1

In the United States Court of Federal Claims 

OFFICE OF SPECIAL MASTERS

No. 18-554V

Filed: November 10, 2022

PUBLISHED

SCOTT ROBERTSON,

 Petitioner,

v.

SECRETARY OF HEALTH AND 

HUMAN SERVICES,

 Respondent.

Ronald Homer, Conway, Homer, P.C., Boston, MA, for petitioner.

Voris Johnson, U.S. Department of Justice, Washington, DC, for respondent.

DECISION1

On April 17, 2018, petitioner filed a petition under the National Childhood Vaccine 

Injury Act, 42 U.S.C. § 300aa-10-34 (2012),2 alleging that the influenza (“flu”) vaccine 

he received on October 28, 2016, caused him to suffer relapsing optic neuropathy 

and/or neuritis. (ECF No. 1, p. 1.) Subsequently, the parties’ experts agreed that the 

best diagnosis for petitioner’s condition is nonarteritic anterior ischemic optic neuropathy 

(“NAION”). (Ex. 30, p. 1; Ex. B, p. 5.) On August 13, 2021, petitioner filed his motion 

for a ruling on the record alleging that the flu vaccine caused-in-fact his NAION. (ECF 

No. 65, pp. 1 n.2, 27-29.) For the reasons set forth below, I conclude that that petitioner 

is not entitled to compensation. 

1 Because this decision contains a reasoned explanation for the special master’s action in this case, it will 

be posted on the United States Court of Federal Claims’ website in accordance with the E-Government 

Act of 2002. See 44 U.S.C. § 3501 note (2012) (Federal Management and Promotion of Electronic 

Government Services). This means the decision will be available to anyone with access to the 

Internet. In accordance with Vaccine Rule 18(b), petitioner has 14 days to identify and move to redact 

medical or other information the disclosure of which would constitute an unwarranted invasion of privacy. 

If the special master, upon review, agrees that the identified material fits within this definition, it will be 

redacted from public access.

2 Within this decision, all citations to § 300aa will be the relevant sections of the Vaccine Act at 42 U.S.C. 

§ 300aa-10-34. 

Special Master Horner

Optic neuritis (“ON”); 

nonarteritic anterior ischemic 

optic neuropathy (“NAION”); 

Influenza (“flu”) vaccine 
2

I. Applicable Statutory Scheme

Under the National Vaccine Injury Compensation Program, compensation 

awards are made to individuals who have suffered injuries after receiving vaccines. In 

general, to gain an award, a petitioner must make a number of factual demonstrations, 

including showing that an individual received a vaccination covered by the statute; 

received it in the United States; suffered a serious, long-standing injury; and has 

received no previous award or settlement on account of the injury. Finally – and the key 

question in most cases under the Program – the petitioner must also establish a causal 

link between the vaccination and the injury. In some cases, the petitioner may simply 

demonstrate the occurrence of what has been called a “Table Injury.” That is, it may be 

shown that the vaccine recipient suffered an injury of the type enumerated in the 

“Vaccine Injury Table,” corresponding to the vaccination in question, within an 

applicable time period following the vaccination also specified in the Table. If so, the 

Table Injury is presumed to have been caused by the vaccination, and the petitioner is 

automatically entitled to compensation, unless it is affirmatively shown that the injury 

was caused by some factor other than the vaccination. § 300aa-13(a)(1)(A); § 300 aa11(c)(1)(C)(i); § 300aa-14(a); § 300aa-13(a)(1)(B).

In many cases, however, the vaccine recipient may have suffered an injury not of 

the type covered in the Vaccine Injury Table. In such instances, an alternative means 

exists to demonstrate entitlement to a Program award. That is, the petitioner may gain 

an award by showing that the recipient’s injury was “caused-in-fact” by the vaccination 

in question. § 300aa-13(a)(1)(B); § 300aa-11(c)(1)(C)(ii). In such a situation, of course, 

the presumptions available under the Vaccine Injury Table are inoperative. The burden 

is on the petitioner to introduce evidence demonstrating that the vaccination actually 

caused the injury in question. Althen v. Sec’y of Health & Human Servs., 418 F.3d 

1274, 1278 (Fed. Cir. 2005); Hines v. Sec’y of Health & Human Servs., 940 F.2d 1518, 

1525 (Fed. Cir. 1991). 

The showing of “causation-in-fact” must satisfy the “preponderance of the 

evidence” standard, the same standard ordinarily used in tort litigation. § 300aa13(a)(1)(A); see also Althen, 418 F.3d at 1279; Hines, 940 F.2d at 1525. Under that 

standard, the petitioner must show that it is “more probable than not” that the 

vaccination was the cause of the injury. Althen, 418 F.3d at 1279. The petitioner need 

not show that the vaccination was the sole cause but must demonstrate that the 

vaccination was at least a “substantial factor” in causing the condition, and was a “but 

for” cause. Shyface v. Sec’y of Health & Human Servs., 165 F.3d 1344, 1352 (Fed. Cir. 

1999). Thus, the petitioner must supply “proof of a logical sequence of cause and effect 

showing that the vaccination was the reason for the injury[,]” with the logical sequence 

being supported by “reputable medical or scientific explanation, i.e., evidence in the 

form of scientific studies or expert medical testimony.” Althen, 418 F.3d at 1278; Grant 

v. Sec’y of Health & Human Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992). A petitioner 

may not receive a Vaccine Program award based solely on his or her assertions; rather, 

the petition must be supported by either medical records or by the opinion of a 

competent physician. § 300aa-13(a)(1).
3

In what has become the predominant framing of this burden of proof, the Althen

court described the “causation-in-fact” standard, as follows:

Concisely stated, Althen’s burden is to show by preponderant evidence that 

the vaccination brought about her injury by providing: (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. If Althen satisfies this burden, she is “entitled to 

recover unless the [government] shows, also by a preponderance of the 

evidence, that the injury was in fact caused by factors unrelated to the 

vaccine.”

Althen, 418 F.3d at 1278 (citations omitted). The Althen court noted that a petitioner 

need not necessarily supply evidence from medical literature supporting petitioner’s 

causation contention, so long as the petitioner supplies the medical opinion of an 

expert. Id. at 1279-80. The court also indicated that, in finding causation, a Program 

factfinder may rely upon “circumstantial evidence,” which the court found to be 

consistent with the “system created by Congress, in which close calls regarding 

causation are resolved in favor of injured claimants.” Id. at 1280.

In this case, petitioner has alleged that the flu vaccine caused him to suffer 

nonarteritic anterior ischemic optic neuropathy (“NAION”). (ECF No. 65, pp. 1 n.2, 27-

29.) Since NAION is not listed on the Vaccine Injury Table relative to the flu vaccine,

petitioner must satisfy the above-described Althen test for establishing causation-in-fact. 

II. Procedural History 

On April 17, 2018, petitioner filed a petition alleging that he received a flu vaccine 

on October 28, 2016, that caused relapsing optic neuropathy and/or neuritis. (ECF No. 

1, p. 1.) This case was originally assigned to Special Master Sanders. (ECF No. 4.) 

On April 20, 2018, petitioner filed his affidavit and medical records. (ECF Nos. 8-10.) 

From May 21, 2018, through April 22, 2019, petitioner subsequently filed additional 

medical records. (ECF Nos. 13, 19, 21, 25.) On May 16, 2019, respondent filed his 

Rule 4(c) report, arguing that the evidence presented did not meet petitioner’s burden 

and recommending against compensation. (ECF No. 28.) Respondent further argued 

that petitioner’s diagnosis appeared to be CRION, a “separate clinical entity from 

monophasic ON and its key clinical features include relapsing inflammatory ON and 

steroid dependency.” (Id. at 7.) 

This case was reassigned to my docket on August 28, 2019. (ECF No. 34.) On 

October 9, 2019, petitioner filed additional medical records. (ECF No. 37.) On 

November 18, 2019, petitioner filed an expert report from Thomas Hedges III, M.D. 

(neuro-ophthalmologist). (ECF No. 40.) On March 31, 2020, respondent filed an expert 

report from Michael Wilson, M.D., MAS (neuroimmunologist). (ECF No. 44.) 
4

Subsequently both parties filed supplemental expert reports on April 29 and June 30, 

2020. (ECF No. 45 (Dr. Hedges); ECF No. 48 (Dr. Wilson).). 

A Rule 5 conference was held on September 18, 2020. (ECF No. 50.) In the 

subsequent Rule 5 Order, I noted that diagnosis was an unresolved issued in this case. 

(Id.) In his petition, petitioner alleged that he suffered either optic neuritis or 

neuropathy; and respondent disputed optic neuritis as a diagnosis but suggested a type 

of neuropathy. (Id.) Petitioner’s expert Dr. Hedges opined that petitioner’s diagnosis is 

nonarteritic ischemic optic neuropathy. (Id.) Respondent’s expert Dr. Wilson agreed 

with the assessment of NAION though he did not dismiss the possible diagnosis of optic 

neuritis. (Id.) With regard to causation, I observed that Dr. Hedges cited four case 

reports showing that NAION can occur post-influenza vaccination (Ex. 24, p. 2), though 

I cautioned that standing alone these case reports are not highly persuasive. (ECF No. 

50.) 

On January 19, 2021, petitioner filed an expert report from Omid Akbari, Ph.D. 

(allergy and immunology). (ECF Nos. 53-57.) Respondent filed a responsive expert 

report from Dr. Wilson on March 23, 2021. (ECF No. 60.) On June 14, 2021, the 

parties filed a joint status report proposing a ruling on the written record. (ECF No. 64.) 

On August 13, 2021, petitioner filed his motion for a ruling on the record. (ECF No. 65.) 

On October 13, 2021, respondent filed his responsive brief. (ECF No. 66.) On 

November 10, 2021, petitioner filed his reply. (ECF No. 68.) 

I have determined that the parties have had a full and fair opportunity to present 

their cases and that it is appropriate to resolve this issue without a hearing. See 

Vaccine Rule 8(d); Vaccine Rule 3(b)(2); Kreizenbeck v. Sec’y of Health & Human 

Servs., 945 F.3d 1362, 1366 (Fed. Cir. 2020) (noting that “special masters must 

determine that the record is comprehensive and fully developed before ruling on the 

record.”). Accordingly, this matter is now ripe for resolution.

III. Factual History 

a. As reflected in the medical records 

Prior to vaccination, petitioner’s history was significant for a motor vehicle 

accident in March 2014 with cervical and lumbar pain. (Exs. 5, 12, 15.) He also had a 

history of tobacco use, hypertension, and hyperlipidemia. (See, e.g., Ex. 5, pp. 1-2 

(4/18/2017 record listing hypertension and hyperlipidemia as active problems, and 

noting “[c]urrent everyday [sic] smoker”); id. at 13 (7/16/2014 record noting “tobacco 

use” under the social history section); Ex. 7, p. 2 (12/22/2016 record noting that 

petitioner “[c]hews tobacco”).) Petitioner also suffers from obstructive sleep apnea.

(Ex. 2, p. 5.) 

