Garcia v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

Filed: April 23, 2025

* * * * * * * * * * * * * * * *

ANA BRUNO GARCIA, *

* No. 19-1927V

*

*

Petitioner, * Special Master Young

*

v. *

*

SECRETARY OF HEALTH *

AND HUMAN SERVICES, *

*

Respondent. *

* * * * * * * * * * * * * * * *

Roberto E. Ruiz-Comas, RC Legal and Litigation Services LLC, Guaynabo, PR, for Petitioner.

Adam Nemeth Muffett, United States Department of Justice, Washington, DC, for Respondent.

DECISION ON ENTITLEMENT 1

On December 19, 2019, Ana Bruno Garcia (“Petitioner”) filed a petition for compensation

in the National Vaccine Injury Compensation Program (“the Program”) 2 alleging that the influenza

(“flu”) vaccine Petitioner received on December 29, 2017, caused her to suffer from “injuries,

including meningoencephalitis.” Pet. at ¶ 1, ECF No. 1. After carefully analyzing and weighing

all the evidence presented in this case in accordance with the applicable legal standards, 3 I find

that Petitioner has failed to provide preponderant evidence that the flu vaccine Petitioner received

1

Because this Decision contains a reasoned explanation for the action taken in this case, it must be made

publicly accessible and will be posted on the United States Court of Federal Claims' website, and/or at

https://www.govinfo.gov/app/collection/uscourts/national/cofc, in accordance with the E-Government Act

of 2002. 44 U.S.C. § 3501 note (2018) (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, upon review, I agree that

the identified material fits within this definition, I will redact such material from public access.

2

National Childhood Vaccine Injury Act of 1986, Pub L. No. 99-660, 100 Stat. 3755 (“the Vaccine Act”

or “Act”). Hereinafter, for ease of citation, all “§” references to the Vaccine Act will be to the pertinent

subparagraph of 42 U.S.C. § 300aa (2018).

3

While I have reviewed all of the information filed in this case, only those filings and records that are most

relevant to the decision will be discussed. Moriarty v. Sec’y of Health & Hum. Servs., 844 F.3d 1322, 1328

(Fed. Cir. 2016) (“We generally presume that a special master considered the relevant record evidence even

though he does not explicitly reference such evidence in his decision.”) (citation omitted); see also Paterek

v. Sec’y of Health & Hum. Servs., 527 F. App’x 875, 884 (Fed. Cir. 2013) (“Finding certain information

not relevant does not lead to—and likely undermines—the conclusion that it was not considered.”).

on December 29, 2017, caused her to develop “meningoencephalitis or possible Acute

Disseminated Encephalomyelitis (“ADEM”).” Pet’r’s Mot. at 2, ECF No. 40. Accordingly,

Petitioner is not entitled to compensation.

I. Procedural History

Petitioner filed her petition on December 19, 2019. Pet. On December 26, 2019, Petitioner

filed Exhibits 1–12, which included a copy of Petitioner’s U.S. Passport, medical records, and an

affidavit from Petitioner. Pet’r’s Exs. 1–12, ECF Nos. 6–7. The same day, she filed her statement

of completion. ECF No. 8. On June 24, 2020, Petitioner filed an additional, legible copy of her

immunization record. Pet’r’s Ex. 13, ECF No. 13.

On December 14, 2020, Respondent filed his Rule 4(c) Report, recommending that

compensation be denied. Resp’t’s Report, ECF No. 19. On July 14, 2021, Petitioner filed an expert

report from Christian E. Schenk, M.D. Pet’r’s Ex. 15, ECF No. 23. Petitioner filed a statement of

completion on July 15, 2021. ECF No. 24. On November 12, 2021, Respondent filed expert reports

from Michael Wilson, M.D., M.A.S., and S. Mark Tompkins, Ph.D., as well as their curriculum

vitae and accompanying medical literature. Resp’t’s Ex. A, Tabs 1–8, B, ECF No. 26; Resp’t’s Ex.

C, Tabs 1–5, D, ECF No. 27. Petitioner filed a rebuttal expert report from Dr. Schenk and

accompanying medical literature on March 17, 2022, along with an expert report from Cristina

Ramos, M.D. Pet’r’s Exs. 16–17, ECF Nos. 29–30. On March 25, 2022, the Court received

accompanying medical literature for Dr. Ramos’ report, which was submitted on a portable storage

disc. See ECF No. 32. On July 11, 2022, Respondent filed supplemental reports from Dr. Wilson

and Dr. Tompkins with accompanying medical literature. Resp’t’s Exs. E, F, Tabs 1–9, ECF No.

33. On October 5, 2022, Petitioner filed a supplemental expert report from Dr. Ramos. Pet’r’s Ex.

18, ECF No. 35.

On November 22, 2022, the parties filed a joint status report agreeing to submit the case

for a ruling on the record. Joint Status Report, ECF No. 37. Petitioner submitted her motion for a

ruling on the record on March 20, 2023. Pet’r’s Mot. Respondent filed a response on May 19,

2023. Resp’t’s Resp., ECF No. 41. Petitioner filed a reply on July 20, 2023. Pet’r’s Reply, ECF

No. 44.

This matter is now ripe for consideration.

II. Factual Background

A. Medical Records

Prior to vaccination, Petitioner’s medical history was significant for hypertension, diabetes,

arthritis, hyperthyroidism, degenerative joint disease, cardiac arrhythmias, and anxiety. Pet’r’s Ex.

3 at 29, 227, ECF No. 7-1; Pet’r’s Ex. 8 at 2, 32, ECF No. 6-7; Pet’r’s Ex. 11 at 5, ECF No. 6-10.

Petitioner was 73 years old at the time of her flu vaccination on December 29, 2017. Pet’r’s Ex. 2

at 2–3, ECF No. 6-2.

2

On December 29, 2017, Petitioner received the subject flu vaccination at Costco Pharmacy

in Milford, Connecticut. Id. at 3. Seven days later, on January 5, 2018, Petitioner’s son brought

her to the emergency room (“ER”) at Yale New Haven Health with symptoms of confusion,

nausea, vomiting, abdominal pain, and tremors. Pet’r’s Ex. 3 at 29. The medical report noted that

she had no symptoms until the day prior to admission, when she was found to be “delirious” with

a recorded fever of 104 degrees Fahrenheit. Id. at 39. Petitioner’s children stated that Petitioner

had received the flu shot one week prior to her appointment. Id. at 29. During the same time,

Petitioner’s children reported to be “down with a viral URI . . .(but no GI symptoms).” Id.

Petitioner was admitted to the hospital, and a geriatric consult was ordered. Id. at 32. During her

stay, Petitioner developed “progressive lethargy[,] followed by seizure activity and

unresponsiveness.” Id. at 33. She was intubated and moved to the intensive care unit (“ICU”). Id.

Petitioner’s temperature remained elevated, at times up to 104 degrees Fahrenheit, and an

infectious disease consult was requested. Id.

On January 7, 2018, Zane Kevin Saul, M.D. performed an infectious disease consultation.

Id. at 37–38. His impression notes identified fever and seizure symptoms and a need to rule out

infectious meningoencephalitis. Id. at 38. Dr. Saul noted that Petitioner’s “[p]ersistent fever curve

[was] more suggestive of CNS fever.” Id. He recommended a lumbar puncture, additional

medications, an MRI when Petitioner was able to be moved, a neurological consultation, and to

monitor temperatures and cultures. Id. The same day, Lawrence Beck, M.D. performed a

neurological consultation. Id. at 39–40. Medical records indicate that Petitioner was intubated and

sedated at the time of her examination and was therefore unresponsive to verbal or noxious stimuli.

Id. at 39. Blood work revealed normal electrolytes; a peripheral white blood cell count of 9,900;

hemoglobin at 12.1; CSF results showed 451 white blood cells, and glucose levels measured 123.

Id. Petitioner’s total protein was 129, her red cells measured 3, and no xanthochromia was noted.

Id. A CT of Petitioner’s brain showed a left temporal arachnoid cyst, but no acute abnormalities.

Id. at 39–40. Petitioner was treated with broad-spectrum antibiotics and antiviral therapy. Id. Dr.

Beck’s impression was acute meningoencephalitis, due to an organism yet to be determined. Id.

Petitioner had a geriatric consult with Mithil Choksey, M.D. on January 8, 2018. Id. at 40.

Dr. Choksey did not observe any discrete thoracic lymphadenopathy nor consolidated pneumonia,

but felt Petitioner likely had advanced degenerative arthritis of the bilateral shoulders with a left-

sided shoulder joint effusion. Id. at 45. He also observed scattered diverticulosis and an

indeterminate 1.7 cm left adrenal nodule. Id. Dr. Choksey noted that Petitioner was likely

encephalopathic from an ongoing infectious process and agreed with infectious and neurological

work-ups. Id. The same day, Petitioner underwent an electroencephalogram (“EEG”) with

abnormal results, due to generalized slowing of the background rhythm consistent with diffuse

cerebral dysfunction. Pet’r’s Ex. 5 at 16, ECF No. 6-4. No focal or paroxysmal features were noted.

Id.

On January 9, 2018, Petitioner had a neurology follow up with James Butler, M.D. Pet’r’s

Ex. 3 at 67. During this evaluation, Petitioner, who awakened to voice and light stimulation,

followed simple commands, and moved both arms and legs. Id. Her grip strength was weak, but

equal in both hands. Id. Geriatric progress notes from the same day listed “acute encephalopathy

in the setting of-URI, seizures, [and] alteration in mental status [with a] working diagnosis [of]

meningeal encephalitis.” Id. Treatment plans included “possible intubation later in the day[,

c]ontinue on board (sic) spectrum antibiotics and antivirals.” Id.

3

Petitioner’s January 10, 2018, laboratory results for West Nile, CMV, HSV, and

Enterovirus were negative. Id. at 103. Critical care notes from the same date contain an impression

of “[s]uspected encephalitis complicated by seizure and resp[iratory] failure.” Pet’r’s Ex. 3 at 72,

76.

