# V. v. Secretary of Health and Human Services

> United States Court of Federal Claims · July 28, 2021

URL: https://www.frixlaw.com/law-library/cases/4707162

## Case

- **Court:** United States Court of Federal Claims
- **Decided:** July 28, 2021
- **Precedential status:** Published
- **Opinion:** Opinion
- **Judges:** Nora Beth Dorsey
- **Cited by:** 0 later opinions in the Frix Law Library

## Citator (automated)

- No negative treatment found by the automated citator. That is not the same as a confirmation that the case is good law; read the citing cases.
- Full citator and citing cases: https://www.frixlaw.com/law-library/cases/4707162

## How later opinions describe it (automated extraction)

- noting that “clear, cogent, and consistent testimony can overcome such missing or contradictory medical records”
- noting that “close calls” are resolved in petitioner’s favor
- noting that special masters are bound by both § 13(b)(1) and Vaccine Rule 8(b)(1) to consider only evidence that is both “relevant” and “reliable”
- stating that an “expert opinion is no better than the soundness of the reasons supporting it” (citing Fehrs v. United States, 620 F.2d 255, 265 (Ct. Cl. 1980))

## Opinion text

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
Originally Filed: June 16, 2021
Refiled in Redacted Form: July 28, 2021

* * * * * * * * * * * * * * *
O.M.V., * PUBLISHED
*
Petitioner, * No. 16-1505V
*
v. * Special Master Nora Beth Dorsey
*
SECRETARY OF HEALTH * Entitlement; Influenza (“Flu”) Vaccine;
AND HUMAN SERVICES, * Acute Disseminated Encephalomyelitis
* (“ADEM”); Multiple Sclerosis (“MS”);
Respondent. * Demyelinating Condition.
*
* * * * * * * * * * * * * * *

Edward M. Kraus, Law Offices of Chicago Kent, Chicago, IL, for petitioner.
Laurie Wiesner, U.S. Department of Justice, Washington, DC, for respondent.

DECISION1

I. INTRODUCTION

On November 14, 2016, O.M.V. (“petitioner”) filed a petition under the National Vaccine
Injury Compensation Program (“Vaccine Act” or “the Program”), 42 U.S.C. § 300aa-10 et seq.
(2012).2 Petitioner alleges he suffers “permanent disabilities [and] permanent neurologic
deficits” as a result of an influenza (“flu”) vaccine administered on November 15, 2013. Petition
at 1 (ECF No. 1). Respondent argued against compensation, stating that “this case is not

1
Because this Decision contains a reasoned explanation for the action in this case, the
undersigned is required to post it on the United States Court of Federal Claims’ website in
accordance with the E-Government Act of 2002. 44 U.S.C. § 3501 note (2012) (Federal
Management and Promotion of Electronic Government Services). This means the Decision will
be available to anyone with access to the Internet. In accordance with Vaccine Rule 18(b),
petitioner has 14 days to identify and move to redact medical or other information, the disclosure
of which would constitute an unwarranted invasion of privacy. If, upon review, the undersigned
agrees that the identified material fits within this definition, the undersigned will redact such
material from public access.
2
The National Vaccine Injury Compensation Program is set forth in Part 2 of the National
Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755, codified as amended,
42 U.S.C. §§ 300aa-10 to -34 (2012). All citations in this Decision to individual sections of the
Vaccine Act are to 42 U.S.C. § 300aa.
appropriate for compensation under the terms of the Act.” Respondent’s Report (“Resp. Rept.”)
at 2 (ECF No. 38).

After carefully analyzing and weighing the evidence presented in this case in accordance
with the applicable legal standards, the undersigned finds petitioner is not entitled to
compensation. Accordingly, petitioner’s case must be dismissed.

II. ISSUES IN AGREEMENT AND IN DISPUTE

The parties agree that petitioner was generally healthy with no known neurological
conditions prior to his flu vaccination on November 15, 2013. Joint Prehearing Submission,
filed Oct. 22, 2020, at 1 (ECF No. 112). “[T]he appropriate diagnosis for [petitioner’s] condition
that began on November 16, 2013 and continues to the present day” is in dispute. Id. at 2.
Additionally, the parties disagree as to whether the flu vaccine was a but-for cause and/or
substantial factor in the development of petitioner’s neurological illness. Id.

III. BACKGROUND

A. Medical Terminology

Acute disseminated encephalomyelitis (“ADEM”) is “an acute or subacute
encephalomyelitis[3] or myelitis[4] characterized by perivascular lymphocyte and mononuclear
cell infiltration and demyelination.”5 Acute Disseminated Encephalomyelitis, Dorland’s Med.
Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=73033 (last visited
Apr. 14, 2021). “It is believed to be a manifestation of an autoimmune attack on the myelin of
the central nervous system [(“CNS”)].” Id.

3
Encephalomyelitis is “inflammation involving both the brain and the spinal cord.”
Encephalomyelitis, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/
definition?id=16191 (last visited May 4, 2021).
4
Myelitis is “inflammation of the spinal cord.” Myelitis, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=32680 (last visited May 4, 2021).
5
Demyelination is the “destruction, removal, or loss of the myelin sheath of a nerve or nerves.”
Demyelination, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/
definition?id=13092 (last visited May 4, 2021).

2
ADEM is a monophasic disease that is “usually triggered by an inflammatory response to
viral infections and vaccinations.” Pet. Ex. 98 at 1;6 see also Pet. Ex. 28 at 3;7 Pet. Ex. 99 at 1;8
Pet. Ex. 102 at 5;9 Pet. Ex. 103 at 1.10 The monophasic nature of ADEM is “defined as a lack of
recurrence (within 3 months) in the absence of treatment or while on appropriate treatment.
Relapse occurring during cessation or tapering of therapy should be considered to belong to one
monophasic episode.” Pet. Ex. 102 at 5 (emphasis omitted). “A single clinical event of ADEM
can evolve over a period of 3 months, with fluctuations in clinical symptoms and severity.”
Resp. Ex. H at 2.11

ADEM “is usually associated with multifocal neurologic symptoms and mental status
change.” Pet. Ex. 101 at 1.12 Symptoms include “decreased level of consciousness varying from
lethargy to coma, convulsions, and multifocal neurologic symptoms such as hemi-, para-, and
tetraparesis, cranial nerve palsies, and movement disorders.” Pet. Ex. 98 at 1. “[B]ehavioral
changes varying from irritability, depression, delusions, and psychosis” dominate symptoms in
some cases. Id. ADEM patients also “commonly have headache, vomiting, drowsiness, and
meningism.” Pet. Ex. 97 at 1-2.13

According to the Brighton Collaboration Working Group (“Brighton Collaboration”),
“[t]he diagnostic hallmark of ADEM is the demonstration of scattered, focal or multifocal
(disseminated) areas of inflammation and demyelination within cerebral subcortical and deep

6
Jari Honkaniemi et al., Delayed MR Imaging Changes in Acute Disseminated
Encephalomyelitis, 22 Am. J. Neuroradiology 1117 (2001).
7
Xinqing Deng & Subramaniam Sriram, Role of Microglia in Multiple Sclerosis, 5 Current
Neurology & Neuroscience Reps. 239 (2005).
8
William Huynh et al., Post-Vaccination Encephalomyelitis: Literature Review and Illustrative
Case, 15 J. Clinical Neuroscience 1315 (2008).
9
James J. Sejvar et al., Encephalitis, Myelitis, and Acute Disseminated Encephalomyelitis
(ADEM): Case Definitions and Guidelines for Collection, Analysis, and Presentation of
Immunization Safety Data, 25 Vaccine 5771 (2007).
10
S. Schwarz et al., Acute Disseminated Encephalomyelitis: A Follow-Up Study of 20 Adult
Patients, 56 Neurology 1313 (2001).
11
Lauren B. Krupp et al., Consensus Definitions Proposed for Pediatric Multiple Sclerosis and
Related Disorders, 68 Neurology 87 (2007).
12
Yann Mikaeloff et al., First Episode of Acute CNS Inflammatory Demyelination in Childhood:
Prognostic Factors for Multiple Sclerosis and Disability, 144 J. Pediatrics 246 (2003).
13
R C Dale & J A Branson, Acute Disseminated Encephalomyelitis or Multiple Sclerosis: Can
the Initial Presentation Help in Establishing a Correct Diagnosis?, 90 Archives Disease
Childhood 636 (2005).

3
cortical white matter.” Pet. Ex. 102 at 5. The Brighton Collaboration developed the following
diagnostic criteria for ADEM:14

Level 1 of (a) Demonstration of diffuse or multifocal areas of demyelination by
Diagnostic histopathology; OR
Certainty (b) Focal or multifocal findings referable to the central nervous system,
including one or more of the following:
(1) Encephalopathy,
(2) Focal cortical signs (including but not limited to: aphasia, alexia,
agraphia, cortical blindness),
(3) Cranial nerve abnormality/abnormalities,
(4) Visual field defect/defects,
(5) Presence of primitive reflexes (Babinski’s sign, glabellar reflex,
snout/sucking reflex),
(6) Motor weakness (either diffuse or focal; more often focal),
(7) Sensory abnormalities (either positive or negative; sensory level),
(8) Altered deep tendon reflexes (hypo- or hyperreflexia, asymmetry of
reflexes), or
(9) Cerebellar dysfunction, including ataxia, dysmetria, cerebellar
nystagmus, AND
(c) Magnetic resonance imaging (“MRI”) findings displaying diffuse or
multifocal white matter lesions; AND
(d) Monophasic pattern to illness (i.e., absence of relapse within a minimum of
3 months of symptomatic nadir).
Level 2 of (a) Focal or multifocal findings referable to the central nervous system (as
Diagnostic outlined in the Level 1 of diagnostic certainty section), AND
Certainty (b) MRI findings displaying diffuse or multifocal white matter lesions, AND
(c) Insufficient follow up time achieved to document absence of relapse within
a minimum period of 3 months following symptomatic nadir.
Level 3 of (a) Focal or multifocal findings referable to the central nervous system (as
Diagnostic outlined in the Level 1 of diagnostic certainty section).
Certainty
Level 3A Insufficient information is available to distinguish case between acute
encephalitis or ADEM; case unable to be definitively classified.
Exclusion • Presence of a clear alternative acute infectious or other diagnosis for illness,
Criteria for • Recurrence or relapse of illness at any point following a 3 month period of
All Levels of clinical improvement from symptomatic nadir, or
Diagnostic • If known, MRI findings or histopathologic data inconsistent with the
Certainty diagnosis of ADEM.

14
Pet. Ex. 102 at 8-9.

4
The Brighton Collaboration defined encephalopathy15 as “depressed or altered level of
consciousness, lethargy, or personality change lasting [more than] 24 h[ours].” Pet. Ex. 102 at 6.
The Group recognized that “ADEM—or any other adverse event—which follows administration
of an inactivated component or live vaccine may be temporally associated with, but is not
necessarily the result of, administration of a vaccine.” Id. at 5.

The International Pediatric Multiple Sclerosis Study Group (“MS Study Group”) also set
forth a list of findings that must all be present to render an ADEM diagnosis:

ADEM (monophasic).
• A first clinical event with a presumed inflammatory or demyelinating cause,
with acute or subacute onset that affects multifocal areas of the CNS. The
clinical presentation must be polysymptomatic and must include
encephalopathy, which is defined as one or more of the following:
o Behavioral change, e.g., confusion, excessive irritability
o Alteration in consciousness, e.g., lethargy, coma
• Event should be followed by improvement either clinically, on MRI, or
both, but there may be residual deficits
• No history of a clinical episode with features of a prior demyelinating event
• No other etiologies can explain the event
• New or fluctuating symptoms, signs, or MRI findings occurring within 3
months of the inciting ADEM event are considered part of the acute event
• Neuroimaging shows focal or multifocal lesion(s), predominantly involving
white matter, without radiologic evidence of previous destructive white
matter changes:
o Brain MRI, with FLAIR or T2-weighted images, reveals large (>1 to 2
cm in size) lesions that are multifocal, hyperintense, and located in the
supratentorial or infratentorial white matter regions; gray matter,
especially basal ganglia and thalamus, is frequently involved
o In rare cases, brain MR images show a large single lesion (≥1 to 2 cm),
predominantly affecting white matter
o Spinal cord MRI may show confluent intramedullary lesion(s) with
variable enhancement, in addition to abnormal brain MRI findings above
specified

Resp. Ex. H at 2. The Group’s definition of ADEM requires both encephalopathy, defined as
“mental status changes and/or behavioral alterations such as marked irritability,” and multifocal
involvement. Id. Additionally, an ADEM diagnosis “must rest on clinical features first,” and

15
Under the Vaccine Injury Table, an acute encephalopathy persists for at least 24 hours and is
characterized by at least two of the following: “(1) a significant change in mental status that is
not medication related (such as a confusional state, delirium, or psychosis); (2) [a] significantly
decreased level of consciousness which is independent of a seizure and cannot be attributed to
the effects of medication; and (3) [a] seizure associated with loss of consciousness.” 42 C.F.R. §
100.3(c)(2)(i)(B).

5
“MRI findings alone are insufficient.” Id. Although the Brighton Collaboration and MS Study
Group differ on the requirement of encephalopathy for ADEM diagnosis, “[e]ncephalopathy . . .
is considered mandatory for definite diagnosis.” Pet. Ex. 35 at 2.16

Multiple sclerosis (“MS”), like ADEM, is a demyelinating and disseminated disease of
the CNS. Pet. Ex. 97 at 1-2. MS is “a disease in which there are foci of demyelination
throughout the white matter of the [CNS], sometimes extending into the gray matter.” Multiple
Sclerosis, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/
definition?id=105130 (last visited Apr. 14, 2021). Symptoms “include weakness,
incoordination, paresthesias, speech disturbances, and visual complaints,” and disease course is
usually prolonged, with “remissions and relapses that occur over a period of many years.” Id.
MS typically presents between 20 and 40 years of age. Resp. Ex. C at 4.17 “A recent extensive
review from the US Institute of Medicine did not find sufficient evidence to support a causal
relationship between the onset of MS and various common vaccinations” including flu. Pet. Ex.
35 at 6.

The International Panel on Diagnosis of Multiple Sclerosis (“International Panel”)
developed the McDonald criteria, which combines clinical, imaging, and laboratory evidence, to
aid in the diagnosis of MS. Resp. Ex. C at 1.

