VICP Registry Case Source Bundle
Canonical URL: https://vicp-registry.org/case/USCOURTS-cofc-1_15-vv-01137
Package ID: USCOURTS-cofc-1_15-vv-01137
Petitioner: Pitey Morgan
Filed: 2015-10-07
Decided: 2020-06-17
Vaccine: influenza
Vaccination date: 2012-10-16
Condition: longitudinally extensive transverse myelitis (LETM) / Neuromyelitis Optica Spectrum Disorder (NMOSD)
Outcome: denied
Award amount USD: 

AI-assisted case summary:
On October 7, 2015, Pitey Morgan filed a petition seeking compensation under the National Vaccine Injury Compensation Program, alleging that he developed longitudinally extensive transverse myelitis (LETM) as a result of an influenza vaccine received on October 16, 2012. Mr. Morgan, who was 54 years old at the time of vaccination, had a history of lower back pain, radiculopathy, degenerative disc disease, and prostatitis predating the vaccination. Following the vaccination, he experienced a rapid decline in leg strength, urinary retention, and numbness. Medical evaluations and imaging suggested an inflammatory process in the spinal cord. Initially, some treating physicians and Mr. Morgan's expert, Dr. Carlo Tornatore, believed he had LETM, possibly caused by the flu vaccine through molecular mimicry. However, respondent's expert, Dr. Subramaniam Sriram, and later treating physicians, concluded that Mr. Morgan's condition was more consistent with Neuromyelitis Optica Spectrum Disorder (NMOSD), a chronic, relapsing demyelinating disease, despite negative tests for the typical AQP4-IgG antibodies. The Chief Special Master denied compensation on December 4, 2019, finding that the evidence preponderated in favor of an NMOSD diagnosis and that Mr. Morgan failed to establish a reliable theory that the flu vaccine caused his NMOSD. The Special Master noted that while acute demyelinating conditions like TM are often monophasic, NMOSD is a chronic, relapsing condition, and that establishing a vaccine link to chronic demyelinating diseases is less consistent in program cases. The Special Master found Mr. Morgan's proposed theory of molecular mimicry lacked sufficient evidence connecting it specifically to the flu vaccine and NMOSD. The Special Master also found that the progression of Mr. Morgan's symptoms over several years was not reasonably attributable to the vaccination. On review, the United States Court of Federal Claims affirmed the Special Master's decision on June 17, 2020. The court found the Special Master's determination that Mr. Morgan suffered from NMOSD was not arbitrary or capricious, as it was supported by expert testimony and medical records, including evidence of dissemination in space and lesions in the periventricular region of the brain. The court also agreed that Mr. Morgan failed to meet the burden of proof for causation under the Althen prongs, particularly regarding the link between the flu vaccine and a chronic demyelinating condition like NMOSD, and that his arguments did not demonstrate the Special Master's conclusion was wholly implausible. Petitioner was represented by Sylvia Chin-Caplan and Timothy J. Mason, and respondent was represented by Joseph H. Hunt, C. Salvatore D’Alessio, Catharine E. Reeves, Heather L. Pearlman, and Zoe Wade. The decision was issued by Chief Special Master Brian H. Corcoran and reviewed by Judge Ryan T. Holte.

Theory of causation field:
Petitioner Pitey Morgan alleged that an influenza vaccine administered on October 16, 2012, caused him to develop longitudinally extensive transverse myelitis (LETM). Petitioner's expert, Dr. Carlo Tornatore, opined that the flu vaccine caused LETM through molecular mimicry, citing medical literature suggesting a link between vaccinations and TM and noting the close temporal relationship between vaccination and symptom onset. Respondent's expert, Dr. Subramaniam Sriram, and treating physicians concluded the diagnosis was Neuromyelitis Optica Spectrum Disorder (NMOSD), a chronic, relapsing demyelinating disease, and opined that the flu vaccine did not cause or contribute to NMOSD, citing a lack of evidence for a causal link between the flu vaccine and chronic demyelinating conditions like NMOSD, particularly when the mechanism proposed was molecular mimicry without specific evidence of antibody production related to the flu vaccine. The Special Master denied the claim, finding the evidence preponderated in favor of an NMOSD diagnosis and that Petitioner failed to establish a reliable theory connecting the flu vaccine to NMOSD. The Court of Federal Claims affirmed, agreeing that Petitioner did not meet the burden of proof for causation under the Althen prongs, specifically the lack of a scientifically reliable theory linking the flu vaccine to NMOSD. The case was litigated by Petitioner's counsel Sylvia Chin-Caplan and Timothy J. Mason, and Respondent's counsel Joseph H. Hunt, C. Salvatore D’Alessio, Catharine E. Reeves, Heather L. Pearlman, and Zoe Wade. Chief Special Master Brian H. Corcoran issued the initial decision, which was reviewed by Judge Ryan T. Holte. The outcome was denied.

Public staged source text:

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DOCUMENT 1: USCOURTS-cofc-1_15-vv-01137-1
Date issued/filed: 2020-01-07
Pages: 28
Docket text: PUBLIC DECISION (Originally filed: 12/04/2019) regarding 62 DECISION of Special Master, Signed by Chief Special Master Brian H. Corcoran. (ypb) Service on parties made.
--------------------------------------------------------------------------------
Case 1:15-vv-01137-RTH Document 68 Filed 01/07/20 Page 1 of 28
In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 15-1137V
(to be published)
* * * * * * * * * * * * * * * * * * * * * * * * *
*
PITEY MORGAN, *
* Chief Special Master Corcoran
Petitioner, *
* Filed: December 4, 2019
v. *
* Influenza Vaccine; Transverse
SECRETARY OF HEALTH AND * Myelitis; Neuromyelitis Optica
HUMAN SERVICES, * Spectrum Disorder; Chronic
* Demyelination; Evidence
Respondent. * Supporting Diagnosis
*
* * * * * * * * * * * * * * * * * * * * * * * * *
Sylvia Chin-Caplan, Law Office of Sylvia Chin-Caplan, LLC, Boston, MA, for Petitioner.
Amy P. Kokot, U.S. Dep’t of Justice, Washington, D.C., for Respondent.
ENTITLEMENT DECISION1
Pitey Morgan filed a petition on October 7, 2015, seeking compensation under the National
Vaccine Injury Compensation Program (“Vaccine Program”).2 Petition (“Pet.”) at 1 (ECF No. 1).
Mr. Morgan alleged that he developed longitudinally extensive transverse myelitis (“LETM”) due
to the influenza (“flu”) vaccine he received on October 16, 2012. Id.
An entitlement hearing was held in this matter on January 23, 2019. After consideration of
1 This Decision will be posted on the Court of Federal Claims’ website in accordance with the E-Government Act of
2002, 44 U.S.C. § 3501 (2012). This means that the Decision will be available to anyone with access to the
internet. As provided by 42 U.S.C. § 300aa-12(d)(4)(B), however, the parties may object to the Decision’s inclusion
of certain kinds of confidential information. Specifically, under Vaccine Rule 18(b), each party has fourteen days
within which to request redaction “of any information furnished by that party: (1) that is a trade secret or commercial
or financial in substance and is privileged or confidential; or (2) that includes medical files or similar files, the
disclosure of which would constitute a clearly unwarranted invasion of privacy.” Vaccine Rule 18(b). Otherwise, the
whole Decision will be available to the public in its current form. Id.
2 The Vaccine Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, 42 U.S.C. §§ 300aa-
10–37 (2012) (hereinafter “Vaccine Act” or “the Act”). Individual section references hereafter shall refer to § 300aa
of the Act.
1

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the record and testimony provided at hearing, I find that Petitioner is not entitled to a compensation
award. As discussed in more detail below, Petitioner has not offered preponderant evidence to
support the alleged diagnosis of LETM, whereas the record evidence preponderates in favor of an
alternative diagnosis: Neuromyelitis Optica Spectrum Disorder (“NMOSD”). He also has not
established a reliable theory explaining how the flu vaccine could have caused his NMOSD.
I. Factual Background
A. Medical History Prior to Vaccination
Prior to receiving the flu vaccine in October 2012, Mr. Morgan had several preexisting
health conditions, including lower back pain, lower extremity radiculopathy, multi-level
degenerative disc disease, lumbar spondylosis, and prostatitis. The nature and basis for these
diagnoses, along with Petitioner’s subsequent disease course, has some bearing on the claims
asserted herein.
The medical record establishes that Mr. Morgan’s lower back pain dated back to August
26, 2009 (three years before vaccination), when he saw Deborah Stayman, PA-C (“PA-C
Stayman”) for worsening lower back pain with onset three weeks prior. Ex. 4 at 6. He also
complained of pain radiating to his left thigh. Id. During a physical examination, PA-C Stayman
noted that Mr. Morgan exhibited decreased reflexes in his left achilles tendon. Id. Suspecting a
herniated or bulging lumbar disc, PA-C Stayman ordered an MRI3 study, which was conducted on
September 1, 2009. Ex. 2 at 1; Ex. 4 at 32–33. The MRI results showed “mild foraminal narrowing
at the L3–L4 and L4–L5 levels…with moderate foraminal narrowing bilaterally at L5–S1 level.
No significant spinal canal narrowing. There are disc bulges involving the lower two lumbar
levels.” Ex. 2 at 1; Ex. 4 at 32–33.
On September 28, 2009, Mr. Morgan was seen by Anthony Wilson, M.D. Ex. 2 at 9–10;
Ex. 4 at 10–11. After reviewing the results of the September MRI, Dr. Wilson referred him to
physical therapy. Ex. 2 at 9; Ex. 4 at 10. He later returned to Dr. Wilson on November 2, 2009,
and complained of persistent pain that the prescribed physical therapy was not assisting. Ex. 2 at
9; Ex. 4 at 13. Dr. Wilson advised Mr. Morgan to temporarily discontinue physical therapy and
3 Magnetic Resonance Imaging (MRI) is a diagnostic scanning tool that places the patient in a magnetic field rather
than exposing him to radiofrequency signals in a traditional x-ray. Mosby’s Manual of Diagnostic and Laboratory
Tests 1106–07 (5th ed. 2014) (hereinafter “Mosby’s”). An MRI provides several benefits over CT scans, such as
providing better contrast between normal and pathologic tissue as well as not being obscured by bone artifacts. Id. at
1107.
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ordered an EMG4 and nerve conduction study5. Ex. 2 at 9; Ex. 4 at 13. Mr. Morgan underwent this
testing on November 24, 2009, but the results of both tests were found to be within normal limits.
Ex. 2 at 12–15; Ex. 4 at 29. He was thereafter given a spinal nerve injection. Ex. 2 at 12; Ex. 4 at
29. He received several more spinal nerve injections between 2009 and 2010. Ex. 2 at 11, 16–17;
Ex. 4 at 24.
On January 13, 2011, Mr. Morgan presented to Shoreline Family Medicine and complained
of muscle stiffness, decreased range of motion, weakness, and radiating lower back pain. Ex. 5 at
44. During this visit, he was diagnosed with chronic lower back pain and degenerative disc disease,
and his Neurontin dosage was increased. Id. at 45. He continued to seek treatment at Shoreline
Family Medicine on a monthly basis. During these visits, he consistently complained of persistent
pain, stiffness, weakness, and radiating lower back pain, though not every symptom was present
at every visit. See id. at 38–43.
On May 16, 2011, Mr. Morgan returned to Shoreline Family Medicine and reported of
dizziness and nausea. Ex. 5 at 36–37. He was diagnosed with vertigo and was treated with
medication. Id. at 37. In the following months, he continued to complain of dizziness as well as
neck pain. Id. at 34–35. Then, on June 30, 2011, Mr. Morgan underwent an MRI of his cervical
spine, the results of which showed “[s]pondylosis causing some mild to moderate spinal canal
stenosis at C5-6 and C6-7. No frank herniated disc is appreciated.” Id. at 92. These results were
reviewed at a follow-up appointment at Shoreline Family Medicine on July 19, 2011, during which
Mr. Morgan complained of stiffness, neck pain, lower back pain, and radiating pain. Id. at 32–33.
The next year, Mr. Morgan underwent another MRI and x-ray on March 11, 2012, for lower
back pain and lower extremity radiculopathy. Ex. 8 at 191, 193. The results of the MRI showed
“[m]ulti level degenerative disc disease and lumbar spondylosis with slight interval progression
and worsening in the appearance of degenerative change at the L4-5 level.” Id. at 193. The x-ray
performed on Mr. Morgan’s lumbar spine demonstrated “no acute disease.” Id. at 192.
On August 6, 2012, Mr. Morgan returned to Shoreline Family Medicine, complaining of
trouble urinating and related concerns. Ex. 5 at 145. Following a physical examination, he was
diagnosed with prostatitis. Id. at 146. He thereafter returned to Shoreline Family Medicine for a
follow-up on September 5, 2012, at which time he complained of stiffness and lower back pain in
4 An EMG, or electromyography, test is a diagnostic method that measures the response to electrical stimulation of
muscle nerves. Dorland’s Illustrated Medical Dictionary 602 (32 ed. 2012) (hereinafter “Dorland’s”).
5 Nerve conduction studies are used in conjunction with EMGs to detect and locate peripheral nerve injuries or disease.
Mosby’s at 514.
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addition to citing the urological symptoms of frequency and oliguria6. Id. at 147. During this visit,
he was again diagnosed with prostatitis as well as lower back pain and bilateral sciatica. Id. at 148.
Mr. Morgan returned to Shoreline Family Medicine on September 24, 2012 and
complained of toe and thigh numbness with an onset of three weeks prior, as well as difficulty
initiating urination and waking up during the night to urinate. Ex. 5 at 149. A physical examination
revealed spinal tenderness and limited range of motion as well as decreased sensation in two of his
right toes. Id. at 150. Following this visit, Mr. Morgan underwent an ultrasound of his prostate.
Ex. 8 at 185. The results of the ultrasound were negative. Id.
On October 9, 2012, Mr. Morgan was again seen at Shoreline Family Medicine where he
reported lower back and pelvic pain, weakness, poor balance, fatigue, and sleep disturbances. Ex.
5 at 151. He was ordered to undergo a CT scan7 of his head. Id. at 152. The CT scan was performed
on October 12, 2012, and the results were unremarkable. Ex. 8 at 166.
B. Vaccination and Subsequent Concerns for Neurologic Injury
Mr. Morgan was 54 when he received the seasonal flu vaccination on October 16, 2012.
Ex. 1 at 1. The next day (October 17, 2012), Mr. Morgan saw Dr. Arthur Golin for a urologic
consultation. Ex. 22 at 7–8. During this visit, Petitioner told Dr. Golin (consistent with the record
in this case) that his urinary symptoms had begun the year before, but that “in the last 2 ½ months
his situation has deteriorated. It has been progressive and he notes marked hesitance, particularly
at night.” Id. at 8. Mr. Morgan also reported “increasing pain and some weakness in the right lower
extremity…numbness, right lateral thigh.” Id. A physical examination revealed an “enlarged,
benign-appearing [prostate] gland” and reduced tone of the anal sphincter. Id. at 7. Dr. Golin’s
assessment was urinary retention—but with a possible neurologic component. Id.
On October 22, 2012, Mr. Morgan returned to Shoreline Family Medicine, where he was
examined for lower back pain, persistent urinary symptoms, weakness, and radiating pain in his
legs. Ex. 5 at 153. He was prescribed medication for his prostatitis and instructed to return in one
week for a follow-up appointment. Id. at 154. The next day, Mr. Morgan was seen by Scott
Greenwald, M.D. at Michigan Pain Consultants for his lower back pain, which Mr. Morgan
described as radiating down both of his legs. Ex. 7 at 15. He also reported new numbness in
bilateral calves. Id. During the visit, he was assessed for bilateral lumbar radiculopathy and lumbar
degenerative disc disease, and he was treated with a lumbar epidural steroid injection. Id. at 17.
6 Oliguria is the diminished production and excretion of urine as compared to fluid intake. Dorland’s at 1318.
7 A computed tomography (CT) scan employs an emergent x-ray beam measured by a scintillation counter, with the
results recorded and processed by a computer for reconstruction display. Dorland’s at 1935. CT scans are useful when
a disease of the central nervous system is implicated and degenerative abnormalities can be identified. Mosby’s at
1026. A CT scan is generally preferable to an MRI during the initial trauma evaluation and the identification of
subarachnoid (hemorrhage) bleeding. Id.
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A few days later, on October 24, 2012, Mr. Morgan was seen by Justin Grill, D.O. in the
emergency room of North Ottawa Community Hospital. Ex. 6 at 20. He was assessed for urinary
retention, and again reported that he had been experiencing urinary incontinence issues for about
a year. Id. During a physical examination, Dr. Grill noted that Mr. Morgan “[m]oves all extremities
well.” Id. at 21. A Foley catheter was placed and Mr. Morgan was instructed to return if he
experienced any problems. Id. Later that same day, however, Mr. Morgan gradually lost the
strength in his legs until he was too weak to ambulate. Id. at 16.
Petitioner was thereafter transported by ambulance to the emergency room at Mercy Health
where he was evaluated by Christopher Hummel, D.O. for leg weakness and urinary retention. Ex.
6 at 13–19; Ex. 8 at 124. A physical evaluation revealed decreased rectal tone, decreased sensation
in his lower legs, saddle paresthesias, and buttocks numbness. Ex. 8 at 125. Following the
examination, Dr. Hummel expressed concern for possible cauda equina syndrome8 and epidural
hematoma given Mr. Morgan’s history of having a lumbar steroid injection the day prior. Id. at
126. An MRI was ordered, and the results showed “[m]ild lumbar disc degeneration, which does
not appear significantly changed as compared to 03/11/2012 . . . conus medullaris appears
somewhat indistinct with a suggestion of some increased T2-weighted signal intensity, of uncertain
significance given the limitations of the low field strength magnet.” Id. at 140, 143.
Mr. Morgan was subsequently transferred to Mercy Health – Hackley Campus (“Hackley”)
just a few hours later. Ex. 9 (ECF Nos. 9-1 to 9-3)9 at 733, 1209. During an initial evaluation
conducted by Christopher Marquart, M.D., Petitioner stated that he had first noticed mild weakness
in his lower extremities in August 2012 (two months before the vaccination in question) while he
was moving his daughter into college. Id. at 896. He explained that the patchy numbness and
tingling he experienced progressively increased over the previous two months and coincided with
his worsening urologic symptoms. Id. Dr. Marquart also noted in the history section of the record
that Petitioner had recently received the flu shot, and that he reported experiencing occasional
blurry vision. Id. at 897.
A physical examination revealed that Petitioner had “crude sensory level at about T12-L1
level,” as well as “patchy decreased pinprick and light touch over the anterior thighs bilaterally,
top of the right foot and bottom both the left heel and patchy over the area of the cath[eter],”
decreased strength, and absent reflexes in his lower extremities. Ex. 9 at 898. Dr. Marquart did not
note any mass, lesion, or herniated disc in Mr. Morgan’s MRI, but he did observe evidence of
nerve root clumping and enhancing in the conus—leading him to question whether Mr. Morgan
8 Cauda equina syndrome is characterized by dull, aching pain of the perineum, bladder, and sacrum that generally
radiates in a sciatic fashion. Dorland’s at 1824. It is typically caused by compression of the spinal nerve roots and is
associated with paresthesias. Id.
9 Exhibit 9 was filed as three separate, consecutively-paginated volumes.
5

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had experienced transverse myelitis (“TM”) or some other acute, neuro-inflammatory process. Id.
at 809, 899. Given these concerns, Mr. Morgan was admitted to the intensive care unit for
observation, “to make certain he does not have any type of ascending paralysis with the recent flu
vaccination.” Id. at 899.
Mr. Morgan underwent a second MRI on October 25, 2012, the results of which showed
“edema within the cord from T8 to the inferior tip of the cord…but no significant contrast
enhancement.” Ex. 5 at 80. That same day, Mr. Morgan was evaluated by an infectious disease
consultant, Roni Devlin, M.D. Ex. 9 at 711. Following a physical evaluation, Dr. Devlin indicated
that the MRI was suggestive of myelitis of indeterminate etiology—though he did later implicate
the flu vaccine, noting that “[c]ase reports of myelitis following vaccination have certainly been
reported, but rarely.” Id. at 714.
A few days later, on October 27, 2012, Mr. Morgan was evaluated by Larry Wahl, D.O,
who noted that Mr. Morgan had experienced “increasing urinary retention and some difficulty with
strength in his lower extremities, climbing stairs as much as 5-1/2 weeks ago that gradually
increased” and “seemed to reach a critical level 1 day after having an epidural steroid injection on
Tuesday [October 23, 2012].” Id. at 715. Within his differential diagnosis, Dr. Wahl included viral
infection, arachnoiditis, and TM, though he did express some skepticism towards TM as
explanatory given the extensive nature of Mr. Morgan’s spinal cord edema. Id. at 717.
While at Hackley, Mr. Morgan was treated with high dose steroids and intensive physical
therapy. Id. at 681. He gradually recovered the ability to stand, bear weight, and walk short
distances with the assistance of a walker, but he continued to experience numbness and tingling in
his lower extremities. Id. On October 29, 2012, he was discharged to outpatient rehabilitation and
was scheduled to return in one week for a follow-up with Dr. Marquart. Id. When Mr. Morgan
returned on November 15, 2012, Dr. Marquart reiterated his belief that Petitioner’s myelitis was
“probably a reaction to his flu vaccine for lack of a better explanation.” Ex. 10 at 1. A repeat MRI
conducted shortly thereafter on November 21, 2012, showed marked improvement in the
appearance of the spinal cord with only “very mild patchy cord edema.” Ex. 5 at 79.
On December 13, 2012, Mr. Morgan presented to Douglas Gelb, M.D. at the University of
Michigan Neurology Clinic. Ex. 14 at 6. While reviewing Mr. Morgan’s history, Dr. Gelb noted
that “[h]e has had low back pain for a few years, radiating into one or both legs at times, but never
causing numbness or weakness.” Id. In addition, before the October 16, 2012 vaccination, Mr.
Morgan “had noticed some numbness in his right fifth toe for about a month, and would tire a little
bit more easily.” Id. Mr. Morgan also reported that since his hospital discharge on October 29,
2012, he had not noticed much improvement in his ability to ambulate and felt as though his
neurologic symptoms were worsening. Id. He now specifically complained of persistent loss of
sensation in his lower extremities, bladder, and bowls, burning pains, the development of a lump
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on his neck, worsening vision, sudden arm jerks, and cramping or spasms in his fingers. Id.