On January 11, 2018, Dr. Butler noted Petitioner’s improvement, despite complaints of

headache and neck pain. Pet’r’s Ex. 5 at 20, ECF No. 6-4. Her diagnosis remained

meningoencephalitis, much improved, and Dr. Butler questioned whether there was a relationship

between Petitioner’s condition and her recent flu shot. Id. An MRI conducted on January 13, 2018,

showed no evidence of infectious or inflammatory processes involving the cervical spine. Pet’r’s

Ex. 3 at 110. Petitioner showed multi-level degenerative changes, no significant canal stenosis or

cord compression, and asymmetric right thyroid lobe enlargement incompletely characterized on

exam. Id. Petitioner was discharged home with therapy services on January 16, 2018. Id. at 119.

Her principal discharge diagnoses were acute encephalopathy, possible viral meningoencephalitis,

and seizures. Id. Petitioner was hemodynamically stable and was ambulating with physical therapy

prior to discharge. Id.

Goran Miljkovic, M.D. evaluated Petitioner for a follow-up visit on January 30, 2018.

Pet’r’s Ex. 9 at 4. Dr. Miljkovic noted viral encephalitis following the flu vaccination. Id. At the

time of her evaluation, Petitioner was without headaches, fevers, or chills, or an altered mental

status. Id. Her diagnosis remained encephalitis, with an unclear etiology- “possibly viral versus

post-[flu] vaccination encephalitis.” Id. Petitioner was advised to avoid the flu vaccine in the

future. Id.

Petitioner was evaluated by neurologist Philip Barasch, M.D., on February 7, 2018. Pet’r’s

Ex. 5 at 17. Dr. Barasch noted Petitioner’s diagnosis of encephalitis, with no clear etiology

determined at the time of her hospital discharge. Id. at 16–17. On physical examination, Petitioner

was alert and oriented and in no acute distress, had normal tone and strength in upper and lower

extremities, mild imbalance, and no sensory loss to light touch bilaterally. Id. at 18–19. Dr. Barasch

agreed with Petitioner’s hospital diagnosis. Id. at 19. Dr. Barasch also noted that he had requested

medical records from the hospital to determine the etiology of her meningoencephalitis. Id. In the

interim, Petitioner was instructed to continue taking Levetracetam 4 500 mg twice a day and began

to taper off if she continued without any seizure activity. Id.

On February 21, 2018, Petitioner was discharged from home physical therapy after meeting

stated goals, including “supervision or less with performing tub transfers for bathing,” independent

“supine to sit to stand transfers and indoor ambulation with appropriate assistive device,” and

ability to “ascend/descend stairs independently.” Pet’r’s Ex. 4 at 84–85.

Petitioner returned for a follow-up with Dr. Barasch on March 23, 2018. Pet’r’s Ex. 5 at

12. Petitioner reported ongoing fatigue and weight loss, which Dr. Barasch thought might be due

4

Levetiracetam is “an anticonvulsant administered orally as an adjunct in the treatment of partial and

myoclonic seizures and idiopathic generalized epilepsy.” Dorland’s Illustrated Medical Dictionary (33rd

ed. 2020) [hereinafter “Dorland’s”].

4

to her seizure medication. Id. at 14. Blood work was ordered, and a taper off the Levetracetam was

recommended. Id. Her diagnosis was viral encephalitis. Id.

On September 10, 2018, Petitioner saw Mitchell Matundan, M.D., an internal medicine

specialist, for an initial evaluation. Pet’r’s Ex. 11 at 2, ECF No. 6-10. Petitioner’s physical

examination revealed urinary incontinence, generalized aches (arthritis low back pain), and anxiety

depressed mood with loss of interest. Id. at 4. Petitioner’s neurological exam was normal. Id. Dr.

Matundan’s diagnoses for Petitioner were diabetes Type II and an adjustment disorder with

anxiety. Id. at 5. On November 26, 2018, Petitioner returned to Dr. Matundan for evaluation of a

rash that occurred after eating seafood. Id. at 8. Petitioner’s neurological examination was normal.

Id. at 9.

Petitioner saw Dr. Matundan for lab and follow-up appointments from February 2019 to

May 2019. Id. at 13, 21, 25. Petitioner’s neurological examinations were normal. Id. at 17, 22, 27.

On July 1, 2019, approximately one year and six months after the subject vaccination,

Petitioner sought treatment with Palmira Martinez Romero, M.D., with the Bayamon

Otolaryngology Group, for nasal congestion and loss of smell “since six months ago.” Pet’r’s Ex.

10 at 2, ECF No. 6-9. Petitioner also reported an altered sense of taste “since six months ago.” Id.

Dr. Romero noted that Petitioner was intubated “due to encephalitis after [flu] vaccine or viral,

since no etiologic agent was identified.” Id. Dr. Romero’s assessment included anosmia, deviated

nasal septum, chronic pansinusitis, and acute pharyngitis. Id. at 3. Dr. Romero prescribed

Petitioner Fluticasone Propionate nasal suspension and Claritin. Id.

Petitioner saw Dr. Matundan for follow-up of laboratory testing on September 9, 2019.

Pet’r’s Ex. 11 at 35. Petitioner’s neurological and musculoskeletal examinations were normal. Id.

On October 15, 2019, Petitioner returned to Dr. Matundan with complaints of generalized aches,

arthritis, low back pain, and gait difficulty. Id. at 42. Petitioner requested a prescription for a

rollator stroller due to gait difficulty. Id. On December 3, 2019, Petitioner was reevaluated by Dr.

Miljkovic, her infectious disease specialist, for seizure and encephalitis. Pet’r’s Ex. 9 at 6.

Petitioner described an absence of smell and taste, and Dr. Miljkovic indicated a possibility that

her symptoms were the result of viral meningoencephalitis. Id. at 6–7. Dr. Miljkovic noted there

was “[n]o ongoing infectious process,” and instructed Petitioner to follow up with ENT and

neurology. Id. at 7.

B. Petitioner’s Affidavit

Petitioner submitted an affidavit that briefly summarized her condition and sequela. Pet’r’s

Ex. 12, ECF No. 6-11. She described “flu-like symptoms, chills, and general malaise” six days

after she received her December 29, 2017, flu vaccine. Id. at ¶ 3. Believing that she may be having

a stroke, Petitioner went by ambulance to Bridgeport Hospital in Connecticut with “abdominal

pain, fever, a mild cough, tremors, nausea, vomiting, and confusion.” Id. When she arrived at the

hospital, she “had a very high fever, suffered a seizure and was transferred to the ICU where [she]

was intubated and sedated.” Id. at ¶ 4. She claimed that she was then diagnosed with viral

meningoencephalitis after a lumbar spine exam. Id. She noted that while hospitalized, an infectious

disease doctor advised her “to never repeat the [flu] vaccine, as it was very likely [her]

meningoencephalitis was caused by the [flu] vaccine.” Id. at ¶ 5. After months of physical

5

rehabilitation, Petitioner has “regain[ed] the ability to be independent again.” Id. at ¶ 6. However,

she still suffers from significant decreases in smell and taste sensitivity, memory loss, appetite,

and weight loss, and constant fatigue. Id. at ¶ 7.

III. Expert Review

A. Petitioner’s Experts

1. Christian E. Schenk, M.D. 5

Dr. Schenk submitted two expert reports in this case. Pet’r’s Ex. 15, ECF No. 23-1. He is

board-certified in psychiatry and neurology, with experience as an expert witness in civil, criminal,

and medical malpractice cases since 2013. Id. at 1. Currently, Dr. Schenk works with patients,

teaches, and conducts research at the University of Puerto Rico, School of Medicine. Id. He has a

general and behavioral neurology practice wherein he sees patients “at both inpatient and

outpatient settings.” Id.

In Dr. Schenk’s first submitted report, he discussed Petitioner’s medical history with a

focus on her January 2018 hospitalization. Id. He inserted direct quotes from the medical record

that detail Petitioner’s initial symptoms when she presented to the hospital on January 5, 2018,

laboratory and diagnostic tests, and Petitioner’s course of treatment. Id. at 1–8. Dr. Schenk then

reviewed several differential diagnoses, including encephalopathy, stroke, vaccine-related neuro-

inflammatory disorders, and the presumptive diagnosis of meningoencephalitis. Id. at 9.

Petitioner’s “neck rigidity, nausea, vomiting and fever, along with signs of encephalitis with the

presence of neurological symptoms and encephalopathy or alteration of consciousness and

seizures.” Id. at 10. Dr. Schenk also cited Petitioner’s CSF analysis as evidence of

meningoencephalitis. Id. Although an extensive infectious disease panel was conducted with no

positive results, Petitioner’s quick recovery contributed to a “final presumptive diagnosis [of] viral

meningoencephalitis.” Id. Dr. Schenk noted that vascular disorders were considered, but

Petitioner’s “neuroimaging with MRI [did] not report evidence of previous ischemic lesions or

signs suggestive of previous hemorrhagic stroke.” Id.

Dr. Schenk described encephalitis as “a severe inflammatory disorder of the brain with

many possible causes and a complex differential diagnosis.” Id. (citing Pet’r’s Ex. 16-23, ECF No.

29-23). 6 He noted that the condition is “frequently caused by a virus,” and “causes focal or multi-

focal neurological deficits and [frequent] seizure activity.” Id. Meningoencephalitis is

characterized by clinical symptoms or findings, “which would be neck rigidity and pain, sensitivity

to light, irritability, altered mental status, fevers, chills, nausea and vomiting, all which develop as

signs of meningeal irritation.” Id. (citing Pet’r’s Ex. 16-10, ECF No. 29-10). 7 Dr. Schenk noted

that Petitioner’s presentation was consistent with “acute and often rapidly progressive” multifocal

5

Dr. Schenk did not submit a curriculum vitae in this case. His qualifications are briefly summarized in his

initial report and are referenced here.