The 2017 McDonald Criteria:18
Number of lesions with Additional data needed for a diagnosis of multiple sclerosis
objective clinical evidence
≥2 clinical ≥2 None
attacks
≥2 clinical 1 (as well as clear-cut None
attacks historical evidence of a
previous attack involving
a lesion in a distinct
anatomical location)
≥2 clinical 1 Dissemination in space demonstrated by an additional
attacks clinical attack implicating a different CNS site or by MRI
1 clinical ≥2 Dissemination in time demonstrated by an additional
attack clinical attack or by MRI OR demonstration of CSF-
specific oligoclonal bands

16
Dimitrios Karussis & Panayiota Petrou, The Spectrum of Post-Vaccination Inflammatory CNS
Demyelinating Syndromes, 13 Autoimmunity Revs. 215 (2014).
17
Alan J. Thompson et al., Diagnosis of Multiple Sclerosis: 2017 Revisions of the McDonald
Criteria, 17 Lancet Neurology 162 (2018).
18
Resp. Ex. C at 6 (emphasis added).

6
1 clinical 1 Dissemination in space demonstrated by an additional
attack clinical attack implicating a different CNS site or by MRI
AND
Dissemination in time demonstrated by an additional
clinical attack or by MRI OR demonstration of CSF-
specific oligoclonal bands

The International Panel defined the first attack as a “clinically isolated syndrome,” or “[a]
monophasic clinical episode with patient-reported symptoms and objective findings reflecting a
focal or multifocal inflammatory demyelinating event in the CNS, developing acutely or
subacutely, with a duration of at least 24 h[ours], with or without recovery, and in the absence of
fever or infection.” Resp. Ex. C at 2. An objective finding consists of “[a]n abnormality on
neurological examination, imaging . . . , or neurophysical testing . . . that corresponds to the
anatomical location suggested by the symptoms of the clinically isolated syndrome.” Id. The
International Panel cautioned against “accepting symptoms accompanied only by patient-
reported subjective alteration as evidence of a current or previous attack.” Id.

“MS is characterized by discrete demyelinating events separated by at least 4 weeks” in
time. Resp. Ex. H at 2. The dissemination in time requirement, described above, is met when
new lesions have developed or appeared over time. Resp. Ex. C at 2. The dissemination in
space requirement is met when lesions have developed in distinct anatomical locations within the
CNS. Id. In certain situations when dissemination in space is met, but there is no dissemination
in time, a finding of oligoclonal bands in the cerebrospinal fluid (“CSF”) can substitute for the
requirement of dissemination in time. Id. at 5. “Oligoclonal bands are present in the CSF of
more than 85% of patients with clinically definite [MS].” Pet. Ex. 11 at 39. However,
oligoclonal bands can be found in a variety of other diseases. Id.

“The pathological hallmark of MS is the demyelinated regions, referred to as plaques” or
lesions. Pet. Ex. 28 at 1. “The lesions in MS are inflammatory in nature, and the underlying
basis for the pathology is considered to be autoimmune and most likely mediated by activated T
cells to the oligodendrocyte/myelin unit.” Id. at 2. Demyelinated regions show “loss of
oligodendrocytes and . . . variable inflammatory responses consisting of lymphocytes and
macrophages,” and contain activated microglia. Id. at 1. Additionally, “[m]icroglial cells
express activation markers and are, therefore, presumed to play a key role in the disease.” Id.

Although ADEM and MS are both demyelinating diseases of the CNS, they have many
differences that aid in diagnosis. ADEM is more common in children, whereas MS is more
common in adults. Pet. Ex. 97 at 1. Both ADEM and MS patients have lesions, however,
lesions in ADEM patients completely or partially resolve, while new lesions are anticipated in
MS patients. Id. at 2; Resp. Ex. H at 5. Unlike ADEM, encephalopathy is typically not
associated with MS. Pet. Ex. 97 at 1-2; Resp. Ex. H at 2. Additionally, ADEM patients tend to
have a polysymptomatic presentation, whereas MS patients have a monosymptomatic
presentation. Pet. Ex. 97 at 2.

“[F]requently[,] patients originally diagnosed with ADEM relapse and are reclassified as
MS.” Pet. Ex. 97 at 3. The Brighton Collaboration recognized that “ADEM may fall along a

7
continuum of CNS demyelinating disorders that includes [MS]” and “a subset of patients with
suspected ADEM will nonetheless progress to MS.” Pet. Ex. 102 at 5. They found “[t]he
absence of recurrence and monophasic nature of ADEM is useful as a distinguishing feature to
discern ADEM from [MS].” Id. at 8 n.17. They “decided that recurrence of illness following a
3-month interval would be more likely representative of MS, and . . . such recurrence would be
operationally considered MS, and thus ‘not a case’ of ADEM.” Id. Others have found that when
inflammation at an isolated CNS site is “followed by a further neurologic episode in another
CNS site, [it] qualif[ies] for conversion to MS.” Pet. Ex. 101 at 1.

B. Procedural History

Petitioner filed his petition requesting compensation under the Vaccine Act on November
14, 2016.19 Petition at 1. Petitioner filed medical records in May, August, and October 2017.
Petitioner’s Exhibits (“Pet. Exs.”) 1-18. On January 19, 2018, respondent filed his Rule 4(c)
Report, arguing against compensation. Resp. Rept. at 2.

On June 11, 2018, petitioner filed an expert report of Dr. Marcel Kinsbourne. Pet. Ex.
25. Thereafter, petitioner filed additional medical records. Pet. Exs. 19-24. On November 7,
2018, respondent filed an expert report of Dr. Subramaniam Sriram. Resp. Ex. A. Petitioner
filed additional medical records and a supplemental expert report of Dr. Kinsbourne on March
19, 2019. Pet. Exs. 45-59.

A status conference was held on April 11, 2019, where the undersigned ordered the
parties to file additional expert reports further addressing the issues in petitioner’s claim. Order
dated Apr. 15, 2019 (ECF No. 61). In May and June 2019, petitioner filed additional medical
records, a second supplemental expert report of Dr. Kinsbourne, and an expert report of Dr. M.
Eric Gershwin. Pet. Exs. 60-69, 95. Respondent filed a supplemental expert report of Dr. Sriram
on September 26, 2019. Resp. Ex. E.

A Rule 5 conference was held on October 22, 2019. The undersigned preliminarily
concluded there was no firm diagnosis in this case although she noted that an exact diagnosis is
not required to rule on causation. Rule 5 Order dated Oct. 24, 2019, at 1-2 (ECF No. 72) (citing
Contreras v. Sec’y of Health & Hum. Servs., 107 Fed. Cl. 280, 293 (2012); Knudsen v. Sec’y of
Health & Hum. Servs., 35 F.3d 543, 549-50 (Fed. Cir. 1994)). The undersigned encouraged the
parties to resolve the case through settlement negotiations. Id. at 2-3.

Petitioner filed a third supplemental expert report of Dr. Kinsbourne on January 6, 2020,
and respondent filed a second supplemental expert report of Dr. Sriram on July 8, 2020. Pet. Ex.
96; Resp. Ex. G. On October 2, 2020, petitioner filed a supplemental expert report from Dr.
Gershwin. Pet. Ex. 107.

19
Petitioner was pro se from November 14, 2016 until March 6, 2017, when a consented motion
to substitute attorney was filed.

8
An entitlement hearing was held on November 5 and 6, 2020. Petitioner, Dr.
Kinsbourne, Dr. Gershwin, and Dr. Sriram testified. Transcript (“Tr.”) 3, 169. Thereafter,
additional records were filed from both parties. Pet. Ex. 114; Resp. Ex. H.

This matter is now ripe for adjudication.

C. Factual History

1. Medical History Prior to Vaccination and Vaccination

Petitioner had no neurological symptoms prior to vaccination. Pet. Prehearing
Memorandum, filed Sept. 17, 2020, at 1 (ECF No. 94); Joint Prehearing Submission at 1. On
November 15, 2013, at thirty-nine years old, petitioner returned from a medical mission trip in
Bolivia and received a flu vaccine. Pet. Ex. 1 at 1; Pet. Ex. 11 at 1.

2. Medical Treatment from November 16, 2013 to November 23, 2013

Post-vaccination, petitioner received medical diagnoses of acute severe migraine
headache, weakness, and cerebrovascular accident (“CVA”)20 at different times.

On November 16, 2013, petitioner presented to Vista Medical Center East Emergency
Department with a chief complaint of generalized weakness. Pet. Ex. 2 at 3. He stated his
symptoms began at 2:00 PM that day and “came on gradually.” Id. at 6. Petitioner reported he
had “bilateral facial numbness [for 15-20 minutes] and left arm weakness. He fell asleep in his
car today and woke up with a headache. Noted difficulty with speech. No trouble swallowing.”
Id. at 3. Review of systems was positive for headache and numbness and negative for altered
mental status, confusion, weakness, and tingling. Id. at 5. Neurologic physical examination by
Physician Assistant (“PA”) Amee Patel revealed petitioner was awake and alert, intact, and had
slightly decreased sensation to light touch in his left cheek, hand, and ankle. Id. at 3, 6. Motor
examination was normal and symmetric. Id. at 6. Blood work was normal, and a computerized
tomography (“CT”) scan of the head showed no signs of acute disease. Id. at 6-7, 16-20.
Petitioner was diagnosed with generalized weakness and an acute severe migraine headache. Id.
at 7. He was discharged home. Id.

On November 22, 2013, petitioner presented to Community Healthcare System
Emergency Department, complaining of left-sided weakness and drooping in face and left arm
weakness. Pet. Ex. 5 at 2. Registered Nurse (“RN”) Renee I. Thurman documented,
“[petitioner’s] speech [was] clear. [Moves all extremities] with equal strength. Pupils [equal and
reactive to light and accommodation]. Ambulatory and steady. Smile symmetrical. Eyes close

20
CVA, or stroke, is “a condition with sudden onset caused by acute vascular lesions of the
brain, such as infarction from hemorrhage, embolism, or thrombosis, or rupturing aneurysm. It
may be marked by any of a variety of symptoms . . . including hemiparesis, vertigo, numbness,
aphasia, and dysarthria.” Stroke Syndrome, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=111462 (last visited May 4, 2021).

9
normally, but [petitioner] state[d] it feels like his eye does not close normally and it ‘waters’
more than usual.” Id. at 3.

Dr. Carrie Lynn Shaffer, in her physical examination, noted petitioner was alert, oriented
to person, place, and time, and in no distress. Pet. Ex. 5 at 5. Her neurological physical
examination found petitioner had normal gait and deep tendon reflexes, a sensory deficit,
weakness in the left hip flexor and intrinsic muscles of the left hand, and abnormal heel to shin
testing. Id. at 5-6. Dr. Shaffer diagnosed petitioner with weakness of left upper extremity. Id. at
6. She advised petitioner to follow up with Dr. Mark Alan Simaga, and discharged petitioner
home. Id.

The following day, on November 23, 2013, petitioner presented to the Emergency
Department at Porter Health System for continued weakness in his arm and difficulty grasping
items, focusing, and putting together words. Pet. Ex. 5 at 8. Petitioner stated he was diagnosed
with a CVA the previous Saturday and his “symptoms were much worse” then. Id. His nursing
assessment placed his NIH stroke score21 at 10. Id. at 9. Petitioner was seen by Dr.
Vishnuvardhan Rao who documented petitioner’s symptoms that began one week prior were
“almost gone.” Id. Physical examinations conducted by RN Tamara Barnes and Dr. Rao were
inconsistent. Id.

[Petitioner] was able to move his legs with strength when the ataxia exam was
done by Dr. Rao, but [petitioner] [was] unable to hold the legs up during [Ms.
Barnes’] exam. [Petitioner] also required re-focusing many times when he was
getting undressed. He kept “forgetting” what he was doing, and was quick to
apologize and restart the task, but became forgetful and needed to be asked again.

Id. During his physical examination, Dr. Rao found petitioner was well-developed, alert, and
oriented to person, place, and time. Id. at 10. Neurological examination noted “Normal speech, .
. . . Able to express self appropriately. Cranial nerves and [extraocular movements] are intact.
Symmetrical smile. . . . Pupils equal round and reactive to light. Normal symmetric muscle
strength and tone. Cerebellar exam grossly intact. Normal finger nose finger exam with
overshooting.” Id. Petitioner complained “pinprick [was] less sharp or [was] dull on the
affected side[] or there [was] a loss of superficial pain with pinprick, but [petitioner] [was] aware
of being touched.” Id. Dr. Rao ordered labs, electrocardiogram (“EKG”), and brain MRI. Id. at
11. All tests were normal. Id. at 12, 18. The MRI showed no evidence of a demyelinating
disorder. Id. at 18. Petitioner was diagnosed with paresthesia and stroke/CVA. Id. at 14-17.
Petitioner was discharged home. Id. at 13.

21
A stroke score is “any of various scoring systems that seek to characterize a patient’s clinical
state following a stroke.” Stroke Score, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=105180 (last visited May 4, 2021); see
also NIH Stroke Scale, Nat’l Insts. Health, https://www.stroke.nih.gov/resources/scale.htm (last
visited May 4, 2021).

10
3. Medical Treatment from January 14, 2014 to May 6, 2014

During this time period, petitioner received diagnoses of transient ischemic attack
(“TIA”),22 hemiplegic migraine,23 and CVA.

Petitioner next sought medical treatment on January 14, 2014 with neurologist, Dr.
Simaga.24 Pet. Ex. 6 at 1. Dr. Simaga diagnosed petitioner with TIA and hemiplegic migraine.
Id. Numerous tests, including labs and MRIs, were ordered, and petitioner was prescribed
Plavix.25 Id.

Petitioner presented to Dr. Krista Molina on January 29, 2014 to establish care with a
primary care physician for insurance purposes. Pet. Ex. 11 at 1; Pet. Ex. 6 at 3. Petitioner
reported he returned from Bolivia in November and had a flu shot the same day.26 Pet. Ex. 11 at
1. Petitioner repeated his history of developing confusion and weakness the day following
vaccination, and complained of continued weakness. Id. Review of systems noted decreased
coordination and residual weakness in left leg and foot. Id. On exam, petitioner was alert and
oriented to person, place, and time. Id. at 1-2. He had a sensory deficit, normal coordination,
decreased grip strength in left hand, and weakness in left lower extremity, hip flexors, and knee
flexors. Id. at 2. He was diagnosed with TIA, left arm weakness, left leg weakness, and left
facial numbness. Id. Dr. Molina was concerned for CVA and CNS vasculitis,27 “especially
given that his symptoms occurred the day after receiving a flu vaccine.” Id. Tests, including

22
TIA is “a brief attack (from a few minutes to an hour) of cerebral dysfunction of vascular
origin, with no persistent neurologic deficit.” Transient Ischemic Attack, Dorland’s Med.
Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=59631 (last visited
May 4, 2021).
23
Hemiplegic migraine is a “migraine associated with varying degrees of transient hemiplegia or
hemiparesis.” Hemiplegic Migraine, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=89344 (last visited May 4, 2021).
24
Petitioner testified that he did not have health insurance until January 2014, and this was the
first available appointment. Tr. 16, 23-24.
25
Plavix, a trademark of clopidogrel bisulfate, is “an inhibitor of platelet aggregation used as an
antithrombotic.” Plavix, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/
dorland/definition?id=39538 (last visited Apr. 14, 2021); Clopidogrel Bisulfate, Dorland’s Med.
Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=10156 (last visited
Apr. 14, 2021).
26
According to petitioner’s testimony at the hearing, he returned from Bolivia on November 11
and received the flu vaccine at issue on November 15, 2013. Tr. 12-13.
27
Vasculitis is the “inflammation of a blood or lymph vessel.” Vasculitis, Dorland’s Med.
Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=52617 (last visited
May 4, 2021).