Following a physical evaluation—in which Mr. Morgan exhibited mild spasticity in both
lower extremities, reduced sensation from the waist down, and absent reflexes in his ankles—Dr.
Gelb proposed that Mr. Morgan was experiencing either an isolated episode of TM or the first
instance of a recurrent, central nervous system (“CNS”) demyelinating disease, such as Multiple
Sclerosis10 (“MS”) or Neuromyelitis Optica11 (“NMO”). Id. at 8–9, 11. He acknowledged that Mr.
Morgan’s pre-vaccination symptoms “raise[d] some concern that he might have had an ongoing
disease process in his nervous system that ‘flared up’ on Oct. 24,” but noted that those earlier
symptoms were non-specific, or could be explained by Mr. Morgan’s degenerative disc disease
and enlarged prostate. Id. at 10–11. Overall, however, Dr. Gelb did not feel that Mr. Morgan’s
neurologic disease was progressing, instead attributing his change in vision to dexamethasone—
one of the medications Mr. Morgan was taking. Id. at 11. He instructed Mr. Morgan to taper off
dexamethasone and suggested a follow-up MRI as well as a serum NMO antibodies test. Id.
On December 20, 2012, Mr. Morgan returned to Dr. Wahl to discuss his progress. Ex. 11
at 5. During this visit, Mr. Morgan described continuing improvement of his neurologic symptoms,
and he demonstrated almost full strength throughout his lower extremities during his physical
evaluation. Id. In accordance with Dr. Gelb’s suggestion, Dr. Wahl ordered laboratory testing—
including an NMO serum antibodies test and a brain MRI. Id.
C. Ongoing Treatment of Neurologic Symptoms and Search for Etiology
Between December 20, 2012 and February 14, 2013, Mr. Morgan exhibited some
improvement in his neurologic symptoms, though Dr. Wahl expressed the view that a complete
recovery was unlikely, and that any further improvements would be small. Id. at 3–5. The result
of the NMO serum antibodies test was negative, but, as the results summary remarked,
“seronegativity does not necessarily preclude a diagnosis of [NMO].” Ex. 5 at 56 (emphasis
added). The results of the brain MRI conducted on January 7, 2013 were also negative. Id. at 76.
On April 29, 2013, Mr. Morgan returned to Dr. Wahl and reported little improvement but
denied any new symptoms. Ex. 11 at 2. On physical examination, he exhibited decreased strength
in both legs. Id. A repeat thoracic MRI was ordered and performed on May 20, 2013. Id.; Ex. 5 at
70. The results showed “[i]nterval change in the appearance of the thoracic spinal cord which
10 Multiple sclerosis is a disease in which there is demyelination of the central nervous system causing weakness,
incoordination, paresthesias, speech disturbances, and visual complaints. Dorland’s at 1680. Its course is characterized
by a series of relapses and remissions. Id.
11 NMO is characterized by the demyelination of the optic nerve and the spinal cord. Dorland’s at 1266. Symptoms
of NMO often include changes in vision, flaccid paralysis of the extremities, and sensory and genitourinary
disturbances. Id.
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demonstrates diffuse but mild expansion and increased intramedullary signal centrally between the
T6 level and the conus, the appearance here is suggestive of [TM].” Ex. 5 at 70.
In the weeks following, Mr. Morgan’s condition deteriorated such that by June 17, 2013,
he was unable to stand independently and exhibited increasingly diminished strength in his
bilateral lower extremities. Ex. 11 at 1. He presented to Ivan Landon, M.D. on July 23, 2013 with
concerns that he was experiencing a relapse of his symptoms. Ex. 12 at 14. Dr. Landon noted that
Mr. Morgan was now paraplegic, whereas he had previously been able to ambulate with the
assistance of a walker or cane. Id. at 14, 16. During his evaluation, Dr. Landon concluded that Mr.
Morgan had suffered at least one, maybe two, relapses and that he was likely suffering from a
polyphasic TM. Id. at 16. He suggested Mr. Morgan begin inpatient therapy as well as
immunoglobulin therapy. Id.
On July 31, 2013, Mr. Morgan was admitted to the inpatient rehabilitation unit at Hackley
for nine days, during which time he was treated with high dose steroids, IVIG, and intensive
physical therapy. Ex. 9 at 2–3. He saw some improvement with these treatments, and was
discharged to outpatient rehabilitation on August 8, 2013. Id. at 4. Petitioner continued his
treatment with Dr. Landon over the ensuing year (between August 2013 and June 2014). Ex. 12 at
1–12. Throughout, Dr. Landon noted that Mr. Morgan’s condition appeared to be deteriorating, as
he continued to experience recurrent symptoms relapses. Id. By June 17, 2014, Mr. Morgan was
restricted to a wheelchair and complained of symptoms in his upper extremities. Id. at 1. Dr.
Landon expressed his frustrations and emphasized that Mr. Morgan seemed to respond best to
IVIG coupled with steroids, but that his insurance company was no longer covering the cost of the
IVIG treatment. Id.
D. Embrace of NMO Diagnosis in 2014
On August 15, 2014, Mr. Morgan returned to the University of Michigan Neurology Clinic.
Ex. 14 at 93. During this appointment, Mr. Morgan reported that he had developed numbness in
his trunk that ascended from his waist to his mid-back, numbness in the tips of his fingers, and
blurry spots of vision within the past few months. Id. at 93–94. Dr. Gelb conducted a physical
examination and found that Mr. Morgan’s lower extremities were completely immobile,
areflexive, and exhibited reduced sensation to light touch and pain. Id. at 95. In his assessment,
Dr. Gelb expressed uncertainty as to “whether his clinical deterioration was due to [a] new episode
of spinal cord inflammation, or simply some systemic illness exacerbating his deficits from his
initial episode (although new episodes of inflammation seem more likely, given the severity and
persistence of the new deficits, and given the higher sensory level).” Id.
Such concerns prompted Dr. Gelb to refer Mr. Morgan to a MS clinic and order repeat
MRIs of Mr. Morgan’s cervical and thoracic spine and brain as well as a repeat serum NMO
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antibodies test. Ex. 14 at 95–96. The result of Mr. Morgan’s serum NMO antibodies test was again
negative, but the MRI of his thoracic spine now showed:
[V]olume retraction/myelomalacia, seen caudal to T8 level and extending down to
the conus, is non masslike abnormal enhancement predominantly involving central
and posterior portions of the spinal cord, which is more conspicuous at T12 and
T10-T11 levels…The spinal cord volume loss likely represent[s] myelomalacia as
the sequela of previous inflammatory process. Areas of T2 signal change and
abnormal enhancement could represent reactivation of inflammatory process, this
possibility should be correlated with deficits on physical exam and paraclinical
test/parameters.
Id. at 135, 137. In addition, Mr. Morgan’s brain MRI revealed “nonspecific small areas of
nonenhancing T2 signal prolongation in predominantly left supratentorial white matter, these
findings may represent sequela from previous inflammatory, infectious or small vessel white
matter ischemic process.” Id. at 137.
Following Dr. Gelb’s recommendation, Mr. Morgan went to the University of Michigan
MS Clinic and was evaluated by Robert Pace, M.D. on November 26, 2014. Ex. 14 at 109. During
a physical examination, Mr. Morgan demonstrated reduced tone, absent movement, and absent
reflexes in bilateral lower extremities, and absent sensation below midthoracic level. Id. at 110.
Dr. Pace also reviewed the MRI results from the August 2014 scans, noting:
[S]everal nonspecific T2/FLAIR hyperintensities seen in the brain. These are not
in a pattern that is strongly suggestive of demyelination such as would be seen with
[MS]. However, there is T2 hyperintensity in the fourth ventricle surrounding the
cerebral aqueduct. This is of unclear significance, but can be seen in [NMO]
spectrum….
Id. He also noted “patchy enhancement of the lower thoracic spine/conus medullaris that appears
to involve some of the cauda equina.” Id.
Based on his review of the laboratory testing and imaging studies, Dr. Pace now diagnosed
Mr. Morgan with “longitudinal myelitis due to [NMO], sero-negative.” Id. Dr. Pace emphasized
that there was a high likelihood that Mr. Morgan’s condition would cause “recurrent and
potentially devastating episodes of myelitis if untreated” and therefore advised him to begin
immune modulation therapy. Id. He remarked that Mr. Morgan had experienced significant
improvement with IVIG treatment in the past but opined that the most effective treatment for
patients with NMO is Rituximab. Id. at 110–11.
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Mr. Morgan did not receive either treatment, although he pursued physical therapy from
July to September 2015. Ex. 23 at 2; Ex. 8 at 1–11. He then returned to Dr. Pace on August 18,
2015 at the University of Michigan MS Clinic. Ex. 23 at 2. The medical records from the visit list
Mr. Morgan’s diagnoses as relapsing-remitting MS, Devic’s disease12, and flaccid paralysis of the
lower extremities. Id. at 1. During the appointment, Mr. Morgan reported persistent paralysis in
his lower extremities and numbness from the midthoracic region down. Id. at 2. He did, however,
feel that he was cognitively doing better than before. Id. Dr. Pace ordered repeat MRIs and hepatitis
serologies. Id. at 3–4. Those MRIs showed that the nonspecific signal hyperintensities located in
the periventricular13 area of the brain were stable since January. Ex. 21 at 1. No cervical spine
abnormalities were noted, however, and the previously documented areas of abnormal signal in
the thoracic region of the spinal cord had resolved. Id. at 5.
Mr. Morgan returned to Dr. Pace on April 20, 2016. Ex. 53 at 40. During this visit, he
explained that he had not pursued Rituximab therapy but was seeing improvement with physical
therapy. Id. at 41. He was still confined to a wheelchair, but he had not developed any new or
worsening symptoms. Id. Following a physical examination, Dr. Pace again opined that Mr.
Morgan’s diagnosis was “most likely seronegative [NMO].” Id. at 42. Mr. Morgan returned for a
follow-up appointment with Dr. Pace the following year, in April 2017. Id. at 18. He again reported
improvement with continued physical therapy and denied any new or worsening symptoms. Id. A
physical exam revealed that Mr. Morgan was able to activate his hip flexors and extensors, which
were actions he was incapable of performing the year prior. Id. at 19. Dr. Pace also reviewed the
results of MRIs performed in 2017 and noted that the changes in Mr. Morgan’s spine were stable
and that there was no evidence of new or enhancing lesions. Id. at 19–20. The final diagnoses
documented in the differential at the conclusion of the appointment were NMO, acute TM,
paralytic syndrome, and spinal stenosis of the cervical region. Id. at 21.
II. Witness Testimony
A. Petitioner’s Expert Witness - Dr. Carlo Tornatore, M.D.
Dr. Tornatore testified at hearing and provided two reports on Petitioner’s behalf. See
generally Ex. 24, filed Oct. 27, 2016 (ECF No. 18-1) (“Tornatore First Rep.”); Ex. 47, filed Oct.
5, 2017 (ECF No. 36-1) (“Tornatore Second Rep.”). Dr. Tornatore opined that Mr. Morgan
developed LETM following his October 16, 2012 vaccination, and that Petitioner’s dramatic post-
vaccination decline could not be attributed to any of his preexisting conditions. Additionally, he
asserted that the close temporal connection between onset and vaccination, plus a lack of alternate
explanation, meant that Mr. Morgan’s vaccination more likely than not was the reason for his
12 NMO is sometimes referred to as Devic’s disease. Dorland’s at 503.
13 The prefix peri- means “near” or “around.” Dorland’s at 1410. Therefore, if a brain lesion is periventricular, it is
located near the ventricles of the brain.
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condition.
Dr. Tornatore is a board-certified neurologist currently employed in the Department of
Neurology of the Georgetown University Medical Center. Curriculum Vitae of Dr. Tornatore, filed
Oct. 28, 2016, at 1 (ECF No. 19-1) (“Tornatore CV”). He received his master’s and medical
degrees from Georgetown University after completing his bachelor’s degree from Cornell
University. Id. at 2. He has been licensed to practice medicine since 1988 and completed an
internship in internal medicine at Providence Hospital, a residency in neurology at Georgetown
University Hospital, and a fellowship in molecular virology at the National Institute of Health. Id.
He currently holds an academic position at the Georgetown University Medical Center where he
serves as the Residency Program Director as well as the Director of the Neurology Clerkship
program for third year medical students. Id. at 7. His clinical experience includes serving as the
Vice Chairman for the Department of Neurology and Director of the Georgetown University
Hospital Multiple Sclerosis Clinic. Id. at 3. He has published numerous articles on various
neurological issues, and he is frequently invited to lecture on topics within the field of neurology.
Id. at 7–19.
At hearing, Dr. Tornatore reviewed Mr. Morgan’s pre- and post-vaccination medical
history in depth. He acknowledged (as several points in the pre-vaccination record reflect) that Mr.
Morgan had a significant medical history of lower back pain, radicular symptoms, and bladder
issues. Trial Transcript (“Tr.”) at 12, 15, 19; Ex. 5 at 146, 148. He emphasized, however, his view
that Mr. Morgan’s preexisting symptoms were likely attributable to his degenerative disc disease,
sciatica and prostatitis—none of which were neurologic in etiology. Tr. 17, 19–20, 25–26; Ex. 4
at 7; Ex. 5 at 148.
In making this distinction, Dr. Tornatore relied on the progression of Mr. Morgan’s
symptoms, and more specifically, the tempo of that progression. Tr. at 11, 58. He opined that Mr.
Morgan’s pre-vaccination symptoms had “a very slow progression” that was incongruent with the
faster tempo typically associated with LETM. Id. at 18, 29. He further explained that a slow,
gradual progression of NMO or NMOSD is very uncommon, and in fact is an exclusionary
characteristic when diagnosing NMOSD. Id. at 30–31; see also D. Wingerchuk, et al.,
International Consensus Diagnostic Criteria for Neuromyelitis Optica Spectrum Disorders, 85
Neurology 177, 179 (2015), filed as Ex. E, June 23, 2017 (ECF No. 33) (“Wingerchuk”).
Therefore, the drawn-out progression of Mr. Morgan’s symptoms prior to vaccination suggested
that Mr. Morgan was not at that time suffering from LETM or NMO. Tr. at 58.
After vaccination, by contrast, Mr. Morgan clearly experienced a catastrophic and abrupt
collapse. Id. at 10, 18; Ex. 9 at 711–12. Dr. Tornatore highlighted the difference between the slow
and steady progression of Mr. Morgan’s lower back pain over several years and his urologic
symptoms over the course of months, versus the accelerated and dramatic deterioration he
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experienced one week after receiving the flu shot. Tr. at 10, 18. In light of this sharp decline, Dr.
Tornatore opined that Mr. Morgan’s pre-vaccination conditions were readily distinguishable from
those he experienced post-vaccination. Tr. at 70–72.
Dr. Tornatore also maintained that Petitioner’s proper diagnosis was LETM rather than
NMOSD. Tr. at 9, 59, 68. Dr. Tornatore described TM as a rare clinical syndrome in which an
immune-mediated process causes inflammation within the spinal cord, resulting in scarring and
neural injury. Tornatore First Rep. at 2–3. This inflammatory process causes varying degrees of
weakness, sensory alterations and autonomic dysfunction. Id. LETM is specifically characterized
by inflammation that extends through three or more segments of the spinal cord. D. Karussis, et
al., The Spectrum of Post-Vaccination Inflammatory CNS Demyelinating Syndromes,
Autoimmunity Reviews 1, 6 (2013), filed as Ex. 55, Dec. 19, 2018 (ECF No. 50-4).
In describing the relationship between LETM and NMOSD, Dr. Tornatore espoused the
opinion that LETM is an umbrella diagnosis that actually encompasses the more discreet diagnosis
of NMOSD. Tr. at 9, 66–67. This position, however, was undercut by the medical literature
submitted in support of Petitioner’s claim, which described NMOSD as “an inflammatory disease
of the [CNS], mostly involving the optic nerve and the spinal cord…and frequently manifest[ing]
as severe bilateral optic neuritis or severe longitudinally extensive transverse myelitis.” S. Kim, et
al., Differential Diagnosis of Neuromyelitis Optica Spectrum Disorders, 10 Therapeutic Advances
in Neurological Disorders 265, 265 (2017) (emphasis added), filed as Ex. 49, Dec. 19, 2018 (ECF
No. 49-2) (“Kim”).
Dr. Tornatore further opined that Mr. Morgan did not meet the strict diagnostic criteria for
NMO or NMOSD. Tr. at 48–49, 69. Because Mr. Morgan tested negative for the serum aquaporin-
4 antibodies (“AQP4-IgG”) normally associated with NMO, and had not been diagnosed with a
related disorder within the spectrum, he would have to meet additional, more stringent, diagnostic
criteria. See Wingerchuk at 179. Patients who are seronegative for AQP4-IgG—like Mr. Morgan—
must exhibit two or more core clinical characteristics such as optic neuritis, acute myelitis, area
postrema syndrome14, acute brainstem syndrome, symptomatic narcolepsy, or acute diencephalic
clinical syndrome with NMOSD-typical diencephalic MRI lesions, or symptomatic cerebral
syndrome with NMOSD-typical brain lesions. Id.
Mr. Morgan, Dr. Tornatore opined, had only exhibited one of these core clinical
characteristics: acute myelitis. But this was insufficient to support a diagnosis of NMO or NMOSD
because there were no other core clinical characteristics observed, nor was there dissemination in
space or time of the transverse myelitis. Tr. at 68. He also noted that Mr. Morgan did not fit the
14 The area postrema is located within the walls of the brain’s fourth ventricle. See E. Benarroch, Circumventricular
Organs: Receptive and Homeostatic Functions and Clinical Implications, 77 Neurology 1198, 1198 (2011), filed on
as Court Exhibit 1, Dec. 6, 2019 (ECF No. 63) (“Benarroch”). In NMO, Area Postrema syndrome is characterized by
“intractable nausea, vomiting, and hiccups in various combinations.” Id. at 1202.
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demographic profile typically associated with an increased risk of developing such an autoimmune
disorder. Id. at 49. While Mr. Morgan’s disease process had proven to be relapsing and remitting,
TM was not always monophasic, and thus a person with TM could experience relapses. Id. at 50.
Accordingly, Dr. Tornatore concluded that the proper diagnosis for Mr. Morgan’s condition was
a relapsing and remitting LETM. Id. at 9, 59, 68.
Besides offering an opinion on diagnosis, Dr. Tornatore posited that Petitioner’s October
2012 flu vaccine likely caused him to develop LETM, through the mechanism of molecular
mimicry. Tornatore First Rep. at 3–4; Tr. at 59–60. In support, he referenced several pieces of
medical literature that discuss the theory of molecular mimicry and its putative relationship to the
development of TM. See D. Kerr, et al., Immunopathogenesis of Acute Transverse Myelitis,
Current Opinion in Neurology 339, 342–43 (2002), filed as Ex. 26, Nov. 7, 2016 (ECF No. 20-1)
(discussing the possibility of an immunologically mediated pathogenesis of ATM following
immunization and the presence of autoantibodies in patients with recurrent ATM); see also N.
Nakamura, et al., Neurologic Complications Associated with Influenza Vaccination: Two Adult
Cases, 42 Internal Med. 191, 193–94 (2003), filed as Ex. 34, Nov. 7, 2016 (ECF No. 20-1)
(discussing the theory of molecular mimicry as it applied to a patient who developed TM following
receipt of the flu vaccine); C. Wu, et al., Hemorrhagic Longitudinally Extensive Transverse
Myelitis, Case Reports Neurologic Med. 1, 3 (2016), filed as Ex. 48, Dec. 19, 2018 (ECF No. 49-
1) (discussing the likelihood of cross-reactivity between infectious agents and the central nervous
system).
Dr. Tornatore also supported his theory of molecular mimicry by referring to statements
made by one of Mr. Morgan’s primary treating physicians, Dr. Gelb. Tr. at 41–42. In particular,
he referenced a note in which Dr. Gelb explained numerous causes of myelitis and proposed that
Mr. Morgan’s condition was most likely associated with “a one-time activation of the immune
system…either triggered by something systemic (such as an immunization, infection, surgery, or
trauma) or apparently spontaneous.” Id. at 42; Ex. 14 at 10–11. This statement, Dr. Tornatore
opined, was reliable treater support for the causal relationship between Mr. Morgan’s flu
immunization and his subsequent condition. Tr. at 42. He emphasized that the time that had elapsed
between Mr. Morgan’s receipt of the flu vaccine and the onset of his LETM-related symptoms—
a period of nine days—was an adequate amount of time for the molecular mimicry mechanism to
initiate a demyelinating autoimmune disease. Id. at 50.
On cross examination, Dr. Tornatore acknowledged that Mr. Morgan might have
experienced a prolonged onset of LETM prior to vaccination. Id. at 57. He also agreed that many
of Mr. Morgan’s pre-vaccination symptoms were associated with neuropathies. Id. at 52–58. He
nevertheless maintained that Mr. Morgan’s pre-vaccination symptoms were more likely
attributable to unrelated, non-neurologic conditions such as prostatitis and/or degenerative disc
disease. Id. at 12, 16–17, 20, 25–26. In addition, he reiterated his belief that the temporal
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progression of Mr. Morgan’s symptoms distinguished his pre- and post-vaccination conditions—
the slow, gradual, progression of his pre-vaccination symptoms over several years was
characterized as markedly different from the post-vaccination deterioration Mr. Morgan
experienced over the course of a few hours on October 24, 2012. Id. at 11, 58.
C. Respondent’s Expert Witness: Dr. Subramaniam Sriram, M.D.
Dr. Sriram testified at hearing and provided two reports on behalf of Respondent. See
generally Ex. A, filed Jun. 23, 2017 (ECF No. 33-1) (“Sriram First Rep.”); Ex. F, filed Dec. 22,
2017 (ECF No. 38-1) (“Sriram Second Rep.”). Dr. Sriram, a specialist in neuroimmunology,
opined that Petitioner did not suffer from a monophasic occurrence of TM, but rather a clinically
relapsing form of LETM, or inflammatory myelitis, nevertheless falling within the overall
diagnostic category of NMOSD. Tr. at 82–84, 104; Sriram First Rep. at 5. He also opined that the
onset of Mr. Morgan’s inflammatory myelitis likely pre-dated his vaccination. Tr. at 96; Ex. A at
6.
