J. v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 19-626V

Special Master Horner

P.J.,

Filed: January 3, 2025

Petitioner, Refiled as Redacted:

v. September 2, 2025

SECRETARY OF HEALTH AND

HUMAN SERVICES,

Respondent.

Danielle Anne Strait, Mctlaw, Seattle, WA, for petitioner.

Zoe Wade, U.S. Department of Justice, Washington, DC, for respondent.

DECISION1

On April 26, 2019, petitioner filed a petition under the National Childhood Vaccine

Injury Act, 42 U.S.C. § 300aa-10, et seq. (2012),2 alleging that she suffered a

cerebrovascular injury as a result of a meningococcal vaccine administered on August

11, 2016. (ECF No. 1.) For the reasons set forth below, I conclude that petitioner is not

entitled to an award of compensation.

I. Applicable Statutory Scheme

Under the National Vaccine Injury Compensation Program, compensation

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

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

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

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

1

When this decision was originally filed the undersigned advised his intent to post it 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). In accordance with Vaccine Rule 18(b), petitioner

filed a timely motion to redact certain information. This decision is being reissued with petitioner’s name

reduced to initials. Except for those changes and this footnote, no other substantive changes have been

made. This decision will be posted on the court’s website with no further opportunity to move for

redaction.

2

All references to “§ 300aa” below refer to the relevant section of the Vaccine Act at 42 U.S.C. § 300aa-

10-34.

1

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

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

link between the vaccination and the injury. § 300aa-11(c)(1); § 300aa-13(a)(1)(A)-(B).

In some cases, the petitioner may simply demonstrate the occurrence of what

has been called a “Table Injury.” That is, it may be shown that the vaccine recipient

suffered an injury of the type enumerated in the “Vaccine Injury Table,” corresponding to

the vaccination in question, within an applicable time period following the vaccination

also specified in the Table. If so, the Table Injury is presumed to have been caused by

the vaccination unless it is affirmatively shown that the injury was caused by some

factor other than the vaccination. § 300aa-13(a)(1)(A)-(B); § 300aa-11(c)(1)(C)(i);

§ 300aa-14(a). In many cases, however, the vaccine recipient may have suffered an

injury not of the type covered in the Vaccine Injury Table. In such instances, an

alternative means exists to demonstrate entitlement to a Program award. That is, the

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

by the vaccination in question. § 300aa-11(c)(1)(C)(ii). In such a situation, the

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

on the petitioner to introduce evidence demonstrating that the vaccination actually

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

1274, 1278 (Fed. Cir. 2005); Hines ex rel. Sevier v. Sec’y of Health & Human Servs.,

940 F.2d 1518, 1525 (Fed. Cir. 1991).

In this case, petitioner has alleged that the meningococcal vaccine caused a

cerebrovascular injury, which is not listed on the Vaccine Injury Table relative to the

meningococcal vaccine. Therefore, petitioner must meet the burden of proof for

establishing causation-in-fact.

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

evidence” standard, the same standard ordinarily used in tort litigation.

§ 300aa-13(a)(1)(A); see also Althen, 418 F.3d at 1279; Hines, 940 F.2d at 1525.

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

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

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

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

for” cause. Shyface ex rel. Shyface v. Sec’y of Health & Human Servs., 165 F.3d 1344,

1352 (Fed. Cir. 1999). Thus, the petitioner must supply “proof of a logical sequence of

cause and effect showing that the vaccination was the reason for the injury[,]” with the

logical sequence being supported by “reputable medical or scientific explanation, i.e.,

evidence in the form of scientific studies or expert medical testimony.” Althen, 418 F.3d

at 1278 (quoting Grant ex rel. Grant v. Sec’y of Health & Human Servs., 956 F.2d 1144,

1148 (Fed. Cir. 1992)). Ultimately, petitioner must satisfy what has come to be known

as the Althen test, which requires: (1) a medical theory causally connecting the

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

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

relationship between vaccination and injury. Id.

2

A petitioner may not receive a Vaccine Program award based solely on his or her

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

opinion of a competent physician. § 300aa-13(a)(1). Medical records are generally

viewed as particularly trustworthy evidence because they are created

contemporaneously with the treatment of the patient. Cucuras ex rel. Cucuras v. Sec’y

of Health & Human Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993). However, medical

records and/or statements of a treating physician’s 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. § 300aa-13(b)(1). A petitioner may rely upon circumstantial

evidence. See Althen, 418 F.3d at 1280. The Althen court noted that a petitioner need

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

contention, so long as the petitioner supplies the medical opinion of an expert. Id. at

1279-80. While scientific certainty is not required, that expert’s opinion must be based

on “sound and reliable” medical or scientific explanation. Boatmon ex rel. J.B. v. Sec’y

of Health & Human Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019).

Cases in the Vaccine Program are assigned to special masters who are

responsible for “conducting all proceedings, including taking such evidence as may be

appropriate, making the requisite findings of fact and conclusions of law, preparing a

decision, and determining the amount of compensation, if any, to be awarded.” Vaccine

Rule 3(b)(1). Special masters must ensure each party has had a “full and fair

opportunity” to develop the record but are empowered to determine the format for taking

evidence based on the circumstances of each case, including having the discretion to

decide cases without an evidentiary hearing. Vaccine Rule 3(b)(2); Vaccine Rule 8(a),

(d). Special masters are not bound by common law or statutory rules of evidence but

must consider all relevant and reliable evidence in keeping with fundamental fairness to

both parties. Vaccine Rule 8(b)(1). The special master is required to consider “all []

relevant medical and scientific evidence contained in the record,” including “any

diagnosis, conclusion, medical judgment, or autopsy or coroner’s report which is

contained in the record regarding the nature, causation, and aggravation of the

petitioner’s illness, disability, injury, condition, or death,” as well as the “results of any

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

conclusions.” § 300aa-13(b)(1). The special master is required to consider all the

relevant evidence of record, draw plausible inferences, and articulate a rational basis for

the decision. Winkler v. Sec’y of Health & Human Servs., 88 F.4th 958, 963 (Fed. Cir.

2023) (citing Hines, 940 F.2d at 1528).

II. Procedural History

This case was originally assigned to another special master. (ECF No. 4.) It was

reassigned to the undersigned on August 26, 2019. (ECF Nos. 11-12.) Petitioner

initially filed medical records marked as Exhibits 1-16. (ECF Nos. 6-7). Respondent

then filed a Rule 4 Report recommending against compensation. (ECF No. 13.)

Respondent did not dispute the fact of petitioner’s alleged cerebrovascular injury, but

3

disputed any causal connection to her vaccination and further suggested that treatment

with sertraline could be a more likely explanation.3 (Id. at 14-16.)

Thereafter, petitioner filed additional medical records (Exs. 17-20) and an expert

report by neurologist Ryan Felling, M.D., Ph.D. (Exs. 21-29). (ECF Nos. 15, 21.)

Respondent filed responsive reports by vascular neurologist Steven Messé, M.D., and

immunologist Ross Kedl, Ph.D. (ECF Nos. 26-27; Exs. A-D.) Petitioner filed a

responsive report by Dr. Felling (Ex. 44) and filed a report by immunologist S. Sohail

Ahmed, M.D. (Exs. 33-42). (ECF Nos. 32, 35.) The parties then exchanged a further

round of reports by all four experts. (ECF Nos. 37-38 (Ex. E (Messé) and Ex. F (Kedl));

ECF Nos. 41-42 (Ex. 45 (Felling) and Ex. 46 (Ahmed)).)

I held a Rule 5 Conference on October 14, 2021. (ECF No. 44.) During the

conference, I confirmed that, despite Dr. Ahmed additionally raising the presence of a

chronic autoimmune condition, petitioner’s claim is limited to her allegedly vaccine-

caused focal cerebral arteriopathy. (Id. at 1.) I also directed the parties to provide

further discussion of four studies likely to be key to petitioner’s Althen prong one

showing (Al Qudah et al., Ex. 23; Kothur et al., Ex. 25; Zughaier et al., Ex. 26; and

Macko et al., Ex. 27).4 Id. at 1-2. Following the conference, petitioner filed further

medical records. (ECF No. 47; Exs. 49-50.) Thereafter, respondent filed further reports

by both of his experts (Ex. G (Kedl) and Ex. H (Messé) and petitioner filed a response

by Dr. Ahmed (Ex. 51-52). (ECF Nos. 53-54, 61.)

The parties were instructed to schedule an entitlement hearing, but instead opted

to resolve entitlement by written briefs pursuant to Vaccine Rule 8(d). (ECF No. 62.)

Petitioner filed a motion for a ruling on the written record on July 28, 2023, which was

fully briefed. (ECF Nos. 65, 67, 69.) Thus, this matter is now ripe for resolution as to

entitlement. I have concluded that the parties have had a full and fair opportunity to

develop the record and that it is appropriate to resolve this case without an entitlement

hearing. See Kreizenbeck ex rel. C.J.K. v. Sec’y of Health & Human Servs., 945 F.3d

1362, 1366 (Fed. Cir. 2020) (citing Simanski v. Sec’y of Health & Human Servs., 671

F.3d 1368, 1385 (Fed. Cir. 2012)); see also Vaccine Rule 8(d); Vaccine Rule 3(b)(2).

III. Factual History

a. As reflected in the medical records

Petitioner received the subject meningococcal (“Menactra”) vaccination on

August 11, 2016, during a primary care encounter. (Ex. 1, p. 7; Ex. 35, pp. 7-8.) At the

time of vaccination, petitioner was eighteen years old and presented with a possible

yeast infection. (Ex. 1, p. 5.) She reported that she was taking an oral contraceptive

3

Respondent’s experts did not ultimately discuss sertraline as a cause of petitioner’s condition and so

this issue will not be addressed further.

4

For Al Qudah et al., only an abstract had been filed. Petitioner subsequently confirmed that no complete

article was ever published. (ECF No. 46.)

4

and Zoloft5 as prescribed. (Id.) Her pre-vaccination medical history was significant for

surgery to repair a torn meniscus, anxiety, hair loss/thinning, hematuria, small kidney,

familial hematuria, and allergic rhinitis. (Id.; Ex. 5.) Petitioner was initially prescribed

fluconazole6 for her suspected yeast infection; however, a subsequent urinalysis

showed mild bacterial vaginosis without the presence of yeast, and a new prescription

was ordered. (Ex. 1, p. 6; Ex. 5, pp. 94-95.) This primary care appointment took place

at some point between 4:00 p.m. and 5:00 p.m. on August 11, 2016. (Ex. 1, p. 5.)

The following day, at around 7:30 p.m. on August 12, 2016, the paramedics were

dispatched for a “possible stroke.” (Ex. 4, pp. 23, 28.) Earlier in the day, petitioner had

been running around and playing soccer. (Id. at 23.) She reported that she did not

drink any water and had barely eaten throughout the day. (Id.) At some point, she

decided to go for a swim in the river when she noticed weakness and paralysis on the

right side of her body, as well as a cold sensation. (Id. at 6, 23.) She was unable to pull

herself out of the water and required assistance, prompting the 911 call. (Id.) When

paramedics arrived, they observed that petitioner could not move the right side of her

body at all, and she was aphasic with a droopy mouth on the right side. (Id. at 23.) On

physical examination, petitioner’s skin was noted to be “cool, pink, dry.” (Id.) After a

few minutes, petitioner was able to sit up and was feeling “totally normal.” (Id.)