11
labs and MRIs, were re-ordered, petitioner was referred to neurology, and he was encouraged to
start taking Plavix daily and continue Pravachol.28 Id.; Pet. Ex. 6 at 3-4.

A duplex carotid doppler was conducted on January 29, 2014 and found no significant
plaque or hemodynamically significant stenosis of the right or left carotid, and vertebral arteries
showed normal antegrade flow. Pet. Ex. 6 at 12-13. An EKG was also conducted on January 29,
2014 and was normal. Id. at 36-37. Petitioner’s symptoms were noted to have “started 1 day
after flu shot, 2 days after a long plane trip.”29 Id. at 36.

On February 8, 2014, multiple tests were conducted. A brain MRI without contrast was
done and compared to petitioner’s November 23, 2013 brain MRI. Pet. Ex. 6 at 14. The MRI
was normal, and no significant changes were noted. Id. at 14-15. A head magnetic resonance
angiography (“MRA”) without contrast showed “hypoplasia of the left anterior cerebral artery
and right vertebral artery . . . which represent anatomic variants. The study [was] otherwise
unremarkable.” Id. at 16 (emphasis omitted). An MRA of the carotid arteries without contrast
was conducted and was unremarkable. Id. at 18. Blood tests were normal, petitioner’s ANA was
negative, and petitioner’s vitamin D level was low. Id. at 20-27.

Petitioner returned to Dr. Simaga on February 20, 2014, who reiterated the diagnoses of
TIA and hemiplegic migraine. Pet. Ex. 6 at 6. Petitioner also saw Dr. Alexander Molina30 at his
primary care physician’s office on February 20, 2014 for a follow-up exam. Pet. Ex. 11 at 4.
Petitioner reiterated his complaints of left-sided weakness and added a complaint of neck pain
that had been present for several months. Id. Dr. Molina added that petitioner was “[n]ot getting
worse but not improving.” Id. Dr. Molina found petitioner was alert and oriented to person,
place, and time, and had a sensory deficit and normal coordination. Id. Physical examination
revealed petitioner continued to have decreased grip strength in his left hand as well as weakness
in his left lower extremity, hip flexors, and knee flexors. Id. at 5. Dr. Molina diagnosed
petitioner with a CVA (cerebral infarction) and cervical pain (neck). Id.

On April 5, 2014, petitioner presented to Porter Regional Hospital Emergency Room
complaining of “[s]udden onset of left parietal headache associated with left facial numbness and
left upper extremity numbness and weakness with abnormal gait” that began at 4:00 AM that
morning. Pet. Ex. 14 at 35. Petitioner reported that “this headache was much different than his
usual migraine headache” and lasted until 8:00 AM. Id. Petitioner added that “his left face was
feeling numb and had abnormal sensation associated with abnormal sensation in the left upper

28
Pravachol, a trademark of pravastatin sodium, is an antihyperlipidemic agent. Pravachol,
Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?
id=40665 (last visited Apr. 14, 2021); Pravastatin Sodium, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=40666 (last visited Apr. 14, 2021).
29
Again, petitioner testified at the hearing that he returned from Bolivia on November 11 and
was vaccinated on November 15, 2013. Tr. 12-13.
30
This is the only visit to Dr. Alexander Molina. The remaining visits to a Dr. Molina were with
Dr. Krista Molina.

12
extremity with left upper extremity feeling weak.” Id. Petitioner reported that he was walking
with a limp. Id. Petitioner reiterated his November 2013 symptoms and reported that he had
“been fairly healthy” since then. Id.

Dr. Swati Singh documented petitioner was alert, oriented to person, place, and time, and
in no distress. Pet. Ex. 14 at 36. Cranial nerves were intact. Id. Motor strength in left upper and
lower extremity were decreased. Id. Petitioner exhibited decreased sensation to touch in left
face and left upper extremity. Id. Cerebellar examination was within normal limits. Id.
Urinalysis, blood work, CT, and MRI were normal. Id. An EKG showed sinus rhythm with
early R-wave transition. Id. Dr. Singh diagnosed petitioner with left face numbness, left face
and left-sided weakness and paresthesia, TIA versus complicated migraine, as well as borderline
dyslipidemia. Id. at 36-37. Petitioner was admitted for observation. Id. at 37.

On the following day, April 6, 2014, petitioner underwent a neurology consult by Dr.
Arkadiy Konyukhov. Pet. Ex. 14 at 38. Dr. Konyukhov noted that a repeat MRI of petitioner’s
brain conducted the day before was normal, “except possible very small FLAIR hyperintensity in
the right parieto-occipital white matter.” Id. Dr. Konyukhov, on physical examination,
documented petitioner was in no acute distress, alert, and oriented to person, place, and time. Id.
at 38-39. Petitioner’s speech and language were normal. Id. at 39. Extraocular movements were
intact, and he had normal tongue and shoulder movements. Id. Dr. Konyukhov noted decreased
facial sensation in the V2 distribution on the left side, and slight weakness in left arm, leg, and
intrinsic muscles of hand. Id. Left side sensory examination was normal. Id. Dr. Konyukhov’s
assessment was “[l]eft-sided weakness resolving as well as numbness.” Id. An MRI of the
cervical spine was recommended. Id. Petitioner’s discharge diagnosis was “probable hemiplegic
migraines” or dyslipidemia. Id. at 40.

MRIs of petitioner’s thoracic and cervical spines with and without contrast were
conducted on May 6, 2014. Pet. Ex. 7 at 30-33. The MRIs were unremarkable, and no lesions
were seen. Id.

4. Medical Treatment from July 1, 2014 to December 23, 2014

Beginning in July 2014, petitioner’s treating physicians considered a diagnosis of a
demyelinating disease.

On July 1, 2014, petitioner returned to Porter Regional Hospital for a lumbar puncture.
Pet. Ex. 7 at 3; Pet. Ex. 11 at 23. Petitioner’s CSF showed normal protein at 32 (range 15-45),
normal glucose at 63 (range 40-70), no cytomegalovirus, no growth or organisms on gram stain,

13
no white blood cells in the CSF, and five well-defined oligoclonal bands in the CSF that were not
present in the corresponding serum sample.31 Pet. Ex. 11 at 23-39.32

Petitioner returned to Dr. Konyukhov on July 14, 2014 to review his test results. Pet. Ex.
7 at 3. Petitioner reported episodes of tingling on left side of body and periodic tingling on right
side of body. Id. Dr. Konyukhov’s examination revealed normal facial sensation, no facial
droop, and normal motor examination. Id. Petitioner’s strength was normal in upper and lower
extremities, “except [for] the subtle and [possibly] effort dependent” slight weakness in left arm
and leg, and “very minimal” weakness in intrinsic muscles of the left hand. Id. at 3-4 (emphasis
omitted). Sensory examination was normal except for decreased sensation in the left ulnar
distribution. Id. at 4. Casual and tandem gait were normal. Id. Dr. Konyukhov noted
“[petitioner’s] age might indicate demyelinating disease. It could be clinically isolated
syndrome. However[,] MRI[s] . . . were normal, as well as MRA.” Id. Some test results from
petitioner’s lumbar puncture remained pending as of this visit. Id. Dr. Konyukhov diagnosed
petitioner with disturbance of skin sensation and left hemiplegia. Id.

On July 24, 2014, petitioner saw Dr. Krista Molina with complaints of residual left-sided
weakness and new complaints of left hip pain for the past two-to-three months. Pet. Ex. 11 at 6.
Dr. Molina documented that petitioner’s hip pain “does not radiate and is intermittent,” but made
worse when standing or walking. Id. “[Petitioner] wonder[ed] if he should see an immunologist
since the neurologist told him he thinks his symptoms were due to an immunologic response to
the flu vaccine.” Id. Review of systems was positive for arthralgias and weakness. Id. Dr.
Molina’s physical examination revealed petitioner was alert and oriented to person, place, and
time. Id. at 6-7. He had normal range of motion and no tenderness to palpitation in left hip. Id.
at 6. Neurological examination was normal. Id. at 7. Dr. Molina diagnosed petitioner with
hyperlipidemia, left-sided weakness and joint pain, left hip pain, and a vitamin D deficiency. Id.
Petitioner was referred to physical therapy33 and rheumatology, and labs were ordered. Id.

Petitioner presented to the emergency room at Advocate Sherman Hospital on July 30,
2014. Pet. Ex. 9 at 4. Petitioner reported feeling paresthesias, weakness, tingling, and loss of
sensation on the left side of his body beginning at 5:00 AM. Id. at 21. Petitioner also reported
difficulty speaking, driving, and walking. Id. Petitioner was admitted for further care and
observation. Id.

31
The test result comment regarding petitioner’s five oligoclonal bands added, “[t]his finding is
supportive evidence of [MS], but should be interpreted in conjunction with all clinical and
laboratory data pertaining to this patient. Oligoclonal bands are present in the CSF of more than
85% of patients with clinically definite [MS].” Pet. Ex. 11 at 39. “Oligoclonal bands can
however be observed in a variety of other diseases . . . . The data should be interpreted in
conjunction with all pertinent clinical laboratory data for this patient.” Id.
32
Dr. Gershwin testified that petitioner tested positive for ANA antibodies in July 2014. Tr. 162.
However, due to the way the records were scanned, the laboratory results are difficult to read and
the undersigned was unable to find ANA results from July 2014.
33
Petitioner did not use this referral to attend physical therapy. Pet. Ex. 11 at 8.

14
Dr. Gilbert Egekeze conducted a physical examination. Pet. Ex. 9 at 22-23. His
examination revealed petitioner was awake, alert, oriented to person, place, and time, in no
cardiopulmonary distress, but “a little bit unstable on his feet.” Id. at 22. His neurologic
examination revealed no focal deficits. Id. at 23.

While at the hospital, petitioner had a neurology consultation by Dr. Syed Munzir on July
30, 2014. Pet. Ex. 9 at 25. Dr. Munzir documented a neurologic examination that showed
petitioner was awake, alert, and oriented to person, place, and time, and his speech was fluent.
Id. at 26. “Motor examination of the extremities revealed poor effort on the left side with hand
grasp. There was some give-way weakness affecting the proximal upper extremity, right
shoulder abduction, but estimated strength was 5/5.” Id. Additionally, “[l]ower extremity
strength, left foot dorsiflexion and plantar flexion was 5/5. Hip flexion and knee flexion was at
least 4/5, but demonstrated give-way weakness. Right-sided strength was normal. Deep tendon
reflexes were 2+ bilaterally and symmetric and plantar responses were flexor bilaterally. Gait
was slow but steady.” Id. Musculoskeletal examination was unremarkable. Id. at 27. Dr.
Munzir suspected petitioner had a complicated migraine and recommended a brain MRI. Id.
MRI, CT, and EKG were normal. Id. at 21, 23.

On July 31, 2014, Dr. Munzir’s neurologic examination revealed petitioner was awake,
alert, and oriented to person, place, and time. Pet. Ex. 9 at 19. He found petitioner “was able to
rise from the bed without any significant difficulty and he stood up on his feet.” Id. “[Petitioner]
walked lifting his left leg up and not dragging, and [Dr. Munzir did] see that he was able to
dorsiflex his foot while walking. While walking, [petitioner] tend[ed] to complain of some
feeling of weakness. Isometric strength testing showed give way weakness of the left lower
extremity.” Id. Dr. Munzir found petitioner was likely presenting with a complex migraine. Id.

On July 31, 2014, after Dr. Munzir’s neurology consultation, Dr. Egekeze’s diagnoses
were left-sided paresthesias and weakness and possible hemiplegic migraine. Pet. Ex. 9 at 23.
Petitioner was discharged home. Id. Dr. Egekeze wrote a note dated July 31, 2014, in which he
stated petitioner’s “etiology [was] currently unclear” and “recommend[ed] the [petitioner]
abstain[] from vaccinations at this time until a clear diagnosis.” Pet. Ex. 8 at 1.

On the following day, August 1, 2014, petitioner saw Dr. Konyukhov. Pet. Ex. 7 at 1.
Petitioner reported his recent hospitalization. Id. Physical examination revealed normal facial
sensation, no facial droop, and normal motor examination. Id. Again, Dr. Konyukhov found
strength normal in upper and lower extremities except for subtle weakness in left arm, leg, and
intrinsic muscles of hand. Id. at 1-2. Some crossing of the reflexes at the knees were noted. Id.
at 2. Sensory examination was normal except for decreased sensation in the left ulnar
distribution. Id. Normal coordination and ambulation were documented. Id. Dr. Konyukhov
noted the presence of oligoclonal bands along with left-sided weakness. Id. at 2. He found the
recent complaint of “right-sided weakness could be indication of 2 different attacks separated in
time. Therefore, [MS], still in the differential. It is somewhat unusual that there is still no
lesion[] present on the MRI.” Id. (emphasis omitted). Diagnoses included disturbance of skin
sensation, left hemiplegia, and MS. Id. Dr. Konyukhov recommended petitioner be evaluated at
Indiana University. Id.

15
On August 18, 2014, petitioner presented to Dr. Jaison A. Grimes34 at Indiana University
due to concern for demyelinating illness. Pet. Ex. 45 at 1. Petitioner repeated his medical
history. Id. Petitioner reported “[h]e continues to have significant issues with his left upper and
lower extremity and . . . his right side has returned to baseline.” Id. Petitioner stated his
symptoms are worse when he is extremely overheated or fatigued. Id. Under review of systems,
petitioner reported fatigue, energy loss, confusion, minor swallowing dysfunction, paresthesias
and weakness in extremities, and occasional difficulties with gait. Id. at 2. Petitioner was alert,
oriented to person, place, situation, and date, and in no acute distress. Id. Neurologic
examination revealed slight weakness of left upper extremity, give way weakness on bilateral hip
flexion, and mild weakness on left knee flexion. Id. “There was some very mild impairment to
tandem gait.” Id. Dr. Grimes reviewed petitioner’s July 30, 2014 MRIs and MRA and found
them unremarkable. Id. He further found petitioner’s remaining testing unremarkable other than
petitioner’s July 1, 2014 CSF, which “note[d] the presence of 5 well-defined gamma restriction
bands that are not present in the corresponding serum sample.” Id. Dr. Grimes found “[i]t a bit
atypical that the patient’s symptoms are so severe without a corresponding lesion on imaging,
but the presence of oligoclonal bands is suggestive that this could be an atypical presentation of
demyelinating disease.” Id. He recommended petitioner wean his corticosteroids and try an
immunomodulating therapy, specifically Tecfidera.35 Id. Dr. Grimes ordered evoked responses
to assess for potential lesions “to aid in diagnosis of [MS], as it does appear that the [petitioner]
has had at least 2 separate events,” and repeat MRIs of brain and spine. Id. at 3.

