Morgan v. Hhs

Case: 20-2107 Document: 33 Page: 1 Filed: 03/24/2021

NOTE: This disposition is nonprecedential.

United States Court of Appeals
for the Federal Circuit
______________________

PITEY MORGAN,
Petitioner-Appellant

v.

SECRETARY OF HEALTH AND HUMAN
SERVICES,
Respondent-Appellee
______________________

2020-2107
______________________

Appeal from the United States Court of Federal Claims
in No. 1:15-vv-01137-RTH, Judge Ryan T. Holte.
______________________

Decided: March 24, 2021
______________________

SYLVIA CHIN-CAPLAN, Law Office of Sylvia Chin-
Caplan, LLC, Boston, MA, for petitioner-appellant. Also
represented by TIMOTHY MASON.

ZOE WADE, Torts Branch, Civil Division, United States
Department of Justice, Washington, DC, for respondent-
appellee. Also represented by JEFFREY B. CLARK, C.
SALVATORE D'ALESSIO, HEATHER LYNN PEARLMAN,
CATHARINE E. REEVES.
______________________
Case: 20-2107 Document: 33 Page: 2 Filed: 03/24/2021

2 MORGAN v. HHS

Before DYK, BRYSON, and HUGHES, Circuit Judges.
BRYSON, Circuit Judge.
Appellant Pitey Morgan filed a petition for compensa-
tion under the National Vaccine Injury Compensation Pro-
gram, 42 U.S.C. §§ 300aa-10–300aa-34 (“Vaccine Act”),
claiming that an influenza vaccination resulted in serious
neurological injury. The chief special master in the Vac-
cine Program’s Office of Special Masters denied his claim
for compensation, and the Court of Federal Claims sus-
tained that decision. We affirm.
I
A
Mr. Morgan has an extensive medical history from well
before his influenza vaccination in 2012. See Morgan v.
Sec’y of Health & Hum. Servs., No. 15-1137V, 2019 WL
7498665, at *1–7 (Fed. Cl. Spec. Mstr. Dec. 4, 2019) (“Spe-
cial Master’s Decision”). The evidence showed that Mr.
Morgan had numerous preexisting conditions, including
persistent lower back pain, lower extremity radiculopathy,
multi-level degenerative disc disease, lumbar spondylosis,
and prostatitis. Nonetheless, the special master agreed
with Mr. Morgan that his neurological injury did not pre-
date his vaccination. Id. at *17.
Mr. Morgan received a flu vaccination on October 16,
2012. Following his vaccination, Mr. Morgan sought treat-
ment from numerous physicians for medical issues. The
reports from those physicians reveal that the assessments
of Mr. Morgan’s illness shifted over time as his symptoms
matured and as the treating physicians received a more
complete picture of his medical condition.
The day after his vaccination, Mr. Morgan saw a urol-
ogist, Dr. Arthur Golin, complaining of urination issues.
Id. at *3. Mr. Morgan told Dr. Golin that his urination
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MORGAN v. HHS 3

issues had begun during the previous year but had acceler-
ated during the past two and a half months. Mr. Morgan
also reported weakness and numbness in his lower extrem-
ities. Dr. Golin assessed his condition as urinary retention
with a possible neurologic component.
Six days later, Mr. Morgan saw Dr. Scott Greenwald,
complaining of lower back pain. Mr. Morgan reported that
the pain was radiating down both of his legs and that he
was experiencing numbness in his calves. Dr. Greenwald
treated Mr. Morgan with a lumbar steroid injection.
The next day, Mr. Morgan was taken to an emergency
room after losing strength in, and the ability to ambulate,
both of his legs. Dr. Christopher Hummel assessed possi-
ble cauda equina syndrome and epidural hematoma in
light of Mr. Morgan’s recent steroid injection. Dr. Hummel
ordered an MRI of Mr. Morgan’s spinal cord.
Later that day, Mr. Morgan was transferred to a neigh-
boring hospital where he was examined by Dr. Christopher
Marquart. A physical examination revealed that Mr. Mor-
gan had poor sensory reception corresponding to the T12
and L1 vertebrae. Id. at *4. Upon reviewing Mr. Morgan’s
most recent MRI results, Dr. Marquart observed evidence
of nerve root clumping at the conus (i.e., the base of the
spinal cord), leading him to suspect that Mr. Morgan was
experiencing transverse myelitis (“TM”) 1 or some other
acute, neuro-inflammatory process. Dr. Marquart admit-
ted Mr. Morgan to the intensive care unit to ensure that
“he [did] not have any type of ascending paralysis with the
recent flu vaccination.” Special Master’s Decision at *4.

