Hock v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 21-945V

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JUSTIN HOCK, * Chief Special Master Corcoran

*

Petitioner, * Dated: July 12, 2024

*

v. *

*

SECRETARY OF HEALTH AND *

HUMAN SERVICES, *

*

Respondent. *

*

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Maximillian J. Muller, Muller Brazil, LLP, Drescher, PA, for Petitioner.

Eleanor Hanson, U.S. Department of Justice, Washington, DC, for Respondent.

RULING ON ENTITLEMENT 1

On February 18, 2021, Justin Hock filed a petition seeking compensation under the

National Vaccine Injury Compensation Program (the “Vaccine Program”). 2 Petitioner alleges

that an influenza (“flu”) vaccine he received on October 8, 2018, caused him to develop myelin

oligodendrocyte glycoprotein antibody-associated disease (“MOGAD”). ECF No. 19. A two-day

Entitlement Hearing was held on December 14-15, 2023. Now, having heard the witnesses at

hearing and reviewed the record, I find Petitioner is entitled to compensation.

1

Under Vaccine Rule 18(b), each party has fourteen (14) 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 Ruling will be available to the public

in its present form. Id.

2

The Vaccine Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660,

100 Stat. 3758, codified as amended at 42 U.S.C. §§ 300aa-10 through 34 (2012) (“Vaccine Act” or “the Act”).

Individual section references hereafter will be to § 300aa of the Act (but will omit that statutory prefix).

I. Factual Background

Pre-Vaccination History

Mr. Hock was born on November 14, 1985. Ex. 2 at 6. Prior to receiving the vaccine at

issue, he had no documented history of neurological disease (although the parties dispute

whether his MOGAD might have predated vaccination). Petitioner was formerly an IV drug user,

and sustained a gunshot wound to his left leg in 2016. Ex. 2 at 10, Ex. 3 at 13 (notes residual

neuropathy from gunshot wound), Ex. 4 at 13–14, Ex. 7 at 11.

On September 18, 2018 (approximately three weeks before receiving the flu vaccine at

issue), Petitioner visited an emergency room with complaints of leg pain, lower back pain, and

neck pain that he reported had begun around 10 days prior. Ex. 4 at 11. He also complained of a

“running sensation” in both thighs. Id. After an examination (but no imaging) yielded normal

results, Petitioner was prescribed muscle relaxers and pain medication and discharged. Id. at 14.

Then, about a week later (September 24, 2024), Mr. Hock saw a provider at Mian Family

Medicine in Rosedale, Maryland, for a sore throat and ear pain. Ex. 3 at 19. He reported that his

neck and back pain had improved since the ER visit. Id. He was diagnosed with an unspecified

upper respiratory infection, and prescribed amoxicillin and a cough suppressant. Id. at 21.

Vaccination and Initial Evidence of Neurologic Symptoms

Petitioner received the flu vaccine during a routine appointment at Mian Family Medicine

on October 8, 2018. Ex. 3 at 18. He did not report any complaints during this visit (and thus did

not reference the seemingly infection-related symptoms he had recently experienced—or his

earlier September issues). Id. at 17. There is no record evidence of any immediate vaccine

reaction, and no symptoms were reported in the period between vaccination and Petitioner’s

temporally-next medical record.

Three weeks later, on October 29, 2018, Petitioner presented to the Franklin Square

emergency room in Baltimore, Maryland, with complaints of constant neck and back pain. Ex. 4

at 65. He did not report numbness or tingling, but had difficulty with motor skills and picking up

objects like his phone. Id. at 74. Petitioner also at this time noted some urination difficulties, and

that he had not urinated since the day before. Id. at 65, 76.

A neurological exam and head CT were normal. Ex. 4 at 75–76. An MRI showed a disc

protrusion at C4-5, and disc bulges at L3-4 and L5-5. Id. There were no other significant spinal

abnormalities (including lesions) identified, but the MRI lumbar imaging revealed that

Petitioner’s bladder was distended to the middle of the lowest lumbar vertebrae. Id. Lab work

showed elevated levels of white blood cells, and mildly elevated C-reactive protein (an

2

inflammation biomarker). Id. at 76–77. Given all of the above, treater impressions centered on

neck pain as the primary concern, and Petitioner was treated with steroids, discharged, and told

to follow up with a neurologist. Id.

The next day, Petitioner saw his primary care provider, Dr. Jamshid Mian. Ex. 3 at 13. Dr.

Mian discussed Petitioner’s ER visit the day prior, and Petitioner now reported that he had

bladder sensitivity, sinus pressure, and postnasal drip. Id. Petitioner was diagnosed with acute

sinusitis, inflammatory spondylopathy, cervical arthritis, white blood cell disorder, and bladder

disorder. Id. at 13–14. He was prescribed Naproxen. Id.

Petitioner thereafter saw a urologist, Dr. Kannan Manickam, on November 1, 2018. Ex.

10 at 13. He specifically complained of “urine problems” (difficulty urinating). Id. His post-void

urine residuals measured 228 ml—an abnormal finding. 3 Id. at 15. Dr. Manickam concluded that

Petitioner’s urinary issues were most likely neurologic in nature. Id. Several days later, on

November 5, 2018, Petitioner saw neurologist Dr. Ali Kooshkabadi, with complaints of hand

weakness and neck pain that he now reported (as the face of this record indicates) had begun “six

months earlier,” but had dramatically worsened in the more recent months. Ex. 11 at 7. A

neurological exam was normal, however, and Petitioner made no mention of the bladder issues

that he had been reporting to other treaters. Id. at 8. Dr. Kooshkabadi diagnosed Petitioner with

cervical spondylosis, left arm weakness, and cervical spine stenosis, and prescribed physical

therapy and anti-inflammatories. Id.

Petitioner saw Dr. Manickam again on November 7, 2018, for an urgent visit, as he was

still unable to urinate. Ex. 10 at 10. On repeat testing, his post-void urine residuals measured

more than 1000 ml. Id. He was prescribed self-catheterization two to three times daily. Id. at 12.

Later that day, Petitioner presented to the MedStar Harbor Hospital ER for his ongoing issues

(neck and back pain plus inability to urinate). Ex. 5 at 12–13. The treating physician, Dr. Neil

Majmundar, noted that a neurological exam was unremarkable, and did not order imaging. Id. at

16–17. Petitioner’s urine tested positive for “rare bacteria, but no other signs of infection.” Id. at

18. Dr. Majmundar attributed Petitioner’s urinary issues to hygiene, but told him to follow up

with a neurologist and PCP. Id.

Hospitalization

Petitioner was hospitalized at Johns Hopkins Hospital in Baltimore, Maryland from

November 9-14, 2018, after going to the ER again on November 9th. Ex. 6 at 8. He reported to

3

A post-void residual volume over 200 mL indicates inadequate emptying. A volume over 300 mL is suggests

urinary retention, and a volume over 400 mL confirms urinary retention. L. Ballstaedt et al., Bladder Post Void

Residual Volume, NCBI Bookshelf at

https://www.ncbi.nlm.nih.gov/books/NBK539839/#:~:text=Less%20than%20100%20mL%20PVR,is%20suggestive

%20of%20urinary%20retention. (last accessed June 24, 2024).

3

initial emergency treaters the same symptoms of neck and back pain and urinary retention, but

also a new symptom of progressive numbness. Id. at 11. Preliminary exams showed sensation

“intact, but diminished distal to the T4 level,” but normal gait and motor strength. Id. at 12–13.

Further neurological exams by neurologist Dr. Carlos Pardo-Villamizar showed hyperreflexia,

sensory loss around T10/11, and pain with eye movement. Ex. 6 at 26.

An MRI performed on November 10, 2018, revealed “multiple small foci of faint

enhancement in the bilateral frontal and temporal lobes, and T2/FLAIR hyper-intensity in the

frontal lobe without cranial nerve enhancement.” Ex. 6 at 29. Lab work showed elevated proteins

in the cerebrospinal fluid, and an elevated white blood cell count. Id. at 18, 49, 53. A

neurosurgeon evaluating these results deemed the imaging to be concerning for a neuro-

inflammatory or infectious process. Id. at 27–30. Dr. Pardo characterized the imaging as “highly

suspicious for a demyelinating myelopathy,’ and considered neuromyelitis optica (“NMO”),

MOGAD, and rheumatic myelopathies as possible diagnostic explanations, to be explored

through further testing. Id. at 21. Petitioner was started on a three-day course of

methylprednisolone. Id.

Petitioner was later examined by a neurology fellow on November 12th and 13th. Ex. 6 at

32. He still reported eye tenderness, neck pain, and urinary retention, but added that his

numbness had improved. Id. at 32–33. An exam showed decreased fine touch and pin prick

sensation on his left leg up to the T12 level. Id. at 35. He continued to receive

methylprednisolone. Id. The next day, Petitioner was able to urinate on his own and have a bowel

movement, and no longer was experiencing numbness. Id. at 39.

Mr. Hock was subsequently discharged, but without a final diagnosis. Ex. 6 at 48–49. Lab

work for NMO and MOG antibodies was still pending at this time. Id. However, an optical

coherence tomography (“OCT”) test 4 performed while Petitioner was hospitalized showed

chronic injury to both optic nerves—supportive of the existence of a demyelinating process that

might have been present for some time. Id. at 49. Petitioner was referred to outpatient neurology

and prescribed a slow prednisone taper. Id.

December 2018 Testing and Treater Opinions on Nature of Presentation

Petitioner’s first post-discharge treater visit occurred on December 5, 2018, when he saw

Dr. Pardo and a neuroimmunology fellow at the Johns Hopkins Outpatient Transverse Myelitis

Center (“Johns Hopkins OTMC”). Ex. 6 at 287–88. Petitioner’s lab work taken during the

hospitalization had resulted in a positive MOG antibody test, with high titers at 1:1000, while

4

An OCT is a non-invasive imaging test that uses light waves to take cross-section pictures of the retina. This

allows ophthalmologists to measure the thickness of the retina, helping to diagnose illnesses like glaucoma and other

retinal diseases. What is Optical Coherence Tomography?, American Academy of Ophthalmology, at

https://www.aao.org/eye-health/treatments/what-is-optical-coherence-tomography (last accessed June 24, 2024).