6

Francesc Graus et al., A Clinical Approach to Diagnosis of Autoimmune Encephalitis, 15 LANCET

NEUROLOGY 391 (2016).

7

Diederik van de Beek et al., Clinical Features and Prognostic Factors in Adults with Bacterial Meningitis,

351 NEW ENG. J. MED. 1849 (2004).

6

neurological deficits. Id. at 11 (citing Pet’r’s Ex. 3 at 5, 28). He included in his report a chart that

outlines the Diagnostic Criteria for Encephalitis and Encephalopathy of Presumed Infectious or

Autoimmune Etiology. Id. Altered mental status lasting less than 24 hours with no alternative

cause identified was the only major required criterion. Id. The chart also included minor criteria

and noted that three or more are “required for probable or confirmed encephalitis.” Id. Dr. Schenk

detailed Petitioner’s individual symptoms of nausea and vomiting, which are indicative of

“increased intracranial pressure and also[] meningitis;” altered mental status or “acute

deterioration of consciousness caused by an internal or provoking condition;” a tremor, in

Petitioner’s case, most likely a “physiological response to an acute process, fever, or related to

seizures;” fever; and neck pain. Id.

Given Petitioner’s “presentation of a monophasic Central Nervous System (CNS)

inflammatory syndrome of unknown etiology,” Dr. Schenk opined that “acute demyelinating

encephalomyelitis (ADEM) must be considered.” Id. This is especially true for Petitioner, “in view

of prior administration of a vaccine.” Id. at 12. ADEM presents similarly to viral encephalitis, but

“encephalopathy is less frequent [in adults] and the clinical presentation is usually dominated by

long tract involvement (corticospinal tract signs and symptoms).” Id. Dr. Schenk explained that

“an autoimmune response is the cause of the inflammatory reaction, and [] a trigger such as a viral

or bacterial infection or a vaccine, is considered in the majority of cases.” Id. He asserted the

timeframe “for ADEM to occur after vaccination (2-30 days)” and explained that in Petitioner’s

case, “[t]he presence of close sick contacts prior to infection, most likely viral infections, were

accounted for with a negative viral panel testing.” Id. (citing Pet’r’s Ex. 16-62, ECF No. 29-62; 8

Pet’r’s Ex. 3 at 64).

Dr. Schenk continued to explain that ADEM, “also known as postinfectious

encephalomyelitis, is an autoimmune demyelinating disease of the central nervous system and may

occur as an immunologically mediated para-infectious phenomenon following a variety of

infections or after vaccination.” Id. It is typically characterized by “multifocal inflammatory

lesions, principally affecting the white matter of the CNS.” Id. (citing Pet’r’s Ex. 16-49, ECF No.

29-49). 9 He proposed one pathogenic mechanism that occurs when “myelin autoantigens such as

myelin basic protein, proteolipid protein, and myelin oligodendrocyte protein share antigenic

determinants with those of an infecting pathogen. Antiviral antibodies or a cell-mediated response

to the pathogen cross-react with the myelin autoantigens, resulting in [postinfectious neurological

syndromes].” Id. at 13.

ADEM is a “diagnosis of exclusion,” but it “require[s] there to be an encephalopathy.” Id.

at 14. Dr. Schenk identified ADEM onset symptoms as “low-grade fever, headache and meningism

preceding the development of drowsiness and encephalopathy which may progress to stupor and

coma, as it evolves rapidly over hours to days.” Id. The diagnosis is considered more readily in the

context of recent illness or vaccination, and “[t]he rare post[-]vaccinal cases typically follow a

8

Romain Sonneville et al., Update on Investigation and Management of Postinfectious Encephalitis, 23

CURRENT OP. NEUROLOGY 300 (2010).

9

Siobhan Leary et al., NEUROLOGY: A QUEEN SQUARE TEXTBOOK 439–40 (Robin Howard et al. eds., 2nd

ed. 2016).

7

primary rather than revaccination.” Id. (citing Pet’r’s Ex. 17-34, ECF No. 29-29). 10 ADEM is

generally diagnosed by neuroimaging, especially MRI, and should be performed when ADEM is

suspected. Id. Dr. Schenk noted that Petitioner did not receive a brain MRI during her

hospitalization. Id. at 15. It could not be performed during her time in critical care “and later was

considered not important once the resolution of symptoms and no seizure recurrence, after a follow

up head CT scan was found without interval changes.” Id. Dr. Schenk acknowledged that “ADEM

after vaccination is a rare complication in children and adults,” but “[m]ore recent surveillance

studies have found little or no association between ADEM and immunization.” Id. at 17 (citing

Pet’r’s Ex. 16-56, ECF No. 29-56; 11 Pet’r’s Ex. 16-34, ECF No. 29-34; 12 Pet’r’s Ex. 16-7, ECF

No. 29-7). 13

Dr. Schenk concluded that “[t]he signs and symptoms [Petitioner] presented during the first

three days of hospitalization were consistent with the diagnosis of acute encephalitis.” Id. at 18.

He noted that “[c]linical and laboratory testing did not reveal a viral pathogen that would have

caused the [meningoencephalitis.]” Id. While “[e]xamining mechanistic evidence to assess

causation remains a challenge,” Dr. Schenk opined that “[t]he cause of [Petitioner’s] acute

encephalitis is most likely due to an autoimmune reaction after a trigger such as administration of

the [flu] vaccine days prior to the events.” Id. Additionally, despite the “relatively short” duration

of Petitioner’s symptoms, ADEM “still remains the most acceptable diagnosis to consider in this

patient.” Id.

In a supplemental report, Dr. Schenk expressed agreement with “the clinical presentation

description of an acute meningoencephalitis,” but noted that “the exact etiological agent or trigger

for the inflammatory process could not be detected.” Pet’r’s Ex. 16 at 1, ECF No. 29-1. Although

there were some tests done to identify a possible pathogen, all results were negative, “and an

infectious etiology could not be completely ruled out.” Id. Dr. Schenk noted that Petitioner’s MRI

did not show signs of ADEM and that her “CSF profile [was] atypical for ADEM.” Id. He

continued that “[a]ntecedent viral infections or vaccinations have been suggested as presenting an

antigenic challenge” leading to ADEM. Id. He suggested that molecular mimicry could be

involved in Petitioner’s case, but deferred to other experts versed in immunology. Id.

Dr. Schenk opined that Petitioner “most likely had a delayed inflammatory neurological

syndrome, either a post-infectious neurological syndrome or an adverse event following

immunization.” Id. at 2. He maintained that there is a differential between “an acute

meningoencephalitis due to either a vaccine or infectious viral or bacterial agent, and ADEM after

immunization.” Id. Although Dr. Schenk cited “the timing of the vaccine and the presentation of

seizures and encephalopathy” to describe Petitioner’s progression as “a clinical presentation,” he

10

William Huynh et al., Post-Vaccination Encephalomyelitis: Literature Review and Illustrative Case, 15

J. CLINICAL 1315 (2008).

11

Margaret Ryan et al., Revisiting Influenza Vaccination Exemption, 24 EMERGING INFECTIOUS DISEASES

1947 (2018).

12

Jorge D. Machicado et al., Acute Disseminated Encephalomyelitis Following Seasonal Influenza

Vaccination in an Elderly Patient, 20 CLINICAL VACCINE 1485 (2013).

13

Roger Baxter et al., Acute Demyelinating Events Following Vaccines: A Case-Centered Analysis, 63

CLINICAL INFECTIOUS DISEASES 1456 (2016).

8

also described her case as atypical “in adult presentation and with a relatively quick recovery.” Id.

He also noted that her recovery was not facilitated by “any treatment for ADEM such as

corticosteroids or immunoglobulin.” Id. In conclusion, Dr. Schenk opined that Petitioner

developed delayed meningoencephalitis, and much less likely an acute demyelinating event such

as ADEM. Id. In either scenario, “a post-vaccination reaction is considered more likely,” despite

“laboratory results [that] point toward a bacterial or fungal etiology.” Id. If Petitioner “had an

infectious etiology for her symptoms, in the frame after her [flu] vaccination, [it] would rather be

a coincidence.” Id.

2. Cristina Ramos-Romey, M.D. 14

Cristina Ramos-Romey received her medical degree from the University of Puerto Rico’s

Medical Sciences Campus. Pet’r’s Ex. 17 at 1, ECF No. 30-1. She specialized in internal medicine

with a subspecialty in geriatrics at the University District Hospital. Id. Dr. Ramos also received

her subspecialty in allergy and immunology at Pennsylvania State University, Hershey Medical

Center. Id. She is board certified in internal medicine, geriatrics, and allergy and immunology. Id.

Dr. Ramos is the Allergy and Immunology Fellowship Program Professor at the University of

Puerto Rico School of Medicine. Id. She is the lead immunology researcher at the Fundación de

Investigación research facility. Id.

In her first report, Dr. Ramos summarized Petitioner’s medical records and stated that she

“will defer to Dr. Schenk [] on the detailed evaluation and diagnostic criteria of [Petitioner’s]

neurological disorder and differential diagnosis.” Id. at 5. As to causation, Dr. Ramos asserted that

“[a]lthough we have already established that it is more likely that her symptoms were caused by

an infection, we cannot discard the possibility that [Petitioner’s] symptoms were caused by an

adverse reaction to the [flu] vaccine, due to the proximity of the onset of symptoms and her recent

[flu] vaccination.” Id. at 7–8.

Dr. Ramos asserted that “[t]he term molecular mimicry and immune cross-reaction is a

theory that has been accepted as a possible and viable explanation of how vaccines may cause

neurological disease.” Id. at 8. She then explained the general concept of molecular mimicry, “as

a process in which there is immune cross-reactivity due to structural homology between pathogens

and self-antigens.” Id. Medical researchers have discovered a “massive overlap” of viral and

bacterial peptides, which are shared with the human genome.” Id. This overlap will not likely result

in autoimmunity, except “in the setting of impaired tolerance, such as environmental causes and

genetic predisposition to autoimmune disease, this homology may induce autoimmunity.” Id.