Petitioner received a Fluvirin vaccine on October 28, 2016. (Ex. 1, p. 1.) On 

December 5, 2016, petitioner presented to Jennifer Roman, O.D., complaining of blurry 

vision in his left eye. (Ex. 13, p. 11.) He reported a sudden onset on Tuesday 
5

(November 29), which had slowly worsened over the last couple of days. (Id.) 

Petitioner indicated that he recently had a cold. (Id. at 11; see also Ex. 3, pp. 4-8 

(petitioner reporting that he had a cold over Thanksgiving).) On examination, the 

optometrist observed left optic disc swelling. (Ex. 13, pp. 11-16; Ex. 3, p. 3.) Dr. 

Roman referred petitioner to the emergency room for suspected NAION. (Ex. 13, p. 

16.) 

That same day, December 5, 2016, petitioner presented to the Emergency 

Department (“ED”) at UF Health Shands. (Ex. 3, p. 3.) He reported noticing floaters /

spots in his left field of vision approximately three-to-four days earlier, which had 

enveloped his whole eye. (Id.) Petitioner also reported eye pressure but denied eye 

pain. (Id. at 4-6.) A review of systems was positive for nasal congestion and discharge. 

(Id. at 4.) His differential diagnoses included papilledema, optic neuropathy, anterior 

ischemic optic neuropathy, and papillophlebitis. (Id. at 5.) An ophthalmologist was 

consulted and ordered a brain MRI, which confirmed the presence of left-sided palpable 

edema without associated enhancement and changes of chronic ischemic white matter 

demyelination in the brain as seen in the setting of chronic small vessel disease. (Id. at

6, 52-53.) There was no evidence of an intracranial mass lesion, infectious /

inflammatory process, or MR findings of intracranial hypertension. (Id. at 6.) The 

ophthalmologist diagnosed petitioner with optic nerve swelling and optic atrophy of the 

left eye of unknown etiology, and recommended Brimonidine eye drops. (Id.) Petitioner 

was discharged the following day to follow up with an ophthalmologist. (Id. at 6, 14.) 

On December 9, 2016, petitioner was evaluated by ophthalmologist Stephen 

Potter, M.D., at the University of Florida (“UF”) Eye Center for painless vision loss and 

optic disc edema in the left eye. (Ex. 8, p. 1.) He also developed atrophy in his left eye. 

(Id. at 10.) The ophthalmologist indicated that petitioner’s differential diagnosis was 

“most likely post-vaccination optic neuritis given flu-shot 1 month prior to presentation vs

post-infectious optic neuritis (less likely given negative labs; baronella [sic] pending) vs 

autoimmune optic neuritis (MS-spectrum).” (Id. at 2; Ex. 4, p. 43.) He recommended 

admission to the hospital for treatment with intravenous (“IV”) steroids. (Ex. 8, p. 2.) 

Petitioner was subsequently admitted to the hospital for three days of treatment with IV 

steroids and then discharged with an oral steroid taper. (Ex. 4, pp. 39-44; Ex. 19, pp. 4-

5.) 

On January 5, 2017, petitioner presented to neuro-ophthalmologist Hazem 

Samy, M.D., at the UF Eye Center. (Ex. 8, pp. 4-5.) Dr. Samy diagnosed petitioner with 

left eye papillitis “[p]ost-vaccination vs post-infectious vs autoimmune optic neuritis (MSspectrum . . . Received flu vaccine 1 month prior to presentation.” (Id.) Petitioner 

reported improved visual acuity and visual field as well as resolved edema. (Id.) Dr. 

Samy ordered petitioner to continue taking Brimonidine and “[a]void flu vaccination in 

future.” (Id.) 

On January 27, 2017, petitioner returned to Dr. Samy with new onset of mild 

swelling / edema of the optic nerve with flame hemorrhage in his right eye. (Ex. 8, pp. 

9-15.) Dr. Samy started petitioner on treatment with oral prednisone. (Id. at 11.) 
6

Petitioner returned to Dr. Samy emergently almost a week later, on February 2, 2017, 

complaining of worsening blurry vision in his right eye. (Id. at 15.) Dr. Samy suspected 

possible sequential NAION of the right eye. (Id. at 15-16.) Petitioner had mild inferior 

optic nerve edema, which was stable since his previous visit. (Id.) Dr. Samy 

recommended continuing treatment with prednisone. (Id. at 16.) In follow-up two 

weeks later, petitioner’s vision was stable. (Id. at 17.) 

Petitioner returned to Dr. Samy’s office on March 12, 2017, complaining of 

worsening visual disturbances in his right eye with decreasing prednisone dosage. (Ex. 

8, p. 22.) The doctor recommended that petitioner go to the hospital to receive another 

round of IV steroids. (Id. at 25; Ex. 3, pp. 82-83.) The ER sent petitioner to the infusion 

center for treatment to avoid having to be admitted to the hospital. (Id. at 87.) 

Petitioner subsequently received two days of IV steroids for right ischemic optic 

neuropathy. (Ex. 10, pp. 1-50.) 

Petitioner followed up with Dr. Samy on March 16, 2017, complaining that his 

right eye seemed worse. (Ex. 8, p. 26.) Dr. Samy’s impression based on petitioner’s 

presentation and clinical course was that he had chronic relapsing AION.

3 (Id. at 30.) 

Petitioner continued to follow up with Dr. Samy for CRON in April, May, and July 2017. 

(Ex. 5, pp. 1-6; Ex. 8, pp. 32-37; Ex. 19, pp. 1-5.) A skin punch biopsy collected on April 

14, 2017, showed no evidence of vasculitis or vasculopathy. (Ex. 8, p. 44.) At a May 

19, 2017 visit, Dr. Samy noted that petitioner had slight improvement in his visual field 

defects and stable visual acuity. (Id. at 38.) 

On April 4, 2017, petitioner established care with a new primary care physician, 

Brian Pecoraro, D.O., at Ocala Family Wellness Center. (Ex. 5, p. 7.) Dr. Pecoraro

noted in petitioner’s active problems optic neuritis—for which he was being monitored 

by ophthalmology and treated with steroids. (See, e.g., Ex. 5, pp. 1-5.)

On July 7, 2017, petitioner complained to Dr. Samy that his vision had been off 

for the past four days after tapering his prednisone. (Ex. 19, pp. 4-5.) Dr. Samy 

recommended starting CellCept, an immune-modulating agent. (Id.) However, 

because it would take about three months for CellCept to be effective, Dr. Samy 

recommended another round of IV steroids followed by increasing petitioner’s 

prednisone in the interim. (Id. at 5.) Consequently, petitioner received three days of IV 

steroids at the infusion center from July 12 through 14, 2017. (Id. at 6; Ex. 10, pp. 50-

110.) 

In follow-up on July 21, 2017, petitioner indicated that his vision was off in the 

previous visit. (Ex. 19, pp. 11-12.) Petitioner underwent subsequent C-spine MRI to 

rule out neuromyelitis optica. (Ex. 22, pp. 1-2.) The impression was “[n]o evidence of 

abnormal T2 signal changes or abnormal contrast enhancement of the cervical or 

thoracic spinal cord which could suggest inflammation/demyelination.” (Id. at 2.) There 

3 Dr. Samy maintained the diagnosis of CRON (chronic relapsing optic neuropathy) throughout 

subsequent visits, noting sequential NAION as a previous impression. (See, e.g., Ex. 5, pp. 1-6; Ex. 8, 

pp. 32-37; Ex. 19, pp. 1-35; Ex. 21, pp. 1-3.) 
7

was no significant disc disease or canal narrowing in the cervical or thoracic spine. (Id.) 

Thereafter, petitioner followed up with Dr. Samy on August 11, September 22, and 

December 14, 2017; and on February 23, May 25, and November 12, 2018, for CRON. 

(Ex. 19, pp. 13-39; Ex. 21, pp. 1-3.) During that time, petitioner experienced some 

improvement in his visual acuity and visual fields on prednisone and CellCept, and there 

was no recurrence of inflammation in the optic nerves. (Id.) Petitioner discontinued 

prednisone in February 2018 without a subsequent change in his vision. (Ex. 19, pp. 

34-35.) In his November 12, 2018, visit Dr. Samy remarked that petitioner developed 

“optic neuropathy [in] early 2017 which was post vaccination but in a pattern suggestive 

of possible ischemia in disc without cup followed by a few months later with the other 

eye.” (Ex. 21, p. 3.) “The clinical course of the optic neuropathy showed recurrences 

after tapering of the oral steroid which made the diagnosis CRION (chronic relapsing 

inflammatory optic neuropathy).” (Id.) Dr. Samy explained to petitioner he would need 

to taper off the CellCept and continue regular blood testing. (Id. at 4.) 

b. Petitioner’s affidavit 

On October 28, 2016, petitioner received a flu vaccine at his local Walgreens. 

(Ex. 16, p. 1.) Several weeks later, shortly after Thanksgiving, petitioner describes 

losing vision in his left eye, “[i]t started as a hazy halo around the outside of my left eye, 

which progressively closed in and led to a complete loss of vision in my left eye when I 

woke up on December 5, 2016.” (Id. at 1-2.) That day petitioner presented to an 

optometrist who sent him to the emergency room at Shands Hospital in Gainesville,

Florida. (Id. at 2.) He was discharged on December 6, 2016, and told to follow up with 

an ophthalmologist. (Id.) 

Petitioner returned to work soon after discharge. (Ex. 16, p. 2.) Petitioner avers 

that he was concerned that his employer would feel that he was unable to work due to 

his vision loss. (Id.) While on the job petitioner suffered a right thumb injury while 

operating a spring-loaded jack. (Id.) In January 2017, petitioner avers that he 

established care with ophthalmologist Dr. Hazem Samy. (Id. at 3.) Despite treatment 

petitioner asserts that he still had significant deficits in his vision in his left eye. (Id.) 

Subsequently petitioner began to experience vision issues in his right eye in 

March 2017. (Ex. 16, p. 3.) He avers that he was “more aware of what was occurring 

with [his] right eye,” so he immediately went to Dr. Samy’s office, where he saw Dr. 

Andres Gonzalez, who sent him directly to Shands Hospital to receive three days of IV 

steroid treatments. (Id.) Petitioner avers that following his onset of optic neuritis, his 

vision loss has been permanent. (Id.) He continued taking steroids to prevent further 

episodes, which caused additional health issues. (Id.) Petitioner describes taking 

Metformin, arnica (due to bruising that developed after taking steroids), vitamin B12 and 

CoQ10 supplements, and using an APAP machine. (Id.) 

Petitioner avers that his condition caused him to miss three to four weeks of 

work, and that he can no longer perform mechanic or welding work because of his 

difficulties with depth perception. (Ex. 16, pp. 3-4.) As a result, petitioner avers that he 
8

“need[s] to be much more cautious at work and [his] end product is not as good as it 

was prior to [his] vision loss.” (Id.) He asserts that he is unable to do his job to the best 

of his ability and is concerned about future employment. (Id.) 