4

Petitioner tested negative for NMO antibodies. Id. Dr. Pardo also reviewed his OCT results from

the November hospitalization, which (as noted above) “suggested there was already some

established damage to both optic nerves” at the time of this testing. Id. at 292 (emphasis added).

Petitioner reported that he was still unable to urinate, and had to self-catheterize five to eight

times a day. Id. at 288.

Based upon the clinical exam, symptoms, as well as recent test results, Dr. Pardo

characterized Mr. Hock’s overall presentation as consistent with a “MOG-related

neuroinflammatory disorder.” Ex. 6 at 287. However, although Dr. Pardo identified onset as

having occurred in mid-October 2018 (manifesting “with inflammation of the spinal cord, nerve

roots, meninges (patchy) and probably optic nerve”) his comment about the results of the OCT

testing suggested a relapsing disease course, which could have begun prior to Petitioner’s initial

complaints. Id. at 292 (“anti-MOG antibodies can be associated with either monophasic or

relapsing disease”). Mr. Hock was prescribed another course of prednisone, and told to come

back for a repeat MRI, OCT, and anti-MOG testing in six weeks, so that it could be determined if

the disease course had subsided (since “there is some evidence that patients who revert to a

negative antibody after an attack are less likely to experience a relapsing disease course”). Id.

The notes from Petitioner’s December 5th visit (prepared principally by Olwen Cait

Murphy, MBChB)5 also memorialize the fact that Petitioner’s case was subsequently discussed

during a neuroimmunology case conference at Johns Hopkins on December 6, 2018. Ex. 6 at

292. Treaters who at this time collectively evaluated Mr. Hock’s overall history since October

“felt that the OCT supports prior inflammation, suggesting that disease may already be

considered relapsing rather than monophasic.” Id. (emphasis added).

Petitioner visited the Johns Hopkins OTMC on December 30, 2018, for a follow-up OCT.

Ex. 6 at 302–03. This second OCT revealed that the “mean peripapillary retinal nerve fiber layer

thickness was normal for each eye,” but “the retinal nerve fiber superior quadrant on the left,”

“average macular thickness on the right,” and both GCIP (ganglion cell inner plexiform layers)

were thinned. Id. The ophthalmologist who performed the OCT testing noted that its results

established “the presence of bilateral optic neuropathies,” and recommended yearly exams. Id.

No comment was made as to how long the damage might have existed, however.

Subsequent Treatment

Despite his somewhat acute post-vaccination presentation and the concerning nature of

his symptoms, Petitioner’s treatment diminished from the start of 2019 thereafter. For example,

5

The MBChB is the equivalent of an MD for countries that adhere to the UK’s higher education system. NEIL M.

DAVIS, MEDICAL ABBREVIATIONS (16th ed. 2020)

5

Mr. Hock saw his PCP on January 28, 2019. Ex. 3 at 7. He reported feeling better, but had

coughing and post-nasal drip. Id. He also reported that a neurologist had told him not to get the

flu vaccine in the future, asking that this be noted on his chart. Id. 6 He saw the same PCP again

on February 25, 2019, but reported no concerns besides asking for a Cialis prescription. Id.

Petitioner underwent MRI imaging again on February 26, 2019. Ex. 9 at 8. Treater notes

in connection with this event stated the existence of “prior episodes of upper and lower extremity

weakness with incontinence. Effects from flu shot.” Id. The brain MRI showed signal

abnormalities in the periventricular and deep white matter of the right parietotemporal area, in

the periventricular white matter of the left periarterial region, and also a tiny signal abnormality

in the deep white matter of the left frontal region. Id. His spinal imaging was unremarkable. Id.

at 9–11. Treaters noted that this might be evidence of CSF suppression, or sequalae of a prior

demyelination or infection, although no active demyelination was observed. Id. at 8.

Petitioner visited the Johns Hopkins OTMC again on March 13, 2019. Ex. 7 at 96. He

reported that he still self-catheterized several times a day, but could sometimes urinate with a

“strange sensation.” Id. at 101. He had no more neck or back pain, but had issues ejaculating. Id.

at 97. He also reported some peripheral vision blurring when looking from left to right. Id. The

neurologist recommended continued monitoring and follow-up MOG testing. Id. at 101.

Petitioner’s most recent records, based on the materials filed in this case, are from a visit

with Dr. Pardo on September 18, 2019. Ex. 7 at 120. He was now stable in terms of symptoms,

but his urinary issues remained. Id. Dr. Pardo recommended repeat MRI and MOG antibody

tests, as well as a test for Sjogren’s antibodies. Id. He also recommended placement of a bladder

stimulation device if Petitioner remained stable. Id. This appears to be the last time Petitioner

received neurologic-specific treatment, and no records from any subsequent temporal period

have been filed.

II. Hearing Witnesses

A. Petitioner’s Witnesses and Experts

1. Justin Hock - Mr. Hock (the sole fact witness) testified that, a few weeks

prior to receiving the vaccine at issue, he had visited the Franklin Square Medical Center

Emergency Room with complaints of back and neck pain, with a running sensation in the thighs.

Tr. at 8. This pain had lasted for around ten days, and intensified when he was sitting or laying

down. Id. at 9. He was prescribed ibuprofen and Flexeril, and the pain subsided shortly after. Id.

at 10. He attributed the pain to long periods of sitting while driving for work, and possibly from

keeping his wallet in his back pocket while sitting. Id. at 9. He noted that he had thereafter

6

I have not been able to identify a record in which this recommendation was made to Petitioner.

6

stopped sitting on his wallet after the ER visit, and speculated that this may have contributed to

his symptoms resolving. Id. at 10. Mr. Hock also saw a primary care physician for a sore throat

and ear pain on September 24, 2018, and was prescribed antibiotics, but remembered nothing

else about this incident. Id. at 10–11.

On October 8, 2018, Mr. Hock visited the same PCP and received the flu vaccine. Tr. at

11. He testified that he did not typically get flu shots, but was “trying to be responsible” after the

birth of his daughter. Id. at 11–12. Toward the end of October, he went to the Franklin Square

Medical Center ER. Id. at 12. He was in “excruciating pain” around his head, neck, and

shoulders. Id. He had been experiencing great difficulty urinating for two days, and had

deteriorating motor skills, with difficulty grabbing objects and picking them up. Id. at 13. At the

ER, he had MRI and CAT scans performed. Id. He was sent home with Motrin (or a similar pain

medication) and steroids. Id.

Thereafter, however, Petitioner continued having “extreme urinary retention,” and visited

a urologist twice during November 2018. Tr. at 14–15. A sonogram showed an extremely full

bladder, and he could not urinate to complete a stream test the doctor requested. Id. at 15. He was

prescribed self-catheterization. Id.

During the same time period, Mr. Hock experienced “excruciating” pain in his neck, pain

in his legs, and continuing loss of motor function in his hands. Tr. at 16. He saw a neurologist

with a referral from his prior hospitalization. Id. Treaters continued prescribing him steroids, but

his symptoms did not improve. Id. at 17. He tried going to a different emergency room where a

relative worked, hoping to get more attentive treatment. Id. at 18. This facility also prescribed

him steroids. Id. at 18. Two days after this visit, he was admitted at Johns Hopkins. Id. at 18.

Treaters ran various tests, such as scans and a spinal tap. Id. at 19. At this point, his peripheral

vision was compromised, and he had very poor balance. Id. at 20.

Mr. Hock expressed some recollection of treaters discussing the neurological root of his

symptoms during his hospitalization. Tr. at 21. He recalls they told him “the sheathing on my

brain stem and my spine was deteriorated,” and cited a possible “infection” as the cause. Id.

They also said his condition was “similar to MS [multiple sclerosis] and that [he] would be

continuously treated as an MS patient.” Id. He was given an IV of high-dose steroids, which

allowed him to make a bowel movement (which he had trouble doing previously, along with

urinating). Id. Some numbness in his feet subsided, but his poor balance and neck pain did not.

Id. at 21–22. He was eventually discharged, and instructed to continue self-catheterization and

follow up with a neurologist at Johns Hopkins. Id. at 22.

After discharge, Petitioner followed up at the Johns Hopkins Transverse Myelitis Center

on December 5, 2018, seeing the same neurologist he saw during his hospitalization. Tr. at 22.

7

At this point, he still had pain, but was experiencing improvement in using the restroom. Id. at

23. He received a formal diagnosis of MOGAD at this visit, and the neurologist said that he

could not rule out the flu vaccine as the cause of his symptoms. Id. at 24–25. He recommended

that Mr. Hock not receive the vaccine again, but that there was no issue with his children

receiving it. Id. at 25. He also advised Mr. Hock to have his eyes monitored regularly, since it

was possible his vision could continue to deteriorate. Id.

Petitioner had follow-up visits with his PCP, the Transverse Myelitis Center, and the

Wilmer Eye Institute over the coming months. Tr. at 26–27. He believes he was tapered off from

steroids during this time, but was not given a comprehensive treatment plan, and was instructed

instead to follow up if symptoms flared. Id. at 27. By September 2019, Petitioner’s neck pain

was gone, although he still had erectile dysfunction, and usually had to self-catheterize to

urinate. Id. at 27–28. He felt as if his body was “adapting” with different muscles, improving his

motor skills and allowing him to urinate normally at times. Id. He had returned to work by that

point, after being out for an unspecified amount of time previously. Id. at 29.

