Goff v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 17-259V

Filed: January 13, 2025

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HEATHER GOFF, *

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Petitioner, *

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v. *

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SECRETARY OF HEALTH AND *

HUMAN SERVICES, *

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Respondent. *

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Alison Haskins, Siri & Glimstad, LLP, Aventura, FL, for Petitioner;

Lara A. Englund, U.S. Department of Justice, Washington, DC, for Respondent.

DECISION DENYING ENTITLEMENT1

Shah, Special Master:

On February 23, 2017, Heather Goff (“Petitioner”) filed a petition for compensation under

the National Vaccine Injury Compensation Program, 42 U.S.C. § 300aa-10, et seq.2 (the “Vaccine

Act” or “Program”). The petition alleges that Ms. Goff suffered strokes caused by an influenza

(“flu”) vaccination she received on March 22, 2016. Pet. at 3 (ECF No. 1).

1

Because this Decision contains a reasoned explanation for the action 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. For ease of citation,

all “§” references to the Vaccine Act in this Decision will be to the pertinent subparagraph of 42 U.S.C. §

300aa (2012).

I have reviewed the evidence presented in this case, and I conclude that Petitioner has not

established by preponderant evidence that the vaccine she received caused her condition. The

petition is accordingly dismissed.

I. PROCEDURAL HISTORY

Petitioner filed a signed statement along with the petition. Ex. 1. Subsequently, Petitioner

filed medical records and a statement of completion. See ECF Nos. 6, 8, 9, 10. On September 11,

2017, Respondent filed a Rule 4(c) Report (“Report”), contending that the case was not appropriate

for compensation and should be dismissed. Report at 7-8 (ECF No. 18).

On November 14, 2017, Petitioner filed an expert report and curriculum vitae from Laura

S. Boylan, M.D. Exs. 16-17. On November 28, 2017, Petitioner filed medical literature in support

of Dr. Boylan’s opinions. Exs. 19-33. On June 14, 2018, Respondent filed an expert report from

Steven Messé, M.D., along with Dr. Messé’s curriculum vitae and medical literature. Exs. A &

Tabs 1-5, B. On November 12, 2019, Petitioner filed a supplemental expert report from Dr.

Boylan. Ex. 35. Respondent declined to file a supplemental expert report from Dr. Messé. ECF

No. 45.

Former Special Master Katherine E. Oler held an entitlement hearing on April 6-7, 2021,

by videoconference. Petitioner, Dr. Boylan, and Dr. Messé testified at the hearing. See generally

Transcript (ECF No. 60). Both parties filed pre- and post-hearing briefs. ECF Nos. 50, 53, 54,

67, 70, 72. After the hearing, Petitioner filed additional medical records and literature, and

Respondent filed additional literature. ECF Nos. 63, 65, 69.

On August 13, 2024, this case was reassigned to me. ECF No. 78. The case is ripe for

adjudication.

II. FACT EVIDENCE

A. Petitioner’s Statement

Petitioner was 43 years old at the time of the subject flu vaccination. Ex. 1 at 1. Her past

medical history included hyperthyroidism that was controlled by medication. Id. Before the

vaccination, she engaged in weightlifting, biking, hiking, and other outdoor activities, and she was

employed as a physiotherapist. Id.

On September 14, 2015, Petitioner was given a flu vaccination that was required by her

employer, Laporte Hospital. Ex. 1 at 1. She said that “[t]his was the first time I had a flu shot in

about 18 years.” Id. She did not have any lingering effects from that vaccination aside from a few

days’ worth of shoulder pain. Id.

In early 2016, Petitioner moved to Arizona and took a job with Banner University Medical

Center (“Banner”) as a physical therapy (“PT”) assistant. Ex. 1 at 1. She was again advised that

she would be required to receive a flu vaccination as a condition of employment. Id. Although

2

she reported she had received a flu vaccination a few months earlier, Banner did not have the

record of that vaccination, so Petitioner was required to be vaccinated again. Id.

Petitioner received the subject flu vaccination on March 22, 2016. Ex. 1 at 1. Her left

deltoid was “sore and pink” for the next few days, but those symptoms “seemed to lessen over the

next week.” Id. at 2.

On March 30, 2016, Petitioner woke up with no feeling or control of her right arm, an

inability to speak, and right-sided facial drooping. Ex. 1 at 2. Petitioner’s roommate took her to

the nearest emergency room (“ER”), where she was diagnosed with a 20-30% blockage in her left

carotid artery, elevated cholesterol, and a transient ischemic attack (“TIA”) in the right parietal

lobe. Id.

Petitioner received PT and occupational therapy (“OT”) in the hospital, and she had a

cardiac loop monitor implanted in her left breast. Ex. 1 at 2. She was discharged from the hospital

on April 3, 2016. Id. On April 20, 2016, she experienced high blood pressure, as well as

“continued” left deltoid soreness that extended into her scapular area, shoulder, and jaw. Id. She

feared that she was having another TIA, so she went to the ER. Id. After medical tests came back

negative, she was discharged home. Id.

On June 24, 2016, Petitioner had a cerebral angiogram, which showed “non-significant

stenosis of the right carotid artery and ulcerated plaque on the left carotid artery, causing a

narrowing of about 35%[.]” Ex. 1 at 2.

On June 30, 2016, while Petitioner was at work, her supervisor noticed a change in her

speech. Ex. 1 at 2. She went to the ER, where she was diagnosed with acute, non-fluent aphasia

and admitted. Id. She underwent a brain biopsy, which revealed hemorrhage but no neoplasm or

infection. Id. at 3. She was hospitalized until July 7, 2016. Id.

In late July 2016, Petitioner returned to work on a restricted schedule. Ex. 1 at 3. She was

unable to fulfill her work duties, however, and was dismissed on September 23, 2016. Id. She

secured a new job in late 2016. Id. She said that she continues to experience numbness and

tingling on the right side of her body, along with memory problems and “trouble with numbers

and letters.” Id.

B. Petitioner’s Testimony

At the entitlement hearing, Petitioner testified that she was in excellent health and active

prior to the subject vaccination. Tr. at 5-6. She was under treatment for her thyroid. Id. at 6. She

had never suffered a stroke before her vaccination. Id.

Petitioner received a flu vaccination on September 14, 2015, at her previous place of

employment. Tr. at 6. She was required to receive the vaccination. Id. She experienced a few

days of arm soreness after that vaccination, but no other symptoms. Id.

3

On March 22, 2016, Petitioner received another flu vaccination that was required by her

new employer, Banner. Tr. at 7. She was feeling well at the time of the vaccination. Id. After

being vaccinated, she had a red, swollen arm for a “couple months.” Id.

The morning of March 30, 2016, Petitioner went into the kitchen to make coffee. Tr. at 8.

She dropped the coffee pod twice. Id. She “was feeling kind of funny.” Id. She then looked in

the mirror and noticed that her “face was drooped” and that she could not speak. Id. When her

roommate saw her, he believed she was having a stroke, so he took her to the hospital. Id.

After Petitioner was discharged from the hospital, she had difficulty keeping up with her

work responsibilities. Tr. at 10. She still experienced impairments from her stroke, including

memory problems and a “constant headache,” along with weight gain and fatigue. Id. at 10, 12,

14.

Petitioner underwent a cerebral angiogram and had to take off work for the test. Tr. at 10-

11. On June 30, 2016, while at work, she was taken to her supervisor’s office because she “wasn’t

talking straight” and was “babbling.” Id. at 12. Her supervisor suspected another stroke and took

her to the ER at Banner. Id.at 12-13. She remained in the hospital for a few days and had to

undergo a brain biopsy, along with PT, OT, and speech therapy. Id. at 13. When she returned to

work after being discharged, she had work restrictions. Id. at 14. Ultimately, she was dismissed

after being unable to keep up with her caseload. Id.

Petitioner testified that, since her strokes, she depleted her retirement savings and had to

file for bankruptcy. Tr. at 14-15. She can work but has limited her patient load. Id. at 14-16. She

has had difficulty maintaining relationships. Id. at 15. She also has facial asymmetry, and the

right side of her face is “droopy and wrinkled.” Id. at 17. She has right-sided weakness. Id. She

takes 325mg of aspirin every day. Id. She rates her daily symptoms at a 6 out of 10 in severity.

Id.

On cross examination, Petitioner testified that she could not recall developing any new

symptoms, including new memory, speech, or numbness problems, between her first and second

strokes. Tr. at 20.

C. Medical Records

The medical records confirm that Petitioner was 43 years old at the time of the subject flu

vaccination. Ex. 2 at 1. Her prior medical history included thyroid disease, for which she took

Synthroid. Ex. 7 at 16. She had no prior history of stroke.

On September 14, 2015, Petitioner was given a flu vaccination at Indiana University

Health. Ex. 14 at 1. On March 22, 2016, she was given another flu vaccination at Banner. Ex. 2

at 1.

There are no medical records between March 22 and 30, 2016. The morning of March 30,

2016, Petitioner was transported to the Abrazo West Campus (“Abrazo”) ER complaining of

slurred speech, facial droop, and right arm weakness and numbness, with an onset of that morning.

4

Ex. 6 at 12-14, 280-82. She recalled going to bed the previous night feeling well except for a

headache. Id. at 14. At the time of triage, the only symptom remaining was right arm numbness.

Id. at 12. She did not have a fever. Id. at 281. An exam showed no evidence of rash, swelling of

the left arm, or skin abnormalities. Id. The working diagnosis in the ER was an acute ischemic

stroke, which was characterized as a “wake-up stroke.” Id. at 13-14, 280-82. Petitioner was

admitted to the hospital. Id. at 282.

During an admission exam on March 30, 2016, Petitioner denied any history of prior

strokes, TIAs, irregular heartbeat, palpitations, or atrial fibrillation. Ex. 6 at 220. She reported

that she had been in “good chronic health.” Id. She stated that she smoked a little more than a

pack of cigarettes daily. Id. She also reported that several months earlier, she had a large

granuloma removed from the base of a tooth. Id. at 221. Again, an exam found no rash or other

skin abnormalities, and her extremities had no signs of clubbing, cyanosis, or edema. Id. at 222.

On March 30, 2016, Petitioner had a neurology consult with Ahmed El-Gengaihy, M.D.,

in the hospital. Ex. 6 at 227. Dr. El-Gengaihy noted that a CT scan of the head was normal, but

an MRI of the brain revealed a left middle cerebral artery acute infarct measuring 5 x 25 mm. Id.

at 230. An MRA of the neck without contrast revealed a possible filling defect of the left internal

carotid artery. Id. An MRA of the head showed no large vessel occlusion. Id. A CT angiogram

of the neck with and without contrast showed mild atherosclerotic changes in the left internal

carotid artery, with a small focal ulcerative plaque and stenosis of 30-40%. Id. A transesophageal

echocardiogram revealed mild atherosclerosis in the descending aorta but was otherwise normal.

Ex. 4 at 25-27; Ex. 6 at 306.

During a consult with cardiologist Rajkumar Sugumaran, M.D., on April 1, 2016,

Petitioner reported that “prior to her ER visit she was in her usual state of health.” Ex. 6 at 224.

She reported the removal of the granuloma and that she had received two flu vaccinations “7

months apart” that year. Id. Dr. Sugumaran implanted a cardiac loop recorder to monitor

Petitioner’s heart for arrhythmias. Ex. 8 at 21.

Lab work undertaken at Abrazo revealed an elevated cholesterol level, and Petitioner was

started on a statin. Ex. 6 at 5. Her troponin test was negative, as was urine toxicology. Id. at 5,

342. Her C-reactive protein3 (“CRP”) and erythrocyte sedimentation rate (“ESR”) levels 4 were

3

C-reactive protein: a globulin that forms a precipitate with the somatic C-polysaccharide of the

pneumococcus in vitro; it is the most predominant of the acute-phase proteins. DORLAND’S MEDICAL

DICTIONARY ONLINE (“DORLAND’S”), https://www.dorlandsonline.com/dorland/definition?id=100489

(last accessed January 2, 2025).

4

Erythrocyte sedimentation rate: the rate at which erythrocytes precipitate out from a well-mixed specimen

of venous blood, measured by the distance the top of the column of erythrocytes falls in a given time interval

under specified conditions; an increase in rate is usually due to elevated levels of plasma proteins, especially

fibrinogen and immunoglobulins, which decrease the zeta potential on erythrocytes by dielectric shielding

and thus promote rouleau formation. It is increased in monoclonal gammopathy, hypergammaglobulinemia

due to inflammatory disease, hyperfibrinogenemia, active inflammatory disease, and anemia. DORLAND’S,

https://www.dorlandsonline.com/dorland/definition?id=102146 (last accessed January 2, 2025).

5

normal. Id. at 342, 350. Her complete blood count (“CBC”) did not reveal any evidence of

inflammation. Id. at 349. Her hypercoagulable workup5 was normal. Id. at 344-48.

