                 In the United States Court of Federal Claims
                                    OFFICE OF SPECIAL MASTERS
                                              No. 15-860V
                                           (to be published)

*************************                                                Chief Special Master Corcoran
REGINA TODD,                *
                            *                                            Filed: January 8, 2020
                Petitioner, *
                            *
          v.                *
                            *                                            Influenza Vaccine; Small Fiber
SECRETARY OF HEALTH AND     *                                            Neuropathy; Skin Biopsy; Expert
HUMAN SERVICES,             *                                            Testimony
                            *
                Respondent. *
                            *
*************************

Amber Wilson, Maglio, Christopher & Tolle, P.C., Washington, D.C., for Petitioner.

Debra A. Filteau Begley, U.S. Dep’t of Justice, Washington, D.C., for Respondent.


                                                   DECISION 1
        On August 12, 2014, Regina Todd filed a petition seeking compensation under the National
Vaccine Injury Compensation Program (“Vaccine Program”) 2 based on the assertion that she
developed a neuropathy (alleged at hearing to be properly diagnosed as a non-length dependent
small fiber neuropathy (“NLDSFN”)) after receiving the influenza (“flu”) vaccine on September
17, 2012. Petition (“Pet.”) (ECF No. 1) at 1. An entitlement hearing was held on March 4–5, 2019,
in Washington, D.C., and the parties subsequently filed post-hearing briefs and supplemental
reports, completing that process in July 2019.


1
  This Decision shall be posted on the Court of Federal Claims’ website in accordance with the E-Government Act of
2002, 44 U.S.C. § 3501 (2012)). This means that the Decision will be available to anyone with access to the
internet. As provided by 42 U.S.C. § 300aa-12(d)(4)(B), however, the parties may object to the Decision’s inclusion
of certain kinds of confidential information. Specifically, under Vaccine Rule 18(b), each party has fourteen days
within which to request redaction “of any information furnished by that party: (1) that is a trade secret or commercial
or financial in substance and is privileged or confidential; or (2) that includes medical files or similar files, the
disclosure of which would constitute a clearly unwarranted invasion of privacy.” Vaccine Rule 18(b). Otherwise, the
whole Decision will be available to the public. Id.
2
 The Vaccine Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660,
100 Stat. 3758, codified as amended at 42 U.S.C. §§ 300aa-10 through 34 (2012) [hereinafter “Vaccine Act” or “the
Act”]. Individual section references hereafter will be to § 300aa of the Act (but will omit that statutory prefix).
        The matter is finally ripe for resolution, and after review of the record and all submissions,
I deny an entitlement award in this case. As discussed in greater detail below, Petitioner has not
successfully established that she more likely than not experienced NLDSFN, or more broadly that
the various symptoms she alleges were the product of a vaccine-initiated injury.

    I.        Factual Background
         A.       Vaccination and Initial Symptoms
        Ms. Todd (a full-time nurse) received the flu vaccine on September 17, 2012. See Ex. 1;
Tr. at 8. At the time, she was in good health, although she had previously been treated for type 2
diabetes. Ex. 8 at 19–20. Approximately three weeks later, on October 8, 2012, Petitioner went to
her primary care provider, Thomas Crosby, M.D., complaining of a three-week history of
intermittent “sciatica” symptoms and cramping in one leg, as well as a burning sensation in her
left leg since the prior Saturday. Id. at 19. The records from this visit do not associate these
symptoms with the vaccination Petitioner had received the prior month. Dr. Crosby diagnosed her
with sciatic neuritis and muscle spasms. Id.
        At the end of that month, on October 31, 2012, Ms. Todd saw an orthopedist, Mark Triana,
D.O., for persisting symptoms associated with those she had initially reported to Dr. Crosby. Ex.
2 at 2. At the time of this visit, she specifically told Dr. Triana that her symptoms first began four
weeks before (meaning the first week of October) as a “burning pain in her left buttock,” that
resolved but then returned the following week, with the sensation radiating down her left leg and
into her foot, along with a constellation of other new symptoms (tingling, weakness, skin
sensitivity akin to a sunburn, and burning feelings) in her right buttock, feet, and arms. Id.
        A physical exam documented normal strength and reflexes. Ex. 2. at 2–3. Testing ordered
by Dr. Triana revealed normal erythrocyte sedimentation rate (“ESR”) and C-reactive protein
(“CRP”), both well-recognized biomarkers establishing the presence of systemic inflammation.
Ex. 6 at 20, 22. Rheumatoid Factor (“RF”) and anti-nuclear antibody (“ANA”) 3 testing also
produced negative results. Id. at 24–25. Dr. Triana assessed Ms. Todd with a disturbance of skin
sensation, “unspecified hereditary and idiopathic peripheral neuropathy,” joint pain, and lumbago,
and he prescribed medication. Ex. 2 at 3. A lumbar x-ray and MRI performed the next day
(November 1, 2012) were both normal. Id. at 2–3, 6.
         B.       2012 Hospitalization
       Within a week of her visit to Dr. Triana, Ms. Todd was admitted to Waccamaw Community
Hospital in Murrells Inlet, South Carolina, on November 6, 2012, due to concerns about the
progression of the symptoms she reported having experienced over the prior five weeks. Ex. 7 at

3
  An antinuclear antibody (“ANA”) test is typically used to assess the presence of Systemic lupus erythematosus
(“SLE”), and other autoimmune diseases. Because healthy individuals often test positive for ANA, however, follow-
up testing is necessary to corroborate the diagnosis of an autoimmune disease, thus a negative result typically excludes
the diagnosis of some autoimmune diseases or an ongoing autoimmune process. See K. Pagana et al., Mosby’s: Manual
of Diagnostic and Laboratory Tests 80 (6th ed. 2018) (hereinafter “Mosby’s”).

                                                           2
4–8, 10–11. She remained hospitalized (albeit at more than one facility) over the next five days.
Ex. 10 at 85–86.
        As Petitioner recounted during an initial assessment at Waccamaw by a neurologist, Paul
Amodeo, M.D., the symptoms course she had been experiencing began in the weeks after receiving
the flu vaccine, and had progressed to burning pain in both her legs and pelvis that spread to her
arms, chest, back, and shoulders. Ex. 7 at 5. The week immediately before seeking hospitalization,
she began to feel unsteady when walking, worsening to the point where she could not walk at all.
Id. Before her admission, Petitioner had sought treatment in the ER on November 5, 2012, and
was administered 60 milligrams of prednisone, but felt that she had not improved with that
medication. Id.
        On exam, Ms. Todd’s strength, reflexes, and sensation were normal. Ex. 7 at 6–7. In
addition, although Petitioner reported hyperesthesia 4 to light touch across her shoulders and along
the dorsal aspect of her arms, her sensation was intact to pinprick and vibratory testing. Id. at 7.
And even though Petitioner reported difficulty standing, in Dr. Amodeo’s assessment her
complaints were “out of proportion with her strength to confrontation testing.” Id. at 8. He thus
concluded that the “etiology for the patient’s presentation is unclear,” but ordered further testing
to evaluate a number of possible diagnoses, including a cervical cord pathology, Guillain-Barré
syndrome (“GBS”), a small fiber neuropathy, or dorsal root ganglionopathy. Id. The subsequent
testing (which included an MRI of Petitioner’s cervical spine and brain, a cerebrospinal fluid
(“CSF”) study, and several autoimmune labs) produced uniformly normal results. Id. at 14, 75–
81, 83; Ex. 8 at 41.
         While at Waccamaw, Petitioner was initially treated with a course of prednisone, but the
medication was discontinued as unnecessary given the absence of evidence of ongoing systemic
inflammation (as reflected in normal CRP and ESR test results). Ex. 7 at 3. On November 8, 2012
(two days after admission), Ms. Todd was transferred to Medical University of South Carolina
(“MUSC”) with a discharge diagnosis of generalized weakness and a disturbance of skin sensation.
Id. at 2. The discharging physician reported his view that her symptoms could be related to her flu
vaccine, but he ultimately deferred to Petitioner’s treating neurologists. Id.
        Thereafter, Ms. Todd was evaluated at MUSC by Paul Pritchard, M.D., a neurologist. Ex.
10 at 103. Upon arrival, it was noted that she was tired and unwilling to fully engage in an
examination (possibly because of a sedative she had received just prior). Id. at 109. Under such
circumstances, Dr. Pritchard was only able to observe that her findings were “limited to subtle
changes consistent with a L5-S1 radiculopathy.” Id. at 111. However, an EMG completed on
November 9, 2011, showed no signs of radiculopathy or neuropathy. Id. at 108. Based on
Petitioner’s overall presentation and testing, Dr. Pritchard concluded that there was no evidence
of a neuropathic process, and started her on an antidepressant. Id. at 180–81.


4
  Hyperesthesia is “a dysesthesia consisting of increased sensitivity, particularly a painful sensation from a normally
painless touch stimulus.” Dorland’s Illustrated Medical Dictionary 888 (32 ed. 2012) (hereinafter “Dorland’s”).