By the time of the hearing, Mr. Hock testified, he no longer needed to self-catheterize,

but still finds urination difficult, and requires medication to treat erectile dysfunction. Tr. at 30,

32. He otherwise does not feel significant lower extremity weakness beyond his legs

occasionally feeling numb, which he proposed may be from sitting too long. Id. He characterized

himself as healthy, and stated that he did not take any medications. Id.

2. Syed Rizvi, M.D. - Dr. Syed Rizvi prepared two reports in this case. Rizvi

First Report, dated April 13, 2022, filed as Ex. 12 (ECF No. 20); Rizvi Second Report, dated

December 15, 2022, filed as Ex. 68 (ECF No. 26). He also testified at the hearing.

Dr. Rizvi is a neuro-immunologist in practice at Brown Neurology, and a Professor of

Clinical Neurology at Alpert School of Medicine at Brown University. Rizvi CV, dated April 13,

2022, filed as Ex. 13 (ECF No. 20-3). He routinely cares for patients with a wide variety of

autoimmune conditions, including but not limited to MS and related disorders such as MOGAD

and NMO. Rizvi First Report at 1. He is board-certified by the American Board of Psychiatry

and Neurology to practice neurology. Id. He received his MD from Dow Medical College in

Karachi, Pakistan, and completed his residency at Stony Brook University Hospital. Rizvi CV at

1. He received post-graduate training in MS and clinical neuro-immunology, and has practiced in

that field since 2000. Rizvi First Report at 1. He teaches medical students, residents, and fellows

about the diagnosis and management of MS and related disorders, and has authored over 20

journal articles in his field. Id.

Dr. Rizvi began his testimony discussing his professional background and experience

seeing MOGAD patients. Tr. at 41–46. He explained that he sees primarily MS patients, with

only about “10 percent” of his patients have related disorders like MOGAD and NMO. Id. at 43.

8

He deemed MOGAD a newer diagnosis, although “[e]very year you see a lot more” MOGAD

patients in practice. Id. at 45. Testing for the disorder did not become commercial until 2017. Id.

at 49. Some patients he treated for MS previously were later diagnosed as having MOGAD after

new testing became available. Id.

Dr. Rizvi then briefly explained the nature of MOGAD. Tr. at 49–50. MOG protein

makes up a small percentage of the myelin sheath and is found on oligodendrocytes (cells

responsible for the creation of myelin in the central nervous system). Id. at 50. When

autoantibodies mistakenly attack the MOG protein, demyelination occurs, leading to the clinical

symptoms of disorders associated with MOGAD. Id. As Dr. Rizvi explained, a “spectrum of

diseases…fall into the MOGAD category,” including optic neuritis, ADEM, and transverse

myelitis (“TM”). Id. at 49. MOGAD patients have a “variety of presentations,” including

seizures and meningitis. Id. at 52. MOGAD is diagnosed with a combination of imaging and

testing - optic neuritis and transverse myelitis may appear on scans, and a MOG titer test

confirms the diagnosis. Id. at 53. Patients are typically treated with steroids, but may also require

IVIG and immunosuppressant drugs if they have relapsing symptoms. Id. at 55.

Dr. Rizvi then testified about a number of the studies cited in his reports. These articles

came to varying conclusions he deemed applicable to Petitioner’s case, either reflecting a similar

timeframe to Petitioner’s symptom onset, or establishing an association between demyelinating

conditions and the flu vaccine more generally (albeit not specifically in connection with

MOGAD itself). Tr. at 59-64; J. Roszkiewicz & Y. Shoenfeld, Vaccines and Optic Neuritis:

Consequence or Coincidence?, 17 Immunome Research 1, 4 (2021) (15-30 days as the most

common time of onset between vaccination and optic neuritis), filed on Nov. 11, 2022, as Ex. 61

(ECF No. 23-25); D. Karussis & P. Petrou, The Spectrum of Post-Vaccination Inflammatory CNS

Demyelinating Syndromes, 13 Autoimmunity Reviews 215, 216 (2014) (mean of 14.2 days

between vaccination and CNS demyelination), filed on Nov. 11, 2022, as Ex. 59 (ECF No. 23-

23) (“Karussis”). He also discussed a few case reports in which authors associated different

demyelinating illnesses with vaccines. Id. at 65, 73–76; C. Alicino et al., Acute Disseminated

Encephalomyelitis with Severe Neurological Outcomes Following Virosomal Seasonal Influenza

Vaccine, 10 Human Vaccines & Immunotherapeutics 1969 (case study of patient with ADEM

after flu vaccine), filed on December 15, 2022, as Ex. 72 (ECF No. 26-6); W. Huynh et al., Post-

Vaccination Encephalomyelitis: Literature Review and Illustrative Case, 15 Journal of Clinical

Neuroscience 1315, 1321 (2008) (case study of patient with optic neuritis and encephalomyelitis,

attributed by authors to flu vaccine), filed on April 13, 2022, as Ex. 17 (ECF No. 20-7).

Many of these studies proposed that molecular mimicry constituted a likely mechanistic

process for autoimmune disease pathology. Tr. at 63–64, 70–72; N. Kumar et al.,

Postvaccination Anti-Myelin Oligodendrocyte Glycoprotein Neuromyelitis Optica Spectrum

Disorder: A Case Report and Literature Review of Postvaccination Demyelination, 22

9

International Journal of MS Care 85, 88 (2020) (discussing molecular mimicry as a mechanism

for autoimmune demyelination), filed on April 13, 2022, as Ex. 23 (ECF No. 20-13). Dr. Rizvi

briefly explained molecular mimicry as a theory, admitting that it is “tough to prove

experimentally.” Id. at 66.

Based on his review of Petitioner’s records, Dr. Rizvi opined that Petitioner had

developed MOGAD as a result of receiving the flu vaccine. He first endeavored to distinguish

evidence of a possible pre-vaccination onset for Petitioner’s symptoms. Petitioner’s reports of

back and neck pain around September 2018, for example, were deemed by Dr. Rizvi to be

musculoskeletal rather than “something more central”—perhaps attributable to a pinched nerve.

Id. at 77. By contrast, he felt that Petitioner first displayed MOGAD symptoms around his ER

visit on October 29, 2018. Id at 81. At that point, Petitioner had headaches (along with the

preexisting neck pain), was having trouble picking up objects, and could not urinate. Id.

This, Dr. Rizvi stated, was “a sign of something going on neurologically.” Tr. at 82. He

acknowledged that Petitioner’s MRI was normal at this time, with no signs of lesions. Id. at 83.

However, Dr. Rizvi deemed this to undercut the conclusion that Petitioner’s condition predated

vaccination. Had Petitioner been at that point in a MOGAD progression that had begun in

September, lesions would not have resolved by October, and thus would definitely have

appeared in this scan. Id. at 84.

Petitioner’s November 2018 hospitalization and the findings made at this time were

further support for MOGAD beginning after vaccination. Tr. at 86. By this time, Petitioner had

significant neurological symptoms, including urinary retention, gait problems, and sensory

abnormalities. Id. Most significantly, an MRI performed in mid-November now showed the

existence of enhancing lesions—a clear indicator of demyelination. Id. at 88. By this time,

Petitioner was reasonably suspected by treaters to have “a myelitis,” and medical professionals

were trying to determine why, through testing such as a spinal tap. Id. at 88. Confirmation was

received by MOG antibody test results from early December. Id. at 89. Petitioner’s ongoing

bladder issues were also typical of a MOGAD disease course. Id. at 91.

Dr. Rizvi rejected the possibility of other explanations for Petitioner’s MOGAD. He

acknowledged that the medical record allowed for the possibility that Mr. Hock had experienced

respiratory symptoms in September 2018, immediately before vaccination, and therefore a post-

infectious autoimmune reaction could not be ruled out. Tr. at 106. But Dr. Rizvi emphasized the

fact that the yellow mucus and treatment with antibiotics for that infection suggested that it was

likely bacterial, rather than viral, and thus would (in his view) have been less likely to cause an

autoimmune reaction. Id. at 107. 7

7

Dr. Rizvi also, however, cited literature involving Guillain-Barré syndrome, a peripheral neuropathy thought to be

autoimmune in mechanistic pathology—but known to have bacterial and viral triggers (reducing the value of his

distinguishing between the two in this context). See, e.g., Harris v. Sec'y of Health & Hum. Servs., No. 18-944V,

10

Dr. Rizvi then discussed the timing of Petitioner’s disease onset. Tr. at 93. He specifically

opined that Petitioner’s MOGAD likely first manifested around October 27th, two days before he

visited an ER, and within three weeks of vaccination. Id. He deemed that timeframe medically

acceptable, noting that a typical onset for demyelinating disorders following vaccines is thought

to be 3-42 days, although he derived this timeframe from articles specific to a distinguishable

peripheral neuropathy, Guillain-Barré syndrome (“GBS”). Id. at 93-94; L. Schonberger et al.,

Guillain-Barré Syndrome Following Vaccination in the National Influenza Immunization

Program, United States, 1976-1977, 110 American Journal of Epidemiology 105 (1979), filed on

November 18, 2022, as Ex. 66 (ECF No. 23-30). But other studies involving central nervous

system demyelinating conditions also supported a 19-day onset. Tr. at 94–96; A. Langer-Gould

et al., Vaccines and the Risk of Multiple Sclerosis and Other Central Nervous System

Demyelinating Diseases, 71 JAMA Neurology 1506, 1510 (2014) (timeline of up to 30 days for

the first symptoms of CNS demyelinating disorders after vaccination), filed on Nov. 11, 2022, as

Ex. 64 (ECF No. 23-28) (“Langer-Gould”); A. Rowhani-Rabar et al., Biologically Plausible and

Evidence-Based Risk Intervals in Immunization Safety Research, 31 Vaccine 271, 273 (2012)

(mean onset of 17 days between vaccination and ADEM), filed on Nov. 11, 2022, as Ex. 67

(ECF No. 23-31) (“Rowhani-Rabar”). 8

At the same time, however, Dr. Rizvi admitted that physicians at Johns Hopkins (taking

into account evidence of chronic optic nerve damage) had classified Petitioner’s illness course as

possibly relapsing, rather than monophasic—thereby allowing for the possibility that Petitioner’s

MOGAD predated vaccination. Tr. at 89, 112. Indeed, Dr. Rizvi admitted that Petitioner had

complained of peripheral vision difficulties during his hospitalization, adding that there was no

way to tell if the optic nerve damage was in fact pre-existing. Id. at 90.