However, she complained of a headache and reported a recent history of hypertension.

(Id.) She was transported to the hospital for further evaluation. (Id. at 23-25.) It is

noted that stroke protocol was initiated but subsequently discontinued after petitioner

began feeling normal. (Id. at 24.)

While at the hospital, petitioner was evaluated for headache with associated

paresthesias, focal weakness, and speech changes, which began approximately one

hour prior but had since resolved. (Ex. 4, p. 4.) Her temperature was recorded as 98.9º

Fahrenheit, and a review of symptoms was negative for chills or fever. (Id. at 5.)

Although her vital signs showed mild tachycardia, petitioner was noted to be emotional

and somewhat anxious. (Id. at 6.) Her neurologic examination was normal, and there

was no evidence of leukocytosis or anemia. (Id. at 5-7, 16-17.) An EKG showed a

normal sinus rhythm and possible left arterial enlargement, and a CT of the head and

CT angiogram of the head and neck were unremarkable with no significant

abnormalities. (Id. at 6-7, 13-16.) During her hospitalization, petitioner reported that

she had never experienced a similar episode, she had no complaints, and “she just

want[ed] to go home.” (Id. at 6.) She was given Toradol and Tylenol for her headache

and advised to return to the hospital if her symptoms returned. (Id. at 7, 18.) Her

5

Zoloft is the brand name for sertraline hydrochloride, which is an orally administered selective serotonin

reuptake inhibitor that is used in the treatment of depressive, obsessive-compulsive, and panic disorders.

Zoloft, DORLAND’S MEDICAL DICTIONARY ONLINE,

https://www.dorlandsonline.com/dorland/definition?id=54076 (last visited Oct. 31, 2024); Sertraline

hydrochloride, DORLAND’S MEDICAL DICTIONARY ONLINE,

https://www.dorlandsonline.com/dorland/definition?id=45550 (last visited Oct. 31, 2024).

6

Fluconazole is an orally or intravenously administered antifungal medication. Fluconazole, DORLAND’S

MEDICAL DICTIONARY ONLINE, https://www.dorlandsonline.com/dorland/definition?id=18848 (last visted

Oct. 31, 2024).

5

differential diagnoses included transient ischemic attack, hemiplegic migraine, atypical

seizure, and cervical artery dissection despite the absence of neck pain. (Id. at 6.) Her

diagnoses on discharge were transient paralysis and unspecified headache. (Id. at 7.)

She was discharged home in a stable condition. (Id.)

On August 14, 2016, petitioner presented to the emergency department with a

two-day history of headache. (Ex. 9, p. 119.) Upon arrival, petitioner was experiencing

a panic attack with heavy breathing and tachycardia. (Id.) She reiterated the events of

August 12, 2016, and reported that, at the time, her symptoms lasted for approximately

30 minutes. (Id.) Petitioner’s systolic blood pressure was elevated. (Id. at 120.)

Intermittent tachycardia was noted but believed to be associated with petitioner's

anxiety. (Id. at 121.) Her physical and neurologic examinations were normal, and an

MRI was considered unnecessary at that time. (Id.) Her laboratory testing was

essentially unremarkable, and a urine sample was apparently contaminated. (Id.)

Although it was noted that petitioner was recently treated for a yeast infection, there

were no significant urinary symptoms as this time. (Id.) Petitioner was again

discharged with diagnoses of transient paralysis and headache. (Id. at 123.) She was

instructed to follow up with a neurologist. (Id. at 121, 123.)

On August 17, 2016, petitioner presented to neurologist Brent Burroughs, M.D.,

for right hemiparesis and aphasia. (Ex. 3, p. 2.) She again reiterated the events of

August 12, 2016, and her mother indicated some concern that petitioner’s symptoms

could be the result of her recent meningococcal vaccination. (Id.) She reported that

she had been feeling “fine” since her August 14, 2016 hospitalization. (Id.) Dr.

Burroughs noted that petitioner received the “meningococcal vaccine on 8/11 then

developed right hemiparesis and aphasia on 8/12 with an associated headache. This

lasted 20 minutes then recurred 2 days later.” (Id. at 3.) His differential diagnoses

included transient ischemic attack, atypical migraine, and panic attack. (Id.) An MRI

was ordered to determine whether petitioner’s oral contraceptive should be switched,

and she was directed to follow up after completing the imaging. (Id.) Petitioner was

prescribed a Medrol (Pak)7 and tramadol HCL.8 (Id.) However, Dr. Burroughs noted

that petitioner’s exam was normal with no significant risk factors for stroke. (Id.)

Petitioner underwent an MRI on August 23, 2016, which showed “[a]cute

ischemic infarct involving the left basal ganglia and left frontal lobe.” (Ex. 3, p. 12.)

There was also “diminutive flow voids involving the left [middle cerebral artery]

distribution as well as the left [internal carotid artery],” which was concerning for

underlying vasculopathy or dissection. (Id.) Based on these results, a repeat CT

7

Medrol is an orally administered “synthetic glucocorticoid derived from progesterone” which is “used in

replacement therapy for adrenocortical insufficiency and as an anti-inflammatory and immunosuppressant

in a wide variety of disorders.” Methylprednisolone, DORLAND’S MEDICAL DICTIONARY ONLINE,

https://www.dorlandsonline.com/dorland/definition?id=31014 (last visited Nov. 4, 2024).

8

Tramadol HCL is an orally administered opioid analgesic that is used to treat moderate to moderately

severe pain. Tramadol hydrochloride, DORLAND’S MEDICAL DICTIONARY ONLINE,

https://www.dorlandsonline.com/dorland/definition?id=50542 (last visited Nov. 4, 2024).

6

angiogram was ordered and revealed “[a]bnormal irregular stenoses” of the left middle

cerebral artery, anterior cerebral artery, internal carotid artery, and posterior cerebral

artery. (Id. at 4-5, 14.) The MRI findings suggested an acute ischemic cerebrovascular

accident; however, given the subsequent CT angiogram findings and petitioner’s age, a

vasculitic process was of primary concern. (Id. at 5, 8; Ex. 6, p. 18.) Petitioner was

subsequently transferred to Oregon Health & Sciences University for further testing.

(Ex. 6, p. 18.)

On admission, petitioner reported no new symptoms but described a remitting,

bilateral posterior headache with occasional pulsation and associated nausea. (Ex. 6,

pp. 18-19.) Although her weakness and sensory changes had resolved, petitioner

reported an additional episode of anxiety a few days prior that was accompanied by a

recurrence of her initial symptoms, although to a lesser extent. (Id. at 39.) It was also

noted that petitioner had been taking Zoloft for the past month and had a family history

of lupus. (Id. at 3, 54.) Her screening bloodwork and initial neurologic exam was

normal, and her lupus inhibitor evaluation was negative. (Id. at 39-46, 107-08.)

Petitioner then underwent a repeat MRI on August 24, 2016, which showed a new focus

of acute infarction involving the left anterior commissure superimposed on the

previously seen infarction in the left lenticulostriate distribution. (Ex. 3, p. 14.) She also

underwent a diagnostic cerebral angiogram that showed improvement in the blood

vessels when compared to the prior CT angiogram. (Id.; Ex. 6, pp. 19, 30; Ex. 10, p.

105.) These results were believed to be consistent with a possible reversable cerebral

vasoconstriction syndrome (“RCVS”). (Ex. 10, p. 105; Ex. 6, p. 19; Ex. 3, p. 14.)

Specifically, neuroradiologist Gary Nesbit, M.D., opined that petitioner’s “significant

resolution over a single day and the overall findings” points to RCVS; however, he was

reluctant to administer intra-arterial verapamil9 due to petitioner’s relatively low blood

pressure. (Ex. 6, p. 19.)

On August 25, 2016, petitioner presented to neurologist Wayne Clark, M.D. (Ex.

6, p. 2.) Dr. Clark noted that vasculitis had been ruled out due to petitioner’s marked

improvement without treatment and that petitioner was likely suffering from RCVS “from

Zoloft or vaccine.” (Id. at 4.) He prescribed verapamil and aspirin, as well as

magnesium glycinate for her headaches. (Id. at 4, 55-56.) Petitioner’s discharge

diagnosis was reversible vasoconstriction syndrome complicated by stroke, but the

cause of the condition remained “unclear.” (Id. at 55.) She was directed to follow up for

additional blood work. (Id.)

In late September 2016, petitioner underwent a follow up CT angiogram of her

head and neck, which showed left internal carotid artery dissection and improved but

diminutive flow within the left middle cerebral artery distribution. (Ex. 5, pp. 106-07.)

9

Verapamil is an orally or intravenously administered calcium channel blocking agent that dilates

coronary arteries and decreases myocardial oxygen demand. Verapamil hydrochloride, DORLAND’S

MEDICAL DICTIONARY ONLINE, https://www.dorlandsonline.com/dorland/definition?id=52873 (last visited

Nov. 5, 2024). When intravenously administered, verapamil is used to treat supraventricular

tachyarrhythmias, and when orally administered, it is used in the treatment and prophylaxis of angina

pectoris, in the treatment of hypertension, and in the prophylaxis of supraventricular tachyarrhythmias. Id.

7

Thereafter, she presented for a follow up with the stroke clinic and complained of daily

headaches, which she described as aching/throbbing and primarily affecting the left

side. (Id. at 158.) It was noted that petitioner’s hypercoagulable labs were

unremarkable and her urine tox screen was negative. (Id.) It was further noted that her

rheumatology labs were unremarkable with the exception of elevated antinuclear

antibodies (“ANA”) at 1:10240 in a speckled pattern and elevated Sjӧgren’s syndrome

antibodies at 420. (Id. at 158-59.) Additionally, her lupus anticoagulant and cardiolipin

tests were negative, and her neurologic exam was normal. (Id. at 159.) Given

petitioner’s presentation, including her workup thus far and continued headaches

despite no new neurologic symptoms, the possibility of cerebral vasculitis was again

suggested. (Id. at 160.) Lupus versus Sjӧgren’s syndrome was also included in the

differential. (Id.) Petitioner was referred to a neuroimmunologist for further evaluation.

(Id.)

On November 2, 2016, petitioner presented to Oregon Health & Science

University. (Ex. 12, p. 66.) She denied recurrence of hemiparesis or speech issues but

reported continued headaches with associated nausea and fatigue. (Id. at 66-67.) She

described two instances in which she experienced a rash that quickly resolved with

allergy medication. (Id. at 67.) Although she had discontinued Zoloft, she continued to

take verapamil and Tramadol, as well as Vicodin. (Id.) It was noted that RCVS

secondary to restarting Zoloft was initially suspected, but persistent stenosis and

abnormal labs suggested a rheumatologic diagnosis. (Id. at 72.) Sjӧgren’s syndrome

was discussed, including its association with leukocytoclastic vasculitis and neurologic

symptoms, such a peripheral neuropathy and encephalopathy. (Id.) Petitioner’s

intermittent rash could be cutaneous vasculitis, which is also sometimes associated with

Sjӧgren’s syndrome; however, further evaluation for vasculitis was necessary at this

juncture. (Id.) Regarding the differential diagnosis of vasculitis, it was suggested that

petitioner suffered from medium to small vessel vasculitis, rather than primary central

nervous system vasculitis, due to her systemic symptoms. (Id.) Petitioner was referred

to a rheumatologist for further evaluation. (Id.)