Petitioner describes difficulty watching his daughter’s softball games and award 

ceremonies. (Ex. 16, p. 4.) His condition also impacts his ability to drive, especially at 

night. (Id. at 5.) He avers that he faces financial instability due to the medical bills he 

incurred during treatment. (Id.) Petitioner continues follow-up treatment with Dr. Samy 

every sixty to ninety days. (Id.) He avers that his vision has stabilized but has not 

improved. (Id. at 6.) Petitioner describes a small area of tunnel vision in the bottom 

right-hand corner of his left eye, a hazy halo around the outside of the eye, and a blind 

spot in the lower right-hand corner of his right eye. (Id.) 

IV. Summary of Expert Opinions 

a. Petitioner’s Experts 

i. Thomas R. Hedges, III, M.D.

Dr. Hedges received his medical degree from Tufts University. (Ex. 25.) He 

completed his residency in ophthalmology at Massachusetts Eye and Ear Infirmary at 

Harvard Medical School. (Id.) Dr. Hedges completed an ophthalmic pathology 

fellowship at that the Massachusetts Eye and Ear Infirmary at Harvard Medical School. 

(Id.) He subsequently completed a fellowship in neuro-ophthalmology at the University 

of California, San Francisco. (Id.) Dr. Hedges is board certified in ophthalmology. (Id.) 

He has served as an ophthalmologist at Tufts Medical Center since 1991. (Id.) He 

currently serves as a professor of ophthalmology and neurology at Tufts University. 

(Id.) His research interests include qualitative and quantitative evaluation of the retinal 

nerve fiber layer using photographic methods, computerized image enhancement, and 

Optical Coherence Tomography; Color Doppler imaging of orbital and extracranial blood 

vessels in vascular diseases affecting the eye; multifocal electroretinography and visual

evoked potential recording. (Id.) He has co-authored several works on optic and 

peripheral neuropathy. (Id.) 

Dr. Hedges opines that petitioner’s correct diagnosis is NAION. (Ex. 24, p. 1.) 

According to Dr. Hedges, anterior ischemic optic neuropathy is relatively common, but 

the exact pathogenesis is unknown. (Id. at 2.) It appears to be multifactorial, with 

various associations, but no one direct cause has been identified. (Id.) Dr. Hedges 

observes that petitioner has some of the associated risk factors, including hypertension 

and sleep apnea, but he stresses that “these are associations, not direct causative 

factors.” (Id.) Dr. Hedges opines that these risk factors combined with a physiologic

response to vaccination “pushed beyond normal function and past regulatory 

mechanisms, more likely than not, resulted in injury to [petitioner’s] optic nerves.” (Id.) 

He asserts that the most plausible mechanism is that of immune complex mediated 

vasculopathy/vasculitis, leading to inflammation and resultant ocular nerve injury. (Id.) 

This is a form of type Ill hypersensitivity whereby proteins contained in the vaccine 
9

stimulate an antibody reaction causing formation of antigen-antibody complexes, which 

can block small blood vessels or attach to the walls of small blood vessels stimulating 

inflammation and then blockage of the vessels leading to damage, in this case, to the 

optic nerve. (Id.) 

In support of his theory, Dr. Hedges observes that post-vaccination optic neuritis 

is well-documented in the medical literature and is believed to be similar to other 

instances of damage to other cranial nerves following vaccination, especially with 

regard to the seventh nerve (Bell’s) palsy following vaccination. (Ex. 24, p. 2 (citing 

Janaki Patel et al., Development of Optic Neuritis After Vaccination, a CDC/FDA 

Vaccine Adverse Event Reporting System (VAERS) Study, 1990-2017, 90 NEUROLOGY

1 (2018) (Ex. 26)).) Dr. Hedges cites four case reports of anterior ischemic neuropathy 

following vaccination. (Id.) In 1998, Kawasaki et al. reported two cases of anterior 

ischemic optic neuropathy following influenza vaccination. (Id. (citing Aki Kawasaki et 

al., Bilateral Anterior Ischemic Optic Neuropathy Following Influenza Vaccination, 18 J.

NEURO-OPHTHALMOLOGY 56 (1998) (Ex. 27)).) The authors postulated that an immune 

complex-mediated vasculopathy caused the optic nerve damage. (Id.) Next, Dr. 

Hedges cites Ray and Dreizin, who reported a case of a 61-year-old man with bilateral 

optic neuropathy “similar to [petitioner] who had some response to steroid treatment.” 

(Id. (citing Cheryl Ray & Ivy Dreizin, Bilateral Optic Neuropathy Associated with 

Influenza Vaccination, 16 J. NEURO-OPHTHALMOLOGY 182 (1996) (Ex. 28)).) Most 

recently, Manasseh et al. reported another case of bilateral sequential NAION following 

repeat influenza vaccination. (Id. (citing Gemma Manasseh et al., Bilateral Sequential 

Non-Arteritic Anterior Ischaemic Optic Neuropathy Following Repeat Influenza 

Vaccination, 5 CASE REP. OPHTHALMOLOGY 267 (2014) (Ex. 29)).) Like Kawasaki et al., 

the authors opined that immune complex vasculitis was a more likely mechanism than 

demyelination damaging the optic nerve. 

Regarding timing, Dr. Hedges opines that petitioner experienced onset of 

symptoms approximately 4.5 weeks post vaccination. (Ex. 24, p. 2.) He opines that this 

is an appropriate timeframe for symptom development because immune-mediated 

disorders typically develop within 6 to 8 weeks following a triggering event. (Id.) 

Moreover, Dr. Hedges represents that this is consistent with the timing of symptom 

onset in the case reports. (Id.) On average those patients experienced onset of NAION 

within one to four weeks post-flu vaccination. (Id.) 

In his supplemental report, Dr. Hedges opines that skin biopsies in patients with 

immune hypersensitivity reactions are “frequently normal, especially when performed 

months later.” (Ex. 30, p. 1.) Petitioner’s skin biopsy was performed in April 2017, over 

six months post-vaccination. (Id.) Respondent’s expert Dr. Wilson argues that a 

temporally proximate viral illness may have equally served as an infectious trigger for 

petitioner’s injury. (Ex. B.) In response, Dr. Hedges opines that any potential illness is 

ill-defined, and no viral or bacterial infection was ever identified. (Ex. 30, p. 1.) 

Furthermore, he stresses that upper respiratory infections are common, frequently 

coincidental and generally not considered to be associated with or causal of ON or 

NAION. (Id. at 1-2.) 
10

ii. Omid Akbari, Ph.D. 

Dr. Akbari received his Master of Science degree from the University College of 

London. (Ex. 32.) He received his Ph.D. in cellular and molecular immunology from the 

National Institute for Medical Research in London. (Id.) Dr. Akbari completed his 

postdoctoral fellowship at Stanford University. (Id.) He currently serves as a professor 

of Allergy and Immunology and professor of Medicine at Keck School of Medicine, 

University of Southern California. (Ex. 31.) Prior to that Dr. Akbari was an assistant 

professor at Harvard Medical School and held an appointment as senior scientist at 

Stanford University. (Id.) Dr. Akbari’s research is focused on the role of immune 

tolerance and how immune cells induce autoimmune and allergic diseases. (Id.) He 

has served on several NIH study sections, including special emphasis panel related to 

research in vaccine, infectious diseases, and immunology. (Id.) 

Regarding petitioner’s diagnosis, Dr. Akbari observed that “[t]he possibility of 

[optic neuritis] was not ruled out as some patients with ON are steroid refractory and do 

not exhibit demyelination in regular MRI scan.” (Ex. 31, p. 3.) He acknowledges that 

Dr. Hedges and Dr. Wilson have opined that petitioner may have atypical optic neuritis, 

though it is more likely that he suffers from NAION. (Id.) Still, in his expert report Dr. 

Akbari discusses how the flu vaccine can cause optic neuritis and/or vasculitis, leading 

to ischemic complications and optic nerve injury. (Id.) 

First Dr. Akbari proposes a theory of molecular mimicry, “which support[s] the 

notion and describe[s] how [the] influenza vaccine can induce immune responses, 

which are often associated with inflammation, vasculitis[,] and optic nerve injury.” (Ex. 

31, p. 6-8.) He cites two studies involving multiple sclerosis, neuromyelitis and 

demyelinating disease. (Id. at 6.) Markovic-Plese et al. proposed cross-reactivity of a 

CD4+ T-cell clone specific for the immunodominant influenza virus hemagglutinin 

peptide (sequence YVKQSTLKL) derived from a patient with neuromyelitis and 

demyelinating disease, including MS. (Silva Markovic-Plese et al., High Level of CrossReactivity in Influenza Virus Hemagglutinin-Specific CD4+ T Cell Response: 

Implications for the Initiation of Autoimmune Response in Multiple Sclerosis, 169 J.

NEUROIMMUNOLOGY 31 (2005) (Ex. 50)).) In another study by Harvard group 

Wucherpfennig et al., a panel of 129 peptides that matched the molecular mimicry motif 

was tested on seven specific T cell clones from patients with neuromyelitis and 

demyelinating disease. (Kai Wucherpfennig et al., Recognition of the Immunodominant 

Myelin Basic Protein Peptide by Autoantibodies and HLA-DR2-Restricted T Cell Clones 

from Multiple Sclerosis Patients, 100 J. CLIN. INVEST. 1114 (1997) (Ex. 54)).) Seven viral 

and one bacterial peptide efficiently activated three of these clones. (Id.) From these 

studies Dr. Akbari proposes that the influenza vaccine petitioner received “contains a 

protein that cross-reacts with myelin based antigens in humans who had demyelinating 

disease.” (Ex. 31, p. 6.) Dr. Akbari draws support for this theory from studies showing 

that self-reactive T cells were also shown to cause optic neuritis in both rat models and 

non-human primates. (Id. (citing F.X. Weilbach et al., T-Cell Receptor V Beta-Element 

Expression in Peripheral Nerves of Lewis Rats Suffering from Experimental 

Autoimmune Neuritis, 79 J. NEUROIMMUNOL. 69 (1997) (Ex. 52); Jeffrey Bajramovic et 
11

al., Oligodendrocyte-Specific Protein Is Encephalitogenic in Rhesus Macaques and 

Induces Specific Demyelination of the Optic Nerve, 38 EUR. J. IMMUNOL. 1452 (2008) 

(Ex. 53)).) Alternatively, Dr. Akbari proposes another peptide to the major protein in the 

myelin sheath known as myelin basic protein in the influenza A vaccines. (Ex. 31, p. 7.) 

The amino acid sequence, FYKNLI, has high homology to myelin basic protein FFKNIV. 

(Id.) He explains that the only variations are one aromatic amino acid “f” for “y” and two 

aliphatic amino acids, leucine and isoleucine. (Id.) This, according to Dr. Akbari, is an 

undeniable example of molecular mimicry with influenza A strains that appear in the 

vaccine petitioner received. 