On a brief rebuttal, Dr. Rizvi reiterated his prior opinion that Petitioner’s September 2018

back and neck pain complaints were distinguishable from his post-vaccine complaints. Tr. at

338. Petitioner had complained of tenderness in his back and neck at these visits, but displayed

full range of movement. Id. at 339. Dr. Rizvi deemed this to indicate a musculoskeletal problem

rather than a neurological one, which would be characterized by weakness, numbness, and reflex

changes. Id. This difference, coupled with the lack of lesions on his October 2018 MRIs,

suggested that Petitioner had not been experiencing MOGAD prior to vaccination. Id. at 340. A

course that relapsed and healed so rapidly within a short period of time would be “very, very

unusual.” Id. at 341.

Dr. Rizvi also deemed it unlikely that medication Petitioner received in September for his

neck and back pain would have masked ongoing neurologic symptoms. Tr. at 341. Otherwise,

2023 WL 2583393, at *22 (Fed. Cl. Spec. Mstr. Feb. 21, 2023) (“GBS is well accepted as an autoimmune condition

with a wide variety of suspected antigenic triggers, inclusive of antigens from both infection and vaccination…”).

8

Petitioner’s counsel inadvertently quoted the wrong sentence from this study during the hearing, citing the mean

time between natural infection and ADEM (range of 6.2-17.8 days) rather than with regard to vaccination (mean

time 17 days, with a range of 9-30).

11

Dr. Rizvi proposed the timeframe from Petitioner’s late-October onset to nadir in November was

consistent with what was known about MOGAD. Tr. at 348, 350; S. Jarius et al., MOG-IgG in

NMO and Related Disorders: A Multicenter Study of 50 Patients. Part 2: Epidemiology, Clinical

Presentation, Radiological and Laboratory Features, Treatment Responses, and Long-Term

Outcome, 13 Journal of Neuroinflammation 280 (2016), filed on April 13, 2022, as Ex. 25 (ECF

No. 20-15) (“Jarius”).

Dr. Rizvi acknowledged that Petitioner’s OCT scans from November-December 2018

showed prior optic nerve damage. Tr. at 354. He agreed that some literature placed the minimum

timeframe for this damage to occur at three months, which would imply that Petitioner’s onset

was earlier than October. Id. And he admitted that other post-vaccination records could indicate

a relapsing course. Id. at 358–64.

3. S. Michael Phillips, M.D. - Dr. Phillips prepared one expert report in this

case, and testified at the hearing. Report, filed November 18, 2022, as Ex. 31 (ECF No. 23).

Dr. Phillips is a Professor of Medicine in the Pulmonary, Allergy, Critical Care Division

of The University of Pennsylvania School of Medicine and a Lead Clinical Physician at the

University of Pennsylvania, Department of Medicine. Phillips CV, filed on Nov. 18, 2022, as Ex.

32 (ECF No. 23-2). He received his medical degree from the University of Wisconsin, and

completed his residency at the University of Pennsylvania. Phillips CV at 1. He is Director of

Allergy and Immunology Services at the University of Pennsylvania and a Consultant in

Medicine and Immunology to the Philadelphia Veterans Administration Hospital. Id. at 1-2. He

is Board Certified in Allergy and Immunology and Internal Medicine. Id. at 2. He is also a

Professor of Neurology in the Neurology Department of the University of Pennsylvania. Id. He

has over 30 years of clinical and scientific experience in the field of internal medicine, allergy

medicine, immunology, and epidemiology. Phillips Report at 2. During his career, he has treated

over 200 cases of GBS and CIDP, as well as over 20 patients with confirmed or suspected

MOGAD. Id. at 3. 9

Dr. Phillips explained at the beginning of his testimony that he had in the past regularly

acted as an expert for Respondent for several years—making this the first instance in which he

offered an opinion for a Program claimant. Tr. at 130. He explained, however, that he felt

comfortable with the change, noting that his views about vaccine injury theories had evolved

with “increasing scientific sophistication”—“I’ve becoming increasingly convinced that through

a number of mechanisms, the vaccines can cause some of these problems.” Id. at 133. In

9

Cross examination identified several issues with Dr. Phillips’s cited credentials as set forth in his previously-filed

2019 CV. Tr. at 168. For example, he is no longer an emeritus professor at the University of Pennsylvania School of

Medicine, and has scaled back his teaching duties to clinicals twice a week. Id. at 169-170. He presently only sees

patients “in a teaching context with interns and residents and fellows.” Id. at 170. And he is no longer a professor of

neurology, going so far to clarify that he does not hold himself out as a “neurology specialist.” Id. at 173. He was

also unaware that his Pennsylvania medical license expired in 2022. Id. at 170. Counsel requested permission during

the hearing to file an updated CV, but did not do so. Id. at 207.

12

addition, Petitioner’s case had “unique” aspects, leading him to “support the causal relationship,”

and they dovetailed with “advances in understanding of molecular mimicry, a newer diagnosis

with limited research available, and timing that matched with established ‘autoimmune models

of demyelination.” Id. at 133–35.

Because of his prior work as an expert for Respondent, Dr. Phillips was cross-examined

closely on opinions he had offered in the past that seemed to contradict his testimony in this case.

Indeed, in past cases Dr. Phillips had harshly criticized molecular mimicry theories. Tr. at 194–

96; see Kelly v. Sec'y of Health & Hum. Servs., No. 16-878V, 2021 WL 5276373, at *14 (Fed.

Cl. Spec. Mstr. Oct. 18, 2021). One of these cases involved MS, a disease Dr. Phillips compared

to MOGAD several times during his testimony. Tr. at 199; Townsend v. Sec'y of Health & Hum.

Servs., No. 14-266V, 2023 WL 6212496 (Fed. Cl. Spec. Mstr. Aug. 29, 2023), mot. for review

den’d, 170 Fed. Cl. 130 (2024). In fact, the Townsend Special Master had described him as the

expert most critical of molecular mimicry theories. Tr. at 201; Townsend, 2023 WL 6212496 at

n.32. It was also noted that Dr. Phillips had cited some of the same literature herein in cases

where he criticized molecular mimicry theories as scientifically unreliable. Tr. at 200; see B.

Trost et al., No Human Protein is Exempt From Bacterial Motifs, Not Even One, 1 Self/Nonself

328 (2010), filed on Nov. 30, 2022, as Ex. 54 (ECF No. 25-6); B. Trost et al., Bacterial Peptides

are Intensively Present Throughout the Human Proteome, 1 Self/Nonself 71 (2010), filed on

November 30, 2022, as Ex. 55 (ECF No. 25-7) (“Trost 2”); M. Sospedra & R. Martin, Molecular

Mimicry in Multiple Sclerosis, 39 Autoimmunity 3 (2006), filed on Nov. 30, 2022, as Ex. 51

(ECF No. 25-5).

The initial part of Dr. Phillips’s testimony involved an explanation of molecular mimicry

as a pathologic mechanism for autoimmune disease. Tr. at 137–39. He also explained the

demyelination process, and how myelin loss interrupts electrical transmission in nerves,

producing neurological symptoms such as paralysis, weakness, and loss of motor skills. Id. at

146. However, Dr. Phillips emphasized that molecular mimicry was only the first step in a

complex autoimmune disease process that was also reliant upon an imbalance of T-regulatory

and T-effector cells. Id. at 143. This creates a destructive autoimmune reaction, where cytotoxic

chemicals damage the myelin sheath. Id. at 149. And Dr. Phillips briefly touched on bystander

activation as an alternative mechanistic explanation leading to autoimmune cross-attack, but

deemed bystander immune cells “only really important as they interfere with the regulatory

pathways which are dependent ultimately on the presence of molecular mimicry.” Id. at 155.

MOGAD, Dr. Phillips emphasized, overlaps with optic neuritis, ADEM, and TM, as all

are central nervous system inflammatory conditions characterized by damaging demyelination.

Tr. at 155. Like Dr. Rizvi, however, Dr. Phillips deemed MOGAD a newer diagnosis, noting that

many cases previously diagnosed as other demyelinating illnesses, like TM, could have actually

been MOGAD. Id. at 157. Thus, studies on the connection between vaccines and these illnesses

13

cited by Dr. Rizvi were relevant to the case at hand, since MOGAD as a diagnostic classification

is still too new to be the basis of large epidemiological studies. Id. at 155–156; see also L.

Mumoli et al., ADEM Anti-MOG Antibody-Positive After SARS-CoV2 Vaccination, 43

Neurological Sciences 763 (2022), filed on April 13, 2022, as Ex. 22 (ECF No. 20-12).

Dr. Phillips then discussed Petitioner’s clinical course. Tr. at 159. He disputed the

possibility that Petitioner’s September, pre-vaccination back pain could have been an initial

presentation of MOGAD, opining that it was more likely due to his disc disease and strenuous

physical activity. Id. At the same time, several treaters had mentioned the flu vaccine in their

notes as possibly causal, with Dr. Phillips stating that “[t]he doctors who are most able to

interpret what’s going on with a patient generally are the doctors who are taking care of that

patient at that point in time.” Id. at 162.

