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

*

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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

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any cross-reactivity via molecular mimicry). See Calise, 2011 WL 1230155, at *12–21 (finding

that petitioner met her burden of proof by providing medical literature and the opinions of a treating

physician which supported her proposed mechanism of causation); but see Davis, 2010 WL

1444056, at *8–9 (finding that petitioner did not carry her burden in the absence of medical

literature and expert opinion to support her proposed theory of causation). Here, by contrast,

Petitioner simply proposes that molecular mimicry between antigens in the vaccine and self-

structures of the CNS caused harm, with less explanation as to how the process occurred.

Day involved a causation theory centered on molecular mimicry, as here, but featured two

different vaccines acting in concert (i.e., the HPV and Flumist vaccines). The presiding special

master decided the claim for petitioner in that case based primarily on record evidence supporting

the potential of components of the HPV vaccine to cause a cross-reaction spurred on by AQP4-

IgG, for which the claimant tested positive. Day, 2015 WL 8028393, at *14. In this case, however,

it is undisputed that Mr. Morgan is seronegative, and he did not receive the HPV vaccine. Day did

not otherwise specifically address the role the flu vaccine by itself might have played in

contributing to the petitioner’s disease course. Day, 2015 WL 8028393, at *14.

The decision most on all fours with the present case is Wei-Ti Chen, which I decided. The

petitioner in that case had a long-standing history of lower back and buttock pain. Wei-Ti Chen,

2019 WL 2121208, at *2. She presented to her chiropractor one week prior to receipt of the flu

vaccine complaining of inner thigh tingling as well as persistent lower back and buttock pain. Id.

Following administration of the flu vaccine, the petitioner developed a demyelinating disease that

resulted in differential diagnoses of ADEM, MS, and NMOSD. Id. at *3–4. Ultimately the medical

record preponderated in favor of an NMOSD diagnosis despite the petitioner’s atypical

presentation—namely her seronegativity. Id. at *20. The petitioner, however, was unable to

present sufficient evidence to credibly support a finding that the flu vaccine could cause NMOSD

through the mechanism of molecular mimicry. Id. at *21–22. 17

II. Petitioner’s Pre-vaccination Symptoms Have Not Been Established to be Associated

With His Neurologic Injury

The parties’ dispute whether Mr. Morgan’s back pain and pre-vaccination urologic

problems reflected the onset of some greater neurologic injury (whether TM, NMOSD, or

otherwise) can be resolved in Petitioner’s favor. The record plainly establishes that Petitioner had

a long-standing medical history of documented degenerative disc disease and an enlarged prostate.

See Ex. 4 at 7; Ex. 5 at 148; Ex. 22 at 9. Some of Petitioner’s post-vaccination treating physicians

repeatedly offered the view that his pre-vaccination symptoms could be attributable to such pre-

existing causes, and it was not unreasonable to consider the possibility that they were related,

especially since some of Petitioner’s pre-vaccination symptoms (like those pertaining to bladder

17

Though similar to the present matter, Wei-Ti Chen is distinguishable in at least one regard—I found the petitioner’s

pre-vaccination symptoms were a part of her overall disease process. Wei-Ti Chen, 2019 WL 2121208, at *23–25.

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