1 Myelitis is inflammation of the spinal cord. Sted-
man’s Medical Dictionary 1268 (28th ed. 2006). Transverse
myelitis is inflammation across the entire thickness of only
one or two segments of the spinal cord. Id.
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4 MORGAN v. HHS

Dr. Roni Devlin, an infectious disease specialist, exam-
ined Mr. Morgan the following day and ordered another
MRI examination. That MRI revealed swelling in the spi-
nal cord from the T8 vertebra to the lower tip of the spinal
cord. Dr. Devlin assessed myelitis of indeterminate etiol-
ogy. He noted that “[c]ase reports of myelitis following vac-
cination have certainly been reported, but rarely.” Id.
Two days later, Mr. Morgan was evaluated by Dr.
Larry Wahl, who noted that Mr. Morgan’s difficulties with
his lower extremities seemed to reach a critical point the
day after the October 23 steroid injection. Dr. Wahl
reached a differential diagnosis of a viral infection, arach-
noiditis, and TM, but he expressed skepticism about TM
given the nature of the swelling in Mr. Morgan’s spinal
cord.
Mr. Morgan was discharged from the hospital on Octo-
ber 29, 2012. By that time, he had recovered the ability to
stand, bear weight, and walk short distances with a
walker. However, he continued to experience numbness
and tingling in his lower extremities. During a follow-up
examination on November 15, 2012, Dr. Marquart reiter-
ated his belief that Mr. Morgan had probably experienced
myelitis as a “reaction to his flu vaccine for lack of a better
explanation.” Id. A third MRI showed improvement in the
appearance of the spinal cord.
On December 13, 2012, Mr. Morgan was examined by
Dr. Douglas Gelb at the University of Michigan Neurology
Clinic. Dr. Gelb proposed that Mr. Morgan had suffered
from either an isolated episode of TM or the first instance
of a recurring, central nervous system disease, such as
multiple sclerosis or neuromyelitis optica (“NMO”). 2

2 Neuromyelitis optica is characterized by the demy-
elination of the optic nerve and the spinal cord. Dorland’s
Medical Dictionary 1249 (33rd ed. 2020). Demyelination
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MORGAN v. HHS 5

Special Master’s Decision at *5. Dr. Gelb ordered an NMO
antibodies test, which returned a negative result but with
the qualification that a negative result did not necessarily
preclude a diagnosis of NMO.
Mr. Morgan’s condition improved from late 2012 into
early 2013. He recovered strength in his lower extremities
and did not experience any new symptoms.
In early 2013, however, Mr. Morgan’s condition once
again began to deteriorate. An examination by Dr. Wahl
revealed decreased strength in both of Mr. Morgan’s legs.
Dr. Wahl ordered an MRI, and the results showed expand-
ing lesions in the thoracic section of the spinal cord, the
appearance of which was suggestive of TM. By June 2013,
Mr. Morgan had lost further strength in his lower extrem-
ities and could no longer stand on his own. On July 23,
2013, Dr. Ivan Landon classified Mr. Morgan as paraplegic
and concluded that Mr. Morgan had “suffered at least one,
maybe two, relapses” and “was likely suffering from a poly-
phasic TM.” Id.
From July 2013 through June 2014, Mr. Morgan saw
occasional improvements in his condition while completing
a treatment and rehabilitation program. Id. at *6. Despite
those occasional improvements, Dr. Landon observed that
Mr. Morgan’s condition was generally deteriorating as he
continued to experience relapses. By June 2014, Mr. Mor-
gan was restricted to a wheelchair and began complaining
of issues with his upper extremities.
On August 15, 2014, Mr. Morgan saw Dr. Gelb again.
An examination revealed that Mr. Morgan’s lower

occurs when myelin, the protective coating on nerve cells,
is damaged. Id. at 480. Symptoms of neuromyelitis optica
often include changes in vision, flaccid paralysis of the ex-
tremities, and sensory and genitourinary disturbances. Id.
at 1249.
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6 MORGAN v. HHS