Dr. Sriram is a board-certified neurologist with a focus in neuroimmunology. See Ex. B,
filed Jun. 23, 2017 (ECF No. 33-2) (“Sriram CV”). He obtained a Bachelor of Medicine and a
Bachelor of Surgery from the University of Madras in Madras India. Id. at 1. He then served as an
intern and resident at Wayne State University and completed a residency in neurology at Stanford
University, where he also served as chief resident and eventually completed a post-doctoral
fellowship in neuroimmunology. Id. Currently, Dr. Sriram serves director of the Vanderbilt
Multiple Sclerosis Clinic. Tr. at 76. He also holds academic positions as a professor of
experimental neurology and therapeutics as well as an associate professor in molecular biology
and immunology. Sriram CV at 1. Dr. Sriram’s clinical practice includes seeing patients two and
a half days a week. Tr. at 76. Additionally, he has published numerous articles about demyelinating
diseases and the neuroimmunological pathogenesis for those conditions. Sriram CV at 9–20.
Much like Dr. Tornatore, Dr. Sriram discussed Mr. Morgan’s pre- and post-vaccination
medical records at length during his testimony. First, Dr. Sriram opined that the neurologic and
urologic symptoms Mr. Morgan was experiencing in the months preceding vaccination were likely
the early manifestations of a demyelinating condition. Sriram First Rep. at 6; Tr. at 92–96. To
support this contention, Dr. Sriram cited several records in which Petitioner sought medical
treatment for difficulty urinating, toe and thigh numbness, numbness and tingling in his legs,
weakness, poor balance, and pelvic pain prior receiving the flu vaccination to October 16, 2012.
Ex. 5 at 145–51; Ex. 22 at 8. While he did acknowledge that a slow neurological worsening over
months to years is very uncommon in NMOSD, Dr. Sriram emphasized that the symptoms Mr.
Morgan experienced signified “a continuum of neurological deficits that began sometime around
the end of August, beginning of September [2012]” and ultimately culminated in what Dr. Sriram
characterized as a clinically relapsing form of LETM within NMOSD. Tr. at 81–84, 127–28, 160.
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Dr. Sriram took issue with Dr. Tornatore’s interpretation of the post-vaccination record,
and in particular what it says about Petitioner’s proper diagnosis. He acknowledged that Mr.
Morgan was seronegative for the hallmark antibody associated with NMOSD—AQP4-IgG. Tr. at
106. He explained, however, that some individuals with NMOSD will present as seronegative15
but still otherwise meet the diagnostic criteria for NMOSD. Tr. at 87–92, 108, 110–113; Sriram
First Rep. at 6; Wingerchuk at 179. For such a patient to be properly diagnosed with NMOSD, Dr.
Sriram explained, they would need to exhibit at least two core clinical characteristics—optic
neuritis, acute myelitis, area postrema syndrome, acute brainstem syndrome, symptomatic
narcolepsy or acute diencephalic syndrome with NMOSD-typical diencephalic MRI lesions, or
symptomatic cerebral syndrome with NMOSD-typical brain lesions—with at least one of the core
characteristics being optic neuritis, acute myelitis with LETM, or area postrema syndrome,
dissemination in space, and fulfillment of additional MRI requirements, as applicable. Sriram First
Rep. at 6; Wingerchuk at 179.
Here, Dr. Sriram maintained, Mr. Morgan met the diagnostic criteria for seronegative
NMOSD because he exhibited two of those core clinical characteristics—myelitis plus an area
postrema brain lesion—and also because the initial lesion extending to T8 on the October 25, 2012
MRI was later found to have extended to T6 on the May 20, 2013 MRI, thereby exhibiting
dissemination in space. Tr. at 108, 110–11, 113; Ex. 5 at 70, 80. On cross examination, however,
Dr. Sriram conceded that none of the MRI reports in the record unquestionably indicated the
presence of a postrema area brain lesion—at most, the record revealed hyperintensity in the
periventricular region of the brain where the area postrema is located. Tr. at 114–15, 117; Ex. 21
at 1. Additionally, while the medical records indicate that a brain lesion existed, Dr. Sriram
acknowledged that Mr. Morgan had not experienced any symptoms typically associated with area
postrema syndrome, though he also noted that it is not uncommon for lesions to be “silent” or
asymptomatic. Tr. at 111–12.
During cross examination, Dr. Sriram agreed that “’[r]ecurrent isolated episodes of optic
neuritis or myelitis do not qualify [for the diagnosis of NMOSD] in the absence of [evidence of]
AQP4-IgG given the broad differential diagnosis of these syndromes.’” Tr. at 115–17 (quoting B,
Weinshenker, et al., Neuromyelitis Spectrum Disorders, 92 Mayo Clinic Proc. 663, 666 (2017),
filed as Ex. G, Dec. 19, 2018 (ECF No. 47). He emphasized, however, that TM is generally
considered a monophasic disease—especially when it has a post-infectious etiology—whereas
15 Dr. Sriram proposed several explanations as to why a patient might be seronegative for this otherwise-critical
biomarker of NMOSD. Tr. at 91–92. One such explanation is that the test used to detect the presence of AQP4-IgG
has low sensitivity. Id. A second explanation is that Mr. Morgan was treated with corticosteroids, which would have
suppressed Mr. Morgan’s immune system. Id. at 92. Additionally, it is understood that, although rare, NMOSD
attributable to an infectious process can initially manifest as LETM. Kim at 279. Under such circumstances, a patient
will be seronegative for AQP4-IgG. Id. at 280.
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NMOSD is typically considered to be a chronic condition, with sixty to seventy percent of patients
with NMOSD experiencing relapse. Tr. at 86, 90. Dr. Sriram also opined that even if Mr. Morgan’s
presentation was initially considered characteristic of TM, his subsequent relapse in June 2013
warranted reconsideration of the initial TM diagnosis. Id. at 90–91. Taking into account the
entirety of Mr. Morgan’s clinical course, Dr. Sriram opined, the record suggested that the proper
diagnosis was actually clinically relapsing LETM within NMOSD. Id. at 82.
III. Procedural History
After this case was initiated and following the filing of pertinent medical records,
Respondent filed his Rule 4(c) Report on May 6, 2016, contesting Mr. Morgan’s entitlement to
damages on May 6, 2016. ECF No. 14. I subsequently ordered the parties to file expert reports in
support of their respective positions, and they did so as set forth above. I thereafter set the matter
for hearing on January 23, 2019 (ECF No. 41). The hearing took place as scheduled and included
testimony from the experts identified above. Following the hearing’s conclusion, the parties
submitted post-hearing briefs on June 17, 2019 (ECF No. 60 and 61). This matter is now ripe for
resolution.
IV. Applicable Legal Standards
A. Claimant’s Burden in Vaccine Program Cases
To receive compensation in the Vaccine Program, a petitioner must prove either: (1) that
he suffered a “Table Injury”—i.e., an injury falling within the Vaccine Injury Table—
corresponding to one of the vaccinations in question within a statutorily prescribed period of time
or, in the alternative, (2) that his illnesses were actually caused by a vaccine (a “Non-Table
Injury”). See Sections 11(c)(1), 13(a)(1)(A), 14(a); see also Moberly v. Sec’y of Health & Human
Servs., 592 F.3d 1315, 1321 (Fed. Cir. 2010); Capizzano v. Sec’y of Health & Human Servs., 440
F.3d 1317, 1320 (Fed. Cir. 2006).16 In this case, Petitioner does not assert a Table claim.
For both Table and Non-Table claims, Vaccine Program petitioners bear a “preponderance
of the evidence” burden of proof. Section 13(a)(1)(a). That is, a petitioner must offer evidence that
leads the “trier of fact to believe that the existence of a fact is more probable than its nonexistence
before [they] may find in favor of the party who has the burden to persuade the judge of the fact’s
existence.” Moberly, 592 F.3d at 1322 n.2; see also Snowbank Enters. v. United States, 6 Cl. Ct.
476, 486 (1984) (mere conjecture or speculation is insufficient under a preponderance standard).
Proof of medical certainty is not required. Bunting v. Sec’y of Health & Human Servs., 931 F.2d
16 Decisions of special masters (some of which I reference in this ruling) constitute persuasive but not binding
authority. Hanlon v. Sec’y of Health & Human Servs., 40 Fed. Cl. 625, 630 (1998). By contrast, Federal Circuit rulings
concerning legal issues are binding on special masters. Guillory v. Sec’y of Health & Human Servs., 59 Fed. Cl. 121,
124 (2003), aff’d 104 F. App’x 712 (Fed. Cir. 2004); see also Spooner v. Sec’y of Health & Human Servs., No. 13-
159V, 2014 WL 504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014).
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867, 873 (Fed. Cir. 1991). In particular, a petitioner must demonstrate that the vaccine was “not
only [the] but-for cause of the injury but also a substantial factor in bringing about the injury.”
Moberly, 592 F.3d at 1321 (quoting Shyface v. Sec’y of Health & Human Servs., 165 F.3d 1344,
1352–53 (Fed. Cir. 1999)); Pafford v. Sec’y of Health & Human Servs., 451 F.3d 1352, 1355 (Fed.
Cir. 2006). A petitioner may not receive a Vaccine Program award based solely on his assertions;
rather, the petition must be supported by either medical records or by the opinion of a competent
physician. Section 13(a)(1).
In attempting to establish entitlement to a Vaccine Program award of compensation for a
Non-Table claim, a petitioner must satisfy all three of the elements established by the Federal
Circuit in Althen v. Secretary of Health & Human Services, 418 F.3d 1274, 1278 (Fed. Cir. 2005):
“(1) a medical theory causally connecting the vaccination and the injury; (2) a logical sequence of
cause and effect showing that the vaccination was the reason for the injury; and (3) a showing of
proximate temporal relationship between vaccination and injury.” Althen, 418 F.3d at 1278.
Each of the Althen prongs requires a different showing. Under Althen prong one, petitioners
must provide a “reputable medical theory,” demonstrating that the vaccine received can cause the
type of injury alleged. Pafford, 451 F.3d at 1355–56 (citations omitted). To satisfy this prong, a
petitioner’s theory must be based on a “sound and reliable medical or scientific explanation.”
Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 548 (Fed. Cir. 1994). Such a theory
must only be “legally probable, not medically or scientifically certain.” Id. at 549.
Petitioners may satisfy the first Althen prong without resort to medical literature,
epidemiological studies, demonstration of a specific mechanism, or a generally accepted medical
theory. Andreu v. Sec’y of Health & Human Servs., 569 F.3d 1367, 1378–79 (Fed. Cir. 2009)
(citing Capizzano, 440 F.3d at 1325–26). Special masters, despite their expertise, are not
empowered by statute to conclusively resolve what are essentially thorny scientific and medical
questions, and thus scientific evidence offered to establish Althen prong one is viewed “not through
the lens of the laboratorian, but instead from the vantage point of the Vaccine Act’s preponderant
evidence standard.” Id. at 1380. Accordingly, special masters must take care not to increase the
burden placed on petitioners in offering a scientific theory linking vaccine to injury. Contreras v.
Sec’y of Health & Human Servs., 121 Fed. Cl. 230, 245 (2015), vacated on other grounds, 844
F.3d 1363 (Fed. Cir. 2017).
In discussing the evidentiary standard applicable to the first Althen prong, many decisions
of the Court of Federal Claims and Federal Circuit have emphasized that petitioners need only
establish a causation theory’s biological plausibility (and thus need not do so with preponderant
proof). Tarsell v. United States, 133 Fed. Cl. 782, 792–93 (2017) (special master committed legal
error by requiring petitioner to establish first Althen prong by preponderance; that standard applied
only to second prong and petitioner’s overall burden); Contreras, 121 Fed. Cl. at 245 (“Plausibility
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. . . in many cases may be enough to satisfy Althen prong one.” (emphasis in original)); see also
Andreu, 569 F.3d at 1375. At the same time, there is contrary authority from the Federal Circuit
suggesting that the same preponderance standard used overall in evaluating a claimant’s success
in a Vaccine Act claim is also applied specifically to the first Althen prong. See, e.g., Broekelschen
v. Sec’y of Health & Human Servs., 618 F.3d 1339, 1350 (Fed. Cir. 2010) (affirming special
master’s determination that expert “had not provided a ‘reliable medical or scientific explanation’
sufficient to prove by a preponderance of the evidence a medical theory linking the [relevant
vaccine to relevant injury].”) (emphasis added). Regardless, one thing remains: petitioners always
have the ultimate burden of establishing their Vaccine Act claim overall with preponderant
evidence. W.C. v. Sec’y of Health & Human Servs., 704 F.3d 1352, 1356 (Fed. Cir. 2013) (citations
omitted); Tarsell, 133 Fed. Cl. at 793 (noting that Moberly “addresses the petitioner’s overall
burden of proving causation-in-fact under the Vaccine Act” by a preponderance standard).
The second Althen prong requires proof of a logical sequence of cause and effect, usually
supported by facts derived from a petitioner’s medical records. Althen, 418 F.3d at 1278; see also
Andreu, 569 F.3d at 1375–77; Capizzano, 440 F.3d at 1326; Grant v. Sec’y of Health & Human
Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992). In establishing that a vaccine “did cause” injury, the
opinions and views of the injured party’s treating physicians are entitled to some weight. Andreu,
569 F.3d at 1367; Capizzano, 440 F.3d at 1326 (“[M]edical records and medical opinion testimony
are favored in vaccine cases, as treating physicians are likely to be in the best position to determine
whether a ‘logical sequence of cause and effect show[s] that the vaccination was the reason for the
injury.’” (quoting Althen, 418 F.3d at 1280)). Medical records are generally viewed as particularly
trustworthy evidence, since they are created contemporaneously with the treatment of the patient.
Cucuras v. Sec’y of Health & Human Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993).
Medical records and/or statements of a treating physician’s views, however, do not per se
bind the special master to adopt the conclusions of such an individual, even if they must be
considered and carefully evaluated. Section 13(b)(1) (providing that “[a]ny such diagnosis,
conclusion, judgment, test result, report, or summary shall not be binding on the special master or
court”); Snyder v. Sec’y of Health & Human Servs., 88 Fed. Cl. 706, 746 n.67 (2009) (“[T]here is
nothing . . . that mandates that the testimony of a treating physician is sacrosanct—that it must be
accepted in its entirety and cannot be rebutted.”). As with expert testimony offered to establish a
theory of causation, the opinions or diagnoses of treating physicians are only as trustworthy as the
reasonableness of their suppositions or bases. The views of treating physicians should also be
weighed against other, contrary evidence present in the record—including conflicting opinions
among such individuals. Hibbard v. Sec’y of Health & Human Servs., 100 Fed. Cl. 742, 749 (2011)
(finding that it is not arbitrary or capricious for special masters to weigh competing treating
physicians’ conclusions against each other), aff’d, 698 F.3d 1355 (Fed. Cir. 2012); Caves v. Sec’y
of Dept. of Health & Human Servs., No. 06-522V, 2011 WL 1935813, at *17 (Fed. Cl. Spec. Mstr.
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Apr. 29, 2011), mot. for review denied, 100 Fed. Cl. 344, 356 (2011), aff’d without op., 475 Fed.
App’x 765 (Fed. Cir. 2012).
The third Althen prong requires establishing a “proximate temporal relationship” between
the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been equated to the
phrase “medically-acceptable temporal relationship.” Id. A petitioner must offer “preponderant
proof that the onset of symptoms occurred within a timeframe which, given the medical
understanding of the disorder’s etiology, it is medically acceptable to infer causation.” de Bazan
v. Sec’y of Health & Human Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for
what is a medically acceptable timeframe must also coincide with the theory of how the relevant
vaccine can cause an injury (Althen prong one’s requirement). Id.; see also Shapiro v. Sec’y of
Health & Human Servs., 101 Fed. Cl. 532, 542 (2011), recons. denied after remand, 105 Fed. Cl.
353 (2012), aff’d mem., 2013 WL 1896173 (Fed. Cir. 2013); Koehn v. Sec’y of Health & Human
Servs., No. 11-355V, 2013 WL 3214877 (Fed. Cl. Spec. Mstr. May 30, 2013), mot. for review
denied (Fed. Cl. Dec. 3, 2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).
B. Law Governing Factual Determinations
The process for making determinations in Vaccine Program cases regarding factual issues
begins with consideration of the medical records. Section 11(c)(2). The special master is required
to consider “all [] relevant medical and scientific evidence contained in the record,” including “any
diagnosis, conclusion, medical judgment, or autopsy or coroner’s report which is contained in the
record regarding the nature, causation, and aggravation of the petitioner’s illness, disability, injury,
condition, or death,” as well as the “results of any diagnostic or evaluative test which are contained
in the record and the summaries and conclusions.” Section 13(b)(1)(A). The special master is then
required to weigh the evidence presented, including contemporaneous medical records and
testimony. See Burns v. Sec’y of Health & Human Servs., 3 F.3d 415, 417 (Fed. Cir. 1993) (it is
within the special master’s discretion to determine whether to afford greater weight to
contemporaneous medical records than to other evidence, such as oral testimony surrounding the
events in question that was given at a later date, provided that such determination is evidenced by
a rational determination).
Medical records that are created contemporaneously with the events they describe are
presumed to be accurate and “complete” (i.e., presenting all relevant information on a patient’s
health problems). Cucuras, 993 F.2d at 1528; see also Doe/70 v. Sec’y of Health & Human Servs.,
95 Fed. Cl. 598, 608 (2010) (“Given the inconsistencies between petitioner’s testimony and his
contemporaneous medical records, the special master’s decision to rely on petitioner’s medical
records was rational and consistent with applicable law”); Rickett v. Sec’y of Health & Human
Servs., 468 F. App’x 952 (Fed. Cir. 2011) (non-precedential opinion). This presumption is based
on the linked propositions that (i) sick people visit medical professionals; (ii) sick people honestly
report their health problems to those professionals; and (iii) medical professionals record what they
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are told or observe when examining their patients in as accurate a manner as possible, so that they
are aware of enough relevant facts to make appropriate treatment decisions. Sanchez v. Sec’y of
Health & Human Servs., No. 11-685V, 2013 WL 1880825, at *2 (Fed. Cl. Spec. Mstr. Apr. 10,
2013); Cucuras v. Sec’y of Health & Human Servs., 26 Cl. Ct. 537, 543 (1992), aff’d, 993 F.2d at
1525 (Fed. Cir. 1993) (“[I]t strains reason to conclude that petitioners would fail to accurately
report the onset of their daughter’s symptoms.”).
Accordingly, if the medical records are clear, consistent, and complete, then they should
be afforded substantial weight. Lowrie v. Sec’y of Health & Human Servs., No. 03-1585V, 2005
WL 6117475, at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed, contemporaneous medical
records are generally found to be deserving of greater evidentiary weight than oral testimony—
especially where such testimony conflicts with the record evidence. Cucuras, 993 F.2d at 1528;
see also Murphy v. Sec’y of Health & Human Servs., 23 Cl. Ct. 726, 733 (1991), aff’d per curiam,
968 F.2d 1226 (Fed. Cir. 1992), cert. denied sub. nom. Murphy v. Sullivan, 506 U.S. 974 (1992)
(“It has generally been held that oral testimony which is in conflict with contemporaneous
documents is entitled to little evidentiary weight.”) (citing United States v. United States Gypsum
Co., 333 U.S. 364, 396 (1948)).
There are, however, situations in which compelling oral testimony may be more persuasive
than written records, such as where records are deemed to be incomplete or inaccurate. Campbell
v. Sec’y of Health & Human Servs., 69 Fed. Cl. 775, 779 (2006) (“[L]ike any norm based upon
common sense and experience, this rule should not be treated as an absolute and must yield where
the factual predicates for its application are weak or lacking.”); Lowrie, 2005 WL 6117475, at *19
(“Written records which are, themselves, inconsistent, should be accorded less deference than
those which are internally consistent.”) (quoting Murphy, 23 Cl. Ct. at 733)). Ultimately, a
determination regarding a witness’s credibility is needed when determining the weight that such
testimony should be afforded. Andreu, 569 F.3d at 1379; Bradley v. Sec’y of Health & Human
Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).
When witness testimony is offered to overcome the presumption of accuracy afforded to
contemporaneous medical records, such testimony must be “consistent, clear, cogent, and
compelling.” Sanchez, 2013 WL 1880825, at *3 (citing Blutstein v. Sec’y of Health & Human
Servs., No. 90-2808V, 1998 WL 408611, at *5 (Fed. Cl. Spec. Mstr. June 30, 1998)). In
determining the accuracy and completeness of medical records, the Court of Federal Claims has
listed four possible explanations for inconsistencies between contemporaneously created medical
records and later testimony: (1) a person’s failure to recount to the medical professional everything
that happened during the relevant time period; (2) the medical professional’s failure to document
everything reported to her or him; (3) a person’s faulty recollection of the events when presenting
testimony; or (4) a person’s purposeful recounting of symptoms that did not exist. La Londe v.
Sec’y of Health & Human Servs., 110 Fed. Cl. 184, 203–04 (2013), aff’d, 746 F.3d 1334 (Fed. Cir.
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2014). In making a determination regarding whether to afford greater weight to contemporaneous
medical records or other evidence, such as testimony at hearing, there must be evidence that this
decision was the result of a rational determination. Burns, 3 F.3d at 417.
C. Analysis of Expert Testimony
Establishing a sound and reliable medical theory often requires a petitioner to present
expert testimony in support of his claim. Lampe v. Sec’y of Health & Human Servs., 219 F.3d
1357, 1361 (Fed. Cir. 2000). Vaccine Program expert testimony is usually evaluated according to
the factors for analyzing scientific reliability set forth in Daubert v. Merrell Dow Pharm., Inc., 509
U.S. 579, 594–96 (1993). See Cedillo v. Sec’y of Health & Human Servs., 617 F.3d 1328, 1339
(Fed. Cir. 2010) (citing Terran v. Sec’y of Health & Human Servs., 195 F.3d 1302, 1316 (Fed. Cir.
1999)).
The Daubert factors for analyzing the reliability of testimony are: (1) whether a
theory or technique can be (and has been) tested; (2) whether the theory or
technique has been subjected to peer review and publication; (3) whether there is a
known or potential rate of error and whether there are standards for controlling the
error; and (4) whether the theory or technique enjoys general acceptance within a
relevant scientific community.
Terran, 195 F.3d at 1316 n.2 (citing Daubert, 509 U.S. at 592–95).