                                                          3
        Petitioner subsequently improved and did not require any physical therapy. Ex. 10 at 85.
At discharge on November 11, 2012, Dr. Pritchard noted that Ms. Todd’s “neurological
examination was not consistent . . . [t]here were no obvious sensory deficits . . . [t]here were no
obvious motor deficits,” and there was no clear basis for her symptoms. Id. at 85. The discharge
diagnoses included “possible viral syndrome” and “lumbar radiculopathy,” but made no mention
of other neuropathic injury, whether caused by the flu vaccine or otherwise. Id. at 86. Nevertheless,
Petitioner’s primary care physician, Dr. Crosby, noted at a follow-up visit on November 19, 2012,
that Ms. Todd might have “a mild case of [GBS]” (although the medical record containing this
notation does not explain the basis for his opinion), and he recommended against her receiving the
flu vaccine in the future. Ex. 8 at 18.
       C.      2013 Treatment
        There is a subsequent five-month gap in the medical records, during which time Ms. Todd
appears not to have experienced any recurrent symptoms associated with her fall 2012
hospitalization. On April 16, 2013, however, Petitioner called Dr. Pritchard’s office reporting that
her symptoms had reappeared about one week earlier, particularly characterized by a burning
sensation when touched in certain parts of her body. Ex. 10 at 3. The following month, Petitioner
saw Dr. Crosby on May 20, 2013, and reported a burning pain in her back, although she also added
that her buttock and leg pain had resolved. Ex. 8 at 13.
         Later that summer, in July 2013, Ms. Todd was evaluated by infectious disease specialist
Joseph Cantley, M.D. Ex. 10 at 6. She reported waxing and waning pain symptoms since she
received the flu vaccine in September 2012, plus a transient rash cluster on her right or left side.
Id. at 6–7. Dr. Cantley’s examination, however, revealed normal reflexes, normal sensation (based
on a vibration test on her upper and lower extremities), and a normal gait. Id. at 8. Dr. Cantley
concluded that Petitioner’s symptoms were inconsistent with a peripheral neuropathy, and
“unlikely” to be attributable to a vaccine reaction, preferring anxiety as an explanation. Id.
        In the second half of that month, Petitioner again saw Dr. Pritchard, and informed him of
the symptoms flares she claimed to have been experiencing since the spring, plus rashes and
fatigue. Ex. 10 at 10. Although examination revealed a slightly awkward gait, Petitioner also
appeared to possess normal strength, normal reflexes, and normal sensory test results. Id. Dr.
Pritchard thus opined that Ms. Todd had “diffuse paresthesias and dysesthesias for which I cannot
determine a cause or anatomical locus.” Id. at 11. He suggested she restart antidepressants, or
consider a consultation with a neuromuscular specialist. Id. Petitioner also saw a dermatologist
that August, who (after examination, culture testing, and a biopsy) opined that her intermittent rash
was more likely attributable to dry skin than to a cutaneous autoimmune condition. Ex. 5 at 2–3,
5–6.
        Acting on Dr. Pritchard’s recommendation, Ms. Todd saw a neuromuscular specialist,
David Stickler, M.D., in September 2013. Ex. 10 at 12. Dr. Stickler’s examination revealed both
normal reflexes and intact “sensory modalities.” Id. at 15. Given Petitioner’s reported history, Dr.
Stickler nevertheless allowed for the possibility that she might have a migratory sensory neuritis
                                                 4
or small fiber neuropathy. However, additional testing to confirm this speculation revealed a
negative ANA of 1:80, a normal CRP, and negative antibodies for a variety of infectious processes.
Id. 15, 248. Based upon such negative testing results, Dr. Stickler rejected his earlier speculation
about the etiology of Petitioner’ condition, adding that he could provide no further treatment for
it. Id. at 16.
       D.      2014 Treatment
         Ms. Todd maintains that she continued into 2014 to suffer from intermittent flares of the
condition that purportedly began with her September 2012 vaccination, although the medical
records suggest only sporadic treatment occurrences. For example, in March 2014, Petitioner
informed Dr. Jeffrey Bush, M.D. at MUSC that her symptoms now encompassed her face and
included difficulty swallowing. Ex. 10 at 19. Testing, however, again revealed a lack of
inflammation biomarkers and no disease-associated antibodies. Ex. 6 at 42–43. Ms. Todd also
had an emergency room visit on March 26, 2014, but her exam was largely normal, and a urinary
tract infection was proposed as the most likely source of her symptoms flare. Id. at 21–23, 247.
Indeed, while Petitioner was in the ER, Dr. Pritchard (her MUSC neurologist) was contacted by
current treaters, and he explained to them that he had previously been unable to propose or
identify a neurologic cause for her symptoms. Id. at 27. Dr. Pritchard directly told Ms. Todd the
same thing at a return visit to him on April 1, 2014, referring her instead to a rheumatologist. Ex.
8 at 2.
         Later that same April, Petitioner sought a second opinion from Dr. Fletcher Hartsell,
 M.D., a neuroimmunologist at Duke University’s Health System. Ex. 9 at 17. His examination,
 however, revealed normal results, including sensory response. Id. at 19. Dr. Hartsell assessed
 Ms. Todd with diffuse pain and disturbance of her skin sensation, adding that her symptoms
 might be consistent with several different underlying conditions: central pain syndrome, SFN,
 or fibromyalgia. To evaluate if any could be the proper explanation for Petitioner’s constellation
 of symptoms, Dr. Hartsell ordered a skin biopsy and additional laboratory testing. Id. at 20. But
 such testing again produced normal results—other than a positive ANA that persisted, as
 reflected in subsequent testing from May. Id. at 8, 32, 99.

        The most recent medical records filed in this matter are from August 2014, around the
time of the case’s initiation. At the end of that month, Ms. Todd was evaluated by Sara
Wasserman, M.D., a rheumatologist. Ex. 12 at 4. Dr. Wasserman’s examination noted many
tender points on Petitioner’s back, upper and lower shoulders, arms, and thighs, but no joint
tenderness, and Petitioner’s strength and reflexes were normal as before. Id. at 7. Although Dr.
Wasserman took note of Petitioner’s positive ANA, she deemed it a nonspecific finding, present
in a significant minority of the population. Id. at 8. Dr. Wasserman ultimately could not provide
an etiology for Petitioner’s condition, and did not deem it reflective of a connective tissue
disease. Id.

       That same month, Ms. Todd saw Thomas Buchheit, M.D., a pain management specialist,

                                                 5
who (taking into account the fact that testing did not suggest an autoimmune process at work)
assessed her with probable fibromyalgia. Ex. 8 at 32. Petitioner was thereafter treated with a
combination of medications based on a working diagnosis of fibromyalgia. See Ex. 13 at 2, 24.
This, plus physical therapy, has led her to report improvement in her pain symptoms. Id. at 26.
She had not, however, followed up with any neurologists since 2015. Tr. at 29.

II.    Witness Testimony
       A.      Ms. Todd
        Petitioner’s testimony was largely consistent with the filed medical record. See generally
Tr. at 8–31. She emphasized her good health prior to receipt of the flu vaccine—in contrast to the
sensations of burning and skin sensitivity she purports to have experienced the month after. Id. at
14–15. She recounted the circumstances of her visit to the ER at Waccamaw Hospital and
subsequent admission, detailing the weakness, pain, and other seeming neuropathic symptoms she
was experiencing, along with how frightening she found the experience. Id. at 15–19. Thereafter,
despite some improvement, Ms. Todd felt that she never returned to baseline, noting that cessation
of her medication could result in a dramatic relapse. Id. at 19–20. She agreed, however, that treaters
never were able to pinpoint an explanation for her condition, and that she never received a
diagnosis of small fiber neuropathy, although she maintained that treaters had speculated that some
of her symptoms resembled GBS. Id. at 20–21, 29–31.

        Some of Ms. Todd’s testimony was intended to expand on the impact her alleged vaccine
injury has had on her life. Thus, she has been unable to complete certain training she had been
participating in to expand her professional capabilities as a nurse (which in turn would have
permitted an increase in income). Tr. at 10–11. She has had to seek accommodations at work that
allow her to rest frequently and/or avoid standing for extended periods of time. Id. at 22–23. Her
ability to engage in leisure activities has also been curtailed due to the burning sensations she
experiences if seated for too long. Id. at 23–24.

       B.      Petitioner’s Expert – Dr. Enrique Aradillas-Lopez
       Dr. Aradillas prepared a single expert report in this case and testified at hearing. See Report,
dated February 27, 2017, filed as Ex. 14 (ECF No. 41-2); Tr. at 33–190. He opined generally that
Ms. Todd’s chronic pain, which he deemed neuropathic in nature, was attributable to an adverse
immunologic reaction produced by her September 2012 flu vaccine. Tr. at 76; Aradillas Rep. at 5.

        As elaborated upon in his filed CV, Dr. Arradillas is a board-certified neurologist
specializing in pain management. Tr. at 34, 43; CV, filed as Ex. 15 on Feb. 27, 2017 (ECF No. 41-
3) (“Arradillas CV”). He does not hold board certification in immunology. Tr. at 157. Previously,
he served as an assistant professor in the Drexel University College of Medicine Department of
Neurology Pain Division. Arradillas CV at 1. Dr. Arradillas received his medical degree from La
Salle University School of Medicine in Mexico City, Mexico. Id. Thereafter, he completed his

                                                  6
residency in internal medicine at Interfaith Medical Center in Brooklyn, New York as well as a
residency in neurology at Drexel University College of Medicine in Philadelphia, Pennsylvania.
Id. He then completed an interventional pain management fellowship at the Milton S. Hershey
Medical Center in Hershey, Pennsylvania. Id.

        The overwhelming majority of Dr. Aradillas’s patients seek treatment from him for
complex regional pain syndrome (“CRPS”) or small fiber neuropathy, and only a small percentage
of his clinical time is spent treating patients on a regular neurology service. Tr. at 87, 160. In
addition to his clinical work, Dr. Arradillas has conducted research related to CRPS and has
published several articles on the subject. Id. at 2–5. His publications, however, do not reflect
research on the subjects of immunology or immunological responses to vaccination or disease. Tr.
at 153–54.

        At the outset of his testimony, Dr. Aradillas began with a general explanation of pain
comparable to what Ms. Todd had experienced. He termed pain an “unpleasant sensory and
emotional experience” that needs to be taken seriously when reported to treaters by a patient. Tr.
at 42–43. He initially defined two kinds of pain: “neuropathic” pain attributable to injury or
nervous system disease, and “somatic” pain (although he did not clearly explain how that truly
differed from the first, and later expanded the field to include other categories). Id. at 44–45.
Relying on the patient’s description, a treater needs to try to ascertain the pain’s source for
treatment purposes. Id. at 43–44. However, Dr. Aradillas ultimately proposed that pain
classifications were unhelpful for purposes of clinical assessment of the causal bases for different
types of pain mechanisms. Id. at 46, 48–49.

         Dr. Aradillas moved on to a review of the categories of conditions that might best describe
Petitioner’s constellation of symptoms. He noted (in agreement with literature filed in support of
this action) 5 that pain deemed “neuropathic” could be the result of a wide variety of diseases—not
all of which would themselves be considered to be the result of direct neurologic injury. Tr. at 52.
CRPS, for example, is a condition that is not readily attributable to an identified structural
abnormality, but is often associated with small fiber neuropathy—a condition that is characterized
by a measurable diminution in nerve fibers (as revealed by skin biopsy). Id. at 49–50. The former
would not be deemed classically neuropathic, but the latter would, simply because the association
with nerve injury could be more easily made. Id. at 51. Some pain syndromes could be considered
neuroimmune disorders in and of themselves, however, in which “the immune system is causing
these aberrant responses to keep going.” Id. at 74.

       From this, Dr. Ardillas embarked on a lengthy discussion of the physiologic structure and
performance of different kinds of nerves in conjunction with the central nervous system (“CNS”)

5
 T. Jensen et al., A New Definition of Neuropathic Pain, 152 PAIN 2204, 2204 (2017), filed as Ex. 64 on Feb. 28,
2019 (ECF No. 68-10) (noting that “[n]europathic pain is not a single disease, but a syndrome caused by a range of
different diseases and lesions, which manifests as an array of symptoms and signs.”).


                                                        7
in causing the sensation of pain. See generally Tr. at 53–65. He particularly focused on how
synapse relay error might produce chronic pain, comparing the situation to a radio whose volume
control could not be turned down—a process he termed “sensitization.” Id. at 60–62. The
peripheral version of sensitization occurs at the dorsal root ganglion (located near, and emanating
from, the spinal cord). Id. at 62, 64–65, 68. In Dr. Aradillas’s view, an “out-of-control
inflammatory response” in the body (instigated by some other initial injury) could cause T cells
central to the immune process and triggered by injury to migrate to the dorsal root, interfering with
nerve signal transmission and leading to peripheral nerve sensitization. Id. at 70–72.

        Dr. Aradillas’s specific theory, as he explained at hearing, involves several interlocking
components. Tr. at 76. He proposed that “minor tissue damage” (as insignificant as a skin prick
from a needle) could in rare circumstances be sufficient to later result in chronic pain. Id. at 76–
77. This could occur whether the damage specifically involved the nerve or occurred around it—
for in either case, the resulting inflammation would have the capacity to cause peripheral
sensitization. Id. at 78. However, Dr. Aradillas seemed to give greater emphasis to damage to a
nerve itself as likely to trigger such a process (although he later also discounted this as the only
way by which a pain syndrome could arise). Id. at 78–79.

        Dr. Aradillas’s theory did not assume that the fact of Ms. Todd’s being vaccinated was an
example of the harm possible from a mere “needle prick,” even though he maintained this was a
plausible explanation for similar kinds of chronic pain. Tr. at 80, 179–80. Rather, in Ms. Todd’s
case it was the components of the vaccine itself that explained her subsequent injuries. The flu
vaccine was designed to trigger an inflammatory response via both the innate and adaptive immune
system, which in his view had a greater capacity to elicit inflammation around nerves than the
needle used to administer the vaccine. Id. at 80–82, 181.