(citing Pet’r’s Ex. 17-11, ECF No. 32). 15 Dr. Ramos described a study done with rabbit tissue

samples that were exposed to a viral peptide and produced a histology “consistent with allergic

encephalomyelitis.” Id. at 8–9 (citing Pet’r’s Ex. 17-8, ECF No. 32). 16 She noted that other

14

Dr. Ramos did not submit a curriculum vitae in this case. Her qualifications are briefly summarized in

her initial report and are referenced here.

15

Darja Kanduc, Quantifying the Possible Cross-Reactivity Risk of an HPV16 Vaccine, 8 J. EXPERIMENTAL

THERAPEUTICS ONCOLOGY 65 (2009).

16

R.S. Fujinami et al., Molecular Mimicry in Virus Infection: Crossreaction of Measles Virus

Phosphoprotein or of Herpes Simplex Virus Protein with Human Intermediate Filaments, 80 PROCS. NAT’L

ACAD. SCIS. U.S. 2346 (1983).

9

“[s]tudies have also shown molecular mimicry resulting in diseases such as uveitis, myocarditis

and myasthenia gravis due to viral proteins.” Id. at 9 (citing N. Neu et al.; 17 Pet’r’s Ex. 17-12, ECF

No. 32; 18 Pet’r’s Ex. 17-13, ECF No. 32; 19 VK Singh et al.). 20 Consequently, “[t]he concept of

molecular mimicry has been widely accepted as a proven concept and is considered to be one of

the mechanisms in which viral or bacterial infections can result in the development or worsening

of autoimmune disease.” Id. at 10.

In addition to molecular mimicry, Dr. Ramos asserted other “proposed mechanisms for

viral and vaccine-induced autoimmunity includ[ing] bystander activation, epitope spreading, []

and polyclonal activation.” Id. She described these processes briefly as follows: “Bystander

activation occurs when T cells recognize viral particles and are activated. Activation lead (sic) to

the secretion of inflammatory mediators that may damage the surrounding tissues. Once damaged

the self-epitopes are released and presented to autoreactive T cells and mediate future damaged,

this is known as epitope spreading.” Id. Dr. Ramos further explained that “[m]olecular mimicry

occurs when T cells bearing [receptors] specific to epitopes derived from foreign pathogens (e.g.,

viruses) are activated during an infection and cross-react with self-antigens inducing autoimmune

diseases.” Id. (citing Pet’r’s Ex. 17-14, ECF No. 32). 21 She noted the postulation by some

researchers that “although molecular mimicry is a common event, it only leads to autoimmunity

disease when it takes place in the context of chronic local inflammation, presentation of self-

antigens and a sufficient number of autoreactive T cells.” Id. at 11 (citing Pet’r’s Ex. 17-19, ECF

No. 32). 22

Dr. Ramos next turned to studies of molecular mimicry “to explain the mechanisms

through which vaccination can cause or worsen neurological conditions.” Id. She noted an

increased concern in the medical community for post-vaccination autoimmune diseases such as

Guillain-Barré Syndrome (“GBS”) and narcolepsy following mass flu vaccinations in 2009. Id.

Specifically, US studies done following the 2009 H1N1 pandemic revealed “consistent

epidemiologic evidence demonstrating an increased risk of GBS following the 2009 H1N1

vaccines across different populations,” and “provid[ing] strong evidence for a causal relationship.”

17

N Neu et al., Cardiac Myosin Induces Myocarditis in Genetically Predisposed Mice, 139 J. IMMUNOLOGY

3630 (1987). Petitioner failed to file this article with the Court, and as a result, I am unable to consider it

within the context of Dr. Ramos’ discussion or incorporate it into my analysis and findings.

18

C.J. Gauntt et al., Coxsackievirus-Induced Chronic Myocarditis in Murine Models, 16 EUR. HEART J. 56

(1995).

19

Schulze K. Schultheiss, The Role of the ADP/ATP Carrier in the Pathogenesis of Viral Heart Disease,

16 EUR. HEART J. 64 (1995).

20

VK Singh et al., Molecular Mimicry Between a Uveitopathogenic Site of S-antigen and Viral Peptides.

Induction of Experimental Autoimmune Uveitis in Lewis Rats, 144 J IMMUNOLOGY 1282 (1990). Petitioner

failed to file this article with the Court, and as a result, I am unable to consider it within the context of Dr.

Ramos’ discussion or incorporate it into my analysis and findings.

21

El Rosario University Press, AUTOIMMUNITY: FROM BENCH TO BEDSIDE (Juan-Manuel Anaya et al.

eds., 1st ed. 2013).

22

Silva Markovic-Plese et al., High Level of Cross-Reactivity in Influenza Virus Hemagglutinin-Specific

CD4+ T-Cell Response: Implications for the Initiation of Autoimmune Response in Multiple Sclerosis, 169

J. NEUROIMMUNOLOGY 31 (2005).

10

Id. at 10–11 (quoting Pet’r’s Ex. 17-24, ECF No. 32). 23 Although vaccines differ from their viral

counterparts, they “have viral protein subunits that may activate self-reactive T cells, especially if

the patient has had prior infection with the virus.” Id. at 11. Dr. Ramos mentioned reports of post-

vaccination encephalitis and ADEM following rabies and Japanese encephalitis virus vaccines,

but she acknowledged that “[w]ith the development of safer vaccines, the incidence of post-

vaccinal encephalomyelitis has decreased.” Id. She also mentioned the Topplak et al. 24 study,

where “researchers found an increased level of autoantibodies or appearance of new autoantibodies

in up to 15% of healthy individuals” one month post flu vaccination. Id. (citing Pet’r’s Ex. 17-27,

ECF No. 32). While the authors “did not find clinical significance to these autoantibodies,” Dr.

Ramos asserted that their increased presence “is of concern for the possibility of developing an

autoimmune disease post-vaccination, especially with an underlying condition or genetic

predisposition.” Id. An appropriate temporal relationship “between vaccine injection and

subsequent activation of an autoimmune condition such as ADEM could be coincidental.

Alternatively, it could reflect a causal association revealing a biological link.” Id.

In the present case, Dr. Ramos opined there is “a logical sequence of events and the timeline

of [Petitioner’s] symptoms consistent with the presentation of neurological complications

following vaccination, reported in the literature to be approximately [two] weeks after

vaccination.” Id. at 12. Petitioner’s “lack of previous symptoms, the evolution of symptoms, and

clinical presentation” support a causal connection.” Id. Dr. Ramos also noted that Petitioner’s

treaters considered whether her vaccination was related to the development of her symptoms. Id.

She noted that an infectious process or a cerebrovascular event “were evaluated and excluded by

the treating physicians.” Id. Relying on “convincing evidence in the literature that vaccination with

[flu] vaccine can cause neurological symptoms ranging from optic neuritis, ADEM, and GB,” Dr.

Ramos concluded that “there is sufficient evidence to support the conclusion that the [Petitioner’s]

symptoms were caused by the [flu] vaccine.” Id.

Following the filing of Respondent’s expert reports, Dr. Ramos submitted a supplemental

expert report reiterating that vaccine-induced injury must be considered in this case “after an

infectious etiology was out by the treating physician.” Pet’r’s Ex. 18 at 1, ECF No. 35-1. Her

second report also followed Dr. Schenck’s supplemental report and acknowledged his revised

opinion that “the clinical presentation of [Petitioner] does not fully support the diagnosis of

ADEM.” Id. Dr. Ramos then questioned whether the specific vaccine Petitioner received is

associated with encephalitis. Id. She noted that “[l]arge cohort studies have not shown an increase

in the risk of neurological complications after [flu] vaccine;” however, case reports “are evidence

of patients that have developed neurological and autoimmune disease post vaccination.” Id. Dr.

Ramos again noted that “[a]dditional studies to determine the clinical implications of [increased

numbers of autoantibodies post flu vaccination] are needed.” Id. at 2. In her final report, Dr. Ramos

stated that she “cannot in sound medical judgment state that vaccination is the most probable cause

of the [Petitioner’s] neurological presentation, but we cannot in all certainty exclude the possibility

that her symptoms were caused by the vaccine.” Id. She maintained her initial assertion that

23

Daniel A. Salmon et al., Did the Influenza A (H1N1) 2009 Monovalent Inactivated Vaccines Increase the

Risk for Guillain-Barré syndrome?, 9 EXPERT REV. CLINICAL IMMUNOLOGY 795 (2013).

24

N. Toplak et al., Autoimmune Response Following Annual Influenza Vaccination in 92 Apparently

Healthy Adults, 8 AUTOIMMUNITY REVS. 134 (2008).

11

Petitioner’s “timeline of the onset of her symptoms does support the theory of a vaccine induce[d]

complication.” Id. She added that “all [agree] that infectious causes are the most common causes

of meningoencephalitis, and it is not surprising and should not be considered conclusive of an

infectious process that the treating physicians treated the patient with antivirals and antimicrobials

upon admission.” Id. Without an alternative plausible cause, the temporal relationship between

Petitioner’s vaccination and neurological condition, Dr. Ramos argued that “[w]e cannot exclude

the possibility that [Petitioner’s] neurological condition was attributed to the [flu] vaccine.” Id.

She concluded that “[t]he clinical implications of eliciting and (sic) autoimmune response in

genetically predisposed individuals cannot be ignored. It is [her] opinion that the treating

physicians excluded other causes of [Petitioner’s] neurological deterioration and a vaccine related

adverse event following the [flu] vaccine is a more probable cause of [Petitioner’s] symptoms.”

Id. at 2–3.