Petitioner was discharged from Abrazo on April 2, 2016. Ex. 6 at 5. Her diagnosis at the

time of discharge was acute cerebrovascular accident (“CVA”). Id.

On April 5, 2016, Petitioner followed up with Dr. Sugumaran. Ex. 8 at 7. Petitioner

reported left arm, shoulder, and left-sided neck tightness, with an onset of that morning. Id. at 7,

9. She also reported decreased facial sensations. Id. at 7. She denied any chest pain, chest

pressure, shortness of breath, orthopnea, dizziness, palpitations, presyncope, or syncope. Id. Her

physical exam was normal except for elevated blood pressure. Id. at 8-9. Dr. Sugumaran assessed

CVA, hyperlipidemia, hypertension, left arm pain, and tobacco abuse. Id. at 10. He counseled

Petitioner about quitting smoking. Id.

On April 15, 2016, Petitioner submitted a VAERS report in which she stated that she

received a flu vaccination on March 22, 2016, and experienced the onset of facial numbness, facial

drooping, difficulty speaking, arm and hand numbness, and decreased object recognition and

processing sensations beginning on March 30, 2016. Ex. 3 at 1.

On April 20, 2016, Petitioner was brought to the ER by ambulance, complaining of left

arm pain that was radiating to her neck and jaw. Ex. 6 at 494. She reported the symptoms began

while she was at home. Id. She also reported that “she received [the] flu vaccine two weeks ago

on [the] affected arm.”6 Id. Her neurological exam was normal, and the examining physician

noted that she was scheduled to see her neurologist two hours later. Id. at 497. Lab results were

normal. Ex. 4 at 10-19. She was discharged home with a diagnosis of arm pain of unknown cause.

Ex. 6 at 497.

Later that day, Petitioner saw Dr. El-Gengaihy. Ex. 10 at 9. On her intake form, she

described her complaint as “[follow-up] after TIA and [left] deltoid flu shot [with] ‘fever’ in my

shoulder, neck, chest and scapular region,” which had been ongoing “since” March 22, 2016. Id.

at 5. She further reported that she had suffered a TIA on March 22, 2016, the day of vaccination.

Id. Her exam was normal, with no evidence of edema or rashes. Id. at 6, 9. Dr. El-Gengaihy

ordered a cerebral angiogram to rule out vasculitis. Id. at 10.

On May 9, 2016, Petitioner had another follow-up with Dr. Sugumaran. Ex. 8 at 1. Her

cardiac loop recorder had detected only one episode of bradycardia since implantation. Id. She

complained of an itchy scalp but was otherwise doing well from a cardiac standpoint. Id. She had

no symptoms of angina. Id. She reported that she had stopped smoking. Id. at 4. Dr. Sugumaran

assessed “unchanged” CVA, hyperlipidemia, and hypertension, “improved” tobacco abuse, and

“resolved” left arm pain. Id. at 3-4.

5

Hypercoagulability: the state of being more readily coagulated than normal. Hypercoagulability,

DORLAND’S, https://www.dorlandsonline.com/dorland/definition?id=23731 (last accessed January 2,

2025).

6

In fact, the vaccine had been given 35 days earlier. Ex. 2 at 1.

6

On June 24, 2016, Petitioner underwent a cerebral angiogram, which found an ulcerated

plaque in the left internal carotid artery, causing about 40% narrowing of the artery. Ex. 15 at 673-

77. She tolerated the procedure well. Id. at 677.

Six days later, on June 30, 2016, Petitioner presented to the ER at Banner with complaints

of expressive aphasia. Ex. 15 at 544. She was seen by neurologist Douglas Franz, M.D. Id. She

could not provide a history due to difficulty speaking. Id. Dr. Franz recorded her NIH stroke

scale7 as 1 for right-sided hemisensory changes and 1 for nonfluent aphasia. Id. On exam,

Petitioner was aphasic but could at times put three words together in a meaningful sentence. Id.

at 545. She had mild dysnomia, but her comprehension appeared intact. Id. She had difficulty

with repetition. Id. Her facial sensation was diminished on the right side, but her face, tongue,

and palate were symmetric. Id. Her motor exam and reflexes were normal, but she had diminished

light-touch sensation on the right side of her body. Id. Dr. Franz noted that Petitioner had a history

of stroke earlier that year, with a “probable residual sensory deficit on the right[.]” Id. at 546. He

recommended admission for treatment with IV tissue plasminogen activator (“tPA”) pursuant to

hospital protocol. Id. at 544-46.

In the hospital, Petitioner underwent another MRI of the brain that showed a 2.3-cm left

thalamic lesion, which was potentially consistent with a subacute infarct but was also concerning

for neoplasm. Ex. 15 at 550. She also had a CT angiogram of the neck, which was interpreted as

showing bilateral carotid webs, with the more prominent web in her left internal carotid artery. Id.

at 473. The interpretation was that neither web appeared hemodynamically significant. Id. at 474.

On July 3, 2016, Petitioner was seen by neurosurgeon Jose Menendez, M.D., who was

concerned she might have a high-grade glioma. Ex. 9 at 5. She underwent a brain biopsy on July

5, 2016, which showed that the tissue exhibited “hemorrhage, reactive gliosis and foamy histocyte

infiltrate.” Id. at 9-11. The foamy cells were felt to be consistent with a history of stroke. Id. at

7. There was no evidence of neoplasm or infection. Id. The pathology report stated that the tissue

showed “an inflammatory-reactive process characterized by sharply demarcated foci of damage

containing clusters of wall-to-wall macrophages, rimmed by enlarged/tortuous axonal profiles

(axonal spheroids), parenchymal and perivascular chronic inflammation and reactive vessels.” Ex.

15 at 785.

On July 7, 2016, Petitioner was discharged from Banner to home. Ex. 15 at 8-9. Her

discharge diagnoses included left thalamus lesion, status post left frontal burr hole for stereotactic

needle biopsy; history of left thalamic stroke; and aphasia, status post IV tPA given for concern

for CVA. Id. She had undergone PT, OT, and speech therapy in the hospital. Id. at 9. At the time

of discharge, she was able to walk without assistance, though she still had aphasia, which had

7

The NIH stroke scale is “widely used [to help] health care providers assess the severity of a stroke. Health

care providers use it to measure neurological function and deficits by asking the person to answer questions

and perform several physical and mental test…. Using a numerical scale to determine stroke severity, health

care providers record the person’s performance in 11 categories, such as sensory and motor ability.” NIH,

NIH Stroke Scale,

https://www.ninds.nih.gov/health-information/stroke/assess-and-treat/nih-stroke-scale (last accessed on

January 2, 2025). A score of 1 is defined as “1 = Not alert; but arousable by minor stimulation to obey,

answer, or respond.” Id.

7

persisted throughout her hospitalization. Id. She was instructed not to drive. Id. She was referred

for outpatient speech therapy. Id.

On July 15, 2016, Petitioner followed up with her primary care physician (“PCP”), Peter

Young, M.D. Ex. 4 at 5. Her exam was normal. Id. at 7-8. Dr. Young advised her to stop

smoking. Id. at 9. On July 18, 2016, Petitioner returned to Dr. Young so that leave-related forms

could be completed. Id. at 1. On October 3, 2016, she saw Dr. Young to discuss lab results relating

to her thyroid condition. Id. at 28. Her exam was normal, but she had low TSH levels. Id. at 30.

The plan was to decrease her Synthroid dosage and recheck her TSH in two months. Id. at 31.

On February 13, 2018, Petitioner saw Dr. Franz. Ex. 37 at 1. Dr. Franz noted that she had

experienced two cryptogenic strokes. Id. He commented that she had a history of carotid web.

Id. At the time of the visit, Petitioner complained of right-sided sensation changes, skin sensitivity

to touch, post-stroke depression, and headaches. Id. Dr. Franz assessed depressive disorder,

central pain syndrome, and stroke. Id. at 2. He noted that Petitioner had a “history of left peri-

insular and left thalamic stroke the former of which may be related to left carotid web and the

second may have been a periprocedural [complication].” Id. He prescribed duloxetine for pain

and depression, along with aspirin, and referred Petitioner to a psychologist. Id.

In 2019, Petitioner was diagnosed with Crohn’s disease, for which she was prescribed

Lialda.8 See Ex. 40 at 159. She moved to California and established care with Kaiser Permanente.

See generally Ex. 40. On July 2, 2020, she had a telehealth visit with Florence Leung, M.D.,

during which she complained of gastrointestinal symptoms but no neurologic ones. Id. at 71. Her

records indicated a remote history of CVA. See, e.g., id. at 159.

On August 28, 2020, Petitioner sent electronic messages to Dr. Leung complaining of

headaches on the side of her head on which she had experienced the strokes. Ex. 40 at 178-79.

She requested a referral to a neurologist. Id. Dr. Leung prescribed nortriptyline, but Petitioner

later reported that the medication gave her unusual dreams and did not work, so she stopped taking

it. Id. at 178. There is no indication that Petitioner saw a neurologist for her headaches. There

are no further relevant medical records.

III. EXPERT EVIDENCE

A. Petitioner’s Expert: Laura S. Boylan, M.D.

1. Qualifications

Dr. Boylan authored two expert reports in this case. Ex. 16 (“First Boylan Rep.”); Ex. 35

(“Second Boylan Rep.”). She received her M.D. in 1994 from the Columbia University College

of Physicians & Surgeons. Ex. 18 (“Updated Boylan CV”) at 1. She completed a residency in

neurology at The Neurological Institute at Columbia-Presbyterian Medical Center, and a post-

doctoral clinical research fellowship at The Neurological Institute and New York State Psychiatric

Institute. Id. at 2.

8

Petitioner’s diagnosis was later changed to ulcerative colitis. Ex. 40 at 200.

8

According to the documents in the record and the hearing testimony, Dr. Boylan is board

certified in neurology and is an attending neurologist at Bellevue Hospital Center in New York

City. Id. She has also worked as a neuro-hospitalist at Essentia Health in Duluth, Minnesota,

where she has covered the stroke service. First Boylan Rep at 1; Tr. at 25-26. She has taught

neurology at New York University School of Medicine in several different roles. Updated Boylan

CV at 2. She estimated that she has diagnosed and treated more than 1,000 patients with stroke

and more than 100 cases of post-infectious neurological symptoms. First Boylan Rep. at 2.

Dr. Boylan is a member of the American Academy of Neurology, the American

Neurological Association, and the Movement Disorder Society. Tr. at 24. She has served as an

ad hoc reviewer for Neurology, Brain, Epilepsia, BMJ Case Reports, Seizure, Epilepsy &

Behavior, and other publications. Updated Boylan CV at 3-4. She also served on the editorial

board of Practical Reviews in Neurology. Id. at 4. She has authored 11 peer-reviewed papers and

10 abstracts. Id. at 8-9, 12.

2. Dr. Boylan’s First Expert Report

Dr. Boylan explained that “[t]here is substantial evidence that inflammation plays a role in

stroke.” First Boylan Rep. at 3. Vaccinations provoke the immune/inflammatory system,

“inducing a series of cellular and molecular events in the body referred to as an ‘inflammatory

cascade.’” Id. Although this response is protective in the “vast majority of individuals,” it rarely

can be harmful. Id.

Dr. Boylan noted that “influenza vaccination has been shown to decrease cardiovascular

risk at the population level[.]” First Boylan Rep. at 3. But “this does not indicate that Ms. Goff’s

influenza vaccinations did not cause or contribute to her stroke.” Id. She observed that acute

infections, including flu infection, have been associated with an increased risk of vascular events.

Id. “[T]his observation has raised concern that vaccination itself could be associated with

increased short term stroke risk,” based on a “plausible scientific basis for causality.” Id.

Although the flu vaccination is generally recommended once a year, Dr. Boylan pointed

out that some populations, like infants and children, are given booster doses to ensure adequate

protection. First Boylan Rep. at 3-4. This suggests that the clinical response to vaccination –

including the potential for adverse response – is affected by the frequency of vaccination and the

total dose of vaccine given. Id. at 4. Petitioner received two flu vaccinations during one season,

which might have produced an enhanced immune provocation and a “higher risk of adverse

events.” Id.

Dr. Boylan stated that the “event of March 30, 2016 was clearly a stroke,” and the “event

of June 30, 2016 was most likely a second stroke, but there is a possibility that it represents

primarily inflammation or progression/extension of the first stroke.” First Boylan Rep. at 5.

Petitioner’s imaging revealed the presence of bilateral carotid webs, worse on the left than the

right. Id. at 9. A carotid web is “a particular abnormality in the wall of one of the major vessels

which provides blood to the brain.” Id. at 5. These carotid webs increased Petitioner’s propensity

for stroke. Id. Notably, “[t]he web is most prominent on Ms. Goff’s left side and that is the side

9

where she had both strokes.” Id.