        To describe the mechanistic process by which the aforementioned would theoretically
occur, Dr. Aradillas cited several items of literature regarding “autoimmune pain disorders,” which
he defined as disorders “that manifest[] as pain, as chronic pain, really,” driven by autoantibodies.
Tr. at 82–84, 89; D. Carr et al., Neuropathic Pain: The Immune Connection, 12 Pain: Clinical
Updates 1, 2 (2014), filed as Ex. 19 on Feb. 27, 2017 (ECF No. 41-7) (“Carr”). Carr specifically
observed that certain antibodies injected into the serum of animal subjects with CRPS would cause
the test subjects to develop a version of CRPS—thus demonstrating an autoimmune process. Tr.
at 83; Carr, supra, at 2. 6

        Another article, in Dr. Aradillas’s view, supported the notion that autoantibodies could
interfere with nerve function even if they did not harm the actual nerves. Tr. at 84–85; M.

6
  Dr. Aradillas differentiated the precise mechanism by which the proposed antibody cross-reactive attack would occur
in such circumstance from the way antibodies might cause other kinds of autoimmune injury, like GBS. Tr. at 83. In
some instances, the antibody in question was thought to bind to a self-structure, causing damage, whereas for CRPS
with concurrent neuropathic pain, it was more likely that the antibody caused nerve malfunction merely by interfering
with the manner in which nerves conduct signals—but without direct harm to the nerve. Id. at 83–84, 89–91.


                                                         8
Talkington, An Autoimmune Basis for Chronic Pain?, Pain Research Forum 1 (Sep. 4, 2012), filed
as Ex. 74 on Feb. 28, 2019 (ECF No. 69-10) (“Talkington”). Talkington discusses an individual
who complained of burning pain but revealed no neurologic injury on testing. Talkington, supra,
at 1. Nevertheless, when the individual was treated with immunotherapies, like intravenous
steroids, as if he suffered from an autoimmune condition, he improved. Tr. at 85–86; Talkington,
supra, at 1–2. Dr. Aradillas himself had confirmed the efficacy of such treatments, like
plasmapheresis, in his own patients suffering from CRPS (with those experiencing small fiber
neuropathy doing even better). Tr. at 86–87. However, Dr. Aradillas later admitted that he was not
proposing that Ms. Todd in fact possessed any autoantibodies that would arguably interfere with
her nervous system signal processing sufficient to cause chronic pain—or that this entire line of
testimony accurately captured her particular circumstances. Id. at 91. Rather, he raised the concept
only to underscore the existence of reliable science supporting the notion that a pain syndrome did
not have to involve direct damage to the nerves. Id. at 92–93. 7

        Dr. Aradillas’s testimony said little directly relevant to the nexus between the flu vaccine
and the aforementioned processes—a point underscored during his cross-examination. He
admitted, for example, that he could identify no direct evidence setting forth how components of
the flu vaccine (which are changed on a yearly basis, in anticipation of what wild version of the
virus is anticipated to be prevalent) could produce the kind of autoantibodies he purported were
interfering or damaging nerve function sufficient to cause Petitioner’s symptoms, relying instead
on the general assertion “that’s how a vaccine works.” Tr. at 155–56.

         Pivoting from the above, Dr. Aradillas returned to a discussion of how he viewed Ms.
Todd’s situation. He characterized the pain syndromes associated with peripheral nerve diseases,
from GBS to other more general polyneuropathies, as falling under the umbrella of
“somatosensory pain system,” which he deemed as responsible for transmitting pain signals “in
the form of peripheral sensitization.” Tr. at 100–02. Peripheral nerve diseases would inherently
involve the dorsal root ganglion (which as Dr. Aradillas previously testified was involved in
peripheral sensitization). Id. at 102. An injury like a small fiber neuropathy would also fit within
this structure, and therefore have the capacity to involve a pain disorder. Id. at 103–04.

        Dr. Aradillas firmly opined that Ms. Todd suffers from some form of small fiber
neuropathy (specifically NLDSFN, attributable in this case to an antibody-driven ganglionopathy).
Tr. at 120, 133. He classified small fiber neuropathy as a kind of sensory peripheral neuropathy
with many possible different presentations, but which would likely implicate interference at the
dorsal root ganglion level. Id. at 103–04, 106. Small fiber neuropathies result in both “positive”

7
  In the course of this testimony, Dr. Aradillas specifically referenced some articles establishing that the CASPR 1 and
2 antibodies have also been recognized as having the capacity to cause the nerve signal conducting interference in
individuals experiencing chronic pain in association with known autoimmune diseases GBS. Tr. at 88–95. But because
Dr. Aradillas acknowledged that he does not contend Ms. Todd has ever been shown to possess such autoantibodies,
and given that none of her treaters ever proposed testing for their presence, I do not include herein a detailed review
of these items of literature. Id. at 177–79.


                                                           9
symptoms (meaning affirmative feelings of painful or unpleasant burning or tingling), and
“negative” symptoms (characterized by numbness and/or the absence of sensitivity to pressure,
heat, and other stimuli), as well as allodynia (pain sensitivity even in the absence of a pain
stimulus) 8 but not impairment of motor function. Id. at 110–11, 113, 120. A symptom of weakness
could be understood as a negative symptom, but could also (if it stemmed from motor difficulties)
reflect an entirely different neuropathy. Id. at 111.

        One distinction in classification of small fiber neuropathies delineated by Dr. Aradillas,
however, involved length-dependent (meaning one that “starts at the feet” and ascends into the
body for a more widespread impact) versus non-length-dependent (one that is more localized to
the ganglion level or impacting only a limited area of the body). Tr. at 107–08, 113–14, 117;
Petitioner’s Glossary of Terms, filed as Ex. 87 on Feb. 28, 2019 (ECF No. 71-3). As he explained,
NLDSFN is less common than its counterpart, and is characterized by a patchy distribution of
symptoms that can vary more widely than in the length-dependent version, and can affect a nerve
anywhere from the root ganglion to a receptor ending at the skin level. Tr. at 113–14, 116–17; S.
Khan et al., Characterization of Non-Length-Dependent Small-Fiber Sensory Neuropathy,
MUSCLE & NERVE 86, 86 (2012), filed as Ex. 58 on Feb. 28, 2019 (ECF No. 68-4) (“Khan”).
He thus asserted that there were “several different types” of NLDSFN, with a ganglionopathy
constituting merely one version. Tr. at 166.

        There are also different diagnostic tests for each. In Dr. Aradillas’s view, length-dependent
small fiber neuropathies are correlated with a positive skin biopsy testing small nerve fiber density
(which reveals the extent of nerve destruction), but such testing has less utility in assessing the
existence of NLDSFN. Id. at 100, 108. 9 Thus, even though Petitioner’s skin biopsy unquestionably
produced normal results, Dr. Aradillas maintained that the possibility of damage to Ms. Todd’s
dorsal root ganglion could not be ruled out. Id. at 127. 10 Indeed, Dr. Aradillas admitted that
NLDSFN can exist even in the face of an otherwise-normal medical exam, and (perhaps as a result)
is often considered a “psychogenic disorder.” Id. at 114–15. Another useful test is qualitative
sensory testing, or “QST,” which provides objective evidence of a patient’s responses to certain
types of stimuli. Id. at 127–28. Overall, Dr. Aradillas proposed that a patient’s clinical presentation

8
  Allodynia is “pain resulting from a non-noxious stimulus to normal skin.” Dorland’s at 51. Dr. Aradillas
acknowledged on cross-examination that allodynia was not unique to small fiber neuropathies. Tr. at 169–70.
9
  Dr. Aradillas later stressed the impossibility of performing the kind of nerve biopsy that might help establish the
existence of an NLPSFN, because the source of the injury (the dorsal root ganglion) could not be tested without the
risk of permanent harm. Tr. at 125–26.
10
   Dr. Aradillas referenced an item of literature that he maintained further diminished the value of the skin biopsy. Tr.
at 128–29, citing A. Truini et al., Does the Epidermal Nerve Fibre Density Measured by Skin Biopsy in Patients with
Peripheral Neuropathies Correlate with Neuropathic Pain?, 155 PAIN 828, 829 (2014), filed as Ex. 50 on Nov. 30,
2018 (ECF No. 63-4). That article, he proposed, demonstrated a lack of association between the degree of pain a
patient with small fiber neuropathy might experience and the degree of nerve destruction measured by the skin biopsy.
Tr. at 128–29.


                                                          10
plus either a positive skin biopsy or QST was sufficient for a small fiber neuropathy diagnosis
(although he maintained a skin biopsy was ultimately “irrelevant” to assessing the existence of
NLDSFN). Id. at 165, 174.

        Dr. Aradillas next discussed his views on a possible etiology for NLDSFN. He deemed
small fiber neuropathies generally to be autoimmune in origin, citing a single item of literature in
support. Tr. at 121; X. Liu et al., IVIg for Apparently Autoimmune Small-Fiber Polyneuropathy:
First Analysis of Efficacy and Safety, 11 Therapeutic Advances in Neurological Disorders 1, 2
(2018), filed as Ex. 52 on Nov. 30, 2018 (ECF No. 63-6) (“Liu”). Liu observed that treating 52
patients believed to be suffering from small fiber neuropathies with IVIg 11 caused them to show
improvement, thereby providing at least circumstantial evidence of the condition’s autoimmune
character. Tr. at 122; Liu, supra, at 7. In so doing, Liu’s authors compared small fiber neuropathy
to other peripheral neuropathies, such as GBS, known to be driven by immunologic processes like
autoantibody attacks on the myelin sheath of nerves. Tr. at 122–23; Liu, supra, at 2. Dr. Aradillas
admitted, however, that the specific targets for a comparable attack on the small, unmyelinated or
thinly-myelinated nerves relevant to a small fiber neuropathy had not yet been identified (although
he attempted to diminish the significance of this fact by stressing how little was still known about
GBS and similar demyelinating conditions). Id. at 123–24.

         Other evidence of small fiber neuropathies likely autoimmune character was established
by the degree to which the condition is experienced by GBS patients (whose neuropathies at the
outset impact large nerves). Tr. at 130–31; A. Uncini et al., Sensory Guillain-Barré Syndrome and
Related Disorders: An Attempt at Systemization, MUSCLE & NERVE, 464, 464 (2012), filed as
Ex. 54 on Nov. 30, 2018 (ECF No. 63-8). Dr. Aradillas went so far to propose that small fiber
neuropathies could reflect a subcategory or variant of more commonly understood peripheral
neuropathies like GBS, with the former having more of a sensory orientation but not featuring all
of the clinical indicia otherwise associated with GBS. Tr. at 131–32. Thus, even though Ms. Todd
herself had not been shown to possess the clinical criteria necessary for a GBS diagnosis (such as
proper CSF readings), her NLDSFN could still be understood to constitute a GBS variant. Id. at
132–33. He later acknowledged, however, that he could not specify the clinical diagnostic criteria
for this proposed variant, although he felt the variant was medically valid. Id. at 161–63.

        To support his diagnostic opinion, Dr. Aradillas provided his read on Ms. Todd’s medical
history. He deemed her early October 2012 visit corroborative of NLDSFN, since Petitioner at this
time complained of patchy symptoms in different places on her body. Tr. at 134–35. Later that
month, Dr. Aradillas argued, there was evidence that Petitioner’s symptoms were progressing in a
more widespread, bilateral manner, with burning pain and sunburn-like skin sensitivity that he
considered reflective of allodynia. Id. at 136–37. Her lumbar spine MRI ruled out other


11
  IVIg—or intravenous immunoglobulin—is a common treatment for demyelinating autoimmune disorders such as
GBS or chronic inflammatory demyelinating polyneuropathy. Liu, supra, at 2. It works by modifying B- and T-cells
thereby inhibiting antibody production. Id.