B. Respondent’s Experts

1. Michael Wilson, M.D.

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

School of Medicine (“UCSF”). Resp’t’s Ex. B at 1, ECF No. 26-10. He completed his neurology

residency at Harvard Neurology Residency Program at Massachusetts General Hospital and

Brigham and Women’s Hospital. Id. Dr. Wilson has completed fellowships in neuro-infectious

diseases, virology, and metagenomics at Massachusetts General, National Emerging Infectious

Diseases Laboratories at Boston University School of Medicine, and UCSF School of Medicine,

respectively. Id. He is board certified in neurology with subspecialty training in neuro-infectious

diseases and neuroimmunology. Resp’t’s Ex. A at 1, ECF No. 26-1. He is currently the Director

of the UCSF Center for Encephalitis and Meningitis, a clinic where he “diagnose[s] and treat[s]

patients with a variety of neuroinflammatory disorders ranging from autoimmune diseases like

multiple sclerosis and neuromyelitis optica to infectious causes of meningitis and encephalitis.”

Id. Dr. Wilson also completes “[four] weeks of inpatient neurology per year at Zuckerberg San

Francisco General Hospital” and commonly encounters patients with acute meningoencephalitis.

Id. He is also an associate professor of neurology at UCSF in the Division of Neuroimmunology

and Glial Biology and a researcher that “has pioneered the development of metagenomic next-

generation sequencing to diagnose neurologic infections in patients with meningitis, encephalitis

and other neuroinflammatory conditions.” Id. His research also includes the development of

“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 has been published in the New England Journal of Medicine in

addition to several other top peer-reviewed journals. Id.

After a brief summary of Petitioner’s medical course, Dr. Wilson agreed “with the

[P]etitioner’s doctors and [] expert that [she] suffered from an acute meningoencephalitis given

the rapid onset of fever, confusion, focal neurologic signs (i.e., word finding difficulty)[,] and

seizure in the setting of a highly inflammatory CSF profile.” Id. at 1–2 (citing Resp’t’s Ex. A, Tab

1, ECF No. 26-2). 25 However, he cautioned, meningoencephalitis “is not a diagnosis[; i]t is a

25

A. Venkatesan et al., Case Definitions, Diagnostic Algorithms, and Priorities in Encephalitis: Consensus

Statement of the International Encephalitis Consortium, 57 CLINICAL INFECTIOUS DISEASES 1114 (2013).

12

syndrome that can be caused by more than 100 different infectious and non-infectious etiologies.”

Id. at 3. Dr. Wilson noted that treaters “frequently fail to identify the etiologic agent in a broad

array of encephalitis syndromes,” and in Petitioner’s case, no definitive diagnosis was made. Id.

(citing Resp’t’s Ex. A, Tab 1; Resp’t’s Ex. A, Tab 2, ECF No. 26-3; 26 Resp’t’s Ex. A, Tab 3, ECF

No. 26-4). 27 Nonetheless, Dr. Wilson agreed with Petitioner’s treaters that an infectious

meningoencephalitis “is much more likely than a non-infectious etiology, including vaccine-

associated ADEM.” Id. Petitioner’s testing of infectious agents was limited to a small number, and

Dr. Wilson asserted that “negative results for this limited number of pathogens by no means ‘rules

out’ an infectious etiology.” Id. He continued that it is still possible to “assess whether the patient

likely had an infectious or non-infectious cause of her meningoencephalitis,” even where the

testing is non-diagnostic. Id.

Dr. Schenk initially opined that Petitioner suffered from ADEM; however, Dr. Wilson

noted that Petitioner “was not known to have ‘the diagnostic hallmark of ADEM . . . , the

demonstration of scattered, focal or multifocal (disseminated) areas of inflammation and

demyelination within cerebral subcortical and deep cortical white matter.” Id. (citing Resp’t’s Ex.

A, Tab 7, ECF No. 26-8; 28 Resp’t’s Ex. A, Tab 8, ECF No. 26-9). 29 He concluded that there is

insufficient information to definitively classify her course as ADEM. Id. Additionally, Dr. Wilson

noted that despite the lack of a brain MRI, Petitioner’s “profile was not consistent with what is

seen in the vast majority of ADEM cases.” Id. at 4. Petitioner made a rapid and “dramatic” recovery

without receipt of any of the immunosuppressant medications “typically required to treat ADEM.”

Id. Her CSF profile was not consistent with ADEM cases, and specifically, her neutrophil cell

count was elevated. Id. Dr. Wilson explained that in ADEM cases, the elevation is usually with

respect to lymphocytes, not neutrophils, while “[n]eutrophils are typically elevated when a patient

is fighting a bacterial or fungal infection or in very early viral meningoencephalitis.” Id. (citing

Resp’t’s Ex. A, Tab 1). Petitioner also “had elevated systemic inflammatory markers (elevated

white blood cell count, erythrocyte sedimentation rate and procalcitonin) which are not elevated

in the context of ADEM,” combined with her high fever and intermittent hypotension, which are

also “consistent with an infectious etiology.” Id. Although Dr. Wilson asserted that there is

overwhelming evidence that Petitioner did not suffer from ADEM, he also argued that “she had

another potential temporally proximate trigger for ADEM: she was exposed to her children who

had viral upper respiratory infections in the week prior to her illness.” Id. (citing Resp’t’s Ex. A,

Tab 8). He acknowledged that “[t]here are rare reports of ADEM occurring in close temporal

association with different vaccines, but as the [P]etitioner’s expert notes, evidence for an increased

risk of ADEM in association with vaccines in general is scant, including for [flu] vaccines.” Id.

Dr. Wilson also acknowledged that the timing of Petitioner’s symptom onset approximately one

week post vaccination “is within the accepted range during which immune-mediated vaccine

26

Prashanth S. Ramachandran & Michael R. Wilson, Metagenomics for Neurological Infections -

Expanding Our Imagination, 16 NATURE REVS. NEUROLOGY 547 (2020).

27

Carol A. Glaser et al., In Search of Encephalitis Etiologies: Diagnostic Challenges in the California

Encephalitis Project, 1998-2000, 36 CLINICAL INFECTIOUS DISEASES 731 (2003).

28

James J. Sejvar et al., Encephalitis, Myelitis, and Acute Disseminated Encephalomyelitis (ADEM): Case

Definitions and Guidelines for Collection, Analysis, and Presentation of Immunization Safety Data, 25

VACCINE 5771 (2007).

29

McGraw-Hill Education, ADAMS AND VICTOR’S PRINCIPLES OF NEUROLOGY (Andrew Moyer & Kim J.

Davis eds., 11th ed. 2019).

13

complications occur.” Id. at 5. Instead, Dr. Wilson argued that Petitioner’s medical history, clinical

presentation, and laboratory workup all “argues strongly for her having an undiagnosed infectious

meningoencephalitis and not ADEM.” Id. at 4.

In Dr. Wilson’s supplemental report, he noted Dr. Schenk’s agreement with his assessment

of Petitioner’s condition, insofar as it is inconsistent with ADEM and “could very well have been”

infectious meningoencephalitis or even a bacterial infection that caused an inflammatory CNS

reaction. Resp’t’s Ex. E at 1, ECF No. 33-1. Dr. Wilson contemplated that, “[i]f we discount the

ADEM diagnosis, we are left wondering what link – if any – exists between [flu] vaccination and

meningoencephalitis.” Id. at 2. He acknowledged Dr. Schenk’s assessment of case reporting of

nervous system disorders, and how he acknowledged Dr. Wilson’s previous assertion that “these

are only case studies and the official surveillance has not found an association with the vaccine.”

Id. (quoting Pet’r’s Ex. 15 at 2). Dr. Schenk’s observation that the timing of the vaccination “would

rather be a coincidence” was dismissed by Dr. Wilson as “not a substantive argument for

affirmatively linking a vaccination to a neurologic event.” Id. (quoting Pet’r’s Ex. 15 at 2). Dr.

Wilson reiterated that “[a]t the time of the vaccination, [P]etitioner was an elderly woman with

multiple medical co-morbidities, including advanced age, hypertension and diabetes mellitus, who

also had recent sick contacts.” Id. He explained that “[t]hese are all risk factors for an infectious

meningoencephalitis from a variety of pathogens so for her to develop an infectious

meningoencephalitis at this time would not just be a ‘coincidence’” Id. Dr. Wilson also noted that

Petitioner filed “more than 100 associated exhibits [], the majority of which are not individually

cited in their opinions. Id. at 1. (citing Pet’r’s Exs. 16-1–16-69, ECF No. 29; Pet’r’s Exs. 17-2–17-

39, ECF No. 32). He concluded that “the expansive literature cited by the [P]etitioner’s experts is

not responsive to this case, and we are left with isolated case reports to speculate about any

potential link between the [P]etitioner’s condition and the [flu] vaccine she received.” Id. at 2.

2. Stephen M. Tompkins, Ph.D.

Dr. Tompkins received his Ph.D. in immunology from Emory University. Resp’t’s Ex. D

at 1, ECF No. 27-7. He completed post doctorate training in immunology and virology at

Northwestern University and the Center for Biologics Evaluation and Research at the United States

Food and Drug Administration. Id. Dr. Tompkins’ fellowships “focused on immunologic

mechanisms of induction of autoimmune disease, specifically interrogating antigen- and virus-

induced models of experimental autoimmune encephalomyelitis[;] and . . . understanding the

immune response to influenza infection and vaccination”. Resp’t’s Ex. C at 1, ECF No. 27-1. He

is currently Professor of Infectious Diseases in the Center for Vaccines and Immunology at the

University of Georgia and conducts research focused on “understanding the interactions of [flu]

virus and [flu] vaccines with the host.” Id. Dr. Tompkins is an ad hoc reviewer for the National

Institutes of Health (“NIH”) study sections and scholarly journals in the fields of virology and

immunology. Id.

Dr. Tompkins reviewed Petitioner’s medical record to complete his report; however, he

did “not comment on [Petitioner’s] diagnosis and [] instead refer[red] to the expert report provided

by [Dr. Wilson].” Id. at 4. In response to Dr. Schenk, Dr. Tompkins answered two questions: “1)

Is inactivated [flu] vaccine associated with meningoencephalitis or ADEM? [and] 2) Is there an

alternative explanation for the onset of disease?” Id. As to the first question, Dr. Tompkins

answered “[n]o.” Id. He argued that, notwithstanding Dr. Schenk’s reference to “literature

14

support[ing] evidence of immune-mediated inflammatory brain disorders following vaccination in

a wide spectrum of vaccines,” the inactivated flu vaccine bears no relationship to that group. Id.