extremities were completely immobile. Dr. Gelb was un-
sure whether Mr. Morgan’s clinical deterioration “was due
to [a] new episode of spinal cord inflammation, or simply
some systemic illness exacerbating his deficits from his in-
itial episode.” Id. Dr. Gelb judged that the former was
more likely because of the severity of Mr. Morgan’s new
symptoms. Dr. Gelb ordered MRIs of Mr. Morgan’s spine
and brain, as well as another NMO antibodies test. The
antibodies test was negative. The spinal MRI revealed a
loss of volume starting at the T8 vertebra and extending
down to the conus, likely caused by prior inflammation.
The spinal MRI also showed signal changes and abnormal
enhancements at the T2 vertebra that were indicative of
spinal inflammation. The brain MRI revealed “nonspecific
small areas of nonenhancing T2 signal prolongation in pre-
dominantly left supratentorial white matter,” possibly as a
result of prior inflammation at the T2 vertebra. Id.
On November 26, 2014, Dr. Robert Pace of the Univer-
sity of Michigan Multiple Sclerosis Clinic further evaluated
Mr. Morgan’s MRIs. Regarding the brain MRI, Dr. Pace
noted that the scans did not reveal patterns that were sug-
gestive of multiple sclerosis. “However, there is T2 hyper-
intensity in the fourth ventricle surrounding the cerebral
aqueduct. This is of unclear significance, but can be seen
in [NMO] spectrum . . . .” Id. Based on his review of the
laboratory tests and imaging studies, Dr. Pace diagnosed
Mr. Morgan with “longitudinal myelitis due to [NMO],
sero-negative.” Id. at *7.
In an August 15, 2015, visit to Dr. Pace, Mr. Morgan
reported persistent paralysis in his lower extremities and
numbness starting at, and extending below, his middle
back. Dr. Pace ordered additional MRIs. The brain MRI
revealed that the “signal hyperintensities located [near the
ventricles] of the brain [had been] stable since January.”
Id. The spinal MRI revealed no abnormalities. Dr. Pace
reported a differential diagnosis of relapsing-remitting
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MORGAN v. HHS 7

multiple sclerosis, NMO, and flaccid paralysis of the lower
extremities.
On April 20, 2016, Mr. Morgan visited Dr. Pace for a
third time. Mr. Morgan was still confined to a wheelchair
but had not developed any new or worsening symptoms.
Following an examination, Dr. Pace once again diagnosed
Mr. Morgan’s condition as “most likely seronegative
[NMO].” Id.
In April 2017, Dr. Pace examined Mr. Morgan for a
fourth and final time. The examination revealed positive
progress with Mr. Morgan’s lower extremities. An MRI
showed no evidence of new or enhanced lesions on the spi-
nal cord. Dr. Pace’s differential diagnosis listed NMO,
acute TM, paralytic syndrome, and spinal stenosis of the
cervical region.
B
Mr. Morgan filed a petition seeking compensation un-
der the Vaccine Act. He alleged that he had developed lon-
gitudinally extensive transverse myelitis (“LETM”) 3
caused by the flu vaccine he received in 2012. At a January
2019 hearing, the special master heard testimony from
both sides’ expert witnesses.
Mr. Morgan’s expert, Dr. Carlo Tornatore, testified
that Mr. Morgan had developed remitting and relapsing
LETM, not NMO or NMO spectrum disorder (“NMOSD”). 4

3 Longitudinally extensive transverse myelitis is
characterized by bilateral spinal cord inflammation (i.e.,
transverse myelitis) that extends vertically through three
or more vertebral segments. D. Karussis et al., The Spec-
trum of Post-Vaccination Inflammatory CNS Demyelinat-
ing Syndromes, Autoimmunity Reviews 1, 6 (2013).
4 The term neuromyelitis optica spectrum disorder
was first introduced in 2007 to cover patient groups with
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8 MORGAN v. HHS