Dr. Akbari explains that NAION is the most common form of ischemic optic 

neuropathy and the second most common form of optic neuropathy. (Ex. 31, p. 7.) He 

writes, “[i]t is presumed to be due to a transient disruption in the circulation of the optic 

nerve head leading to hypoperfusion and ischemia.” (Id.) Several hypotheses have 

been proposed including generalized hypoperfusion, nocturnal hypotension, local 

autoregulation failure, vasospasm, venous inflammation, vasculitis and thrombosis. (Id.

(citing Shauna Berry et al., Nonarteritic Anterior Ischemic Optic Neuropathy: Cause, 

Effect, and Management, 9 EYE & BRAIN 23 (2017) (Ex. 56)).) Although rare, Dr. Akbari 

opines that vasculitis has been reported as an adverse event following influenza 

vaccination. (Id.) Among 45 published reports, Watanabe identified 65 patients who

developed vasculitis after influenza vaccination. (Id. (citing Toru Watanabe, Vasculitis 

Following Influenza Vaccination: A Review of Literature, 13 CURR. RHEUMATOL. REV. 188 

(2017) (Ex. 57)).) Hadden et al. also reported several case reports with vasculitic

neuropathy after influenza vaccination. (Id. (citing Robert Hadden et al., Vasculitic 

Peripheral Neuropathy: Case Definition and Guidelines for Collection, Analysis, and 

Presentation of Immunization Safety Data, 35 VACCINE 1567 (2017) (Ex. 58)).) Still

other investigators also reported cases associating flu vaccination with optic

neuropathy. (Id. (citing Emily Li & Adeniyi Fisayo, Bilateral Reversible Optic Neuropathy 

After Influenza Vaccination, 39 J. NEURO-OPHTHALMOL. 496 (2019) (Ex. 59); Kawasaki et 

al., supra, at Ex. 27 (also filed as Ex. 60)).) 

Dr. Akbari further opines that cytokines may also play a role in inducing 

vasculitis. (Ex. 31, p. 8.) He observes that Song et al. published a meta-analysis to 

investigate possible associations between IL-1ɑ, IL-1β, and IL-1 receptor antagonist 

(IL1RN) polymorphisms and vasculitis. (Id. (citing Song et al., Associations Between 

Interleukin-1 Polymorphisms and Susceptibility to Vasculitis: A Meta-Analysis, 75 Z.

RHEUMATOL. 406 (2016) (Ex. 67)).) According to Dr. Akbari, the results strongly suggest 

that IL-1 polymorphism is associated with susceptibility to vasculitis. (Id.) Besides the

IL-1 cytokine family, Dr. Akbari identifies other pro-inflammatory cytokines such as IL-6 

which were associated with a strong ability to polarize immune cells to produce IL-17 

and induce vasculitis and optic neuropathy. (Id. (citing Hajime Yoshifjui, 

Pathophysiology of Large Vessel Vasculitis and Utility of Interleukin-6 Inhibition 

Therapy, 29 MODERN RHEUMATOL. 287 (2019) (Ex. 68)).) Since these cytokines are 

“potent stimulators of adaptive responses,” Dr. Akbari concludes that the inflammasome 

is likely a primary target causing vascular inflammation. (Id. (citing G.A. Ramirez et al., 
12

Intravascular Immunity as a Key to Systemic Vasculitis: A Work in Progress, Gaining 

Momentum, 175 CLIN. EXP. IMMUNOL. 150 (2014) (Ex. 69)).) 

Still further, Dr. Akbari proposes a mechanism involving T cell dysfunction. (Ex. 

31, pp. 8-9.) He opines that the influenza vaccine has been shown to stimulate 

regulatory T cells and T effector cells in normal individuals post-vaccination. (Id. at 9.) 

A balance in the levels of regulatory T cells and T effector cells maintains the

homeostatic and disease-free state. (Id.) A shift in the balance towards T regulatory 

cells causes a decrease in anti-cancer immunity, resulting in cancer. (Id.) In contrast, a 

shift in the balance towards T effector cells causes a decrease in T regulatory cell levels 

and T effector cells hyperactivation—leading to autoimmune disorders, such as optic

neuropathy. (Id.) In petitioner’s case, Dr. Akbari proposes pathogenic T effector cells 

caused injury directly to the nerve or, alternatively, caused inflammation in the vascular 

system that resulted in optic nerve injury—simply due to T regulatory cells. (Id. (citing 

Huabin Zheng et al., Increased Th17 Cells and IL-17 in Rats with Traumatic Optic 

Neuropathy, 10 MOL. MED. REP. 1954 (2014) (Ex. 48); Shin-Min Wang et al., The 

Regulatory T Cells in Antiinfluenza Antibody Response Post Influenza Vaccination, 8 

HUM. VACCIN. IMMUNOTHER. 1243 (2012) (Ex. 71); Thi Hong Khanh Vu et al., CD4(+) TCell Responses Mediate Progressive Neurodegeneration in Experimental Ischemic 

Retinopathy, 190 AM. J. PATHOL. 1723 (2020) (Ex. 72)).) Moreover, Dr. Akbari cites a 

cohort study of elderly patients who received the flu vaccine who demonstrated only a 

limited responsiveness to the vaccine, but a higher inflammatory status. (Ex. 31, p. 9 

(citing I. Herrero-Fernandez et al., Effect of Homeostatic T-Cell Proliferation in the 

Vaccine Responsiveness Against Influenza in Elderly People, 16 IMMUNITY & AGEING 1 

(2019) (Ex. 73)).) Dr. Akbari concludes that T regulatory cells post-flu vaccination “may 

trigger autoimmune diseases such as optic associated inflammation result[ing] in 

neuropathies in some individuals.”

Lastly, Dr. Akbari opines that host susceptibility to the development of optic 

neuropathy is one of the most important factors in the development of the disease—and 

independent of the initiating pathologic cause. (Ex. 31, p. 9.) Specifically, he points to 

animal models, one using rodents and one using primates, of NAION that demonstrate 

the role of immune cells in creating inflammation leading to ocular damage. (Id. at 10-

11 (citing Steven Bernstein et al., Functional and Cellular Responses in a Novel Rodent 

Model of Anterior Ischemic Optic Neuropathy, 44 INVEST. OPTHALMOL. VIS. SCI. 4153 

(2003) (Ex. 78); Celia Chen et al., A Primate Model of Nonarteritic Anterior Ischemic 

Optic Neuropathy, 49 INVEST. OPHTHALMOL. VIS. SCI. 2985 (2008) (Ex. 79)).) Dr. Akbari 

acknowledges that these animal models have been criticized as not reflecting the true 

NAION because the experimental ischemic lesions are induced primarily in the 

intraretinal region of the central retinal artery circulation, rather than in the deeper 

posterior ciliary artery circulation. (See id.) While a model of the optic nerve injury that 

includes ON and NAION with conformity to the features of the human disease has yet to

be created, Dr. Akbari stresses that “the cooperation between immune cells causing 

inflammation suggests it is likely that [the] genetic background of the host is a critical 

component to the pathogenesis of optic neuritis and NAION.” (Id. at 11.) 
13

b. Respondent’s Expert, Michael Wilson, M.D., MAS

Dr. Wilson received his medical degree from the University of California, San 

Francisco School of Medicine. (Ex. C.) He completed his residency in neurology at the 

Harvard Neurology Residency Program at Massachusetts General Hospital and

Brigham and Women's Hospital. (Id.) Dr. Wilson completed his clinical fellowship in 

neuro-infectious diseases at Massachusetts General Hospital. (Id.) Subsequently, he 

completed postdoctoral fellowships in neurovirology and metagenomics. (Id.) Dr. 

Wilson received his Master of Applied Science degree from the University of California, 

San Francisco. (Id.) He is a board-certified neurologist with subspecialty training in 

neuro-infectious diseases and neuroimmunology. (Ex. B, p. 1.) He serves as an 

associate professor of Neurology at UCSF in the Division of Neuroimmunology and Glial 

Biology and is a Principal Investigator of a lab “that has pioneered the development of 

metagenomic next-generation sequencing to diagnose neurologic infections in patients 

with meningitis, encephalitis and other neuroinflammatory conditions.” (Id.) He has coauthored three New England Journal of Medicine publications and multiple publications 

in other top peer-reviewed journals. (Id.) In addition, his lab has developed

comprehensive autoantibody and viral antibody discovery assays to search for antigenic 

targets and triggers of neuroinflammatory diseases, including multiple sclerosis and 

autoimmune encephalitis. (Id.) Dr. Wilson’s research is funded by the National 

Institutes of Health, the National Multiple Sclerosis Society as well as several private

foundations. (Id.) 

Dr. Wilson agrees that “it is not clear that [petitioner’s] clinical presentation was

consistent with optic neuritis.” (Ex. B, p. 4.) Dr. Wilson opines that “sequential NAION 

is a more likely diagnosis.” (Id. at 5.) He summarizes, “[t]he petitioner’s expert and I 

are in agreement that although optic neuritis cannot be completely excluded, the weight 

of the evidence favors the alternate diagnosis entertained by [petitioner’s] treating

physicians,” NAION. (Ex. D, p. 1.) 

Although Dr. Hedges opines that an immune complex vasculitis triggered by the 

influenza vaccine led to ischemic complications, Dr. Wilson stresses that petitioner’s 

skin biopsy showed no clear evidence of vasculitis. (Ex. B, p. 4.) Moreover, Dr. Wilson 

observes that there is no record of a fluorescein angiogram to look for evidence of 

vasculitis in the retina, and systemic markers commonly associated with immune 

complex deposition, such as complement levels, are not available. (Id.) 

Dr. Wilson also distinguishes petitioner’s case from the case reports cited by Dr. 

Hedges. (Ex. B, p. 4.) Dr. Wilson stresses that the case reports of bilateral NAION 

cited by Dr. Hedges occurred sequentially after two separate influenza vaccinations 

whereas petitioner’s bilateral optic nerve injury occurred after a single vaccination. (Id.

(citing Manasseh et al., supra, at Ex. 29).) Both patients reported in Kawasaki et al. had 

eye pain which Dr. Wilson opines is more consistent with an optic neuritis than NAION. 

(Id. (citing Kawasaki et al., supra, at Ex. 27).) Moreover, the second case report by 

Kawasaki et al., had a coincident febrile systemic illness suggesting that in addition to 

the vaccination the patient also had an acute infection. (Id.) Lastly, the two cases 
14

described in Kawasaki and the case reported by Ray and Dreizin had bilateral vision 

loss either occur simultaneously or within days of each other whereas petitioner’s vision 

loss was truly sequential with his right eye becoming symptomatic only 2 months after 

the symptoms appeared in the left eye. (Ex. B, pp. 4-5.) According to Dr. Wilson “[i]t is 

this aspect of [petitioner’s] case – the progressive and evolving illness over multiple 

months – that is importantly inconsistent with the short-lived, monophasic inflammatory 

reactions like optic neuritis and Guillain-Barré syndrome that are typically associated 

with vaccine complications.” (Ex. D, p. 1.) 