Petitioner’s June 30, 2016 brain imaging “showed a stroke in the territory supplied with

blood which passes through the carotid web.” First Boylan Rep. at 9. That imaging showed a

second lesion that was distinct from the first stroke on March 30, 2016, but adjacent to the previous

stroke. Id. Dr. Boylan agreed with Petitioner’s treating physicians that the lesion from the second

event “did not look like a stroke,” because it was deep and irregular, suggesting that it might have

been caused by a tumor or infection. Id.

Dr. Boylan explained that repeated strokes in a woman in her forties are “extremely rare,”

and the decision to perform a biopsy of the lesion illustrates “how atypical and unusual Ms. Goff’s

clinical situation and brain imaging were.” First Boylan Rep. at 9. The biopsy revealed abundant

inflammatory cells and demonstrated an active inflammatory process that was sufficient to light

up on an MRI, another unusual occurrence. Id. at 9-10. Dr. Boylan concluded that “[t]he tissue

biopsy provided [a] definitive diagnosis of an active inflammatory process and did not show

changes associated with tumors or infections.” Id. at 10.

Dr. Boylan noted that Petitioner’s “extensive stroke evaluation did not reveal any apparent

cause of stroke other than the carotid webs.” First Boylan Rep. at 10. The role of carotid webs in

predisposition to stroke is an “emerging area” of medicine. Id. In Dr. Boylan’s opinion, the carotid

webs made Petitioner particularly vulnerable to strokes. Id.

Dr. Boylan also identified a tendency toward inflammation as a risk factor for Petitioner.

Inflammation promotes blood clotting, or thrombosis, increasing the risk of stroke. First Boylan

Rep. at 10. Petitioner had a history of allergies, recurrent shingles, and thyroid disease, all of

which are “associated with abnormalities in the immune/inflammatory system and may have

predisposed her to stroke from either or both excessive clot formation or abnormalities in the vessel

walls in the setting of carotid webs.” Id. Furthermore, her history of granuloma requiring surgical

removal signified a propensity toward inflammation. Id.

Dr. Boylan noted that, according to the National Stroke Association Stroke Risk Calculator,

Petitioner’s history of smoking increased her risk of stroke by only 0.4% over ten years.9 First

Boylan Rep. at 10. Overall, her risk as a young adult was low. Id.

Dr. Boylan observed that flu infections are associated with strokes, but she acknowledged

that there have been few cases of stroke after the flu vaccine. First Boylan Rep. at 11. Nonetheless,

“in rare individuals, [stroke] will occur as a post-vaccine phenomenon even though vaccination

reduces overall risk in the population.” Id.

Dr. Boylan concluded that the September 14, 2015 and March 22, 2016 flu vaccines

together “most likely provoked an immune/inflammatory response which caused or contributed to

the occurrence and severity of the strokes [Petitioner suffered].” First Boylan Rep. at 11.

Petitioner had several risk factors that might have predisposed her to a stroke triggered by the

9

Dr. Boylan pointed out that this stroke risk calculator does not even permit calculation of risk for people

under age 45. First Boylan Rep. at 10.

10

inflammatory response initiated by the vaccines. Id. Petitioner’s inflammation was “particularly

strong,” particularly with her second stroke, as evidenced by her imaging. Id.

3. Dr. Boylan’s Second Expert Report

In a brief response to Dr. Messé’s expert report (discussed below), Dr. Boylan clarified

that, in her opinion, Petitioner’s brain MRI following the second event was unusual because it

showed sufficient inflammation to cause a suspicion of tumor or infection, requiring biopsy.

Second Boylan Rep. at 1. Her conclusions were unchanged.

4. Dr. Boylan’s Testimony

Dr. Boylan was recognized as an expert in neurology. Tr. at 31. She defined a stroke as

“local damage to the brain in a particular area related to the blood flow and the vascular structures

of the brain.” Id. Strokes are generally categorized as either ischemic, characterized by choking

off blood supply to the brain, or hemorrhagic, characterized by bleeding into the brain. Id. at 32.

They can be caused by emboli that develop in the heart or other parts of the body, including arteries

or veins, and then break off and travel to the brain. Id. at 32-33. Dr. Boylan’s opinion was that

Petitioner suffered from an ischemic, artery-to-artery, thromboembolic stroke, likely arising in the

artery with the carotid web. Id. at 33-34.

Dr. Boylan testified that both chronic and acute inflammation play a major role in stroke.

Tr. at 34. Patients with severe systemic inflammation can develop strokes. Id. Inflammation from

non-infectious causes also can trigger stroke. Id. at 36. The walls of the blood vessels in the brain

are “very sensitive to the effects of inflammation.” Id. at 37. The more inflammation a person

experiences in response to a stroke, the worse the outcome might be. Id. at 50. Medications with

anti-inflammatory properties are given to treat strokes. Id. However, “not every inflammation

will provoke a stroke, and not every stroke will be caused by inflammation[.]” Id. at 39.

Furthermore, stroke itself causes an inflammatory response. Id.

According to Dr. Boylan, one of the main sources of inflammation is the endothelium,

which is the innermost lining of the blood vessels. Tr. at 40. The endothelium within the brain is

proximate to immune cells called glial cells. Id. at 52. The glial cells excrete endothelium-related

growth factor, along with chemokines and cytokines that “are actively in communication with the

blood and with messengers within the blood.” Id. Inflammation will cause changes in vascular

reactivity, or endothelial-dependent relaxation, which can impair the ability of blood to circulate

through the brain. Id. at 53-54. Dr. Boylan testified that a study showed that certain biomarkers

and changes in vascular reactivity were evident two weeks after flu vaccination in healthy

individuals. Id. (referencing Smeeth L, et al., Risk of Myocardial Infection and Stroke after Acute

Infection or Vaccination, N. ENGL. J. MED. (2004);351(25):2611-2618 (Ex. 31) (“Smeeth”)).

Dr. Boylan stated that Smeeth explored the possible association between vaccination and

stroke. Tr. at 37. The authors posited that systemic inflammation could “pull the trigger” for a

vascular event, such as a stroke, that might not have otherwise occurred. Id. at 37-38. Both

infections and vaccines are pro-inflammatory and could, theoretically, cause a stroke. Id. at 38.

Although the Smeeth study found that the flu vaccine reduced the risk of stroke in the population

11

by 40-60%, according to Dr. Boylan, that finding does not rule out the possibility that “rare

individuals” will experience adverse effects from the vaccine, including stroke. Id. at 38.

Dr. Boylan testified that systemic inflammation affects stroke risk. Tr. at 54. She stated

that it was “conventional wisdom to the point of dogma[] that infection promotes thrombosis.” Id.

Also, according to the Cardenas paper, both viral infection and vaccination could promote blood-

brain barrier dysfunction, “producing neuroinflammation and neurological disorders.” Id. at 44;

see Cardenas G, et al., Neurological events related to influenza A (H1N1) pdm09, INFLUENZA AND

OTHER RESPIRATORY VIRUSES (2014);8(3):339-346 (Ex. 19) (“Cardenas”). The inflammatory

response in a given individual “may be modulated by individual biological factors, like age, sex,

[and] genetic background.” Tr. at 42-43. Additionally, the McColl article supported the notion

that an inflammatory response unfolds in a cascade of events, and people will have a broad range

of symptoms as a result. Id. at 45-46; see McColl BW, et al., Systemic Infection, Inflammation

and Acute Ischemic Stroke, NEUROSCIENCE (2009);158:1049-1061 (Ex. 27) (“McColl”). McColl

observed that the highest risk period for stroke occurs during the greatest pro-inflammatory phase

of the immune response. Tr. at 45.

Dr. Boylan next explained that a carotid web “is an abnormal formation on a vessel, like

a little ledge within the vessel.” Tr. at 56. Carotid webs are a risk factor for stroke because vascular

abnormalities “promote the creation of thrombus.” Id. at 55-56. The abnormal formation of the

vessel disturbs the usual flow within the vessel, similar to rocks disturbing the flow of water in a

river. Id. at 56, 61. Carotid webs are “one of the causes of stroke and recurring stroke in young

women who you would not otherwise expect to have a stroke.” Id. at 57. Even small carotid webs

are associated with increased stroke risk. Id. at 65.

Based on her review of Petitioner’s imaging, Dr. Boylan agreed that Petitioner had bilateral

carotid webs, with the larger one in her left internal carotid artery, which was located upstream

from where her first stroke occurred. Id. at 64. These carotid webs predisposed Petitioner to

strokes and would be classified as an “anatomic prothrombotic substrate.”10 Id. at 77. Further, the

combination of this anomaly with the inflammation induced by a vaccination would enhance this

risk. Id. at 79.

Dr. Boylan referenced the Lin case report, in which the authors broadly stated that

“vaccination provokes a variable magnitude of inflammatory and immunological response that

modifies the risk for ischemic stroke,” and “an inflammatory/immunological response after

vaccination may trigger thrombosis superimposing a preexisting prothrombotic state.” Tr. at 77-

78; see Lin YP, et al., Ischaemic stroke and influenza A H1N1 vaccination: a case report, ARCH

MED. SCI. (2011);7(2):345-348) (Ex. 26) (“Lin”). Furthermore, the fact that Petitioner had not had

a stroke prior to vaccination made it “very hard to say” that the vaccination and the stroke were

unrelated. Tr. at 77-78. Additionally, the March 22, 2016 vaccination could have elicited a booster

10

Dr. Boylan testified that she was somewhat confused by Petitioner’s June 30, 2016 CT angiogram, which

reported multiple infarcts or an “embolic shower” from multiple sources. Tr. at 74-75. The scan also

showed that Petitioner’s second stroke did not seem to have occurred downstream from the left carotid web.

Id. at 76. This confusion did not alter her opinion that Petitioner suffered from carotid webs, which

predisposed her to strokes. Id. at 77.

12

effect, given that it was administered only six months after her previous flu vaccination. Id. at 83.

This could have produced additional inflammation. Id.

Dr. Boylan testified that carotid webs “are quite dangerous” and can cause recurrent

strokes. Tr. at 83. The fact that Petitioner had a stroke after receiving the vaccination, but had not

experienced any strokes since 2016, caused Dr. Boylan to conclude that “the vaccine triggered the

stroke to a level of certainty that I would make a clinical decision on that basis.” Id. at 84.

Dr. Boylan testified that Petitioner was feeling unwell and experienced localized arm pain

and swelling after vaccination, indicating a clinically notable inflammatory response to the

vaccination. Tr. at 47-48. Petitioner did not have any contemporaneous triggers for an acute

inflammatory response other than the flu vaccination. Id. at 69. A stroke occurring eight days

after vaccination was within the expected time frame for such an event. Id. at 48.

Dr. Boylan opined that she would recommend against Petitioner receiving future flu

vaccinations. Tr. at 85. Petitioner had a low risk of dying from the flu; therefore, the protection

she would receive from the flu vaccine would not outweigh the risk of another stroke. Id.

Regarding Petitioner’s second stroke, Dr. Boylan noted that it was “strange in a number of

ways.” Tr. at 85. That episode occurred after a needle angiogram, which is associated with a risk

of stroke. Id. at 86. The event did not occur in the carotid artery or around any anomalous

vasculature. Id. Dr. Boylan opined that the second stroke might have been triggered by the

angiogram procedure. Id. She clarified that she did not believe the second stroke was directly

caused by the vaccination; instead, it resulted from the treatment given for the first stroke, which

she maintained was vaccine caused. Id. at 87.

Dr. Boylan did not believe Petitioner’s history of smoking caused her stroke. Tr. at 88.

Based on her evaluation of Petitioner’s smoking habits, her carotid webs, and her flu vaccination,

Dr. Boylan did not think Petitioner’s smoking or carotid webs were enough to cause the first stroke

without the catalyst of the vaccination. Id. at 91.

In summary, Dr. Boylan opined:

[The vaccination,] through a direct effect or through its pro-

inflammatory stimulation possibly, and also with the booster effect,

adduced an acute inflammatory response, which, in turn, triggered

an inflammatory cascade, which includes a prothrombotic state, and

that triggered abnormal blood flow over her preexisting carotid

webs, formed a thrombus, which flew downstream and caused a

stroke.

Tr. at 94. She added that “the vaccine induced a pro-inflammatory state which promoted the

formation of a clot in Ms. Goff’s preexisting carotid web and that there was a subsequent breakup

of that clot, and it went downstream and caused her stroke.” Id. at 129.