Petitioner presented for a rheumatology evaluation on November 7, 2016. (Ex.

5, p. 150.) The history of present illness lists that petitioner suffered from two strokes,

as evidenced on MRI, but the later stroke was mistakenly believed to be a panic attack.

(Id.) It is also noted that petitioner experienced random numbness in her fingers that

generally lasts 10-30 minutes before spontaneously resolving. (Id.) Petitioner also

reported general fatigue and weakness. (Id.) Although it was observed that petitioner’s

presentation was not consistent with any systemic autoimmune disorder or other

condition, such as Sjӧgren’s syndrome, it was suggested that she could be suffering

from drug-induced lupus based on her prior use of Zoloft and declining antibodies

following discontinuation of the drug. (Id. at 153-54.) However, it was also noted that

these antibodies can be found in healthy adults so additional bloodwork was ordered.

(Id. at 154.) In a follow up email, petitioner’s rheumatologist confirmed that her

bloodwork did not demonstrate evidence of any of the common systemic autoimmune

disorders. (Ex. 12, p. 207.)

8

A few days later, petitioner presented for a follow up with the stroke clinic at

Oregon Health & Science University. (Ex. 10, p. 84.) She reported continued

headaches and fatigue. (Id.) She also reported a facial rash with associated hives. (Id.

at 85.) A neurologic exam was normal. (Id.) Additionally, her ANA was elevated at

1:1280 and in speckled pattern, her Sjӧgren’s syndrome antibodies were only slightly

elevated at 248, and her lupus anticoagulant and anticardiolipin were negative. (Id. at

86, 105.) Her normal CSF results ruled out CSF inflammation or vasculitis, and her

working diagnoses remained RCVS or drug-induced lupus secondary to Zoloft. (Id. at

87.) She was continued on aspirin and magnesium, directed to wean off verapamil, and

directed to follow up for repeat imaging. (Id. at 87-88.) She was also referred to a

headache specialist for further evaluation. (Id. at 88.)

Petitioner had a neuroimmunology follow up on January 1, 2017. (Ex. 10, p.

105.) She reported that, in attempting to wean off verapamil, she experienced daily

throbbing headaches over the back of the head with associated nausea and

photophobia. (Id.) It was noted that petitioner was infrequently taking Tramadol and

Vicodin, but she was advised that these medications can cause medication overuse

headaches. (Id. at 107-08.) She was prescribed an increased dose of verapamil and

directed to undergo an MRI of the cervical spine to evaluate for a possible cervicogenic

component. (Id. at 108.) It was also noted that there was “no evidence of a

Neuroimmunological problem contributing to her clinical picture” and therefore a

neuroimmunology follow up was not necessary at this time. (Id.)

Further imaging was performed in February of 2017. (Ex. 9, pp. 11-16.) An MRI

of the cervical spine showed no significant central canal and neural foraminal stenosis,

and an MRI of the brain showed no evidence of mass, hemorrhage, or acute stroke.

(Id. at 11, 16.) An MRA of the head was normal with the exception of decreased flow

through the left middle cerebral and temporal lobe branches. (Id. at 14.)

On February 9, 2017, petitioner presented to neurologist Juliette Preston, M.D.,

for management of chronic headaches. (Ex. 10, p. 131.) Petitioner described her

headaches as throbbing; affecting the back, left side of the head; and associated with

nausea, sensitivity to light and sound, fatigue, dizziness, and difficulty concentrating.

(Id.) However, she reported mild improvement in her headaches after increasing her

verapamil prescription. (Id.) A neurologic exam was normal. (Id. at 133-34.) She

prescribed Topamax for her headaches and directed to follow up in two months. (Id. at

134.) On February 17, 2017, petitioner presented to the stroke clinic for a follow up.

(Id. at 146.) She reported significant improvement in her headaches with her new

prescription. (Id. at 147.) A neurologic exam was normal. (Id. at 147-48.) It was noted

that the lack of improvement on repeat CT angiogram and MRA did not support a

diagnosis of RCVS. (Id. at 150.) It was suggested that petitioner could have thrombus

or congenital vessel abnormality, although the negative CT angiogram does not support

the latter diagnosis. (Id.) She was directed to follow up for repeat imaging. (Id.)

9

Petitioner followed up with Dr. Preston on April 17, 2017, and reported reduced

headaches with diclofenac.10 (Ex. 10, p. 162.) She was assessed with “chronic daily

migraine headache triggered by vascular event last August.” (Id. at 163.) She was

directed to continue taking her medication as prescribed, to keep a headache diary, to

increase her intake of potassium rich foods (to alleviate paresthesia), and to follow up in

three months. (Id. at 163-64.)

On September 17, 2017, petitioner underwent an MRA of her head, which

showed “[n]arrowing of the left M1 segment with decreased number of vessels in the left

sylvian fissure,” which was consistent with an old middle cerebral artery infarct. (Ex. 13,

p. 22.) Petitioner followed up with the stroke clinic on September 22, 2017, and it was

noted that her rheumatologist initially believed that her elevated ANA and Sjӧgren’s

syndrome antibodies were the result of drug-induced lupus secondary to Zoloft. (Ex.

12, p. 323.) However, her working diagnoses were “RCVS vs drug-induced Lupus

vasculitis.” (Id.) It was noted that petitioner successfully weaned off verapamil without

worsening symptoms, that her headaches had improved on topiramate,11 and that she

had not experienced any further episodes of focal neurologic symptoms. (Id.)

Petitioner’s September 17, 2017 MRA showed stable narrowing predominantly affecting

the distal left middle cerebral artery. (Id.) Her neurologic exam was normal during this

encounter. (Id. at 324.) Petitioner was assessed with acute ischemic stroke and, based

on stable narrowing of the left middle cerebral artery, the etiology of petitioner’s

condition was suspected to represent drug-induced lupus vasculitis or RCVS. (Id. at

325.) Although both working diagnoses were possibly related to petitioner’s treatment

with Zoloft, drug-induced lupus was favored, given the persistence of vessel narrowing.

(Id.)

On November 21, 2017, petitioner presented to the emergency department,

complaining of headache with associated nausea and vomiting. (Ex. 13, p. 9.) She

reported that her headache was “worse than normal and similar to after her stroke.”

(Id.) A neurologic exam was normal, as was a CT scan of the head. (Id. at 10-11, 15.)

The attending physician neither believed that a repeat MRI was necessary nor

suspected an acute repeat or worsening cerebrovascular accident or other intracranial

vascular abnormality. (Id. at 11.) Petitioner was not in acute distress and was

discharged. (Id.)

Throughout the rest of 2017, 2018, and 2019, petitioner continued to seek

evaluation and care for her headaches. (Ex. 15, pp. 4-10, 33-36, 68-71; Ex. 16, pp. 31-

36, 49-52, 96-103; Ex. 32, pp. 105-09.) Her treaters remained puzzled by her

presentation, noting that it was not clear why she suffered the cerebrovascular accident.

10

Diclofenac potassium is an orally administered “treatment of rheumatoid arthritis, osteoarthritis, and

ankylosing spondylitis, a variety of nonrheumatic inflammatory conditions, pain, and dysmenorrhea.

Diclofenac potassium, DORLAND’S MEDICAL DICTIONARY ONLINE,

https://www.dorlandsonline.com/dorland/definition?id=69744 (last visited Nov. 6, 2024).

11

Topiramate is an orally administered anticonvulsant that is used in the treatment of partial seizures.

Topiramate, DORLAND’S MEDICAL DICTIONARY ONLINE,

https://www.dorlandsonline.com/dorland/definition?id=50310 (last visited Nov. 6, 2024).

10

(E.g., Ex. 15, p. 10; Ex. 16, p. 102.) The consensus seemed to be drug-induced lupus

vasculitis related to Zoloft as the suspected etiology of her condition with RCVS

appearing less likely as time went on. (E.g., Ex. 15, pp. 36, 70; Ex. 16, pp. 35, 51; Ex.

32, p. 109.) This determination was primarily based on the persistence of vessel

narrowing; however, it was repeatedly noted that the continued elevation of ANA and

Sjӧgren’s syndrome antibodies following discontinuation of Zoloft was “puzzling.” (Ex.

15, pp. 36, 70; Ex. 16, p. 35; Ex. 32, p. 109.) Additionally, while other diagnoses were

discussed, such as connective tissue disease, Sjӧgren’s syndrome, Moyamoya disease,

and fibromuscular dysplasia, these conditions were considered less likely or not

detectable at that time, given petitioner’s overall clinical presentation. (Ex. 15, pp. 10,

36, 70-71; Ex. 16, p. 35; Ex. 32, p. 109.)

In early 2020, petitioner returned to the stroke clinic at Oregon Health & Science

University. (Ex. 32, pp. 44.) Her ANA and Sjӧgren’s syndrome antibody levels were

rechecked and remained stable when compared to the 2017 results. (Id.) Petitioner

reported a new headache type affecting the left eye and ear, which improved with rest.

(Id.) She described this headache as including a burning and throbbing sensation, as

well as associated nausea. (Id.) She further described an episode of dizziness,

nausea, diaphoresis, paleness, and generalized weakness that last for approximately

one hour and improved after she ate some ice cream. (Id.) The suspected etiology of

petitioner’s condition was lupus vasculitis or systemic lupus. (Id. at 46.) At this point,

RCVS appeared unlikely in the setting of persistent vessel narrowing and drug-induced

lupus appeared unlikely due to consistently elevated ANA and Sjӧgren’s syndrome

antibodies following discontinuation of Zoloft. (Id.) The etiology of petitioner’s new

headache type was unclear, but repeat imaging was not ordered in the absence of new

focal neurologic symptoms or headache that is both progressive/severe and

unresponsive to therapy. (Id.)

Petitioner followed up with the stroke clinic on August 6, 2020. (Ex. 34, p. 4.)

She reported a headache frequency of 1-2 per week. (Id. at 5.) Petitioner’s neurologic

exam was normal. (Id. at 5, 7.) In the assessment, the following was noted:

Interval imaging showed stable narrowing. . . . Etiology of narrowing is

unclear. Suspected initially to be vasculitis process, [lumbar puncture]

unrevealing, and there has been no evidence for progression. Did not

reverse to suspect RCVS. May represent a Focal Cerebral Arteriopathy

(FCA) that can occur in young adults. Etiology of FCA not well understood,

but its hallmark is that it is not progressive. There is conjecture that it may

be due to a viral infection, and of note patient did have a vaccination the

day prior to her event.

(Id. at 7.) Repeat vascular imaging was ordered to evaluate for a progressive

inflammatory process. (Id.) Petitioner underwent an MRA of the head on October 14,

2020, which was normal. (Ex. 49, pp. 102, 107.) During subsequent encounters

throughout the rest of 2020, petitioner reported that she was “doing well” overall, and

her assessment remained the same. (Ex. 50, pp. 55-57, 90-93.)

11

In February of 2021, petitioner presented to the stroke clinic and reported that

she had experienced a bad migraine that incapacitated her for a week following receipt

of a COVID-19 vaccine. (Ex. 50, pp. 34-35.) It was noted that interval imaging showed

improved vessel narrowing, but her assessment remained the same. (Id. at 37.) Her

diagnoses included history of left middle cerebral artery stroke, left middle cerebral

artery stenosis, possible Sjӧgren’s syndrome vs. lupus, and chronic refractory migraine.