Dr. Wilson agrees that symptom onset 4 weeks post-vaccination is within the 

time window for post-vaccination syndromes. (Ex. B, p. 5.) However, Dr. Wilson 

contends that petitioner had a viral upper respiratory tract infection (“URI”) even more 

proximate temporally to the onset of his vision symptoms. (Id.) He opines that there is 

no evidence suggesting that an influenza vaccination would be any more likely to trigger 

this process than a viral URI. (Id.) Moreover, he stresses that petitioner had a number 

of non-inflammatory risk factors for NAION. (Ex. D, p. 2.) 

In response to Dr. Akbari, Dr. Wilson acknowledges that scientific literature might 

support the theory that rare immune responses to vaccination(s) can cause vascular 

inflammation. (Ex. E, p. 1.) However, he again stresses that petitioner’s skin biopsy 

showed no clear evidence of vasculitis, nor are there any other results demonstrating an 

immune complex deposition. (Id.) Dr. Wilson suggests that petitioner’s poor clinical 

response to a variety of immunosuppressive agents argues against his condition as 

having a significant inflammatory component as well. (Id. at 2.) 

Dr. Akbari relies on literature demonstrating the association between nonvasculitic, demyelinating complications (e.g., optic neuritis) and influenza vaccination. 

In response, Dr. Wilson stresses that although petitioner’s doctors reasonably 

speculated at various stages of his illness that optic neuritis was a diagnostic possibility, 

he continues to agree with petitioner’s treating physicians that the evidence favors the 

alternate diagnosis of NAION. (Ex. E, p. 2.) 

V. Discussion 

a. Diagnosis 

“The function of a special master is not to ‘diagnose’ vaccine-related injuries, but

instead to determine ‘based on the record as a whole and the totality of the case,

whether it has been shown by a preponderance of the evidence that a vaccine caused

the [petitioner]’s injury.’” Andreu v. Sec’y of Health & Human Servs., 569 F.3d 1367,

1382 (Fed. Cir. 2009) (quoting Knudsen v. Sec’y of Health & Human Servs., 35 F.3d

543, 549 (Fed. Cir. 1994)). “Although the Vaccine Act does not require absolute

precision, it does require the petitioner to establish an injury – the Act specifically

creates a claim for compensation for ‘vaccine-related injury or death.’” Stillwell v. Sec’y

of Health & Human Servs., 118 Fed. Cl. 47, 56 (2014) (quoting 42.U.S.C. § 300aa11(c)). Accordingly, the Federal Circuit has concluded that it is “appropriate for the
15

special master to first determine what injury, if any, [is] supported by the evidence

presented in the record before applying the Althen test to determine causation.” 

Lombardi v. Sec’y of Health & Human Servs., 656 F.3d 1343, 1351-53 (Fed. Cir. 2011).

As noted during my prior Rule 5 conference, there was some uncertainty among 

petitioner’s treating physicians as to petitioner’s correct diagnosis – in particular optic

neuritis versus NAION. (ECF No. 50.) In that regard, petitioner’s motion for a ruling on 

the record includes some argumentation in his opening brief addressing optic neuritis. 

(ECF No. 65, pp. 29-30 n.16 (medical literature demonstrating a connection between 

vaccination and optic neuritis).) Additionally, petitioner suggests “should the Court find 

an expanded Althen analysis applied to the development of optic neuritis helpful to its 

consideration of petitioner’s claim, petitioner can comply with such a request in his reply 

brief.” (Id. at 29 n.15.) Such an expanded analysis is not warranted, however, because 

there is preponderant evidence on this record that petitioner suffered NAION. In fact, 

both parties have sections addressing diagnosis in their respective briefs in which they 

both explicitly confirm there is no dispute as to diagnosis – that diagnosis being NAION. 

(Id. at 27-29; ECF No. 66, p. 7.) 

While petitioner’s treating physicians were not definitive in their diagnosis, among 

the expert opinions offered in this case, both parties’ experts agree that petitioner’s 

correct diagnosis is NAION. (Ex. 30, p. 1; Ex. 31, p. 3; Ex. D, p. 1.) According to Dr. 

Hedges, NAION and optic neuritis have “overlapping clinical profiles.” (Ex. 30, p. 1.) 

However, Dr. Hedges concludes on petitioner’s behalf that petitioner suffers from an 

atypical presentation of NAION. (Ex. 24, p. 2.) Additionally, Dr. Wilson opines for 

respondent “petitioner’s expert and I are in agreement that although optic neuritis 

cannot be completely excluded, the weight of the evidence favors the alternate 

diagnosis entered by [petitioner’s] treating physicians,” NAION. (Ex. D, p. 1.) Dr. Akbari 

noted that the possibility of optic neuritis was not ruled out, but likewise accepted the 

NAION diagnosis. (Ex. 31, pp. 1, 3.)

Importantly, the literature makes clear that optic neuritis and NAION are not the 

same condition and do not have the same etiology—NAION is ischemic / vascular 

rather than demyelinating. (Chen et al., supra, at Ex. 79, p. 1 (NAION “is an optic nerve 

(ON) stroke and a leading cause of sudden ON-related vision loss”).) NAION is 

presumed to be due a transient disruption in the circulation of the optic nerve head 

leading to hypoperfusion and ischemia. (Berry et al., supra, at Ex. 56, p. 24.) The 

transient disruption is thought to be caused by generalized hypoperfusion, nocturnal 

hypotension, local autoregulation failure, vasospasm, venous occlusion, or thrombosis, 

though the exact cause remains unclear. (Id.) Still other patients are thought to be 

predisposed to NAION because of their small cup-to-disc ratio, or “crowded optic disk 

head.” (Id.) When localized swelling occurs in a fixed space anterior to the rigid lamina 

cribosa, Barry et al. explain that the capillaries could become more easily compressed 

and secondary ischemia may result. (Id.) Systemic diseases, such as hypertension, 

diabetes, and hypercholesterolemia can cause decreased perfusion to the optic nerve 

head, secondary to microvascular compromise that puts individuals with these diseases 

at risk of NAION. (Id.) Dr. Wilson also draws this distinction between optic neuritis and 
16

NAION in his report. (Ex. E, p. 2 (optic neuritis is “a non-vasculitic, demyelinating 

complication[]” unlike NAION).) 

Prior cases in the Vaccine Program where petitioners have alleged vaccinecaused optic neuritis have addressed causation in terms of autoimmune demyelination. 

Reinhardt v. Sec’y of Health & Human Servs., No. 17-1257V, 2021 WL 1851491, at *16 

(Fed. Cl. Spec. Mstr. Apr. 2, 2021); Althen v. Sec’y of Health & Human Servs., 58 Fed. 

Cl. 270, 285 (2003) (recognizing that optic neuritis represents a central demyelinating 

disease of the optic nerve and is not a “vasculitis” illness), aff’d, 418 F.3d 1274 (Fed. 

Cir. 2005). However, even setting aside a specific diagnosis, petitioner in this case 

exhibited no evidence of demyelination on MRI. (Ex. 3, pp. 52-55.) Moreover, given the 

record as a whole, the evidence favors the diagnosis of NAION entertained by 

petitioner’s treating physicians and favored by both parties’ experts, including most 

notably petitioner’s own expert in neuro-ophthalmology. This points to a different 

underlying disease process. Thus, the fact that petitioner’s NAION is preponderantly 

established does affect the resulting Althen analysis.4

b. Althen prong one 

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, petitioner’s theory must 

be based on a “sound and reliable medical or scientific explanation.” Knudsen v. Sec’y 

of Health & Human Servs., 35 F.3d 543, 548 (Fed. Cir. 1994). Such a theory must only 

be “legally probable, not medically or scientifically certain.” Id. at 549. However, 

petitioners may satisfy the first Althen prong without resort to medical literature, 

epidemiological studies, demonstration of a specific mechanism, or a generally 

accepted medical theory. Andreu v. Sec’y of Health & Human Servs., 569 F.3d 1367, 

1378-79 (Fed. Cir. 2009) (citing Capizzano v. Sec’y of Health & Human Servs., 440 

F.3d 1317, 1325-26 (Fed. Cir. 2006)). 

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 

4 For example: In Katz v. Secretary of Health & Human Services, petitioner alleged that he suffered optic 

neuritis caused in fact by his hepatitis B vaccination. No. 04-714V, 2005 WL 6117659 (Fed. Cl. Spec. 

Mstr. Nov. 30, 2005). Petitioner’s first expert proposed a diagnosis of optic neuritis, which was disputed

by respondent’s expert, who advocated an alternate diagnosis of ischemic optic neuropathy. Id. at *6. 

The special master found that petitioner more likely than not suffered from a non-demyelinating 

inflammatory optic neuritis. Id. at *18. Petitioner’s expert was charged with explaining how petitioner's 

hepatitis B vaccination can cause and did cause her optic neuritis. Id. He offered the molecular mimicry 

theory to explain how the vaccine might have caused the production of antibodies, which then attacked 

healthy tissue. Id. However, the molecular mimicry theory proposed by Dr. Waisbren relied upon a 

similarity between a substance in the hep B vaccine and the myelin of the human nervous system. Id. 

The fatal flaw with this proposed mechanism was that petitioner exhibited no evidence of demyelination. 

Id. Without any evidence of demyelination, the special master found that “Dr. Waisbren's molecular 

mimicry proposal is of no use to explain how the hepatitis B vaccine may have caused petitioner’s optic 

neuritis. Dr. Stivelman's diagnosis and Dr. Waisbren's theory of causation are mismatched.” Id. 
17

preponderant evidence standard.” Id. at 1380. Accordingly, special masters must take 

care not to increase the burden placed on petitioners in offering a scientific theory 

linking vaccine to injury. Contreras v. Sec’y of Health & Human Servs., 121 Fed. Cl. 

230, 245 (2015) (“Plausibility . . . in many cases may be enough to satisfy Althen prong 

one.”). But this does not negate or reduce a petitioner’s ultimate burden to establish his 

entitlement to damages by preponderant evidence. W.C. v. Sec’y of Health & Human 

Servs., 704 F.3d 1352, 1356 (Fed. Cir. 2013) (citations omitted). Nonetheless, although 

petitioners cannot be required to show “epidemiologic studies, rechallenge, the 

presence of pathological markers or genetic disposition, or general acceptance in the 

scientific or medical communities to establish a logical sequence of cause and effect” 

(Capizzano, 440 F.3d at 1325), the special master may consider and evaluate such 

evidence when filed. Andreu, 569 F.3d at 1379 (special masters may consider medical 

literature and epidemiological evidence, when it is submitted, in “reaching an informed 

judgment as to whether a particular vaccine likely caused a particular injury”). 