Special Master’s Decision at *8. Dr. Tornatore described
TM/LETM as a syndrome in which an immune-mediated
process causes inflammation of the spinal cord, resulting
in scarring and neural injury. That inflammatory process,
according to Dr. Tornatore, is known to cause symptoms
that align with Mr. Morgan’s symptoms, including weak-
ness in limbs, sensory alterations, and autonomic dysfunc-
tion.
Dr. Tornatore stated that Mr. Morgan did not meet the
diagnostic criteria for NMOSD. Because Mr. Morgan
tested negative for NMO-related antibodies, Dr. Tornatore
testified, he needed to exhibit an additional clinical char-
acteristic besides acute myelitis to justify a diagnosis of
NMOSD, but his medical records did not reveal such a
characteristic. Id. at *9. Dr. Tornatore added that in his
view Mr. Morgan did not fit the typical demographic for
NMOSD and that, although the remitting-relapsing nature
of Mr. Morgan’s disease did not fit the typical TM case, TM
could be polyphasic in certain individuals.
As for causation, Dr. Tornatore testified that the close
connection in time between Mr. Morgan’s vaccination and
the onset of his symptoms meant that Mr. Morgan’s vac-
cination was more likely than not the cause of his LETM.
Id. at *7. Dr. Tornatore proposed molecular mimicry as the
medical theory for causation. Id. at *9. In support of that

various clinical features and AQP4-IgG antibody test re-
sults. See Wingerchuk et al., International Consensus Di-
agnostic Criteria for Neuromyelitis Optica Spectrum
Disorders, 85 Neurology 177, 178 (2015). In 2013, a panel
of experts decided that the term “NMO would be subsumed
into the single descriptive term NMOSD because the clini-
cal behavior, immunopathogenesis, and treatment of pa-
tients who have NMOSD are not demonstrably different
than for those with NMO and patients with incomplete
forms of NMO frequently later fulfill NMO criteria.” Id.
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MORGAN v. HHS 9

theory, Dr. Tornatore cited medical literature discussing
molecular mimicry and its role in the development of TM
following vaccinations. See, e.g., N. Nakamura et al., Neu-
rologic Complications Associated with Influenza Vaccina-
tion: Two Adult Cases, 42 Internal Med. 191, 193–94
(2003). Dr. Tornatore also relied on statements from Mr.
Morgan’s treating physicians indicating a possible connec-
tion between Mr. Morgan’s vaccination and the onset of his
disease. Dr. Tornatore did not, however, point to any evi-
dence suggesting a connection between the influenza vac-
cine and NMOSD.
The government’s expert, Dr. Subramaniam Sriram,
disagreed with Dr. Tornatore and testified that in his opin-
ion Mr. Morgan’s condition was NMOSD featuring relaps-
ing LETM, not merely LETM. 5 Special Master’s Decision
at *10. Regarding the NMOSD diagnostic criteria, Dr. Sri-
ram agreed with Dr. Tornatore that Mr. Morgan was sero-
negative and thus needed to exhibit a second clinical
characteristic in addition to acute myelitis in order to jus-
tify a diagnosis of NMOSD under the NMOSD diagnostic
criteria. However, Dr. Sriram asserted that the additional
characteristic was present. He pointed to Dr. Pace’s anal-
ysis of the two brain MRIs, which supported the existence
of an area postrema brain lesion. He also pointed to the
MRI ordered by Dr. Wahl, which showed expansion of my-
elitis along the spinal cord, thus evincing dissemination in
space. Id. at *11. Dr. Sriram also noted that the NMOSD
diagnostic criteria were “guidelines” for treating

5 The government asserted, and the special master
agreed, that LETM can be an acute condition or a feature
of a chronic disorder, such as NMOSD or multiple sclerosis,
both of which result from hyperactivity of the immune sys-
tem directed to the central nervous system. See Special
Master’s Decision at *16. Dr. Tornatore’s testimony is con-
sistent with that conclusion. See J.A. 107–08.
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10 MORGAN v. HHS