Dr. Phillips further embraced the onset timeframe of Petitioner’s MOGAD as medically

acceptable. Petitioner’s initial symptoms of clumsiness and neck pain were the “first obvious

neurological symptoms,” although the disease process could have started a few days before (but

nevertheless still after vaccination). A 19-day, post-vaccination onset timeframe was, in his

opinion, “perfect” for vaccine-induced MOGAD, as supported by studies cited in both expert

reports. See Karussis at 216 (mean of 14.2 days between vaccination and CNS demyelination);

Rowhani-Rabar at 273 (17-day mean onset for ADEM after vaccination). Dr. Phillips denied that

Petitioner’s upper respiratory infection during that time period could have triggered his

MOGAD. Id. at 161. In his view, it was “very unlikely” that Petitioner would have had an MRI

scan (like the one he had during his initial hospitalization) without signs of demyelination, had

the disease onset already begun prior to vaccination. Id. at 160.

Dr. Phillips was then asked about several studies that seemed to potentially contradict his

conclusions. Trost 2, for example, concluded that the high amount of homologies between

human and viral and bacterial peptides made it difficult to support molecular mimicry as a theory

in autoimmunity, given how common it was (but without leading to disease). Tr. at 178; Trost 2

at 73. Dr. Phillips contended, however, that Trost 2 (authored in 2010) was outdated, and that he

no longer accepted its conclusions about molecular mimicry. Id. He was also asked about a study

finding that there was no statistically significant relationship between vaccination and MS, a

demyelinating disease Dr. Phillips compared to MOGAD several times in his testimony. Id. at

185; Langer-Gould at 1509 (“In this nested case-control study, we found no long-term

association between vaccines and MS or other CNS [diseases].”).

Respondent’s cross-examination of Dr. Phillips further delved into certain record

evidence—in particular, the November treatment record from Dr. Kooshkabadi (Ex. 11 at 7)—

and whether it suggested that Petitioner’s MOGAD-related symptoms actually began well before

vaccination. Tr. at 190, 211. Dr. Phillips did not gainsay what the record indicated Petitioner had

14

told Dr. Kooshkabadi, but allowed only that it was “theoretically possible,” not likely, that

Petitioner had experienced a relapsing form of MOGAD that began pre-vaccination. Id. at 212.

In so doing, he emphasized again that molecular mimicry was just the beginning of the

autoimmune process, with an imbalance of T-cells thereafter “ultimately responsible for the

problem.” Id. at 217. (This contention would, however, only explain why Petitioner’s course

might have been erratic or relapsing after vaccination—and not whether it could have been based

on a pre-vaccination onset).

B. Respondent’s Experts

1. Brian Callaghan, M.D. - Dr. Callaghan authored one report in this case,

and testified at the hearing. Callaghan Report, filed on July 29, 2022, as Ex. A (ECF No. 21-1)

(“Callaghan Rep.”).

Dr. Callaghan is an Associate Professor of Neurology at the University of Michigan.

Callaghan CV, filed on July 29, 2022, as Ex. C (ECF No. 21-7). He received his medical degree

from the University of Pennsylvania, and completed his neurology residency there as well.

Callaghan CV at 1. He is American Board of Psychiatry and Neurology (ABPN) and American

Board of Electrodiagnostic Medicine (ABEM) certified. Id. He has published more than 120

articles on neurologic diseases. Id. at 14–24. In his clinical practice, he has encountered and

treated at least 50 patients with CNS demyelinating disorders. He has testified in four vaccine

injury compensation program hearings to date. Callaghan Report at 1.

Although Dr. Callaghan accepted Petitioner’s MOGAD diagnosis, he disputed that the flu

vaccine had caused it. Tr. at 227, 257. He started by discussing several of the articles filed on

both sides in the case. Id. at 232. One, which discusses the research landscape on MOGAD, does

not mention vaccine causation. Id. at 233; R. Marignier et al., Myelin-Oligodendrocyte

Glycoprotein Antibody-Associated Disease, 20 Lancet Neurology 762 (2021), filed on July 29,

2022, as Ex. A1 (ECF No. 21-2) (“Marignier”). Two others concluded that there was no

significant association between the flu vaccine and MS (a parallel central nervous system

demyelinating disease). Id. at 233-35; M. Mailand & J. Frederiksen, Vaccines and Multiple

Sclerosis: A Systematic Review, 264 Journal of Neurology 1035 (2017), filed on July 29, 2022,

as Ex. A2 (ECF No. 21-3); L. Belbasis et al., Environmental Risk Factors and Multiple

Sclerosis: An Umbrella Review of Systematic Reviews and Meta-Analysis, 14 Lancet Neurology

263 (2015), filed on July 29, 2022 as Ex. A3 (ECF No. 21-4). Rather, filed literature far better

associated infections with MOGAD, especially since a live infection would have much more of a

stimulative impact on the immune system. Tr. at 258; see, e.g., D. Dubey et al., Clinical,

Radiologic, and Prognostic Features of Myelitis Associated with Myelin Oligodendrocyte

Glycoprotein Autoantibody, 76 JAMA Neurology 301 (2019), filed on Nov. 18, 2022, as Ex. 40

(ECF No. 23-9). Case reports purporting to make a more direct association deserved less weight,

15

in Dr. Callaghan’s view, and he deemed them “the lowest levels of evidence.” Tr. at 236. Dr.

Callaghan also stated that he did not find literature studying GBS or other central nervous system

conditions to be particularly helpful, due to the differences in those conditions and MOGAD. Id.

at 228–29.

Dr. Callaghan then discussed Petitioner’s clinical course, and what it suggested to him

about possible onset timeframe. Tr. at 237. He characterized Petitioner’s MOGAD as relapsing

in nature, with onset likely in early September 2018, when he visited an emergency room with

complaints of neck and back pain. Callaghan Rep. at 6; Tr. at 238. He did not agree with Dr.

Phillips that Petitioner had disc issues, as this was not indicated on the MRI. Tr. at 239. When

asked why Petitioner had reported that his neck and back pain had improved at the October 8,

2018 appointment (when he received the vaccine), Dr. Callaghan proposed that Petitioner likely

had MOGAD lesions that “came and went.” Id. at 241, 263. And Dr. Callaghan did not deem the

absence of lesion evidence in late-October to be significant, opining that “MRIs are not perfect,”

and could well have been missed by the reviewing radiologist. Id. at 242. He otherwise stated

that he had seen patients where lesions were suspected but whose imaging showed no lesions,

only appearing on later scans. Id.

Dr. Callaghan further emphasized the record of Petitioner’s November 5, 2018

neurologist visit, at which time Petitioner reported that his symptoms began six months prior. Tr.

at 243. Dr. Callaghan characterized this to be possibly “when it started,” in contrast to the

October symptoms (such as pain, numbness, and loss of motor skills), which occurred “when it

became dramatically worse.” Id. at 243–44. The fact that Petitioner’s MRI during the November

2018 hospitalization showed spinal cord lesions did not impact his contention of a pre-vaccine

disease onset. Id. at 245–46.

Another significant factor suggesting to Dr. Callaghan that Petitioner’s MOGAD

predated onset were the results of the OCT testing from November-December 2018. Tr. at 248.

As Dr. Callaghan explained, it takes three to six months for optic neuropathy to manifest—

meaning the OCT findings were inconsistent with a more recent October onset. Id. at 248–49. In

fact, the Johns Hopkins neuroimmunology case conference notes from December 6, 2018,

concluded that Petitioner’s course was likely relapsing over time, as opposed to recent and

monophasic, based on the OCT findings. Tr. at 250; see also Ex. 6 at 292. Thus, while the optical

nerve findings “aren’t typical in MOGAD,” they did “indicate that this has been going on for at

least three to six months.” Tr. at 249.

On cross, Dr. Callaghan was confronted with his conflicting statements that Petitioner’s

MOGAD may have been caused by infection (which the record suggested had possibly occurred

in two or so weeks before vaccination), versus an idiopathic onset of months before (a conflict

also seemingly present when comparing Drs. Callaghan’s and He’s opinions). Tr. at 259–60. He

16

agreed that the record had “more obvious” evidence of neurologic-like symptoms in September

than earlier. Id. But Dr. Callaghan would not state that he outrightly disagreed with Dr. He’s

theory that Petitioner’s MOGAD was caused by an upper respiratory infection. Id. at 269. At

best, Dr. Callaghan opined that he “would place the onset before the vaccine and the infection.

But if one was to say that [onset] was in late October, then I pointed to multiple exhibits that

show infections are way more common than vaccines prior to the onset of MOGAD.” Id.

In addition, Dr. Callaghan could not opine as to what length of time would typically

separate MOGAD symptoms flares, stating only that it “could be all over the place. You can, you

know, have relapses that happen in short order. It can happen months and years later.” Tr. at 262.

He otherwise agreed, however, that Petitioner’s November 2018 hospitalization was the “nadir”

of his illness. Id. at 269. He also suggested the possibility that Petitioner’s MOGAD was

continuous even in times when he had no symptoms, but that he was “taking symptomatic

treatments that were masking some of his symptoms.” Id. at 271.

2. You-Wen He, M.D., Ph.D. - Dr. He wrote one report in this case, and

testified at the hearing. Report, filed July 29, 2022, as Ex. B (ECF No. 22). Dr. He denied the flu

vaccine could have caused Petitioner’s MOGAD.

Dr. He is a Professor of Immunology in the Department of Immunology at Duke

University School of Medicine. Curriculum Vitae of You-Wen He, M.D., Ph.D., filed July 29,

2022, as Ex. D (ECF No. 22-19) (“He CV”). He earned his medical degree in 1986 from the

Fourth Military Medical University in Xian, China. He CV at 1. He went on to earn a Ph.D. in

Microbiology and Immunology from the University of Miami School of Medicine in 1996. Id.

He has been conducting research in immunology since 1986 after completing his MD training.

Id. His research areas include both innate and adaptive immunity against viral and bacterial

infections as well as tumors. He Report at 1. He has directed research on human immune

responses to viral infections including influenza, HIV, HBV and HCV. Id. He has been the

Director for an advanced immunology course (IMM601), Immunology of Human Diseases, at

Duke University Medical Center for 10 years. Id. He has also served as a co-Principal

Investigator for four clinical trials focusing on cancer immunotherapy using personalized cancer

vaccine. Id. He is a reviewer for more than 30 scientific journals, and an editor for several more.