Petitioner’s theory derives primarily from Dr. Akbari while Dr. Hedges principally

relied on case reports. (Ex. 31, pp. 6-10; Ex. 24, p. 2.) Dr. Akbari proposes several 

theories ranging from molecular mimicry to vaccine-induced vasculitis to T-cell 

dysfunction. (Ex. 31, pp. 6-10.) However, as explained above, given that petitioner’s 

NAION is preponderantly established, Dr. Akbari’s extended discussion of 

demyelinating optic neuritis is irrelevant. On the whole, the literature filed in this case

supports that NAION is likely due to a stroke-like mechanism affecting blood supply to 

the retina. (Chen et al., supra, at Ex. 79; Berry et al., supra, at Ex. 56; A.H. Ropper et 

al., eds. Chapter 12: Disturbances of Vision, in VICTOR’S PRINCIPLES OF NEUROLOGY

(11th ed. 2019) (Ex. B, Tab 2); D. Vaughan et al., eds. Chapter 14: NeuroOphthalmology, in VAUGHAN & ASHBURY’S GENERAL OPHTHALMOLOGY (19th ed. 2004) 

(Ex. B, Tab 3); Nathan Kerr et al., Non-Arteritic Anterior Ischaemic Optic Neuropathy: A

Review and Update: 16 J. CLIN. NEUROSCIENCE 994 (2009) (Ex. B, Tab 4).) 

Both of petitioner’s experts acknowledge that the pathophysiology of NAION is 

unknown. (Ex. 24, p. 3; Ex. 31, p. 8.) However, as the name suggests, both 

acknowledge that it results from ischemia. (Ex. 30, p. 1; Ex. 31, p. 8.) Dr. Akbari

supports ischemia as underlying cause of NAION based on a number of publications, 

including experimental animal models. (Ex. 31 (citing Berry et al., supra, at Ex. 56; 

Khanh et al., supra, at Ex. 72; Chen et al., supra, at Ex. 79).) Notably, however, the 

animal models do not themselves include any studies examining vaccine-causation. 

(Khanh et al., supra, at Ex. 72; Bernstein et al., supra, at Ex. 78; Chen et al., supra, at 

Ex. 79; Hayreh, supra, at Ex. 80.) Moreover, gaps in petitioner’s theory are further 

drawn out in Dr. Akbari’s own concession that the animal models of NAION that he 

relies on “have been criticized as not reflecting true NAION.” (Ex. 31, pp. 7, 10-11; see

also Chen et al., supra, at Ex. 79; Hayreh, supra, at Ex. 80.) Additionally, in both Khanh 

et al. and Chen et al., the authors discuss how the retinal injury itself recruits 

inflammation to the eye in NAION. (Khanh, supra, at Ex. 72, p. 1732; Chen et al., 

supra, at Ex. 79, p. 7 (“the inflammation can cause increased tissue destruction, edema, 

and compression of adjacent vessels and axons, resulting in further loss of visual 

sensory function and decreasing the likelihood of significant visual recovery”).) This 
18

complicates any discussion of inflammation associated with NAION as being part of the 

etiology of the condition as opposed to a consequence of the condition. 

Dr. Akbari’s resulting theory otherwise turns largely on his broader discussion of 

post-vaccination vasculitis. (Ex. 31, pp. 7-8.) Importantly, however, not all vasculitides 

are the same. The vasculitides are a heterogenous group of disorders associated with 

organ dysfunction caused by inflammatory disease of blood vessels. (Hadden et al., 

supra, at Ex. 58, p. 1567.) The various clinical manifestations of different vasculitides 

depend on local immunologic environments, tissue vulnerabilities, and blood flow 

distributions. (Id.) Systemic vasculitis involves multiple organs and tissues, whereas in 

some patients, vasculitis is restricted to a single organ or tissue. (Id.) Thus, while Dr. 

Wilson conceded on respondent’s behalf that “the scientific literature might support this 

general assertion about rare maladaptive immune responses to vaccinations causing 

vascular inflammation” (Ex. E, p. 1 (emphasis removed)), he was clear in opining that 

the fact that the flu vaccine might be capable of causing vasculitis in some contexts is 

not in itself evidence that it causes NAION.5 (Id.) Rather, Dr. Wilson stresses that 

NAION is of unknown pathogenesis. (Id. at 1-2.) Examining the vasculitide literature 

relied upon by Dr. Akbari, he is not persuasive in linking vaccines to NAION. 

Watanabe et al. (2017), sought reports of vasculitides following influenza 

vaccination. (Watanabe et al., supra, at Ex. 57.) Among 45 published reports the 

authors identified 65 patients. (Id. at 189.) As the study makes clear, not all forms of 

vasculitis have the same consequences. The authors divided the vasculitides of total 

cases into six major categories according to the predominant size of the vessel involved 

(large vessel, medium vessel, and small vessel vasculitis), single organ-involved 

vasculitis compared to systemic disease (rheumatoid vasculitis), and finally vasculitis 

associated with a probable etiology (HBV-associated vasculitis). (Id.) The small vessel 

vasculitides were further subdivided to ANCA-associated vasculitis, immune complex 

vasculitis, and unclassified. (Id.) The most frequently reported symptom was skin rash 

(37/57), followed by arthralgia or arthritis (31/57), fever (20/57) and malaise (15/57). 

(Id.) Unsurprisingly, the highest reported involved organ was skin (37/57), followed by 

joints (31/57), kidney (24/57), muscle (16/57), gastrointestinal tract (13/57), lung (10/57),

peripheral nervous system (7/57), eye (8/57), central nervous system (7/57), and nose 

or mouth (3/57). (Id.) Dr. Akbari relies on this paper for the proposition that there were 

eight reports of ocular involvement. (Ex. 31, p. 7.) However, the eight cases he cites

5 Special masters have likewise distinguished between different vasculitides in prior cases. See Kelly v. 

Sec’y of Health & Human Servs., No. 17-1475V, slip op. (Fed. Cl. Spec. Mstr. Oct. 12, 2022) 

(distinguishing polymyalgia rheumatica and giant cell arteritis); Suliman v. Sec’y of Health & Human 

Servs., No. 13-993V, 2018 WL 6803697 (Fed. Cl. Spec. Mstr. Nov. 27, 2018) (same); see also Temes v. 

Sec’y of Health & Human Servs., No.16-1465V, 2020 WL 4198036 at *19-20 (Fed. Cl. Spec. Mstr. May 

12, 2020) (distinguishing cryoglobulinemia and leukocytoclastic vasculitis); Schultz v. Sec’y of Health & 

Human Servs., No. 16-539V, 2020 WL 1039161, at *7 (Fed. Cl. Spec. Mstr. Jan. 24, 2020) (criticizing Dr. 

Shoenfeld’s opinion, in part, for conflating petitioner’s stroke with vasculitis); Guzman v. Sec’y of Health & 

Human Servs., No. 15-736V, 2019 WL 2723392, at *20 (Fed. Cl. Spec. Mstr. May 14, 2019) 

(distinguishing cutaneous vasculitis and chronic urticaria).
19

occurred in the context of ANCA-associated vasculitis, a broader systemic vasculitis.6

(Watanabe et al., supra, at Ex. 57, p. 191.) That is not analogous to NAION. Only five 

cases overall involved single organ vasculitis and of those only one involved retinal 

arteritis. (Id.) None involved ischemic optic neuropathy, either arteritic or nonarteritic. 

(See id.) There was no indication that any particular vasculitis demonstrated a higher 

probability of vaccine-causation, though the most common type of vasculitis was small 

vessel vasculitis—somehow leading the authors to conclude that caution should be 

required for patients with small vessel vasculitis (in particular those with ANCAassociated or reactivated-IgAV vasculitis). (Id. at 193-94.) Among all the reported postinfluenza vaccination vasculitides, Watanabe et al. concluded that the majority of 

studies did not find a causal association between vaccination and subsequent 

development of vasculitis. (Id. at 193.) 

Hadden et al. (2017), reviewed twelve case reports proposing a possible 

association of vasculitis with previous immunization. (Hadden et al., supra, at Ex. 58, p. 

1568.) Dr. Akbari cites this article presumably for the six cases reported post influenza 

vaccination. (Id.) However, this paper addresses the case definition and analysis for 

vasculitic peripheral neuropathy. (Id.) NAION is specifically identified as a CNS 

condition.7 (Chen et al., supra, at Ex. 79, p. 2.) Vasculitic peripheral neuropathy 

typically manifests as an asymmetric neuropathy resulting from ischemic axonal injury. 

(Hadden et al., supra, at Ex. 58, p. 1567.) Unlike NAION, vasculitic neuropathies 

typically manifest with subacute stepwise progression or progressive worsening, 

although some patients exhibit more insidious chronic progression over many years. 

(Id. at 1568.) Even setting aside this distinction, Hadden et al. concluded that no causal 

relationship existed between immunization and systemic or nonsystemic (single-organ)

vasculitic neuropathy has been established. (Id.)

Given the above, Dr. Akbari ultimately concludes only that “the scientific research 

supports the assertion that stimulation of the immune system following vaccinations is a 

plausible medical theory causally linking the influenza vaccination with the development 

of vasculitis and inflammation that resulted in symptoms in [petitioner] including optic 

neuropathy and vision loss.” (Ex. 31, p. 10 (emphasis added).) Given that Dr. Akbari 

has only opined that petitioner’s medical theory is “plausible,” his opinion less helpful to 

petitioner in meeting his legal burden. See, e.g., Boatmon v. Sec’y of Health & Human 

Servs., 941 F.3d 1351, 1360 (Fed. Cir. 2019) (citing Moberly v. Sec’y of Health & 

Human Servs., 592 F.3d 1315, 1322 (Fed. Cir. 2010)) (reaffirming that a “plausible” or 

“possible” causal theory does not satisfy a petitioner’s burden). 

6 ANCA-associated vasculitides are a subgroup of small vessel vasculitis in which there are circulating 

antineutrophil cytoplasmic autoantibodies (ANCA). ANCA-associated vasculitis, DORLAND’S MEDICAL 

DICTIONARY ONLINE, https://www.dorlandsonline.com/dorland/definition?id=116898 (last accessed Nov. 9, 

2022). 

7 NAION is an isolated infarct of the anterior optic nerve—the optic nerve “is a central nervous system 

(CNS) tract composed of retinal ganglion cell (RGC) axons that synapse in the lateral geniculate nuclei.” 

(Chen et al., supra, at Ex. 79, p. 2.) 
20

The remaining supporting evidence consists of case reports. Ray and Dreizin 

(1996) reported a 61-year-old woman who developed progressive visual loss in both 

eyes within three weeks following influenza vaccination. (Ray & Dreizin, supra, at Ex. 

28.) Among the possible causes, the authors note the strong possibility of temporal 

arteritis, given the patient’s age. (Id. at 183.) Temporal arteritis was ruled out, however, 

given the patient had no jaw claudication, headaches, fevers, or myalgias, or 

arthralgias. (Id.) Two separate sedimentation rates were normal and both temporal

artery biopsies were negative. (Id.) Other ischemic causes such as small vessel 

disease associated with hypertensive disease were reportedly considered, however, the 

authors indicated that “these rarely occur in both eyes simultaneously, and the patient

[here] was healthy.” (Id. at 183-84.) A compressive mass or infiltrative tumor was 

excluded on MRI and by the normal histopathology of the optic nerve sheath. (Id. at

184.) Laboratory tests also ruled out meningeal carcinomatosis, sarcoid, Lyme disease, 

Leber’s optic neuropathy, and systemic lupus. (Id.) A heavy metal screening revealed 

elevated mercury—and while mercury has been reportedly associated with peripheral 

neuropathies and cerebellar symptoms, the authors stress that it has not been causally 

associated with optic neuropathies. (Id.) The authors stress that optic neuropathy is a 

diagnosis of exclusion. (Id.) While Ray and Dreizin suggest it is possible their patient’s 

abrupt onset of bilateral vision loss was caused by the influenza vaccine, the authors 

acknowledge several caveats. (Id.) First, optic neuropathy does not follow influenza 

vaccination as often as acute inflammatory demyelinating polyneuropathy (GBS). (Id.) 