On cross examination, Dr. Boylan acknowledged that the Smeeth study, which included

19,000 subjects, revealed a decreased risk of stroke after flu vaccination compared to after

13

infection. Tr. at 95. She broadly agreed with the authors’ finding that flu vaccination is not

associated with a detectable increase in the risk of vascular events at the population level, but she

did not believe that finding was applicable to Petitioner, because the study was “not designed to

detect or capable of detecting rare events or exclusion of events.” Id. at 97-98. She allowed that,

in general, a natural flu infection would produce a more robust inflammatory response than the

typical response to a vaccination. Id. at 103.

Dr. Boylan testified that she did not believe every stroke was caused by inflammation. Tr.

at 101. It is difficult to ascertain whether a stroke has been caused by an inflammatory trigger. Id.

To make that determination, one would “look at certain inflammatory markers” like ESR and CRP.

Id. Dr. Boylan maintained that Petitioner “had all of the classical symptoms of an inflammatory

response of some magnitude, undefined magnitude, before she had a stroke,” but she

acknowledged that there was no evidence in the medical records that she had a fever, flu-like

symptoms, or lab work showing inflammation or a prothrombotic state. Id. at 101-02, 113.

Instead, she pointed out that Petitioner self-reported experiencing a “fever” in her shoulder, neck,

chest, and scapular region after the March 22, 2016 vaccination. Id. at 121-23.

Dr. Boylan acknowledged that her causal theory was not specific to the flu vaccine. Tr. at

104. Her theory suggests that any inflammatory stimulus could trigger a stroke, but she admitted

that other inflammatory events, such as poison ivy exposure, seasonal allergies, and bee stings, are

not associated with stroke. Id. at 104-05. She confirmed that most strokes in patients under 50

are idiopathic, and she agreed that none of Petitioner’s treating physicians attributed her stroke to

her vaccination. Id. at 106-07. She acknowledged that the studies she submitted involved strokes

in younger patients with carotid webs who had no identified inflammatory triggers. Id. at 106-09.

Dr. Boylan testified that her proposed causal mechanism involved both the innate and

adaptive immune systems, but primarily the innate immune system. Tr. at 114. She stated that

there was no specific time frame during which she would expect an inflammatory process to occur

and trigger a stroke. Id. at 115-16. She stated that the Vaccine Injury Table gives some guidance,

and she believed any injury occurring within six to eight weeks of vaccination might be considered

autoimmune in nature. Id. at 116. Any injury occurring six months after vaccination would not

be attributable to the vaccine. Id. She could not say how long the innate immune system response

to a flu vaccination would continue, but she was “confident that it lasts at least as long as the time

period from the second vaccine to the first stroke.” Id. at 119.

In response to a question from Special Master Oler, Dr. Boylan testified that certain types

of infections increase the risk of stroke, including flu, zoster, bacterial blood infections, syphilis,

tuberculosis, cryptococcus, and fungal infections. Tr. at 126. She opined that in principle, if a

viral infection can induce stroke, then the vaccination against that infection could as well. Id.

On redirect examination, Dr. Boylan clarified that the McColl study showed that the

highest risk of stroke occurred within one week of infection. Tr. at 130-31. This corresponded to

the time during which the systemic inflammatory response was strongest. Id.

14

B. Respondent’s Expert: Steven Messé, M.D.

1. Qualifications

Dr. Messé authored one expert report in this case. See Ex. A (“Messé Rep.”). According

to the documents in the record and the hearing testimony, he is an Associate Professor in the

Division of Vascular Neurology at the University of Pennsylvania. Messé Rep. at 1. He received

his M.D. from the University of Michigan School of Medicine. Ex. B (“Messé CV”) at 1. He

completed his neurology residency and a stroke and neurocritical care fellowship at the University

of Pennsylvania. Id. He is board certified in neurology and vascular neurology, which is the area

of neurology that focuses on cerebrovascular diseases such as stroke. Id. at 2; Tr. at 142. His

clinical practice specializes in patients with cerebrovascular disease, and he has treated thousands

of stroke patients. Tr. at 142, 221. He also conducts clinical research, primarily focused on stroke.

Id. at 142.

Dr. Messé has served as an ad hoc reviewer for publications such as Neurology, Stroke,

Journal of Neuroimaging, The New England Journal of Medicine, and Lancet. Messé CV at 2-3.

He has published about 70 peer-reviewed papers. Id. at 6-13. He is a member of the American

Academy of Neurology, the American Heart Association, and the American Stroke Association.

Tr. at 144. At the time of the hearing in this case, he was serving as the chair of the American

Stroke Association’s Stroke Systems of Care Advisory group, which oversees a large database of

stroke incidents used by clinicians to improve treatment. Id. at 144-45.

2. Dr. Messé’s Expert Report

Dr. Messé opined that Petitioner’s recurrent ischemic strokes were not related to the March

22, 2016 flu vaccination. Messé Rep. at 3. He stated that the literature “strongly supports the

notion that influenza vaccination is associated with a reduced, not increased, risk of stroke.” Id.

(emphasis in original). For example, the Grau study showed that vaccination was less common in

stroke patients compared to control subjects. Id.; see also Grau AJ, et al., Influenza Vaccination

Is Associated With a Reduced Risk of Stroke, STROKE (2005);36:1501-1506 (Ex. 23) (“Grau”).

The Siriwardena study similarly reported a 24% reduced risk of stroke in those who were

vaccinated. Messé Rep.at 3; see also Siriwardena AN, et al., Influenza and pneumococcal

vaccination and risk of stroke or transient ischemic attack – Matched case control study, VACCINE

(2014);1354-1361 (Ex. 30) (“Siriwardena”). The Smeeth study found no increased risk of stroke

after flu vaccination. Id. The medical literature supplied by Dr. Boylan also mostly supported

the notion that flu vaccinations are “robustly protective” against stroke. Id. Dr. Boylan cited just

two case reports for her claim that a causal association exists between vaccination and stroke; one

of those involved a varicella vaccination, not flu. Id. at 3-4.

In describing Petitioner’s imaging, Dr. Messé noted that Petitioner’s first stroke was a “left

middle cerebral artery embolic-appearing stroke.” Messé Rep. at 4. She had an ulcerated plaque

in the internal carotid artery, resulting in 30-40% stenosis. Id. The risk of stroke is significantly

increased when there is greater than 50% stenosis, but lesser degrees of stenosis are also associated

with an increased risk. Id. Furthermore, ulcerated plaque is associated with an even higher risk

of stroke, because “[t]he rupture or endothelial erosion of an unstable, atherosclerotic plaque leads

15

to thrombus formation, which then may embolize distally.” Id. Dr. Messé’s opinion was that

Petitioner’s stroke was related to her carotid lesion. Id.

In his report, Dr. Messé disagreed that Petitioner had a carotid web. Messé Rep. at 4. He

noted that she underwent a conventional angiogram, which is the gold standard for evaluation of

blood vessel abnormalities, and the radiologist interpreting the study concluded that her carotid

stenosis was caused by an ulcerated atherosclerotic plaque, not a carotid web. Id. Furthermore,

regardless of whether she had stenosis caused by a carotid web or plaque, “it seems unnecessary

to blame the vaccination . . . [which] is associated with a reduced stroke risk.” Id.

Dr. Messé strongly disagreed with the claim that Petitioner had an unusual degree of

inflammation in the brain following her second stroke. Messé Rep. at 4. He noted that

“[e]nhancement on MRI after stroke is very common after the first day or two, and typically

persists for weeks.” Id. Petitioner’s biopsy was clearly consistent with a subacute infarction, and

the pathologists analyzing the biopsied tissue did not report finding abnormal inflammation. Id.

Dr. Messé opined that the MRI indicated that Petitioner’s second, thalamic infarct occurred

at the time of her cerebral angiogram on June 24, 2016. Messé Rep. at 4. He noted that infarcts

visible on MRI are common after cerebral angiograms. Id. He concluded that the second stroke

was iatrogenic, meaning it was caused by the medical care given to her for the first stroke. Id. at

4-5.

Dr. Messé pointed out that it is very common for strokes to be cryptogenic, with no clear

cause identified, particularly in younger patients. Messé Rep. at 5. “This uncertainty . . . does not

provide support for the notion that the stroke was caused by the vaccination, particularly when the

evidence suggests that vaccinations are protective overall.” Id. He concluded that Petitioner’s

history as a tobacco user, coupled with her mild hyperlipidemia and ulcerated atherosclerotic

plaque, likely caused her initial stroke. Id. Further, if she did have a left carotid web, “that also

would be a plausible mechanism for the stroke.” Id. He opined that it was “highly likely that the

second stroke was related to the cerebral angiogram that [Petitioner] received one week prior to

the MRI.” Id.

3. Dr. Messé’s Testimony

Dr. Messé was recognized as an expert in neurology and vascular neurology. Tr. at 145.

He characterized Petitioner’s stroke on March 30, 2016, as a left middle cerebral artery stroke. Id.

at 155.

Dr. Messé testified that Petitioner had a number of risk factors for stroke, including

elevated LDL cholesterol, smoking, and an anomaly in her carotid artery, which was either a

carotid web or atherosclerosis. Tr. at 155. Addressing the imaging of Petitioner’s carotid arteries,

Dr. Messé explained that Petitioner had a conventional angiogram on June 24, 2016. Id. at 155.

A conventional angiogram is an invasive procedure during which a radiologist or interventional

neurologist inserts a catheter through the groin and into the blood vessels in the neck. Id. at 156.

Although this procedure is considered the gold standard for assessing the blood vessels, it does not

image the walls of the blood vessels, and it carries the risk of brain injury caused by the catheter

16

dislodging a blood clot or plaque. Id. In Petitioner’s June 24, 2016 angiogram, a neurosurgeon

found a complex ulcerated atherosclerotic plaque, causing a 40% narrowing of the carotid artery.

Id. at 156-57.

When Petitioner went to the hospital on June 30, 2016, she had a CT angiogram of the head

and neck. Tr. at 157. Dr. Messé testified that a CT angiogram is a noninvasive procedure in which

contrast is injected into the blood vessels while the patient is in a CT scanner. Id. Petitioner’s

radiologist interpreted her CT angiogram to show a carotid web, not atherosclerosis. Id. at 158.

At the hearing, and in contrast to his expert report, Dr. Messé favored carotid web as the proper

diagnosis. Id. at 159; compare Messé Rep. at 4. This was, in part, because he did not see a

significant overall atherosclerosis burden in Petitioner’s body. Id. He clarified that the physicians

performing the June 24 and June 30, 2016 studies both observed the same lesion in Petitioner’s

carotid artery, but they interpreted it differently. Id.

Dr. Messé opined that ultimately, the characterization of Petitioner’s carotid abnormality

was irrelevant, because either a carotid web or an ulcerated atherosclerotic plaque with 30-40%

stenosis could be a plausible mechanism for stroke. Tr. at 160. Dr. Messé defined a carotid web

as an abnormal growth in the lining of a blood vessel, caused by abnormal collagen deposition in

the lining. Id. at 160-61. A carotid web tends to develop at the carotid bifurcation, where the

common carotid artery splits into the external and internal arteries. Id. at 161. A carotid web

could, by itself, cause a stroke, without the need for a catalyzing trigger such as a vaccination. Id.

Dr. Messé opined that typically stroke patients are older, but about 30% of strokes occur

in patients under the age of 65. Tr. at 166-67. The mechanisms for stroke in older patients are

typically different than in younger patients. Id. at 167. There is ample literature supporting carotid

web being a risk factor for stroke in younger people. Id. Petitioner was in the appropriate age

group for a carotid web-caused stroke. Id.

Dr. Messé also discussed the thalamic lesion on Petitioner’s June 30, 2016 MRI. Tr. at

167. He noted that Petitioner’s clinical presentation was consistent with a subacute stroke, rather

than an acute stroke. Id. at 168. The biopsy was performed because her treating physicians were

concerned the lesion was a tumor, not because of a concern about inflammation or vasculitis. Id.

A suspicion of an inflammatory or vasculitis-related stroke would not have required a biopsy. Id.

Dr. Messé testified that the biopsy was “completely consistent” with a subacute stroke and did not

show a tumor; the biopsy also confirmed there was inflammation, but, in his opinion, that

inflammation was a natural response to the stroke and not its cause. Id. at 168-69.

Dr. Messé opined that there was no evidence in the literature that the flu vaccine can cause

a stroke. Tr. at 169. He identified Smeeth as the best study addressing this question. Id. at 169-

70. That study was conducted in the United Kingdom, which has a nationalized health system and

a large collection of patient records. Id. at 170. The study subjects had an exposure to either an

infection, a tetanus vaccination, a pneumococcal vaccination, or a flu vaccination, and had suffered

a stroke within a year of exposure. Id. at 171. The investigators compared the risk of stroke during

the 90-day period following infection/vaccination with the risk during a baseline period with no

such exposures. Id. The study assessed more than 19,000 patients who had a flu vaccination and

a stroke. Id. at 171-72. The incidence of stroke was lower for flu vaccinated patients during the

17

risk period than during the baseline period. Id. at 172. Conversely, subjects who had infections

were at increased risk of stroke during the risk period compared to the baseline period. Id. at 173.