Id. at 2.

Dr. He started by explaining the difference in immune system stimulation caused by

vaccines versus wild-type viruses. Tr. at 284. He defined “PAMPs” (pathogen-associated

molecular patterns) as “the individual component from microbe pathogens, and our host use[s]

the receptor called a pattern recognition receptors” in reacting to PAMPS. Id. at 288. A flu

vaccine, however, is much “simpler” than a wild-type virus, as it has been stripped down to

contain only one PAMP. Id. at 286, 292. This allows it to create a “controlled immune process.”

17

Id. at 291. In contrast, a wild-type virus contains many more PAMPS; the flu virus, for example,

contains at least “five different categories” of PAMP. Id. at 290. Thus, “[t]he magnitude, the

breadth, the depth of the immune response is fundamentally different.” Id. at 292. Though no

testing revealed the cause of Petitioner’s upper respiratory symptoms, any wild bacteria or virus

would have stimulated his immune system with more PAMPs than a vaccine. Id. at 294.

Dr. He next criticized molecular mimicry as a theory of autoimmune injury. Tr. at 295.

He noted that molecular mimicry theories had initially emerged before the existence of

technology sufficient to uncover massive sequence sharing in genomes. Id. at 296. When this

genome sequencing became possible on a large scale, evidence emerged weakening the concept

that sequence sharing would likely be pathogenic. Id. Instead, Dr. He explained, “self-reactive

lymphocytes [are] the nature of our immune system,” constantly communicating with peripheral

immune cells to function.” Id. at 298. Thus, “the majority of the time, you know, [cross-

reactivity]’s not pathogenic at all, and actually most cases are protective even.” Id. at 299. In

support, Dr. He referenced three studies discussing significant sequence similarities between

viral and human genomes. Id. at 299-302; Trost 2 at 71; A. Kusalik et al., Widespread and Ample

Peptide Overlapping Between HCV and Homo Sapiens Proteomes, 28 Peptides 1260 (2007),

filed on July 29, 2022, as Ex. B6 (ECF No. 22-7); D. Li & M. Wu, Pattern Recognition

Receptors in Health and Diseases, 6 Signal Transduction and Targeted Therapy 291 (2021), filed

on July 29, 2022, as Ex. 7 (ECF No. 22-8).

Petitioner’s cited studies did not, in Dr. He’s reading, suggest molecular mimicry was a

likely driver of most instances of autoimmune disease. Some studies, for example, involved an

animal model—experimental autoimmune encephalomyelitis (“EAE”)—applicable mainly to

MS, and which requires use of a highly-stimulative laboratory-specific additive, “complete

Freund’s adjuvant” (“CFA”). Tr. at 303; K. O’Connor et al., Self-Antigen Tetramers

Discriminate Between Myelin Autoantibodies to Native or Denatured Protein, 13 Nature

Medicine 211 (2007), filed on Nov. 18, 2022, as Ex. 34 (ECF No. 23-5) (“O’Connor”). But there

is currently no animal model for MOGAD, and CFA is a “nasty adjuvant” not approved for use

on humans (while the version of the flu vaccine at issue contains no adjuvant at all). Id. at 303,

304. Accordingly, EAE studies were not helpful in establishing causation. He also criticized the

use of case studies, stating that while a series of case reports may be useful, a single case report

is not reliable evidence for establishing causality. Id. at 307.

While denying the vaccine was causal, Dr. He (although not a neurologist or treating

expert) deemed infection a far more likely explanation for Petitioner’s MOGAD. Tr. at 309. He

opined that antibodies (such as the MOG antibody Petitioner unquestionably had) would take up

to seven days to develop post-infection. Id. at 310. But at a primary care visit on October 30,

2018, Petitioner complained of sinus pressure and post-nasal drip. Id. at 312; Ex. 3 at 13.

Petitioner’s hospitalization in November 2018 began nine days after this visit, matching the

18

timeline in which an adaptive immune response. Id. at 313. This timeframe was not consistent

with the longer period separating Petitioner’s vaccination and likely MOGAD onset. Id. at 315.

On cross, Dr. He refused to disagree with Dr. Callaghan’s assertions that Petitioner’s

MOGAD onset likely predated vaccination. Tr. at 318. Dr. He in fact argued that their somewhat

competing etiologic explanations were not contradictory, while adding that he could not

comment on Dr. Callaghan’s opinion overall because he was not a neurologist. Id. at 319. He

was then asked about two of his cited studies, which expressly mentioned vaccines as a potential

causes for MOGAD or other central nervous system demyelinating injuries. Id. at 323–27; E.

Flanagan et al., Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease (MOGAD):

Clinical Features and Diagnosis, Wolters Kluwer (2022), filed on July 29, 2022, as Ex. B1 (ECF

No. 22-2) (“Flanagan”); O’Connor at 211. In response, Dr. He only pointed out that O’Connor

involved EAE, reiterating his prior contentions that results from this animal stud would not

translate to humans. Tr. at 326. He also acknowledged that several articles filed in this case did

discuss molecular mimicry as a viable mechanism for at least some autoimmune diseases. Id. at

328–29. And Dr. He conceded that cross-reactivity could serve as the first step in a far more

complex autoimmune process. Id. at 330.

III. Procedural History

Although the Petition originally alleged that Mr. Hock had developed “demyelinating

disease” as a result of receiving the flu vaccine, he later amended his petition to specify

MOGAD as his injury. Amended Petition, dated March 30, 2022 (ECF No. 19). Respondent filed

his Rule 4(c) Report on December 16, 2021, recommending against compensation. (ECF No.

17). Expert reports were filed through the end of 2022, and then trial was set in the matter for

December 2023. The parties opted not to submit post-hearing briefs, and the claim is ripe for

resolution.

IV. Applicable Legal Standards

A. Petitioner’s Overall 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 13(a)(1)(A), 11(c)(1), and 14(a), as amended by 42 C.F.R. § 100.3; §

11(c)(1)(C)(ii)(I); see also Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1321 (Fed.

19

Cir. 2010); Capizzano v. Sec’y of Health & Hum. Servs., 440 F.3d 1317, 1320 (Fed. Cir. 2006). 10

There is no Table injury for MOGAD, so Petitioner can only proceed herein with a causation-in-

fact claim.

For both Table and Non-Table claims, Vaccine Program petitioners bear a

“preponderance of the evidence” burden of proof. Section 13(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 [he] 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 Enter. 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 &

Hum. Servs., 931 F.2d 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 &

Hum. Servs., 165 F.3d 1344, 1352–53 (Fed. Cir. 1999)); Pafford v. Sec’y of Health & Hum.

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. Sec'y of Health and Hum. Servs., 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.”

Each Althen prong 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 & Hum. 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 & Hum. Servs., 569 F.3d 1367, 1378–79 (Fed. Cir. 2009)

10

Decisions of special masters (some of which I reference in this ruling) constitute persuasive but not binding

authority. Hanlon v. Sec’y of Health & Hum. 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 & Hum. 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 & Hum. Servs.,

No. 13-159V, 2014 WL 504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014).

20

(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, 121 Fed. Cl. at 245 (“[p]lausibility . . . in many cases may be enough to satisfy Althen

prong one” (emphasis in original)).

In discussing the evidentiary standard applicable to the first Althen prong, the Federal

Circuit has consistently rejected the contention that it can be satisfied merely by establishing the

proposed causal theory’s scientific or medical plausibility. See Kalajdzic v. Sec’y of Health &

Hum. Servs., No. 2023-1321, 2024 WL 3064398, at *2 (Fed. Cir. June 20, 2024) (arguments “for

a less than preponderance standard” deemed “plainly inconsistent with our precedent” (citing

Moberly, 592 F.3d at 1322)); Boatmon v. Sec’y of Health & Hum. Servs., 941 F.3d 1351, 1359

(Fed. Cir. 2019); see also Howard v. Sec'y of Health & Hum. Servs., 2023 WL 4117370, at *4

(Fed. Cl. May 18, 2023) (“[t]he standard has been preponderance for nearly four decades”),

aff’d, 2024 WL 2873301 (Fed. Cir. June 7, 2024) (unpublished). And petitioners always have the

ultimate burden of establishing their overall Vaccine Act claim with preponderant evidence.

W.C. v. Sec’y of Health & Hum. Servs., 704 F.3d 1352, 1356 (Fed. Cir. 2013) (citations omitted);

Tarsell v. United States, 133 Fed. Cl. 782, 793 (2017) (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; Andreu,

569 F.3d at 1375–77; Capizzano, 440 F.3d at 1326; Grant v. Sec’y of Health & Hum. 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 (“medical records and medical opinion testimony are

favored in vaccine cases, as treating physicians are likely to be in the best position to determine

whether a ‘logical sequence of cause and effect show[s] that the vaccination was the reason for

the injury’”) (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 & Hum. Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993).

Medical records and statements of a treating physician, 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”);

21

Snyder v. Sec’y of Health & Hum. Servs., 88 Fed. Cl. 706, 746 n.67 (2009) (“there 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 be

weighed against other, contrary evidence also present in the record—including conflicting

opinions among such individuals. Hibbard v. Sec’y of Health & Hum. Servs., 100 Fed. Cl. 742,

749 (2011) (not arbitrary or capricious for special master to weigh competing treating

physicians’ conclusions against each other), aff’d, 698 F.3d 1355 (Fed. Cir. 2012); Veryzer v.

Sec’y of Dept. of Health & Hum. Servs., No. 06-522V, 2011 WL 1935813, at *17 (Fed. Cl. Spec.