(Id. at 36.) There are no further medical records related to petitioner’s post-vaccination

condition.

IV. Summary of Expert Opinions

a. Petitioner’s neurologist, Ryan Felling, M.D., Ph.D.12

Dr. Felling opines that petitioner suffered a stroke, and more specifically a form of

inflammatory arteriopathy known as a focal cerebral arteriopathy, rather than a RCVS

as initially suspected. (Ex. 21, p. 3.) Although he acknowledges that petitioner’s initial

presentation was consistent with RCVS, the persistence of her condition over time and

the focality of her vascular abnormalities are inconsistent with RCVS. (Id.) Further, Dr.

Felling opines that petitioner’s meningococcal vaccination “was at the very least an

important contributor” to her arteriopathy. (Id.)

Dr. Felling acknowledges that vaccination is generally thought to reduce the risk

of stroke (Ex. 21, p. 3), but indicates that this is because the infections they prevent are

an even greater risk factor for stroke, which does not suggest vaccines cannot also lead

to adverse events more rarely even as they are protective at the population level (Ex.

44, pp. 1-2). In particular, Dr. Felling challenges the methodology of a study by

Fullerton et al., cited by Dr. Messé, that reported a protective effect of vaccination

against pediatric stroke. (Id. at 2 (citing Heather J. Fullerton et al., Infection,

Vaccination, and Childhood Arterial Ischemic Stroke: Results of the VIPS Study, 85

NEUROLOGY 1459 (2015) (Ex. 28; Ex. A, Tab 6)).) He is also critical of a study by

Wintermark et al. because it did not apply the same level of analysis for potentially

associating vaccinations to pediatric stroke that it did for infections. (Ex. 45, p. 2 (citing

12

Dr. Felling received his medical degree and Ph.D. in neuroscience from Penn State University College

of Medicine in 2007, before going on to complete a pediatric internship and residency at Children’s

Hospital of Philadelphia in 2008 and 2009, respectively, and a child neurology residency and vascular

neurology fellowship at The Johns Hopkins Hospital in 2012 and 2013, respectively. (Ex. 22, p. 1.) He is

board certified in neurology with special qualification in child neurology and vascular neurology, and he

maintains an active medical license in Maryland. (Ex. 21, p. 1.) He currently works as an assistant

professor in the Department of Neurology at The Johns Hopkins University School of Medicine, director of

the Pediatric Stoke Program, and co-director of the Neuro-PICU. (Ex. 22, p. 1.) He also maintains a joint

appointment in the Department of Neurology. (Id.) In his clinical work, Dr. Felling regularly diagnoses

and treats pediatric stroke patients, in addition to patients with a full range of pediatric neurological

diseases. (Ex. 21, p. 1.) He also has an active research program related to clinical aspects of pediatric

stroke and the basic biological mechanisms of recovery after brain injury in children. (Id.) In his research

capacity, he has authored 16 original research papers, 10 review articles, 8 case reports, and 6 book

chapters. (Ex. 22, pp. 1-4.)

12

Max Wintermark et al., Arteriopathy Diagnosis in Childhood Arterial Ischemic Stroke:

Results of the Vascular Effects of Infection in Pediatric Stroke Study, 45 STROKE 3597

(2014) (Ex. A, Tab 10)).)

Dr. Felling indicates that focal cerebral arteriopathy is associated with elevated

cytokines including IL-6, IL-8, and CXCL10, which are also induced by the

meningococcal vaccine. (Ex. 21, p. 3-4 (citing Kavitha Kothur et al., Elevation of

Cerebrospinal Fluid Cytokine/Chemokines Involved in Innate, T Cell, and Granulocyte

Inflammation in Pediatric Focal Cerebral Arteriopathy, 14 INT’L J. STROKE 154 (2019)

(Ex. 25); Susu M. Zughaier, Neisseria Meningitidis Capsular Polysaccharides Induce

Inflammatory Response via TLR2 and TLR4-MD-2, 89 J. LEUKOCYTE BIOLOGY 469

(2011) (Ex. 26)).) He opines that petitioner’s cerebral arteriopathy occurred at a time

consistent with a post-vaccination inflammatory response (approximately 24 hours post-

vaccination). (Id. at 4.) Dr. Felling indicates that multiple studies have shown increased

risk of brain infarction within the week following an infection or inflammatory syndrome.

(Id. (citing Richard F. Macko et al., Precipitants of Brain Infection: Roles of Preceding

Infection/Inflammation and Recent Psychological Stress, 27 STROKE 1999 (1996) (Ex.

27); Fullerton et al., supra, at Ex. 28; Ex. A, Tab 6).) He further suggests that no other

likely trigger is evidenced. (Id.) In particular, he disagrees with Dr. Messe’s suggestion

that a yeast infection13 at the time of vaccination was a likely contributor to petitioner’s

stroke, stressing that there is no literature available to suggest any causal association

between a localized infection and stroke. (Ex. 44, pp. 2-3.) Dr. Felling is critical of Dr.

Messé’s conclusion that petitioner’s stroke was “cryptogenic,” i.e., having no cause

whatsoever, both because arteriopathy is a defined etiology for stroke and because it

merely represents a preconceived bias against her vaccination as a cause of the stroke.

(Ex. 45, p. 1.)

b. Respondent’s neurologist, Steven Messé, M.D.14

Dr. Messé agrees that RCVS is a less likely diagnosis for this petitioner. (Ex. A,

pp. 4-5.) He also acknowledges that Dr. Felling’s proposed diagnosis of focal cerebral

13

The immunology experts would subsequently clarify that what is at issue is a bacterial vaginosis, rather

than a yeast infection. (Ex. G, p. 9; Ex. 51, pp. 2-4.)

14

Dr. Messé received his medical degree from the University of Michigan School of Medicine in 1998,

before going on to complete an internship, residency, and fellowship at the Hospital of the University of

Pennsylvania in 1999, 2002, and 2003, respectively. (Ex. B, p. 1.) He is board certified in neurology and

vascular neurology. (Id.) He currently works as an associate professor of Neurology at the Hospital of

the University of Pennsylvania, University of Pennsylvania School of Medicine. (Id.) In that position, he

has cared for thousands of stroke patients in the inpatient and outpatient setting, as well as published

extensively on issues related to cerebrovascular disease. (Ex. A, p. 1.) Dr. Messé has also served as a

member of the Academy of Neurology Guideline Development Committee. (Id.; Ex. B, p. 2.) In that

capacity, he has authored multiple clinical practice guidelines that are based upon systemic literature

reviews requiring critical assessments of study methodology and risk bias. (Ex. A, p. 1.) Additionally, Dr.

Messé has served on the Classification of Evidence review panel for Neurology and as an ad hoc

reviewed on several relevant journals. (Id.; Ex. B, pp. 2-3.) In his research capacity, Dr. Messé has

authored 84 peer-reviewed research publications, 23 reviews, and 31 editorials, reviews, and chapters,

including committee reports. (Ex. B, pp. 8-28.)

13

arteriopathy is “possible.” (Id. at 4.) He stresses, however, that stroke is a

heterogeneous disorder with numerous pathophysiologic mechanisms and that,

especially among children, it is not unusual for even thorough work ups to fail to find any

obvious proximate cause of the stroke. (Id. at 3.) He cites a study indicating that,

among young stroke patients, 24-36% will have no determined cause of their stroke.

(Id. (citing Jukka Putaala et al., Analysis of 1008 Consecutive Patients Aged 15 to 49

with First-Ever Ischemic Stroke: The Helsinki Young Stroke Registry, 40 STROKE 1195

(2009) (Ex. A, Tab 1)).)

Dr. Messé cites several studies for the proposition that vaccines reduce, rather

than increase, the risk of stroke, especially in children. (Ex. A, pp. 3-4 (citing Armin J.

Grau et al., Influenza Vaccine is Associated with a Reduced Risk of Stroke, 36 STROKE

1501 (2005) (Ex. A, Tab 2); A. Niroshan Siriwardena et al., Influenza and

Pneumococcal Vaccination and Risk of Stroke or Transient Ischaemic Attack–Matched

Case Control Study, 32 VACCINE 1354 (2014) (Ex. A, Tab 3); Pai-Feng Kao et al.,

Influenza Vaccination Might Reduce the Risk of Ischemic Stroke in Patients with Atrial

Fibrillation: A Population-Based Cohort Study, 8 ONCOTARGET 112697 (2017) (Ex. A,

Tab 4); Liam Smeeth et al., Risk of Myocardial Infarction and Stroke After Acute

Infection or Vaccination, 351 NEW ENG. J. MED. 2611 (2004) (Ex. A, Tab 5; Ex. G, Tab

14); Fullerton et al., supra, at Ex. 28; Ex. A, Tab 6; Nancy K. Hills et al., Recent Trauma

and Acute Infection as Risk Factors for Childhood Arterial Ischemic Stroke, 72 ANNALS

NEUROLOGY 850 (2012) (Ex. A, Tab 7)).) Discussing a study by Smeeth et al., Dr.

Messé acknowledges that vaccine-preventable infections were found to increase stroke

risk but asserts that the separate finding of a decreased risk of stroke within 28 days of

vaccination evidences an actual protective effect from vaccination. (Id. at 3 (discussing

Smeeth et al., supra, at Ex. A, Tab 5; Ex. G, Tab 14).) He also highlighted a finding by

Fullerton et al. that both prior infection and under-vaccination were risk factors for stroke

in children. (Id. at 4 (citing Fullerton et al., supra, at Ex. 28; Ex. A, Tab 6).) Dr. Messé

stresses in particular that the Fullerton study found that children who received the

meningococcal vaccine were less likely to experience a stroke. (Id. (citing Fullerton et

al., supra, at Ex. 28; Ex. A, Tab 6).) He also cited two other studies for the proposition

that stroke has not been reported as an adverse event associated with the

meningococcal vaccine. (Id. (citing Hung-Fu Tseng et al., Safety of Quadrivalent

Meningococcal Conjugate Vaccine in 11- to 21-Year-Olds, 139 PEDIATRICS, January

2017, at 1 (Ex. A, Tab 8); Rongxia Li et al., Meningococcal Conjugate Vaccine Safety

Surveillance in the Vaccine Safety Datalink Using a Tree-Temporal Scan Data Mining

Method, 27 PHARMACOEPIDEMIOLOGY DRUG SAFETY 391 (2018) (Ex. A, Tab 9)).)

In his first report, Dr. Messé notes, in contrast to a complete lack of literature

supporting any association between vaccination and the focal cerebral arteriopathy

proposed by Dr. Felling, that recent or ongoing infection is the most common

explanation for focal cerebral arteriopathy. (Ex. A, pp. 4-5 (citing Fullerton et al., supra,

at Ex. 28; Ex. A, Tab 6; Catherine Amlie-Lefond et al., Predictors of Cerebral

Arteriopathy in Children with Arterial Ischemic Stroke: Results of the International

Pediatric Stroke Study, 119 CIRCULATION 1417 (2009) (Ex. A, Tab 11)).) Thus,

assuming petitioner suffered a focal cerebral arteriopathy, Dr. Messé proposes that

14

petitioner’s ongoing yeast infection would be a more likely cause as compared to

vaccination. (Id. at 5.) In his second report, however, Dr. Messé indicates in response

to Dr. Felling’s criticism that “[i]t is probably most accurate to conclude that neither of

these issues are likely to have caused her stroke and that this was a cryptogenic stroke,

without a clear etiology.” (Ex. E, p. 2.)