The Daubert factors play a slightly different role in Vaccine Program cases than they do
when applied in other federal judicial fora (such as the district courts). Daubert factors are usually
employed by judges (in the performance of their evidentiary gatekeeper roles) to exclude evidence
that is unreliable and/or could confuse a jury. In Vaccine Program cases, by contrast, these factors
are used in the weighing of the reliability of scientific evidence proffered. Davis v. Sec’y of Health
& Human Servs., 94 Fed. Cl. 53, 66–67 (2010) (“[U]niquely in this Circuit, the Daubert factors
have been employed also as an acceptable evidentiary-gauging tool with respect to persuasiveness
of expert testimony already admitted.”). The flexible use of the Daubert factors to evaluate the
persuasiveness and reliability of expert testimony has routinely been upheld. See, e.g., Snyder, 88
Fed. Cl. at 742–45. In this matter (as in numerous other Vaccine Program cases), Daubert has not
been employed at the threshold, to determine what evidence should be admitted, but instead to
determine whether expert testimony offered is reliable and/or persuasive.
Respondent frequently offers one or more experts of his own in order to rebut a petitioner’s
case. Where both sides offer expert testimony, a special master’s decision may be “based on the
credibility of the experts and the relative persuasiveness of their competing theories.”
Broekelschen v. Sec’y of Health & Human Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (citing
Lampe, 219 F.3d at 1362). But nothing requires the acceptance of an expert’s conclusion
“connected to existing data only by the ipse dixit of the expert,” especially if “there is simply too
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great an analytical gap between the data and the opinion proffered.” Snyder, 88 Fed. Cl. at 743
(quoting Gen. Elec. Co. v. Joiner, 522 U.S. 146 (1997)); see also Isaac v. Sec’y of Health & Human
Servs., No. 08-601V, 2012 WL 3609993, at *17 (Fed. Cl. Spec. Mstr. July 30, 2012), mot. for
review denied, 108 Fed. Cl. 743 (2013), aff’d, 540 Fed. App’x 999 (Fed. Cir. 2013) (citing Cedillo,
617 F.3d at 1339). Weighing the relative persuasiveness of competing expert testimony, based on
a particular expert’s credibility, is part of the overall reliability analysis to which special masters
must subject expert testimony in Vaccine Program cases. Moberly, 592 F.3d at 1325–26
(“Assessments as to the reliability of expert testimony often turn on credibility
determinations….”); see also Porter v. Sec’y of Health & Human Servs., 663 F.3d 1242, 1250
(Fed. Cir. 2011) (“[T]his court has unambiguously explained that special masters are expected to
consider the credibility of expert witnesses in evaluating petitions for compensation under the
Vaccine Act.”).
D. Consideration of Medical Literature
Both parties filed medical and scientific literature in this case, but not every filed item
factors into the outcome of this decision. While I have reviewed all of the medical literature
submitted in this case, I discuss only those articles that are most relevant to my determination
and/or are central to Petitioner’s case—just as I have not exhaustively discussed every individual
medical record filed. See Moriarty v. Sec’y of Health & Human Servs., 844 F.3d 1322, 1328 (Fed.
Cir. 2016) (“We generally presume that a special master considered the relevant record evidence
even though he does not explicitly reference such evidence in his decision.”) (citation omitted);
see also Paterek v. Sec’y of Health & Human Servs., 527 F. App’x 875, 884 (Fed. Cir. 2013)
(“Finding certain information not relevant does not lead to—and likely undermines—the
conclusion that it was not considered”).
ANALYSIS
I. Overview of TM, NMOSD, and Relevant Prior Decisions
The experts largely defined the competing diagnoses in this case correctly, but a few
additional points are in order. First, it should be noted that acute demyelinating neurologic
conditions like TM are understood to occur rapidly, proceed in a monophasic manner, and often
resolve without recurrence (even though they can leave lasting sequelae). See Palattao v. Sec’y of
Health & Human Servs., No. 13-591V, 2019 WL 989380, at *11 (Fed. Cl. Spec. Mstr. Feb. 4,
2019) (describing TM’s course as “abrupt[]” and “monophasic”). By contrast, chronic
demyelinating conditions affecting the CNS, like MS, can initially present as if they were TM but
will invariably recur. See, e.g., Hunt v. Sec’y of Health & Human Servs., No. 12-232V, 2015 WL
1263356, at *11 (Fed. Cl. Spec. Mstr. Feb. 23, 2015) (noting that an MS diagnosis traditionally
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requires “at least two events disseminated in time and space”) (internal quotation marks omitted)),
mot. for review den’d, 123 Fed. Cl. 509 (2015).
NMOSD is understood to be a relapsing and chronic CNS disease, like MS. It is therefore
distinguishable from monophasic conditions like TM, even though both involve CNS
demyelination. Wingerchuk at 185 (noting that only “5%–10% of contemporary cases [of
NMOSD] are described as monophasic” and requiring five years of relapse-free clinical
observation in order to confirm a monophasic course). While a chronic CNS demyelinating disease
may begin with an occurrence that appears discrete, like TM, the later overall course of disease
will establish that the patient did not only experience a one-time event.
Such distinctions are critical for purposes of evaluating causation in this case. Program
petitioners have on many occasions successfully established that acute forms of CNS
demyelinating conditions (e.g., TM or acute disseminated encephalomyelitis (“ADEM”)) were
likely vaccine-caused. See, e.g., Raymo v. Sec’y of Health & Human Servs., No. 11-0654V, 2014
WL 1092274, at *23 (Fed. Cl. Spec. Mstr. Feb. 24, 2014) (TM injury found to be vaccine caused);
Brown v. Sec’y of Health & Human Servs., No. 09-426V, 2011 WL 5029865, at *41 (Fed. Cl.
Spec. Mstr. Sept. 30, 2011) (flu vaccine caused Petitioner’s ADEM injury); Banks v. Sec’y of
Health & Human Servs., No. 02-0738V, 2007 WL 2296047, at *25 (Fed. Cl. Spec. Mstr. July 20,
2007) (awarding compensation for ADEM linked to MMR vaccine); Kuperus v. Sec’y of Health
& Human Servs., No. 01-0060V, 2003 WL 22912885, at *11 (Fed. Cl. Spec. Mstr. Oct. 23, 2003)
(awarding compensation for ADEM linked to the DTaP vaccine).
By contrast, Program claimants have less consistently succeeded in establishing that a
vaccine (including the flu vaccine) could cause a person to develop a chronic demyelinating
condition, like MS or NMOSD. See, e.g., Day v. Sec’y of Health & Human Servs., No. 12-630,
2015 WL 8028393 (Fed. Cl. Spec. Mstr. Nov. 13, 2015) (awarding entitlement where HPV and
Flumist vaccines were shown to have caused petitioner to develop NMOSD); Calise v. Sec’y of
Health & Human Servs., No. 08-85V, 2011 WL 1230155 (Fed. Cl. Spec. Mstr. Mar. 14, 2011)
(awarding entitlement for flu/NMOSD injury); but compare Wei-Ti Chen v. Sec’y of Health &
Human Servs., No. 16-634V, 2019 WL 2121208, at *22 (Fed. Cl. Spec. Mstr. Apr. 19, 2019)
(finding that insufficient evidence was provided to support causal connection between the flu
vaccine and petitioner’s subsequent development of seronegative NMOSD); Davis v. Sec’y of
Health & Human Servs., No. 07-451V, 2010 WL 1444056, aff’d, 94 Fed. Cl. 53 (upholding special
master’s decision that the flu vaccine did not cause NMOSD). Although the results of some of
these decisions are consistent with Petitioner’s favored outcome, the theories offered are not.
In Calise and Davis, for example, the theories offered in both cases associating the flu
vaccine with NMOSD relied on the concept that the components of the flu vaccine first caused
direct injury to the endothelial cells in the body, thereby producing a breach in the blood brain
barrier, and resulting in further injury via a subsequent antibody attack on the myelin sheath (absent
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any cross-reactivity via molecular mimicry). See Calise, 2011 WL 1230155, at *12–21 (finding
that petitioner met her burden of proof by providing medical literature and the opinions of a treating
physician which supported her proposed mechanism of causation); but see Davis, 2010 WL
1444056, at *8–9 (finding that petitioner did not carry her burden in the absence of medical
literature and expert opinion to support her proposed theory of causation). Here, by contrast,
Petitioner simply proposes that molecular mimicry between antigens in the vaccine and self-
structures of the CNS caused harm, with less explanation as to how the process occurred.
Day involved a causation theory centered on molecular mimicry, as here, but featured two
different vaccines acting in concert (i.e., the HPV and Flumist vaccines). The presiding special
master decided the claim for petitioner in that case based primarily on record evidence supporting
the potential of components of the HPV vaccine to cause a cross-reaction spurred on by AQP4-
IgG, for which the claimant tested positive. Day, 2015 WL 8028393, at *14. In this case, however,
it is undisputed that Mr. Morgan is seronegative, and he did not receive the HPV vaccine. Day did
not otherwise specifically address the role the flu vaccine by itself might have played in
contributing to the petitioner’s disease course. Day, 2015 WL 8028393, at *14.
The decision most on all fours with the present case is Wei-Ti Chen, which I decided. The
petitioner in that case had a long-standing history of lower back and buttock pain. Wei-Ti Chen,
2019 WL 2121208, at *2. She presented to her chiropractor one week prior to receipt of the flu
vaccine complaining of inner thigh tingling as well as persistent lower back and buttock pain. Id.
Following administration of the flu vaccine, the petitioner developed a demyelinating disease that
resulted in differential diagnoses of ADEM, MS, and NMOSD. Id. at *3–4. Ultimately the medical
record preponderated in favor of an NMOSD diagnosis despite the petitioner’s atypical
presentation—namely her seronegativity. Id. at *20. The petitioner, however, was unable to
present sufficient evidence to credibly support a finding that the flu vaccine could cause NMOSD
through the mechanism of molecular mimicry. Id. at *21–22.17
II. Petitioner’s Pre-vaccination Symptoms Have Not Been Established to be Associated
With His Neurologic Injury
The parties’ dispute whether Mr. Morgan’s back pain and pre-vaccination urologic
problems reflected the onset of some greater neurologic injury (whether TM, NMOSD, or
otherwise) can be resolved in Petitioner’s favor. The record plainly establishes that Petitioner had
a long-standing medical history of documented degenerative disc disease and an enlarged prostate.
See Ex. 4 at 7; Ex. 5 at 148; Ex. 22 at 9. Some of Petitioner’s post-vaccination treating physicians
repeatedly offered the view that his pre-vaccination symptoms could be attributable to such pre-
existing causes, and it was not unreasonable to consider the possibility that they were related,
especially since some of Petitioner’s pre-vaccination symptoms (like those pertaining to bladder
17 Though similar to the present matter, Wei-Ti Chen is distinguishable in at least one regard—I found the petitioner’s
pre-vaccination symptoms were a part of her overall disease process. Wei-Ti Chen, 2019 WL 2121208, at *23–25.
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control) can be neurologic.
Nevertheless, the record preponderates against the conclusion that Petitioner’s injury,
however characterized, predated his receipt of the flu vaccine. See, e.g., Ex. 14 at 10–11. Dr.
Tornatore persuasively established that there was a difference between the tempo of Petitioner’s
long-standing pre-vaccination symptoms and those he experienced thereafter. In addition, Dr.
Sriram seems to have conceded the low likelihood that an individual with his preferred diagnosis
of NMOSD would experience a slow and progressive series of symptoms over the relevant time
period at issue. Tr. at 127. I therefore do not find, based on this record, that Petitioner’s neurologic
injury likely predated his October 2012 receipt of the flu vaccine.
III. The Medical Record Best Supports an NMOSD Diagnosis
The parties strenuously disagree on the proper diagnosis of Mr. Morgan. Here, the evidence
preponderates against Petitioner. Consideration of the record as a whole -- from the time of
Petitioner’s October 2012 vaccination through the 2016 medical records -- establishes persuasive
support for a seronegative NMOSD diagnosis (although admittedly the matter cannot be
conclusively determined).
First, there is no doubt that treater views support that diagnosis (especially those from
physicians who saw Petitioner later in time). See Ex. 14 at 110; Ex. 53 at 42. While they are not
dispositive of the question by themselves, they offer reliable proof, even in the face of contrary
assertions by Dr. Tornatore. See Andreu, 569 F.3d at 1367; Capizzano, 440 F.3d at 1326; see also
Snyder, 88 Fed. Cl. at 746 n.67. Those treaters did not conclude, as Dr. Tornatore urges, that
Petitioner experienced a one-time event that resembled TM, or even (as he allowed) that
Petitioner’s subsequent course reflected a relapsing form of TM. Indeed, NMO was suspected as
early as December 2012 (just two months after onset). Ex. 14 at 10.
Second, the record upon which treaters based the NMOSD diagnosis preponderantly
supports Respondent’s position. The University of Michigan MS Clinic records set forth a
comprehensive history that strongly supports the NMOSD diagnosis. Ex. 14 at 109–11. Its treaters,
including Dr. Pace, acknowledged that Mr. Morgan was seronegative and took into account his
initial presentation, but placed it in the context of his greater condition. Id. Additionally, the
relapsing and remitting nature of Mr. Morgan’s disease process, plus the existence of a lesion in
the area of the brain most commonly associated with NMOSD, lend further credence to Dr. Pace’s
conclusion that Mr. Morgan’s condition was properly diagnosed as NMOSD. Id. at 110. Petitioner
is correct in pointing out the criteria that apply in the context of a seronegative patient, as well as
the difficulty in establishing those criteria, but there was still evidence to fit each criterion—
Petitioner initially exhibited acute myelitis with LETM, and demonstrated brain lesions in the area
postrema region of the brain. See Ex. 5 at 56; Ex. 14 at 110, 135; Ex. 21 at 1; Ex. 53 at 21; see also
Wingerchuk at 179.
In response, Petitioner reasonably argued that one of these criteria—evidence of area
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postrema syndrome—is not strongly supported by the record. Ex. E at 3. Indeed, Mr. Morgan did
not even receive such a specific diagnosis. There is, however, as Dr. Sriram proposed, evidence of
dissemination in space, because later MRI reports from September 2015 show a brain lesion in the
periventricular region of the brain (Ex. 14 at 110; Ex. 21 at 1), as well as a lesion extending to T6,
where it had previously extended only to T8 before resolving. Ex. 14 at 137; Ex. 5 at 70, 80. In
addition, while Petitioner did not experience some of the symptoms that would be associated with
an area postrema lesion (Tr. at 111), his treating physicians nevertheless noted that the mere
existence of an area postrema lesion supported a diagnosis of NMOSD by itself. See Ex. 14 at 110.
This, along with the overall thrust of treater opinion, better supports the NMOSD diagnosis than
Petitioner’s arguments to the contrary.
Third, and by contrast, the overall record does not preponderate in favor of the TM
diagnosis proposed by Petitioner. Treaters initially, and rationally, interpreted Petitioner’s
symptoms and test results (like MRIs) as supportive of LETM. Moreover, some of the therapies
utilized (steroids or PT) proved effective, and Mr. Morgan’s improving course, coupled with what
appeared to be a lack of radiologic evidence of further lesion activity, all suggested that he had
experienced a one-time, monophasic event. Ex. 5 at 79; Ex. 9 at 681. But over time, Petitioner
began experiencing a progressive course of symptoms that suggested a relapse, and certainly
resulted in more severe symptoms that impacted his ambulation. Ex. 14 at 109. Thereafter, other
evidence (as extensively referenced above) undermined the initial conclusion about the possible
nature of Petitioner’s injury. The overall progressive course of Petitioner’s symptoms from
October 2012 to 2016 is not supportive of the conclusion that he experienced a one-time acute
injury and thereafter suffered its sequelae; rather, the record suggests Petitioner’s initial symptoms
were part of something chronic that took time to unfold.
Dr. Tornatore’s interpretation of the overall record, and Petitioner’s symptoms within it,
was reasonable but ultimately not persuasive. He allowed that at a minimum, Petitioner had
experienced what he deemed a “relapsing” form of LETM—thus implicitly acknowledging that
the medical record did not reflect a single monophasic injury, as normally would be associated
with TM. Tr. at 43–44. He also erred somewhat in asserting that this version of TM would subsume
NMOSD - when in fact, as literature filed by Petitioner establishes, the opposite is the case. Kim
at 265. It is simply more likely than not that NMOSD could present as it did for Petitioner—a
conclusion that Mr. Morgan’s treaters later embraced, after Petitioner had lived with his symptoms
for several years.
Admittedly, the overall record in this case makes it difficult to establish with certainty
Petitioner’s correct diagnosis (a task that I am not even called upon to perform, since diagnosing
an illness falls well beyond the purview of the special masters in resolving Vaccine Act claims).
Petitioner has raised reasonable objections to this diagnosis, such that I could not find that the
NMOSD diagnosis is supported by even 75 percent of the record. However, the evidence still
preponderates in favor of the NMOSD diagnosis (a determination that merely means more than
50 percent of the record favors that determination).
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IV. Petitioner Has Not Satisfied the Althen Prongs
This case largely turns on Petitioner’s inability to satisfy the first and second Althen
prongs.18 With respect to the first, “can cause” prong, I note that Petitioner’s causation theory
includes elements that are routinely deemed valid in the Vaccine Program. For example, molecular
mimicry has repeatedly been embraced in Program cases as a reliable scientific mechanism for
explaining the pathophysiology of certain immune-mediated conditions, including many
demyelinating disorders. See, e.g., Tompkins v. Sec’y of Health & Human Servs., No. 10-261V,
2013 WL 3498652, at *22 (Fed. Cl. Spec. Mstr. June 21, 2013) (“[t]he molecular mimicry theory
is the one most widely accepted for the agents most frequently accepted as causal”), mot. for review
den’d, 117 Fed. Cl. 713 (2014). Molecular mimicry has been invoked to explain how a vaccine
might cause TM. See, e.g., Hargrove v. Sec’y of Health & Human Servs., No.05-0694V, 2009 WL
1220986, at *38 (Fed. Cl. Spec. Mstr. Apr. 14, 2009).
However, I find preponderant evidence supports a different injury—NMOSD. And, as
noted above, there is a lack of persuasive authority (in the form of prior Vaccine Act decisions)
that suggests this kind of chronic, progressive CNS demyelinating injury has credibly been shown
to be associated with vaccination. This is particularly the case if the mechanism of molecular
mimicry is considered closely.19 For molecular mimicry to have utility herein as a reliable
mechanism, there should be some evidence that the relevant autoantibodies that are known to
drive, or are at least associated with, the resulting demyelinating disease are likely produced as a
result of the flu vaccine (or the comparable wild virus) - and it is reasonable to require a petitioner
to offer some evidence in support of such a contention when evaluating the success of the
claimant’s prong one showing. See, e.g., W.C., 704 F.3d at 1361. Petitioner could have established
this with a variety of circumstantial evidence involving the flu vaccine (or wild flu virus) and its
association with NMOSD, or proof that immune system stimulation can at least initiate a chronic
process that would indirectly result in the down-stream, continued production of the relevant
autoantibodies.
Petitioner, however, offered little such evidence. At best, there are some references in the
18 Mr. Morgan’s LETM-like symptoms arguably first manifested within nine days of vaccination (although it is
difficult to distinguish during this period between symptoms of his prior, non-neurologic problems and new distinct
symptoms). Nevertheless, a timeframe of two to three weeks is both consistent with his causation theory as well as
reasonable in light of other cases involving the onset of autoimmune demyelinating injuries, suggesting that the third
Althen prong has been met. However, because the theory itself—that the flu vaccine could cause what the evidence
established Petitioner was ultimately diagnosed with (NMOSD)—is evidentiarily deficient, the satisfaction of this
single Althen prong does not assist Petitioner in satisfying his overall burden of proof.
19 Although petitioners are not obligated to establish a mechanism in their efforts to prove entitlement, they often try
to do so—and in such circumstances (as is the case here), it is reasonable to evaluate if they have succeeded. See, e.g.,
McKown v. Sec’y of Health & Human Servs., No. 15-1451V, 2019 WL 4072113, at *49 n.75 (Fed. Cl. Spec. Mstr.
July 15, 2019).
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literature indicating that NMOSD initially manifesting as LETM could be caused by a variety of
infectious agents (i.e., the herpes virus, dengue fever, tuberculosis, etc.). Kim at 279–80. But this
list does not also include the influenza wild virus. Nor did Petitioner’s filings establish how an
initial reaction to vaccination might be sufficient to create the kind of chronic, CNS-oriented
inflammatory process that would ultimately morph into NMOSD. Thus, Petitioner has not offered
sufficient reliable and persuasive evidence suggesting that the flu vaccine could cause a chronic
form of CNS demyelinating disease such as NMOSD, that would unfold over a lengthy period of
time.
Petitioner’s efforts to satisfy the second Althen prong similarly founder on the facts—and
especially my determination that his disease is best understood as NMOSD. Although the treaters
who first saw Mr. Morgan post-vaccination may reasonably have understood his presentation to
be comparable to LETM, over time it was evident that he more likely suffered from a related, but
different, chronic condition. The record does not support the conclusion that the progression of
Mr. Morgan’s symptoms over a period of four or more years could reasonably be attributed to a
vaccination received at the outset of that timeframe. Nor is it evident from the record that the
vaccine, even if it had played some role in his initial presentation, continued to drive a pathologic
process over such a lengthy period of time. Admittedly, several of Mr. Morgan’s treating
physicians reference the fact that he had received a flu vaccine one week prior to the onset of his
symptoms. See Ex. 9 at 714, 897, 899; Ex. 10 at 1. But while these treaters may have so opined
based on speculation that in turn deemed significant the temporal relationship between onset and
vaccination, none later proffered the opinion that the vaccine could have caused the chronic
condition of NMOSD. See Ex. 9 at 714, 897, 899; Ex 10 at 1. Again, consideration of the record’s
scope is not supportive of the conclusion that the vaccine caused Petitioner’s overall course.
CONCLUSION
The Vaccine Act permits me to award compensation only if a Petitioner alleging a “non-
Table Injury” can show by medical records or competent medical opinion that the injury was more
likely than not vaccine-caused. Here, there is insufficient evidence to support an award of
compensation, leaving me no choice but to hereby DENY this claim.
In the absence of a timely-filed motion for review (see Appendix B to the Rules of the
Court), the Clerk shall enter judgment in accord with this decision.20
IT IS SO ORDERED.
