Morgan v. Secretary of Health and Human Services

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 DECISION 1

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
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 MRI 3 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.

2
ordered an EMG 4 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.

3
addition to citing the urological symptoms of frequency and oliguria 6. 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 scan 7 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.

4
 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 syndrome 8 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
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

6
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
Sclerosis 10 (“MS”) or Neuromyelitis Optica 11 (“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.

7
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

8
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.

9
 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 disease 12, 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 periventricular 13 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.

10
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

11
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 syndrome 14, 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.

12
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

13
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.

14
 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.

15
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).

16
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

17
. . . 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.

18
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

19
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.

20
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

21
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

22
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

23
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.

24
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

25
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).

26
 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).

27
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