                                                      11
explanations for her symptoms, while her subsequent stay at Waccamaw eliminated the possibility
of “classic” GBS. Id. at 137–39. And a Waccamaw neurologist seemed to allow that some kind of
sensory GBS variant/small fiber neuropathy caused by vaccination could explain Petitioner’s
constellation of symptoms. Id. at 140–41; Ex. 7 at 8.

        Dr. Aradillas found additional support for his diagnostic conclusions from Ms. Todd’s
MUSC records. Testing performed at MUSC revealed a lack of responsiveness to sensory stimuli,
allodynia, and a few other symptoms—not all of which (like areflexia) correspond to a small fiber
neuropathy. Tr. at 141–43. Nevertheless, treaters later began to actively explore the possibility of
such a diagnosis (although some time after vaccination). Id. at 143–44 (discussing Duke treatment
from 2014). The consistency of Ms. Todd’s characterization of her ongoing pain and allodynia
was telling in his view. Id. at 146–47. At the same time, however, Dr. Aradillas downplayed the
lack of testing corroboration for an autoimmune condition, along with the negative skin biopsy, as
not precluding his NLDSFN diagnosis—pointing out some specific positive inflammation
biomarker results (although these kinds of tests were, taken as a whole, overwhelmingly negative).
Id. at 148–49. He found especially significant the fluctuating nature of some of this inflammation
testing, since it was consistent with his view that an autoimmune condition would be expected to
follow a variable course. Id. at 149. And he deemed the timing of onset of Petitioner’s symptoms
(12 days post-vaccination) to be biologically reasonable, based on how long he expected it would
take for symptoms to begin after the initiation nerve function interference. Id. at 151–52; P. Austin
& G. Moalem-Taylor, The Neuro-immune Balance in Neuropathic Pain: Involvement of
Inflammatory Immune Cells, Immune-like Glial Cells and Cytokines, 229 J. of Neuroimmunology
26, 36 (2010), filed as Ex. 44 at on Nov. 11, 2018 (ECF No. 62-8).

        On cross, Dr. Aradillas admitted that his embrace of NLDSFN as the proper diagnosis
(which he acknowledged none of Petitioner’s treaters ever proposed) came only after preparation
of his original report. Tr. at 163–64, 172–73. He admitted that some other neuropathic conditions
that he deemed falling on the same overall spectrum as Petitioner’s symptoms, like CRPS, were
not applicable to this case. Id. at 161–62. He also noted that Petitioner did not in fact display some
of the clinical criteria he had deemed critical to an NLDSFN diagnosis. Id. at 171. Thus, Ms. Todd
tested negative on a skin biopsy—and although Dr. Aradillas steadfastly maintained that this test
only ruled out nerve fiber “destruction,” rather than the malfunction he maintained she had
experienced, he accepted that some of the literature he had filed actually contradicted his assertion
that skin biopsies were not useful in establishing NLDSFNs. Tr. at 100, 166–67, 187–88, 190; K.
Gorson, et al., Non-length Dependent Small Fibre Neuropathy/Ganglionopathy, 79 J.
Neurosurgery Psychiatry 163, 163 (2008), filed as Ex. 56 on Feb. 28, 2019 (ECF No. 68-2) (finding
that skin biopsies could help establish whether study participants had a non-length-dependent
small fiber ganglionopathy).

        Dr. Aradillas also agreed that Petitioner had never received QST testing, while proposing
that she nevertheless did display some altered sensation testing results (and arguing that the overall
record still supported the conclusion that she suffered from some kind of neuropathic pain
                                                 12
syndrome). Tr. at 170–73. He reiterated his opinion on cross that a QST test result plus clinical
evidence of a neuropathic pain syndrome was enough to support a NLDSFN diagnosis, relying on
Gorson for this assertion (and despite demonstration by Respondent that Gorson did not mention
QST testing as a clinical criteria for the diagnosis). Id. at 174–76.

        Cross examination revealed other evidentiary deficiencies in Dr. Aradillas’s theories. For
example, although Dr. Aradillas proposed that a vaccine could cause the kind of neuropathic injury
that Ms. Todd allegedly suffered simply as a result of “profound inflammation” generated by the
innate immune response, he admitted there was a lack of direct evidence establishing the
contention, and that it could likely not be measured by normal medical standards (such as the
inflammation biomarker tests administered to Ms. Todd, which had consistently not revealed any
alarming post-vaccination inflammation). Tr. at 181–83. Rather, this particular theory was (in Dr.
Aradillas’s view) corroborated by Petitioner’s clinical symptoms, and the fact that she displayed a
positive ANA in 2014—almost two years after vaccination. Id. at 186. He later, however, proposed
that it was more likely Ms. Todd’s condition was the product of an adaptive immune response,
mediated by antibodies—even though (at the same time) he could not specify the relevant
antibodies in her case, and noted that many of the antibodies that arguably were associated with
an autoimmune-derived neuropathy did not apply to her. Id. at 188–90.

        C.       Respondent’s Experts
                 1.      Dr. Eric Lancaster
       Dr. Lancaster submitted two reports and testified on Respondent’s behalf at hearing. Expert
Report of Dr. Lancaster, dated Aug. 11, 2017, filed as Ex. B (ECF No. 51-4) (“Lancaster Rep.”);
Supplemental Expert Report of Dr. Lancaster, dated Feb. 21, 2019, filed as Ex. D (ECF No. 66-1)
(“Lancaster Supp. Rep.”); Tr. at 198–334. Dr. Lancaster rejected Petitioner’s contention that she
suffered from NLDSFN, as well as the broader contention that her symptoms were attributable to
a vaccine-caused, antibody-driven autoimmune process.

        Dr. Lancaster is a clinical physician at the Center for Autoimmune Neurology at the
University of Pennsylvania, as well as an assistant professor of neurology at the University of
Pennsylvania. Dr. Eric Lancaster Updated CV, filed as Ex. E on March 3, 2019 (ECF No. 72-1)
(“Lancaster CV”). He completed a neurology residency at the University of Pennsylvania from
2004–07, and is board certified in neurology, with subspecialties in neuromuscular medicine and
electrodiagnostic medicine. Id.; Tr. at 199. His research focuses on antibody-mediated
neurological disorders, and he sees patients with complex autoimmune neurologic disorders on a
regular basis. Lancaster CV at 1; Tr. at 202–04. He has significant expertise performing the tests
used to evaluate peripheral neuropathies (e.g., EMGs, nerve conduction studies) 12, and also has a

12
  An EMG, or electromyography test, is a diagnostic procedure used to assess the health of muscles and the nerve
cells that control them (motor neurons). Dorland’s at 602. Nerve conduction studies are used in conjunction with
EMGs to detect and locate peripheral nerve injuries or disease. Mosby’s at 514.


                                                      13
clinical practice. Tr. at 200–02; Lancaster Rep. at 1. Dr. Lancaster has treated patients with small
fiber neuropathies. Tr. at 202.

        Dr. Lancaster began with an overview of small fiber neuropathies. The term “neuropathy”
refers to damage to the peripheral nerve fibers. Tr. at 208. While large nerve fibers are mostly
associated with motor function and control in the human body (although they also play a role in
detecting position and some other sensations, like vibration), the small fibers (which are either
unmyelinated or thinly myelinated) 13 generally “detect pain, cold, heat, and other modalities,” such
as injuries. Tr. at 208. Although many neuropathies will impact both large and small fibers, small
fiber neuropathies are “exclusively” relevant to the small fibers and the functions they serve,
preserving the function of the large fibers. Id. at 210–11. Dr. Lancaster largely accepted Dr.
Aradillas’s contentions about the kinds of symptoms a person with a small fiber neuropathy would
experience (e.g., burning pain, tingling, loss of sensation/numbness, etc.). Id. at 327–28.

        “Length-dependent” small fiber neuropathies, in which “the longest fibers get affected first
and most predominantly,” were in Dr. Lancaster’s estimation most common. Tr. at 208–09. In
such cases (perhaps due in part to the metabolic strain placed on longer nerve fibers), symptoms
ascend from distal portions of the body, like the feet and hands, and move toward the chest (hence
closer to the spine and brain stem, where nerve signals would be processed). Id. at 209. Length-
dependent small fiber neuropathies were more likely to occur than NLDSFNs. 209–11.

         A NLDSFN, by contrast, is “a much more variable category.” Tr. at 210, 213–14. Dr.
Lancaster did not accept (although he did not completely rule out) the possibility that an NLDSFN
could be caused by a virus, but he directly disputed that NLDSFNs were properly considered “in
general” autoimmune conditions. 14 He acknowledged there existed hypotheses that an NLDSFN
could have an autoimmune etiology in some cases, but noted the existence of many more
recognized etiologies that were not, including metabolic dysfunction, diabetes, and other illnesses.
Id. at 215–16. He also deemed significant the total number of individuals with neuropathies, which
he placed in the millions, that were considered either attributable to diabetes or an idiopathic
source. Id. at 216. Because of the usual etiologies for NLDSFN, the condition is most effectively
addressed with treatments aimed at the underlying cause, such as control of blood sugar where
diabetes is at issue, or vitamins to treat underlying vitamin deficiencies believed to be causing the

13
  Myelination is the process by which the body produces a fatty substance that coils around nerve cells providing a
protective sheath and electrical insulator. Dorland’s at 1218.
14
   Dr. Lancaster also questioned whether there existed definitive evidence establishing a particular autoantibody as
capable of causing NLDSFN without other neurologic symptoms, although he allowed it might be established
someday. Tr. at 234. He also emphasized (based upon his experience studying antibody-mediated neuropathies) that
the kind of syndromes where a particular antibody, like CASPR2, is thought to result in some symptoms comparable
to a NLDSFN involve a broader and more complex presentation than what Petitioner claims to have experienced. Id.
at 283–95, 297–304.


                                                        14
neuropathy. Id. at 230–32. Where the source for the neuropathy was deemed idiopathic, by
contrast, the best course was to attempt to reduce pain symptoms, but not with immune therapies.
Id. at 233.

         The NLDSFN subtype most relevant herein is a ganglionopathy, in which “the cell body
itself [of the dorsal root ganglia] is injured in the ganglia root 15 and dies, or becomes impaired or
defective in some way,” independent of the length of the targeted nerve. Id. at 211, 214. This
results in symptoms presenting as changes in sensation sensitivity occurring in a “non-length-
dependent pattern.” Id. Like Dr. Aradillas, Dr. Lancaster agreed that such changes could result in
positive as well as negative phenomena, combining a loss of feeling sensitivity to various stimuli
with abnormal pain elsewhere plus allodynia, all caused by neuron-signaling malfunction. Id. at
215, 217–18, 221. Dr. Lancaster proposed that there was no functional difference between the
terms NLDSFN, “non-length-dependent ganglionopathy,” and “dorsal root ganglionopathy,” since
all three described a process exclusively affecting small fiber nerves, with an unproven
“presumption” that the ganglia are the target. Id. at 212–13. However, existing literature in Dr.
Lancaster’s view (including what Petitioner offered) did not reliably demonstrate that “the ganglia
is actually the site of any particular pathology,” and that what research that did support the concept
involved “excruciatingly rare” diseases. Id. at 212.