/s/ Brian H. Corcoran
Brian H. Corcoran
Chief Special Master
20 Pursuant to Vaccine Rule 11(a), the parties may expedite entry of judgment by filing a joint notice renouncing their
right to seek review.
28

================================================================================
DOCUMENT 2: USCOURTS-cofc-1_15-vv-01137-2
Date issued/filed: 2020-06-17
Pages: 27
Docket text: **RE-DOCKETED 77 TO CORRECT FILING ERROR**JUDGE VACCINE REPORTED OPINION re: 76 Judge Vaccine Order/Opinion, Signed by Judge Ryan T. Holte. (fm) Service on parties made.
--------------------------------------------------------------------------------
Case 1:15-vv-01137-RTH Document 78 Filed 06/17/20 Page 1 of 27
In the United States Court of Federal Claims
No. 15-1137
(Filed: 17 June 2020*)
***************************************
PITEY MORGAN, *
*
Petitioner, * Vaccine Act; off-table case; influenza
* vaccine; longitudinally-extensive transverse
v. * myelitis (“LETM”); neuromyelitis optica
* spectrum disorder (“NMOSD”).
SECRETARY OF HEALTH AND HUMAN *
SERVICES, *
*
Respondent. *
*
***************************************
Sylvia Chin-Caplan, of Law Office of Sylvia Chin-Caplan, with whom was Timothy J.
Mason, both of Boston, MA for petitioner.
Zoe Wade, Trial Attorney, Torts Branch, Civil Division, U.S. Department of Justice, with
whom were Joseph H. Hunt, Assistant Attorney General, C. Salvatore D’Alessio, Acting
Director, Catharine E. Reeves, Deputy Director, Heather L. Pearlman, Assistant Director, all of
Washington, DC, for respondent.
OPINION AND ORDER
Petitioner Pitey Morgan (“petitioner”) moved for review of Chief Special Master
Corcoran’s decision that petitioner is not entitled to compensation under the National Vaccine
Injury Compensation Program, 42 U.S.C. §§ 300aa-10–300aa-34 (“Vaccine Act”). Petitioner
claims he suffered longitudinally extensive transverse myelitis (“LETM”) caused by the
influenza (“flu”) vaccine he received on 16 October 2012. The Special Master denied
compensation and found petitioner did not “offer[] preponderant evidence to support the alleged
diagnosis of LETM, whereas the record evidence preponderates in favor of an alternative
diagnosis: Neuromyelitis Optica Spectrum Disorder (“NMOSD”).” Morgan v. Sec’y of Health
& Human Servs., No. 15-1137V, 2019 WL 7498665, at *1 (Fed. Cl. Spec. Mstr. Dec. 4, 2019).
Petitioner contends this decision was arbitrary and capricious because it ignored factual evidence
in the record, particularly portions of the expert reports and testimony, as well as medical
literature. For the following reasons, the Court DENIES petitioner’s motion and SUSTAINS
* This opinion was initially filed under seal pursuant to Vaccine Rule 18(b) of the Rules of the Court of Federal
Claims. The Court provided the parties 14 days to submit proposed redactions, if any, before the opinion was
released for publication. Neither party proposed redactions. This opinion is now reissued for publication in its
original form.

Case 1:15-vv-01137-RTH Document 78 Filed 06/17/20 Page 2 of 27
the decision of the Chief Special Master. Additionally, the Court GRANTS petitioner’s motion
for leave to exceed the page limit.1
I. Background
A brief recitation of the facts provides necessary context.2
A. Petitioner’s Medical History and the Vaccination
Petitioner, who was 54 at the time of his October 2012 flu vaccination, suffered
preexisting conditions, including: “lower back pain, lower extremity radiculopathy, multi-level
degenerative disc disease, lumbar spondylosis, and prostatitis.” Id. at *1, *3. Beginning in
August 2009, petitioner was under the care of Physician Assistant Deborah Stayman (“PA
Stayman”) and Dr. Anthony Wilson, M.D. of Orthopaedic Associates of Muskegon for lower
back pain. Id. Petitioner “complained of pain radiating to his left thigh,” and PA Stayman noted
petitioner “exhibited decreased reflexes in his left achilles tendon.” Id. A Magnetic Resonance
Imaging (“MRI”) study conducted on 1 September 2009 showed “mild foraminal narrowing at
the L3–L4 and L4–L5 levels . . . with moderate foraminal narrowing bilaterally at L5–S1 level.
No significant spinal canal narrowing. There are disc bulges involving the lower two lumbar
levels.” Id. (quoting Pet’r’s Ex. 2, at 1; Pet’r’s Ex. 4, at 32–33). Petitioner was referred to
physical therapy for his pain but complained the physical therapy “was not assisting.” Morgan,
2019 WL 7498665, at *2. An electromyography test (“EMG”) and nerve conduction study, both
conducted on 24 November 2009, returned normal results. Id. Throughout 2009 and 2010,
petitioner received spinal nerve injections. Id.
In January 2011, petitioner began to visit Shoreline Family Medicine, complaining of
“muscle stiffness, decreased range of motion, weakness, and radiating lower back pain.” Id. At
that time, “he was diagnosed with chronic lower back pain and degenerative disc disease.” Id.
Thereafter, he was seen monthly and “consistently complained of persistent pain, stiffness,
weakness, and radiating lower back pain, though not every symptom was present at every visit.”
Id. In May 2011, he began to complain of dizziness and neck pain. Morgan, 2019 WL 7498665,
at *2. On 30 June 2011, petitioner underwent another MRI, which showed “[s]pondylosis
causing some mild to moderate spinal canal stenosis at C5-6 and C6-7. No frank herniated disc
is appreciated.” Id. (quoting Pet’r’s Ex. 5, at 92).
On 11 March 2012, petitioner underwent an additional MRI “for continued lower back
pain and lower extremity radiculopathy.”3 Id. The MRI “showed ‘[m]ulti-level degenerative
1 Petitioner also filed a motion for leave to exceed the page limit contemporaneously with filing his motion for
review. See Pet’r’s Mot. for Leave of Court to Exceed the Page Limit, ECF No. 66. Respondent indicated during
oral argument he does not oppose the motion. See Tr. at 5:8–10, ECF No. 73.
2 As the basic facts in this case have not changed significantly since the Special Master’s 4 December 2019 decision
in this case, the Court’s recitation of the background facts herein draws from that decision.
3 Radiculopathy is a “[d]isorder of the spinal nerve roots.” Radiculopathy, Stedmans Medical Dictionary (Westlaw,
last updated Nov. 2014). “Radiculopathy describes a range of symptoms produced by the pinching of a nerve root in
the spinal column. The pinched nerve can occur at different areas along the spine.” Radiculopathy, John’s Hopkins
Medicine, https://www.hopkinsmedicine.org/health/conditions-and-diseases/radiculopathy (last visited May 21,
2020).
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disc disease and lumbar spondylosis with slight interval progression and worsening in the
appearance of degenerative change at the L4-5 level.’” Id. (quoting Pet’r’s Ex. 8, at 193).
On 6 August 2012, petitioner was diagnosed with prostatitis4 after being seen for his
“trouble urinating and related concerns.” Id. (citing Pet’r’s Ex. 5, at 145). A month later, he was
also diagnosed with “lower back pain and bilateral sciatica” during a follow-up visit when he
“complained of stiffness and lower back pain in addition to citing the urological symptoms of
frequency and oliguria.” Id. On 24 September 2012, petitioner was seen for “toe and thigh
numbness with an onset of three weeks prior, as well as difficulty initiating urination and waking
up during the night to urinate.” Morgan, 2019 WL 7498665, at *2. Petitioner “underwent an
ultrasound of his prostate,” which returned negative results. Id.
On 9 October 2012, petitioner was seen again at Shoreline Family Medicine for “lower
back and pelvic pain, weakness, poor balance, fatigue, and sleep disturbances.” Id. Petitioner
underwent a CT scan on 12 October 2012, but “the results were unremarkable.” Id.
On 16 October 2012, petitioner received the flu vaccination at issue in this case. Id. at 3.
The next day, he was seen for a urologic consultation with Dr. Arthur Golin, M.D. Id. Petitioner
explained to the physician his urinary symptoms began a year prior but had worsened over the
previous two and a half months. Morgan, 2019 WL 7498665, at *3. He also noted “increasing
pain and some weakness in the right lower extremity . . . numbness, right lateral thigh.” Id. Dr.
Golin found an “‘enlarged, benign-appearing [prostate] gland’ and reduced tone of the anal
sphincter” during a physical examination and determined petitioner suffered “urinary retention—
but with a possible neurologic component.” Id. (quoting Pet’r’s Ex. 22, at 7). On 22 October
2012, petitioner was seen for persistent symptoms at Shoreline Family Medicine and “was
prescribed medication for his prostatitis and instructed to return in one week for a follow-up
appointment.” Id. The next day, petitioner “was seen by Scott Greenwald, M.D. at Michigan
Pain Consultants for his lower back pain.” Id. He complained of lower back pain with pain
“radiating down both of his legs,” as well as “new numbness in bilateral calves.” Id. Petitioner
“was treated with a lumbar epidural steroid injection.” Morgan, 2019 WL 7498665, at *3.
On 24 October 2012, petitioner went to the emergency room complaining of urinary
retention and “again reported that he had been experiencing urinary incontinence issues for about
a year.” Id. A catheter was placed. Id. “Later that same day, however, [petitioner] gradually
lost the strength in his legs until he was too weak to ambulate.” Id.
Petitioner was taken by ambulance to the emergency room of a different hospital, where
he was seen “for leg weakness and urinary retention.” Id. Petitioner underwent an MRI, which
showed “[m]ild lumbar disc degeneration, which does not appear significantly changed as
compared to 3/11/2012 . . . conus medullaris appears somewhat indistinct with a suggestion of
some increased T2-weighted signal intensity, of uncertain significance given the limitations of
the low field strength magnet.” Id.
4 Prostatitis is “[i]nflammation of the prostate.” Prostatitis, Stedmans Medical Dictionary (Westlaw, last updated
Nov. 2014).
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Petitioner was thereafter transferred to a different hospital. Morgan, 2019 WL 7498665,
at *3. He reported “that he had first noticed mild weakness in his lower extremities in August
2012 (two months before the vaccination in question)” and “patchy numbness and tingling he
experienced progressively increased over the previous two months and coincided with his
worsening urologic symptoms.” Id. Dr. Christopher Marquart, M.D., the treating physician,
noted, after physical examination, petitioner had “crude sensory level at about T12-L1 level” and
“‘patchy decreased pinprick and light touch over the anterior thighs bilaterally, top of the right
foot and bottom both the left heel and patchy over the area of the cath[eter],’ decreased strength,
and absent reflexes in his lower extremities.” Id. at *4 (quoting Pet’r’s Ex. 9, at 898). Dr.
Marquart “observe[d] evidence of nerve root clumping and enhancing in the conus—leading him
to question whether [petitioner] had experienced transverse myelitis (“TM”) or some other acute,
neuro-inflammatory process.” Id. Petitioner “was admitted to the intensive care unit for
observation, ‘to make certain he does not have any type of ascending paralysis with the recent flu
vaccination.’” Id. (quoting Pet’r’s Ex. 9, at 899).
On 25 October 2012, petitioner underwent another MRI, which showed “edema within
the cord from T8 to the inferior tip of the cord . . . but no significant contrast enhancement.” Id.
An infectious disease consultant, Dr. Roni Devlin, M.D. saw petitioner the same day and
“indicated that the MRI was suggestive of myelitis of indeterminate etiology—though he did
later implicate the flu vaccine, noting that ‘[c]ase reports of myelitis following vaccination have
certainly been reported, but rarely.’” Id. (quoting Pet’r’s Ex. 9, at 714).
On 27 October 2012, while still at the same hospital, petitioner was seen by Dr. Larry
Wahl, D.O. at Mercy Health “who noted that [petitioner] had experienced ‘increasing urinary
retention and some difficulty with strength in his lower extremities, climbing stairs as much as 5-
1/2 weeks ago that gradually increased’ and ‘seemed to reach a critical level 1 day after having
an epidural steroid injection on Tuesday [October 23, 2012].’” Morgan, 2019 WL 7498665, at
*4 (quoting Pet’r’s Ex. 9, at 715). Dr. Wahl’s differential diagnosis included TM, but the
physician “express[ed] some skepticism towards TM as explanatory given the extensive nature
of [petitioner’s] spinal cord edema.” Id. While in the hospital, petitioner “gradually recovered
the ability to stand, bear weight, and walk short distances with the assistance of a walker, but he
continued to experience numbness and tingling in his lower extremities.” Id.
On 29 October 2012, petitioner was discharged from the hospital to outpatient
rehabilitation. Id. During a follow-up visit on 15 November 2012, Dr. Marquart “reiterated his
belief that Petitioner’s myelitis was ‘probably a reaction to his flu vaccine for lack of a better
explanation.’” Id. (quoting Pet’r’s Ex. 10, at 1). Another MRI conducted on 21 November 2012
“showed marked improvement in the appearance of the spinal cord with only ‘very mild patchy
cord edema.’” Id. (quoting Pet’r’s Ex. 5, at 79).
On 13 December 2012, petitioner was seen by Dr. Douglas Gelb, M.D. at the University
of Michigan Neurology Clinic. Morgan, 2019 WL 7498665, at *4. Petitioner noted during this
visit, “since his hospital discharge on October 29, 2012, he had not noticed much improvement
in his ability to ambulate and felt as though his neurologic symptoms were worsening.” Id. At
this time, he “complained of persistent loss of sensation in his lower extremities, bladder, and
[bowels], burning pains, the development of a lump on his neck, worsening vision, sudden arm
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jerks, and cramping or spasms in his fingers.” Id. During a physical examination, petitioner
“exhibited mild spasticity in both lower extremities, reduced sensation from the waist down, and
absent reflexes in his ankles.” Id. at *5. Dr. Gelb “proposed that [petitioner] was experiencing
either an isolated episode of TM or the first instance of a recurrent, central nervous system
(“CNS”) demyelinating disease, such as Multiple Sclerosis (“MS”) or Neuromyelitis Optica
(“NMO”).” Id. Dr. Gelb “acknowledged that [petitioner’s] pre-vaccination symptoms ‘raise[d]
some concern that he might have had an ongoing disease process in his nervous system that
“flared up” on Oct. 24,’ but noted that those earlier symptoms were non-specific, or could be
explained by [petitioner’s] degenerative disc disease and enlarged prostate.” Id. (quoting Pet’r’s
Ex. 14, at 10–11). Dr. Gelb determined petitioner’s neurologic disease was not progressing, and
“attribut[ed] his change in vision to . . . one of the medications [petitioner] was taking.” Morgan,
2019 WL 7498665, at *5 (citing Pet’r’s Ex. 14, at 10–11). Dr. Gelb subsequently directed
petitioner to “taper off” the medication “and suggested a follow-up MRI as well as a serum
NMO antibodies test.” Id.
On 20 December 2012, petitioner had a follow-up visit with Dr. Wahl. Id. Petitioner
“described continuing improvement of his neurologic symptoms, and he demonstrated almost
full strength throughout his lower extremities during his physical evaluation.” Id. Dr. Wahl
“ordered laboratory testing—including an NMO serum antibodies test and a brain MRI.” Id.
Between this visit and 14 February 2013, petitioner experienced some improvement in his
neurologic symptoms. Id. Both his NMO serum antibodies test and a 7 January 2013 brain MRI
returned negative results, although the NMO serum antibodies test results summary noted,
“seronegativity does not necessarily preclude a diagnosis of [NMO].” Morgan, 2019 WL
7498665, at *5 (quoting Pet’r’s Ex. 5, at 56).
On 29 April 2013, petitioner returned to Dr. Wahl, where “he exhibited decreased
strength in both legs.” Id. Another MRI was performed on 20 May 2013, which showed,
“[i]nterval change in the appearance of the thoracic spinal cord which demonstrates diffuse but
mild expansion and increased intermedullary signal centrally between the T6 level and the
conus,” which appearance was “suggestive of [TM].” Id. (quoting Pet’r’s Ex. 5, at 70).
Petitioner’s condition continued to deteriorate. Id. “[B]y June 17, 2013, he was unable
to stand independently and exhibited increasingly diminished strength in his bilateral lower
extremities.” Id. On 23 July 2013, petitioner, “concern[ed] that he was experiencing a relapse of
his symptoms,” was seen by a neurologist, Dr. Ivan Landon, M.D. Id. “Dr. Landon concluded
that [petitioner] had suffered at least one, maybe two, relapses and that he was likely suffering
from a polyphasic TM.” Morgan, 2019 WL 7498665, at *5.
On 31 July 2013, petitioner “was admitted to . . . inpatient rehabilitation” for nine days,
“during which time he was treated with high dose steroids, [intravenous immunoglobin
(“IVIG”)], and intensive physical therapy.” Id. at *6. Petitioner “saw some improvement with
these treatments.” Id. Over the next year, petitioner was continually seen by Dr. Landon, who
“noted that [petitioner’s] condition appeared to be deteriorating, as he continued to experience
recurrent symptoms relapses.” Id. By 17 June 2014, petitioner became “restricted to a
wheelchair and complained of symptoms in his upper extremities.” Id. Dr. Landon observed
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petitioner “seemed to respond best to IVIG coupled with steroids, but [petitioner’s] insurance
company was no longer covering the cost of the IVIG treatment.” Id.
On 15 August 2014, petitioner returned to the University of Michigan Neurology Clinic,
where he “reported that he had developed numbness in his trunk that ascended from his waist to
his mid-back, numbness in the tips of his fingers, and blurry spots of vision within the past few
months.” Morgan, 2019 WL 7498665, at *6. Dr. Gelb was uncertain “whether [petitioner’s]
clinical deterioration was due to [a] new episode of spinal cord inflammation, or simply some
systemic illness exacerbating his deficits from his initial episode (although new episodes of
inflammation seem more likely, given the severity and persistence of the new deficits, and given
the higher sensory level).” Id. (quoting Pet’r’s Ex. 14, at 95).
Dr. Gelb therefore referred petitioner to a MS clinic and ordered “repeat MRIs of
[petitioner’s] cervical and thoracic spine and brain as well as a repeat serum NMO antibodies
test.” Id. The NMO antibodies test returned negative results, but the MRI of his thoracic MRI
showed:
[V]olume retraction/myelomalacia, seen caudal to T8 level and extending down to
the conus, is non masslike abnormal enhancement predominantly involving central
and posterior portions of the spinal cord, which is more conspicuous at T12 and
T10-T11 levels . . . The spinal cord volume loss likely represent[s] myelomalacia
as the sequela of previous inflammatory process. Areas of T2 signal change and
abnormal enhancement could represent reactivation of inflammatory process, this
possibility should be correlated with deficits on physical exam and paraclinical
test/parameters.
Id. (quoting Pet’r’s Ex. 14, at 135, 137). Petitioner’s brain MRI also showed “nonspecific small
areas of nonenhancing T2 signal prolongation in predominantly left supratentorial white matter,
these findings may represent sequela from previous inflammatory, infectious or small vessel
white matter ischemic process.” Id. (quoting Pet’r’s Ex. 14, at 137).
On 26 November 2014, petitioner was seen by Dr. Robert Pace, M.D. at the University of
Michigan MS Clinic. Id. Dr. Pace reviewed the August 2014 MRI scans and noted:
[S]everal nonspecific T2/FLAIR hyperintensities seen in the brain. These are not
in a pattern that is strongly suggestive of demyelination such as would be seen with
[MS]. However, there is a T2 hyperintensity in the fourth ventricle surrounding the
cerebral aqueduct. This is of unclear significance, but can be seen in [NMO]
spectrum.
Morgan, 2019 WL 7498665, at *6 (quoting Pet’r’s Ex. 14, at 110). Dr. Pace also observed
“patchy enhancement of the lower thoracic spine/conus medullaris that appears to involve some
of the cauda equina.” Id.
Based on his review of the August 2014 MRIs and laboratory testing, Dr. Pace formally
diagnosed petitioner with “longitudinal myelitis due to [NMO], sero-negative.” Id. at *7
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(quoting Pet’r’s Ex. 14, at 110). Dr. Pace “advised [petitioner] to begin immune modulation
therapy” given the “high likelihood that [petitioner’s] condition would cause ‘recurrent and
potentially devastating episodes of myelitis if untreated.’” Id. (quoting Pet’r’s Ex. 14, at 110).
Although petitioner “had experienced significant improvement with IVIG treatment in the past,”
Dr. Pace “opined that the most effective treatment for patients with NMO is Rituximab.” Id.
Petitioner did not pursue either recommended treatment, but “he pursued physical therapy
from July to September 2015.” Id. On 18 August 2015, petitioner returned to Dr. Pace, who
listed his diagnoses as “relapsing-remitting MS, Devic’s disease, and flaccid paralysis of the
lower extremities.”5 Morgan, 2019 WL 7498665, at *7. Petitioner “reported persistent paralysis
in his lower extremities and numbness from the midthoracic region down,” but noted he felt “he
was cognitively doing better than before.” Id. Dr. Pace again ordered “MRIs and hepatitis
serologies.” Id. The MRIs “showed that the nonspecific signal hyperintensities located in the
periventricular area of the brain were stable since January.” Id. There were no reported
abnormalities of the cervical spine, “and the previously documented areas of abnormal signal in
the thoracic region of the spinal cord had resolved.” Id.
On 20 April 2016, petitioner again returned to Dr. Pace, and reported he “was seeing
improvement with physical therapy.” Id. Although he was still wheelchair-bound, “he had not
developed any new or worsening symptoms.” Morgan, 2019 WL 7498665, at *7. “Dr. Pace
again opined that [petitioner’s] diagnosis was ‘most likely seronegative [NMO].’” Id. (quoting
Pet’r’s Ex. 53, at 42).
Petitioner had a follow-up appointment with Dr. Pace in April 2017 with similar reports
that he continued to improve with physical therapy and did not experience new or worsening
symptoms. Id. “A physical exam revealed that [petitioner] was able to activate his hip flexors
and extensors, . . . actions he was incapable of performing the year prior.” Id. Dr. Pace also
“noted that the changes in [petitioner’s] spine were stable and that there was no evidence of new
or enhancing lesions.” Id. Dr. Pace included the following diagnoses after the appointment:
“NMO, acute TM, paralytic syndrome, and spinal stenosis of the cervical region.” Id.