While the patient’s visual recovery coincided with restarting steroids—the authors 

question: “Was her recovery due just to time or was it from the combined use of 

prednisone, or from the prednisone alone?” (Id.) Lastly, the authors note that their 

patient underwent a left optic nerve sheath fenestration (“ONSF”) at the time she 

restarted prednisone—“which too may have played a role in her recovery.” (Id.) 

Kawasaki et al. (1998), reported two cases of anterior ischemic optic neuropathy 

following influenza vaccination. (Kawasaki et al., supra, at Ex. 27.) The first case was a 

47-year-old woman who complained of decreased vision in her right eye one week after 

her influenza vaccination—associated with transient eye pain. (Id. at 56.) Five days 

later she developed blurriness in the left eye. (Id.) The patient demonstrated 

moderately edematous optic discs with splinter hemorrhages and cotton-wool spots. 

(Id.) Her laboratory tests were largely normal. (Id.) She was treated with prednisone 

and subsequently developed segmental disc atrophy—the results of her examination 

remained unchanged at one year. (Id.) The second case involved a 51-year-old 

woman who became febrile with chills and myalgias one-day post vaccination. (Id.) 

These symptoms resolved over three weeks. (Id.) Four weeks later, she complained of 

ear pain, headache, and blurry vision—first in her right eye then in her left eye. (Id.) 

Both optic discs were edematous. (Id.) Despite IV methylprednisolone, her vision 

progressively worsened over several weeks. (Id.) Lab tests were all normal except for 

disc edema. (Id.) Her visual function was unchanged at two months, and bilateral optic 

disc atrophy had developed. (Id. at 57.) The authors proposed two possible 

mechanisms for the lack of visual recovery, either (1) an allergic cross-reaction to viral 

antigens stimulating optic nerve inflammation and demyelination severe enough to 

cause direct axonal injury or (2) immune-mediated vasculitis causing ischemic optic 
21

neuropathy. (Id. at 58.) However, the authors expressly note that “[n]o pathologic 

examination of vaccination-associated optic neuritis currently exists to help differentiate 

these two mechanisms.” (Id. at 58-59.) 

Manasseh et al. (2014), reported a case of a 68-year-old man who developed 

bilateral NAION, with each episode occurring in close temporal proximity to influenza 

vaccination. (Manasseh et al., supra, at Ex. 29.) The patient reported a two-day history 

of reduced visual acuity ten days after receiving an influenza vaccine. (Id. at 267.) The 

patient was subsequently diagnosed with AION, which was later refined to NAION. (Id. 

at 268.) Over the next three months the patient’s visual acuity in the left eye recovered 

with a persistent field defect. However, the following year, six days after receiving the 

influenza vaccine, he returned with a new-onset visual field defect in his right eye. (Id.) 

Ocular findings were again normal apart from swelling in the superior disc margin in the 

right eye, and laboratory studies excluded giant cell arteritis. (Id.) The patient was 

treated with a prednisone taper. (Id.) The authors observed that the patient was over 

65, had a history of diabetes mellitus and was hypermetropic with small optic discs and 

taking tadalafil—“all of which are known or potential risk factors for NA-AION.” (Id.) 

Moreover, the authors point out that the cumulative incidence of second-eye 

involvement in NA-AION is 18% at one year and 25% at three years. (Id.) Taken 

together, Manasseh et al. report “our case probably represents a chance occurrence, 

especially as there is some evidence that within-season influenza vaccination leads to a 

reduced incidence of stroke and other cardiovascular events.” (Id.) 

Li & Fisayo (2019) reported a case of bilateral optic neuritis occurring one week 

after influenza vaccination in a previously healthy six-year-old child. (Li & Fisayo, supra, 

at Ex. 59, p. 496.) Examination revealed severe optic disc swelling with vessel 

obscuration bilaterally and peripapillary hemorrhages on the left. (Id.) MRI of the brain, 

orbits, and spinal cord showed increased T2/FLAIR signal and abnormal enhancement 

in the retrobulbar optic nerves bilaterally, but no white matter lesions in the brain or 

spinal cord. (Id.) Six days after the last dose of IV steroids, the patient experienced 

decreased vision in the left eye. (Id.) The patient started oral prednisone, and two 

weeks later visual acuities returned to 20/20 with normal color vision in each eye. (Id.) 

There is no indication that this patient had NAION. 

Generally, case reports offer circumstantial evidence of vaccine causation and 

therefore should not be summarily rejected. Case reports “‘do not[, however,] purport to 

establish causation definitively, and this deficiency does indeed reduce their evidentiary 

value’. . . [but] ‘the fact that case reports can by their nature only present indicia of 

causation does not deprive them of all evidentiary weight.’” Paluck v. Sec’y of Health & 

Human Servs., 104 Fed. Cl. 457, 475 (2012) (quoting Campbell v. Sec’y of Health & 

Human Servs., 97 Fed. Cl. 650, 668 (2011), aff’d, 786 F.3d 1373 (Fed. Cir. 2015)). 

Case reports often present a detailed report of symptoms, signs, diagnosis, treatment, 

and follow-up care. Oftentimes petitioners in the Program will highlight the usefulness 

of case reports in cases of novel, unusual or rare diseases. See Patton v. Sec’y of 

Health & Human Servs., 157 Fed. Cl. 159, 166-67 (2021). But see Crutchfield v. Sec’y 

of Health & Human Servs., No. 09-39V, 2014 WL 1665227, at *19 (Fed. Cl. Spec. Mstr. 
22

Apr. 7, 2014) (“single case reports of Disease X occurring after Factor Y . . . do not 

offer strong evidence that the temporal relationship is a causal one—the temporal 

relationship could be pure random chance”), aff’d, 125 Fed. Cl. 251 (2014). 

Here, I am not persuaded by respondent’s contention that eye pain suggestive of 

optic neuritis is dispositive where Kawasaki et al. are clear in concluding that the 

diagnosis is NAION. Both patients suffered eye pain which Dr. Wilson opines is more 

consistent with an optic neuritis than NAION. (Ex. B, p. 4 (citing Kawasaki et al., supra, 

at Ex. 27).) Indeed, some researchers consider eye pain to be an atypical feature for 

NAION. (Berry et al., supra, at Ex. 56, p. 24.) Moreover, Kawasaki et al. acknowledge 

that optic neuritis can present with bilateral vision loss and optic disc edema may or 

may not present acutely. (Kawasaki et al., supra, at Ex. 27, p. 56.) The presentation of 

both patients in Kawasaki’s case report would have been seemingly atypical for both 

AION and optic neuritis. (See id.) Yet, Kawasaki et al. concluded that in their two 

patients, the pattern of visual field loss, segmental disc changes, and failure of visual 

recovery is more consistent with AION than with a demyelinating optic neuritis. (Id. at

59.) However, I am persuaded by the fact that the case reports filed in this case 

describe acute onset—whereas petitioner had sequential onset approximately two

months after the symptoms appeared in the left eye. (Kawasaki et al., supra, at Ex. 27; 

Ray & Dreizin, supra, at Ex. 28.) In his second report, Dr. Wilson notes this is in 

contrast to acute monophasic conditions that are typically associated with vaccines.

(Ex. D, p. 1.) The issue here is that a fluctuating condition in one eye might be 

explained by the resulting nerve damage from the initial inflammatory event. But to 

have a new onset occurring in a separate eye at a separate time speaks to some kind of 

chronicity in the underlying cause that is not necessarily consistent with vaccine 

causation.8

At first blush, the case report from Manasseh suggests the possibility for a 

challenge-rechallenge event.

9 Respondent argues this is immaterial because there is 

no evidence petitioner experienced a recurrence of NAION after a second dose of flu 

vaccine. (ECF No. 66, p. 11 n.4.) However, I find that this is a factor that increases the 

evidentiary value of that case report. The Institute of Medicine (IOM) “has stated that 

rechallenge is proof of causation . . . The IOM has also stated that where causation is 

8 Relatedly, Dr. Akbari observes that petitioner experienced optic disc swelling in his right eye 

approximately one month after the steroid taper. (Ex. 31, p. 4 (citing Ex. 8, pp. 6-10).) Though, on the 

other hand, Dr. Wilson stresses that petitioner only ever had an incomplete response to steroid treatment. 

(Ex. B, p. 4.) When patients respond well to steroids, it is support of an inflammatory etiology (e.g., optic 

neuritis). (Id.) 

9 Within the context of the Vaccine Program, the Federal Circuit has described:

A rechallenge event occurs when a patient who had an adverse reaction to a vaccine 

suffers worsened symptoms after an additional injection of the vaccine. The chief special 

master stated that this evidence of rechallenge constituted ‘such strong proof of causality 

that it is unnecessary to determine the mechanism of cause—it is understood to be 

occurring.’

Capizzano, 440 F.3d at 1322 (internal citation omitted). 
23

proven, biologic plausibility is a given.” Capizzano v. Sec’y of Health & Human Servs., 

2004 WL 1399178, *2 (Fed. Cl. Spec. Mstr. 2004) (citing Christopher P. Howson et al., 

Institute of Medicine, Adverse Effects of Pertussis and Rubella Vaccines, 48, 53 (1991); 

Kathleen R. Stratton et al., Institute of Medicine, Adverse Events Associated with 

Childhood Vaccines: Evidence Bearing on Causality, 21 (1994)). It was not disputed 

that the petitioner in Capizzano did not suffer a challenge-rechallenge event. 

Capizzano v. Sec’y of Health & Human Servs., 2006 WL 3419789, at *12 (Fed. Cl.

Spec. Mstr. 2006). However, what I find most critical in this case report is the authors’ 

overall conclusion that the patient’s development of sequential bilateral NAION was a 

chance occurrence—noting the patient’s risk factors for developing NAION independent 

of the vaccine administered. (Manasseh et al., supra, at Ex. 29, p. 268.) 

On balance, the case reports provide some support for petitioner’s claim, but not 

enough without more given that the causes of NAION are unknown. See, e.g., W.C. v. 

Sec’y of Health & Human Servs., No. 07-456V, 2011 WL 4537887, at *13 (Fed. Cl. 

Spec. Mstr. Feb. 22, 2011) (“case reports are generally weak evidence of causation 

because case reports cannot distinguish a temporal relationship from a causal 

relationship”), mot. for review den’d, 100 Fed. Cl. 440 (2011), aff’d, 704 F.3d 1352 (Fed. 