(citing Pet’r’s Ex. 15 at 16). Dr. Tompkins then shifted to Dr. Schenk’s reliance on the Institute of

Medicine’s (“IOM”) assessment that the available “epidemiologic evidence [is] insufficient and

mechanistic evidence [is] weak for establishing a causal association between [flu] vaccination and

encephalitis or ADEM.” Id. (quoting Pet’r’s Ex. 15 at 17). Dr. Tompkins acknowledged that this

was “a reasonable representation of the findings of the IOM committee[;]” however, “it fail[ed] to

consider the basis for these assessments.” Id. According to Dr. Tompkins, the studies referenced

by the committee “utilized passive surveillance systems and did not have unvaccinated comparison

populations.” Id. Furthermore, “[m]echanistic evidence of a possible association between [flu]

vaccination and ADEM is entirely based upon reports of temporal associations and rare

associations between [flu] infection and ADEM.” Id. Dr. Tompkins also criticized Dr. Schenk’s

reliance on VAERS “due to the inherent limitations of passive surveillance.” Id. at 5. Specific to

ADEM, Dr. Tompkins cited Baxter et al. 30 as a work that “provides compelling evidence that [the

flu] vaccination is not associated with ADEM.” Id. (citing Resp’t’s Ex. C, Tab 3, ECF No. 27-4).

In response to the second question, Dr. Tompkins discussed Shukla et al., 31 “[a]n

assessment including clinical epidemiology and diagnostic evaluation of aseptic meningitis in the

United States [that showed] 81% of etiologies remained unknown.” Id. (citing Resp’t’s Ex. C, Tab

4, ECF No. 27-7). He noted other studies with similar percentages, including Aldriweesh et al., 32

with a 60% pathogen identification rate in aseptic meningitis patients. Id. (Resp’t’s Ex. C, Tab 5,

ECF No. 27-6). The literature suggests that “[b]ased upon the rate of undiagnosed viral infections

associated with meningoencephalitis, it is probable that a viral infection was not detected.” Id. at

6. Dr. Tompkins argued that this is consistent with the present case. Id. He noted that Petitioner’s

exposure to “the reported infections by two children the week before onset of symptoms,”

Petitioner’s “gastrointestinal symptoms and URI [are] indicative of a viral infection [as] the most

likely cause of [Petitioner’s] meningoencephalitis.” Id. (citing Pet’r’s Ex. 1 at 29, 27, 33).

Despite ultimately discounting ADEM as Petitioner’s correct diagnosis, Dr. Schenk’s

expert reports discussed the condition in depth. See Pet’r’s Exs. 15–16. Consequently, Dr.

Tompkins authored a supplemental report wherein he discussed “the likelihood that the [flu]

vaccine was associated with onset of ADEM.” Resp’t’s Ex. F at 2, ECF No. 33-2. Dr. Tompkins

clarified that he was not conceding that Petitioner “developed ADEM following receipt of the [flu]

vaccine.” Id. Indeed, he reasoned that “[b]oth Dr. Wilson and Dr. Schenk note[d] that ADEM was

unlikely,” and reiterated that he would defer to Dr. Wilson’s opinion on diagnosis. Id.

Dr. Tompkins opined that there is no evidence “that the 2017-2018 Afluria Quadrivalent

[flu] vaccine is associated with ADEM,” nor is there “evidence of molecular mimicry by the 2017-

2018 Afluria Quadrivalent [flu] vaccine eliciting ADEM.” Id. at 6. He reiterated his previously

stated position that the flu vaccine is not associated with encephalitis, and that a more likely cause

for Petitioner’s condition is an infectious process. Id. at 6–7. Dr. Tompkins concluded that

30

Baxter, surpa note 13.

31

Bhavarth Shukla et al., Aseptic Meningitis in Adults and Children: Diagnostic and Management

Challenges, 94 J. CLINICAL VIROLOGY 110 (2017).

32

Mohammed A. Aldriweesh et al., Viruses Causing Aseptic Meningitis: A Tertiary Medical Center

Experience with a Multiplex PCR Assay, 11 FRONTIERS NEUROLOGY 1 (2020).

15

Petitioner’s gastrointestinal symptoms and proximity to individuals with URI symptoms provides

the best evidence for a viral cause. Id. at 8. Furthermore, Petitioner’s “recovery from encephalitis

following the intravenous antibiotics and antiviral drug treatment suggest resolution of an

infectious process causing the acute meningoencephalitis.” Id. Dr. Tompkins asserted that “many

if not a majority of infection encephalitis cases remain undiagnosed,” but in Petitioner’s case, “the

medical records provide compelling evidence of an . . . infection [as] the most likely cause of

[Petitioner’s] acute meningoencephalitis.” Id.

IV. Applicable Legal Standards

I am resolving Petitioner’s claim on the filed record. The Vaccine Act and Rules not only

contemplate but encourage special masters to decide petitions on the papers where, in the exercise

of their discretion, they conclude that doing so will properly and fairly resolve the case. See 42

U.S.C. § 12(d)(2)(D); Vaccine Rule 8(d). The decision to rule on the record in lieu of a hearing

has been affirmed on appeal. Kreizenbeck v. Sec’y of Health & Hum. Servs., 945 F.3d 1362, 1366

(Fed. Cir. 2020); see also Hooker v. Sec’y of Health & Hum. Servs., No. 02-472V, 2016 WL

3456435, at *21 n.19 (Fed. Cl. Spec. Mstr. May 19, 2016) (citing numerous cases where special

masters decided cases on the papers in lieu of hearing and those decisions were upheld). I am

simply not required to hold a hearing in every matter, no matter the preferences of the parties.

Hovey v. Sec’y of Health & Hum. Servs., 38 Fed. Cl. 397, 402–03 (1997) (determining that the

special master acted within his discretion in denying an evidentiary hearing); Burns v. Sec’y of

Health & Hum. Servs., 3 F.3d 415, 417 (Fed. Cir. 1993); Murphy v. Sec’y of Health & Hum. Servs.,

No. 90-882V, 1991 WL 71500, at *2 (Fed. Cl. Spec. Mstr. Apr. 19, 1991).

To receive compensation under the Vaccine Act, a petitioner must demonstrate either that:

(1) the petitioner suffered a “Table injury” by receiving a covered vaccine and subsequently

developing a listed injury within the time frame prescribed by the Vaccine Injury Table set forth

at 42 U.S.C. § 300aa-14, as modified by 42 C.F.R. § 100.3; or (2) that petitioner suffered an “off-

Table injury,” one not listed on the Table, as a result of receiving a covered vaccine. See 42 U.S.C.

§§ 300aa-11(c)(1)(C); Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1321 (Fed. Cir.

2010); Capizzano v. Sec’y of Health & Hum. Servs., 440 F.3d 1317, 1319–20 (Fed. Cir. 2006). In

this case, Petitioner does not allege a Table injury and must prove that her injury was caused-in-

fact by a Table vaccine.

To establish causation-in-fact, a petitioner must demonstrate by a preponderance of the

evidence that the vaccine was the cause of the injury. 42 U.S.C. § 300aa-13(a)(1)(A). A petitioner

is required to prove that the vaccine was “not only a but-for cause of the injury but also a substantial

factor in bringing about the injury.” Moberly, 592 F.3d at 1321–22 (quoting Shyface v. Sec’y of

Health & Hum. Servs., 165 F.3d 1344, 1352–53 (Fed. Cir. 1999)).

16

In the seminal case of Althen v. Sec’y of the Dept. of Health & Hum. Servs, the Federal

Circuit set forth a three-pronged test used to determine whether a petitioner has established a causal

link between a vaccine and the claimed injury. 418 F.3d 1274, 1278–79 (Fed. Cir. 2005). In

Broekelschen v. Sec’y of Health and Hum. Servs., the Federal Circuit recognized that in some

circumstances, the special master may “first determine which injury was best supported by the

evidence in the record before applying the Althen test.” 618 F.3d 1339, 1346 (Fed. Cir. 2010). This

principle also means that a petitioner must establish that the vaccinee suffers the injury allegedly

linked to the vaccination. Lombardi v. Sec’y of Health & Hum. Servs., 656 F.3d 1343, 1353–54

(Fed. Cir. 2011).

The Althen test requires petitioners to set forth: “(1) a medical theory causally connecting

the vaccination and the injury; (2) a logical sequence of cause and effect showing that the

vaccination was the reason for the injury; and (3) a showing of a proximate temporal relationship

between vaccination and injury.” Althen, 418 F.3d at 1278. To establish entitlement to

compensation under the Program, a petitioner is required to establish each of the three prongs of

Althen by a preponderance of the evidence. Id. “[C]lose calls regarding causation are resolved in

favor of injured claimants.” Id. at 1280. Further, evidence used to satisfy one prong of the test may

overlap to satisfy another prong. Capizzano, 440 F.3d at 1326.

Under the first prong of Althen, a petitioner must offer a scientific or medical theory that

answers in the affirmative the question: “can the vaccine[] at issue cause the type of injury

alleged?” See Pafford v. Sec’y of Health & Hum. Servs., No. 01-0165V, 2004 WL 1717359, at *4

(Fed. Cl. Spec. Mstr. July 16, 2004), mot. for rev. denied, 64 Fed. Cl. 19 (2005), aff’d, 451 F.3d

1352 (Fed. Cir. 2006). 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 548–49. Petitioners are not required to identify “specific biological

mechanisms” to establish causation, nor are they required to present “epidemiologic studies,

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

the scientific or medical communities.” Capizzano, 440 F.3d at 1325 (quoting Althen, 418 F.3d at

1280). Scientific and “objective confirmation” of the medical theory with additional medical

documentation is unnecessary. Althen, 418 F.3d at 1278–81; see also Moberly, 592 F.3d at 1322.