B. The Petition and Hearing Before the Special Master
Petitioner filed his vaccine petition against the Secretary of Health and Human Services
(“respondent”) on 7 October 2015. See Pet., ECF No. 1. Petitioner requested compensation for
the transverse myelitis he allegedly developed after receipt of a flu vaccination on 16 October
2012. See id. at 1.
1. Expert Reports
Petitioner filed his first expert report authored by Dr. Carlo Tornatore, M.D. on 27
October 2016. See Pet’r’s Ex. 24, ECF No. 18-1. Dr. Tornatore is Professor and Chairman of
the Department of Neurology at the Georgetown University Medical Center. Id. at 7. He is also
5 The Special Master’s decision noted that “NMO is sometimes referred to as Devic’s disease.” Morgan, 2019 WL
7498665, at *7 n.12.
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the Chairman, Neurologist-in-Chief, and Executive Director of the Multiple Sclerosis Patient
Centered Specialty Home at Medstar Georgetown University Hospital. Id. Upon reviewing
petitioner’s medical history, Dr. Tornatore asserted:
I agree with the treating physicians that [petitioner] suffered a profound
demyelinating event within a week of receiving an influenza vaccination. This
event was characterized by symptoms of lower extremity weakness and bladder
dysfunction that were subsequently diagnosed as longitudinally extensive
transverse myelitis. Notably[,] the spinal cord was edematous at multiple levels in
October 2012, consistent with an acute event.
Id. at 2. Dr. Tornatore explained the physiology of his preferred diagnosis:
Transverse Myelitis (TM) is a rare clinical syndrome in which an immune-mediated
process causes neural injury to the spinal cord, resulting in varying degrees of
weakness, sensory alterations[,] and autonomic dysfunction. The term myelitis
refers to inflammation of the spinal cord; transverse describes the position of the
inflammation, across the width of the spinal cord. In TM, inflammation damages
or destroys myelin, the fatty insulating substance that covers nerve cell fibers,
causing scars that interrupt communications between the nerves and the rest of the
body.
Id. at 2–3. Dr. Tornatore stated “[t]he immunopathogenesis of TM is not fully understood,” but
“[i]t is thought that a variety of immune stimuli, through such processes as molecular mimicry or
superantigen-mediated immune activation, may trigger the immune system to injure the nervous
system.” Id. at 3. Based on this background, Dr. Tornatore cited to various medical journal
articles, which state “TM has been reported following vaccinations,” including the influenza
vaccination. Id. Quoting another medical journal article, Dr. Tornatore highlighted that “it is
widely reported in neurology texts that [acute TM] is a post-vaccination event.” Id. at 3–4. Dr.
Tornatore further emphasized that “the Johns Hopkins Transverse Myelitis Center’s model
diagnostic approach for evaluating patients with acute myelopathies[] includes determining
whether there is a history of recent vaccination or systemic illness.” Id. at 4. A
neuroimmunology textbook, in addition to a study of MRIs following flu vaccines, also show an
association between the flu vaccine and acute TM.6 Id. at 5–6. Based on petitioner’s medical
history and the various cited medical journal articles, Dr. Tornatore concluded:
[I]t is my opinion, to a reasonable degree of medical probability, that the influenza
vaccine [petitioner] received on 10/16/2012 resulted in transverse myelitis, within
a week of vaccination. . . . [T]here was no evidence in [his] medical record for any
alternate cause for his condition and the temporal relationship between the
vaccination and the onset of [his] symptoms was in an appropriate time frame . . .
6 The authors of the Bakshi et al. article Dr. Tornatore cites in his report concluded, however, “association of TM
following the influenza vaccination does not prove cause and effect, however, because no other known causes of
[acute TM] were identified, [and] a postvaccination syndrome was diagnosed by exclusion. Pet’r’s Ex. 24, at 6.
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Lastly, [his] treating physician also speculated that the vaccination could have been
the etiology of the transverse myelitis.
Id. at 6–7.
On 23 June 2017, respondent filed an expert report authored by Dr. Subramaniam Sriram.
See Resp’t’s Ex. A, ECF No. 33-1. Dr. Sriram is “a Professor of Neurology and Microbiology,
Immunology and head of the Multiple Sclerosis (MS) Clinic at Vanderbilt Medical Center.” Id.
at 1. He cares for “over 1,000 patients with MS and allied neuro-inflammatory disorders
including NMO,” in addition to performing “research on the causes and treatment of MS.” Id.
After detailing petitioner’s medical history, Dr. Sriram opined “the final diagnosis in [petitioner]
is not transverse myelitis, which is attributed to monophasic disease; rather[,] his diagnosis is
relapsing longitudinal myelitis, which suggests that the condition that [petitioner] had was a
recurring relapsing disease of the spinal cord.” Id. at 5.
Dr. Sriram “agree[d] with the final assessment of Dr. Pace from the University of
Michigan that the most likely diagnosis is longitudinal extensive myelitis seronegative
Neuromyelitis Optica.” Id. Dr. Sriram laid out the diagnostic criteria for Seronegative NMO as
follows:
1. At least 2 core clinical characteristics occurring as a result of one or more
clinical attacks and meeting all of the following requirements:
a. At least 1 core clinical characteristic must be optic neuritis, acute
myelitis with LETM, or area post-rema syndrome.
b. Dissemination in space (2 or more different core clinical
characteristics).
c. Fulfillment of additional MRI requirements, as applicable.
2. Negative tests for AQP4-IgG using best available detection method, or testing
unavailable
3. Exclusion of alternative diagnoses.
Id. at 6. Dr. Sriram determined petitioner “most likely satisfies the criteria for seronegative
neuromyelitis optica,” satisfying subsection 1(a), but expressed uncertainty “as to the
definitiveness of the diagnoses . . . because [he has] not been able to look at the MRI scans to
ensure that he has had dissemination in space (Item 1b above).” Id. Dr. Sriram suggested “anti-
Myelin Oligodendrocyte Protein (MOG) antibody mediated longitudinal transverse extensive
myelitis” as an alternative diagnosis, but “[a]t present, the serological tests for the MOG
antibody are not available, and hence will be diagnosis of exclusion.” Id. Dr. Sriram further
emphasized “[n]one of the neurologists [who treated petitioner] suggested that the vaccination
played a role in his disease,” and petitioner’s neurologic symptoms predated his vaccination. Id.
Dr. Sriram also opined, contrary to Dr. Tornatore’s report, that “[t]he current literature
does not support a causal connection between influenza vaccine and a relapsing myelitis of any
cause.” Id. Dr. Sriram distinguished two of the case reports Dr. Tornatore cited because neither
of the patients studied in each report suffered “isolated cases of Transverse Myelitis.” Id. at 6–7.
Dr. Sriram distinguished the other case study cited for the association between flu vaccination
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and TM because “the clinical findings [in that study] are very suggestive of Neuromyelitis
Spectrum disorder and not an isolated TM,” also noting that report “preceded the advent of our
current understanding of NMO.” Id. at 7. Dr. Sriram further responded to Dr. Tornatore’s
report, stating he did “not provide a causal connection between TM and the influenza vaccine,
and he provides no supporting evidence to show that the influenza vaccine can cause TM.” Id.
Regarding causation, Dr. Sriram contended, “[t]he prevailing opinion on the neurological
condition of [petitioner] is that he has Neuromyelitis Optica Spectrum disorder (NMOSD), a
condition caused by an auto- antibody response to Aquaporin IV, a protein in brain cells. There
is no evidence that there is any cross reactivity between Influenza vaccine and Aquaporin IV
protein.” Id. Dr. Sriram therefore concluded: “It is my opinion that [petitioner] most likely had
NMOSD. In addition, [petitioner’s] receipt of the influenza vaccine on 10/16/2012 did not cause
or contribute to the development or the subsequent course of the disease. I hold these opinions to
a reasonable degree of medical probability.” Id.
Petitioner filed a responsive expert report also authored by Dr. Tornatore on 5 October
2017. See Pet’r’s Ex. 47, ECF No. 36-1. In this report, Dr. Tornatore focused his analysis on
“whether [petitioner’s] disc disease could have been the etiology of his myelitis.” Id. at 1. He
answered this question in the negative because the disc disease petitioner suffered was in the
lumbar region, lower on the spine than the level at which he suffered myelitis. Id. at 1–2.
According to the 1 September 2009 MRI, petitioner had “mild foraminal narrowing at the L3-L4
and L4-L5 levels with moderate foraminal narrowing bilaterally at the L5-S1 level,” and there
were “disc bulges involving the lower two lumbar levels.” Id. at 2. The 25 October 2012 MRI,
on the other hand, identified “evidence of edema within the cord from T8 to the inferior tip of the
cord,” with the spinal cord ending at the L1 level. Id. Therefore, “from an anatomical
standpoint, the myelitis cannot be attributed to lumbar disc disease.” Id. Dr. Tornatore also
opined petitioner’s “symptoms of weakness, bladder changes[,] and sensory symptoms are due to
the myelitis and not lumbar disc disease” based on the discharge summary from petitioner’s 25
October 2012 hospital admission because “[t]he abrupt change in neurologic symptoms, in the
absence of lumbar disc disease that encroached upon the spinal canal, clearly speaks to the
myelitis as the etiology of the acute symptoms and subsequent disability.” Id. at 3.
On 17 October 2017, the Chief Special Master ordered respondent to file a supplemental
expert report “addressing a) the distinction made by Petitioner’s Expert regarding Petitioner’s
preexisting pain, b) the recently filed MRIs and c) stating if there is a meaningful difference
between the injuries claimed by the experts for the purposes of causation.” Respondent filed this
supplemental expert report, also authored by Dr. Sriram, on 22 December 2017, responding to
the Chief Special Master’s inquiries. Resp’t’s Ex. F at 1, ECF No. 38-1. Given petitioner’s
“long history of low back pain,” Dr. Sriram agreed with Dr. Tornatore’s assessment that “the
back pain was from degenerative lumbo-sacral disc disease and does not have any bearing on the
diagnosis of inflammatory thoracic myelopathy.” Id. Dr. Sriram summarized the timeline from
when petitioner was hospitalized 24 October 2012, his continued neurologic deterioration
throughout 2013, and the 30 August 2014 MRI, which “showed abnormal enhancement
predominantly involving the central and posterior portions of the spinal cord which is more
conspicuous at thoracic 12 and thoracic 10 and thoracic 11 levels.” Id. at 2. Based on this
summary, Dr. Sriram stated:
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The sum of these observations suggests that [petitioner’s] symptoms of spinal cord
dysfunction:
• Preceded the receipt of the flu vaccination on 10/16/2012;
• Was relapsing remitting in nature;
• At least one clinical relapse and two radiological relapses were observed;
and
• Was not the consequence of his back pain or the local steroid therapy.
Id. Therefore, Dr. Sriram asserted:
Any causal connection between [petitioner’s] receipt of the flu vaccine and the
development of neurological deficits consistent with transverse myelitis is unlikely
since the development of gait instability and bladder complaints preceded the
receipt of the vaccine. Furthermore, the underlying diagnosis of [petitioner’s]
condition is relapsing myelitis, and the clinical relapse and the radiological relapse
were seen 6-9 months after his initial presentation. Therefore, it is my opinion that
there is no causal connection between the vaccine and the neurological problems
that followed, given [petitioner’s] chronic course. I agree with the physicians who
evaluated [petitioner] at the University of Michigan that he has neuromyelitis optica
spectrum disorder.
Id.
2. Expert Testimony
The Chief Special Master held a one-day entitlement hearing on 23 January 2019. See
Order, ECF No. 41. Both parties’ experts testified during the hearing.
i. Testimony of Dr. Tornatore
Dr. Tornatore began his testimony recognizing the complexities of petitioner’s medical
record due to his preexisting symptoms but stated there was “no question” petitioner had LETM.
Hr’g Tr. at 9:7–15, ECF No. 57. He asserted that the dramatic change between the slow tempo
of petitioner’s symptoms before the vaccination and petitioner’s condition a week after the
vaccination suggested to him the vaccine caused petitioner’s LETM. See id. at 10:16–11:25.
In contrasting petitioner’s post-vaccination condition from his pre-vaccination condition,
Dr. Tornatore emphasized the progression of petitioner’s symptoms. See id. at 11:5–8. Dr.
Tornatore opined petitioner’s long-standing bladder issues and lower back pain were likely
attributable to petitioner’s history of prostatitis, bilateral sciatica, and degenerative disc disease.
See id. at 12:18–23, 26:20–24. He also acknowledged petitioner’s neurological exams were
“checked off as negative” until the week after the vaccination. Id. at 15:25–16:1; see also id. at
24:4. Dr. Tornatore further emphasized the importance of the tempo of change in petitioner’s
symptoms by explaining that petitioner’s spinal inflammation was so profound it could not have
predated the vaccine because petitioner would have experienced more symptoms than his bladder
issues and lower back pain with that degree of inflammation. See id. at 29:11–30:2. Dr.
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Tornatore similarly urged that the slow progression of petitioner’s pre-vaccination symptoms is
inconsistent with the “profound inflammatory event” characteristic of either LETM or NMOSD.
Hr’g Tr. at 30:3–18.
Dr. Tornatore cited an article authored by Dr. Kerr, petitioner’s Exhibit 26, which states
“acute transverse myelitis [“ATM”] exists on a continuum of neuroinflammatory disorders,”
including NMOSD, all of which are “related to an autoimmune response.” Id. at 35:18–36:15.
Dr. Kerr writes that “it is widely reported in neurology text that ATM is a post-vaccination
event,” and it is important for a physician treating these neuroinflammatory disorders to
“determine if there’s a recent history of vaccination or systemic illness.” Id. at 37:7–8, 37:21–
38:4. Relying on the Kerr article, Dr. Tornatore invoked the theory of molecular mimicry to
explain how the flu vaccination caused petitioner’s LETM. See id. at 38:18–39:1. According to
this theory, bacteria “triggers an immune system and then the immune system attacks the heart
and the brain, as well as the joints.” Id. at 39:20–23.
Dr. Tornatore contended it did not matter whether petitioner had LETM or NMO for
purposes of determining whether the vaccination caused the injury. See id. at 46:6–18. The
significance of diagnosis, Dr. Tornatore maintained, was merely for finding the proper treatment.
See id. at 46:19–47:9. He further explained the uncertainties with treating and diagnosing
patients with neuroinflammatory conditions, but test negative for the Aquaporin-4 antibodies that
are typical of NMOSD. Hr’g Tr. at 47:10–49:1. Moreover, Dr. Tornatore suggested petitioner,
as a male in his fifties, does not fit the typical demographic for NMOSD. See id. at 49:2–16.
Dr. Tornatore opined the “temporal relationship . . . between the antigenic exposure and
the onset” of petitioner’s spinal inflammation was suggestive of vaccine-induced TM because it
made sense “from an immune standpoint” that petitioner’s spinal cord inflammation would begin
“roughly seven or eight days following the vaccination.” Id. at 50:5–14.
Lastly, Dr. Tornatore noted TM is not always monophasic, meaning “it can relapse,
whether it’s from NMO or other things that can cause transverse myelitis,” and petitioner’s
relapse did not affect his assessment of petitioner’s condition. Id. at 50:18–51:9.
On cross examination, Dr. Tornatore acknowledged petitioner’s pre-vaccination
symptoms could be symptoms of demyelinating disease, but conditioned that they could also be
attributed to other causes. See id. at 54:18–55:22, 56:19–57:8. Despite this, Dr. Tornatore
reiterated his opinion that “the greater probability is that these were preexisting symptoms that
were not referable to the spinal cord” due to the difference in the tempo of petitioner’s pre-
vaccination symptoms versus his post-vaccination symptoms. Id. at 57:20–22, 58:9–16, 59:2–6.
ii. Testimony of Dr. Sriram
Dr. Sriram opined petitioner had a relapsing form of Aquaporin-4 negative NMOSD, also
called serologically negative or seronegative NMOSD. Id. at 82:18–83:6. He began his
testimony by providing an overview of the different types of demyelinating disorders of the
central nervous system. Id. at 84:5–89:10. Dr. Sriram explained “there is not a typical course”
of NMOSD, but it is considered a chronic condition because “[a]bout 60 to 70 percent of patients
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will relapse.” Id. at 90:2, 90:9–10. He also indicated a physician would reconsider his initial
diagnosis of TM if the patient relapsed because TM is monophasic. Id. at 90:20–91:4.
Addressing the testing for NMOSD, Dr. Sriram explained there is a blood test used to
detect Aquaporin-4 autoantibodies, the autoantibodies which tend to be elevated in NMOSD
patients. Id. at 91:15–18. Dr. Sriram indicated, though, the test is “not very sensitive,” and
estimated “20 to 25 percent [of patients] are seronegative. . . . for a number of reasons.” Id. at
91:19–23. Therefore, notwithstanding petitioner’s negative Aquaporin-4 test, it was likely his
physicians “missed the window of opportunity where [they were] more likely to have the test
come [back] positive.” Id. at 92:7–9. Dr. Sriram opined petitioner’s pre-vaccination symptoms
“were indicative of NMOSD.” Id. at 92:17–19. Reviewing the progression of petitioner’s pre-
vaccination symptoms, Dr. Sriram asserted “[t]hey represent an ongoing process that began in
the spinal cord sometime in August [2012].” Id. at 96:6–7.
Dr. Sriram contended there was no “scientifically reliable evidence to show that flu
vaccine can cause TM . . . [o]r NMOSD” or that show the “flu vaccine can worsen an
individual’s clinical course if he has TM . . . [o]r NMOSD.” Id. at 97:16–20, 98:14–19.
Discussing the Kerr article Dr. Tornatore relied on to assert the flu vaccine can cause TM, Dr.
Sriram warned “that extreme caution should be exercised in drawing a causal connection”
because it was a case report and “case reports must be viewed with caution as it is entirely
possible that the two events occurred in close proximity by chance alone.” Id. at 99:8–17.
Dr. Sriram also addressed the timeline of the progression of petitioner’s symptoms,
contending that an onset of six to eight weeks would be a reasonable progression for petitioner’s
demyelinating condition. Id. at 100:20–101:24.
Lastly, Dr. Sriram stated he did not believe petitioner’s vaccination caused or worsened
his condition. Id. at 105:2–4.
On cross examination, Dr. Sriram agreed that in patients who test negative for
Aquaporin-4, the diagnostic criteria for NMSOD are more stringent. Id. at 107:10–17.
According to the seronegative NMOSD diagnostic criteria, individuals must exhibit two or more
different core clinical characteristics. Id. at 107:18–20. Dr. Sriram agreed petitioner had
myelitis, but he did not have optic neuritis or any other core clinical characteristics of
seronegative NMOSD. Id. at 108:1–4, 9–20. Further, although Dr. Sriram agreed petitioner did
not have symptoms associated with the area postrema of the brain, “he had a lesion there.” Id. at
108:5–8. Dr. Sriram therefore maintained petitioner has seronegative NMOSD based on
petitioner’s myelitis and an extending spinal lesion. Id. at 108:21–109:9. While Dr. Sriram
acknowledged petitioner’s spinal lesion having extended is not considered dissemination in
space for purposes of satisfying a second requisite core clinical characteristic of seronegative
NMOSD, he asserted the lesion “[l]iterally . . . disseminated from one region of the spinal cord
to an additional region of the spinal cord.” Id. at 109:3–15. Admittedly using the diagnostic
criteria as “guidelines,” and conceding that petitioner did not have symptoms related to the area
postrema of the brain, Dr. Sriram asserted it is “an unusual place to develop a T2 lesion” and
“[i]t’s not uncommon to have silent lesions.” Id. at 110:10, 111:21–112:20. Dr. Sriram
recognized it is uncommon for NMOSD to progress over a course of months or years but
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contended petitioner’s symptoms progressed over a six-week period, which he considered a
reasonable timeframe for NMOSD onset. Id. at 127:12–129:20.
Finally, Dr. Sriram asserted there is no human evidence, nor is there epidemiological
evidence, that the flu vaccine can cause demyelinating disorders. Id. at 138:12–139:12.
C. The Special Master’s Decision Denying Compensation
On 4 December 2019, Chief Special Master Corcoran issued his decision denying
petitioner’s claim and denying compensation because petitioner did not “offer[] preponderant
evidence to support the alleged diagnosis of LETM, whereas the record evidence preponderates
in favor of an alternative diagnosis: [NMOSD],” and petitioner did not “establish[] a reliable
theory explaining how the flu vaccine could have caused his NMOSD.” Morgan, 2019 WL
7498665, at *1.
The Chief Special Master began by defining TM and NMOSD because “[s]uch
distinctions are critical for purposes of evaluating causation in this case.” Id. at *16. The Chief
Special Master first “noted that acute demyelinating neurologic conditions like TM are
understood to occur rapidly, proceed in a monophasic manner, and often resolve without
recurrence.” Id. The Chief Special Master contrasted this with “chronic demyelinating
conditions affecting the [central nervous system (“CNS”)], like MS, [which] can initially present
as if they were TM but will invariably recur.” Id. He thus differentiated NMOSD, which “is
understood to be a relapsing and chronic CNS disease, like MS,” from “monophasic conditions
like TM, even though both involve CNS demyelination.” Id. Therefore, “[w]hile a chronic CNS
demyelinating disease may begin with an occurrence that appears discrete, like TM, the later
overall course of disease will establish that the patient did not only experience a one-time event.”
Id. This distinction was important to the Chief Special Master’s decision because although
“petitioners have on many occasions successfully established that acute forms of CNS
demyelinating conditions . . . were likely vaccine-caused[,]. . . . claimants have less consistently
succeeded in establishing that a vaccine . . . could cause a person to develop a chronic
demyelinating condition, like MS or NMOSD.” Morgan, 2019 WL 7498665, at *16.
With this background, the Chief Special Master distinguished cases in which
compensation was awarded where the petitioner showed a flu vaccination caused NMOSD
because the theories offered in those cases were not the same as the medical theory of causation
posited in this case. Id. For example, in two of the cited cases, “the theories offered in both
cases associating the flu vaccine with NMOSD relied on the concept that the components of the
flu vaccine first caused direct injury to the endothelial cells in the body, thereby producing a
breach in the blood brain barrier, and resulting in further injury via a subsequent antibody attack
on the myelin sheath.” Id. at *17 (citing Calise v. Sec’y of Health & Human Servs., No. 08-85V,
2011 WL 1230155, at *12–21 (Fed. Cl. Spec. Mstr. Mar. 14, 2011); Davis v. Sec’y of Health &
Human Servs., No. 07-451V, 2010 WL 1444056, at *8–9 (Fed. Cl. Spec. Mstr. Mar. 16, 2010),
aff’d, 94 Fed. Cl. 53). In this case, however, “[p]etitioner simply proposes that molecular
mimicry between antigens in the vaccine and self-structures of the CNS caused harm, with less
explanation as to how the process occurred.” Id.