physicians and did not have to be applied rigidly in order
to reach a correct diagnosis.
Dr. Sriram testified that TM is generally considered a
monophasic disease, not a polyphasic disease, especially
when connected to an infection or vaccination event, as al-
leged in this case. On the other hand, NMOSD is typically
considered a chronic condition, with 60 to 70 percent of pa-
tients suffering relapses, according to Dr. Sriram. In sum,
Dr. Sriram concluded from the totality of Mr. Morgan’s
medical history, including the remitting and relapsing na-
ture of his disease, that the proper diagnosis was NMOSD
with clinically relapsing LETM.
The special master issued a decision denying Mr. Mor-
gan’s claim for compensation. Special Master’s Decision at
*20. As a preliminary matter, the special master agreed
with Mr. Morgan that his neurologic condition did not pre-
date his flu vaccination. Id. at *17. The special master
found, however, that the record best supported a diagnosis
of NMOSD, not LETM. Id. at *18. The special master then
reviewed Mr. Morgan’s showing on causation regarding the
flu vaccine and NMOSD. Id. at *19. The special master
concluded that Mr. Morgan failed to carry his burden with
respect to the first two prongs of the causation test set out
in Althen v. Secretary of Health & Hum. Servs., 418 F.3d
1274 (Fed. Cir. 2005).
Mr. Morgan moved for review of the special master’s
decision, but the Court of Federal Claims affirmed. Mor-
gan v. Sec’y of Health & Hum. Servs., 148 Fed. Cl. 454, 477
(2020).
Mr. Morgan appeals to this court. We have jurisdiction
pursuant to 42 U.S.C. § 300aa-12(f).
II
On appeal, Mr. Morgan challenges the special master’s
conclusion that the evidence best supports a diagnosis of
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MORGAN v. HHS 11

NMOSD, and he argues that the special master’s findings
on causation were tainted by that erroneous conclusion.
A petitioner seeking compensation under the Vaccine
Act for an injury not listed in the Vaccine Injury Table (see
42 U.S.C. § 300aa-14) must prove by a preponderance of
the evidence that the vaccine was the cause in fact of the
injury. Broekelschen v. Sec’y of Health & Hum. Servs., 618
F.3d 1339, 1341 (Fed. Cir. 2010); see 42 U.S.C. §§ 300aa-
13(a)(1)(A) and 300aa-11(c)(1)(C)(ii). To prove causation in
fact, the petitioner must establish by a preponderance of
the evidence “(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 rela-
tionship between vaccination and injury.” De Bazan v.
Sec’y of Health & Hum. Servs., 539 F.3d 1347, 1352 (Fed.
Cir. 2008) (quoting the “Althen test” from 418 F.3d at
1278). In cases in which the nature of the claimant’s injury
is in dispute, a fundamental first step in the causation
analysis is to determine the nature of the injury based on
a preponderance of the evidence. See Lombardi v. Sec’y of
Health & Hum. Servs., 656 F.3d 1343, 1352 (Fed. Cir.
2011).
In Vaccine Act cases, we review a decision by the Court
of Federal Claims de novo, applying the same standard of
review as that court applies in reviewing a decision of a
special master. Broekelschen, 618 F.3d at 1345. Although
we review legal determinations without deference, we re-
view the special master’s factual findings under the arbi-
trary and capricious standard. Milik v. Sec’y of Health &
Hum. Servs., 822 F.3d 1367, 1375 (Fed. Cir. 2016). “The
arbitrary and capricious standard is difficult for an appel-
lant to satisfy with respect to any issue, but particularly
with respect to an issue that turns on the weighing of evi-
dence by the trier of fact.” Id. (internal quotation marks
omitted).
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12 MORGAN v. HHS

A
Mr. Morgan argues that the special master’s diagnosis
of NMOSD was arbitrary and capricious because it relied
on factual findings that had no basis in the evidence of rec-
ord. More specifically, Mr. Morgan argues that the special
master erred in finding that Mr. Morgan’s condition satis-
fied the diagnostic criteria for NMOSD, seronegative type.
The NMOSD diagnostic criteria for seronegative adult
patients are as follows: First, the patient must exhibit two
or more core clinical characteristics along with the corre-
sponding MRI components. Second, at least one of the core
clinical characteristics must be optic neuritis, TM, or area
postrema clinical syndrome. Third, the two required core
clinical characteristics must occur across different neuro-
anatomic regions, i.e., they must exhibit “dissemination in
space.” Wingerchuk et al., International Consensus Diag-
nostic Criteria for Neuromyelitis Optica Spectrum Disor-
ders, 85 Neurology 177, 179 (2015); see also Weinshenker
et al., Neuromyelitis Spectrum Disorders, 92 Mayo Clinic
Proc. 663, 666 (2017). It is undisputed that Mr. Morgan’s
injury satisfied the clinical characteristic of TM and its
MRI component. The characteristic in dispute is the area
postrema syndrome and its corresponding MRI component
requiring a lesion in a specific area of the brain. See Wing-
erchuk et al., supra, at 179.
The special master found that Mr. Morgan’s medical
history “demonstrated brain lesions in the area postrema
region of the brain” and that the “mere existence of an area
postrema lesion supported a diagnosis of NMOSD by it-
self.” Special Master’s Decision at *18. That finding was
clearly erroneous, Mr. Morgan contends, because the
NMOSD diagnostic criteria require area postrema syn-
drome, and Dr. Sriram admitted that Mr. Morgan did not
have any of the clinical symptoms evincing that syndrome,
namely hiccups, nausea, or vomiting. According to Mr.
Morgan, the special master’s finding was also clearly
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MORGAN v. HHS 13