Dr. Messé concluded that the Smeeth study was “very reassuring that the vaccinations are not

causing strokes.” Id. He felt that, if there was a safety signal of increased risk of stroke from flu

vaccination, it would have been detected by the study. Id. at 172-73.

Dr. Messé also discussed the Siriwardena paper, a retrospective case-control study that

compared vaccinated patients who suffered strokes to those who did not. Tr. at 173-74; see

generally Siriwardena. He explained that, “after adjusting for all known and obvious and known

risk factors for stroke . . . people who got the vaccination had much lower risk of stroke, and it

actually is kind of the opposite, because people who had a stroke were much less likely to have

been vaccinated[.]” Tr. at 174. The Siriwardena study concluded that vaccinated subjects had a

24% reduction in stroke risk. Id. Dr. Messé characterized the study as “well done.” Id. The Grau

study was similarly constructed and found that the odds of stroke were reduced by “more than

half” in vaccinated patients compared to unvaccinated patients. Id. at 174-75; see Grau at 1504.

This finding was “very reassuring[] that vaccinations are not causing strokes.” Tr. at 175.

Dr. Messé also discussed the Lin case report, which described a 75-year-old who

experienced a stroke after vaccination. Tr. at 175; see Lin at 345. He found the case report

“uncompelling,” stating that “a 75-year-old having a stroke is not a big surprise.” Tr. at 175. The

subject of the report had experienced a prior stroke, had hypertension, and was not taking aspirin,

all of which heightened his stroke risk. Id. at 224. The authors provided no evidence for their

statement that “an inflammatory immunological response after vaccination may trigger

thrombosis, superimposing a preexisting prothrombotic state.” Id. at 175. Dr. Messé pointed out

that flu vaccination is not contraindicated in patients with a preexisting prothrombotic state; in

fact, they are “important for people at risk of vascular disease in particular.” Id. at 176, 206.

Dr. Messé testified that the Cardenas paper addressed autoimmune responses to

vaccination, but it provided “no evidence that vaccinations are actually causing these disorders,”

other than observational case reports. Tr. at 176-77.

Contrary to Dr. Boylan’s view, Dr. Messé did not find any evidence in Petitioner’s medical

records that she had an inflammatory reaction to the subject flu vaccination prior to the stroke,

such as redness or swelling in her arm, edema, purpura, ecchymoses, rash, or fever. Tr. at 162-65.

He stated: “I didn’t see anything that a doctor or nurse documented about recently feeling unwell

prior to the stroke.” Id. at 162. Her records on the day of admission indicated that she had been

in her “usual state of health” before the onset of the stroke, indicating that she had no complaints

between the vaccination and the stroke. Id. at 162-63. Petitioner’s CRP, ESR, white blood cell

(“WBC”) count, and platelet levels were all normal at the time of her March 30, 2016 admission.

Id. at 165-66. Her hypercoagulable studies, which were done to check whether she had a condition

predisposing her to blood clots, were also normal. Id. at 166.

On cross examination, Dr. Messé maintained that Petitioner’s smoking habit was another

likely risk factor for stroke, despite her relatively young age. Tr. at 178. He explained that

smoking increases the risks of atherosclerosis and blood clots. Id. at 179.

18

Dr. Messé testified that flu infection can contribute to stroke risk, in part due to

inflammation. Tr. at 182, 194. He agreed that inflammation plays a role in stroke and that the

Smeeth study was at least indirectly looking at the association between inflammatory conditions

and stroke. Id. at 181. He opined that strokes caused by a recent or ongoing inflammatory state

are “rare.” Id. at 221.

Dr. Messé acknowledged that in the Smeeth study, more than 170 subjects experienced a

stroke within a week of receiving a flu vaccination. Tr. at 181. In his view, this was coincidental,

but he conceded that these cases were not assessed individually. Id. at 182. He further agreed that

the study was not powered to detect rare adverse events. Id. at 192. He pointed out, however, that

the risk of stroke was most reduced in the first one to three days following flu vaccination; he

surmised that this could be because people receiving the flu vaccination tend to be healthier. Id.

at 222-23.

Dr. Messé disagreed with Dr. Boylan’s opinion that, if a wild-type infection has been

associated with a harm, it is reasonable to presume that vaccination against that infection could

cause the same harm. Tr. at 189. He explained that the body’s responses to infection and

vaccination are “different in severity and extent.” Id. at 190. He generally agreed, however, that

“immune system activation” can contribute to stroke risk and that vaccination is specifically

designed to activate the immune system. Id. at 191-92.

Regarding Petitioner’s second episode, Dr. Messé testified that there was some uncertainty

whether she suffered a second acute stroke caused by her carotid web or a vascular event due to

the June 24, 2016 angiogram procedure. Tr. at 204-05. He favored the procedure as the

precipitating event, in agreement with Dr. Boylan. Id. at 205.

Dr. Messé agreed that a carotid web is a preexisting thrombotic condition, but he

distinguished that from a hypercoagulable state or a generalized prothrombotic state. Tr. at 206-

07. He explained that the web increases the likelihood of developing a clot in the web’s location,

not elsewhere the body. Id. at 207. He allowed that recurrent strokes are seen in patients with

carotid webs, but he disagreed that the presence of a web would guarantee recurrent strokes. Tr.

at 214-15. Instead, he opined that carotid web is a meaningful risk factor for stroke. Id. at 215.

Regarding Petitioner’s presentation at the time of her first stroke, Dr. Messé agreed that

her CRP level might have been normal even in the presence of inflammation. Tr. at 219. However,

he maintained that there was no evidence of inflammation in Petitioner’s case. Id. He testified

that for “a systemic inflammatory state that’s bad enough to cause a stroke, I would expect to see

something.” Id. at 220.

Dr. Messé testified that the timing of Petitioner’s initial stroke fell within the range during

which the risk of stroke is increased due to the body’s “inflammatory and immunological ramp-up

responding to infection.” Tr. at 212. But he pointed out that her stroke also occurred in the

timeframe “where we saw a reduced risk of stroke in people who are vaccinated.” Id. at 212-13.

19

IV. LEGAL FRAMEWORK

A. Petitioner’s Burden in Vaccine Program Cases

Under the Vaccine Act, a petitioner may prevail in one of two ways. First, a petitioner may

demonstrate that she suffered a “Table” injury—i.e., an injury listed on the Vaccine Injury Table

—that occurred within the time provided in the Table. § 11(c)(1)(C)(i). “In such a case, causation

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

see § 13(a)(1)(B). Second, where the alleged injury is not listed in the Vaccine Injury Table, a

petitioner may demonstrate that she suffered an “off-Table” injury caused by the vaccination.

§ 11(c)(1)(C)(ii).

For both Table and non-Table claims, Vaccine Program petitioners bear a “preponderance

of the evidence” burden of proof. § 13(a)(1). That is, a petitioner must offer evidence that leads

the “trier of fact to believe that the existence of a fact is more probable than its nonexistence before

[he] may find in favor of the party who has the burden to persuade the judge of the fact’s

existence.” Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1322 (Fed. Cir. 2010); see

also Snowbank Enter. v. United States, 6 Cl. Ct. 476, 486 (1984) (mere conjecture or speculation

is insufficient under a preponderance standard). The petitioner must demonstrate that the vaccine

was “not only [the] but-for cause of the injury but also a substantial factor in bringing about the

injury.” Moberly, 592 F.3d at 1321 (quoting Shyface v. Sec’y of Health & Hum. Servs., 165 F.3d

1344, 1352-53 (Fed. Cir. 1999)); Pafford v. Sec’y of Health & Hum. Servs., 451 F.3d 1352, 1355

(Fed. Cir. 2006). A petitioner may not receive a Vaccine Program award based solely on her own

assertions; rather, the petition must be supported by either medical records or the opinion of a

competent physician. § 13(a)(1).

To establish entitlement to a Vaccine Program award of compensation for a non-Table

claim, a petitioner must satisfy all three of the elements established by the Federal Circuit in Althen

v. Secretary of Health and Human Services, 418 F.3d 1274 (Fed. Cir. 2005). Althen requires a

petitioner to establish by preponderant evidence that the vaccination she received caused 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 a proximate temporal relationship between vaccination and injury.” Id. at 1278.

Each of the Althen prongs requires a different showing. Under Althen prong one, petitioner

must provide a “reputable medical theory,” demonstrating that the vaccine received can cause the

type of injury alleged. Pafford, 451 F.3d at 1355-56 (citations omitted). To satisfy this prong, a

petitioner’s theory must be based on a “sound and reliable medical or scientific explanation.”

Knudsen v. Sec’y of Health & Hum. Servs., 35 F.3d 543, 548-49 (Fed. Cir. 1994). Such a theory

must only be “legally probable, not medically or scientifically certain.” Id. at 549; Bunting v. Sec’y

of Health & Hum. Servs., 931 F.2d 867, 873 (Fed. Cir. 1991) (proof of medical certainty is not

required).

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

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

accepted medical theory. Andreu v. Sec’y of Health & Hum. Servs., 569 F.3d 1367, 1378-79 (Fed.

20

Cir. 2009) (citing Capizzano, 440 F.3d at 1325-26). Special masters, despite their expertise, are

not empowered by statute to conclusively resolve what are complex scientific and medical

questions, and thus the scientific evidence offered to establish Althen prong one is viewed “not

through the lens of the laboratorian, but instead from the vantage point of the Vaccine Act’s

preponderant evidence standard.” Id. at 1380. Special masters must take care not to increase the

burden placed on petitioners in offering a scientific theory linking vaccine to injury, but this does

not negate or reduce a petitioner’s ultimate burden to establish her overall entitlement to damages

by preponderant evidence. W.C. v. Sec’y of Health & Hum. Servs., 704 F.3d 1352, 1356 (Fed. Cir.

2013) (citations omitted).

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 (“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 1278). Medical records are generally viewed

as particularly trustworthy evidence, because they are created contemporaneously with the

treatment of the patient. Cucuras v. Sec’y of Health & Hum. Servs., 993 F.2d 1525, 1528 (Fed.

Cir. 1993). However, medical records and/or statements of a treating physician’s views 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. § 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 & Hum. Servs., 88 Fed. Cl. 706, 746 n.67 (2009) (“there is nothing …

that mandates that the testimony of a treating physician is sacrosanct–- that it must be accepted in

its entirety and cannot be rebutted”). As with expert testimony offered to establish a theory of

causation, the opinions or diagnoses of treating physicians are only as trustworthy as the

reasonableness of their suppositions or bases. The views of treating physicians should also be

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

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

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

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

& Hum. Servs., No. 06-522V, 2011 WL 1935813 at *17 (Fed. Cl. Spec. Mstr. Apr. 29, 2011), mot.

for review den’d, 100 Fed. Cl. 344, 356 (2011), aff’d without opinion, 475 Fed. App’x. 765 (Fed.

Cir. 2012).

The third Althen prong requires establishing a “proximate temporal relationship” between

the vaccination and the injury alleged. Althen, 418 F.3d at 1278. That term has been equated to

the phrase “medically acceptable temporal relationship.” Id. at 1281. A petitioner must offer

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

medical understanding of the disorder’s etiology, it is medically acceptable to infer causation.” de

Bazan v. Sec’y of Health & Hum. Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation

for what is a medically acceptable timeframe must 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 & Hum. Servs., 101 Fed. Cl. 532, 542 (2011), recons. den’d after remand on other grounds,

105 Fed. Cl. 353 (2012), aff’d without op., 503 F. App’x. 952 (Fed. Cir. 2013); Koehn v. Sec’y of

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

21

mot. for review den’d, 113 Fed. Cl. 757 (Fed. Cl. Dec. 3, 2013), aff’d, 773 F.3d 1239 (Fed. Cir.

2014).

B. Law Governing Analysis of Fact Evidence

The process for making factual determinations in Vaccine Program cases begins with

analyzing the medical records, which are required to be filed with the petition. § 11(c)(2). The

special master is required to consider “all [] relevant medical and scientific evidence contained in

the record.” § 13(b)(1)(A). This includes “any diagnosis, conclusion, medical judgment, or

autopsy or coroner’s report which is contained in the record regarding the nature, causation, and

aggravation of the petitioner’s illness, disability, injury, condition, or death,” and the “results of

any diagnostic or evaluative test which are contained in the record and the summaries and

conclusions.” Id. The special master is then required to weigh the evidence presented, including

contemporaneous medical records and testimony. See Burns v. Sec’y of Health & Hum. Servs., 3

F.3d 415, 417 (Fed. Cir. 1993) (it is within the special master’s discretion to determine whether to

afford greater weight to contemporaneous medical records than to other evidence, such as oral

testimony surrounding the events in question that was given at a later date, provided that such

determination is evidenced by a rational determination).