On August 29, 2014, brainstem auditory, visual, and somatosensory evoked potentials36
were normal. Pet. Ex. 7 at 35. On August 30, 2014, petitioner underwent MRIs of his lumbar,
cervical, and thoracic spine with and without contrast. Pet. Ex. 62 at 13-17. The MRI of his
lumbar spine showed degenerative disc disease at L5-S1. Id. at 14. The MRI of his cervical

34
Dr. Jaison A. Grimes is an MS specialist at Indiana University. Tr. 35-36, 199.
35
Tecfidera is a drug used to treat patients with MS. Tr. 92, 205-07.
36
An evoked potential is “the electrical signal recorded from a sensory receptor, nerve, muscle,
or area of the central nervous system that has been stimulated, usually by electricity.” Evoked
Potential, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/
definition?id=99671 (last visited May 4, 2021). A brainstem auditory evoked potential is “that
portion of the auditory evoked potential which comes from the brainstem” and can be used “to
support diagnosis of [MS].” Brainstem Auditory Evoked Potential, Dorland’s Med. Dictionary
Online, https://www.dorlandsonline.com/dorland/definition?id=99675 (last visited May 4, 2021).
A visual evoked potential looks at “changes in the evoked cortical potential when the eye is
stimulated by light” and “variations are diagnostic for . . . neurologic disorders such as [MS].”
Visual Evoked Potential, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/
dorland/definition?id=99729 (last visited May 4, 2021). Lastly, a somatosensory evoked
potential looks at “waves recorded from the spinal cord or cerebral hemisphere after electrical
stimulation or physiologic activation of peripheral sensory fibers” and “deviations in latency or
amplitude can detect or characterize lesions.” Somatosensory Evoked Potential, Dorland’s Med.
Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=99723 (last visited
May 4, 2021).

16
spine revealed a mild disc bulges with no focal disc protrusion or central canal stenosis, as well
as bilateral foraminal narrowing in C6-7. Id. at 16. His thoracic spine MRI also showed minor
disc bulges with no spinal canal stenosis. Id. at 17. There were no lesions characteristic of MS
reported.

On October 1, 2014, petitioner was tested for neuromyelitis optica (“NMO”)37 antibodies,
which were not detected. Pet. Ex. 7 at 43-44. It was noted that “seronegativity does not
necessarily preclude a diagnosis of [NMO].” Id.

On December 10, 2014, petitioner saw Dr. Molina for a follow up and complaints of
continued left-sided weakness as well as new onset of right-sided weakness that began in July.
Pet. Ex. 11 at 8. Review of systems was positive for arthralgias, myalgias, confusion, and
weakness. Id. Petitioner reported “[r]ight arm and hand always feel colder than the left,
occasional tingling on the left of the head.” Id. Dr. Molina’s physical examination noted
petitioner was alert and oriented to person, place, and time. Id. Musculoskeletal examination
noted petitioner had weakness of left upper and lower extremity. Id. Neurological examination
was normal. Id. at 8-9. Dr. Molina diagnosed petitioner with left-sided weakness, history of
TIA, hyperlipidemia, and a Vitamin D deficiency. Id. at 9. Upon request, Dr. Molina provided
petitioner with a new referral to physical therapy. Id. at 8-9.

Dr. Molina provided a letter dated December 10, 2014, stating petitioner “had a severe
reaction to the flu vaccine previously which resulted in long-lasting neurological deficits.
Because of this, further [flu] vaccination is contraindicated.” Pet. Ex. 8 at 2. Similarly, Dr.
Gillespie provided a letter dated December 10, 2014, recommending petitioner “avoid any
vaccines” at this time. Id. at 3.

On December 23, 2014, petitioner underwent an MRI of his cervical spine with and
without contrast. Pet. Ex. 62 at 9. Mild degenerative disc disease at C4-5 and C5-6 was found,
otherwise the MRI was normal. Id. A brain MRI with and without contrast was also conducted
and was unremarkable. Id. at 11.

5. Medical Treatment in 2015

Petitioner returned to Dr. Gillespie on January 14, 2015, complaining of fatigue, joint
pain, and back pain. Pet. Ex. 10 at 10. Petitioner had been off steroids for three weeks and
stated he was at 90% of baseline and feeling generally well. Id. at 11. Petitioner was alert and in
no acute distress. Id. Dr. Gillespie’s assessment was weakness and pain in face, upper
extremity, lower extremity, abnormal liver function tests, reactive arthritis,
hypogammaglobulinemia, and back pain. Id. at 12. She recommended intermittent steroid
dosing and a neurology follow up with Dr. Grimes. Id.

37
NMO is the “combined, but not usually clinically simultaneous, demyelination of the optic
nerve and the spinal cord; it is marked by diminution of vision and possibly blindness, flaccid
paralysis of the extremities, and sensory and genitourinary disturbances.” Neuromyelitis Optica,
Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=
92610 (last visited May 4, 2021).

17
On February 5, 2015, petitioner followed up with Dr. Grimes. Pet. Ex. 52 at 6. Dr.
Grimes noted petitioner started taking dimethyl fumarate (Tecfidera), but if he missed a dose, he
had a recrudescence of his symptoms. Id. at 6-7. He reviewed petitioner’s December 2014
MRIs and found the studies unremarkable. Id. at 7. Petitioner was in no acute distress, alert, and
oriented to person, place, situation, and date. Id. Neurological examination revealed petitioner
had “full power” in right extremities, and almost full strength in the left extremities.38 Id. Dr.
Grimes opined petitioner had “dysesthesias and transient weakness of unclear etiology.” Id. He
found petitioner did not meet criteria for MS. Id. If he did, it would likely be a progressive
form. Id. He recommended petitioner see a neuromuscular specialist. Id.

Petitioner returned to Dr. Gillespie on March 20, 2015. Pet. Ex. 10 at 8. Petitioner
continued to have “persistent” left-sided weakness. Id. Petitioner was “[w]orried about vascular
causes” and vasculitis. Id. at 9. On examination, Dr. Gillespie noted petitioner was alert, in no
acute distress, “able to rise from a seated position but more difficulty from low seated position,”
had no distal weakness, and some decreased range of motion at his left hip. Id. at 9. Her
assessment was “neurologic symptoms of weakness and pain in face, [upper extremity], [lower
extremity], abnormal [liver function tests], reactive arthritis, hypogammaglobulinemia now with
features of myopathy and labs consistent with myopathy.” Id. at 10. She noted that petitioner’s
ANA was positive. Id. Dr. Gillespie’s plan included an MRI of left lower extremity and likely a
muscle biopsy. Id.

An MRI of petitioner’s left hip and thigh was conducted on March 23, 2015, and it was
normal. Pet. Ex. 10 at 23-24. Incidentally, petitioner had an allergic reaction to the intravenous
contrast used. Id. Petitioner underwent an EMG of the left arm and leg on April 24, 2015,
which were both normal. Pet. Ex. 52 at 11-13.

On May 6, 2015, petitioner returned to Dr. Gillespie with complaints of persistent
episodes of hip weakness, dorsiflexion weakness, persistent intermittent facial asymmetry,
slower thought process, and feeling very sleepy. Pet. Ex. 10 at 6. Petitioner reported having
pruritus and erythema prior to this episode of muscle weakness. Id. Petitioner had been taking
prednisone for the past three days. Id. Dr. Gillespie’s physical examination revealed petitioner
was alert and in no acute distress. Id. at 7. Examination was normal other than slight facial
asymmetry. Id. Assessment was “positive ANA, neuropathic symptoms, myopathic symptoms,
oligoclonal bands.” Id. Dr. Gillespie’s gave petitioner a referral for a muscle biopsy, agreed
with his prednisone use, ordered an ANA panel, and planned to follow up with EMG results. Id.

Petitioner next saw Dr. Gillespie on June 10, 2015. Pet. Ex. 10 at 3. Petitioner was
“feeling generally well,” but complained of “some persistent pain and weakness in left leg,”
“some [mild] residual weakness in left arm and legs,” and “some decreased grip strength.” Id. at
4. Petitioner was off prednisone for two months and was on propranolol for tremors. Id.
Physical examination was normal. Id. at 5. Petitioner’s muscle biopsy showed no evidence of
inflammatory changes. Id. Dr. Gillespie believed petitioner had a “primary neurologic process.”
Id.

38
Dr. Grimes’ record stated, “[petitioner] has full power in the right upper and lower extremity.
The left upper and lower extremity have grade diffusely as a 5/-5.” Pet. Ex. 52 at 7.

18
On October 1, 2015, petitioner underwent a brain MRI that showed a 2 mm focus of
signal abnormality within the periventricular white matter, which was noted to be an isolated
finding and nonspecific. Pet. Ex. 62 at 8. The same day, a cervical spine MRI revealed no
significant change from prior study and no signal alteration within the spinal cord to suggest a
demyelinating process. Id. at 6-7. A thoracic spine MRI was also unremarkable. Id. at 5.

Petitioner saw Dr. Molina on October 29, 2015 for a follow up and medication refill. Pet.
Ex. 11 at 10. Petitioner reported “recurrent episodes of muscle pain and weakness.” Id.
Petitioner stated he was taking Tecfidera for presumed MS even though Dr. Grimes’ records
indicated that they did not suspect MS. Id. Petitioner was also “taking propranolol for a
question of hemiplegic migraines.” Id. He reported going to the emergency room one week
earlier for racing heart and a high heart rate, and all testing was normal. Id. Dr. Molina’s
physical examination was normal. Id. Diagnoses included hyperlipidemia; essential tremor;
“[m]igraine without aura and without status migrainosus, not intractable;” palpitations; left-sided
weakness; history of Vitamin D deficiency; and dyspnea on exertion. Id.

6. Medical Treatment in 2016

Petitioner returned to Dr. Gillespie on February 11, 2016, reporting that he started
treatment for MS in the past six months with “some benefit.” Pet. Ex. 10 at 1. He reported an
episode of upper extremity weakness over Thanksgiving, which improved with steroids. Id. He
complained of joint pain in hands and chronic neck pain. Id. Petitioner was alert and in no acute
distress, he had no swollen joints, but was tender at the right 3-5 proximal interphalangeal joints.
Id. at 2. Dr. Gillespie attributed petitioner’s symptoms to an “[a]pparent response to MS
treatment.” Id. She recommended petitioner follow up with neurology and ordered more labs.
Id.

On September 8, 2016, petitioner underwent repeat MRIs of his cervical and thoracic
spine as well as his brain. Pet. Ex. 62 at 1-4. Petitioner’s cervical spine MRI revealed C4-5
central disc protrusion, no evidence of central canal stenosis, and no abnormal signal within the
cervical spinal cord. Id. at 2. MRI of his thoracic spine was normal. Id. at 3. Petitioner’s MRI
of his brain showed “nonspecific T2 flair signal hyperintensities within the frontal periventricular
white matter regions bilaterally similar to the prior exam.” Id. at 4 (emphasis omitted).

Petitioner presented to Dr. Konyukhov on October 20, 2016 for “possible MS follow up.”
Pet. Ex. 12 at 1. Petitioner reported the history of intermittent episodes of weakness, numbness,
and tingling, mostly on the left side, which “[h]e originally attributed to the [flu] vaccination.”
Id. He reported getting better every time he was treated with steroids. Id. Dr. Konyukhov noted
repeat MRIs did not show any abnormalities, and a MS specialist from Indiana University
“considered possibility of [MS] even without any lesions and therefore placed [petitioner] on
Tecfidera.” Id. Dr. Konyukhov reviewed the September 2016 MRIs and did not see any
nonspecific white matter lesions. Id. Petitioner was in no apparent distress, alert, and oriented to
person, place, and time. Id. at 2-3. Dr. Konyukhov’s neurological examination was normal
except for mild decreased strength in left arm and leg. Id. at 3. In his assessment, Dr.
Konyukhov wrote petitioner’s “intermittent episodes of weakness and numbness . . . could be
suggestive of some kind of problem in the brain (MS), but so far MRIs not showing any clear

19
lesions.” Id. at 4. He recommended petitioner continue taking Tecfidera and have a repeat MRI
in one year. Id.

7. Medical Treatment in 2017

On March 23, 2017, petitioner had a follow up visit with Dr. Konyukhov. Pet. Ex. 12 at
5. Petitioner reported an episode of weakness in his legs and problems swallowing in November
2016. Id. Petitioner was alert and oriented to person, place, and time during physical
examination. Id. at 7. Neurologic examination performed by Dr. Konyukhov revealed mild
weakness in the left arm and leg. Id. Dr. Konyukhov’s assessment was unchanged since
petitioner’s last visit in October 2016. Id.

In May and June 2017, petitioner presented to the emergency room on multiple occasions
for throat tightness and itching thought to be due to an allergic reaction. Pet. Ex. 15 at 5-6, 22-
23, 69-70, 88-89.

On August 18, 2017, petitioner presented to Nurse Practitioner, Jennifer Davison. Pet.
Ex. 16 at 1. Petitioner reported “he probably has MS after a flu vaccine and had a reaction and
was paralyzed on the left side.” Id. Petitioner also said that in the one to two years following
vaccination, he developed allergies to everything, making breathing and swallowing difficult,
and requested a referral to an allergist. Id. He reported difficulty breathing while sleeping. Id.
Under review of symptoms, Ms. Davison noted “[petitioner] report[ed] MS” and petitioner was
concerned that “MS flares also cause difficulty swallowing.” Id. Physical examination was
normal. Id. at 1-2. Diagnoses included history of allergic reactions, sleep apnea, and MS. Id. at
2.

On August 23, 2017, petitioner saw allergist Dr. Jatinder K. Kansal, who documented
petitioner’s report of onset of neurological symptoms one day after his flu vaccine in 2013, and
added “[f]inal conclusion might be reaction to flu.” Pet. Ex. 17 at 1. Allergy testing conducted
on September 15, 2017 was negative for everything except histamine. Id. at 8.