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The Chief Special Master next considered whether petitioner’s pre-vaccination symptoms
were related to his neurologic injury. Id. Although some of petitioner’s post-vaccination
treating physicians considered his pre-vaccination symptoms related to his post-vaccination
symptoms, the Chief Special Master determined “the record preponderates against the
conclusion that Petitioner’s injury, however characterized, predated his receipt of the flu
vaccine.” Id. (emphasis added). The Chief Special Master based this determination on Dr.
Tornatore’s testimony “that there was a difference between the tempo of Petitioner’s long-
standing pre-vaccination symptoms and those he experienced thereafter.” Id. The Chief Special
Master additionally noted, “Dr. Sriram seems to have conceded the low likelihood that an
individual with his preferred diagnosis of NMOSD would experience a slow and progressive
series of symptoms over the relevant time period at issue.” Morgan, 2019 WL 7498665, at *17
(citing Hr’g Tr. at 127).
Next, the Chief Special Master determined, based on his “[c]onsideration of the record as
a whole” that the record preponderates in favor of a “seronegative NMOSD diagnosis.” Id. at
*18. The Chief Special Master cited treating physicians’ views, “especially those from
physicians who saw Petitioner later in time” for persuasive evidence that petitioner suffered
NMOSD. Id. Additionally, the Chief Special Master reasoned “the record upon which treaters
based the NMOSD diagnosis preponderantly supports Respondent’s position.” Id. For example,
“the relapsing and remitting nature of [petitioner’s] disease process, plus the existence of a lesion
in the area of the brain most commonly associated with NMOSD” made Dr. Pace’s diagnosis of
NMOSD persuasive. Id. Considering the diagnostic criteria for seronegative NMOSD, the Chief
Special Master indicated despite “the difficulty in establishing those criteria, . . . there was still
evidence to fit each criterion—Petitioner initially exhibited acute myelitis with LETM, and
demonstrated brain lesions in the area postrema region of the brain.” Id. Further, responding to
petitioner’s argument that evidence of area postrema syndrome was not supported by the record,
the Chief Special Master cited “evidence of dissemination in space, because later MRI reports
from September 2015 show a brain lesion in the periventricular region of the brain . . . , as well
as a lesion extending to T6, where it had previously extended only to T8 before resolving.”
Morgan, 2019 WL 7498665, at *18. Moreover, “while Petitioner did not experience some of the
symptoms that would be associated with an area postrema lesion . . . , his treating physicians
nevertheless noted that the mere existence of an area postrema lesion supported a diagnosis of
NMOSD by itself.”7 Id.
The Chief Special Master determined “the overall record does not preponderate in favor
of the TM diagnosis proposed by Petitioner.” Id. While at first petitioner’s treating physicians
thought petitioner “experienced a one-time, monophasic event,” which would support a TM
diagnosis, “over time, Petitioner began experiencing a progressive course of symptoms that
suggested a relapse, and certainly resulted in more severe symptoms that impacted his
ambulation.” Id. Thus, “[t]he overall progressive course of Petitioner’s symptoms from October
2012 to 2016 . . . suggests Petitioner’s initial symptoms were part of something chronic that took
7 As discussed infra, the record also shows the international consensus diagnostic criteria for seronegative NMOSD
merely provides guidelines for treating physicians. See Hr’g Tr. at 110:8–14. Petitioner’s treating physicians,
especially the later treating physicians, could interpret the criteria in light of their expertise treating NMO-spectrum
diseases.
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time to unfold,” which the Chief Special Master deemed more suggestive of NMOSD than TM.
Id.
Applying the three-pronged test for causation the Federal Circuit articulated in Althen v.
Secretary of Health & Human Services, 418 F.3d 1274, 1278 (Fed. Cir. 2005), the Chief Special
Master decided “[t]his case largely turns on Petitioner’s inability to satisfy the first and second
Althen prongs.” Id. at *19. These prongs require a petitioner to demonstrate: “(1) a medical
theory causally connecting the vaccination and the injury; (2) a logical sequence of cause and
effect showing that the vaccination was the reason for the injury; and (3) a showing of a
proximate temporal relationship between vaccination and injury.” Althen, 418 F.3d at 1278.
Concerning the first prong, the Chief Special Master noted “that Petitioner’s causation theory
includes elements that are routinely deemed valid in the Vaccine Program[;] . . . molecular
mimicry has repeatedly been embraced in Program cases as a reliable scientific mechanism for
explaining the pathophysiology of certain immune-mediated conditions, including many
demyelinating disorders.” Morgan, 2019 WL 7498665, at *19. Notwithstanding the general
recognition of molecular mimicry as a reliable medical theory in vaccine cases, “[f]or molecular
mimicry to have utility herein as a reliable mechanism, there should be some evidence that the
relevant autoantibodies that are known to drive, or are at least associated with, the resulting
demyelinating disease are likely produced as a result of the flu vaccine.” Id. The Chief Special
Master indicated, “[p]etitioner, however, offered little such evidence.” Id. at *20. Petitioner’s
medical literature “indicat[ed] that NMOSD initially manifesting as LETM could be caused by a
variety of infectious agents,” but not the influenza vaccine, and petitioner’s filings did not
“establish how an initial reaction to vaccination might be sufficient to create the kind of chronic,
CNS-oriented inflammatory process that would ultimately morph into NMOSD.” Id. The Chief
Special Master similarly found petitioner failed to satisfy the second prong because “[t]he record
does not support the conclusion that the progression of [petitioner’s] symptoms over a period of
four or more years could reasonably be attributed to a vaccination received at the outset of that
timeframe.” Id. Moreover, the Chief Special Master determined it was not “evident from the
record that the vaccine, even if it had played some role in his initial presentation, continued to
drive a pathologic process over such a lengthy period of time.” Id.
Importantly, the Chief Special Master acknowledged “the overall record in this case
makes it difficult to establish with certainty Petitioner’s correct diagnosis (a task that I am not
even called upon to perform, since diagnosing an illness falls well beyond the purview of the
special masters in resolving Vaccine Act claims).” Morgan, 2019 WL 7498665, at *19.
D. Petitioner’s Motion for Review
On 3 January 2020, petitioner filed his motion for review. See Pet’r’s Mot. for Review,
ECF No. 65. Petitioner argues “[t]he Chief Special Master abused his discretion, and erred as a
matter of law, in ruling that the Petitioner’s injury was [NMOSD].” Id. at 13. Petitioner points
to the diagnostic criteria for seronegative NMOSD as set out in the article entitled, “International
consensus diagnostic criteria for neuromyelitis optica spectrum disorders,” written by Dr. Dean
M. Wingerchuk, MD, FRCP(C) et al. (“Wingerchuk”), respondent’s Exhibit E. Id. at 14.
Wingerchuk provides, in relevant part, a patient who tests seronegative must exhibit:
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1. At least 2 core clinical characteristics occurring as a result of one or more clinical
attacks and meeting all of the following requirements:
a. At least 1 core clinical characteristic must be optic neuritis, acute myelitis
with LETM, or area postrema syndrome
b. Dissemination in space (2 or more different core clinical characteristics)
c. Fulfillment of additional MRI requirements, as applicable
2. Negative tests for AQP4-IgG using best available detection method, or testing
unavailable
3. Exclusion of alternative diagnoses
Resp’t’s Ex. E, at 3, ECF No. 33-5. Wingerchuk also lists the following core clinical
characteristics:
1. Optic neuritis
2. Acute myelitis
3. Area postrema syndrome: episode of otherwise unexplained hiccups or nausea
and vomiting
4. Acute brainstem syndrome
5. Symptomatic narcolepsy or acute diencephalic clinical syndrome with NMOSD-
typical diencephalic MRI lesions . . .
6. Symptomatic cerebral syndrome with NMOSD-typical brain lesions
Id. Quoting expert testimony from the hearing, petitioner contends “the testimony of both
experts demonstrated that the Petitioner did not meet the diagnostic criteria for seronegative
NMOSD” due to what petitioner characterizes as “major concessions during cross examination”
of respondent’s expert, Dr. Sriram. Pet’r’s Mot. for Review at 17, 18. While both experts
agreed petitioner had acute myelitis, satisfying one of the above diagnostic criteria, petitioner
emphasizes Dr. Sriram’s testimony that petitioner’s “thoracic spinal cord lesion (i.e., his
myelitis), and the extension thereof over time, did not constitute dissemination in space.” Id. at
19 (emphasis and internal quotation marks omitted). Petitioner contends the diagnostic
requirement that a patient exhibit “2 or more different core clinical characteristics” means the
dissemination in space must “affect[] different neuroanatomic regions”—“[t]hus, by definition,
an extensive spinal cord lesion, on its own, is not evidence of dissemination in space.” Id.
(emphasis omitted). Similarly, “despite Dr. Sriram’s contention that the Petitioner had a brain
lesion ‘at the floor of the fourth ventricle,’ he conceded that the Petitioner lacked an ‘[area]
postrema syndrome, which is nausea, vomiting[,] or hiccups, which he did not have[.]’” Id. at 20
(quoting Hr’g Tr. at 83) (emphasis omitted). Petitioner therefore argues, “[d]espite this
testimony and the undisputed literature, the Chief Special Master, citing to Wingerchuk, found
that there was ‘still evidence to fit each criterion,’” a finding which petitioner claims had “no
basis in the record.” Id. at 21 (emphasis omitted).
Petitioner further asserts the Chief Special Master’s reasoning that petitioner “had
evidence of a ‘brain lesion in the periventricular region of the brain’ based upon a September
2015 brain MRI” was contrary to the record because area postrema syndrome “requires
associated dorsal medulla/area postrema lesions,” which is a smaller region of the CNS than the
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periventricular region.8 Id. at 24 (emphasis omitted). Petitioner maintains this finding was
accordingly contrary to portions of the record, such as Dr. Pace’s notes reviewing petitioner’s
brain MRIs. Id. at 25–26. Petitioner points to Dr. Tornatore’s testimony to show the Chief
Special Master’s “discussion that TM is a strictly ‘monophasic condition’ whereas MS and
NMOSD are ‘relapsing and chronic CNS’ diseases” was likewise unsupported by the record. Id.
at 26. Furthermore, petitioner argues “[t]he Chief Special Master’s overreliance on Dr. Pace’s
diagnosis is misplaced” because Dr. Pace “did not always adhere” to his diagnosis that petitioner
suffered “longitudinal myelitis due to [NMO], seronegative.” Id. at 28 (emphasis omitted).
Finally, petitioner asserts “[b]y ignoring expert agreement that the diagnostic criteria for
seronegative NMOSD had not been met, and relying on his own broader criteria, for which there
was no basis in the record, the Chief Special Master substituted his own judgment for that of the
medical community.” Id. at 29. Petitioner claims the Chief Special Master’s decision
constituted legal error warranting reversal. Id.
On 3 February 2020, respondent filed its response to petitioner’s motion for review. See
Resp’t’s Resp. to Pet’r’s Mot. for Review, ECF No. 69. Respondent argues “[p]etitioner makes
only one objection that the Chief Special Master erred in concluding that petitioner’s injury was
NMOSD, an argument that amounts to nothing more than a request that this Court impermissibly
reweigh the evidence regarding the nature of his condition.” Id. at 12. Respondent asserts,
“[c]onsistent with the Chief Special Master’s duty to determine which injury petitioner suffered
from, but ‘not through the lens of the laboratorian,’ he admitted that not all of the evidence on
diagnosis was one-sided.” Id. at 14 (quoting Morgan, 2019 WL 7498665, at *12). Therefore, “it
is unsurprising that petitioner can point to evidence in the record that cuts against the Chief
Special Master’s ultimate determination that petitioner suffered from NMOSD, but those
arguments fall far short of demonstrating that the Chief Special Master’s conclusion was based
on evidence that is ‘wholly implausible.’” Id. Pointing to Dr. Sriram’s testimony and medical
records from petitioner’s visits with Dr. Pace, respondent maintains “even though petitioner
disagrees with the Chief Special Master’s weighing of the evidence, the record provides—at
minimum—a basis for his determination that petitioner suffered from NMOSD that is not
‘wholly implausible’ and must be affirmed.” Id. at 16. Additionally, respondent argues “[e]ven
if petitioner did not have NMOSD, he has not established by preponderant evidence that he had
TM, much less that his TM was caused by an influenza vaccine.” Id. at 17. Respondent suggests
that “petitioner appears to assume that the nature of his condition is an either/or proposition: if it
is not NMOSD, it must be TM. But the record does not support this assumption.” Id. Lastly,
respondent contends “regardless of the diagnosis for petitioner’s alleged injury, his claim would
have failed because he could not have satisfied either Althen prong one or prong two based on
the evidence provided.” Id. at 19.
The Court held oral argument on 20 May 2020. Order, ECF No. 71. Petitioner’s motion
for review is now ripe for decision.
8 Petitioner explains the periventricular region “refers to the entire region near or around any of the cerebral
ventricles, rather than the fourth ventricle specifically. . . . [T]he fourth ventricle is the only ventricle that houses the
area postrema.” Pet’r’s Mot. for Review at 24, n.10.
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II. Discussion
A. Legal Standards
1. The Court’s Standard of Review of a Special Master’s Decision
The Vaccine Act provides this Court jurisdiction to review a Special Master’s decision
upon timely motion of either party. See 42 U.S.C. § 300aa-12(e)(1)–(2). In reviewing the record
of the proceedings before the Special Master, the Court may: (1) “uphold the findings of fact
and conclusions of law of the special master and sustain the special master’s decision;” (2) “set
aside any findings of fact or conclusion of law of the special master found to be arbitrary,
capricious, an abuse of discretion, or otherwise not in accordance with law and issue its own
findings of fact and conclusions of law;” or (3) “remand the petition to the special master for
further action in accordance with the court’s direction.” Id. § 300aa-12(e)(2). “Fact findings are
reviewed . . . under the arbitrary and capricious standard; legal questions under the ‘not in
accordance with law’ standard; and discretionary rulings under the abuse of discretion standard.”
Saunders v. Sec’y of Dept. of Health & Human Servs., 25 F.3d 1031, 1033 (Fed. Cir. 1994)
(quoting Munn v. Sec’y of Dept. of Health & Human Servs., 970 F.2d 863, 870 n.10 (Fed. Cir.
1992)).
It is not the Court’s role “to reweigh the factual evidence, or to assess whether the special
master correctly evaluated the evidence.” Lampe v. Sec’y of Health & Human Servs., 219 F.3d
1357, 1360 (Fed. Cir. 2000) (quoting Munn, 970 F.2d at 871). The Court also does “not examine
the probative value of the evidence or the credibility of the witnesses. These are all matters
within the purview of the fact finder.” Id. (quoting Munn, 970 F.2d at 871). “Reversal is
appropriate only when the special master’s decision is arbitrary, capricious, an abuse of
discretion, or not in accordance with the law.” Snyder ex rel. Snyder v. Sec’y of Dept. of Health
& Human Servs., 88 Fed. Cl. 706, 718 (2009). The arbitrary and capricious standard “is a highly
deferential standard of review:” “[i]f the special master has considered the relevant evidence of
record, drawn plausible inferences and articulated a rational basis for the decision, reversible
error will be extremely difficult to demonstrate.” Hines ex rel. Sevier v. Sec’y of Dept. of Health
& Human Servs., 940 F.2d 1518, 1528 (Fed. Cir. 1991).
2. The Standard of Causation in Vaccine Cases
“A petitioner seeking compensation under the Vaccine Act must prove by a
preponderance of the evidence that the injury or death at issue was caused by a vaccine.”
Broekelschen v. Sec’y of Health & Human Servs., 618 F.3d 1339, 1341 (Fed. Cir. 2010) (citing
42 U.S.C. §§ 300aa-11(c)(1), -13(a)(1)). “A petitioner can show causation under the Vaccine
Act in one of two ways:” (1) “by showing that she sustained an injury in association with a
vaccine listed in the Vaccine Injury Table,” in which case “causation is presumed;” or (2) “if the
complained-of injury is not listed in the Vaccine Injury Table . . . the petitioner may seek
compensation by proving causation in fact.” Id. at 1341–42 (internal citations omitted). Vaccine
cases employ a burden shifting standard: “[o]nce the petitioner has demonstrated causation, she
is entitled to compensation unless the government can show by a preponderance of the evidence
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that the injury is due to factors unrelated to the vaccine.” Id. at 1342 (citing Doe v. Sec’y of
Health & Human Servs., 601 F.3d 1349, 1351 (Fed. Cir. 2010); 42 U.S.C. § 300aa-13(a)(1)(B)).
“When a petitioner has suffered an off-Table injury, as is the case here, [the Federal
Circuit] has established the following test for showing causation in fact under the Vaccine Act:”
[The petitioner’s] burden is to show by preponderant evidence that the vaccination
brought about her injury by providing: (1) a medical theory causally connecting
the vaccination and the injury; (2) a logical sequence of cause and effect showing
that the vaccination was the reason for the injury; and (3) a showing of a proximate
temporal relationship between vaccination and injury.
Broekelschen, 618 F.3d at 1345 (quoting Althen, 418 F.3d at 1278). Under the first prong, “[a]
petitioner must provide a ‘reputable medical or scientific explanation’ for its theory.” Boatmon
v. Sec’y of Health & Human Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019) (quoting Moberly ex
rel. Moberly v. Sec’y of Health & Human Servs., 592 F.3d 1315, 1322 (Fed. Cir. 2010)). “While
it does not require medical or scientific certainty, it must still be ‘sound and reliable.’” Id.
(quoting Knudsen ex rel. Knudsen v. Sec’y of Dept. of Health & Human Servs., 35 F.3d 543,
548–49 (Fed. Cir. 1994)). Petitioners “need not produce medical literature or epidemiological
evidence to establish causation under the Vaccine Act.” Andreu ex rel. Andreu v. Sec’y of Dept.
of Health & Human Servs., 569 F.3d 1367, 1379 (Fed. Cir. 2009). Where such evidence is
introduced, however, it must not be viewed “through the lens of the laboratorian, but instead
from the vantage point of the Vaccine Act’s preponderant evidence standard.” Id. at 1380. For
satisfying the second prong, “medical records and medical opinion testimony are favored in
vaccine cases, as treating physicians are likely to be in the best position to determine whether ‘a
logical sequence of cause and effect show[s] that the vaccination was the reason for the injury.’”
Capizzano v. Sec’y of Health & Human Servs., 440 F.3d 1317, 1326 (Fed. Cir. 2006) (quoting
Althen, 418 F.3d at 1280). Lastly, “the proximate temporal relationship prong requires
preponderant proof that the onset of symptoms occurred within a timeframe for which, given the
medical understanding of the disorder’s etiology, it is medically acceptable to infer causation-in-
fact.” de Bazan v. Sec’y of Health & Human Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008).
B. Analysis
Petitioner argues the Chief Special Master erred in determining petitioner’s injury was
NMOSD because in doing so, he “relied upon broader diagnostic criteria, for which there was no
basis in the record.” Pet’r’s Mot. for Review at 13. Petitioner identifies three findings in the
Chief Special Master’s decision he claims were not in accordance with law because they were
not “based ‘on the record as a whole:’” (1) that petitioner had dissemination in space due to the
extension of his thoracic spinal lesion; (2) that petitioner had dissemination in space because he
had a lesion in the periventricular region of his brain; and (3) petitioner had an area postrema
lesion due to the lesion at the floor of the fourth ventricle. Id. at 12, 13, 24 (quoting 42 U.S.C. §
300aa-12(e), § 300aa-13(a)(1)).
Respondent responds, highlighting the Chief Special Master’s acknowledgment that
“‘[p]etitioner has raised reasonable objections’ to the NMOSD diagnosis, ‘such that I could not
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find that the NMOSD diagnosis is supported by even 75 percent of the record. However, the
evidence still preponderates in favor of the NMOSD diagnosis (a determination that merely
means more than 50 percent of the record favors that determination).” Resp’t’s Resp. to Pet’r’s
Mot. for Review at 14 (quoting Morgan, 2019 WL 7498665, at *19). Respondent therefore
argues “it is unsurprising that petitioner can point to evidence in the record that cuts against the
Chief Special Master’s ultimate determination that petitioner suffered from NMOSD, but those
arguments fall far short of demonstrating that the Chief Special Master’s conclusion was based
on evidence that is ‘wholly implausible.’” Id.
The Chief Special Master stated, “[p]etitioner is correct in pointing out the criteria that
apply in the context of a seronegative [NMOSD] patient, as well as the difficulty in establishing
those criteria, but there was still evidence to fit each criterion—Petitioner initially exhibited
acute myelitis with LETM, and demonstrated brain lesions in the area postrema region of the
brain.” Morgan, 2019 WL 7498665, at *18 (citing Pet’r’s Ex. 5, at 56; Pet’r’s Ex. 14, at 110,
135; Pet’r’s Ex. 21, at 1; Pet’r’s Ex. 53, at 21; Resp’t’s Ex. E at 3). As previously discussed, the
diagnostic criteria for seronegative NMOSD, as outlined by Wingerchuk, require an individual
experience two or more different core clinical characteristics, in addition to MRI imagery
showing NMOSD lesions. See Resp’t’s Ex. E, at 3. Wingerchuk provides “[a]t least 1 core
clinical characteristic must be optic neuritis, acute myelitis with LETM, or area postrema
syndrome.” Id. Both experts agreed petitioner had acute myelitis, fulfilling this requirement.
See Hr’g Tr. at 68:11–12 (Dr. Tornatore); 108:1–2 (Dr. Sriram).