Medical records created contemporaneously with the events they describe are generally

trustworthy, because they “contain information supplied to or by health professionals to facilitate

diagnosis and treatment of medical conditions,” where “accuracy has an extra premium.” Kirby

v. Sec’y of Health & Hum. Servs., 997 F.3d 1378, 1382 (Fed. Cir. 2021) (citing Cucuras, 993 F.2d

at 1528). Accordingly, if the medical records are clear, consistent, and complete, then they should

be afforded substantial weight. See generally Lowrie v. Sec’y of Health & Hum. Servs., No. 03-

1585V, 2005 WL 6117475 at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed, contemporaneous

medical records are often found to be deserving of greater evidentiary weight than oral testimony–

- especially where such testimony conflicts with the record evidence. Cucuras, 993 F.2d at 1528;

see also Murphy v. Sec’y of Health & Hum. Servs., 23 Cl. Ct. 726, 733 (1991), aff’d per curiam,

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

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

testimony which is in conflict with contemporaneous documents is entitled to little evidentiary

weight.”)).

However, there are situations in which compelling oral testimony may be more persuasive

than written records, such as where records are deemed to be incomplete or inaccurate. Campbell

v. Sec’y of Health & Hum. Servs., 69 Fed. Cl. 775, 779 (2006) (“like any norm based upon common

sense and experience, this rule should not be treated as an absolute and must yield where the factual

predicates for its application are weak or lacking”); Lowrie, 2005 WL 6117475 at *19 (“[w]ritten

records which are, themselves, inconsistent, should be accorded less deference than those which

are internally consistent”) (quoting Murphy, 23 Cl. Ct. at 733)). Ultimately, a determination

regarding a witness’s credibility is needed when determining the weight that such testimony should

be afforded. Andreu, 569 F.3d at 1379; Bradley v. Sec’y of Health & Hum. Servs., 991 F.2d 1570,

1575 (Fed. Cir. 1993).

In determining the accuracy and completeness of medical records, the Court of Federal

22

Claims has listed four possible explanations for inconsistencies between contemporaneously

created medical records and later testimony: (1) a person’s failure to recount to the medical

professional everything that happened during the relevant time period; (2) the medical

professional’s failure to document everything reported to her or him; (3) a person’s faulty

recollection of the events when presenting testimony; or (4) a person’s purposeful recounting of

symptoms that did not exist. LaLonde v. Sec’y of Health & Hum. Servs., 110 Fed. Cl. 184, 203-

04 (2013), aff’d, 746 F.3d 1334 (Fed. Cir. 2014). In deciding whether to afford greater weight to

contemporaneous medical records or other evidence, such as testimony, a rational analysis must

be explicated. Burns, 3 F.3d at 417.

C. Analysis of Expert Testimony

Establishing a sound and reliable medical theory connecting the vaccine to the injury often

requires a petitioner to present expert testimony in support of his or her claim. Lampe v. Sec’y of

Health & Hum. Servs., 219 F.3d 1357, 1361 (Fed. Cir. 2000). Vaccine Program expert testimony

is usually evaluated according to the factors for analyzing scientific reliability set forth in Daubert

v. Merrell Dow Pharm., Inc., 509 U.S. 579, 594-96 (1993). See Cedillo v. Sec’y of Health & Hum.

Servs., 617 F.3d 1328, 1339 (Fed. Cir. 2010) (citing Terran v. Sec’y of Health & Hum. Servs., 195

F.3d 1302, 1316 (Fed. Cir. 1999)). “The Daubert factors for analyzing the reliability of testimony

are: (1) whether a theory or technique can be (and has been) tested; (2) whether the theory or

technique has been subjected to peer review and publication; (3) whether there is a known or

potential rate of error and whether there are standards for controlling the error; and (4) whether the

theory or technique enjoys general acceptance within a relevant scientific community.” Terran,

195 F.3d at 1316 n.2 (citing Daubert, 509 U.S. at 592-95).

The Daubert factors play a slightly different role in Vaccine Program cases than in other

federal judicial proceedings. Those factors are employed by judges to exclude evidence that is

unreliable and potentially confusing to a jury. In Vaccine Program cases, the factors are used in

the weighing of the reliability of scientific evidence. Davis v. Sec’y of Health & Hum. Servs., 94

Fed. Cl. 53, 66-67 (2010) (“uniquely in this Circuit, the Daubert factors have been employed also

as an acceptable evidentiary-gauging tool with respect to persuasiveness of expert testimony

already admitted”). The flexible use of the Daubert factors to evaluate persuasiveness and

reliability of expert testimony has routinely been upheld. See, e.g., Snyder, 88 Fed. Cl. at 743. In

this matter (as in numerous other Vaccine Program cases), Daubert has not been employed at the

threshold to determine what evidence should be admitted, but instead to determine whether expert

testimony offered is reliable and/or persuasive.

Respondent frequently offers one or more experts of his own to rebut a petitioner’s case.

Where both sides offer expert testimony, a special master’s decision may be “based on the

credibility of the experts and the relative persuasiveness of their competing theories.”

Broekelschen v. Sec’y of Health & Hum. Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (citing

Lampe, 219 F.3d at 1362). Nothing requires the acceptance of an expert’s conclusion “connected

to existing data only by the ipse dixit of the expert,” especially if “there is simply too great an

analytical gap between the data and the opinion proffered.” Snyder, 88 Fed. Cl. at 743 (quoting

Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997)). 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.

23

Weighing the relative persuasiveness of competing expert testimony, based on a particular expert’s

credibility, is part of the overall reliability analysis to which special masters must subject expert

testimony in Vaccine Program cases. Id. at 1325-26 (“[a]ssessments as to the reliability of expert

testimony often turn on credibility determinations”); see also Porter v. Sec’y of Health & Hum.

Servs., 663 F.3d 1242, 1250 (Fed. Cir. 2011) (“this court has unambiguously explained that special

masters are expected to consider the credibility of expert witnesses in evaluating petitions for

compensation under the Vaccine Act”).

D. Consideration of Medical Literature

Finally, although this decision discusses some but not all the record evidence in detail, I

have reviewed and considered all the materials submitted in this matter. See 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 [s]he does not explicitly reference

such evidence in h[er] decision.”); Simanski v. Sec’y of Health & Hum. Servs., 115 Fed. Cl. 407,

436 (2014) (“[A] Special Master is ‘not required to discuss every piece of evidence or testimony

in her decision.’” (citation omitted)), aff’d, 601 F. App’x. 982 (Fed. Cir. 2015).

V. ANALYSIS

A. Diagnosis

Initially, it is important to clarify some areas of agreement between the parties concerning

Petitioner’s condition. Drs. Boylan and Messé agreed that Petitioner suffered an ischemic stroke

on March 30, 2016. First Boylan Rep. at 5; Messé Rep. at 4. They further agreed that she suffered

a stroke in late June 2016, which was either a new stroke or a continuation/expansion of the first

stroke. Id. Neither expert felt that the June 2016 stroke was a direct result of the March 22, 2016

flu vaccination. Instead, they concurred that the second stroke was likely triggered by the cerebral

angiogram Petitioner underwent on June 24, 2016, because stroke is a known risk of that

procedure.11 First Boylan Rep. at 5; Messé Rep. at 4-5; Tr. at 87, 207.

The operative question to resolve, then, is whether Petitioner’s first stroke on March 30,

2016, was caused by the subject flu vaccination.

B. Althen Prong One

1. Causation Theory

Petitioner has asserted an off-Table claim and thus must prove by preponderant evidence

that she suffered an injury caused by the vaccination at issue, satisfying all of the Althen prongs.

See Capizzano, 440 F.3d at 1320. Under Althen prong one, Petitioner must provide a reputable,

sound, and reliable medical theory that the vaccine can cause the injury. Boatmon v. Sec’y of

11

There also appears to be no dispute that the cerebral angiogram was necessitated by the first stroke. After

that event, Petitioner continued being seen by neurologist Dr. El-Gengaihy, who ordered the angiogram.

See Ex. 10 at 10.

24

Health & Hum. Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2013). “[T]o establish causation, the

standard of proof is preponderance of evidence, not scientific certainty.” Langland v. Sec’y of

Health & Hum. Serv., 109 Fed. Cl. 421, 441 (2013).

Petitioner’s theory of causation centers on the interaction of the inflammatory response

elicited by flu vaccination with a preexisting prothrombotic condition -- in this case, a carotid web.

Dr. Boylan opined that this combination of factors can lead to clot formation and embolization,

causing stroke. See Tr. at 94.

Petitioner provided some support for the proposition that inflammation, including from an

acute infection, can play a role in stroke. Dr. Boylan testified that patients with acute, severe

systemic illnesses, such as sepsis, are at higher risk of stroke. Tr. at 34-35. The more inflammation

a person experiences, the worse the outcome of a stroke might be. Id. at 50. Medications with

anti-inflammatory properties are given to treat strokes. Id.

Dr. Boylan cited to some medical literature that purports to support her theory. In Smeeth,

an increased risk of stroke was found across the first 90 days following diagnosis of a systemic

respiratory infection, with the highest risk during the first three days. Smeeth at 2614. In the

Esenwa review, the authors stated that proinflammatory conditions, “including acute and chronic

infections,” are associated with an increased risk of stroke. Esenwa CC, et al., Inflammatory risk

factors, biomarkers and associated therapy in ischaemic stroke, NATURE REVIEWS (NEUROLOGY)

(2016);12:594-604 (Ex. 42) (“Esenwa”) at 594. Moreover, the enhanced risk appears to be

temporally related to the inflammation produced by those conditions. Id. at 595. Esenwa discussed

studies reporting that the risk of stroke was associated with elevated levels of several inflammatory

markers, including CRP and IL-6.12 Id. at 597. The authors posited that the innate immune system

shares targets with the coagulation system, “with the potential to induce a hypercoagulable state

whenever the system is acutely activated.” Id. at 602.

Likewise, the McColl review reported that inflammation, including that produced by

infection, is implicated in “multiple phases of stroke etiology and pathology.” McColl at 1.

Discussing infections generally, the authors noted that “numerous clinical studies have suggested

a link between peripheral infection and increased stroke susceptibility and recent data have

provided compelling evidence to support these earlier studies.” Id. at 2. The Murray review

reported similar observations, concluding that “stroke risk and outcome can be modified by a pre-

existing inflammatory burden, be it from chronic disease or acute infection.” Murray KN, et al.,

Systemic immune activation shapes stroke outcome, MOLECULAR AND CELLULAR NEUROSCIENCE

(2013);14-25 (Ex. 28) (“Murray”) at 22. Cardenas proposed that neuroinflammation could result

from vaccination or infection; through a literature review, the authors identified seven cases of

stroke following H1N1 flu vaccination. Cardenas at 340, 343.

12

Interleukin-6: a lymphokine produced by antigen- or mitogen-activated T cells, fibroblasts, macrophages,

and adipose and other cells that serves as a differentiation factor for B cells and thymocytes and stimulates

immunoglobulin production by B cells; it also induces hepatocytes to synthesize various plasma proteins

involved in the acute phase response and is a cofactor in initiation of the cell cycle in primitive

hematopoietic cells in vitro. Interleukin-6, DORLAND’S,

https://www.dorlandsonline.com/dorland/definition?id=83023 (last accessed on December 31, 2024).

25

It is not enough, however, to point to an association between stroke and inflammation

without providing some evidence characterizing the inflammatory properties of the subject

vaccine. On cross, Dr. Boylan acknowledged that “not every inflammation will provoke a stroke,

and not every stroke will be caused by inflammation[.]” Tr. at 39. She further conceded that

strokes after vaccination are coincidental “in most cases.” See id. at 104-06. She admitted that

inflammatory triggers like bee stings, seasonal allergies, and poison ivy are not associated with

stroke. Id. at 104-05; see also id. at 180, 221 (Dr. Messé stating that, although inflammation plays

a role in stroke, it is “rare” to see a stroke caused by an acute inflammatory condition). She also

admitted that the immune response to a natural flu infection would be more inflammatory than the

response to a vaccine. Id. at 103.

Notably, Petitioner failed to provide any evidence of the type, quantity, or duration of the

inflammatory products of the flu vaccine. None of the submitted literature addresses this question.

Dr. Boylan testified that inflammation affects the endothelium in the blood vessels, impairing the

ability of the vessels to relax, which in turn causes dysfunction of blood flow, inducing clotting.