Petitioner returned to Dr. Molina on September 18, 2017 “for medically necessary follow
up of MS and with [complaints of] dysphagia/difficulty swallowing.” Pet. Ex. 16 at 3. Petitioner
reported his MS was bad over the summer. Id. Petitioner reported that he went to the emergency
room a couple of times for “what he thought was due to some type of systemic allergic reaction”
but “he was told that his symptoms were not due to allergies and more likely to be due to the
MS.” Id. Petitioner stated he had “several exacerbations of the MS where he has been unable to
walk and has had to use a wheelchair.” Id. He added that he was taking Tecfidera. Id. Dr.
Molina, on examination, stated petitioner was oriented to person, place, and time. Id. Her
neurologic examination revealed “[m]ildly decreased grip strength in left hand [and] mildly
decreased flexor strength in legs bilaterally (R>L).” Id. at 4. Diagnoses included MS and
dysphagia. Id. MRIs and labs were ordered, petitioner was referred to speech therapy and
gastroenterology, and petitioner was prescribed Tecfidera. Id.

A brain MRI conducted on September 26, 2017 revealed “a few tiny faint punctate
FLAIR hyperintense foci in the bifrontal periventricular white matter,” but it was otherwise

20
unremarkable. Pet. Ex. 61 at 1. The impression was “[s]table brain MRI with very minimal
nonspecific supratentorial white matter changes.” Id. Petitioner’s MRI of his cervical spine
found no evidence of plaques in the spinal cord, and his thoracic spine MRI was unremarkable.
Id. at 2-3. Petitioner began speech therapy on September 27, 2017. Pet. Ex. 25 at 11.

Petitioner returned to Dr. Gillespie on October 10, 2017 reporting a flare up in March,
including difficulty swallowing and weakness in lower extremity and hands. Pet. Ex. 21 at 1.
Petitioner reported persistent weakness in hands and worsening difficulty with swallowing. Id.
Physical examination was normal. Id. at 2-3. Dr. Gillespie recommended petitioner follow up
with neurology for “[a]pparent MS variant.” Id. at 3.

On October 16, 2017, petitioner was seen by PA John S. Emmett at Indiana University
for a follow up. Pet. Ex. 19 at 1. Mr. Emmett noted the “few nonspecific punctate white matter
hyperintensities” on petitioner’s September 26, 2017 MRI that were unchanged from petitioner’s
last MRI. Id. Petitioner reported taking Tecfidera for the past three years. Id. Petitioner
reported several episodes of weakness over the past year as well as episodic swallowing
difficulties. Id. Mr. Emmett’s neurological examination of petitioner was normal, noting full
strength in all extremities. Id. at 1-2. Mr. Emmett wrote petitioner has a “self reported [history]
of relapsing MS,” and “[w]hen Dr. Grimes saw him, MS was not suspected given lack of exam
findings and relative lack of typical MRI changes.” Id. at 2. He was concerned about the risk of
progressive multifocal leukoencephalopathy (“PML”), and planned to test for John Cunningham
(“JC”) virus,39 noting that the results may require petitioner to be taken off Tecfidera. Id. Mr.
Emmett’s assessment was weakness. Id. at 2.

Petitioner began physical therapy and occupational therapy in October 2017. Pet. Ex. 24
at 42, 45. Petitioner underwent a swallow study on October 31, 2017, which was normal. Pet.
Ex. 23 at 15.

8. Medical Treatment from 2018 to 2019

On January 12, 2018, petitioner saw Dr. Gillespie, who noted that petitioner reported
testing positive for the JC virus and thus, he was taken off Tecfidera. Pet. Ex. 95 at 5.

Petitioner visited Dr. Chad Glazer, an otolarynologist, on February 21, 2018 to establish
care. Pet. Ex. 49 at 7. He requested an evaluation of dysphagia and difficulty breathing at night.
Id. Petitioner underwent an esophageal motility study and the impression was ineffective
esophageal motility. Id. Physical examination indicated bilateral small tonsil stones. Id. at 10.
Dr. Glazer explained to petitioner that “MS can cause difficulty with swallowing as this takes the
coordination of multiple muscles.” Id. at 11. Dr. Glazer’s assessment was dysphagia, sleep
disorder breathing, tonsil stones, and MS. Id.

39
JC virus “is the cause of progressive multifocal leukoencephalopathy,” which has been known
to occur in MS patients treated with Tecfidera. JC Polyomavirus, Dorland’s Med. Dictionary
Online, https://www.dorlandsonline.com/dorland/definition?id=99364 (last visited Apr. 14,
2021); see Tecfidera, RxList, https://www.rxlist.com/tecfidera-drug.htm (last reviewed Mar. 13,
2020).

21
On March 12, 2018, petitioner visited Dr. Molina for a follow up examination of a recent
hospitalization due to an allergic reaction. Pet. Ex. 48 at 19. Petitioner did not complain of any
weakness. See id. Dr. Molina noted petitioner was not taking Tecfidera. Id. at 20.

Petitioner followed up with Dr. Glazer on April 18, 2018. Pet. Ex. 49 at 1. A flexible
laryngoscopy was performed. Id. at 5. The post-operative diagnoses were dysphasia and
paradoxical vocal cord motion. Id. Dr. Glazer’s assessment was left tinnitus, dysphasia, sleep
disorder breathing, and paradoxical vocal cord motion. Id. at 5-6.

Petitioner returned to Dr. Konyukhov on January 22, 2019 for a follow up. Pet. Ex. 53 at
5. Petitioner reported an MS flare up in February 2018 where he was hospitalized and had
trouble walking, swallowing, and speaking. Id. On physical examination, Dr. Konyukhov found
“some exaggerated physiological tremor . . . in both hands, [but] worse on the right side,” and
decreased strength in lower extremities with “somewhat poor effect.” Id. at 7-8. He assessed
petitioner with weakness. Id. at 8. Dr. Konyukhov noted “[n]o obvious diagnosis [so] far
despite seeing multiple different physicians.” Id.

The following day, on January 23, 2019, petitioner saw Dr. Molina. Pet. Ex. 48 at 1.
Petitioner reported one relapse since February 2018 and complained of continued swallowing
difficulty. Id. Physical examination was normal. Id. at 4-5. Under diagnoses, Dr. Molina listed
hyperlipidemia, MS, muscle spasm, Vitamin D deficiency, osteoporosis of lumbar spine, and
“[a]dverse reaction to [flu] vaccine, sequela.” Id. at 5.

Dr. Molina authored a letter, dated January 23, 2019, stating, “[petitioner] should be
excluded from routine required [flu] vaccination due to a previous history of adverse reaction to
the vaccine. Shortly after receiving the seasonal [flu] vaccine in 2013[,] he developed significant
neurologic symptoms, some of which are persisting even today.” Pet. Ex. 48 at 63.

No more recent medical records were filed.

D. Petitioner’s Affidavit and Testimony

Petitioner averred that prior to receiving the flu vaccine at issue, he “was in excellent
health with no chronic health conditions and no neurological symptoms.” Pet. Ex. 51 at ¶ 3. He
was feeling well, strong, and energetic. Tr. 10-11. He had back pain, high cholesterol, possible
allergies, elevated liver enzymes, “a couple [of] migraines in [his] life,” and prior tendinitis and
arthritis in his left shoulder. Tr. 11, 58-60. At the time of vaccination, he was working as a
pediatric hospitalist and did not have health insurance. Tr. 9-10.

In November 2013, petitioner completed a medical mission trip to Bolivia. Tr. 11.
While in Bolivia, he had no health issues. Tr. 12. He returned from Bolivia on November 11,
2013. Id. During his first shift at the hospital, on November 15, 2013, petitioner received a flu
vaccine around 2:30 or 3:00 PM. Tr. 12-13, 60. He testified that he “probably” received a flu
vaccine every year since 2000 and had never had an adverse reaction besides a sore arm. Tr. 13.

22
Around 24 hours later, on November 16, 2013, he “began to experience weakness and
[paresthesia] on the left side of [his] body, including [his] hand, arm, leg, face[,] and scalp. [He]
also had dysphonia and dysphagia, confusion, and problems with gait and balance.” Pet. Ex. 51
at ¶¶ 4-5; see also Tr. 14. When his symptoms began, he was driving to meet his wife and
daughter and stopped at a rest stop off the road for about 30 minutes. Tr. 14-15. He testified that
everything was spinning, and he felt weak. Tr. 14. “[He] noticed the left side of [his] body was
weak, but [his] right side was fine.” Tr. 15. Once “[he] was feeling a little bit better,” he drove
to meet his wife at a hotel. Id.

Once he arrived at the hotel, “[his wife] immediately told [him] . . . that [his] left side of
[his] face was kind of droopy.” Tr. 15. He asked her to test his strength, and she noted his left
side was weak. Tr. 15-16. Because he did not have health insurance, petitioner drove himself to
the hospital. Tr. 16.

Petitioner arrived at Vista Medical Center and received an extensive work up to rule out
stroke. Tr. 16; Pet. Ex. 51 at ¶ 5. Petitioner contended that he was never examined by the
treating emergency room doctor, nor did he receive a follow up examination before discharge.
Pet. Ex. 51 at ¶ 15; Tr. 17-18. On discharge, he stated “[his] symptoms had not improved.” Pet.
Ex. 51 at ¶ 15. He testified that he still had brain fog and weakness, and that he crashed his car
on the way home from the hospital. Id.; Tr. 18-19, 64-65. He added that he did not remember
how he got back to the hotel where he was staying. Tr. 19, 64. When he woke up the next
morning, he still had weakness, which lingered for the next few days. Tr. 19.

From November 16 to November 22, 2013, petitioner did not return to work due to the
lingering symptoms he was experiencing. Tr. 20. On November 22, 2013, he visited an urgent
care clinic, where a doctor told him that he likely experienced a stoke and needed to see a
neurologist. Tr. 19-20. The following day, on November 23, 2013, petitioner was having
trouble using his arm and holding a fork and went to the emergency room at Porter Hospital. Tr.
21-22.

Petitioner submitted a Vaccine Adverse Event Reporting System (“VAERS”) Report on
November 26, 2013 when he returned to work. Pet. Ex. 3 at 1; Tr. 22. Petitioner wrote that one
day after his flu vaccine, he had confusion; left-sided weakness in his face, arm, hand, and leg;
tremors; dysphasia; dysphonia; and problems with his gait. Pet. Ex. 3 at 1. He indicated that all
symptoms persisted. Id. His flu vaccination was noted to be administered on November 15,
2013 at 3:20 PM, and the adverse event onset was noted to have occurred at 3:00 PM on
November 16, 2013. Id.

Petitioner saw neurologist, Dr. Simaga, on January 14, 2014. Tr. 23. He testified that
this was the first available appointment he could make with a neurologist once he got health
insurance. Tr. 23-24. On January 14, he was still experiencing weakness on his left side and
decreased sensation on the left side of his face. Tr. 24. He was still working at this time, but it
was hard to walk around the hospital and focus on a computer screen, and he felt he was not
strong enough to hold a newborn baby. Tr. 25-26. Petitioner stated that after Dr. Simaga
completed “a very thorough history and exam, . . . he told [petitioner] that [he] possibly [] had a
small stroke” or a hemiplegic migraine. Tr. 24-25.

23
On January 29, 2014, petitioner began seeing Dr. Molina as his primary care physician.
Tr. 26. Dr. Molina noted “concern for CNS vasculitis, especially given that [petitioner’s]
symptoms occurred the day after receiving a flu vaccine.” Tr. 28. Petitioner returned to Porter
Hospital on April 5, 2014 and was admitted. Tr. 29, 31. He testified that he had a sensation on
the left side of his face, and despite what the medical records state, he contended it was not a
headache or migraine. Tr. 29-31. While admitted to the hospital, Dr. Konyukhov, a neurologist,
examined petitioner. Tr. 31-32. Petitioner testified that Dr. Konyukhov has been his treating
neurologist since April 2014. Tr. 32.

Petitioner averred that based on his symptoms, medical treatment, and testing, it is “[his]
understanding from [his] doctors [] that [he] [is] suffering from a form of [MS].” Pet. Ex. 51 at ¶
8. Petitioner testified that beginning in July 2014, he began to experience periodic weakness on
his right side that began in his legs. Tr. 33. Dr. Konyukhov ordered a lumbar puncture, which
showed oligoclonal bands. Tr. 34. Dr. Konyukhov told petitioner that he could have MS, but
because petitioner’s MRIs did not show any findings consistent with MS, he referred petitioner
to MS specialist Dr. Grimes. Tr. 35-36. Dr. Konyukhov explained to petitioner that he “based
his diagnosis of MS [] on the McDonald[] criteria . . . since [his] clinical picture included more
than 2 different episodes, in more than 2 different areas of [his] body (which accounts for
dissemination in space and time), presence of specific oligoclonal bands, and excluding a very
extensive list of neurological conditions.” Pet. Ex. 51 at ¶¶ 8-9. Additionally, Dr. Konyukhov,
along with Dr. Gillespie, found no other diagnostic possibilities. Id. at ¶ 9; Tr. 40-41.

Petitioner saw Dr. Grimes on August 18, 2014. Tr. 36. Petitioner testified that Dr.
Grimes told him he most likely had a demyelinating disease, most similar to primary progressive
MS. Tr. 36-37. Petitioner was “recommended Tecfidera, a medication specific to treat MS,
which [he] took for about 3 years and which helped [him] by reducing the number of relapses
from 6-7 per year to 2-3 relapses per year.” Pet. Ex. 51 at ¶ 10; see also Tr. 37-38, 41-42. On
February 5, 2015, at petitioner’s next visit to Dr. Grimes, Dr. Grimes told petitioner he did not
meet the criteria for MS. Tr. 39.

At the end of 2017, petitioner tested positive for the JC virus, and therefore, Dr. Grimes
recommended petitioner stop taking Tecfidera. Pet. Ex. 51 at ¶ 11; Tr. 46-47. After he stopped
taking Tecfidera, he averred that “all of [his] symptoms began to worsen.” Pet. Ex. 51 at ¶ 12.
The right side of his body started getting weak and had poor grip strength. Tr. 47. In February
2018, petitioner experienced a relapse that left him unable to work until June 2018. Id.; Pet. Ex.
51 at ¶ 12. Thereafter, Dr. Konyukhov recommended high dose Biotin,40 which improved
petitioner’s symptoms and which petitioner was still taking at the time of the hearing. Pet. Ex.
51 at ¶ 12; Tr. 47-48. Petitioner testified that Dr. Konyukhov explained that “many neurologists
now consider the McDonald[] criteria to be outdated, as there is constantly new knowledge on
MS.” Pet. Ex. 51 at ¶ 13.

40
Biotin is “a water-soluble dicyclic monocarboxylic acid considered to be part of the vitamin B
complex.” Biotin, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/
definition?id=6292 (last visited May 4, 2021). Deficiencies in humans can manifest as
“dermatologic, neurologic, and ocular disorders.” Id.