erroneous because the official interpretation of the brain
MRIs in Mr. Morgan’s medical records did not indicate a
lesion in the area postrema. Finally, beyond the dispute
over the area postrema characteristic, Mr. Morgan con-
tends that the special master erred in concluding that the
April 2013 MRI showing the expansion of myelitis along
the spinal cord satisfied the requirement of dissemination
in space. That was error, Mr. Morgan argues, because dis-
semination in space requires two or more clinical charac-
teristics that affect different neuroanatomic regions, not
merely different segments of the spinal cord.
Even assuming Mr. Morgan is correct in arguing that
his injury did not satisfy the technical requirements of the
NMOSD diagnostic criteria, the special master’s conclusion
that Mr. Morgan was suffering from NMOSD is still sup-
ported by ample evidence, for several reasons.
First, the remitting and relapsing nature of Mr. Mor-
gan’s condition strongly supports a diagnosis of NMOSD as
opposed to LETM. Dr. Sriram explained that TM can be a
stand-alone condition or a feature of NMOSD. He testified
that TM, manifesting on its own, is typically a monophasic
event, while “60 to 70 percent” of patients with NMOSD
will relapse. J.A. 156. He also explained that physicians
will reconsider an initial diagnosis of TM if a relapse oc-
curs.
While Dr. Tornatore testified that in his opinion an in-
dividual with TM can experience relapses and that Mr.
Morgan had LETM, see J.A. 116 and 125, the special mas-
ter was entitled to credit Dr. Sriram’s testimony over Dr.
Tornatore’s conflicting testimony and to conclude that the
overall course of Mr. Morgan’s symptoms fit best with a di-
agnosis of NMOSD. See Special Master’s Decision at *18–
19. The special master’s decision in that regard is not an
outlier. Other special masters have reached the same con-
clusion on similar facts. See, e.g., Doles v. Sec’y of Health
& Hum. Servs., No. 17-642V, 2021 WL 750416, at *16 (Fed.
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14 MORGAN v. HHS

Cl. Spec. Mstr. Feb. 1, 2021) (noting a “distinction between
acute demyelinating injuries such as transverse myelitis
and chronic, relapsing demyelinating injuries such as mul-
tiple sclerosis”); Wei-Ti Chen v. Sec’y of Health & Hum.
Servs., No. 16-634V, 2019 WL 2121208, at *19 (Fed. Cl.
Spec. Mstr. Apr. 19, 2019) (collecting cases); see also Crosby
v. Sec’y of Health & Hum. Servs., No. 08-799V, 2012 WL
13036266, at *5 n.7 (Fed. Cl. Spec. Mstr. June 20, 2012)
(citing various medical journals that describe TM as
“acute” and “generally monophasic”).
Second, there is significant evidence in Mr. Morgan’s
medical history other than acute myelitis that is suggestive
of NMOSD. In particular, Dr. Sriram pointed to the expan-
sion of myelitis vertically along the spinal cord and a brain
abnormality in an area most commonly associated with
NMOSD. The MRI ordered by Dr. Wahl showed that mye-
litis had expanded along Mr. Morgan’s spinal cord over a
period of roughly seven months. That expansion was very
relevant to an NMOSD diagnosis, Dr. Sriram testified, re-
gardless of whether it fit within the technical conditions of
the NMOSD diagnostic criteria. In addition, Dr. Pace’s
analysis of Mr. Morgan’s brain MRI noted signal hyperin-
tensities located near the ventricles of the brain. Dr. Pace
described those hypersensitivities as having “unclear sig-
nificance,” but noted that they “can be seen in [NMO] spec-
trum.” J.A. 269. Regarding Dr. Pace’s notes, Dr. Sriram
testified that there are very few diseases that produce an
abnormality near the fourth ventricle of the brain, that
NMOSD is one of those diseases, and that such an abnor-
mality would be something treating physicians would “pay
attention to” with respect to an NMOSD diagnosis. J.A.
176–77.
Mr. Morgan argues that his medical history does not
reflect the presence of all the symptoms normally associ-
ated with NMOSD, particularly those symptoms associ-
ated with area postrema syndrome. As Dr. Sriram testified
and the special master found, however, the symptoms
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MORGAN v. HHS 15