In his third report, Dr. Messé addresses the four studies referenced in my prior

Rule 5 Order and confirms that review of the studies does not change his opinion. (Ex.

H.) Dr. Messé suggests that the Al Qudah et al. study never went beyond the abstract

phase because it was unlikely to survive peer review, given that it is merely a review of

voluntary Vaccine Adverse Event Reporting System (VAERS) submissions with no

review for accuracy or relevancy and no comparison to the general population. (Id. at 1-

2 (discussing Zaid Al Qudah et al., Stroke After Vaccination in United States. A Report

from the CDC/FDA Vaccine Adverse Event Reporting System. [1990-2010] (P01.009),

NEUROLOGY, Apr. 23, 2012, at 1 (Ex. 23)).) Regarding Kothur et al., Dr. Messé

acknowledges that it found higher levels of certain cytokines among those suffering

focal cerebral arteriopathy, but stresses that this does not necessarily point to

vaccination as the cause of inflammation given that ischemic brain injury is inflammatory

in itself and infection-related inflammation is otherwise believed to play a role in focal

cerebral arteriopathy. (Id. at 2 (discussing Kothur et al., supra, at Ex. 25).) Moreover,

the study is small, failed to disclose key data, and failed to acknowledge that stroke

itself produces an inflammatory response. (Id. (citing Klaus Fassbender et al.,

Proinflammatory Cytokines in Serum of Patients with Acute Cerebral Ischemia: Kinetics

of Secretion and Relation to the Extent of Brain Damage and Outcome of Disease, 122

J. NEUROLOGICAL SCIS. 135 (1994) (Ex. H, Tab 1)).) Dr. Messé concludes that the

Macko et al. study, which found infection and inflammation was more common in the

week preceding hospitalization for stroke as compared to controls, is concordant with

his opinion. (Id. at 3 (discussing Macko et al., supra, at Ex. 27.) He defers to Dr. Kedl

with respect to the Zughaier et al. study. (Id. at 2-3.)

c. Petitioner’s immunologist, Sohail Ahmed, M.D.15

Dr. Ahmed begins with the premise that the meningococcal vaccine does

produce systemic inflammation. (Ex. 42, p. 5.) He notes that the package insert for the

Menactra vaccine (the meningococcal vaccine at issue) demonstrates that anorexia,

diarrhea, headache, fatigue, malaise, and arthralgia are among the common solicited

adverse events following vaccination. (Id. (citing Menactra, Meningococcal (Groups A,

15

Dr. Ahmed received his medical degree from the University of Texas at Houston in 1998 and completed

a research fellowship at the National Institutes of Health (NIH), as well as a research fellowship in

immunology at MD Anderson Cancer Center in Houston, Texas. (Ex. 43, p. 4; Ex. 42, p. 2.) He returned

to the University of Texas to complete a combined residency in general medicine, rheumatology, and

rheumatology research. (Ex. 43, p. 4; Ex. 42, p. 2.) Dr. Ahmed is board certified in internal medicine and

rheumatology, and he maintains an active medical license in Massachusetts. (Ex. 43, p. 3.) He has held

faculty positions in rheumatology and immunology, but he currently works as Senior Vice President of

Global Health of Translational Medicine at Galapagos, where he oversees the development of small

molecules and vaccines. (Id. at 2-3; Ex. 42, pp. 2-3.) He has published 29 original articles, reviews,

letters, editorials, and textbook chapters. (Ex. 43, pp. 4-5.)

15

C, Y. and W-135) Polysaccharide Diphtheria Toxoid Conjugate Vaccine Prescribing

Information, [hereinafter Menactra Package Insert], Ex. 36).) According to Dr. Ahmed,

these are systemic effects consistent with cytokine production. (Id.) Dr. Ahmed

acknowledges that Menactra has not been associated with focal cerebral arteriolopathy

specifically, but contends that post-marketing experience and epidemiology have

difficulty capturing short-duration events with delayed pathologic confirmation (i.e., in

this case, petitioner suffered a stroke on August 12, but vasculopathy was not confirmed

until August 23). (Id. at 8-9.)

As part of the clinical trials, adverse events to Menactra were compared against

another meningococcal vaccine, Menomune. (Ex. 42, pp. 5-6.) Menactra had higher

rates of systemic adverse reactions. (Id. (discussing Menactra Package Insert, supra,

at Ex. 36, pp. 6-7, 14).) Thus, “[t]his evidence makes it more likely that the petitioner

experienced systemic inflammation from Menactra vaccination on August 11, 2016 that

would induce levels of inflammation substantial enough to induce focal cerebral

arteriopathy.” (Id. at 6.) Citing a study by McDonald et al., Dr. Ahmed stresses that

non-adjuvanted vaccines are capable of producing a detectable systemic cytokine

response. (Id. at 6-7 (citing Jacqueline U. McDonald et al., Inflammatory Responses to

Influenza Vaccination at the Extremes of Age, 151 IMMUNOLOGY 451 (2017) (Ex. 37)).)

Based on that same study, Dr. Ahmed asserts that a local infection, such as a vaginal

infection, is unlikely to similarly produce a systemic cytokine response. (Id. at 7-8

(citing McDonald et al., supra, at Ex. 37).) Dr. Ahmed is critical of Dr. Kedl for conflating

bacterial vaginosis with infections “more broadly.” (Ex. 51, pp. 3-4.) He also disagrees

with Dr. Kedl’s characterization of petitioner’s infection as “fulminant.” (Id. at 2-3.)

Therefore, petitioner’s vaccination was the more likely cause the of the systemic

inflammation that would lead to focal cerebral arteriopathy. (Ex. 42, p. 8.)

Dr. Ahmed acknowledges that, in petitioner’s own case, there is a lack of

evidence of symptoms consistent with a systemic cytokine response, such as fever,

aches, and flu-like symptoms, but stresses that, at the time of petitioner’s focal cerebral

arteriolopathy, petitioner was swimming in a cold river and was then treated with

acetaminophen, which is anti-inflammatory. Both of these factors could help explain the

absence of such symptoms, especially fever. (Ex. 42, p. 7; Ex. 46, pp. 5-6; Ex. 51, pp.

8-9.) He opines that petitioner’s stroke occurred within an appropriate temporal window

for an inference of causation. (Ex. 42, pp. 6-8.) That is, her stroke occurred about 27

hours post-vaccination and the McDonald study showed that post-vaccination cytokine

elevations plateau at about 24 hours. (Id.)

In his final report, Dr. Ahmed addresses the four papers referenced in my Rule 5

Order. (Ex. 51, pp. 4-8.) Dr. Ahmed defends reliance on the Al Qudah et al. abstract

because it is regularly cited, suggesting the authors’ statements are generally viewed as

supported by the cited data, and the abstract was presented at a neurology conference,

which includes its own form of review and scrutiny. (Id. at 4-5 (discussing Al Qudah et

al., supra, at Ex. 23).) He asserts that the Kothur et al. study does support an

inflammatory milieu in focal cerebral arteriopathy. (Id. at 5-6 (discussing Kothur et al.,

supra, at Ex. 25).) Whereas Dr. Kedl had cited a study by Li et al. as refuting the

16

Zughaier study, Dr. Ahmed opines that the Li authors do not reach the conclusion

suggested by Dr. Kedl, namely that the meningococcal vaccine did not reliably induce

an inflammatory response. (Id. at 6-7 (discussing Zughaier, supra, at Ex. 26; Shuzhao

Li et al., Molecular Signatures of Antibody Responses Derived from a Systems Biology

Study of Five Human Vaccines, 15 NATURE: IMMUNOLOGY 195 (2014) (Ex. C, Tab 5)).)

To the extent Dr. Kedl endorsed the Macko et al. study initially filed by petitioner as

further evidence that infections can cause focal cerebral arteriopathy, Dr. Ahmed again

stresses the distinction between localized bacterial vaginosis and other types of

infections, stressing that Macko et al. examined respiratory infections, rather than

infections of the vaginal tract. (Id. at 7-8 (discussing Macko et al., supra, at Ex. 27).)

Dr. Ahmed also expresses broader disagreement with Dr. Kedl regarding the relative

value of different types of control groups in vaccine studies. (Id. at 9-10; Ex. 46, pp. 2-

4.)

Dr. Ahmed additionally indicates that petitioner separately developed an

undifferentiated connective tissue disease post-vaccination. (Ex. 42, p. 10.) However,

petitioner has not pursued any claim that this represents a compensable injury. (ECF

No. 44; see also ECF Nos. 1, 65, 69.)

d. Respondent’s immunologist, Ross Kedl, M.D.16

Dr. Kedl opines that there is not reliable scientific evidence to support a

connection between the subject vaccination and petitioner’s condition. (Ex. F, p. 8.) He

prefaces his discussion by noting that the association between vaccination and

prevention of stroke is well established in the literature. (Ex. C, p. 2; Ex. G, p. 9 (citing

Smeeth et al., supra, Ex. A, Tab 5, Ex. G, Tab 14; Mitchell S. V. Elkind et al., Infectious

Burden and Risk of Stroke: The Northern Manhattan Study, 67 ARCHIVES NEUROLOGY 33

(2010) (Ex. G, Tab 3); Jaume Roquer et al., Previous Infection and Stroke: A

Prospective Study, 33 CEREBROVASCULAR DISEASE 310 (2012) (Ex. G, Tab 12); Fullerton

et al., supra, Ex. 28, Ex. A, Tab 6).) Because strokes have been associated with

infection and vaccines prevent infections, it follows that vaccination prevent strokes.

(Ex. C, p. 2; Ex. G, pp. 9-10 (citing Nadine McCrea et al., Genetic and Environmental

Associations with Pediatric Cerebral Arteriopathy: Insights into Disease Mechanisms, 50

STROKE 257 (2019) (Ex. G, Tab 10)).) For example, observational studies have found

no increased risk of stroke following influenza, tetanus, or pneumococcal vaccinations.

(Ex. G, p. 9 (citing Smeeth et al., supra, Ex. A, Tab 5; Ex. G, Tab 14).)17

16

Dr. Kedl received his Ph.D. in pathobiology from the University of Minnesota Medical School in 1997,

before going on to complete a post-doctoral fellowship at Howard Hughes Medical Institute in 2001. (Ex.

D, p. 1.) Dr. Kedl went on to be the Senior Immunologist in the Immune Response Modifier program at

3M pharmaceuticals. (Id. at 2; Ex. C, p. 1.) Since joining the faculty at the University of Colorado in

2004, Dr. Kedl has maintain an NIH funded research program centered on the biology of vaccine

adjuvants and their capacity to induce robust and enduring cellular immunity. (Ex. D, p. 2; Ex. C, p. 1.)

Dr. Kedl has authored 72 peer-reviewed publications, 14 invited reviews and commentaries, and 2 book

chapters. (Ex. D, pp. 12-20.)

17

Dr. Kedl asserts that the lack of association between stroke and pneumococcal vaccination is

significant because, like the meningococcal vaccine, the pneumococcal vaccine is a carbohydrate-based

vaccine. (Ex. G, p. 9.)