        In describing the clinical or testing indicia relevant to diagnosing NLDSFN, Dr. Lancaster
reviewed several items of literature, including Gorson. Tr. at 213–30. Most individuals suffering
from NLDSFN would likely experience persistent symptoms in the same area—consistent with
the loss of nerve fibers in the presenting area of the body, causing “fixed deficits” reflecting the
destruction of the nerve cells. Id. at 224–25. Patients would also likely have a loss of pin prick
sensation in the presenting areas. Id. at 229. Reflexes, since they pertain to motor nerve function,
would not bear on a NLDSFN diagnosis. Id. at 269–71.

        With respect to testing, Dr. Lancaster maintained that one article filed by Petitioner very
plainly endorsed the skin biopsy test 16 for diagnosing NLDSFN. Tr. at 221–23, 229–30; see
generally Khan, supra (discussing study design that only included patients with a skin biopsy
diagnosis of NLDSFN). 17 Also, and contrary to Dr. Aradillas, he argued that direct biopsy of the


15
  Although Dr. Aradillas spoke of nerve “dysfunction” as possible even without direct nerve damage, Dr. Lancaster
expressed skepticism that this was the most common accurate explanation for SFN, deeming nerve malfunction absent
damage a “super rare phenomenon.” Tr. at 333. In the majority of SFN cases, actual nerve damage (as reflected in
skin biopsies) was the more likely culprit. Id. at 333–34.
16
   In his testimony, Dr. Lancaster described how a skin biopsy testing for SFN is performed, and what it captures. Tr.
at 223–24.
17
  In response to cross-examination questioning, Dr. Lancaster disputed Petitioner’s contention that Khan in fact did
not completely establish the efficacy of the skin biopsy test, given that a small percentage of tested individuals did not
display abnormal results. Tr. at 317–18. Dr. Lancaster proposed that the proper reading of this part of Khan was that

                                                           15
dorsal root ganglion was possible, although he admitted that it was generally not done due to the
burdensome nature of such testing. Tr. at 311–12. Nevertheless, the skin biopsy test was still
valuable (and more easily performed), even if it was somewhat indirect, and even if it was not 100
percent predictive in all cases. Id. at 311, 319–20. QST, testing, by contrast, was not in Dr.
Lancaster’s opinion useful for diagnosing NLDSFN. Tr. at 226. While he allowed that QST testing
had some value, it largely overlapped a neurologist’s own examination of a patient, was more
illustrative of symptoms, and overall had “lower specificity” and “lower sensitivity” than a biopsy,
which provided objective evidence of nerve injury. Id. at 226–28. He also noted that literature like
Khan reflected the lower significance given to QST testing in comparison to the biopsy. Id. at 228.

        Dr. Lancaster relied on several record facts for concluding that Ms. Todd likely did not
have NLDSFN. He granted that her symptoms “at least made it something reasonable to think
about.” Tr. at 230. But he found more compelling the objective evidence—the lack of a positive
skin biopsy, as well as inconsistency in her “areas of confirmed loss of sensation”—pointing in
the opposite direction. Id. He characterized her overall presentation (which coupled neuropathic-
like symptoms without other neurologic complaints) as “quite a common phenomena” in his
experience, but attributing the cause of symptoms in such cases to an unidentified idiopathic
source. Id. at 235.

        To support his opinion, Dr. Lancaster provided a detailed review of Petitioner’s medical
history. See generally Tr. at 235–83. He noted first that the late-October 2012 record set forth
symptoms that in his view were not consistent with a small fiber neuropathy, such as decreased
sensation of a pin prick or temperature “in a particular distribution,” and thus the relevant treater
(Dr. Triana) did not propose any kind of small fiber neuropathy as explanatory. Tr. at 238. The
neurologist Petitioner subsequently saw at Waccamaw, Dr. Amodeo, “documented a pretty
detailed neurologic examination” that did not reveal meaningful weakness, but did establish some
touch sensitivity, and although he allowed for the possibility of an autoimmune peripheral
neuropathy, like GBS, or a dorsal root ganglionopathy (which would be closer to what Petitioner
alleges she experienced), he could not provide a certain diagnosis (and did not otherwise propose
NLDSFN). Id. at 243–45, 247. Dr. Lancaster, however, stressed that his personal view (based on
consideration of such records) was that Ms. Todd’s sensory symptoms at that time were by
themselves insufficient to support a NLDSFN diagnosis. Id. at 245–46.

        At MUSC, Dr. Lancaster noted, Petitioner again received a neurologic exam from Dr.
Pritchard that came back largely normal, although she was suffering from sufficient pain to
interfere with the exam’s completion. Tr. at 247–51. However, even under such circumstances Dr.
Lancaster felt the exam did not suggest “definitive” weakness. Id. at 252–53. He also felt that the
evidence of loss of sensation at this time was insufficient to establish the existence of a neuropathy,


a small group of patients did not display nerve density abnormality in both tested sites (proximal and distal thigh), but
that all showed abnormality in at least one tested location consistent with NLDSFN. Id. at 319.

                                                          16
and this plus the lack of other “objective deficits,” (including close-to-normal reflexes) reasonably
led treaters to be inconclusive in their assessment of Petitioner’s condition. Id. at 254–55, 257–58.
At a minimum, however, Dr. Lancaster felt the results of this examination did not support a
NLDSFN diagnosis, or any other neuropathy. Id. at 255. Petitioner’s discharge confirmed the fact
that even taking into account her touch sensitivity, treaters “did not find those sort[s] of sensory
deficits that you would want to diagnose neuropathy or another neurologic disorder.” Id. at 261.

        Nearly a year later, Dr. Lancaster observed, Ms. Todd returned to Dr. Pritchard at MUSC
in June 2013. See generally Tr. at 262–64; Ex. 82 at 6. At this time, she reported some flareups of
her skin sensations, tingling, plus a skin eruption that raised concerns about a dermatomal
distribution that could establish shingles. Id. at 263. 18 However, her exam was again largely
normal, and Dr. Pitchard was unable to offer a diagnosis. Id. at 264. Then, at a later visit in
September 2013 with a neuromuscular neurologist (a specialist Dr. Lancaster deemed qualified to
evaluate the existence of small fiber neuropathies), another comprehensive workup established
insufficient objective evidence of neuropathy (although treaters seemed willing to explore the
matter further). Id. at 265–68; Ex. 10 at 12–15. Notably, Petitioner reported symptoms prior to this
examination but was asymptomatic on exam—something that Dr. Lancaster deemed inconsistent
with NLDSFN, which we felt (as previously noted) would involve persistence of at least sensory
deficits rather than variable “acute attacks” of pain followed by lulls. Tr. at 268.

         Dr. Lancaster observed the same lack of support for the NLDSFN diagnosis in records
from 2014. Tr. at 272–83. Petitioner’s examination in the spring of 2014 from Dr. Hartsell at Duke
did not produce evidence of neuropathy. Id. at 274–76. And the skin biopsy test Dr. Hartsell
ordered produced normal density results. Id. at 275–77. Dr. Lancaster’s own reading of the test
results, as set forth in the medical record, led him to opine that they were unsupportive of a
NLDSFN diagnosis. Id. at 278–79. Petitioner’s subsequent follow-up visit with Dr. Hartsell that
fall resulted in his identifying fibromyalgia (and not NLDSFN) as a working diagnosis, something
Dr. Lancaster felt was a generic diagnostic determination in the absence of any more specific,
neuropathic explanation. Id. at 280–83. 19

       Besides addressing the nature of Petitioner’s injury and its purported autoimmune cause,
Dr. Lancaster’s testimony also covered some of the other core elements of any Vaccine Program

18
   Dr. Lancaster explained that the varicella virus that causes shingles can be dormant in the dorsal root ganglia but,
upon reactivation, will follow a pattern in the skin “supplied by the sensory fibers in the dorsal root ganglia” resulting
in a blistering rash. Tr. at 263.
19
   Dr. Lancaster did note that although the records from Petitioner’s November 2014 visit to Dr. Hartsell suggested
the possibility that she has “overlapping post-AIDP [acute inflammatory demyelinating polyneuropathy] neuralgia,”
he did not find support in the record that in fact she was ever previously diagnosed with AIDP, which is essentially
“the most common form of GBS.” Tr. at 279–80. I similarly find no evidence that this note reference has any pre-
existing evidentiary basis in the record, and would not be able to conclude that Petitioner’s symptoms were attributable
to GBS even had she so alleged.

                                                           17
claim. He thus disputed directly whether the flu vaccine could cause any form of small fiber
neuropathy (and did not find persuasive case reports filed by Petitioner that purportedly established
the contrary). Tr. at 234, 329–30. Consistent with Dr. Aradillas’s admission, he observed that not
only was there no evidence that Petitioner possessed any of the antibodies that could potentially
cause a neuropathic syndrome featuring some of the symptoms Petitioner experienced, but they
could easily have been tested for—something no treater who saw Ms. Todd ever proposed (and he
added that he would not have either had he treated her). Id. at 295–96, 307–08. He did not believe
the record supported the conclusion that Ms. Todd otherwise had such a syndrome. Id. at 307–09.
And he maintained that he was not aware of reliable evidence establishing the capacity of the flu
vaccine to even cause the production of such antibodies. Id. at 296–97.

       On cross-examination, Dr. Lancaster admitted that some autoimmune conditions could
possibly involve viral-caused flares. Tr. at 315. But he did not accept the proposition that the
possession of one kind of autoimmune biomarker, such as a positive ANA, invariably led to the
conclusion that the individual in question had an autoimmune condition. Id. at 325. Similarly, he
discounted the evidentiary value of IVIg treatment as indirectly corroborating that a person likely
had an underlying autoimmune illness, noting that such treatments had a “massive placebo effect,”
making it difficult to conclude merely from a patient’s reported improvement, and absent some
other objective corroboration (like a reduction in suspected antibodies believed to be causing the
condition) that the treatment was likely addressing the true cause of her symptoms. Id. at 326–27.

        In addition, Dr. Lancaster accepted the possibility of vaccine-caused adverse events, such
as GBS caused by the flu vaccine. Tr. at 321–23. He also agreed that the medical records
established that Ms. Todd had repeatedly complained of burning pain. Id. at 329. He disagreed,
however, with the statement of Ms. Todd’s primary care physician, Dr. Crosby, that she should
not in the future receive the flu vaccine. Id. at 324–25.

                   2. Dr. Penelope Morel
        Dr. Morel, a research and teaching immunologist, served as Respondent’s second expert,
filing two reports and testifying at hearing. First Report of Dr. Morel, dated Aug. 11, 2017, filed
as Ex. A (ECF No. 49-1) (“Morel First Rep.”); Second Report of Dr. Morel, dated Feb. 18, 2019,
filed as Ex. C (ECF No. 65-1); Tr. at 335–380. She offered the opinion that the flu vaccine Ms.
Todd received did not play a role in the neurologic symptoms she subsequently experienced. Tr.
at 342.

         Dr. Morel is currently employed by the University of Pittsburgh School of Medicine
Department of Immunology and the University of Pittsburgh Cancer Institute. Dr. Penelope Morel
CV, filed as Ex. A Tab 1 on Aug. 14, 2017 (ECF No. 49-2) (“Morel CV”). She also serves as an
affiliate member at the University of Pittsburgh Center for Vaccine Research. Morel CV at 2. Dr.
Morel obtained a Bachelor of Medicine degree from the University of South Hampton in the

                                                 18
United Kingdom. Id. at 1. She then obtained a Doctor of Medicine degree from the University of
Geneva in Switzerland while performing research in the World Health Organization Immunology
and Training Lab. Morel CV at 1; Tr. at 336. She later completed a postdoctoral fellowship at
Scripps Clinic and Research Foundation in La Jolla, California as well as a fellowship in
immunology at Stanford University Medical Center in Stanford, California. Morel CV at 2. She
completed a second postdoctoral fellowship in molecular genetics at the University of Pittsburgh
Cancer Institute. Id.