Cir. 2013); Caves v. Sec’y of Health & Human Servs., No. 07-443V, 2010 WL 5557542, 

at *14 (Fed. Cl. Spec. Mstr. Nov. 29, 2010) (“case reports do[] not help [petitioners] 

meet [their] burden of demonstrating a persuasive and reliable theory causally 

connecting” vaccine to injury), mot. for review den’d, 100 Fed. Cl. 119 (2011), aff’d, 463 

Fed. App’x 932 (Fed. Cir. 2012); Ryman v. Sec’y of Health & Human Servs., 65 Fed. Cl. 

35, 39 (2005) (“case reports are the least reliable type of evidence for establishing 

vaccine injury causation”); Pearson v. Sec’y of Health & Human Servs., No. 17-489V, 

2019 WL 1150044, at *11 (Fed. Cl. Spec. Mstr. Feb. 7, 2019) (noting that “probative 

weight given to [case reports] in Program cases is limited”); Knorr v. Sec’y of Health & 

Human Servs., No. 15-1169V, 2018 WL 6991548, at *30 (Fed. Cl. Spec. Mstr. Dec. 7, 

2018) (“substantial authority also notes that case reports are not robust evidence 

favoring causation (even under the Program’s comparatively lenient preponderance 

evidentiary standard)”). 

Taking all of this together, petitioner’s claim that the flu vaccine can cause

NAION is not preponderantly supported. Dr. Akbari offered molecular mimicry to 

explain how the vaccine might have caused the production of antibodies, which 

subsequently attacked healthy tissue. However, the molecular mimicry theory proposed 

by Dr. Akbari relies upon a similarity between a substance in the flu vaccine and the 

myelin of the human nervous system. The fatal flaw with this proposed mechanism is 

that NAION is ischemic / vascular rather than demyelinating. Without any evidence of 

demyelination, Dr. Akbari’s molecular mimicry proposal is of no use to explain how the 

flu vaccine may have caused petitioner’s NAION. Dr. Akbari’s further reliance on a 

broader discussion of vasculitis is likewise unpersuasive. Nor do the case reports cited 

by Drs. Akbari and Hedges provide preponderant support. Thus, for all these reasons, 

petitioner has not met his burden under Althen prong one. 
24

c. Althen prong two 

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 & Human Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992). In establishing 

that a vaccine “did cause” the 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 & 

Human Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993).

However, medical records and/or statements of a treating physician’s opinion 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. See § 13(b)(1) (providing that “[a]ny 

such diagnosis, conclusion, judgment, test result, report, or summary shall not be 

binding on the special master or court”); Snyder v. Sec’y of Health & Human Servs., 88 

Fed. Cl. 706, 746 n.67 (2009) (“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 

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

conflicting opinions among such individuals. Hibbard v. Sec’y of Health & Human 

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); Caves v. Sec'y of Health & Human Servs., 100 Fed. Cl. 119, 136 

(2011), aff’d, 463 Fed. App’x 932 (Fed. Cir. 2012); Veryzer v. Sec’y of Health & Human 

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 Fed. 

App’x 765 (Fed. Cir. 2012).

Petitioner stresses that his treating physicians documented the onset of his vision 

loss “in the context of his recent flu vaccination repeatedly.” (ECF No. 65, p. 37 (citing 

Ex. 8, p. 2 (Dr. Potter 12/9/2016); Ex. 4, p. 43 (Dr. Sharma 12/9/2016); Ex. 8, p. 5 (Dr. 

Samy 1/5/2017); Ex. 8, p. 10 (Dr. Samy 1/27/2017); Ex. 8, p. 15 (Dr. Samy 2/2/2017); 

Ex. 8, p. 21 (Dr. Samy 2/17/2017); Ex. 8, p. 38 (Dr. Samy 5/19/2017); Ex. 21, p. 3 (Dr. 

Samy 11/12/2018)).) However, the context of those records reveals that his treaters 

considered vaccine-causation within the context of a differential diagnosis that 

concurrently considered the possibility of infectious and autoimmune etiologies. In each 

of Dr. Samy’s reports he additionally notes “suspected post-vaccination vs postinfectious vs autoimmune optic neuritis (MS-spectrum).” (Ex. 8, pp. 2, 5, 10, 15, 21, 
25

38.) The notation from Dr. Sharma in the emergency department similarly reflects “[a]s 

per ophthalmology he has most likely post-vaccination optic neuritis . . . vs postinfectious optic neuritis . . . vs autoimmune optic neuritis.” (Ex. 4, p. 43.) In petitioner’s 

final visit with Dr. Samy on November 11, 2018, he noted that petitioner “developed 

optic neuropathy [in] early 2017 which was post vaccination but in a pattern suggestive 

of possible ischemia in disc without cup followed by a few months later with the other 

eye.” (Ex. 21, p. 3 (emphasis added).) Considering Dr. Samy’s records as a whole, his

statements of mere suspicion fall short of an opinion supporting a vaccine-causation of 

petitioner’s condition. See Cedillo v. Sec’y of Health & Human Servs., 617 F.3d 1328, 

1348 (Fed. Cir. 2010) (special master did not err in affording little weight to the opinions 

of petitioner’s treating physicians where “none of the treating physicians concluded that 

the MMR vaccine caused [petitioner’s] autism”); Moberly, 592 F.3d at 1324-25 (finding 

no treating physician evidence to support the claim of causation where the “medical 

records regarding the temporal proximity of the [vaccination] to the seizures were all 

speculative”); Stapleford v. Sec’y of Health & Human Servs., No. 03-234V, 2009 WL 

1456441, at *17 n.24 (Fed. Cl. Spec. Mstr. May 1, 2009) (referencing medical record “is 

quite different from an indication that such physician has reached a conclusion 

concerning a causal relationship”) (emphasis in original), aff’d, 89 Fed. Cl. 456 (Fed. Cl. 

2009). Moreover, “[a] treating physician’s recognition of a temporal relationship does 

not advance the analysis of causation.” Isaac v. Sec’y of Health & Human Servs., No. 

08-601V, 2012 WL 3609993, at *26 (Fed. Cl. Spec. Mstr. July 30, 2012); see also 

Devonshire v. Sec’y of Health & Human Servs., No. 99-031V, 2006 WL 2970418, at *19 

(Fed. Cl. Spec. Mstr. Sept. 28, 2006) (medical expert’s “post hoc ergo prompter hoc 

reasoning . . . has been consistently rejected by the Court and is ‘regarded as neither 

good logic nor good law’”) (quoting Fricano v. U.S., 22 Cl. Ct. 796, 800 (1991) 

(emphasis in original)).

However, I am also not persuaded that respondent has presented petitioner’s 

prior infection as a significant consideration. Respondent stresses that petitioner had 

an upper respiratory infection roughly two weeks prior to the onset of his symptoms, 

“which under his experts’ causation theory would be just as likely to have caused 

petitioner’s NAION.” (ECF No. 66, p. 1.) In his second report, however, Dr. Wilson 

agrees the relationship between infection and NAION is unclear. (Ex. D, p. 1.) Nor 

does the medical literature filed in this case bear out any suspected infectious etiology. 

Indeed, upon initial presentation, petitioner’s treating physicians felt a post-infectious 

injury was less likely given his negative labs. (Ex. 8, p. 2.) 

However, Dr. Wilson also discussed other factors relevant to Althen prong two. 

First, and most notably, petitioner had other non-inflammatory risk factors for NAION

including hypertension, smoking, age, and sleep apnea. (Ex. 5, pp. 1-2, 13; Ex. 7, p. 2; 

Ex. 2, p. 5.) As Berry et al. explained: 

Systemic diseases that may cause decreased perfusion to the optic nerve 

head secondary to microvascular compromise might increase the patient’s 

risk of NAION. These include hypertension, diabetes, and 

hypercholesterolemia. Other risk factors noted in the literature are 
26

nocturnal hypotension, smoking, obstructive sleep apnea, anemia, 

hypercoagulable states, disc drusen, ocular and nonocular surgery, and 

migraines.

(Berry et al., supra, at Ex. 56, p. 2; see also Kerr et al., supra, at Ex. B, Tab 4, pp. 2-3; 

Vaughan et al., supra, at Ex. B, Tab 3, pp. 25-26.) Dr. Hedges acknowledges that 

petitioner had risk factors for NAION but attempts to minimize this fact by suggesting

“these are associations, not direct causative factors.” (Ex. 24, p. 2.) However, this is 

not persuasive given that Dr. Hedges nonetheless further opines that the risk factors 

were contributory in petitioner’s own case. Specifically, he opined that “[t]hese risk 

factors combined with a physiologic response to vaccination” ultimately caused

petitioner’s optic nerve injury. (Id.) Dr. Wilson also stresses that petitioner’s skin biopsy 

showed no clear evidence of vasculitis. (Ex. B, p. 4.) Moreover, Dr. Wilson observes 

that there is no record of a fluorescein angiogram to look for evidence of vasculitis in the 

retina, and systemic markers commonly associated with immune complex deposition, 

such as complement levels, are not available. (Id.) 

Overall, petitioner has not preponderantly proven that his flu vaccination did 

cause his NAION. Though some of his treating physicians considered and reported a 

temporal association, none concluded that his vision loss was caused by his flu 

vaccination. Moreover, petitioner has not preponderantly demonstrated a logical 

sequence of cause and effect implicating his vaccination as a cause of his injury. Thus, 

petitioner has not met his burden under Althen prong two. 

d. Althen prong three 

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.” Bazan v. Sec’y of Health & Human Servs., 

539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for what is a medically 

acceptable timeframe must also coincide with the theory of how the relevant vaccine 

can cause an injury (Althen prong one’s requirement). Id. at 1352; Shapiro v. Sec’y of 

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

Fed. Cl. 353 (2012), aff’d mem., 503 Fed. App’x 952 (Fed. Cir. 2013); Koehn v. Sec’y of 

Health & Human Servs., No. 11-355V, 2013 WL 3214877 (Fed. Cl. Spec. Mstr. May 30, 

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

2014).

Here, because petitioner has failed to meet his preponderant burden pursuant to 

Althen prongs one and two, he cannot prevail. In the interest of completeness, 

however, I note briefly that respondent’s expert, Dr. Wilson, agrees with the contention

that “symptom onset approximately 4 weeks after vaccination is within the time window 

for post-vaccination syndromes.” (Ex. B, p. 5.) He specifically stated that the timing of

petitioner’s symptoms “could be consistent with a vaccine-triggered complication.” (Id.) 
27

Accordingly, had petitioner proven his case with respect to the first two Althen prongs, it 

is likely he would have also prevailed with regard to Althen prong three. 

VI. Conclusion 

Petitioner has my sympathy for the injury he endured. Considering the record as 

a whole under the standards applicable in this Program, however, petitioner has not 

preponderantly established either that his October 28, 2016, flu vaccination caused his 

condition. Accordingly, petitioner is not entitled to compensation. Therefore, this case 

is dismissed.

10 

IT IS SO ORDERED.

s/Daniel T. Horner

Daniel T. Horner

Special Master

10 In the absence of a timely-filed motion for review of this Decision, the Clerk of the Court shall enter 

judgment accordingly.