1. Whether the Chief Special Master’s Finding that Petitioner had
Dissemination in Space due to the Extension of his Thoracic Lesion was
Supported by the Record
The Wingerchuk diagnostic criteria require “[d]issemination in space (2 or more different
core clinical characteristics).” Resp’t’s Ex. E, at 3. Besides acute myelitis, the other core
clinical characteristics a seronegative NMOSD patient might exhibit include: (1) “Optic
neuritis;” (2) “Area postrema syndrome: episode of otherwise unexplained hiccups or nausea
and vomiting;” (3) “Acute brainstem syndrome;” (4) “Symptomatic narcolepsy or acute
diencephalic clinical syndrome with NMOSD-typical diencephalic MRI lesions;” and (5)
“Symptomatic cerebral syndrome with NMOSD-typical brain lesions.”9 Id. The Chief Special
Master noted, however, there was, “as Dr. Sriram proposed, evidence of dissemination in space,
because later MRI reports from September 2015 show . . . a lesion extending to T6, where it had
previously extended only to T8 before resolving.” Morgan, 2019 WL 7498665, at *18 (citing
Pet’r’s Ex. 5, at 70, 80; Pet’r’s Ex. 14, at 110, 137; Pet’r’s Ex. 21, at 1). Dr. Sriram testified on
cross-examination during the hearing that he would diagnose petitioner with seronegative
NMOSD due to petitioner’s myelitis and lesions. Hr’g Tr. at 108:21–109:9. Dr. Sriram
explained, describing the visible progression of petitioner’s disease: “He had an old lesion that
stopped at T8. His new lesion in the relapse involved up to T6. So there was an extension of the
old – or a new lesion, T6 down.” Id. at 109:4–7. While Dr. Sriram acknowledged that
9 Dr. Sriram testified that petitioner did not have any symptoms representative of acute brain syndrome,
symptomatic narcolepsy or acute diencephalic clinical syndrome, or symptomatic cerebral syndrome with NMOSD-
typical brain lesions. Hr’g Tr. at 108:9–19.
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progression is “not typically” considered dissemination in space, the lesion “disseminated from
one region of the spinal cord to an additional region of the spinal cord.” Id. at 109:12–15.
Petitioner quotes portions of Wingerchuk to argue Dr. Sriram’s and the Chief Special
Master’s determinations that petitioner’s spinal lesion growth satisfied the dissemination in space
requirement was contrary to evidence in the record. Pet’r’s Mot. for Review at 19–20. For
example, petitioner clarifies Wingerchuk’s requirement that a seronegative NMOSD patient
exhibit dissemination in space means “dissemination in space, affecting different neuroanatomic
regions;” in other words, “an extensive spinal cord lesion, on its own, is not evidence of
dissemination in space.” Id. at 19 (quoting Resp’t’s Ex. E, at 3) (emphasis omitted). Further,
petitioner quotes from Dr. Brian G. Weinshenker’s article titled “Neuromyelitis Spectrum
Disorders,” respondent’s Exhibit G (“Weinshenker”)10: “[r]ecurrent isolated episodes of . . .
myelitis do not qualify [as NMOSD] [for seronegative patients].” Id. (quoting Resp’t’s Ex. G, at
4, ECF No. 47-1). Weinshenker continues, however: “NMOSD cannot be excluded in this
situation . . . .” Resp’t’s Ex. G, at 4 (emphasis added).
To the extent petitioner contends the Chief Special Master disregarded the medical
literature in finding petitioner had dissemination in space, “[w]e generally presume that a special
master considered the relevant record evidence even though he does not explicitly reference such
evidence in his decision.” Moriarty ex rel. Moriarty v. Sec’y of Health & Human Servs., 844
F.3d 1322, 1328 (Fed. Cir. 2016) (citing Hazlehurst v. Sec’y of Health & Human Servs., 604
F.3d 1343, 1352 (Fed. Cir. 2010)). In fact, the Chief Special Master wrote, “[w]hile I have
reviewed all of the medical literature submitted in this case, I discuss only those articles that are
most relevant to my determination and/or are central to Petitioner’s case.” Morgan, 2019 WL
7498665, at *16.
Moreover, there was sufficient evidence in the record to support the Chief Special
Master’s determination that petitioner satisfied the dissemination in space requirement for a
seronegative NMOSD diagnosis. Dr. Sriram testified petitioner’s “myelitis also involved . . . an
extension of an old lesion,” which although is “not typically” considered dissemination in space,
“[l]iterally . . . disseminated from one region of the spinal cord to an additional region of the
spinal cord.” Hr’g Tr. at 109:3–4, 10–15. Further, despite acknowledging he was “probably a
little more liberal with the interpretation of the criteria,” Dr. Sriram explained the diagnostic
criteria “are usually guidelines to physicians” and “we are not necessarily . . . boxed into this
alone.” Id. at 109:23–24, 110:9–10, 13–14. While petitioner contends there was no basis in the
record for the Chief Special Master’s findings, Dr. Sriram’s testimony provides a basis in the
record. It is not the Court’s role “to reweigh the factual evidence, or to assess whether the
special master correctly evaluated the evidence. And of course we do not examine the probative
value of the evidence or the credibility of the witnesses. These are all matters within the purview
10 Dr. Dean M. Wingerchuk, M.D., is also an author of the Weinshenker article, respondent’s Exhibit G. See
Resp’t’s Ex. G, at 1. Both Wingerchuk and Weinshenker outline the diagnostic criteria for NMOSD. Compare
Resp’t’s Ex. E, at 3, with Resp’t’s Ex. G, at 4. Throughout the Chief Special Master’s decision and subsequent
briefing, respondent’s Exhibit E is referred to as “Wingerchuk” and respondent’s Exhibit G as “Weinshenker.” See,
e.g., Morgan, 2019 WL 7498665, at *8; Pet’r’s Mot. for Review at 14–15.
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of the fact finder.” Munn v. Sec’y of Dept. of Health & Human Servs., 970 F.2d 863, 871 (Fed.
Cir. 1992).
With Dr. Sriram’s testimony, based on treating physician’s records, the Court cannot say
the Chief Special Master’s finding that petitioner had dissemination in space was “wholly
implausible.” See Lampe, 219 F.3d at 1363 (“Since the special master’s conclusion was based
on evidence in the record that was not wholly implausible, we are compelled to uphold that
finding as not being arbitrary and capricious.”). The Chief Special Master reasonably relied on
expert testimony and evidence of dissemination in space to support his finding that petitioner
suffered from seronegative NMOSD. See Broekelschen, 618 F.3d at 1348 (quoting Hines, 940
F.2d at 1528) (“‘[R]eversible error is “extremely difficult to demonstrate” if the special master
“has considered the relevant evidence of record, drawn plausible inferences and articulated a
rational basis for the decision.”’”). The Chief Special Master’s finding that evidence supported
dissemination in space was accordingly not “arbitrary, capricious, an abuse of discretion, or
otherwise not in accordance with law” because it was supported by the record. 42 U.S.C. §
300aa-12(e)(2)(B).
2. Whether the Chief Special Master’s Finding that Petitioner had
Dissemination in Space Because of a Periventricular Brain Lesion was Based
in the Record
Petitioner similarly challenges the Chief Special Master’s finding that there was, “as Dr.
Sriram proposed, evidence of dissemination in space, because later MRI reports from September
2015 show a brain lesion in the periventricular region of the brain.” Morgan, 2019 WL
7498665, at *18 (citing Pet’r’s Ex. 14, at 110; Ex. 21, at 1). Petitioner quotes the Wingerchuk
criteria, which state “area postrema syndrome ‘requires associated dorsal medulla/area postrema
lesions,’” and explains “[t]he periventricular region, by contrast, expands beyond the dorsal
medulla and area postrema.” Pet’r’s Mot. for Review at 24. Petitioner therefore argues “the
Chief Special Master appears to have conflated the ‘periventricular region of the brain’ with the
more specific MRI requirements for area postrema syndrome.” Id. (quoting Resp’t’s Ex. E, at 3).
Additionally, petitioner claims although the Chief Special Master suggested Dr. Sriram proposed
a periventricular lesion constitutes evidence of dissemination in space, there is no evidence in the
record of Dr. Sriram “rel[ying] upon a ‘periventricular lesion’ in his opinion.” Id. Petitioner
quotes from Dr. Pace’s notes where he states the MRIs show “nonspecific . . . hyperintensities
seen in the brain,” which he specifies are “not in a pattern that is strongly suggestive of
demyelination such as would be seen with multiple sclerosis.” Id. at 25 (quoting Pet’r’s Ex. 14,
at 110).
Petitioner cites Dr. Pace’s notes to support his contention; however, reviewing the MRI
images of hyperintensities in petitioner’s brain, Dr. Pace noted they “can be seen in
neuromyelitis optica spectrum, as this is the location of high concentration Aquaporin 4
channels.” Pet’r’s Ex. 14, at 110. Additionally, the Chief Special Master cites petitioner’s 19
September 2015 MRI report. See Morgan, 2019 WL 7498665, at *18; Pet’r’s Ex. 21. That
report notes, ‘[t]here are scattered foci of hyperintense FLAIR and T2-weighted signal identified
within the bilateral periventricular and subcortical white matter.” Pet’r’s Ex. 21, at 1 (emphasis
added). Contrary to petitioner’s contentions, this report suggests petitioner had lesions in the
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periventricular region of the brain. Moreover, Dr. Sriram testified that “very few diseases . . .
give you a postrema lesion in the floor of the fourth ventricle.” Hr’g Tr. at 110:15–17.
To the extent petitioner disagrees with the terminology the Chief Special Master used,
this does not rise to the level of arbitrary or capricious that would justify setting aside factual
findings. Given Dr. Pace’s notes suggesting petitioner’s brain lesion could be seen with
NMOSD , the radiology report of petitioner’s September 2015 MRI suggesting petitioner had a
bilateral periventricular lesion, and Dr. Sriram’s testimony, the Court cannot say the Chief
Special Master’s finding was “wholly implausible.” Cedillo v. Sec’y of Health & Human Servs.,
617 F.3d 1328, 1338 (Fed. Cir. 2010) (quoting Lampe, 219 F.3d at 1363). Petitioner’s arguments
amount to a request that the Court reweigh the evidence—a task the Chief Special Master
completed. Since the Chief Special Master’s finding that petitioner had a periventricular lesion
suggestive of NMOSD was based in the record, the Court must uphold it as not arbitrary or
capricious. Id. (quoting Lampe, 219 F.3d at 1363) (“We ‘do not sit to reweigh evidence. [If] the
Special Master’s conclusion [is] based on evidence in the record that [is] not wholly implausible,
we are compelled to uphold that finding as not arbitrary or capricious.’”).
3. Whether the Chief Special Master’s Finding that Petitioner’s Area
Postrema Lesion Supported a NMOSD Diagnosis was Based in the Record
Petitioner also challenges the Chief Special Master’s finding that petitioner’s “brain
lesions in the area postrema region of the brain” supported a seronegative NMOSD diagnosis by
satisfying area postrema syndrome as the second core clinical characteristic. See Pet’r’s Mot. for
Review at 21; Morgan, 2019 WL 7498665, at *18. Petitioner points to Wingerchuk’s criteria,
which explain that area postrema syndrome, a core clinical characteristic of seronegative
NMOSD, “requires both a presentation of symptoms (i.e., ‘intractable hiccups or nausea and
vomiting’) and MRI findings ‘meant to enhance diagnostic specificity [that] must also be
present.’” Pet’r’s Mot. for Review at 20 (quoting Resp’t’s Ex. E, at 3) (emphasis and internal
footnotes omitted). The Chief Special Master acknowledged petitioner’s argument that
“evidence of area postrema syndrome [was] not strongly supported by the record.” Morgan,
2019 WL 7498665, at *18 (emphasis omitted). The Chief Special Master also noted, however,
“while Petitioner did not experience some of the symptoms that would be associated with an area
postrema lesion . . . , his treating physicians nevertheless noted that the mere existence of an area
postrema lesion supported a diagnosis of NMOSD by itself.” Id. (citing Pet’r’s Ex. 14, at 110).
During oral argument, petitioner argued the exhibit the Chief Special Master cited for the
proposition that petitioner’s “treating physicians note[d] that the mere existence of . . . [an] area
of postrema lesion supported a diagnosis of NMO by itself” did not in fact support that assertion.
Tr. at 21:23–22:10, ECF No. 73. Respondent conceded the Chief Special Master likely conflated
treating physician statements with Dr. Sriram’s testimony during the hearing. See id. at 26:24–
28:2. While the exhibit the Chief Special Master cited—Dr. Pace’s notes from petitioner’s 26
November 2014 visit—does not state the mere existence of an area postrema lesion meant
petitioner had NMOSD, Dr. Pace noted in his review of petitioner’s 31 August 2014 MRI:
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There are several nonspecific T2/FLAIR hyperintensities seen in the brain.11 These
are not in a pattern that is strongly suggestive of demyelination such as would be
seen with multiple sclerosis. However, there is T2 hyperintensity in the fourth
ventricle surrounding the cerebral aqueduct. This is of unclear significance, but
can be seen in neuromyelitis optica spectrum, as this is the location of high
concentration of Aquaporin 4 channels.
Pet’r’s Ex. 14, at 110 (emphasis added). Dr. Sriram testified on cross-examination during the
hearing “there are very few diseases that give you a postrema lesion in the floor of the fourth
ventricle.” Hr’g Tr. at 110:15–17. Dr. Sriram continued: “[I]rrespective if the patient did not
have hiccups and did not have vomiting and nausea, this is something that clinicians pay
attention to.” Id. at 110:19–21. He also testified the lesion in the floor of the fourth ventricle
was “very persuasive for an NMO spectrum disorder.” Id. at 111:12–13. Further, he testified
that although petitioner did not exhibit the clinical systems of area postrema syndrome (hiccups
or nausea and vomiting), “[i]t’s not uncommon to have silent lesions.” Id. at 112:20.
As previously discussed, to the extent petitioner claims the Chief Special Master
disregarded the Wingerchuk criteria, the Court “presume[s] that a special master considered the
relevant record evidence even though he does not explicitly reference such evidence in his
decision.” Moriarty ex rel. Moriarty, 844 F.3d at 1328 (citing Hazlehurst, 604 F.3d at 1352).
Additionally, although citation to one treating physician’s records does not support the
proposition that petitioner’s area postrema lesion standing alone supports a NMOSD diagnosis,
there is ample evidence in the record to support the Chief Special Master’s finding that
petitioner’s area postrema lesion supported a seronegative NMOSD diagnosis. Both Dr. Pace’s
notes from reviewing petitioner’s MRIs and Dr. Sriram’s testimony lend further support for the
Chief Special Master’s finding. Petitioner’s argument asks the Court to reweigh which pieces of
evidence support discrete findings, but that is not the Court’s role in reviewing a special master’s
decision. “We ‘do not sit to reweigh the evidence. [If] the Special Master’s conclusion [is]
based on evidence in the record that [is] not wholly implausible, we are compelled to uphold that
finding as not being arbitrary or capricious.’” Cedillo v. Sec’y of Health & Human Servs., 617
F.3d 1328, 1338 (Fed. Cir. 2010) (quoting Lampe, 219 F.3d at 1363). The Chief Special
Master’s finding, based on the evidence, is not “wholly implausible.” Id. The Court therefore
finds the Chief Special Master’s finding was not arbitrary or capricious and was supported by the
record. Lampe, 219 F.3d at 1360 (“The arbitrary and capricious standard of review is difficult
for an appellant to satisfy with respect to any issue, but particularly with respect to an issue that
turns on the weighing of evidence by the trier of fact.”).
4. Petitioner’s Burden to Prove the Flu Vaccine Caused LETM
11 Upon further review by the Court, it seems the confusion may be that Dr. Pace notes T2/FLAIR “hyperintensities”
rather than “lesions.” Hyperintensities on T2-weighted MRI images of the brain depict white matter lesions, as
“[w]hite matter lesions are considered present if hyperintense on T2 weighted . . . images.” See Stéphanie Debette
& H.S. Markus, The clinical importance of white matter hyperintensities on brain magnetic resonance imaging:
systematic review and meta-analysis, The BMJ (July 26, 2010), https://www.bmj.com/content/341/bmj.c3666.
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Respondent argued in its response to petitioner’s motion for review “[m]erely attempting
to cast doubt about the Chief Special Master’s conclusion regarding the diagnosis does not
address” the requirements that “petitioner . . . prove by preponderant evidence which injury he
suffered, and that the injury was caused by a vaccine.” Resp’t’s Resp. to Pet’r’s Mot. for Review
at 17. Respondent thus asserted “petitioner appears to assume that the nature of his condition is
an either/or proposition: if it is not NMOSD, it must be TM. But the record does not support
this assumption.” Id. During oral argument, respondent expounded on these arguments,
contending it was not sufficient for petitioner to allege molecular mimicry, a medical theory
which has been accepted in Vaccine Program cases before, establishes the link of causation
between the vaccine and injury. See Tr. at 60:14–61:3. Respondent explained, “irrespective of
which diagnosis the [Chief] Special Master ultimately landed on, one of the things that he did
note was that for molecular mimicry to have utility in this case, there should be some evidence of
the relevant antibodies that are known to drive or at least are associated with the resulting
demyelinating disease are likely produced as a result of the flu vaccine.” Id. at 61:4–11. Dr.
Tornatore’s testimony, in contrast, was “exceptionally vague,” respondent contends, and “[t]here
was really nothing sufficient to tether this theory to the flu vaccine that the Petitioner received
and this theory does not explain the presence of the lesion that was in the Petitioner’s brain.” Id.
at 62:1–5. Respondent therefore argued, even if “the Court were to rule that NMOSD is not the
correct diagnosis, that does not mean that LETM is the correct diagnosis.” Id. at 62:6–8.
In response, petitioner argued “[w]hat the [Chief] Special Master is looking for here is, in
fact, direct contradiction to his own finding from just three years ago,” citing Johnson v.
Secretary of Health & Human Services, No. 14-113V, 2017 WL 772534 (Fed. Cl. Spec. Mstr.
Jan. 6, 2017). Id. at 63:22–25. Petitioner pointed to footnote 25 of that case, where the Chief
Special Master wrote: “Petitioner did not show exactly which antigen would be involved in the
proposed cross-reactivity process, nor did she offer any studies showing molecular mimicry
could happen between [immune thrombocytopenic purpura (“ITP”)] and [human papillomavirus
(“HPV”)]. But to require Petitioner to have done so amounts to heightening the burden of proof
beyond what a claimant need offer.” Johnson, 2017 WL 772534, at *19 n.25. Petitioner
therefore asserted, “[a] petitioner does not have to show a precise, exact biological mechanism of
injury. To do so inappropriately heightens the petitioner’s burden to the level of scientific
certainty, a level that’s not required under preponderant evidence.” Tr. at 64:14–18.
The Chief Special Master recognized “molecular mimicry has repeatedly been embraced
in Program cases as a reliable scientific mechanism for explaining the pathophysiology of certain
immune-mediated conditions, including many demyelinating disorders.” Morgan, 2019 WL
7498665, at *19. As applied to petitioner’s case, however, the Chief Special Master found
petitioner offered little evidence to show “the relevant autoantibodies that are known to drive, or
at least associated with, the resulting demyelinating disease are likely produced as a result of the
flu vaccine,” which the Chief Special Master noted was “reasonable to require” of a petitioner
“when evaluating the success of the claimant’s [Althen] prong one showing.” Id. (citing W.C. v.
Sec’y of Health & Human Servs., 704 F.3d 1352, 1361 (Fed. Cir. 2013)). The Chief Special
Master observed, “[a]t best, there are some references in the literature indicating that NMOSD
initially manifesting as LETM could be caused be a variety of infectious agents (i.e., the herpes
virus, dengue fever, tuberculosis, etc.). But this list does not also include the influenza wild
virus. Nor did petitioner’s filings establish how an initial reaction to a vaccination might be
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Case 1:15-vv-01137-RTH Document 78 Filed 06/17/20 Page 27 of 27
sufficient to create the kind of chronic, CNS-oriented inflammatory process that would
ultimately morph into NMOSD.” Id. at *20. The Chief Special Master therefore found
petitioner failed to demonstrate with “reliable and persuasive evidence . . . that the flu vaccine
could cause a chronic form of CNS demyelinating disease such as NMOSD, that would unfold
over a lengthy period of time.” Id.
The Johnson case is inapposite to the instant case. In Johnson, the parties largely agreed
the petitioner suffered from ITP; they merely disagreed whether the HPV vaccine was a
contributing factor to the petitioner’s condition. Johnson, 2017 WL 772534, at *15. Here, the
parties dispute what petitioner’s injury was, and this is the crux of petitioner’s motion for review.
Notably, however, petitioner does not argue in his motion for review the flu vaccine caused
LETM, nor does he challenge the Chief Special Master’s holding that petitioner failed to meet
his burden to prove the flu vaccine caused his injury. Respondent therefore asserted during oral
argument “even if [the Court] determine[s] that it’s not NMOSD, . . . it’s not necessarily the case
that that finding would translate to a finding that the Petitioner has met his burden to demonstrate
a legally cognizable injury.” Tr. at 13:25–14:4. Likewise, respondent argued “ruling out
NMOSD does not automatically rule in LETM as the Petitioner’s ultimate diagnosis. And,
again, it is the Petitioner that bears the burden of demonstrating that and they did not challenge
or raise an appeal” of the Chief Special Master’s “finding that petitioner failed to meet its burden
of showing a cognizable injury.” Id. at 28:11–12, 19–23. Contrary to petitioner’s argument, the
Chief Special Master did not raise the burden of causation in this case; petitioner simply failed to
meet it. As the Chief Special Master stated, the medical literature petitioner offered did not
connect the flu vaccine or influenza wild virus to a demyelinating disorder that eventually
manifests as NMOSD. Morgan, 2019 WL 7498665, at *20. The Chief Special Master was not
requiring petitioner to “show exactly which antigen would be involved in the proposed-cross
reactivity process.” Johnson, 2017 WL 772534, at *19 n.25. The Chief Special Master was
looking for evidence “involving the flu vaccine . . . and its association with NMOSD, or proof
that immune system stimulation can at least initiate a chronic process.” Morgan, 2019 WL
7498665, at *19. Therefore, even if the Court found the Chief Special Master’s finding that
petitioner suffered from NMOSD was arbitrary and capricious, that does not mean petitioner met
his burden of proof to show the flu vaccine caused LETM.
III. Conclusion
For the foregoing reasons, the Court SUSTAINS the Chief Special Master’s decision
because it was not arbitrary, capricious, or not otherwise in accordance with law. The Court
therefore DENIES petitioner’s motion for review. The Clerk of Court is directed to enter
judgment for respondent.
IT IS SO ORDERED.
s/ Ryan T. Holte
RYAN T. HOLTE
Judge
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