24
Petitioner’s symptoms, which he averred have persisted since November 2013 and “many
of which have waxed and waned at different times,” include

1) weakness on the left side of [his] body, including weakness of [his] left arm,
hand, gluteal area, leg, and foot; 2) weakness on the right side of [his] body,
including [his] right gluteal area, quadriceps, and ankle; 3) decreased grip strength
in both hands; 4) tingling on the scalp, left arm and left leg, tingling on other
areas, and electricity sensation down [his] spine; 5) numbness on [his]
extremities, loss of sensation on the left side of [his] face and left arm; 6) tremors;
7) loss of coordination and balance; 8) confusion or brain fog, including slowed
thought process at times and problems with memory; 9) double vision and
difficulty focusing vision; 10) face drop and drooling, initially on the left side of
the mouth, but now mostly drooling on the right side; 11) paresthesia on left side
of the scalp and face; 12) difficulty swallowing and advancing food past the
stomach (gastroparesis, decreased esophageal motility and uncoordinated swallow
demonstrated in Motility study); 13) difficulty with speech at times, both in
pronouncing words and getting words out; 14) problems dropping things; 15)
episodes of dizziness; 16) tinnitus; 17) sudden pain in my legs; 18) spasticity in
legs and toes; 19) fluctuating blood pressure and tachycardia (referred to by
neurologist as dysautonomia); 20) episodes of tiredness and fatigue; 21) heat
intolerance/sensitivity, worsening weakness and other symptoms when exposed to
heat, for example, having to use cooling bands and a cooling vest to deal with
heat and prevent symptoms in the Summer time; 22) difficulty walking to the
bathroom at night; 23) frequent urinary tract infections and frequent urinating at
night; 24) difficulty breathing at night at times; 25) vocal cord dysfunction (also
related to dysautonomia); 26) intermittent constipation alternated with inability to
hold it; 27) hypotonic bladder; 28) problems with erection; 29) difficulty climbing
stairs, walking long distances, running, prolonged standing, exercising, and
participating in sports; 30) difficulty with hand writing and typing at times; 31)
difficulty with handling silverware and other small objects; and 32) difficulty
sleeping well (lack of sleep also makes all symptoms worse).

Pet. Ex. 51 at ¶ 7. As of the hearing, petitioner testified that he continues to experience
paresthesia, weakness, problems with balance and gait, difficulty focusing, slurred speech, issues
swallowing, and issues with his memory. Tr. 48-50.

Petitioner averred that his condition has had a significant impact on his life. Pet. Ex. 51
at ¶ 17. He described having difficulty getting through the day, requiring cooling bands and
vests in the summer to prevent symptoms from worsening, and experiencing fatigue, weakness,
and overheating in the winter. Id. Because he gets tired easily and has difficulty handling stress,
he has had to decrease his hours at work because his symptoms interfered with his job. Id.; Tr.
51-52. He testified that he also has not been able to care for his daughter properly or participate
fully in her life. Tr. 53.

25
Petitioner contended that many of his medical records, particularly those at Vista Medical
Center, Sherman Hospital, and Porter Hospital, inaccurately documented his symptoms. Pet. Ex.
51 at ¶ 14. He further asserted that on many visits, doctors or nurses “failed to examine [him] or
improperly or inadequately examined [him].” Id.; see also Tr. 61-62. He asserted that he never
had a headache during his relapses, despite many medical records stating this fact. Pet. Ex. 51 at
¶ 16.

Petitioner testified that he has not visited Dr. Konyukhov since January 2019. Tr. 55.
And since March 2020, the start of the Covid-19 pandemic, he has not seen any of his treating
physicians. Tr. 55-56.

E. Expert Reports

1. Petitioner – Dr. Marcel Kinsbourne41

a. Background and Qualifications

Dr. Kinsbourne earned his B.A. from Christ Church at Oxford University in 1952, his
Bachelor of Medicine (B.M.) and Bachelor of Surgery (B.Ch.) from Oxford University Medical
School in 1955, his M.A. and Doctor of Medicine (D.M.) from Oxford University in 1956 and
1963, and his M.D. from State of North Carolina in 1967. Pet. Ex. 44 at 1. From 1955 to the
early 1990s, he regularly treated patients. Tr. 74. Throughout his career, Dr. Kinsbourne has
also held teaching positions at various institutions. Pet. Ex. 44 at 2-3. Dr. Kinsbourne has held
medical licenses in the United Kingdom, Canada, North Carolina, Massachusetts, and Virginia.
Id. at 2. He has been bestowed numerous honors and awards, has served and is currently serving
on a number of editorial boards, and has authored or co-authored more than 400 publications. Id.
at 3-39.

b. Opinion

i. Diagnosis

Based on petitioner’s testimony and medical records, Dr. Kinsbourne opined that
petitioner “has an inflammatory autoimmune encephalopathy”42 that is most like MS with an
ADEM-like onset, and with symptoms consistent with a demyelinating disorder. Tr. 99-100,
102; see also Pet. Ex. 25 at 4. Dr. Kinsbourne found petitioner “most likely . . . began with an
ADEM-like presentation which morphed into [a] [MS]-like disorder.” Tr. 78; see also Pet. Ex.
96 at 1-3.

41
Petitioner filed four expert reports authored by Dr. Kinsbourne. Pet. Exs. 25, 54, 63, 96.
42
Dr. Kinsbourne clarified that “inflammatory autoimmune encephalopathy” is a description of
his condition that “encompasses a number of entities.” Tr. 102, 129. Dr. Kinsbourne did not
enumerate the “number of entities” or otherwise define them.

26
At the hearing, Dr. Kinsbourne testified that he would not have diagnosed petitioner with
MS or ADEM, and that petitioner’s condition is most like a cross between MS and ADEM. Tr.
78, 102. However, on cross-examination, Dr. Kinsbourne testified that as a practical matter, he
would have diagnosed petitioner with MS, as his treating physicians did. Tr. 129. And in his
fourth expert report, he wrote, “there is no question that the subsequent course was that of MS.”
Pet. Ex. 96 at 3.

Prior to vaccination, petitioner was generally in good health with no record or history of
any neurological illness. Tr. 78-79. Looking at petitioner’s medical records from November
2013, Dr. Kinsbourne testified that he most likely would have thought petitioner suffered a
stroke. Tr. 80-81. He found petitioner’s complaint of difficulty focusing would not be unlikely
with a stroke. Tr. 82. Additionally, petitioner complained of difficulty speaking due to the
numbness and weakness in the left side of his face. Tr. 82-83. Dr. Kinsbourne did not believe
that petitioner had a TIA or a hemiplegic migraine. Tr. 83, 88, 103; Pet. Ex. 25 at 4. However,
he did think that CNS vasculitis was a reasonable possibility in early 2014. Tr. 85-87.

Although he agreed that petitioner had symptoms of a stroke, Dr. Kinsbourne testified
that it would have been appropriate to consider a diagnosis of ADEM at onset. Tr. 131-32. Dr.
Kinsbourne opined that petitioner’s presentation at onset was polysymptomatic, a feature
“typical of ADEM, which develops acutely with multiple symptoms appearing at the same time.”
Pet. Ex. 96 at 1-2; see also Tr. 108. He opined that petitioner’s “disease onset conformed to
ADEM, as an encephalopathy that featured headache and confusion.” Pet. Ex. 96 at 2. For
support that petitioner suffered from ADEM at onset, Dr. Kinsbourne pointed to petitioner’s
November 2013 complaints of numbness and tingling in his left face and arm, trouble walking on
his left leg, and cognitive issues. Tr. 108.

Dr. Kinsbourne opined that MRI evidence is not required for a diagnosis of ADEM. Tr.
110. He also stated that there is a delay between ADEM symptoms and associated MRI changes,
and thus, petitioner’s MRI would not reflect lesions typically identified in ADEM. Pet. Ex. 96 at
2; Tr. 110.

However, Dr. Kinsbourne believed the remainder of petitioner’s clinical course, after
onset, conformed to MS. Pet. Ex. 96 at 2; see also Tr. 78. Dr. Kinsbourne opined that
petitioner’s clinical manifestations at onset relapsed and conformed to the McDonald criteria,
specifically, episodes differing in time and space. Pet. Ex. 25 at 4. Additionally, petitioner had
heat sensitivity, five oligoclonal bands in his CSF, a positive response to steroids, and positive
ANA antibodies, which Dr. Kinsbourne opined supported a diagnosis of MS. Id. Because
petitioner’s treating physicians started petitioner on Tecfidera, Dr. Kinsbourne assumed they
believed petitioner had MS. Id. Although petitioner was taken off Tecfidera, he found it
appropriate to discontinue the medication due to petitioner’s positive test result for the JC virus.
Tr. 96.

Dr. Kinsbourne opined that it is appropriate to consider a diagnosis of MS after three
months, and that a diagnosis is clear once there is dissemination in space—here, when petitioner
first reported symptoms on the right side of his body in July 2014. Tr. 132.

27
He also argued that a brain MRI is often normal when clinical diagnostic criteria for MS
are first met. Pet. Ex. 25 at 4. He conceded that “normal-appearing white matter on MRI of the
MS brain can be quite abnormal.” Pet. Ex. 63 at 1. However, he asserted that advanced MRI
techniques were not used on petitioner that could have revealed underlying pathology. Pet. Ex.
54 at 1-2; Tr. 116. He opined that in petitioner’s case, his normal-looking white matter would
likely have been abnormal if appropriate advanced techniques had been used. Tr. 116.

Further, Dr. Kinsbourne argued that “MRI abnormalities are not essential for the
diagnosis for MS if there are oligoclonal bands.” Pet. Ex. 54 at 1. In fact, 90-95% of MS
patients have oligoclonal bands according to Dr. Kinsbourne. Id. at 2; Tr. 117. David Keren43
wrote, “examination of the CSF for the presence of [oligoclonal]-bands is still the best single
laboratory test providing support for the diagnosis of MS because many of the non-MS
conditions in which they appear can be distinguished clinically from MS.” Pet. Ex. 65 at 1.
Keren added that “[i]n the appropriate clinical setting, the presence of the [oligoclonal]-bands
provides powerful supportive evidence for the diagnosis.” Id.

Additionally, Dr. Kinsbourne testified that “if these oligoclonal bands occur only in the
CSF and not in the serum, that is probably convincing evidence of an inflammatory autoimmune
. . . or infectious condition of the brain.” Tr. 89. Dr. Kinsbourne noted petitioner’s CSF showed
five oligoclonal bands, which is “strong evidence of inflammatory disease of his brain.” Id.; see
also Pet. Ex. 54 at 1. He conceded that other conditions can exhibit oligoclonal bands, but
opined that there is no evidence that petitioner has any of those conditions. Tr. 117. He
reiterated that it is “very possible” for someone to suffer from a CNS demyelinating condition
even when there are no visible lesions on MRI. Tr. 118-20.

And at petitioner’s most recent visit to Dr. Konyukhov in January 2019, Dr. Konyukhov
documented symptoms that Dr. Kinsbourne opined are consistent with someone who is suffering
from a demyelinating illness. Tr. 98-100.

In summary, Dr. Kinsbourne concluded that petitioner has a primary inflammatory CNS
white matter demyelinating disease. Tr. 106. He opined it is primary because there is no
evidence that his condition is secondary to any systemic disease. Tr. 106, 112-13. It is
inflammatory because there is no evidence that petitioner had an infection, nor is there any
evidence of any other cause. Tr. 106.

ii. Althen Prong One

Dr. Kinsbourne opined that petitioner’s November 15, 2013 flu vaccination more likely
than not caused petitioner’s demyelinating illness. Tr. 103; Pet. Ex. 25 at 8. At the hearing and
in his expert reports, Dr. Kinsbourne opined as how the flu vaccine can cause or trigger the
innate immune system and lead to a demyelinating condition.

43
David F. Keren, Optimizing Detection of Oligoclonal Bands in Cerebrospinal Fluid by Use of
Isoelectric Focusing with IgG Immunoblotting, 120 Am. Soc’y for Clinical Pathology 649
(2003).

28
He opined generally that vaccinations can cause demyelinating disorders, like ADEM,
but deferred to Dr. Gershwin as to the mechanism. Pet. Ex. 96 at 2-5; Tr. 104; see also Pet. Ex.
99 at 2; Pet. Ex. 102 at 5; Pet. Ex. 104 at 2, 3 tbl.1.44

Dr. Kinsbourne next opined that ADEM can “morph” into MS. Tr. 78; Pet. Ex. 96 at 1-3.
He did not explain the process or mechanism by which ADEM can morph into MS other than to
say it can happen. He did, however, cite to medical literature in support of this opinion.

In Schwarz et al., for example, the authors conducted a long-term follow-up study of 40
adults originally diagnosed with ADEM to determine possible diagnostic criteria to distinguish
ADEM from MS. Pet. Ex. 103 at 1. Those originally diagnosed with ADEM had (1) “[a]cute
neurologic symptoms without a history of previous, unexplained neurologic symptoms,” (2) one
or more lesions on MRI, and (3) “exclusion of CNS infection, vasculitis, or other autoimmune
disease with CSF analysis.” Id. at 2. A final diagnosis of ADEM was established only if “there
was no evidence of a second clinical episode of CNS demyelination.” Id. The authors found 14
of the 40 patients (35%) originally diagnosed with ADEM had a second clinical episode within
one year of initial presentation and thus, were ultimately diagnosed with MS.45 Id. at 3. They
determined “the presence of oligoclonal bands of IgG did not discriminate ADEM from MS.”
Id. All 40 patients exhibited at least one lesion on MRI, and 13 of the 14 patients with definite
MS developed additional lesions. Id. Schwarz et al. concluded that “[m]any patients initially
diagnosed with ADEM develop clinically definite MS upon long-term follow-up.” Id. at 1.
They “found no useful diagnostic criteria for the differentiation of a first episode of MS from
monophasic ADEM.” Id. The authors did not hypothesize as to whether ADEM “morphs” into
MS, nor did the authors provide a mechanism by which ADEM can “morph” into MS. But the
authors demonstrated that an original diagnosis of ADEM can change to a diagnosis of MS based
on long-term follow-up.

Mikaeloff et al. conducted a study of 296 children with a first episode of acute
inflammatory demyelination of the CNS. Pet. Ex. 101 at 2. Those who received a diagnosis of
ADEM at presentation had “a polysymptomatic onset with mental status change and [a]
suggestive brain MRI.” Id. Diagnosis of definite or probable MS was made using the Poser
criteria,46 with MRI suggestive of MS when multiple lesions were seen in periventricular and/or
subcortical locations. Id. Suspected MS diagnosis was given to those who met the MRI criteria
and had compatible clinical criteria. Id. Children with ADEM at onset who had a second attack
were reclassified as clinically definite MS. Id. Initial diagnosis was suggestive of MS in 96
patients (33%) and suggestive of ADEM in 119 patients (40%). Id. at 4. At the end of the
follow-up period, the authors found 168 of 296 of the patients (57%) met the criteria for a final
diagnosis of MS, 34 (20%) of which had ADEM at onset, but when they experienced a second

44
A. Shoamanesh & A. Traboulsee, Acute Disseminated Encephalomyelitis Following Influenza
Vaccination, 29 Vaccine 8182 (2011).
45
The authors used the outdated Poser criteria for diagnosing MS.
46
The authors note they did not use the McDonald criteria because it is not recommended for
those below the age of 10. Pet. Ex. 101 at 2.