        Dr. Morel does not have a clinical practice, and instead focuses on research. Tr. at 363–64.
She has published numerous articles on immunological responses to vaccination, and she has
specifically focused on immune response regulation, autoimmune diseases and the genetic
predisposition to such diseases, and the immunologic mechanisms that prevent them. Tr. at 338–
41. While Dr. Morel indicated that she was familiar with immunological responses to vaccination,
including inflammation, she does not consider herself to be an expert on pain medicine and has
not dedicated her research to the topic. Id. at 371. She also indicated that she would defer to the
opinions of Dr. Lancaster and Petitioner’s treating physicians regarding Petitioner’s proper
diagnosis. Id. at 342.

        Although Dr. Morel did not offer an opinion as to the proper diagnostic understanding of
Petitioner’s symptoms, she commented on the association between those kinds of symptoms and
what she knows about autoimmunity in general. Thus, she emphasized that not all chronic
neuropathic pain can be deemed autoimmune in nature. Tr. at 343. Where autoimmunity was a
likely cause, testing would reveal “evidence of an aberrant immune response,” such as the presence
of biomarkers or test results associated with systemic inflammation. Id.; First Morel Rep. at 3. She
allowed that an immune-associated neuropathic condition would prove responsive to “immune-
modulating therapies.” Tr. at 354; First Morel Rep. at 3.

        Turning to the record in this case, Dr. Morel noted the extent to which various testing
results did not suggest Ms. Todd was in fact experiencing the kind of inflammation that would be
expected in an autoimmune-driven pathologic process. For example, hematology results from
testing performed at the end of October 2012 (five weeks after the vaccination in question)
revealed a normal ESR—a well-recognized, albeit nonspecific, test for the presence of systemic
inflammation occurring in the context of an autoimmune process. Tr. at 344–45, 351. The CRP
test (another kind of inflammation test) was also unsupportive of active inflammation. Id. at 345.
Dr. Morel would have expected elevated readings if in fact Petitioner had at this time been
suffering from an autoimmune process. Id.

       Testing performed in early November 2012 (when Petitioner was at Waccamaw) for certain
autoantibodies associated with inflammatory vascular illnesses also revealed normal results, as
well as several other known autoimmune conditions. Tr. at 346–47. Then, additional testing
performed almost two years later yielded results consistent with what had been seen more
contemporaneously with Ms. Todd’s vaccination. Tr. at 350. Thus, inflammation testing continued

                                                19
to produce normal readings 20 and Petitioner tested negative for Lyme disease antibodies. Id. at
348. Petitioner did display a low positive ANA, but Dr. Morel considered this nonspecific
(especially since a meaningful number of otherwise-healthy individuals can test positive for this
antibody) and therefore not necessarily “clinically relevant.” Id.; see also Tr. at 364–65. 21 The
result nevertheless led Petitioner’s treaters to propose a rheumatologic consult in August 2014, but
(as the records reflect) she was ultimately not found to be likely suffering from any such injury
despite her ongoing symptoms. Id. at 349–50.

        Besides serologic testing, Dr. Morel also found significant Petitioner’s nerve biopsy results
from her spring 2014 workup at Duke. She noted that the results did not reveal vasculitis or any
other “histological abnormalities.” Tr. at 352–53; Ex. 88 at 14. In addition, the skin biopsy
performed on May 9, 2014 was only consistent with immune infiltrates that would be associated
with a localized rash, as opposed to the broader neurologic/sensory symptoms of which Petitioner
primarily complains. Tr. at 353, 366–67.

         Another way of understanding the lack of support for the contention that Petitioner’s
condition was autoimmune-derived, Dr. Morel reasoned, was how Petitioner’s physicians
approached treatment and testing generally. Ms. Todd was never tested for the autoantibodies
known to be associated with neurologic diseases—something Dr. Morel felt would have occurred
if Petitioner’s treaters had even entertained the possibility that her symptoms were autoimmune in
origin. Id. at 352. In addition, treaters never proposed that she receive any immune-modulating
therapies. Id. at 354. She did, however, admit that Petitioner had reported some immediate
improvement after such treatment, although she would need to see sustained improvement if she
was going to accept that the treatment revealed the autoimmune nature of Petitioner’s claimed
injury. Id. a 368–69.

        Besides the above, Dr. Morel commented, from her vantage as an immunologist, on certain
aspects of Dr. Aradillas’s opinion. She noted one article Petitioner filed that seemed to associate
high-positive ANA results plus evidence of positive CRP testing with individuals suffering from
small fiber neuropathies. Tr. at 351; M. Lang et al., Diagnostic Value of Blood Tests for Occult
Causes of Initially Idiopathic Small-Fiber Polyneuropathy, 263 J. of Neurology 1, 6 (2016), filed
as Ex. 86 on Feb. 28, 2019 (ECF No. 71-2)(“Lang”). In this case, however, not only was
Petitioner’s positive ANA (measured in 2014) much lower than what Lang proposed, but Petitioner
herself had never been unequivocally diagnosed with a small fiber neuropathy—unlike Lang’s
subjects. Tr. at 351–52; Lang at 3. She also emphasized her overall view (consistent with her

20
   Dr. Morel acknowledged that Petitioner did display a slightly elevated CRP reading in August 2014, but she deemed
it marginal since it was barely over the high end of the normal range. Tr. at 350. She also noted (along with the positive
ANA) that these findings occurred were two years after vaccination—too long to deem likely associated. Id. at 355.
21
  On cross, Dr. Morel noted that she did not find significant the fact that Ms. Todd had initially had a negative ANA,
followed by a positive one later, given the lack of corroborative evidence of systemic inflammation from other testing.
Tr. at 365. She also noted that a person with a rheumatic condition would possess a positive ANA plus other evidence
specific to conditions. Id. at 366.

                                                           20
reading of the medical record) that, contrary to certain assertions in Dr. Aradillas’s report, there
was a lack of evidence (such as proof of nonspecific inflammation) suggesting that Ms. Todd’s
receipt of the flu vaccine resulted in an initial aberrant innate immune response. Id. at 361–62.

III.     Procedural History
        After the case’s initiation in August 2015, medical records were filed until the spring of
2016. Thereafter, the parties began obtaining and filing their expert reports (as referenced above),
completing the process by January 2018. In the interim period, the case was reassigned to me, and
after a status conference with the parties I set the matter down for a hearing to be held in March
2019. See Prehearing Order, dated June 1, 2018 (ECF No. 59). The hearing occurred as scheduled,
with the parties filing simultaneous post-trial briefs in early July 2019. The matter is now ripe for
resolution.

IV.      Relevant Law
         A.       Petitioner’s Overall Burden in Vaccine Program Cases

        To receive compensation in the Vaccine Program, a petitioner must prove either: (1) that
he suffered a “Table Injury”—i.e., an injury falling within the Vaccine Injury Table—
corresponding to one of the vaccinations in question within a statutorily prescribed period of time
or, in the alternative, (2) that his illnesses were actually caused by a vaccine (a “Non-Table
Injury”). See Sections 11(c)(1), 13(a)(1)(A), 14(a); see also Moberly v. Sec’y of Health & Human
Servs., 592 F.3d 1315, 1321 (Fed. Cir. 2010); Capizzano v. Sec’y of Health & Human Servs., 440
F.3d 1317, 1320 (Fed. Cir. 2006). 22 In this case, Petitioner does not assert a Table claim.

        For both Table and Non-Table claims, Vaccine Program petitioners bear a “preponderance
of the evidence” burden of proof. Section 13(a)(1)(a). That is, a petitioner must offer evidence that
leads the “trier of fact to believe that the existence of a fact is more probable than its nonexistence
before [he] may find in favor of the party who has the burden to persuade the judge of the fact’s
existence.” Moberly, 592 F.3d at 1322 n.2; see also Snowbank Enters. v. United States, 6 Cl. Ct.
476, 486 (1984) (mere conjecture or speculation is insufficient under a preponderance standard).
Proof of medical certainty is not required. Bunting v. Sec’y of Health & Human Servs., 931 F.2d
867, 873 (Fed. Cir. 1991). In particular, a petitioner must demonstrate that the vaccine was “not
only [the] but-for cause of the injury but also a substantial factor in bringing about the injury.”
Moberly, 592 F.3d at 1321 (quoting Shyface v. Sec’y of Health & Human Servs., 165 F.3d 1344,
1352–53 (Fed. Cir. 1999)); Pafford v. Sec’y of Health & Human Servs., 451 F.3d 1352, 1355 (Fed.
Cir. 2006). A petitioner may not receive a Vaccine Program award based solely on his assertions;

22
  Decisions of special masters (some of which I reference in this ruling) constitute persuasive but not binding
authority. Hanlon v. Sec’y of Health & Human Servs., 40 Fed. Cl. 625, 630 (1998). By contrast, Federal Circuit rulings
concerning legal issues are binding on special masters. Guillory v. Sec’y of Health & Human Servs., 59 Fed. Cl. 121,
124 (2003), aff’d 104 F. App’x 712 (Fed. Cir. 2004); see also Spooner v. Sec’y of Health & Human Servs., No. 13-
159V, 2014 WL 504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014).

                                                         21
rather, the petition must be supported by either medical records or by the opinion of a competent
physician. Section 13(a)(1).

        In attempting to establish entitlement to a Vaccine Program award of compensation for a
Non-Table claim, a petitioner must satisfy all three of the elements established by the Federal
Circuit in Althen v. Secretary of Health & Human Services, 418 F.3d 1274, 1278 (Fed. Cir. 2005):
“(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.” Althen, 418 F.3d at 1278.

        Each of the Althen prongs requires a different showing. Under Althen prong one, petitioners
must provide a “reputable medical theory,” demonstrating that the vaccine received can cause the
type of injury alleged. Pafford, 451 F.3d at 1355–56 (citations omitted). To satisfy this prong, a
petitioner’s theory must be based on a “sound and reliable medical or scientific explanation.”
Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 548 (Fed. Cir. 1994). Such a theory
must only be “legally probable, not medically or scientifically certain.” Id. at 549.

        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 v. Sec’y of Health & Human Servs., 569 F.3d 1367, 1378–79 (Fed. Cir. 2009)
(citing Capizzano, 440 F.3d at 1325–26). Special masters, despite their expertise, are not
empowered by statute to conclusively resolve what are essentially thorny scientific and medical
questions, and thus 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. Accordingly, special masters must take care not to increase the
burden placed on petitioners in offering a scientific theory linking vaccine to injury. Contreras v.
Sec’y of Health & Human Servs., 121 Fed. Cl. 230, 245 (2015), vacated on other grounds, 844
F.3d 1363 (Fed. Cir. 2017).