reported by the treating physicians were strongly sugges-
tive of NMOSD rather than LETM. Mr. Morgan thor-
oughly explored the ways in which his symptoms departed
from the classic symptoms of NMOSD, both on cross-exam-
ination of Dr. Sriram and in his briefing to the special mas-
ter. Notwithstanding the absence of some symptoms
generally associated with NMOSD, the special master con-
cluded that the evidence summarized by both experts sup-
ported Dr. Sriram’s proposed diagnosis of NMOSD better
than Dr. Tornatore’s proposed diagnosis of LETM. We are
not inclined to second-guess that weighing of the evidence.
Third, the diagnoses and assessments of Mr. Morgan’s
condition by his treating physicians, on balance, favor a di-
agnosis of NMOSD. There were 13 such diagnoses and as-
sessments between the day after Mr. Morgan’s vaccination
and the spring of 2017. Six of those diagnoses and assess-
ments suggested stand-alone TM/LETM, while five sug-
gested NMOSD. Importantly, however, four of the five
suggesting NMOSD were provided after all of Mr. Morgan’s
relapses, which occurred in the spring of 2013 and thereaf-
ter. On the other hand, only two of the six suggesting TM
were provided after the first relapse in the spring of 2013.
Based on that record, the special master concluded that
“[t]reaters initially, and rationally, interpreted [Mr. Mor-
gan’s] symptoms and test results (like MRIs) as supportive
of LETM. . . . But over time, [Mr. Morgan] began experi-
encing a progressive course of symptoms that suggested a
relapse, and certainly resulted in more severe symptoms
that impacted his ambulation. . . . Thereafter, other evi-
dence (as extensively referenced above) undermined the in-
itial conclusion about the possible nature of [Mr. Morgan’s]
injury,” and the more likely diagnosis became NMOSD.
Special Master’s Decision at *18. The special master’s con-
clusion was not unreasonable.
Finally, contrary to Mr. Morgan’s suggestion, the evi-
dence did not show that the NMOSD diagnostic criteria are
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16 MORGAN v. HHS

the definitive metric for diagnosing NMOSD, to the exclu-
sion of all other evidence in the record. The primary pur-
pose of the NMOSD diagnostic criteria was to differentiate
NMOSD from multiple sclerosis, because treatments for ei-
ther of those two diseases are known to have detrimental
effects on patients suffering from the other disease. See
Weinshenker et al., supra, at 666. The purpose was not to
distinguish NMOSD from relapsing LETM. See id. 6
In contrast to the purpose for which the NMOSD diag-
nostic criteria were created, the special master’s focus was
not to distinguish between NMOSD and multiple sclerosis,
but to determine whether Mr. Morgan suffered from the
alleged injury, LETM. For that purpose, the NMOSD di-
agnostic criteria served as a relevant data point but were
not dispositive. The diagnostic criteria themselves recog-
nize that in the case of a seronegative patient experiencing
recurring myelitis, “NMOSD cannot be excluded.” Weins-
henker et al., supra, at 666–67. Thus, even if Mr. Morgan’s
injury did not fully satisfy the NMOSD diagnostic criteria,
the special master’s diagnosis of NMOSD is well supported
by the evidence of record, including the remitting-relapsing
nature of Mr. Morgan’s condition, the MRIs showing fea-
tures unique to NMOSD, the sum of the treating physi-
cians’ diagnoses, and expert testimony from Dr. Sriram.
For those reasons, we hold that, based on the record as a