Mstr. Apr. 29, 2011), mot. for review den’d, 100 Fed. Cl. 344, 356 (2011), aff’d without opinion,

475 F. Appx. 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 & Hum. Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The

explanation for what is a medically acceptable timeframe must align with the theory of how the

relevant vaccine can cause an injury (Althen prong one’s requirement). Id. at 1352; Shapiro v.

Sec’y of Health & Hum. Servs., 101 Fed. Cl. 532, 542 (2011), recons. den’d after remand, 105

Fed. Cl. 353 (2012), aff’d mem., 503 F. Appx. 952 (Fed. Cir. 2013); Koehn v. Sec’y of Health &

Hum. Servs., No. 11-355V, 2013 WL 3214877 (Fed. Cl. Spec. Mstr. May 30, 2013), mot. for rev.

den’d (Fed. Cl. Dec. 3, 2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).

B. Legal Standards 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 & Hum. Servs., 3 F.3d 415, 417

(Fed. Cir. 1993) (determining that 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

22

that such determination is evidenced by a rational determination).

As noted by the Federal Circuit, “[m]edical records, in general, warrant consideration as

trustworthy evidence.” Cucuras, 993 F.2d at 1528; Doe/70 v. Sec'y of Health & Hum. Servs., 95

Fed. Cl. 598, 608 (2010) (“[g]iven 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”), aff'd, Rickett v. Sec'y of Health &

Hum. Servs., 468 F. App’x 952 (Fed. Cir. 2011) (non-precedential opinion). A series of linked

propositions explains why such records deserve some weight: (i) sick people visit medical

professionals; (ii) sick people attempt to honestly report their health problems to those

professionals; and (iii) medical professionals record what they 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 & Hum.

Servs., No. 11–685V, 2013 WL 1880825, at *2 (Fed. Cl. Spec. Mstr. Apr. 10, 2013); Cucuras v.

Sec'y of Health & Hum. 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 & Hum. Servs., No. 03–1585V, 2005

WL 6117475, at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed, contemporaneous medical

records are often 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 & Hum. Servs., 23 Cl. Ct. 726, 733 (1991), aff'd per curiam,

968 F.2d 1226 (Fed. Cir. 1992), cert. den'd, Murphy v. Sullivan, 506 U.S. 974 (1992) (citing

United States v. United States Gypsum Co., 333 U.S. 364, 396 (1947) (“[i]t has generally been

held that oral testimony which is in conflict with contemporaneous documents is entitled to little

evidentiary weight.”)).

However, the Federal Circuit has also noted that there is no formal “presumption” that

records are accurate or superior on their face to other forms of evidence. Kirby v. Sec’y of Health

& Hum. Servs., 997 F.3d 1378, 1383 (Fed. Cir. 2021). There are certainly situations in which

compelling oral or written testimony (provided in the form of an affidavit or declaration) may be

more persuasive than written records, such as where records are deemed to be incomplete or

inaccurate. Campbell v. Sec'y of Health & Hum. Servs., 69 Fed. Cl. 775, 779 (2006) (“like 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 (“[w]ritten 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

23

determining the weight that such testimony should be afforded. Andreu, 569 F.3d at 1379;

Bradley v. Sec'y of Health & Hum. 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 & Hum.

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 & Hum. Servs., 110 Fed. Cl. 184, 203–04 (2013), aff'd, 746 F.3d 1334

(Fed. Cir. 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 & Hum. 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 & Hum. Servs., 617 F.3d 1328,

1339 (Fed. Cir. 2010) (citing Terran v. Sec’y of Health & Hum. Servs., 195 F.3d 1302, 1316

(Fed. Cir. 1999). Under Daubert, the 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).

In the Vaccine Program the Daubert factors play a slightly different role than they do

when applied in other federal judicial settings, like the district courts. Typically, Daubert factors

are employed by judges (in the performance of their evidentiary gatekeeper roles) to exclude

24

evidence that is unreliable or could confuse a jury. By contrast, in Vaccine Program cases these

factors are used in the weighing of the reliability of scientific evidence proffered. Davis v. Sec'y

of Health & Hum. Servs., 94 Fed. Cl. 53, 66–67 (2010) (“uniquely 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 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 & Hum. Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (citing

Lampe, 219 F.3d at 1362). However, 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

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 &

Hum. Servs., No. 08–601V, 2012 WL 3609993, at *17 (Fed. Cl. Spec. Mstr. July 30, 2012), mot.

for review den'd, 108 Fed. Cl. 743 (2013), aff'd, 540 F. 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

(“[a]ssessments as to the reliability of expert testimony often turn on credibility

determinations”); see also Porter v. Sec'y of Health & Hum. Servs., 663 F.3d 1242, 1250 (Fed.

Cir. 2011) (“this 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 all such items

factor into the outcome of this decision. While I have reviewed all the medical literature

submitted, 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. Moriarty v. Sec’y of Health & Hum. Servs., No. 2015–5072, 2016 WL 1358616, at

*5 (Fed. Cir. Apr. 6, 2016) (“[w]e generally presume that a special master considered the

relevant record evidence even though he does not explicitly reference such evidence in his

decision”) (citation omitted); see also Paterek v. Sec’y of Health & Hum. Servs., 527 F. App’x

25

875, 884 (Fed. Cir. 2013) (“[f]inding certain information not relevant does not lead to—and

likely undermines—the conclusion that it was not considered”).

ANALYSIS

I. MOGAD as a Putative Vaccine Injury

In keeping with the fact that medical science has only recently identified the MOGAD-

associated autoantibodies, and in turn proposed their possible link to certain CNS-oriented

demyelinating injuries, there are few Program decisions addressing MOGAD. I awarded

entitlement in one such case, however. L.C. v. Sec'y of Health & Hum. Servs., No. 17-722V,

2021 WL 3630315 (Fed. Cl. Spec. Mstr. July 2, 2021) (Tdap vaccine found to have caused

MOGAD in minor). The overall evidence offered therein was limited, with only neurologic

treaters testifying, allowing me to conclude that in that case preponderant evidence was

presented in favor of causation (albeit barely). Another petitioner, however, was previously able

to demonstrate that the anti-MOG antibody was vaccine-induced, causing an individual to

experience a CNS demyelinating injury. White v. Sec'y of Health & Hum. Servs., No. 15-1521V,

2019 WL 7563239 (Fed. Cl. Spec. Mstr. Dec. 19, 2019) (HPV vaccine caused anti-MOG

antibody-mediated TM).

Thus, while there is nascent Program recognition that vaccination might play a role in the

propagation of these antibodies, the question is far from resolved. It cannot be said based on

these two decisions that the Program favors a vaccine-MOGAD connection. And I am not

otherwise prepared to adopt the flu-GBS “template” as my analysis, applying it rotely simply

because MOGAD also involves demyelination and is believed in part to be associated with

certain autoimmune neuroinflammatory conditions.

All experts in this case agreed that Petitioner had MOGAD, and the record establishes a

persuasive basis for that conclusion. Petitioner tested positive for MOG antibodies after

experiencing a cluster of neurological symptoms characteristic of MOGAD—pain, weakness,

loss of motor function, bladder dysfunction, and visual loss. Tr. at 53; Ex. 6 at 8. Imaging

showed spinal cord lesions and evidence of optic neuritis, while laboratory testing showed the

presence of the MOG antibodies. Ex. 6 at 287. The diagnosis has solid evidentiary support.

Literature specific to MOGAD is very limited, given that widespread commercial testing

for the autoantibody has only been available for less than a decade. Experts in this case agreed

that there are no large epidemiological studies focusing on MOGAD (though some experts

discussed MS studies, a condition that I have not generally found to be credibly linked to any

covered vaccine). However, a few findings regarding MOGAD can be gleaned from what does

exist. Importantly, expert witnesses and cited articles note that the MOG antibody itself has not

26

been proven to be pathogenic—hence the name “MOG-antibody-associated disease (MOGAD).”

Tr. at 306; Marignier at 762.

There is also some evidence about the nature of MOGAD that might distinguish it from

other central nervous system demyelinating conditions. For example, one 50-patient study on

MOG-IgG positive patients found that 80% of the sample experienced a relapsing disease course

(rather than monophasic). Jarius at 3. In addition, the median time between the first and second

attacks in these patients with a relapsing course was five months, and the median annualized

relapse rate was 0.83. Id. at 8. The most common symptom at onset was optic neuritis (74%),

followed by myelitis (34%). Id. at 6. Two patients in this study received different vaccines

shortly before onset—one 12 days prior, and one two weeks prior. Id. at 14. In addition, tissue

studies have shown a CD4+ T-helper cell-driven reaction with granulocytic inflammation is the

likely pathogenesis of the disease. Flanagan at 2–3.

II. Petitioner Has Carried His Burden of Proof

A. Althen Prong One

Petitioner’s “can cause” showing was thin, but nevertheless sufficiently preponderant to

carry his burden—and the balance of factors that lead me to so conclude were not rebutted by

Respondent.

An overarching consideration underlying my analysis is the fact that the flu vaccine has

often been found in past Program cases to be associated with comparable central nervous system

inflammatory demyelinating diseases, like ADEM, TM, or optic neuritis. See, e.g., Schmidt v.

Sec'y of Dep't of Health & Hum. Servs., No. 07-20V, 2009 WL 5196169 (Fed. Cl. Spec. Mstr.

Dec. 17, 2009) (finding that flu vaccine caused acute transverse myelitis); Daniels v. Sec'y of the

Dep't of Health & Hum. Servs., No. 07-462V, 2012 WL 763175 (Fed. Cl. Spec. Mstr. Feb. 16,

2012) (finding that flu vaccine caused ADEM); Calise v. Sec'y of Dep't of Health & Hum. Servs.,

No. 08-865V, 2011 WL 1230155 (Fed. Cl. Spec. Mstr. Mar. 14, 2011) (finding that flu vaccine

caused neuromyelitis optica). As noted at hearing, many of these diseases might today be

categorized as MOGAD instead, even if MOGAD is not wholly congruent (or even yet fully

understood).