         In discussing the evidentiary standard applicable to the first Althen prong, many decisions
of the Court of Federal Claims and Federal Circuit have emphasized that petitioners need only
establish a causation theory’s biological plausibility (and thus need not do so with preponderant
proof). Tarsell v. United States, 133 Fed. Cl. 782, 792–93 (2017) (special master committed legal
error by requiring petitioner to establish first Althen prong by preponderance; that standard applied
only to second prong and petitioner’s overall burden); Contreras, 121 Fed. Cl. at 245 (“Plausibility
. . . in many cases may be enough to satisfy Althen prong one.” (emphasis in original)); see also
Andreu, 569 F.3d at 1375. At the same time, there is contrary authority from the Federal Circuit
suggesting that the same preponderance standard used overall in evaluating a claimant’s success
in a Vaccine Act claim is also applied specifically to the first Althen prong. See, e.g., Broekelschen
v. Sec’y of Health & Human Servs., 618 F.3d 1339, 1350 (Fed. Cir. 2010) (affirming special


                                                 22
master’s determination that expert “had not provided a ‘reliable medical or scientific explanation’
sufficient to prove by a preponderance of the evidence a medical theory linking the [relevant
vaccine to relevant injury].”) (emphasis added). Regardless, one thing remains: petitioners always
have the ultimate burden of establishing their Vaccine Act claim overall with preponderant
evidence. W.C. v. Sec’y of Health & Human Servs., 704 F.3d 1352, 1356 (Fed. Cir. 2013) (citations
omitted); Tarsell, 133 Fed. Cl. at 793 (noting that Moberly “addresses the petitioner’s overall
burden of proving causation-in-fact under the Vaccine Act” by a preponderance standard).

        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; see also
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 (“[M]edical 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.’” (quoting Althen, 418 F.3d at 1280)). Medical records are generally viewed as particularly
trustworthy evidence, since 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).

        Medical records and/or statements of a treating physician’s views, however, 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. Section 13(b)(1) (providing that “[a]ny such diagnosis,
conclusion, judgment, test result, report, or summary shall not be binding on the special master or
court”); Snyder v. Sec’y of Health & Human Servs., 88 Fed. Cl. 706, 746 n.67 (2009) (“[T]here 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 present in the record—including conflicting opinions
among such individuals. Hibbard v. Sec’y of Health & Human Servs., 100 Fed. Cl. 742, 749 (2011)
(finding that it is not arbitrary or capricious for special masters to weigh competing treating
physicians’ conclusions against each other), aff’d, 698 F.3d 1355 (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), mot. for review denied, 100 Fed. Cl. 344, 356 (2011), aff’d without op., 475 Fed. App’x
765 (Fed. Cir. 2012).

       The third Althen prong requires establishing a “proximate temporal relationship” between
the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been equated to the
phrase “medically-acceptable temporal relationship.” Id. A petitioner must offer “preponderant


                                                  23
proof that the onset of symptoms occurred within a timeframe which, given the medical
understanding of the disorder’s etiology, it is medically acceptable to infer causation.” de Bazan
v. Sec’y of Health & Human Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for
what is a medically acceptable timeframe must also coincide with the theory of how the relevant
vaccine can cause an injury (Althen prong one’s requirement). Id.; see also Shapiro v. Sec’y of
Health & Human Servs., 101 Fed. Cl. 532, 542 (2011), recons. denied after remand, 105 Fed. Cl.
353 (2012), aff’d mem., 2013 WL 1896173 (Fed. Cir. 2013); Koehn v. Sec’y of Health & Human
Servs., No. 11-355V, 2013 WL 3214877 (Fed. Cl. Spec. Mstr. May 30, 2013), mot. for review
denied (Fed. Cl. Dec. 3, 2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).

       B.      Law Governing Analysis of Fact Evidence

        The process for making determinations in Vaccine Program cases regarding factual issues
begins with consideration of the medical records. Section 11(c)(2). The special master is required
to consider “all [] relevant medical and scientific evidence contained in the record,” including “any
diagnosis, conclusion, medical judgment, or autopsy or coroner’s report which is contained in the
record regarding the nature, causation, and aggravation of the petitioner’s illness, disability, injury,
condition, or death,” as well as the “results of any diagnostic or evaluative test which are contained
in the record and the summaries and conclusions.” Section 13(b)(1)(A). The special master is then
required to weigh the evidence presented, including contemporaneous medical records and
testimony. See Burns v. Sec’y of Health & Human Servs., 3 F.3d 415, 417 (Fed. Cir. 1993) (it is
within the special master’s discretion to determine whether to afford greater weight to
contemporaneous medical records than to other evidence, such as oral testimony surrounding the
events in question that was given at a later date, provided that such determination is evidenced by
a rational determination).

        Medical records that are created contemporaneously with the events they describe are
presumed to be accurate and “complete” (i.e., presenting all relevant information on a patient’s
health problems). Cucuras, 993 F.2d at 1528; see also Doe/70 v. Sec’y of Health & Human Servs.,
95 Fed. Cl. 598, 608 (2010) (“Given the inconsistencies between petitioner’s testimony and his
contemporaneous medical records, the special master’s decision to rely on petitioner’s medical
records was rational and consistent with applicable law”); Rickett v. Sec’y of Health & Human
Servs., 468 F. App’x 952 (Fed. Cir. 2011) (non-precedential opinion). This presumption is based
on the linked propositions that (i) sick people visit medical professionals; (ii) sick people honestly
report their health problems to those professionals; and (iii) medical professionals record what they
are told or observe when examining their patients in as accurate a manner as possible, so that they
are aware of enough relevant facts to make appropriate treatment decisions. Sanchez v. Sec’y of
Health & Human Servs., No. 11-685V, 2013 WL 1880825, at *2 (Fed. Cl. Spec. Mstr. Apr. 10,
2013); Cucuras v. Sec’y of Health & Human Servs., 26 Cl. Ct. 537, 543 (1992), aff’d, 993 F.2d at



                                                  24
1525 (Fed. Cir. 1993) (“[I]t strains reason to conclude that petitioners would fail to accurately
report the onset of their daughter’s symptoms.”).

        Accordingly, if the medical records are clear, consistent, and complete, then they should
be afforded substantial weight. Lowrie v. Sec’y of Health & Human Servs., No. 03-1585V, 2005
WL 6117475, at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed, contemporaneous medical
records are generally found to be deserving of greater evidentiary weight than oral testimony—
especially where such testimony conflicts with the record evidence. Cucuras, 993 F.2d at 1528;
see also Murphy v. Sec’y of Health & Human Servs., 23 Cl. Ct. 726, 733 (1991), aff’d per curiam,
968 F.2d 1226 (Fed. Cir. 1992), cert. denied sub. nom. Murphy v. Sullivan, 506 U.S. 974 (1992)
(“It has generally been held that oral testimony which is in conflict with contemporaneous
documents is entitled to little evidentiary weight.”) (citing United States v. United States Gypsum
Co., 333 U.S. 364, 396 (1948)).

        There are, however, situations in which compelling oral testimony may be more persuasive
than written records, such as where records are deemed to be incomplete or inaccurate. Campbell
v. Sec’y of Health & Human Servs., 69 Fed. Cl. 775, 779 (2006) (“[L]ike any norm based upon
common sense and experience, this rule should not be treated as an absolute and must yield where
the factual predicates for its application are weak or lacking.”); Lowrie, 2005 WL 6117475, at *19
(“Written records which are, themselves, inconsistent, should be accorded less deference than
those which are internally consistent.”) (quoting Murphy, 23 Cl. Ct. at 733)). Ultimately, a
determination regarding a witness’s credibility is needed when determining the weight that such
testimony should be afforded. Andreu, 569 F.3d at 1379; Bradley v. Sec’y of Health & Human
Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).

        When witness testimony is offered to overcome the presumption of accuracy afforded to
contemporaneous medical records, such testimony must be “consistent, clear, cogent, and
compelling.” Sanchez, 2013 WL 1880825, at *3 (citing Blutstein v. Sec’y of Health & Human
Servs., No. 90-2808V, 1998 WL 408611, at *5 (Fed. Cl. Spec. Mstr. June 30, 1998)). In
determining the accuracy and completeness of medical records, the Court of Federal Claims has
listed four possible explanations for inconsistencies between contemporaneously created medical
records and later testimony: (1) a person’s failure to recount to the medical professional everything
that happened during the relevant time period; (2) the medical professional’s failure to document
everything reported to her or him; (3) a person’s faulty recollection of the events when presenting
testimony; or (4) a person’s purposeful recounting of symptoms that did not exist. La Londe v.
Sec’y of Health & Human Servs., 110 Fed. Cl. 184, 203–04 (2013), aff’d, 746 F.3d 1334 (Fed. Cir.
2014). In making a determination regarding whether to afford greater weight to contemporaneous
medical records or other evidence, such as testimony at hearing, there must be evidence that this
decision was the result of a rational determination. Burns, 3 F.3d at 417.



                                                 25
       C.      Analysis of Expert Testimony

        Establishing a sound and reliable medical theory often requires a petitioner to present
expert testimony in support of his claim. Lampe v. Sec’y of Health & Human Servs., 219 F.3d
1357, 1361 (Fed. Cir. 2000). Vaccine Program expert testimony is usually evaluated according to
the factors for analyzing scientific reliability set forth in Daubert v. Merrell Dow Pharm., Inc., 509
U.S. 579, 594–96 (1993). See Cedillo v. Sec’y of Health & Human Servs., 617 F.3d 1328, 1339
(Fed. Cir. 2010) (citing Terran v. Sec’y of Health & Human Servs., 195 F.3d 1302, 1316 (Fed. Cir.
1999)). “The Daubert factors for analyzing the reliability of testimony are: (1) whether a theory or
technique can be (and has been) tested; (2) whether the theory or technique has been subjected to
peer review and publication; (3) whether there is a known or potential rate of error and whether
there are standards for controlling the error; and (4) whether the theory or technique enjoys general
acceptance within a relevant scientific community.” Terran, 195 F.3d at 1316 n.2 (citing Daubert,
509 U.S. at 592–95).

         The Daubert factors play a slightly different role in Vaccine Program cases than they do
when applied in other federal judicial fora (such as the district courts). Daubert factors are usually
employed by judges (in the performance of their evidentiary gatekeeper roles) to exclude evidence
that is unreliable and/or could confuse a jury. In Vaccine Program cases, by contrast, these factors
are used in the weighing of the reliability of scientific evidence proffered. Davis v. Sec’y of Health
& Human Servs., 94 Fed. Cl. 53, 66–67 (2010) (“[U]niquely in this Circuit, the Daubert factors
have been employed also as an acceptable evidentiary-gauging tool with respect to persuasiveness
of expert testimony already admitted.”). The flexible use of the Daubert factors to evaluate the
persuasiveness and reliability of expert testimony has routinely been upheld. See, e.g., Snyder, 88
Fed. Cl. at 742–45. In this matter (as in numerous other Vaccine Program cases), Daubert has not
been employed at the threshold, to determine what evidence should be admitted, but instead to
determine whether expert testimony offered is reliable and/or persuasive.

        Respondent frequently offers one or more experts of his own in order to rebut a petitioner’s
case. Where both sides offer expert testimony, a special master’s decision may be “based on the
credibility of the experts and the relative persuasiveness of their competing theories.”
Broekelschen v. Sec’y of Health & Human Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (citing
Lampe, 219 F.3d at 1362). But nothing requires the acceptance of an expert’s conclusion
“connected to existing data only by the ipse dixit of the expert,” especially if “there is simply too
great an analytical gap between the data and the opinion proffered.” Snyder, 88 Fed. Cl. at 743
(quoting Gen. Elec. Co. v. Joiner, 522 U.S. 146 (1997)); see also Isaac v. Sec’y of Health & Human
Servs., No. 08-601V, 2012 WL 3609993, at *17 (Fed. Cl. Spec. Mstr. July 30, 2012), mot. for
review denied, 108 Fed. Cl. 743 (2013), aff’d, 540 Fed. App’x 999 (Fed. Cir. 2013) (citing Cedillo,
617 F.3d at 1339). Weighing the relative persuasiveness of competing expert testimony, based on
a particular expert’s credibility, is part of the overall reliability analysis to which special masters


                                                  26
must subject expert testimony in Vaccine Program cases. Moberly, 592 F.3d at 1325–26
(“Assessments as to the reliability of expert testimony often turn on credibility
determinations….”); see also Porter v. Sec’y of Health & Human Servs., 663 F.3d 1242, 1250
(Fed. Cir. 2011) (“[T]his court has unambiguously explained that special masters are expected to
consider the credibility of expert witnesses in evaluating petitions for compensation under the
Vaccine Act.”).