However, as the Federal Circuit has made clear, “simply identifying a ‘plausible’ theory of

causation is insufficient for a petitioner to meet her burden of proof.” LaLonde v. Sec’y of Health

& Hum. Servs., 746 F.3d 1334, 1339 (Fed. Cir. 2014) (citing Moberly, 592 F.3d at 1322). Indeed,

the Federal Circuit has “consistently rejected theories that the vaccine only ‘likely caused’ the

injury and reiterated that a ‘plausible’ or ‘possible’ causal theory does not satisfy the standard.”

Boatmon v. Sec’y of Health & Hum. Servs., 941 F.3d 1351, (Fed. Cir. 2019) (citing Moberly, 592

F.3d at 1322 and LaLonde, 746 F.3d at 1339). Rather, “[a] petitioner must provide a reputable

medical or scientific explanation that pertains specifically to the petitioner’s case.” Moberly, 592

F.3d at 1322. In general, “the statutory standard of preponderance of the evidence requires a

petitioner to demonstrate that the vaccine more likely than not caused the condition alleged.”

LaLonde, 746 F.3d at 1339.

Furthermore, establishing a sound and reliable medical theory connecting the vaccine to

the injury often requires a petitioner to present expert testimony in support of her claim. Lampe v.

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Sec’y of Health & Hum. Servs., 219 F.3d 1357,1361 (Fed. Cir. 2000). The Supreme Court’s

opinion in Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579 (1993), requires that

courts determine the reliability of an expert opinion before it may be considered as evidence.

However, in the Vaccine Program, the Daubert 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) (“[U]niquely in this Circuit, the Daubert factors have been employed also as an acceptable

evidentiary-gauging tool with respect to persuasiveness of expert testimony already admitted.”);

see also 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).

The Daubert factors are “meant to be helpful, not definitive.” Kumho Tire Co. v.

Carmichael, 526 U.S. 137, 151 (1999). The factors do not “constitute ‘a definitive checklist or

test’” and may be applied differently depending on the facts of a particular case. Id. at 150 (quoting

Daubert, 509 U.S. at 593).

“In short, the requirement that an expert’s testimony pertain to ‘scientific knowledge’

establishes a standard of evidentiary reliability.” Daubert, 509 U.S. at 590 (citation omitted). Thus,

for Vaccine Act claims, a “special master is entitled to require some indicia of reliability to support

the assertion of the expert witness.” Moberly, 592 F.3d at 1324. 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 v. Sec’y of Health & Hum. Servs., 88 Fed. Cl. 706, 743 (2009) (quoting Gen.

Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997)); see also D’Tiole v. Sec’y of Health & Hum. Servs.,

No. 15-085V, 2016 WL 7664475, at *24 (Fed. Cl. Spec. Mstr. Nov. 28, 2016) (stating that the

Vaccine Act “require[s] a chain of reliable propositions supporting [a] petitioner’s theory”).

Under the second prong of Althen, a petitioner must prove that the vaccine actually did

cause the alleged injury in a particular case. See Pafford, 2004 WL 1717359, at *4; Althen, 418

F.3d at 1279. 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;

Capizzano, 440 F.3d at 1326; Grant v. Sec’y of Health & Hum. Servs., 956 F.2d 1144, 1148 (Fed.

Cir. 1992). A petitioner does not meet this obligation by showing only a temporal association

between the vaccination and the injury; instead, the petitioner “must explain how and why the

injury occurred.” Pafford, 2004 WL 1717359, at *4 (emphasis in original). The special master in

Pafford noted petitioners “must prove [] both that her vaccinations were a substantial factor in

causing the illness . . . and that the harm would not have occurred in the absence of the

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vaccination.” 2004 WL 1717359, at *4 (citing Shyface, 165 F.3d at 1352). A reputable medical or

scientific explanation must support this logical sequence of cause and effect. Hodges v. Sec’y of

Health & Hum. Servs., 9 F.3d 958, 961 (Fed Cir. 1993) (citation omitted). Nevertheless,

“[r]equiring epidemiologic studies . . . or general acceptance in the scientific or medical

communities . . . impermissibly raises a claimant’s burden under the Vaccine Act and hinders the

system created by Congress . . . .” Capizzano, 440 F.3d at 1325–26. “[C]lose calls regarding

causation are resolved in favor of injured claimants.” Althen, 418 F.3d at 1280.

In Program cases, contemporaneous medical records and the opinions of treating

physicians are favored. Capizzano, 440 F.3d at 1326 (citing Althen, 418 F.3d at 1280). Indeed,

when reviewing the record, a special master must consider the opinions of treating physicians.

Capizzano, 440 F.3d at 1326. This is because “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.’” Id. In addition, “[m]edical records, in general, warrant

consideration as trustworthy evidence. The records contain information supplied to or by health

professionals to facilitate diagnosis and treatment of medical conditions. With proper treatment

hanging in the balance, accuracy has an extra premium. These records are also generally

contemporaneous to the medical events.” Cucuras v. Sec’y of Health & Hum. Servs., 993 F.2d

1525, 1528 (Fed. Cir. 1993). While a special master must consider these opinions and records,

they are not “binding on the special master or court.” 42 U.S.C. § 300aa-13(b)(1). Rather, when

“evaluating the weight to be afforded to any such . . . [evidence], the special master . . . shall

consider the entire record . . . .” Id.

To satisfy the third Althen prong, a petitioner must establish a “proximate temporal

relationship” between the vaccination and the alleged injury. Althen, 418 F.3d at 1281. This

“requires preponderant proof that the onset of symptoms occurred within a timeframe for which,

given the medical understanding of the disorder’s etiology, it is medically acceptable to infer

causation-in-fact.” de Bazan, 539 F.3d at 1352. Typically, “a petitioner’s failure to satisfy the

proximate temporal relationship prong is due to the fact that onset was too late after the

administration of a vaccine for the vaccine to be the cause.” Id. However, “cases in which onset is

too soon” also fail this prong; “in either case, the temporal relationship is not such that it is

medically acceptable to conclude that the vaccination and the injury are causally linked.” Id.; see

also Locane v. Sec’y of Health & Hum. Servs., 685 F.3d 1375, 1381 (Fed. Cir. 2012) (“[If] the

illness was present before the vaccine was administered, logically, the vaccine could not have

caused the illness.”).

Although a temporal association alone is insufficient to establish causation, under the third

prong of Althen, a petitioner must show that the timing of the injury fits with the causal theory.

See Althen, 418 F.3d at 1278. The special master cannot infer causation from temporal proximity

alone. See Thibaudeau v. Sec’y of Health & Hum. Servs., 24 Cl. Ct. 400, 403–04 (1991); see also

Grant, 956 F.2d at 1148 (“[T]he inoculation is not the cause of every event that occurs within the

ten[-]day period . . . [w]ithout more, this proximate temporal relationship will not support a finding

of causation.” (quoting Hasler v. United States, 718 F.2d 202, 205 (6th Cir. 1983))).

A petitioner who satisfies all three prongs of the Althen test has established a prima facie

showing of causation. Hammitt v. Sec’y of Health & Hum. Servs., 98 Fed. Cl. 719, 726 (2011). A

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petitioner who demonstrates by a preponderance of the evidence that she suffered an injury caused

by vaccination is entitled to compensation unless the respondent can demonstrate by a

preponderance of the evidence that the injury was caused by factors unrelated to the vaccination.

See Althen, 418 F.3d at 1278; Knudsen,., 35 F.3d 543at 547.In such a case, the government must

not merely prove the existence of an alternative cause, but that such an alternative actually caused

the injury. Knudsen, 35 F.3d at 549. Consequently, when and if the petitioner establishes a prima

facie case, the burden then shifts to the government to prove that an alternative cause, unrelated to

the administration of the vaccine, was the “sole substantial factor” in causing the alleged injury.

See de Bazan v. Sec’y of Health & Hum. Servs., 539 F.3d 1347, 1354 (Fed. Cir. 2008); see also

Hammitt, 98 Fed. Cl. at 726 (explaining that the respondent’s burden is to show that the “factor

unrelated” was the “sole substantial factor” in causing the injury). Additionally, a factor unrelated

“may not include ‘any idiopathic, unexplained, unknown, hypothetical, or undocumentable cause,

factor, injury, illness or condition.’” 42 U.S.C. § 300aa-13(a)(2); see also Doe v. Sec’y of Health

& Hum. Servs., 601 F.3d 1349 (Fed. Cir. 2010) (stating that an idiopathic diagnosis cannot be a

“factor unrelated,” as it is idiopathic).

V. Discussion

A. Diagnosis

Petitioner presented to the hospital seven days post vaccination, on January 5, 2018, with

symptoms of confusion, nausea, vomiting, abdominal pain, and tremors. Pet’r’s Ex. 3 at 29. She

further complained of high fever and deliriousness that began the previous day. Id. On January 7,

2018, Petitioner was seen by a geriatric specialist, whose preliminary impression included a

notation to “rule out infectious meningoencephalitis,” and who opined that Petitioner’s “persistent

fever curve [was] more suggestive of CNS fever.” Id. at 38. Throughout Petitioner’s

hospitalization, multiple treaters sought to determine her condition’s etiology, but there is no

evidence that they ever considered ADEM or any other demyelinating disorder as a differential

diagnosis. See id. at 5. Petitioner’s expert neurologist, Dr. Schenk, originally opined that ADEM

was “the most acceptable diagnosis” to consider despite her presentation’s divergence with a

typical ADEM clinical course. Pet’r’s Ex. 15 at 18. Dr. Schenk provided a comprehensive

explanation of the symptoms, progression, and diagnosis of ADEM in support of his assertion. Id.

11–18. It is not necessary, however, to consider Dr. Schenk’s argument on this matter, because in

a subsequent report, Dr. Schenk modified his opinion. Pet’r’s Ex. 16 at 2. He noted that Petitioner’s

MRI and CSF profile did not support an ADEM diagnosis and described her case as atypical. Id.