17

Although Dr. Kedl concedes that the Menactra vaccine may induce some degree

of inflammation on rare occasion in a rare individual, he contends that the Menactra

vaccine cannot reliably induce the level of systemic inflammation necessary to play a

causal role in the etiology of petitioner’s condition. (Ex. C, pp. 3-5; Ex. F, p. 6.) The

Menactra vaccine contains antigens (molecular targets against which an immune

response should be generated) in the form of polysaccharides associated with four

different strains of meningococcus and diphtheria toxoid conjugated to polysaccharides,

but no added adjuvant. (Ex. C, pp. 3-4.) The inclusion of diphtheria toxoid and lack of

added adjuvant suggests that the diphtheria toxoid conjugation can “make up for the

usual need for an adjuvant, thereby bypassing the need for an acute inflammatory

response.” (Id. at 4 (citing Michael Brӧker et al., Factors Contributing to the

Immunogenicity of Meningococcal Conjugate Vaccines, 12 HUMAN VACCINES &

IMMUNOTHERAPEUTICS 1808 (2016) (Ex. C, Tab 1; Ex. G, Tab 1)).) Dr. Kedl further

opines that the lack of adjuvant in the Menactra vaccine suggests that there was “no

corresponding or consequent innate immune activation sufficient for the arterial

pathology diagnosed.” (Id.) Additionally, the meningococcal capsular polysaccharides

that are used in the vaccine are subject to a process that removes any acute

inflammatory capacity, likely through depolarization of the carbohydrates into oligomers.

(Id. (citing Brӧker et al., supra, at Ex. C, Tab 1).) Dr. Kedl disagrees with Dr. Ahmed’s

reliance on the study by McDonald et al., noting that the study involved the flu vaccine,

which contains minor constituents that are “widely speculated” to induce some minimal

degree of inflammation as a way to promote immunity without the help of any additional

adjuvants. (Ex. F, pp. 4-5 (discussing McDonald et al., supra, at Ex. 37).) He also

observes that there was a noted elevation in only 4 out of 27 cytokines studied and

suggested that the findings of post-vaccination inflammation in a mouse model may not

be especially useful for predicting post-vaccination inflammation in humans. (Id.)

Instead, Dr. Kedl cites a study showing that Menactra did not reliably induce an

inflammatory response when examined in vitro and in vivo. (Id. at 5 (citing Li et al.,

supra, at Ex. C, Tab 5); Ex. C, p. 4.)

Dr. Kedl acknowledges that petitioner’s symptoms do not necessarily exclude

systemically elevated cytokines; however, he notes that petitioner did not display any

symptoms that are typically associated with vaccine-induced inflammation, including

fever. (Ex. C, p. 5; Ex. F, p. 5.) Of the systemic adverse events that are typically

associated with vaccination (e.g., fever, malaise, irritability, headache, arthralgia,

fatigue), only fever was reliably linked to vaccination. (Ex. F, pp. 3, 5-6 (citing Martti

Virtanen et al., Day-to-Day Reactogenicity and the Healthy Vaccinee Effect of Measles-

Mumps-Rubella Vaccination, 106 PEDIATRICS, no. 5, Nov. 2000, at 1 (Ex. F, Tab 3)).)

Dr. Kedl opines that “it is inconceivable that levels of secondary inflammatory mediators

sufficient for the induction of focal cerebral arteriopathy” could have been induced in the

complete absence of symptoms, such as fever, aches, and flu-like symptoms, that are

most associated with elevated cytokine production. (Ex. C, p. 5 (citing Stephanie C.

Eisenbarth et al., Crucial Role for the Nalp3 Inflammasome in the Immunostimulatory

Properties of Aluminum Adjuvants, 453 NATURE 1122 (2008) (Ex. C, Tab 4); Amy S.

McKee et al., Alum Induces Innate Immune Responses Through Macrophages and

18

Mast Cell Sensors, but These Sensors are not Required for Alum to Act as an Adjuvant

for Specific Immunity, 183 J. IMMUNOLOGY 4403 (2009) (Ex. C, Tab 6); Natalia Muñoz-

Wolf & Ed C. Lavelle, A Guide to IL-1 Family Cytokines in Adjuvanticity, 285 FED’N EUR.

BIOCHEMICAL SOC’IES J. 2377 (2018) (Ex. C, Tab 7)).) In his supplemental report, Dr.

Kedl cautions against overreliance on the reporting of specific symptoms, as local side

effects could be unrelated to any inflammatory response to the constituents of the

vaccine. (Ex. F, pp. 2-4.) He explains that the study contained within the package

insert for the Menactra vaccine and relied upon by Dr. Ahmed did not contain a placebo,

making it difficult to determine what side effects can be reliably related to vaccination.

(Ex. F, pp. 2-3; Ex. G, pp. 5-6.)

Dr. Kedl opines that the relationship between the subject vaccination and onset

of petitioner’s symptoms is mere coincidence. (Ex. C, p. 5.) He observes that

petitioner’s symptoms were also in close temporal proximity to onset of bacterial

vaginosis and suggested that she had a genetic predisposition to immune overactivation

as evidenced by elevated autoantibodies. (Id. at 6; Ex. G, p. 9.) He explains that, given

the available scientific information connecting a broad spectrum of infections with

stroke, petitioner’s prior infection is “a far more likely, however implausible, cause than

the alleged vaccine,” though he admits that any relationship between the vaginosis and

stroke is speculative. (Ex. F, p. 7; Ex. C, p. 6.)

Finally, Dr. Kedl addresses the four papers referenced in my Rule 5 Order. (Ex.

G, pp. 1-4.) Regarding Al Qudah et al., he explains that the abstract used VAERS data,

which is a passive surveillance system that may inappropriately conflate correlation with

causation and is not peer-reviewed or verified by a subsequently published, peer-

reviewed paper. (Id. at 1 (citing Al Qudah et al., supra, Ex. 23).) Dr. Kedl describes

Kothur et al. as a “highly preliminary study” as the number of control samples was

insufficient to make any concrete causal claims. (Id. at 2 (citing Kothur et al., supra, at

Ex. 25).) Moreover, none of the inflammatory factors observed in the study were

identified in petitioner. (Id.) Dr. Kedl acknowledges that data contained in the Zughaier

study is relevant because capsular polysaccharides from N. meningitidis can stimulate

some innate immune receptors; however, the capsular polysaccharides studied were

not the same as those used in preparation of the polysaccharides in the Menactra

vaccine; the experiment utilized human and mouse cell lines, rather than actual immune

cells; and the capsular polysaccharides were not administered in vivo to determine the

biological relevance of the purported inflammatory potential. (Id. at 2-3 (citing Zughaier,

supra, at Ex. 26).) Finally, Dr. Kedl stresses the relevance of the article by Macko et al.

because, while the majority of the infections studied were upper respiratory infections, a

broad range of inflammatory events were documented, suggesting that other types of

infections may be associated with stroke, which Dr. Kedl explains is more evidence of a

connection between petitioner’s bacterial infection and her vascular pathology. (Id. at 3-

4 (citing Macko et al., supra. at Ex. 27).)

19

V. Analysis

a. Medical theory of causation (Althen prong one)

Under Althen prong one, petitioner must provide a “reputable medical theory,”

demonstrating that the vaccine received can cause the type of injury alleged. Pafford

ex rel. Pafford ex rel. v. Sec’y of Health & Human Servs., 451 F.3d 1352, 1355-56 (Fed.

Cir. 2006) (quoting Pafford ex rel. Pafford v. Sec’y of Health & Human Servs., No. 01-

0165V, 2004 WL 1717359, at *4 (Fed. Cl. Spec. Mstr. July 16, 2004)). Such a theory

must only be “legally probable, not medically or scientifically certain.” Knudsen ex rel.

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

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

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

accepted medical theory. See Andreu ex rel. Andreu v. Sec’y of Health & Human

Servs., 569 F.3d 1367, 1378 (Fed. Cir. 2009) (citing Capizzano v. Sec’y of Health &

Human Servs., 440 F.3d 1317, 1325-26 (Fed. Cir. 2006)). However, “[a] petitioner must

provide a ‘reputable medical or scientific explanation’ for [her] theory. While it does not

require medical or scientific certainty, it must still be ‘sound and reliable.’” Boatmon,

941 F.3d at 1359 (quoting Moberly ex rel. Moberly v. Sec’y of Health & Human Servs.,

592 F.3d 1315, 1322 (Fed. Cir. 2010); Knudsen, 35 F.3d at 548-49).

As explained in her motion papers, petitioner’s medical theory is based on the

proposition, advanced by her experts, that cytokines shown to be induced by the

Menactra vaccine (IL-6, IL-8, and CXCL10) are also hypothesized to be involved in the

development of focal cerebral arteriopathy. (ECF No. 65, p. 26.) This assertion is

primarily based on two papers initially cited by Dr. Felling – Kothur et al. and Zughaier,

respectively. (Id. at 27-28, 30.) At first blush, these two articles do appear to dovetail.

However, respondent’s experts are persuasive in explaining why they are not ultimately

robust or persuasive evidence.

Kothur et al. set out to examine whether inflammation plays any role in the

development of focal cerebral arteriopathy. (Kothur et al., supra, at Ex. 25.) They

examined 32 cytokines and chemokines from cerebrospinal fluid collected from five

post-stroke pediatric patients diagnosed with focal cerebral arteriopathy and compared

them against three control groups, a group of two patients suffering other forms of

stroke; a group of 43 patients with proven inflammatory brain disease, i.e., forms of

encephalitis; and a group of 20 negative controls. (Id. at 1-2.) They found that most of

the cytokines examined were not elevated among the focal cerebral arteriopathy group

as compared to the encephalitis group. (Id. at 4-5.) However, IL-6, IL-8, CXCL1, and

CXCL10, were higher among the focal cerebral arteriopathy group than among the two

controls suffering other types of stroke. (Id.)

On respondent’s behalf, both Drs. Kedl and Messé explained that this study is

“highly preliminary,” especially given the small number of control samples. (Ex. G, p. 2;

Ex. H, p. 2.) Dr. Messé further observed that the study’s findings are of limited

significance with regard to causation, given that other literature has demonstrated that

20

ischemic brain injury itself leads to an inflammatory response. (Ex. H, p. 2 (citing

Fassbender et al., supra, at Ex. H, Tab 1).) Fassbender et al., as cited by Dr. Messé,

took serial cytokine measurements from peripheral blood samples of acute cerebral

ischemia patients and found increasing elevations in cytokines subsequent to onset that

correlated to lesion volume. (Fassbender et al., supra, Ex. H, Tab 1, pp. 1, 4.) The

Fassbender authors acknowledged that stroke can often be caused by infection, which

can generate proinflammatory cytokines, but concluded that the increase in cytokines

following onset allowed for a “high probability attribution” of the cytokines to the lesion

itself. (Id. at 4.) Respondent’s expert’s criticisms of the Kothur et al. study are

consistent with the limitations acknowledged by the study authors themselves. Kothur

et al. indicated that “[e]ven though the cyto/chemokine elevation is higher in [focal

cerebral arteriopathy] compared to non-[focal cerebral arteriopathy] stroke, it is difficult

to differentiate if these elevated inflammatory markers are causally associated with the

arteriopathy, or secondary to the infarct itself due to the small sample sizes in both

groups.” (Kothur et al., supra, at Ex. 25, p. 5.) They conclude that, absent a larger

study, their study is inadequate to determine whether their observations have specificity

as biomarkers of focal cerebral arteriopathy. (Id.)