29
attack, their final diagnosis was modified to MS. Id. Again, the authors did not opine as to
whether ADEM can “morph” into MS, nor did they opine to the mechanism by which this could
occur. Mikaeloff et al. showed that after a follow-up period, an initial diagnosis of ADEM can
change to MS once there is a second flare or attack.

As for the mechanism of causation, Dr. Kinsbourne opined that the flu vaccine can cause
MS through the innate immune system. Pet. Ex. 25 at 6. Although he noted that “MS is thought
frequently to involve molecular mimicry between the infectious antigen and self-antigens,” Dr.
Kinsbourne expressly rejected the mechanism of molecular mimicry in this case and opined that
molecular mimicry would not occur within 24 hours. Id.

Dr. Kinsbourne testified that when the flu vaccine is administered, it elicits the
development of pro-inflammatory cytokines that stimulate inflammatory changes. Tr. 77-78.
For a vaccine to be effective, it must activate the innate immune system, which responds within a
few hours. Tr. 103. He asserts that the innate immune system produces pro-inflammatory
cytokines that pass the blood-brain barrier and activate inflammation, which can subsequently
result in demyelination. Id.; Pet. Ex. 25 at 6.

Specifically, he opined that the flu vaccine “prompt[s] activation of the macrophages of
the innate immune system within minutes.” Pet. Ex. 25 at 6. Subsequently, lymphocytes travel
to key sites, resulting in the production of proinflammatory cytokines that “cause endothelial
damage and activate intra-cranial astrocytes and microglial cells. These immune cells of the
[CNS] release more proinflammatory cytokines intracranially . . . causing demyelination.” Id.
Dr. Kinsbourne added that “innate immunity is also characterized by memory of previous
immune reaction to similar antigens, resulting in anamnestic responses by [toll-like receptors
(“TLRs”)] and an enhanced cytokine-initiated cascade.” Id. at 7.

Dr. Kinsbourne cited to Deng and Sriram47 to support the premise that an innate as
opposed to an adaptive autoimmune etiology is favored for MS because according to Dr.
Kinsbourne, “Deng and Sriram [] favored an autoimmune etiology for MS other than molecular
mimicry.” Pet. Ex. 25 at 6. However, his characterization of the article is misleading. Deng and
Sriram did not state that an innate immune etiology is the favored mechanism for MS. Instead,
they stated that “lesions in MS are inflammatory in nature, and the underlying basis for the
pathology is considered to be autoimmune and most likely mediated by activated T cells to the
oligodendrocyte/myelin unit.”48 Id. at 2. Within that frame of reference, Deng and Sriram
examined the role of microglia in the development of demyelination. They hypothesized that

47
The Deng and Sriram article is co-authored by Dr. Sriram, the respondent’s expert in this case.
48
T cells, or lymphocytes, are “cells primarily responsible for cell-mediated immunity.” T
Lymphocytes, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/
definition? id=87562 (last visited May 4, 2021). “When activated by antigen, T lymphocytes
proliferate and differentiate into T memory cells and the various types of regulatory and effector
T cells.” Id. Adaptive, not innate, immunity is “mediated by B and T lymphocytes following
exposure to a specific antigen.” Illustrated Dictionary of Immunology 18 (3d ed. 2009).

30
“microglia may play a role in both presentation of an autoantigen and in secretion of
proinflammatory cytokines.” Id. They proposed three models of demyelination in inflammatory
disorders, “where microglial activation is evident and [] an important feature of the pathologic
process.” Id. at 1, 3-5.

The first model described by Deng and Sriram implicates “antibody-mediated destruction
of the myelin unit.” Pet. Ex. 28 at 4 fig.1A, 3, 5. This model fits the paradigm of molecular
mimicry and/or the adaptive immune system. The second model contemplates “activation of
microglia as the primary event leading to secondary recruitment of lymphocytes and damage to
myelin.” Id. at 4 fig.1B, 5. This model does not include activation of T cells. Id. However, it
does require “[a]ctivation of microglial by [lipopolysaccharides], toll receptor agonists, [or]
super antigens.” Id. at 4 fig.1B. Dr. Kinsbourne did not suggest that the flu vaccine at issue
contained lipopolysaccharides, a toll receptor agonist, or a super antigen.

The third model proposed by Deng and Sriram is “characterized by oligodendrocyte
death.” Pet. Ex. 28 at 4 fig.1C, 5. “All other immunological . . . processes that follow, including
the development of an immune response to myelin antigens, are secondary events following
oligodendrocyte death.” Id. at 5. In this model, “activation of microglia [is] an unintended
consequence of extensive myelin destruction.” Id. Therefore, this model does not suggest that
microglia or the innate immune system causes demyelination.

To support his opinion that cytokines play a role in triggering the inflammation seen in
MS, Dr. Kinsbourne also cited to Graber et al.,49 whom Dr. Kinsbourne found “attribute MS
lesions to inflammation triggered by cytokines” and “demonstrated that the levels of
proinflammatory cytokine IL-6 are increased in the CSF of MS patients.” Pet. Ex. 25 at 6. In
Graber et al., the authors investigated the role of IL-17 and its possible link with IL-6 in
autoimmune inflammation of the CNS by examining IL-17 and other cytokine levels in
peripheral blood mononuclear cells. Pet. Ex. 32 at 2. The authors determined that IL-17 and IL-
6 production were increased in the peripheral blood mononuclear cells of patients with transverse
myelitis (“TM”) compared to the control group and those with MS. Id. at 5. Notably, there were
limitations to the study in that all MS patients in the study had clinically definite relapsing-
remitting MS at the time of participation in the study. Thus, it was impossible to determine
cytokine levels at the time of onset because they were not tested. Regardless, the authors stated
that IL-17 is made by activated memory CD4+ cells, and that “IL-17 in turn stimulate[d]
macrophage production of IL-6, TNF α and IL-1B.” Id. at 2, 8. While they speculated that, it is
“possible that IL-17 is an early triggering event in autoimmune CNS diseases,” this possibility
appears to be put into the context of the adaptive immune response. See id. at 7. They
recommended additional studies to address the “temporal relationships between the cytokines
studied and disease activity.” Id.

49
Jerome J. Graber et al., Interleukin-17 in Transverse Myelitis and Multiple Sclerosis, 196 J.
Neuroimmunology 124 (2008).

31
iii. Althen Prong Two

Dr. Kinsbourne opined that, in petitioner’s case, “[t]he flu vaccination caused an
outpouring of pro-inflammatory cytokines, which stimulated inflammatory change in the
microglia in [petitioner’s] brain, and caused him to have an acute polysymptomatic neurological
disorder, which was more like what happens in ADEM than in any other alternative condition.”
Tr. 77-78. However, Dr. Kinsbourne testified that over time, petitioner had multiple relapses,
which were most similar to a form of MS, and his condition morphed into MS. Tr. 78; Pet. Ex.
96 at 3. Dr. Kinsbourne maintained petitioner’s current condition is most like MS because
petitioner has experienced dissemination in space and time. Tr. 102, 132; Pet. Ex. 25 at 4.
However, it is not essential to his theory of causation that petitioner’s condition fits neatly into
the technical definition of MS. Tr. 104-05.

Dr. Kinsbourne conceded that petitioner’s condition is atypical because there is no MRI
confirmation of MS. Tr. 124. However, he opined that it is “very possible” for someone to
suffer from a CNS demyelinating condition even when there are no visible lesions on MRI. Tr.
118-20.

First, Dr. Kinsbourne opined that MRI evidence is not required for a diagnosis of ADEM.
Tr. 110. He argued there is a delay between ADEM symptoms and associated MRI changes, and
thus, MRIs do not always reflect lesions typically identified in ADEM. Pet. Ex. 96 at 2; Tr. 110.
He cited to Honkaniemi et al., which examined MRIs of four adult patients with ADEM from a
few days of onset for up to eight months. Pet. Ex. 98 at 1. The authors found “a delay of about 1
to 6 weeks between the onset of clinical symptoms and the appearance of the lesions in MR
images.” Id. at 7. Additionally, new lesions appeared during the recovery period. Id. at 6-7.
However, this article does not address the situation were MRIs are done over a period of years,
and still do not show evidence of lesions.

In Dale et al.,50 another article cited by Dr. Kinsbourne, the authors noted “[h]istological
studies of patients with ADEM [performed] at various intervals up to a month after clinical onset
have shown that microscopic lesions are very numerous, appear within days of clinical
presentation[,] and do not increase in size or number.” Pet. Ex. 27 at 12.

Next, Dr. Kinsbourne opined that MS patients can have normal MRIs, and cited Thorpe
51
et al., which looked 170 patients with possible, probable, or definite MS who had undergone
brain and spinal cord MRIs. Pet. Ex. 42 at 2. Of the 170 patients, 20 had minimal or no
abnormalities on their brain MRIs and abnormal spinal MRIs. Id. at 1. Eight patients, three of
which were diagnosed with MS, had completely normal brain MRIs. Id. at 3, 3tbl.1. The
authors “conclude[d] that the finding of a normal brain MRI, although rare, is nevertheless quite
compatible with a diagnosis of [MS].” Id. at 5. However, all eight patients exhibited at least one

50
R. C. Dale et al., Acute Disseminated Encephalomyelitis, Multiphasic Disseminated
Encephalomyelitis and Multiple Sclerosis in Children, 123 Brain 2407 (2000).
51
J. W. Thorpe et al., Spinal MRI in Patients with Suspected Multiple Sclerosis and Negative
Brain MRI, 119 Brain 709 (1996).

32
spinal cord lesion. Id. at 3, 3tbl.1. Thus, while patients may have normal brain MRIs, their
spinal cord MRIs may show cord lesions, which aid in the diagnosis of MS. Id. at 5.

The authors in Healy et al.52 discussed the dissociation between clinical symptoms and
MRI findings in MS patients. Pet. Ex. 55 at 1. The authors separated their subjects into three
groups: (1) low lesion load/high disability; (2) high lesion load/low disability; and (3) non
dissociated.53 Id. at 1-2. They found 13.5% of patients had a clinical/MRI dissociation, with
4.1% having a low lesion load and high disability and 9.4% having a high lesion load and low
disability. Id. at 4. The low lesion load group was more likely to have progressive MS and
cervical cord lesions, while all but one patient in the high lesion group had relapsing MS. Id. at
3-4. The authors noted that their study did not use high resolution and higher field MRI to
measure lesions, which they acknowledged “might show important differences between the
dissociation groups.” Id. at 5.

Additionally, Dr. Kinsbourne argued “MRI abnormalities are not essential for the
diagnosis for MS if there are oligoclonal bands,” and petitioner’s CSF showed five oligoclonal
bands. Pet. Ex. 54 at 1. At the hearing, Dr. Kinsbourne cited Thompson et al., an article from
respondent’s expert, where the International Panel recommended that when dissemination in
space is met and there is “no better explanation for the clinical presentation,” oligoclonal bands
in CSF can fulfill the dissemination in time requirement, meeting the criteria for a diagnosis of
MS. Resp. Ex. C at 5.

Because petitioner had been exposed to the flu vaccine before, Dr. Kinsbourne opined
that petitioner’s innate immune memory was accelerated and amplified by the flu vaccine which
initiated activation of TLRs.54 Pet. Ex. 25 at 5, 7. He asserted that the flu vaccine activated
TLRs that “stimulate[d] immunity by triggering the release of proinflammatory cytokines . . .
capable of triggering an autoimmune cascade against the white matter of the brain.” Id. at 7.

Lastly, Dr. Kinsbourne opined that there were no other triggers other than vaccination
that could have caused petitioner’s condition. Pet. Ex. 25 at 7.

52
Brian C. Healy et al., Characterizing Clinical and MRI Dissociation in Patients with Multiple
Sclerosis, 27 J. Neuroimaging 481 (2017).
53
Individuals placed into the low lesion load/high disability group were patients with less than 2
ml in T2 hyperintense lesion volume and more than or equal to 3 on the Expanded Disability
Status Scale. Pet. Ex. 55 at 2. High lesion load/low disability patients were those with more
than 6 ml in T2 hyperintense lesion volume and less than 2 on the Expanded Disability Status
Scale. Id.
54
TLRs are “[a] type of pattern recognition receptor that recognizes unique structures derived
from microorganisms. [Signaling] through TLRs promotes inflammatory immune responses,
cytokine production[,] and cell activation in response to microorganisms.” Pet. Ex. 89 at 1
(Serge Rivest, Regulation of Innate Immune Responses in the Brain, 9 Nature Revs.
Immunology 429 (2009)).

33
iv. Althen Prong Three

Dr. Kinsbourne opined that petitioner’s neurological symptoms appeared 24 hours after
his flu vaccination. Tr. 124. He attributed such rapid onset “to an anamnestic response
involving the innate immune system, induced by frequent prior exposure to [flu] vaccination.”
Pet. Ex. 25 at 7. Based on his proposed mechanism involving the innate immune system, he
found the time frame to be medically reasonable. Id.

He opined petitioner’s “clinical presentation one day following vaccination closely
approximated the clinical characteristics of a[n] onset of ADEM.” Pet. Ex. 96 at 3.

For support of a 24-hour onset in ADEM, Dr. Kinsbourne cited Huynh et al., who
examined ADEM cases and noted that “[d]epending on the inciting agent, the onset of symptoms
may vary . . . from 1 to 14 days.” Pet. Ex. 99 at 5. The authors examined a 61-year-old male
who received a flu vaccine three weeks prior to symptom onset and found his “clinical
presentation was most likely due to post-[flu] vaccination.” Id. at 7-8. The authors also noted
“[a] 14-year-old female developed ADEM 2 weeks after [a flu] vaccination, while 2 adult males,
ages 62 and 70, were diagnosed with ADEM and TM with acute motor axonal neuropathy
respectively within 1 week of vaccination,” but did not discuss these cases in more detail. Id. at
3. Mechanisms for these specific cases were not noted. However, the authors did briefly discuss
the pathogenesis of ADEM, specifically noting molecular mimicry.55 Id. at 4.

Shoamanesh and Traboulsee examined an ADEM case with an onset of two days
following flu vaccination. Pet. Ex. 104 at 1. The authors also examined 10 cases of
encephalomyelitis or ADEM following flu vaccination and found “neurological symptoms
typically developed within 3 weeks of vaccination.” Id. at 2, 3 tbl.1. A mechanism was not
discussed by the authors.

