Court Opinion

ID: 4670896
Source: CourtListenerOpinion
Date Created: 2021-03-24 15:00:45.539423+00
Date Added: 2024-06-11T08:02:15.581380
License: Public Domain

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        NOTE: This disposition is nonprecedential.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