Petitioner has not offered any additional evidence to support a causal

relationship between the specified cytokines and focal cerebral arteriopathy or stroke.

Focal cerebral arteriopathy is an increasingly recognized cause of pediatric ischemic

stroke. (Kothur et al., supra, at Ex. 25, p. 1; Amlie-Lefond et al., supra, at Ex. A, Tab

11, p. 1.) However, though believed to be inflammatory, the pathophysiology of

condition is otherwise not well understood. (Kothur et al., supra, at Ex. 25, pp. 1-2;

Wintermark et al., supra, at Ex. A, Tab 10, p. 3.) Apart from citation to Kothur et al.,

petitioner’s experts acknowledge that there is a lack of medical literature associating

focal cerebral arteriopathy or stroke with Menactra vaccination. (Ex. 42, pp. 8-9; Ex. 44,

p. 2.) Although Macko et al. hypothesized that non-infectious causes of inflammation

may be predisposing factors to stroke, that paper only involved patient questionnaires,

with no measurement of purportedly causal cytokines or any significant discussion of

pathophysiology. (Macko et al., supra, at Ex. 27.) Moreover, the non-infectious causes

of inflammation observed by the study related to other types of inflammatory

syndromes, such as gout exacerbation, psoriasis, and urticaria. (Id. at 4.) No instances

of vaccination preceding stroke were reported. (Id. at 9-10.)

Dr. Ahmed opines that the vaccine can cause “clearly systemic effects,” such as

anorexia, diarrhea, headache, fatigue, malaise, and arthralgia, as evidenced in the

package insert. (Ex. 42, p. 5 (citing Menactra Package Insert, supra, at Ex. 36).) He

explains that these common adverse events “typically occur through the production of

cytokines at the local site that are transmitted systemically” and further notes increased

events following vaccination with Menactra, when compared to a different formulation of

meningococcal vaccine, demonstrating the potency of the Menactra vaccine and its

ability to induce systemic inflammation. (Id.) However, this is not a substitute for some

kind of demonstration that the Menactra vaccine can cause focal cerebral arteriopathy

in particular. Even acknowledging that the vaccine can induce some inflammatory

immune response, mere invocation of a vaccine’s intended immune response is not in

21

and of itself sufficient to carry petitioner’s burden under Althen prong one. See Elvira ex

rel. D.E. v. Sec’y of Health & Human Servs., No. 17-531V, 2024 WL 4966035, at *20

(Fed. Cl. Spec. Mstr. Nov. 6, 2024); Vanore v. Sec’y of Health & Human Servs., No. 21-

0870V, 2024 WL 3200287, at *18 (Fed. Cl. Spec. Mstr. May 31, 2024); Kalajdzic ex rel.

A.K. v. Sec’y of Health & Human Servs., No. 17-792V, 2022 WL 2678877, at *23 (Fed.

Cl. Spec. Mstr. June 17, 2022), mot. for rev. den’d, No. 17-792V, 2024 WL 4524777

(Fed. Cl. Oct. 18, 2024), aff’d, No. 2023-1321, 2024 WL 3064398 (Fed. Cir. June 20,

2024); Cordova v. Sec’y of Health & Human Servs., No. 17-1282V, 2021 WL 3285367,

at *17 (Fed. Cl. Spec. Mstr. June 23, 2021). There must be some additional evidence

linking the vaccine’s immune response to the pathology of petitioner’s actual condition.

Given the limitations of the Kothur study, Dr. Ahmed’s reliance on other types of

reported adverse events following Menactra vaccination, as discussed in post-marketing

experience, is unpersuasive as any evidence that the inflammatory response to

vaccination can produce focal cerebral arteriopathy in particular. (Ex. 42, pp. 5-6 (citing

Menactra Package Insert, supra, at Ex. 36).)

Zughaier did find that capsular polysaccharides from N. meningitis infection

induced inter alia IL-6, IL-8, and CXCL10 in human macrophage-like cells. (Zughaier,

supra, at Ex. 26, p. 6.) Again, however, as a threshold matter, the potential value of this

study is dependent on acceptance of the Kothur study as persuasive evidence that

these particular cytokines are causally important in the development of focal cerebral

arteriopathy. Yet, for the reasons discussed above, it is not. Thus, even if fully

credited, the Zughaier findings are insufficient to support a theory of causation

consistent with petitioner’s burden of proof. Moreover, although Dr. Kedl concedes on

behalf of respondent that it may be possible for non-adjuvanted vaccines to “induce

some degree of inflammation on exceptionally rare occasions that may be detectable in

an exceptionally rare individual,” he disputes the ability of the Menactra vaccine to

produce a robust inflammatory response in general. (Ex. F, pp. 4-5.) He explains that

the Menactra vaccine is a non-adjuvanted vaccine that contains meningococcal

polysaccharide capsule antigens that are conjugated to diphtheria toxoid and subjected

to a process of purification and chemical modification that removes inflammatory

potential. (Ex. C, pp. 3-4; Ex. G, p. 3 (citing Brӧker et al., supra, at Ex. C, Tab 1).)

Thus, Dr. Kedl raises additional criticism of the Zughaier study. (Ex. C, p. 4; Ex. G, p.

9.) Most notably, Dr. Kedl observes that the Zughaier findings are based on capsular

polysaccharides from the N. meningitis bacteria that are not equivalent to those used in

the vaccine, which lack the lipooligosaccharide that is key to the virulence of

meningococcal infections. (Ex. G, p. 2.) Thus, he contends that the resultant

inflammatory response to the capsular polysaccharides studied by Zughaier is not

comparable to what would be expected following vaccination with Menactra. (Id. at 3.)

For example, Figure 2 within the study compared the two types of capsular

polysaccharides and showed that the capsular polysaccharides from N. meningitis

induced levels of IL-8 that far exceeded levels induced by the vaccine-grade

meningococcal capsular polysaccharide polymer. (Id. (discussing Zughaier, supra, at

Ex. 26, pp. 6, 18 fig.2).) This is not necessarily surprising, because both parties’

experts otherwise agree that infection is a risk factor for stroke and that vaccination

potentially has a protective effect at a population level precisely because it prevents

22

infections. (Id. at 10; Ex. 21, p. 3; Ex. 44, p. 1; Ex. A, pp. 3-4; Ex. C, p. 2.) Even

assuming arguendo that pro-inflammatory cytokines were implicated in the

pathogenesis of focal cerebral arteriopathy as discussed by Kothur et al., then it would

still stand to reason that the immune response to vaccination must constitute a lesser

risk than infection if a protective effect is potentially observable. Accord Druery v. Sec’y

of Health & Human Servs., No. 17-1213V, 2023 WL 5094088, at *16 (Fed. Cl. Spec.

Mstr. Jul. 11, 2023) (finding that epidemiology establishing a cardio-protective effect of

the flu vaccine “does not in itself mean the flu vaccine is incapable of causing acute

cardiac events such as myocardial infarction. However, it does mean that the

inflammatory response to vaccination cannot be merely equated in its cardiovascular

effects with infection.”), mot. rev. den’d 169 Fed. Cl. 557 (2024).

Although petitioner need not present epidemiology to carry her burden,

Capizzano, 440 F.3d at 1325-26, it is also true that special master need not ignore

relevant epidemiology that undermines petitioner’s theory, D’Tiole v. Sec’y of Health &

Human Servs., 726 F. App’x 809, 811 (Fed. Cir. 2018). Here, petitioner concedes that

epidemiologically vaccination, in general, is either not a risk factor for stroke or is

protective against stroke. (Ex. 21, p. 3.) For example, Smeeth et al. found that there

was no increased risk of stroke following influenza, tetanus, and pneumococcal

vaccination (Smeeth et al., supra, at Ex. G, Tab 14, pp. 4, 6), and Fullerton et al. found

“only a protective effect of vaccination” notwithstanding the type of vaccine administered

(Fullerton et al., supra, at Ex. A, Tab 6, pp. 4-6 (explaining that vaccination “of any type”

within the prior week was associated with reduced risk of stroke)). Similarly, in a study

cohort of over one million meningococcal vaccinations, Li et al. found that there was no

statistically significant risk of focal cerebral arteriopathy or stroke following vaccination.

(Li et al., supra, at Ex. A, Tab 9, pp. 1, 5.) Another study by Tseng et al. found no

statistically significant risk of focal cerebral arteriopathy or stroke in a cohort of nearly

49,000 individuals that were vaccinated with the meningococcal conjugate vaccine.

(Tseng et al., supra, at Ex. A, Tab 8, pp. 1, 5-6.)

Petitioner also cited a paper by Al Qudah et al., which observed 306 cases of

stroke from the VAERS18 database. (Al Qudah et al., supra, at Ex. 23.) However, there

are several problems with this. First, VAERS represents passive surveillance and is

therefore generally viewed skeptically. Analla v. Sec’y of Health & Human Servs., 70

Fed. Cl. 552, 558 (2006); Ryman v. Sec’y of Health & Human Servs., 65 Fed. Cl. 35,

39-40, 43 (2005); Manville v. Sec’y of Health & Human Servs., 63 Fed. Cl. 482, 494

(2004); Carrington ex rel. Carrington v. Sec’y of Health & Human Servs., No. 99-495V,

2008 WL 2683632, at *11 n.19 (Fed. Cl. Spec. Mstr. June 18, 2008), mot. for rev.

denied, 85 Fed. Cl. 319 (2008); Jane Doe/03 v. Sec’y of Health & Human Servs., 2007

18

The Vaccine Adverse Reporting System or VAERS is a national early warning system that is co-

managed by the Centers for Disease Control and Prevention (CDC) and the U.S. Food and Drug

Administration (FDA) and was established to detect possible safety problems in U.S.-licensed vaccines.

About VAERS: Background and Public Health Important, VAERS, https://vaers.hhs.gov/about.html (last

visited Dec. 23, 2024). VAERS is a passive reporting system, meaning that it relies on individuals to

submit reports of adverse events following vaccination. Id. Anyone can submit a VAERS report. Id. As

a result, “VAERS is not designed to determine if a vaccine caused a health problem,” but it can be “useful

for detecting unusual or unexpected patterns of adverse event reporting.” Id.

23

WL 2350645, at *4 (Fed. Cl. Spec. Mstr. Aug. 14, 2007). Additionally, and relatedly,

only the abstract of this proposed paper was ever produced. Notwithstanding Dr.

Ahmed’s defense of the abstract (Ex. 51, pp. 4-5), the lack of a complete analysis

cannot be ignored, especially in light of the limitations of the VAERS data more

generally. Ultimately, petitioner asserts that the Al Qudah abstract stands “simply for

the proposition that members of the medical community have suggested stroke as a

rare adverse event after vaccination.” (ECF No. 65, p. 27.) In that regard, Dr. Felling

asserts that the population-level efficacy of vaccines in reducing the occurrence of

stroke does not necessarily exclude the possibility of rare cases of vaccine-caused

adverse events leading to stroke. (Ex. 44, p. 1; see also Al Qudah et al., supra, at Ex.