I am of course not bound herein to find that the flu vaccine likely causes MOGAD simply

on the basis of these prior determinations. But I am reluctant to ignore them at the same time. I

have noted in other contexts that relevant prior determinations should be taken seriously,

especially in the absence of compelling proof counseling a different outcome. See, e.g., Nieves v.

Sec'y of Health & Hum. Servs., No. 18-1602V, 2023 WL 3580148, at *36 (Fed. Cl. May 22,

2023), mot. for review den’d, 167 Fed. Cl. 422 (2023) (prior cases with favorable results relevant

to CIDP-flu vaccine association deemed “persuasive guidance,” despite issues with causation

27

theory overall). 11 It is reasonable to consider and be guided by a history of relevant reasoned

decisions involving the same theory and vaccine, especially when the injury at hand is consistent

with one that has been repeatedly deemed vaccine-caused in prior cases. Doe v. Sec'y of Health

& Hum. Servs., 76 Fed. Cl. 328, 338–39 (2007) (“[o]ne reason that proceedings are more

expeditious in the hands of special masters is that the special masters have the expertise and

experience to know the type of information that is most probative of a claim”) (emphasis added).

In addition, Petitioner has offered just enough other evidence in support of causation to

find his burden of proof was met (although barely). Dr. Phillips made several reasonable points

about the potential pathologic results of an aberrant immune process triggered by molecular

mimicry between a vaccine’s antigens and self-structures. He explained that the flu vaccine could

stimulate production of anti-MOG antibodies through molecular mimicry—a theory that has

been accepted in other Program cases as a scientifically-valid mechanistic explanation for how

some autoimmune-mediated demyelinating illnesses might unfold. Raymo v. Sec'y of Health &

Hum. Servs., No. 11-0654V, 2014 WL 1092274 (Fed. Cl. Spec. Mstr. Feb. 24, 2014), mot. for

review den’d, 129 Fed.Cl. 691 (Fed. Cl. 2016). And it can be the instigating factor leading to an

autoimmune disease process. Tr. at 143, 149.

Respondent’s primary immunology expert, Dr. He, raised valid arguments about the

limits of molecular mimicry as explanatory of all autoimmune injuries, and the more stimulative

effects of a wild-type virus. I certainly never rule for petitioners simply because they have

invoked molecular mimicry, but without other corroborative evidence. McKown v. Sec'y of

Health & Hum. Servs., No. 15-1451V, 2019 WL 4072113, at *50 (Fed. Cl. Spec. Mstr. July 15,

2019) (“But merely chanting the magic words “molecular mimicry” in a Vaccine Act case does

not render a causation theory scientifically reliable, absent additional evidence specifically tying

the mechanism to the injury and/or vaccine in question.”). But Dr. He’s criticisms, while

reasonable in a broad sense, were themselves not specific enough to the context at hand to rebut

Petitioner’s showing. And impeachment of Dr. Phillips and his late-career “team switching” did

not persuasively call into question his expertise or the specific opinion he offered. (It would

actually be to the Program’s benefit overall if experts more commonly worked for both sides in

Vaccine Act cases).

Thus, and as in L.C., I find that Petitioner’s showing on prong one was just preponderant

enough to make this a “close” case, presenting the kind of circumstances in which special

masters usually resolve the disputed question in the petitioner’s favor. L.C., 2021 WL 3630315 at

20; Andreu, 569 F.3d at 1378. My resolution of this aspect of Petitioner’s overall burden,

however, does not in any regard resolve the question of whether MOGAD is, or is not, likely

11

By the same token, I frequently follow prior reasoned decisions when dismissing claims that repeat theories also

aired in the dismissed matters, while not offering new evidentiary bases for taking a fourth or fifth look at the

theory. See, e.g., Kalajdzic v. Sec'y of Health & Hum. Servs., No. 17-792V, 2022 WL 2678877 (Fed. Cl. Spec. Mstr.

June 17, 2022), mot. for review den’d, Dkt. No. 79 (Fed. Cl. Oct. 27, 2022), aff’d, No. 2023-1321, 2024 WL

3064398 (Fed. Cir. June 20, 2024) (rejecting theory that flu vaccine caused type II narcolepsy, where theory was

largely identical to one offered in prior cases that had also been dismissed).

28

vaccine-caused. It is very possible the anti-MOG antibody does not pathogenically drive the

disease—and if so, a vaccine’s encouragement of this antibody’s production could not be causal.

Indeed—it is far from established with any degree of certainty that vaccines cause the production

of this antibody at all. MOGAD’s novelty as a diagnosis, coupled with the extremely limited

number of Program decisions addressing the topic, mean that the subject remains open to

debate—and additional evidence on the topic (not offered in this case) will be required before

special masters can more confidently state a MOGAD-vaccine association exists. But for present

purposes, what matters is the evidence adduced in this case.

B. Althen Prong Two

The record preponderates in favor of the conclusion that Petitioner’s MOGAD was likely

vaccine-caused. Petitioner began to experience symptoms that were largely neurologic in

character shortly before his ER visit in October 2018. Ex. 4 at 65. At this time, he presented with

headaches, pain in his back and neck, and trouble urinating. Id. at 65, 74, 76. He was prescribed

steroids and discharged with instructions to follow up with a neurologist. Id. at 76–77. In the

weeks following, his symptoms continued, and his bladder issues worsened. He visited a

urologist multiple times, and was eventually prescribed self-catheterization as he could not

urinate. Ex. 10 at 12–15. Petitioner attempted to visit another ER to address these issues, but was

again discharged and advised to follow up with a neurologist. Ex. 5 at 18. His symptoms

progressed, he obtained more focused neurologic treatment, and then was diagnosed with

MOGAD on the basis of a number of reliable and relevant tests. Ex. 6 at 8, 11, 21, 26, 287–88.

And Petitioner’s medical treaters attributed his symptoms to the flu vaccine at least once. Ex. 9 at

8.

Respondent did identify some record evidence that suggested onset of Petitioner’s

MOGAD could have predated vaccination, but it was ultimately too inconclusive when balanced

against the overall record. For example, symptoms reported at Petitioner’s pre-vaccination

medical visit (back and neck pain) were convincingly distinguished by Dr. Rizvi from

Petitioner’s post-vaccination constellation of concerns (which were overall more neurologic in

character). Tr. at 77. Given that Petitioner had evidence of disc disease on MRIs, and worked a

physical job that required several hours of driving per day, it is not difficult to see how he could

have experienced musculoskeletal issues resulting in back and neck pain. His symptoms after

vaccination, in contrast, were distinctly neurologic—Petitioner displayed loss of motor function,

significant pain, gait problems, and sensory abnormalities. And importantly, he could not urinate

on his own, and his bladder symptoms were noted to be neurological by several treaters.

In addition, the reference in a record to Petitioner reporting symptoms predating

vaccination was a one-time occurrence, never corroborated with other proof suggesting he had

been suffering from neurologic concerns for so long. Proposals of an infectious cause for

MOGAD were based on evidence that the Petitioner likely experienced an upper respiratory

infection in September and October 2018, but were never later confirmed during Petitioner’s

29

extensive treatment. 12 And imaging performed in October did not identify active demyelinating

lesions—which if present would have been consistent with a disease process that likely started

before vaccination. Tr. at 84. By contrast, Petitioner’s scan in mid-November revealed enhancing

lesions—a clear indicator of active demyelination that would have begun in October. Id. at 88.

This lends further support to the theory that Petitioner’s MOGAD onset occurred after

vaccination in October.

A stronger argument marshalled by Respondent in favor of an earlier onset was rooted in

the OCT test results. Respondent correctly noted that treaters concluded that these tests

established “chronic” damage to Petitioner’s optic nerves, suggesting that a neuroinflammatory

condition may have been present for some time. Ex. 6 at 48–49, 292. But Dr. Callaghan’s

repeated assertion that this meant Petitioner’s MOGAD had been going on “at least three to six

months” is unsupported. Tr. at 249. And a further look into these results (to the extent the

medical record allows that) finds that they are less clear and robust than at first glance. No

explanation is provided, for example, of what “chronic” really means—or how long the process

causing the optic nerve damage was thought to have predated its discovery.

Literature cited by Petitioner raised additional questions about these findings. Flanagan,

for example, notes that the optic nerves contain two different tissue layers (the peripapillary

retinal nerve fiber layer (pRNFL) and inner plexiform layer (mGICPL)) that thin at different

rates—“mGICPL thinning emerges within a few weeks, while pRNFL takes longer to develop,

possibly due to the optic nerve head edema, which masks initial thinning in the pRNFL.”

Flanagan at 16. A treater note from his December 2018 scan called Petitioner’s pRNFL normal,

but noted that his mGICPL was thinned (“[m]ean peripapillary retinal nerve fiber layer thickness

was normal for each eye”). Ex. 6 at 302–03. And Petitioner never even complained of any vision

associated symptoms until his November hospitalization. Thus, the evidence from this testing of

a long-existing condition is ultimately too inconclusive to support the determination that

Petitioner’s MOGAD likely preceded vaccination.

C. Althen Prong Three/Onset

Petitioner offered persuasive and reliable evidence that a post-vaccination onset of 19

days was medically acceptable. That timeframe would be sufficient for the production of cross-

reactive autoantibodies to occur and thereafter cause the MOG antibody-driven demyelination

characteristic of MOGAD. See Karussis at 216; Rowhani-Rabar at 273. Petitioner’s experience

of acute, neurologic symptoms in late October, progressing to nadir in November, was consistent

with such an onset timeframe.

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Respondent’s experts’ disagreement on etiology also undermined the strength of arguments than an infection was

causal.

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CONCLUSION

Petitioner has established entitlement to a damages award. An order setting forth a

schedule for the resolution of damages in this matter shall shortly follow.

IT IS SO ORDERED.

s/ Brian H. Corcoran

Brian H. Corcoran

Chief Special Master

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