Tr. at 53-54. She attempted to tie this to the flu vaccine, but her testimony on this point was

unpersuasive. Discussing Smeeth, she referenced a different study (the Hingorani paper, cited

below), which she said involved healthy individuals who were given the flu vaccine and

experienced inflammation that suppressed endothelium-dependent relaxation for “two weeks after

the vaccination.” Id. at 54. However, Dr. Boylan incorrectly recited Smeeth’s description of the

Hingorani study: the Smeeth authors simply reported that “in an experimental model, the

vaccination of healthy volunteers induced a short-lived inflammation that was associated with

profound suppression of endothelium-dependent relaxation.” Smeeth at 2612. In fact, the

Hingorani study, which was submitted into evidence after the hearing, did not investigate

endothelium-dependent relaxation following flu vaccination. Instead, it tested the inflammatory

effects of the Salmonella typhi vaccine and found that the inflammatory markers returned to normal

within 32 hours after that vaccination. Hingorani AD, et al., Acute Systemic Inflammation Impairs

Endothelium-Dependent Dilatation in Humans, CIRCULATION (2000);994-999 (Ex. C)

(“Hingorani”) at 997; see Resp’t’s Post-Hr’g Br. at 6-7. Thus, it appears that Dr. Boylan’s

testimony on this topic was erroneous, weakening her opinion.13

2. “Booster effect” of repeated vaccinations

Pointing to the fact that Petitioner received a flu vaccination six months before the subject

vaccination, Dr. Boylan opined that repeated flu vaccinations might produce a “booster effect”

that amplified Petitioner’s inflammatory response and the risk of stroke. See Tr. at 92-93. But Dr.

Boylan admittedly had no evidence supporting this proposition. Id. at 93. No literature was

provided. Instead, she relied on the fact that, in her personal experience, COVID-19 vaccine

recipients have experienced strong reactions to second doses of that vaccine. Id. at 92-93. Her

testimony on this question was unpersuasive.

13

Even accepting that the Hingorani study did show a transient effect of vaccination on endothelium-

dependent relaxation of the vessels, Smeeth found a significantly reduced risk of stroke during the period

of inflammatory response for flu vaccination. Smeeth at 2615 (Table 1) (reporting a 23% reduction in

stroke risk in the first three days after flu vaccination, a 28% reduction in risk from days 4-7, and a 16%

reduction in risk from days 8-14).

26

When given the opportunity to submit additional evidence after the entitlement hearing,

Petitioner filed a printout of a CDC webpage entitled “Children, the Flu, and the Flu Vaccine,”

which reported that children between six months and eight years old require two doses of the

influenza vaccine to receive full protection. Ex. 41 at 1-2. On the same webpage, though, the

CDC stated that “[d]ifferent products are approved for different age groups, including children as

young as 6 months of age.” Id. at 1. In other words, childhood vaccines are typically formulated

differently from those for adults. Further, this site provides no evidence that a second dose of flu

vaccine in anyone amplifies the inflammatory response. This reference does not support Dr.

Boylan’s claim about a “booster effect” in this case, nor has Petitioner submitted any other

evidence to support this opinion.

3. Interaction between flu vaccination and carotid webs

Dr. Boylan further opined that flu vaccination can cause stroke in a person with a carotid

web. She hypothesized that the inflammation elicited by the vaccine can exacerbate thrombosis

in the carotid artery, leading to clotting, embolization, and stroke. Tr. at 94.

There was some disagreement among Petitioner’s treating physicians about whether the

appropriate diagnosis was carotid web or an ulcerated atherosclerotic plaque in the left carotid

artery. Compare Ex. 6 at 230 with Ex. 15 at 473, 673-77. Dr. Messé initially interpreted the

imaging to show an ulcerated plaque. Messé Rep. at 4. Ultimately, though, both parties’ experts

agreed Petitioner had a carotid web, a conclusion that is supported by the medical records. Tr. at

64, 158-59.

The experts concurred that carotid web is associated with an increased risk of stroke, due

to a heightened tendency toward thrombosis. Tr. at 78-79, 83, 161. This proposition is uniformly

supported by the literature. See Choi PMC, et al., Carotid Webs and Recurrent Ischemic Strokes

in the Era of CT Angiography, AM. J. NEURORADIOL. (2015);36:2134-2139 (Ex. 21) (“Choi”) at

2134 (surmising that carotid web contributes to stroke due to impaired blood flow and

thrombogenicity); Haussen DC, et al., Carotid Web (Intimal Fibromuscular Dysplasia) Has High

Stroke Recurrence Risk and Is Amenable to Stenting, STROKE (2017);48:1-4 (Ex. 24) (“Haussen”)

at 1 (reporting an association between carotid web and high risk of recurrent stroke/TIA; carotid

webs are “high-risk lesions,” likely due to a causing a predisposition to thromboembolism); Sajedi

PI, et al., Carotid Bulb Webs as a Cause of “Cryptogenic” Ischemic Stroke, AM. J. NEURORADIOL.

(2017);38:1399-1404 (Ex. 29) (“Sajedi”) at 1399 (study finding a statistically significant

association between cryptogenic stroke and carotid web).14 Similar to other parts of her theory,

though, Dr. Boylan failed to submit any supportive evidence illustrating how the flu vaccine could

produce a stroke in a person with this condition. She did not present any clinical or other data

concerning the putative interaction of vaccination, carotid web, and stroke. None of the literature

on carotid web and stroke hypothesized that any type of vaccination could exacerbate the risk. See

generally Choi, Haussen, Sajedi.

14

As Dr. Messé clarified, although a carotid web predisposes one to thrombosis in the location of the web,

that condition does not equate to a generalized prothrombotic state. Tr. at 206-07.

27

Dr. Boylan also suggested that a carotid web in someone Petitioner’s age would not itself

be sufficient to cause a stroke. Tr. at 91. Instead, a catalyst, such as the inflammation produced

by a vaccination, would be needed. Id. But the literature she submitted identified carotid web as

an independent risk factor for stroke in Petitioner’s age group. The authors in Choi, for example,

concluded that “[t]he carotid web may be an important cause of ischemic stroke in patients with

otherwise no determined mechanism of stroke and present a high risk of recurrent stroke.” Choi

at 2138; see also Haussen at 1 (“Carotid web is associated with high recurrent stroke/TIA risk,

despite antithrombotic use”); Sajedi at 1399 (noting that “carotid webs exhibit a strong association

with ischemic stroke, and their presence should be suspected in patients lacking other risk factors,

particularly African American women”).

4. Epidemiologic Data

Epidemiologic evidence is not required to prove a Vaccine Act case. It is appropriate,

however, for a special master to consider such evidence as part of the overall assessment of the

case. See Druery v. Sec'y of Health & Hum. Servs., No. 17-1213V, 2023 WL 5094088, at *17

(Fed. Cl. July 11, 2023), mot. for rev. den’d, 169 Fed. Cl. 557 (2024) (observing that “[n]othing in

Althen or Capizzano requires the Special Master to ignore probative epidemiological evidence that

undermines petitioner's theory.”) (quoting D'Tiole v. Sec'y of Health & Hum. Servs., 726 F. App'x.

809, 811 (Fed. Cir. 2018)). “Although Althen and Capizzano make clear that a claimant need not

produce medical literature or epidemiological evidence to establish causation under the Vaccine

Act, where such evidence is submitted, the Special Master can consider it in reaching an informed

judgment as to whether a particular vaccination likely caused a particular injury.” Andreu, 569

F.3d at 1379.

The epidemiologic literature in the record strongly indicates that flu vaccination is

associated with a reduced, not increased, risk of stroke. The Smeeth study, which included more

than 19,000 flu-vaccinated patients, found that there was no increase in the rate of stroke during

the first 90 days following vaccination, compared to the baseline period.15 Smeeth at 2614-15.

Moreover, as Dr. Messé explained, the study found a significantly reduced risk of stroke during

the first 28 days following flu vaccination. Tr. at 172; see also Smeeth at 2615 (Table 1) (reporting

significantly decreased risks of stroke at 1-3 days, 4-7 days, 8-14 days, and 15-28 days after flu

vaccination). Petitioner’s stroke occurred during this initial timeframe. Notably, Dr. Boylan did

not question the Smeeth study’s methodology, and she agreed with the authors’ finding that the

vaccine is not associated with an increased stroke risk at the population level. Id. at 97-98.

In the Siriwardena study, the authors compared stroke patients to controls to assess the

potential association between flu vaccination and stroke. Siriwardena at 1354. The study reported

that flu-vaccinated patients had a 24% reduction in the risk of stroke compared to unvaccinated

15

For the flu-vaccinated participants in Smeeth, the baseline period for assessing the risk of stroke did not

include any time preceding a first flu vaccination. This is because one of the indications for receiving the

flu vaccination is preexisting cardiovascular disease; thus, the receipt of a flu vaccination is “itself

associated with the risk of vascular events.” Smeeth at 2613. The authors explained that “[t]o ensure that

during the observation period there was minimal variation in the opportunity to be vaccinated, the

observation period used in the analysis with regard to influenza vaccination did not include the time before

a participant’s first influenza vaccination.” Id.

28

patients. Id. at 1354, 1358 (Table 3). Dr. Messé testified that this study was “well done” and was

“very reassuring that there’s no association at all with stroke risk.” Tr. at 174. The Grau study

similarly found that the risk of stroke following flu vaccination was reduced compared to the risk

in unvaccinated controls. Grau at 1501. Dr. Boylan did not dispute the methodologies or findings

of these studies.

Dr. Boylan referenced the Lin case report as a clinical example of the possibility that a flu

vaccine can trigger stroke. Lin at 345. Lin described a 75-year-old patient who suffered an

ischemic stroke the same day as an influenza A/H1N1 vaccination. Id. at 345-346. Lin is

distinguishable in several ways from this case. The patient was substantially older than Petitioner,

had suffered a previous stroke, and had several comorbidities. Id. The other case report produced

by Petitioner, Wirrell, is also distinguishable, as it described strokes following varicella

vaccinations in two children. Wirrell E, et al., Stroke After Varicella Vaccination, J PEDIATR

(2004);145:845-47 (Ex. 33) (“Wirrell”) at 845. Furthermore, case reports are inferior scientific

evidence of causation and generally do not, on their own, support a causal attribution. See, e.g.,

R.V. v. Sec’y of Health & Hum. Servs., No. 11-504V, 2016 WL 3882519, *41 (Fed. Cl. Spec. Mstr.

Feb. 19, 2016) (noting that “individual patient case reports . . . are not in general, strong evidence

of causation”) (internal quotation marks omitted)), mot. for rev. den'd, 127 Fed. Cl. 136 (2016).

Overall, I conclude that Petitioner failed to produce preponderant evidence of a sound,

reliable theory demonstrating how the flu vaccine is capable of causing stroke. Instead, she offered

disjointed evidence of risk factors for stroke, without evidence tying them to the properties of the

flu vaccine, with respect to which the epidemiologic data is reassuring. Althen prong one was not

satisfied.

C. Althen Prong Two

Under Althen’s second prong, a petitioner must “prove a logical sequence of cause and

effect showing that the vaccination was the reason for the injury.” Althen, 418 F.3d at 1278. The

sequence of cause and effect must be “'logical' and legally probable, not medically or scientifically

certain.” Id. A petitioner is not 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.” Id. (omitting internal citations);

Capizzano v. Sec'y of Health & Hum. Servs., 440 F.3d 1317, 1325 (Fed. Cir. 2006). Instead,

circumstantial evidence and reliable medical opinions may be sufficient to satisfy the second

Althen prong. Isaac v. Sec'y of Health & Hum. Servs., No. 08-601V, 2012 WL 3609993, at *24

(Fed. Cl. Spec. Mstr. July 30, 2012), mot. for rev. den'd, 108 Fed. Cl. 743 (2013), aff'd, 540 F.

App'x. 999 (Fed. Cir. 2013).

I conclude that Petitioner has not demonstrated a logical sequence of cause and effect

between her March 22, 2016 flu vaccination and her initial stroke on March 30, 2016. Initially, it

is undisputed that, although Petitioner was diagnosed and treated by a number of specialists,

including several neurologists, no treating physician attributed her stroke to her flu vaccination.

Dr. Boylan acknowledged this. Tr. at 106. Moreover, the contemporaneous medical records do

not indicate that Petitioner suffered a significant inflammatory response to the vaccination, as

would be expected under Dr. Boylan’s mechanistic theory. See id. at 220 (Dr. Messé testifying

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that for “a systemic inflammatory state that’s bad enough to cause a stroke, I would expect to see

something.”); see also Hibbard v. Sec’y of Health & Hum. Servs., No. 07-446V, 2011 WL

1766033, at *9 (Fed. Cl. Spec. Mstr. Apr. 12, 2011) (finding Althen prong two unsatisfied where

the petitioner failed to prove her injury was consistent with the mechanistic theory of vaccine

causation she advanced), mot. for rev. den’d, 100 Fed. Cl. 742, 749 (2011), aff’d, 698 F.3d 1355

(Fed. Cir. 2012).