       D.      Consideration of Medical Literature

        Both parties filed medical and scientific literature in this case, but not every filed item
factors into the outcome of this decision. While I have reviewed all of the medical literature
submitted in this case, I discuss only those articles that are most relevant to my determination
and/or are central to Petitioner’s case—just as I have not exhaustively discussed every individual
medical record filed. See Moriarty v. Sec’y of Health & Human Servs., 844 F.3d 1322, 1328 (Fed.
Cir. 2016) (“We generally presume that a special master considered the relevant record evidence
even though he does not explicitly reference such evidence in his decision.”) (citation omitted);
see also Paterek v. Sec’y of Health & Human Servs., 527 F. App’x 875, 884 (Fed. Cir. 2013)
(“Finding certain information not relevant does not lead to—and likely undermines—the
conclusion that it was not considered”).

                                           ANALYSIS
I. The Record Does Not Support the Conclusion that Petitioner Had an NLDSFN
        In many Vaccine Act cases, determining whether the evidence supports the injury alleged
by the petitioner is a precursor to (and can even supplant) evaluation of the petitioner’s success in
satisfying the Althen prongs. LaPierre v. Sec’y of Health & Human Servs., No. 17-227V, 2019
WL 6490730, at *16–17 (Fed. Cl. Spec. Mstr. Oct. 18, 2019) (citing Broekelschen, 618 F.3d at
1346. This is especially critical where the claimant’s theory of causation relies on a fact finding
for the alleged injury, i.e. where the theory articulates a vaccine-initiated process that invariably
leads to a particular kind of injury, and/or where it is accepted by science and medicine that a
particular injury results from an immunologic process associated with the vaccine at issue.
Lapierre, 2019 WL 6490730, at *17. This is the case herein—not only did Dr. Aradillas plainly
embrace NLDSFN as the best diagnostic descriptor for Ms. Todd’s constellation of symptoms, but
the scientific and medical theories he proposed for how the flu vaccine could have brought about
this injury were fairly specific to this kind of small fiber neuropathy.

        Here, however, the record and expert testimony taken together do not support the
conclusion that Petitioner suffered from NLDSFN. Critically, no treater ever proposed that
Petitioner had such a neuropathy. Nor does the record suggest the existence of any of the indicia
that would bulwark Petitioner’s diagnostic contention. Numerous test results—especially those
performed close in time to Ms. Todd’s receipt of the flu vaccine—do not establish the existence

                                                 27
of the sort of systematic inflammation that would be associated with an autoimmune neuropathy.
Petitioner never tested positive for any autoantibodies that could even possibly be linked to a small
fiber neuropathy. And Respondent’s experts persuasively established that a positive ANA finding
(almost two years post-vaccination, moreover) is too nonspecific to constitute even indirect
evidence of a small fiber neuropathy. Dr. Lancaster also persuasively established that the
inconsistent, waxing and waning nature of Petitioner’s symptomatic complaints for him was
another factor ruling out NLDSFN as the proper diagnosis. Tr. at 224–25. Finally, the evidence in
this case strongly supports the conclusion that a skin biopsy is in fact the most accurate test for
small fiber neuropathies. Khan, supra, at 89. But Petitioner’s test results were negative. Ex. 88 at
14. 23

        Dr. Aradillas could not overcome what the record plainly shows with his alternative view
of the proper diagnosis. First, his expertise is mainly in the treatment of pain syndromes and
disorders, as opposed to the clinical assessment of neuropathic injury—so, although he had
sufficient expertise and background in neurology to offer an opinion in this case, he did not have
the specific grounding in neuropathies generally to offer a persuasive opinion. Second, his opinion
tried unsuccessfully to navigate around inconvenient facts in the record—for example, by arguing
with limited reliable scientific support) that even though Ms. Todd’s record does not establish the
kind of actual nerve injury that would be associated with an autoimmune neuropathy, nerve
“malfunction” can also explain NLDSFN. This contention, while not implausible, was not
demonstrated to establish what most commonly causes NLDSFN, let alone that this characterized
Ms. Todd’s condition. Dr. Aradillas also was not credible in suggesting other proper diagnostic
and clinical criteria for the condition.

        Dr. Lancaster, by contrast, more persuasively undermined Petitioner’s injury contentions.
He noted that Petitioner’s negative skin biopsy as well as the inconsistency in her “areas of
confirmed loss of sensation” were not indicative of NLDSFN. Tr. at 230. He also noted that many
of the physicians who treated Petitioner documented normal or insignificant examination findings.
Tr. at 238, 243–45, 247–51, 274–77. And he, along with Dr. Morel, showed how the overall record
did not support the conclusion that Petitioner was suffering from the kind of persistent
inflammation that would be congruent with the conclusion that she had an autoimmune-caused
illness (which Dr. Aradillas largely seemed to contend characterized NLDSFN). Though Dr.
Lancaster allowed that NLDSFN was not an unreasonable proposal under the circumstances, given
the nature of some of Petitioner’s symptoms, he ultimately concluded that it was not supported by
the record, and I give greater weight to his testimony and opinion in this case.




23
  By contrast, the literature and more persuasive expert testimony does not support Dr. Aradillas’s contention that a
positive QST test could support an NLDSFN diagnosis—and in any event, Petitioner does not appear to have ever
received such a test.

                                                        28
II.    Petitioner Has Not Satisfied the Althen Test for Entitlement

        As noted, Petitioner’s case depended on a finding that she experienced NLDSFN. I find
instead that the record evidence only preponderates in the determination that her symptoms had an
idiopathic origin—thus obviating the need for a complete Althen analysis, since Petitioner’s theory
required that I find the existence of a specific injury. Nevertheless, even if my determination had
been otherwise, or I had found that Petitioner suffered from some kind of generalized neuropathy
arguably autoimmune in origin, I would still be unable to rule that Petitioner carried her overall
burden of proof under Althen.

         First, Petitioner’s showing on the “can cause” Althen prong was insufficient. The best
understanding of the theory espoused by Petitioner is that the flu vaccine could cause general
interference with nerve function (as opposed to direct injury to the small fibers, given that Dr.
Aradillas seemed to concede there is no evidence in this case that this occurred), via an adaptive
immune response to the flu vaccine attributable to the production of autoantibodies. Some
literature support was offered detailing other contexts in which autoantibodies are thought to
interfere with other biologic processes, such as when the patients experiencing GBS produce
antibodies against the CASPR1 antigen resulting in subsequent pain. Tr. at 90–93; A. Goebel,
Autoantibody Pain, 15 Autoimmunity Reviews 552, 555 (2016), filed as Ex. 62 on Feb. 28, 2018
(ECF No. 68-8).

        But numerous links of the theory as applicable in this specific case were wanting or
nonexistent. Thus, little reliable evidence was offered showing that (a) the flu vaccine has been
shown to cause the creation of antibodies of the sort capable of interfering with nerve function, or
(b) that this kind of interference has been offered to explain NLDSFN, as opposed to the kind of
direct, demyelinating harm known to be implicated in other peripheral neuropathies, like GBS
(which of course it is undisputed Petitioner did not have). And Dr. Aradillas was at the limit of his
expertise in opining how a flu vaccine could produce a NLDSFN, further reducing the
effectiveness of his explanations. Dr. Lancaster, by contrast, was effective and persuasive in
establishing that NLDSFN was more likely than not in most cases the product of the kind of direct
nerve damage that Petitioner concedes is absent here, and that it is otherwise not properly
considered an autoimmune-caused injury, at least directly.

        I acknowledge, however, that other decisions have found that a vaccine can precipitate a
small fiber neuropathy—albeit via the kind of direct, demyelinating injury that is plainly not
demonstrated by the record in this case. See, e.g., Swaiss v. Sec’y of Health & Human Servs., No.
15-286V, 2019 WL 6520791 (Fed. Cl. Spec. Mstr. Nov. 4, 2019) (finding that a petitioner claiming
small fiber neuropathy following receipt of the tetanus-diphtheria-acellular pertussis vaccine was
entitled to compensation). Accordingly, and despite the overall unpersuasive showing on the first
Althen prong made herein, there does exist some reasoned support for the theory.




                                                 29
        But even if I had simply adopted the reasoning from such other cases, and found that
Petitioner preponderantly established the first Althen prong, Petitioner’s case would then run
aground on the second, “did cause” prong. For the record does not confirm the working out in Ms.
Todd’s case of the proposed theory for how the flu vaccine arguably could have injured her. Thus,
there is no evidence that Petitioner possessed any of the primary autoantibodies that might
arguably be associated with the kind of nerve function interference proposed by Petitioner—and
she was tested for some. Ex. 6 at 20, 22, 24–25; Ex. 12 at 8. 24 There was no other indirect evidence
of inflammation that would normally be associated with an autoimmune condition—and even the
weak evidence of it was from too much later in her medical history post-vaccination to link it
persuasively to the September 2012 vaccination. And, as already noted, the symptoms complained
of by Petitioner, while suggestive of some kind of neuropathy, resisted a formal diagnosis, nor did
her treaters ultimately conclude that her injury was autoimmune generally or vaccine-caused
specifically. Whatever Petitioner suffers from, its nature and cause remains unidentified—and
preponderantly has not been associated with her receipt of the flu vaccine. 25

                                                  CONCLUSION

        The Vaccine Act permits me to award compensation only if a Petitioner alleging a “non-
Table Injury” can show by medical records or competent medical opinion that the injury was more
likely than not vaccine-caused. Here, Petitioner has not established with preponderant evidence
her proposed diagnosis, nor has she demonstrated the flu vaccine could bring it (or something
comparable) about. I therefore DENY entitlement in this case.

        In the absence of a timely-filed motion for review (see Appendix B to the Rules of the
Court), the Clerk shall enter judgment in accord with this decision. 26




24
   Although the evidence of successful immunosuppressive treatments might also be circumstantial evidence
supporting Petitioner’s autoimmune contentions, this must be weighed against both the affirmative absence of
evidence of persistent inflammation in Petitioner, as well as the fact that treaters largely did not conclude her symptoms
had an autoimmune origin.
25
   With respect to the third Althen prong, the onset of Petitioner’s putatively neuropathic symptoms—two to three
weeks post-vaccination—is not inconsistent with the timeframe for clinical manifestations of an autoimmune response
after causal trigger and is also consistent with Petitioner’s theory. However, the theory itself, as noted above, is
insufficiently supported with reliable scientific or medical evidence—nor did Petitioner establish in the first place she
had NLDSFN, or any other neuropathic injury for that matter. Regardless, my determination herein turns more on the
first and second prongs, so Petitioner’s success or failure at establishing evidence to support this one does not alter
my conclusion.
26
   Pursuant to Vaccine Rule 11(a), the parties may expedite entry of judgment by filing a joint notice renouncing their
right to seek review.

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IT IS SO ORDERED.

                         /s/ Brian H. Corcoran
                           Brian H. Corcoran
                           Chief Special Master




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