Dale and Branson noted a mean onset period of two weeks in 51-74% of ADEM patients
with a history of a precipitating infection. Pet. Ex. 97 at 1. The authors did not note the
mechanism by which ADEM is thought to be caused.

In Schwarz et al., the authors noted that one patient, who was originally diagnosed with
ADEM and later diagnosed with MS, “experienced the first symptoms a few days after active
immunization against diphtheria and tetanus.” Pet. Ex. 103 at 3. The authors indicated the
length of time their patients experienced symptoms before admission, but did not otherwise
indicate onset. Id. at 3, 3 tbl.1. The authors wrote that “[a]lthough the pathophysiology of

55
The authors also discussed the immuno-inflammatory model. Pet. Ex. 99 at 4. The immuno-
inflammatory model combines molecular mimicry with an inflammatory cascade process. Id.
Under this model, “[a] ‘first hit’ is experienced after an antecedent infection with a virus that
expresses determinants allowing molecular mimicry. . . . A second infection with an unrelated
virus results in sufficient reactivation of the primed autoreactive T cells to eventuate in
demyelination of the CNS. This constitutes the ‘second hit.’” Id. Petitioner’s experts have not
asserted this theory characterized by two unrelated viral infections.

34
ADEM is not known, an autoimmune response to myelin basic protein triggered by infection or
immunization is considered to be a possible etiologic factor.” Id. at 1.

Of the 296 children studied by Mikaeloff et al., 94 had an infection during the month
preceding onset and 16 had a vaccination during the six months preceding onset. Pet. Ex. 101 at
3 tbl.1. The authors did not otherwise discuss onset after an inciting event. Nor did the authors
discuss a mechanism by which ADEM occurs.

Dr. Kinsbourne cited to an article from Karussis and Petrou. See Pet. Ex. 35. Karussis
and Petrou conducted a PubMed search from 1979 to 2013 and found 71 cases of a temporal
association between an inflammatory CNS demyelinating disease and the administration of a
vaccine. Id. at 2. Of these 71 cases, 21 were associated with the flu vaccine. Id. For those cases
of ADEM post-flu vaccination, onset was between 8 days and 3 weeks. Id. at 4 tbl.2. The
authors noted “[t]he current pathogenetic hypothesis in post-vaccination ADEM is that antigens
of viral origin cross-react with myelin components (molecular mimicry) and in a secondary
manner induce a hyperergic reaction, that leads to the development of disseminated
demyelination.”56 Id. at 3.

With regard to a 24-hour onset of MS after flu vaccination, Dr. Kinsbourne deferred to an
immunologist. Pet. Ex. 54 at 3. He testified that it would have been appropriate to consider a
diagnosis of MS three months after onset, once there is dissemination in time and space. Tr. 132.
According to Dr. Kinsbourne, dissemination in petitioner’s case occurred in July 2014 when he
first reported right-sided weakness and five oligoclonal bands were found in his CSF. Id.

2. Petitioner – Dr. M. Eric Gershwin57

a. Background and Qualifications

Dr. Gershwin is board-certified in internal medicine, rheumatology, and allergy and
clinical immunology. Pet. Ex. 94 at 2. He received his A.B., summa cum laude, from Syracuse
University in 1966 and his M.D. from Stanford University in 1971, and holds various honorary
degrees and special awards for his work in immunology. Id. at 1. Thereafter, he completed his
internship and residency at Tufts-New England Medical Center. Id. at 2. Since 2003, Dr.

56
The authors further hypothesized “that vaccination may activate in a non-specific way distinct
clones of antimyelin T-cells and that suppressor or regulatory cells that are aimed to control this
abnormal reactivity are compromised or malfunctioning.” Pet. Ex. 35 at 3. The authors noted
“[t]he inflammatory process in MS is propagated by an autoimmune cascade, involving mainly
T-cells that target myelin self antigens, possibly mediated by mechanisms of molecular mimicry
(cross-reactive antigens expressed by viruses or other microorganisms and myelin components).”
Id. Alternatively, “‘naturally’ existing myelin-specific T-cells, especially of the Th17
phenotype, may expand to critical pathogenic quantities due to malfunctioning
immunoregulatory mechanisms.” Id.
57
Petitioner filed two expert reports authored by Dr. Gershwin. Pet. Exs. 69, 107.

35
Gershwin has been a Distinguished Professor of Medicine with the University of California,
Davis, where he currently holds a chaired professorship in honor of Jack and Donald Chia. Id. at
1. Throughout his career, he has been presented various honors and awards, served as an editor
and reviewer on journals and publications, and authored or co-authored articles, papers,
editorials, and books. Id. at 3-134.

b. Opinion

Dr. Gershwin opined that petitioner’s November 15, 2013 flu vaccine more likely than
not caused his demyelinating neurological condition. Tr. 139. He deferred to Dr. Kinsbourne as
to petitioner’s diagnosis, and thus, did not provide an opinion other than that petitioner suffers
from a neurologic disease. Tr. 139, 275; Pet. Ex. 69 at 1. His opinion focused on “whether
inflammation in the [CNS] can occur within 24 hours of an antigen challenge.” Pet. Ex. 69 at 1.

i. Althen Prong One

Dr. Gershwin opined that the underlying mechanism at play is inflammatory in nature.
Tr. 139. He explained that the immune system is divided into innate and adaptive responses. Tr.
141. The innate immune system acts as a first responder to anything that is foreign in the body.
Id. He also testified that there must be an innate response before an adaptive response occurs.
Tr. 142; Pet. Ex. 69 at 2.

Dr. Gershwin testified that the flu vaccine is a “heat-killed vaccine” containing both an
adjuvant and polysorbate 80. Tr. 140. He opined that the vaccine caused a rapid release of
cytokines and other mediators upon administration.58 Tr. 140, 145; Pet. Ex. 107 at 1. The
mediators, which peak 24 hours after vaccination, go from the lymph node, to the blood, and
then into the brain, and produce an inflammatory response. Tr. 140; Pet. Ex. 107 at 1. He
opined that the “activated cells can cross the blood brain barrier, even in the absence of
neuroinflammation.” Pet. Ex. 69 at 2.

Dr. Gershwin described the brain as a lymphoid organ with innate immune cells,
including microglia and astrocytes, that can respond to and produce cytokines. Tr. 144, 149; Pet.
Ex. 69 at 2. Specifically, the brain contains mononuclear-like cells that are capable of cytokine
production and other inflammatory mediators that lead to inflammation. Tr. 140. “In some
organs, these changes in innate immunity may not be clinically apparent, but in the case of the
brain, they would have more profound clinical implications.” Pet. Ex. 69 at 2.

58
Dr. Gershwin testified that the flu vaccine here contained an adjuvant and polysorbate 80,
however, the petitioner did not file any evidence to support this testimony. Petitioner filed a
package insert for the Fluzone vaccine for 2020-2021, not the formula administered to petitioner.
See Pet. Ex. 114. The insert describes how the vaccine was prepared, and lists the ingredients.
See id. at 20-22. No adjuvants are listed or otherwise identified. Id. at 22. Polysorbate 80 is
also not identified in the list of ingredients. Id.

36
To support the premise that both antigens and cytokines are involved in the immune
response, Dr. Gershwin cited to Hervé et al.59 Pet. Ex. 107 at 1-2; Tr. 146-47. Hervé et al.
explained, “[v]accine antigens and immune enhancers (as adjuvants) injected into the muscle are
[recognized] by the body as potential pathogens and/or danger signals.” Pet. Ex. 108 at 3 fig.1.
This “leads to the stimulation of local cells, followed by the recruitment of blood immune cells
to the local site and the production of different soluble factors including vasodilators and
cytokines, which may trigger the development of signs and symptoms of local inflammation.”
Id. Those factors, like cytokines, travel into the bloodstream and “may contribute to the
development of general symptoms (fever, myalgia, headache etc) in the vaccinee.” Id.

Hervé et al. further explained that after vaccination, TLRs recognize and bind antigens
and potential immune enhancers in the vaccine to trigger inflammation. Pet. Ex. 108 at 4 fig.2.
“Resident immune cells, mast cells, monocytes[,] and macrophages are activated within minutes
of injection and release soluble factors” such as proinflammatory cytokines. Id. “These newly
recruited immune cells, mainly composed of blood-born neutrophils, monocytes[,] and T
lymphocytes, also contribute to pain sensation by releasing soluble factors, such as cytokines, . . .
that can directly interact with local sensory receptors.” Id. Once cytokines are produced, they
“act both locally . . . and may act systemically at distant organs.” Id. “Several immune-to-brain
signaling pathways may propagate an inflammatory response to the [CNS] after peripheral
activation of the innate immune system . . . leading to the development of fever and sickness
[behaviors].” Id.

To further support his argument that cytokines may be present in the brain after
vaccination, Dr. Gershwin cited Wendeln et al.60 Pet. Ex. 69 at 2. In Wendeln et al., the authors
gave mice low dose injections of lipopolysaccharides61 on four consecutive days, leading to mild
sickness and temporary weight loss. Pet. Ex. 88 at 1. They found that three hours after the first
injection, “there was a pronounced increase in blood cytokine levels, but only modest increases
in brain cytokines.” Id. After the second injection, blood levels of certain pro-inflammatory
cytokines reduced, while brain cytokines markedly increased, “indicating a brain-specific
training effect induced by the first [injection].” Id. A change in microglia occurred after the
second injection, while astrocytes increased only after the third injection. Id. Their results
“indicat[ed] the immune memory in the brain is predominantly mediated by microglia.” Id. at 1,

59
Caroline Hervé et al., The How’s and What’s of Vaccine Reactogenicity, 39 NPJ Vaccines 1
(2019).
60
Ann-Christin Wendeln et al., Innate Immune Memory in the Brain Shapes Neurological
Disease Hallmarks, 556 Nature 332 (2018).
61
Lipopolysaccharide is “a major component of the cell wall of gram-negative bacteria, a type of
endotoxin and important group-specific antigen (O antigen). The lipopolysaccharide molecule
consists of three parts: lipid A, a glycolipid responsible for the endotoxic activity, which is
covalently linked to a heteropolysaccharide chain.” Lipopolysaccharide, Dorland’s Med.
Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=28471 (last visited
May 4, 2021).

37
6. The authors also “found that individual cytokines applied peripherally may also elicit immune
memory effects in the brain.” Id. at 6.

The Wendeln et al. study, however, does not appear to be relevant here, since there is no
evidence that petitioner’s vaccine contained lipopolysaccharides.62 See Pet. Ex. 114 at 22, 40-
41. Dr. Gershwin testified that the reaction described in Wendeln et al. can apply to “other
instigators” or “generic materials,” and is not specific to lipopolysaccharides. Tr. 148. But he
did not describe what he meant by “other instigators” or “generic materials.”63

On cross-examination, Dr. Gershwin reiterated that inflammation that causes neurologic
diseases are caused by a combination of innate immune responses. Tr. 156. He testified that for
most people, cytokines developed after vaccination do not cause demyelination. Id. But he
emphasized that microglia and mononuclear cells can be actors in demyelination. Tr. 270. Th1
cytokines, for example, are inflammatory cytokines, and “the more inflammatory the cytokine is,
the more likely it is to produce neurotoxicity.” Tr. 156-57.

Dr. Gershwin agreed with Dr. Sriram that innate immunity is not T-cell mediated, but
disagreed with Dr. Sriram that T cells are required for demyelination to occur. Tr. 271. He
testified that innate immunity can cause demyelination. Tr. 157. However, petitioner provided a
number of medical articles that supported Dr. Sriram’s opinion that the adaptive immune system,
and T-cell mediated processes, are involved in the pathogenesis of MS. See, e.g., Pet. Ex. 87 at
29-32;64 Pet. Ex. 91 at 11-13.65

62
See Pet. Ex. 114 at 22 (noting the ingredients for the 2020-2021 Fluzone vaccine); Pet. Status
Rept., filed Dec. 7, 2020, at 1 (stating “petitioner’s counsel [was] unable to locate the ingredient
list or package insert for the 2013 Fluzone vaccine by Sanofi”).
63
Petitioner also cited an animal study where lipopolysaccharide was used to activate microglia,
resulting in the release of pro-inflammatory cytokines. See Pet. Ex. 29 (Alessandra di Penta et
al., Oxidative Stress and Proinflammatory Cytokines Contribute to Demyelination and Axonal
Damage in a Cerebellar Culture Model of Neuroinflammation, 8 PLoS ONE e54722 (2013)).
The activation was “associated with demyelination and axonal damage” within 24 hours in
mouse brain tissue in the in vitro study. Id. at 1, 10-11.
64
Scott S. Zamvil & Lawrence Steinman, The T Lymphocyte in Experimental Allergic
Encephalomyelitis, 8 Ann. Rev. Immunology 579 (1990).
65
Antoine Lamprone et al., Innate Immunity in the CNS: Redefining the Relationship Between
the CNS and Its Environment, 78 Neuron Rev. 214 (2013).

38
Additional articles supporting Dr. Sriram’s opinion were provided by petitioner’s other
expert, Dr. Kinsbourne. See, e.g., Pet. Ex. 35 at 3, 7; Pet. Ex. 38;66 Pet. Ex. 41.67 For example,
petitioner cited Karussis and Petrou, a 2014 article, which stated that “[t]he current pathogenetic
hypothesis in post-vaccination ADEM is that antigens of viral origin cross-react with myelin
components (molecular mimicry) and in a secondary manner induce a hyperergic reaction, that
leads to the development of disseminated demyelination.” Pet. Ex. 35 at 3. Molecular mimicry
is “the molecular similarity between the proteins of the viruses used for the vaccination and self-
antigens.” Id. at 7. In the context of vaccinations, “[it] also represents one of the main
immunopathogenetic mechanisms in post-vaccination CNS demyelination.” Id.

Dr. Gershwin also discussed the theory of trained immunity.68 Tr. 152-54; Pet. Ex. 107 at
3. He explained that trained immunity “implies that previous exposure to an infection or a
vaccine can accelerate innate immune responses.” Pet. Ex. 107 at 5; see also Tr. 153. Thus, “the
more things you’re exposed to, the faster your response is.” Tr. 153.

Netea et al.69 defined trained immunity as “an enhanced innate immune response to
different pathogens after an initial challenge, such as vaccination or infection.” Pet. Ex. 112 at 5.
The innate immune cells “display adaptive characteristics after certain infections or vaccines, a
property that is functionally similar to building immunological memory.” Id. at 3. This
“[g]reater protection against reinfection . . . has also been reported in plants and invertebrates,
which lack an adaptive immune system.” Id.

ii. Althen Prong Two

Dr. Gershwin opined that petitioner did not have an aberrant local response, but that he
did have an aberrant response in his brain to the flu vaccine

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Source: Frix Law Library, https://www.frixlaw.com/law-library/cases/4707162. Public record. Not legal advice.