6 Dr. Sriram testified that although Mr. Morgan’s
brain abnormality persuaded him that NMOSD was the
correct diagnosis, the existence of that brain abnormality
was not pertinent to the proper treatment—“[Mr. Morgan
was] going to be treated similarly” with or without the
brain lesion. J.A. 177.
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MORGAN v. HHS 17

whole, the special master’s diagnosis was not arbitrary or
capricious. See 42 U.S.C. § 300a-13(a)(1). 7
B
Mr. Morgan argues that the special master’s findings
on causation were erroneous because they relied upon the
special master’s improper conclusion that Mr. Morgan suf-
fered from NMOSD. Because we reject Mr. Morgan’s argu-
ment that the special master’s finding regarding NMOSD
was arbitrary and capricious, we review the special mas-
ter’s causation findings with respect to whether Mr. Mor-
gan’s vaccination caused his NMOSD.
In his causation analysis, the special master first noted
that Mr. Morgan’s theory of molecular mimicry was an ac-
cepted scientific theory for explaining how a vaccine could
cause TM. Special Master’s Decision at *19. Despite the
acceptability of molecular mimicry, the special master
found an absence of evidence in the record and a lack of
authority in prior Vaccine Act decisions supporting molec-
ular mimicry as a viable mechanism for causing NMOSD
and, more generally, supporting the hypothesis that a flu
vaccine could cause NMOSD. Id. at *19–20. For those rea-
sons, the special master concluded that Mr. Morgan had
not satisfied the first two prongs of the Althen test.

7 Mr. Morgan asserts that the government aban-
doned its theory that the NMOSD diagnostic criteria were
satisfied, and that the special master erred by “credit[ing]
an argument that [the government] clearly elected to
waive.” Appellant’s Opening Br. 21. We reject that argu-
ment. The special master was entitled to weigh the totality
of the evidence, regardless of the position taken by the gov-
ernment as to particular pieces of evidence. The question
before us is whether the evidence as a whole was sufficient
to support the special master’s conclusion, and we hold that
it was.
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18 MORGAN v. HHS

We discern no error in the special master’s causation
analysis. To carry his burden on causation, Mr. Morgan
needed to provide a reputable medical or scientific expla-
nation pertaining to his alleged vaccine injury, although
that explanation needed only to be “legally probable, not
medically or scientifically certain.” Moberly v. Sec’y of
Health & Hum. Servs., 592 F.3d 1315, 1322 (Fed. Cir. 2010)
(citation omitted). Mr. Morgan failed to show how his flu
vaccination could have caused his NMOSD through the
mechanism of molecular mimicry. The most Mr. Morgan
offered on that question was a reference listing various in-
fectious agents that could play a role in triggering NMOSD.
See S. Kim et al., Differential Diagnosis of Neuromyelitis
Optica Spectrum Disorders, 10 Therapeutic Advances in
Neurological Disorders 265, 279 (2017). That list of infec-
tious agents does not, however, include the influenza virus.
Additionally, while Dr. Tornatore testified regarding the
possible relationship between molecular mimicry and
NMOSD, his testimony did not implicate the flu vaccine.
See J.A. 104–07.
Given the lack of evidence supporting a connection be-
tween the flu vaccine and NMOSD, it is clear that Mr. Mor-
gan has not established, by a preponderance of the
evidence, that his flu vaccination was causally connected to
his NMOSD through the medical theory of molecular mim-
icry. Nor has he established by a preponderance of the ev-
idence that there was a logical sequence of cause and effect
showing that his vaccination was the reason for his remit-
ting-relapsing NMOSD.
In sum, as in Broekelschen, 618 F.3d 1339 (Fed. Cir.
2010), the causation inquiry in this case largely turns on
which injury the claimant has suffered. See id. at 1346.
Because Mr. Morgan was found to have suffered from
NMOSD, and because Mr. Morgan has not provided suffi-
cient evidence to support a legally probable connection be-
tween his vaccination and his NMOSD, we hold that the
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MORGAN v. HHS 19

special master’s findings on causation were not arbitrary
or capricious.
We therefore uphold the judgment of the Court of Fed-
eral Claims.
AFFIRMED