During the eight days between the vaccination and Petitioner’s stroke, she made no

complaints to any medical providers of symptoms that might be indicative of inflammation, such

as fever, rash, edema, bruising, or purpura, which are common post-vaccination reactions.16

Likewise, when she went to the hospital on March 30, 2016, the records show she did not report

recently feeling unwell. To the contrary, she reported being in “good chronic health” and that

“[p]rior to her ER visit she was in her usual state of health.”17 Ex. 6 at 220, 224. She underwent

multiple examinations at the hospital, with no observations of clinical signs of inflammation. See

id. at 222 (admission exam on March 30, 2016, finding no signs of skin abnormalities or rash); id.

at 281 (March 30, 2016 ER exam showing no evidence of fever, rash, or impaired range of motion).

Lab work done in the hospital showed normal levels of inflammatory markers such as CRP and

ESR, as well as a negative hypercoagulable workup, signifying that she did not have a blood

condition predisposing her to thrombosis.18 Id. at 342, 344-48, 349, 350; Tr. at 165-66. There are

some records in which Petitioner reported having some continuing left-arm soreness/tightness in

the weeks after her stroke, but the most contemporaneous records – those from her initial

presentation to the hospital – consistently reflected no complaints or findings indicative of

inflammation before or at the time of the stroke. See Tr. at 121-23; Ex. 6 at 594; Ex. 10 at 5. Her

VAERS report also failed to mention any symptoms consistent with inflammation in the days

between the vaccination and the stroke. Ex. 3.

At the hearing, Petitioner testified that she experienced left arm redness, swelling, and

soreness for a “couple months” after vaccination. Tr. at 7. This testimony contravened her earlier

sworn statement in this litigation, where she stated that her left arm was “sore and pink” for a few

days after the vaccination, but those symptoms lessened over the next week. Ex. 1 at 2. I do not

find Petitioner’s testimony on this subject persuasive, particularly given her admitted memory

problems since her stroke, and it is insufficient to overcome the contemporaneous medical records.

See Tr. at 14; Cucuras, 993 F.2d at 1528.

16

CDC, Possible Side Effects from Vaccines, https://www.cdc.gov/vaccines/basics/possible-side-

effects.html (last accessed on January 6, 2025).

17

Dr. Messé explained that the note that Petitioner was in her “usual state of health” signified that she had

no other complaints prior to the stroke. Tr. at 163.

18

As discussed above, the Esenwa review proposed that elevated inflammatory markers like CRP are

associated with stroke. Esenwa at 594, 597. The authors surmised that the inflammatory products of the

innate immune system might induce a hypercoagulable state, leading to stroke. Id. at 602. Petitioner,

however, had normal inflammatory markers and a negative hypercoagulable workup, suggesting her stroke

was not causally related to acute inflammation.

30

Dr. Boylan did not dispute that the hospital records did not show clinical or laboratory

indications of inflammation before or at the time of the initial stroke. Tr. at 101-02, 113. She

instead cited the intake form completed by Petitioner for her April 20, 2016 visit with Dr. El-

Gengaihy. Id. at 121-23. On that form, Petitioner described her complaint as “[follow-up] after

TIA and [left] deltoid flu shot [with] ‘fever’ in my shoulder, neck, chest and scapular region,”

which had been ongoing “since” March 22, 2016. Ex. 10 at 5. But on the same form, Petitioner

stated that she had experienced a TIA on March 22, 2016, when her stroke actually occurred on

March 30. Id. This suggests a faulty memory of the events preceding this visit, which is consistent

with Petitioner’s testimony that she had had memory problems since her stroke. See Tr. at 14. An

exam conducted by Dr. El-Gengaihy that day showed no evidence of ongoing inflammatory

symptoms. Ex. 10 at 9. This form is unpersuasive evidence of pre-stroke inflammation and

insufficient to override the contemporaneous records.

There is also evidence of an alternative cause of Petitioner’s stroke: her carotid web.

Although a petitioner does not bear the burden of eliminating all alternative causes for her injury,

it is appropriate for a special master to consider evidence relating to such alternative causes in

assessing the Althen prongs. See, e.g., Doe 11 v. Sec’y of Health & Hum. Servs., 601 F.3d 1349,

1357-58 (Fed. Cir. 2010); Walther v. Sec’y of Health & Hum. Servs., 485 F.3d 1146, 1151 (Fed.

Cir. 2007). As discussed above, both experts agreed that Petitioner had this condition and that it

is a risk factor for stroke. Furthermore, according to the literature supplied by Dr. Boylan, that

risk affects patients around Petitioner’s age, even if the general risk of stroke is low in younger

patients. See Choi at 2135 (reporting that the mean age of the patients with carotid web who

suffered stroke was 50, with an age range of 41-55); Haussen at 1 (reporting that the median age

of 24 patients with carotid web and stroke was 46, with an age range of 41-59); Sajedi at 1399

(reporting that the mean age of patients with stroke and carotid web was 38.9, with an age range

of 30-48). And, as discussed, the literature does not suggest that a catalyzing agent is needed to

trigger a stroke in a person with carotid web.19

For the reasons articulated above, I find that Petitioner has not preponderantly

demonstrated a logical cause-and-effect sequence connecting the subject vaccination and her initial

stroke, and therefore she has not established the second prong of Althen.

D. Althen Prong Three

The timing prong contains two parts. First, a petitioner must establish the “timeframe for

which it is medically acceptable to infer causation,” and second, he must demonstrate that the onset

of the disease occurred in this period. Shapiro v. Secʼy of Health & Hum. Servs., 101 Fed. Cl. 532,

542-43 (2011), recons. denied after remand on other grounds, 105 Fed. Cl. 353 (2012), aff’d

without op., 503 F. App’x. 952 (Fed. Cir. 2013). Here, it is undisputed that Petitioner suffered her

initial stroke eight days after her March 22, 2016 flu vaccination. Thus, the operative question is

19

Dr. Boylan opined that because Petitioner did not have strokes before or after the events in 2016, her

vaccine was probably the causal factor precipitating her initial stroke. Tr. at 84. This is unpersuasive. The

mere temporal relationship between a vaccination and an injury is insufficient to establish causation.

Moreover, Dr. Messé persuasively explained that a carotid web poses a risk of, but does not “guarantee,”

recurrent strokes. Tr. at 214-15. He pointed out that although Petitioner had not yet experienced any further

strokes, she remained at risk for further strokes due to her carotid webs. Id. at 215.

31

whether this onset was within the appropriate interval.

Dr. Boylan gave inconsistent opinions on the medically appropriate time for onset of stroke

following vaccination. In her expert report, she stated that post-infectious neurological symptoms

“typically start within 2-6 weeks following exposure.” First Boylan Rep. at 3. That is longer than

the onset period here. Also, the basis for Dr. Boylan’s opinion was the Marchioni paper, which

concerned encephalitis, myelitis, and encephalomyelitis, not stroke. Marchioni E, et al.,

Postinfectious neurological syndromes, NEUROLOGY (2013);80:882-889 (Ex. 32) (“Marchioni”)

at 883. Moreover, Marchioni did not report a 2-6-week timeframe for onset of those conditions

following exposure. Instead, the inclusion criteria for the study specified that onset had to have

occurred within 30 days of infection/vaccination.20 Id.

At hearing, Dr. Boylan testified that she could not identify a specific time frame during

which the inflammation from vaccination – her proposed causal mechanism – could precipitate a

stroke. Tr. at 115-16. She stated: “The timing . . . on the inflammation is really not known[.]” Id.

at 115. She maintained, however, that an eight-day onset following flu vaccination was medically

appropriate and consistent with her mechanistic theory. Id. at 48. Dr. Messé agreed that the stroke

occurred during the period that the body would produce an inflammatory response to an infection,

but he noted that the Smeeth study showed a reduced risk of stroke during that same period

following vaccination. Id. at 212-13.

Overall, Dr. Boylan’s equivocation on the appropriate onset timeframe further undermined

the persuasiveness of her testimony. She did not attempt to characterize the inflammatory

properties of the flu vaccine, and thus she also could not define the timeframe during which

vaccine-caused inflammation could trigger a stroke. Because Petitioner did not supply reliable

expert testimony or other evidence supporting an eight-day onset of stroke following flu

vaccination, I conclude that she has not satisfied Althen prong three.

E. Other Vaccine Cases

A limited number of cases alleging stroke caused by flu vaccination have been filed in the

Vaccine Program. Although prior decisions from different cases do not control the outcome here,

they can inform my analysis. See Boatmon, 941 F.3d at 1358-59.

First, Petitioner submitted Irwin, in which Special Master Gowen found entitlement to

compensation, as an additional authority for my consideration. Irwin v. Sec’y of Health & Hum.

Servs., No. 16-1454V, 2024 WL 863690 (Fed. Cl. Spec. Mstr. Jan. 23, 2024). Unlike this case,

the petitioner in Irwin felt ill immediately after receiving a seasonal flu vaccination and suffered a

stroke two days later. Id. at *2-3. The petitioner’s expert relied on two case reports describing

patients who had strokes within two days of vaccination, along with the Hingorani study. Id. at

*17-18. Here, Dr. Boylan did not adequately substantiate her causal theory. Moreover, the theory

she advanced is not consistent with the facts of this case, which, as noted, involved a stroke eight

days after vaccination, without evidence of a significant inflammatory response in the interim.

20

The study also identified an average period of 8.2 days from onset to maximum dysfunction, which is

irrelevant to the question posed here. Marchioni at 883.

32

Another case I have identified is Sokol. Sokol v. Sec’y of Health & Hum. Servs., No. 16-

1631V, 2020 WL 553842 (Fed. Cl. Spec. Mstr. Jan. 9, 2020). The petitioner in Sokol suffered

from a subarachnoid hemorrhagic stroke approximately 10 days after vaccination. Id. at *2.

Special Master Moran found that the theory of causation, which was similar to that presented here,

was inadequate. Id. at *6. Specifically, he found that the theory that “inflammation” can cause

stroke to be too generalized to satisfy Althen prong one. Id. at *5. Further, although a cytokine-

driven response within four days of vaccination was medically acceptable, that timeline was

inconsistent with the 10-day onset of the petitioner’s stroke. Id. at *8.

Another case involving the flu vaccine and hemorrhagic stroke is Schultz. Schultz v. Sec’y

of Health & Hum. Servs., No. 16-539V, 2020 WL 1039161 (Fed. Cl. Spec. Mstr. Jan. 24, 2020).

In Schultz, Dr. Boylan served as a petitioner’s expert and, as here, relied on case reports and broad

generalizations, without specific evidence tying the flu vaccination to the injury. Id. at *22. Chief

Special Master Corcoran was unpersuaded by Dr. Boylan and found Dr. Messé more credible. Id.

at *22-23. Further, although the petitioner in Schultz suffered from normal arm soreness and a

low-grade fever after vaccination, her stroke occurred more than 30 days after vaccination, which

was too nonspecific a course to support vaccine causation. Id. at *13, 24.

Although none of these decisions are binding here, I am persuaded by the reasoning in

Sokol and Schultz. As in Schultz, Dr. Boylan here failed to substantiate her theory of causation

with vaccine-specific information. Instead, she rested on the broad proposition that inflammation

can cause stroke, and vaccines produce an inflammatory response of some kind. Tellingly, it

appears that Dr. Boylan presented a similar theory in this ischemic stroke case as she did in Schultz,

a hemorrhagic stroke case, even though she testified that hemorrhagic stroke is mechanistically

distinct from ischemic stroke. See Tr. at 32 (testifying that a hemorrhagic stroke is caused by

rupture of a blood vessel, while ischemic stroke is caused by choking off the blood supply to the

brain). This broad-brush theorizing across different fact patterns and conditions lessens the

persuasiveness of Dr. Boylan’s opinions here. Cf. Schultz, 2020 WL 1039161, at *22 (“Petitioner’s

experts too often relied on literature that conflated ischemic with hemorrhagic strokes, or other

types of vasculitis, without showing that the specific kind at issue in this case could reliably be

associated with the flu vaccine.”). Furthermore, as in both Sokol and Schultz, the records in this

case do not comport with the mechanistic theory advanced, in that they do not signify a significant

inflammatory response in the days following Petitioner’s vaccination.

VI. CONCLUSION

I am sympathetic to Petitioner’s ordeal. However, upon careful evaluation of all the

evidence submitted in this matter, including the medical records, Petitioner’s statement, the expert

reports, the testimony, and the medical literature, I conclude that she has not shown by

preponderant evidence that she is entitled to compensation under the Vaccine Act. Her petition

is therefore DISMISSED. The clerk shall enter judgment accordingly.21

IT IS SO ORDERED.

21

Pursuant to Vaccine Rule 11(a), the parties may expedite entry of judgment by each filing (either jointly

or separately) a notice renouncing their right to seek review.

33

s/ Jennifer A. Shah

Jennifer A. Shah

Special Master

34