Despite his acknowledgment that common ADEM treatments were not administered and did not

factor into her dramatic and rapid recovery, he maintained that ADEM was a potential differential

diagnosis. Id. Ultimately, he conceded that meningoencephalitis was the correct diagnosis, and it

was much less likely that Petitioner suffered from an acute demyelinating event such as ADEM.

Id. Respondent’s expert, Dr. Wilson, agreed with the infectious meningoencephalitis diagnosis

from Petitioner’s hospitalization. Resp’t’s Ex. B at 3. He identified the inconsistencies between

Petitioner’s condition and what is commonly seen in ADEM patients. Id. Presently, there is no

material dispute as to Petitioner’s meningoencephalitis diagnosis, but Petitioner and Respondent

do dispute whether her condition is due to a vaccine-initiated, autoimmune response or an

unidentified infection. Notwithstanding the agreement on Petitioner’s underlying condition, it is

important to note how Petitioner’s theory of injury has evolved. Dr. Schenk’s opinion is directly

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at odds with Dr. Wilson’s, and their respective expertise on the nature of Petitioner’s condition

and its pathogenesis cannot be separated from the ability to correctly diagnose her condition as a

preliminary matter. I find that there is preponderant evidence that Petitioner suffered from

meningoencephalitis.

B. Althen Prong One – Medical Theory

The biological mechanism in this case is initially presented by Dr. Schenk but expanded

on by Dr. Ramos, a geriatric specialist with expertise in allergy and immunology. See Pet’r’s Ex.

15; Pet’r’s Ex. 17. In his first report, Dr. Schenk described a cross-reaction process wherein

proteins that protect and support the function of the myelin sheath in the CNS are attacked by

antiviral antibodies or a cell-mediated response and cause neurological dysfunction. Pet’r’s Ex. 15

at 1. This theory is specific to neurological conditions, but it is only relevant to conditions that

include demyelination. While demyelination does occur in some cases of meningoencephalitis, the

lack of demyelination in the present case was a key factor in determining Petitioner’s diagnosis.

In Dr. Schenk’s second report, he conceded that it is less likely that Petitioner suffered from an

atypical ADEM case, but he maintained that her flu vaccine “appeared to be a contributing factor

to the development of a delayed meningoencephalitis.” Pet’r’s Ex. 16 at 2. Dr. Schenk did not

expound further on the biological mechanism but noted that he “agree[d] with Dr. Cristina Ramos’

reported observations and defer[ed] to the evidence included in the details of the theory included

in [her] report.” Id. at 1.

Dr. Ramos identified molecular mimicry and immune cross-reaction as a “possible and

viable explanation of how vaccines may cause neurological disease.” Pet’r’s Ex. 17at 8. Dr. Ramos

described the general theory of cross-reactivity due to structural homology between pathogens and

self-antigens. Id. She then asserted that “molecular mimicry has been widely accepted as a proven

concept and is considered to be one of the mechanisms in which viral or bacterial infection can

result in the development or worsening of autoimmune disease.” Id. at 9. Specifically, Dr. Ramos

discussed molecular mimicry in the context of GBS and narcolepsy following flu vaccines. Id. at

10–11. She also discussed case reports of encephalitis following rabies and Japanese encephalitis

vaccines. Id. at 11. Although she discussed a possible link between vaccines and the category of

neurological disease, Dr. Ramos did not articulate a theory that links the flu vaccine administered

in this case to meningoencephalitis. Indeed, her entire general causation argument could be

inserted into any case that alleges any vaccine caused any autoimmune disease. See Dennington

v. Sec’y of Health & Hum. Servs., 167 Fed. Cl. 640 (Fed. Cl. Sept. 20, 2023), appeal withdrawn,

No. 2024-1214 (Fed. Cir. 2024). In addition to molecular mimicry, Dr. Ramos also briefly

mentioned bystander activation, epitope spreading, and polyclonal activation. Id. at 10. However,

she did not explain how one or more of these processes worked to form a chain of reliable

propositions supporting vaccine causation. Dr. Ramos highlighted a study that found increased

autoantibody levels post flu vaccination, but she was unable to articulate any clinical significance

or relevance to encephalitis pathogenesis. Id. at 11 (citing Pet’r’s Ex. 17-27). Drs. Schenk and

Ramos identified medical theories, but did not persuasively explain how these offered mechanisms

of vaccine causation are relevant to this case. Accordingly, Petitioner has not presented

preponderant evidence of a sound and reliable medical theory connecting the flu vaccine to

meningoencephalitis.

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C. Althen Prong Two – Actual Causation

Upon presentation to the hospital, Petitioner was treated with broad spectrum antibiotics

and antiviral therapies, despite her physicians’ inability to identify a particular infectious agent.

Pet’r’s Ex. 3 at 39–40, 45. Petitioner was continued on this treatment as testing for West Nile,

CMV, HSV, and Enterovirus came back negative, and her condition improved. Id. at 103.

Petitioner’s symptoms were severe and required life-saving treatments, including ICU care and

intubation. Id. at 32. Approximately six days into her hospitalization, or around January 11, 2018,

Dr. Butler questioned the potential effect of Petitioner’s vaccination on her condition. Pet’r’s Ex.

5 at 20. Her treaters explored many possible causes but ultimately proceeded as though her

condition had an infectious etiology. Id. This is further reflected in her discharge diagnosis on

January 16, 2018, which notes a possible viral cause, but no relationship to her flu vaccine. Pet’r’s

Ex. 3 at 119. Dr. Miljkovic saw Petitioner for follow up at the end of January and agreed with

Petitioner’s encephalitis diagnosis but was unclear on the etiology noting possibly viral versus post

vaccination. Pet’r’s Ex. 9 at 4. Petitioner was later seen by Dr. Barasch, who also agreed with her

discharge diagnosis. Pet’r’s Ex. 5 at 19. Following assessment, she recorded Petitioner’s condition

as viral encephalitis. Id. at 14. The mention and consideration of a possible relationship between

her vaccination and meningoencephalitis illustrates that Petitioner’s treaters were open and

dedicated to determining the cause of her symptoms. That does not mean that they believed her

condition to be more likely than not caused by the flu vaccine. In fact, although more than one of

her treaters concluded that her encephalitis was viral, any mention of vaccine causation was tied

to the temporal relationship or noted as a possibility.

Petitioner’s inability to meet her burden of articulating a general theory of causation is fatal

to her claim, but the strongest evidence in support of dismissal is her own expert’s statements

regarding actual causation. In her first expert report, Dr. Ramos opined that “we have already

established that it is more likely that [Petitioner’s] symptoms were caused by an infection.” Pet’r’s

Ex. 17 at 7. She added that the temporal relationship between vaccination and symptom onset

creates the possibility of vaccine causation. Id. 7–8. However, the plain meaning of Dr. Ramos’

former statement precludes any finding that it is more likely than not Petitioner’s symptoms were

caused by her vaccine. Evidence of mere possibility is not enough. Dr. Ramos went on to assert

that there was “sufficient evidence to support the conclusion that [Petitioner’s] symptoms were

caused by the [flu] vaccine.” Id. at 13. Dr. Ramos did not simply say that Petitioner’s symptoms

were caused by the flu vaccine. Then, in her supplemental report, Dr. Ramos again undercut

Petitioner’s ultimate contention and stated that she “cannot in sound medical judgement state that

vaccination is the most probable cause of [Petitioner’s] neurological presentation.” Pet’r’s Ex. 18

at 2. Dr. Ramos offered a disclaimer, noting that “we cannot in all certainty exclude the possibility

that [Petitioner’s] symptoms were caused by the vaccine.” Id. However, that is not the standard for

establishing any fact within the Program. Again, it is curious how Dr. Ramos reconciled her

medical judgment with her later opinion that “a vaccine related adverse event following the [flu]

vaccine is a more probable cause of [Petitioner’s] symptoms.” Id. Considering Petitioner’s

complete medical record and that Petitioner’s own immunologist is unable to attribute her

condition to vaccination, I do not find there is preponderant evidence that Petitioner’s

meningoencephalitis was vaccine caused.

D. Althen Prong Three – Temporal Relationship

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Drs. Schenk and Ramos both relied heavily on the timing of Petitioner’s symptoms in

support of vaccine causation. See Pet’r’s Ex. 15; Pet’r’s Ex. 17. Petitioner’s experts focused their

opinions on ADEM and argued that Petitioner’s symptom manifestation approximately one week

post vaccination was strong evidence of causation. However, both experts conceded that ADEM

is likely not the proper diagnosis, and I have found that there is no preponderant evidence of this

condition in the record. Therefore, a timeline for vaccine-caused ADEM would be analogous at

best. Instead, the medical records, which are favored and presumed trustworthy, are determinative

here. During Petitioner’s hospitalization and follow up, multiple treaters noted that the timing of

her symptoms was consistent with vaccine-caused encephalitis. It appeared to be the driving factor

for consideration of a vaccine etiology after testing did not reveal a specific infectious cause.

Therefore, despite Petitioner’s lack of preponderant evidence of a biological mechanism linking

flu vaccine to meningoencephalitis, I find there is preponderant evidence of an appropriate

temporal relationship between her vaccination and the onset of symptoms approximately seven

days later. This relationship is insufficient however, to cure the evidentiary shortcomings under

Althen prongs one and two. See Grant, 956 F.2d at 1148 (“Temporal association is not sufficient,

however, to establish causation in fact.”).

VI. Conclusion

After a careful review of the record, Petitioner has failed to prove by preponderant evidence

that her injuries, including meningoencephalitis, were caused by her December 29, 2017, flu

vaccination. Accordingly, I DENY Petitioner’s claim and DISMISS her petition. 33

IT IS SO ORDERED.

s/Herbrina D.S. Young

Herbrina D.S. Young

Special Master

33

Pursuant to Vaccine Rule 11(a), entry of judgment is expedited by the parties’ joint filing of a notice

renouncing the right to seek review.

23