23, p. 2 (noting that “some” stroke cases “may be triggered by vaccination”).) While this

point is well-taken, especially given the overall rarity of adverse events following

vaccination, see D’Tiole, 728 F. App’x at 811 (“[B]ecause vaccine injuries are rare

events, the fact that a particular epidemiological study suggests a vaccine is generally

safe should not prevent a claimant from prevailing.”) (quoting D’Tiole v. Sec’y of Health

& Human Servs., No. 15-085V, 2016 WL 7664475, at *29 (Fed. Cl. Spec. Mstr. Nov. 28,

2016), mot. for rev. denied, 132 Fed. Cl. 421 (2017), aff’d, 726 F. App’x 809 (Fed. Cir.

2018)), Dr. Felling’s observation does not amount to affirmative evidence of causation.

See Crutchfield v. Sec’y of Health & Human Servs., No. 09-0039V, 2014 WL 1665227,

at *14-15 (Fed. Cl. Spec. Mstr. Apr. 7, 2014) (reasoning that “the studies, like all

epidemiological studies, do not prove that the MMR vaccine can never cause Type 1

diabetes. But they offer no support at all to Petitioner in carrying her burden of showing

that the MMR vaccine can cause Type 1 diabetes.”), aff’d, 125 Fed. Cl. 251 (2014); see

also Holmes v. Sec’y of Health & Human Servs., 115 Fed. Cl. 469, 486 (2014) (“Absent

epidemiological evidence to support causation, it remained the job of petitioner, not

respondent, to supply a reputable medical scientific explanation of causation.”); Bender

v. Sec’y of Health & Human Servs., No. 11-693V, 2018 WL 3679637, at *30 (Fed. Cl.

Spec. Mstr. July 2, 2018) (“While I take note of Petitioner’s general point that the fact

that vaccine injuries are rare means that such epidemiologic evidence cannot

conclusively refute a causation theory that is otherwise reliable and/or scientifically

plausible, this argument does not diminish the value such evidence can have in

appropriate cases.”). While not dispositive, epidemiology submitted on this record

overall casts at least some doubt on petitioner’s assertion that the Menactra vaccine

can cause focal cerebral arteriopathy and stroke.

Finally, Dr. Ahmed cites a study by McDonald et al., which found that

immunization with and without an adjuvant induced an elevation in various cytokines

(McDonald et al., supra, at Ex. 37, pp. 4-5), to show that non-adjuvanted vaccines, like

the Menactra vaccine, can induce systemic inflammation. (Ex. 42, pp. 6-7.) However,

this paper involved the flu vaccine, rather than the Menactra vaccine. (McDonald et al.,

supra, at Ex. 37.) Accordingly, while this paper may add nuance to the experts’

discussion regarding the significance of non-adjuvanted vaccine responses, it does not

refute Dr. Kedl’s opinion that there is a lack of evidence to suggest that the Menactra

vaccine, in particular, reliably produces systemic inflammation. (Ex. F, pp. 4-6.) Nor

does the McDonald paper meaningfully bolster petitioner’s claim in light of the

24

limitations of the Kothur and Zughaier papers that form the crux of petitioner’s Althen

prong one showing.

Accordingly, petitioner has not preponderantly established that the Menactra

vaccine can cause focal cerebral arteriopathy leading to stroke under Althen prong one.

b. Logical sequence of cause and effect (Althen prong two)

The second Althen prong requires proof of a logical sequence of cause and

effect, usually supported by facts derived from a petitioner’s medical records. Althen,

418 F.3d at 1278; Andreu, 569 F.3d at 1375-77; Capizzano, 440 F.3d at 1326-27;

Grant, 956 F.2d at 1147-48. Medical records are generally viewed as particularly

trustworthy evidence. Cucuras, 993 F.2d at 1528. However, medical records and/or

statements of a treating physician’s views do not per se bind the special master. See

§ 300aa-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 ex rel.

Snyder v. Sec’y of Health & Human Servs., 88 Fed. Cl. 706, 745 n.67 (2009) (“[T]here is

nothing . . . that mandates that the testimony of a treating physician is sacrosanct—that

it must be accepted in its entirety and cannot be rebutted.”). A petitioner may support a

cause-in-fact claim through either medical records or expert medical opinion. § 300aa-

13(a). The special master is required to consider all the relevant evidence of record,

draw plausible inferences, and articulate a rational basis for the decision. Winkler, 88

F.4th at 963 (citing Hines, 940 F.2d at 1528).

As previously explained, Althen prong one requires a preponderant showing that

the subject vaccine can cause the alleged condition while Althen prong two requires a

preponderant showing that the subject vaccine actually did cause the alleged condition.

Althen, 418 F.3d at 1278; Pafford, 451 F.3d at 1355-56 (approving the special master’s

querying under Althen regarding, first, whether the vaccine “can cause” the alleged

injury and, second, whether it “actually caused” the injury in the particular case).

Because I am not persuaded that the Menactra vaccine can cause focal cerebral

arteriopathy leading to stroke, petitioner necessarily cannot demonstrate that the

vaccine did cause the injury at issue in this case. Therefore, Althen prong two is

addressed below only in the interest of completeness. Of note, nothing in petitioner’s

own medical history lends any further credence to petitioner’s theory under Althen prong

one. Capizzano, 440 F.3d at 1326 (evidence used to satisfy one of the Althen prongs

can be used to satisfy another Althen prong); but see Althen, 418 F.3d at 1278

(temporal association alone is insufficient to establish causation).

In briefing, the parties appear to agree that petitioner suffered an infarct and

respondent concedes vascular pathology; however, the parties’ respective positions

deviate regarding whether petitioner has substantiated a diagnosis of focal cerebral

arteriopathy. (ECF No. 65, pp. 24-25; ECF No. 67, pp. 22-24.) Because the question of

whether petitioner suffered focal cerebral arteriopathy is an integral part of her causal

theory, it is appropriate to first determine whether petitioner has substantiated the

proposed injury as a prerequisite to the analysis of whether petitioner has carried her

25

burden under Althen prong two. Broekelschen v. Sec’y of Health & Human Servs., 618

F.3d 1339, 1346 (Fed. Cir. 2010). I find that petitioner has preponderantly established a

diagnosis of focal cerebral arteriopathy based on the medical records and expert

opinion. Petitioner’s expert, Dr. Felling, opines that focal cerebral arteriopathy is a more

likely diagnosis for petitioner’s condition. (Ex. 21, p. 3.) While respondent asserts that

Dr. Messé’s opinion was limited to concluding that petitioner suffered a cryptogenic

stroke of unclear etiology (ECF No. 67, p. 23), Dr. Messé specifically states that a

diagnosis of focal cerebral arteriopathy is “possible” and that the other diagnoses

explored by petitioner’s treaters are “perhaps less likely.” (Ex. A, pp. 4-5.) There is also

treater opinion, albeit later in the course of her injury, to support a diagnosis of focal

cerebral arteriopathy. (Ex. 34, p. 7.) While Dr. Messé makes it clear that no definitive

diagnosis is available, I find that petitioner has preponderantly established a diagnosis

of focal cerebral arteriopathy.

Petitioner contends that the Menactra vaccine caused systemic inflammation,

which led to focal cerebral arteriopathy and, ultimately, stroke. As previously indicated,

focal cerebral arteriopathy has been recognized as a cause of stroke in pediatric

patients and is believed to have an inflammatory etiology. (Kothur et al., supra, at Ex.

25, p. 1; Amlie-Lefond et al., supra, at Ex. A, Tab 11, p. 1; Wintermark et al., supra, at

Ex. A, Tab 10, p. 4.) However, despite opining on an inflammatory mechanism, Dr.

Ahmed concedes that there is a lack of medical record evidence of symptoms that are

generally associated with a systemic cytokine response, such as fever, aches, and flu-

like symptoms. (Ex. 42, p. 7; Ex. 46, pp. 5-6.) Dr. Kedl asserts that it is unlikely that

petitioner could suffer from systemic inflammation that was sufficient to invoke focal

cerebral arteriopathy leading to stroke in the absence of other symptoms that are

consistent with systemic inflammation. (Ex. C, p. 5 (citing Eisenbarth et al., supra, at

Ex. C, Tab 4; McKee et al., supra, at Ex. C, Tab 6; Muñoz-Wofl & Lavelle, supra, at Ex.

C, Tab 7); Ex. F, p. 5.) Moreover, he cautions against overreliance on subjective

symptoms, such as headache, in favor of objective fever, which he contends is the only

commonly reported post-vaccination symptom that has been reliably linked to

vaccination.19 (Ex. F, pp. 3, 5-6 (citing Virtanen et al., supra, at Ex. F, Tab 3).) In

attempting to overcome this hurdle, Dr. Ahmed offers several explanations that each

require at least some degree of speculation. And, in any event, even if crediting Dr.

Ahmed’s opinion, this allows only a possible explanation for an absence of clinical

19

A study by Virtanen et al. looked at a series of commonly reported post-vaccination symptoms,

including fever, respiratory symptoms, nausea or vomiting, diarrhea, rash, arthralgia, conjunctivitis,

staying in bed, drowsiness, irritability, and “other potential symptoms,” in pediatric patients. (Virtanen et

al., supra, at Ex. F, Tab 3, pp. 1-2.) The authors found that fever was the “clearest vaccine-attributable

effect.” (Virtanen et al., supra, at Ex. F, Tab 3, pp. 1, 3-4.) Although Dr. Ahmed does not dispute the

findings contained in the Virtanen study, he notes that clinical trials for the Menactra vaccine found

injection site pain, headache, and fatigue to be the most common adverse reactions in adolescents aged

11-18 – an age range that is more comparable to petitioner’s age at the time of vaccination. (Ex. 42, pp.

5-6.) Headache was not specifically addressed by the Virtanen study. However, despite petitioner’s

complaints of headache prior to onset of her stroke, this symptom does not play a significant role in

petitioner’s causal theory as the bulk of her expert’s discussion relative to Althen prong two concerns her

fever or lack thereof. Dr. Ahmed initially associated petitioner’s headache with connective tissue disease,

but he otherwise treats this symptom as sequela of her injury. (Id. at 10; Ex. 51, p. 11.)

26

evidence supporting his opinion. Dr. Ahmed’s explanations would still leave a dearth of

evidence affirmatively supporting the application of his theory to the facts of this case.

Accord Baldwin v. Sec’y of Health & Human Servs., 151 Fed. Cl. 431, 447 (2020)

(finding that “Petitioner’s experts theorized that the Fluvirin vaccine can induce various

inflammatory responses which can lead to cardiac arrest . . . Petitioner was required to

prove by a preponderance of the evidence that one of her expert’s theories actually

occurred . . . Petitioner did not identify anything in her medical records to support any of

her exerts’ various theories by a preponderance of the evidence.”) The Federal Circuit

has explained that “[a]lthough probative, neither a mere showing of a proximate

temporal relationship between vaccination and injury, nor a simplistic elimination of

other potential causes of the injury suffices, without more, to meet the burden of

showing actual causation.” Althen, 418 F.3d at 1278 (citing Grant, 956 F.2d at 1149).

First, Dr. Ahmed suggests that petitioner’s fever may have been masked by

external factors. (Ex. 42, p. 7; Ex. 46, p. 5.) One such factor is a non-steroidal anti-

inflammatory medication received in treatment of her condition. (Ex. 42, p. 7; Ex. 46, p.

5.) However, a close reading of the medical records shows that petitioner did not report

taking any over-the-counter medications to paramedics upon their arrival (Ex. 4, p. 23);

received acetaminophen at the hospital only after her temperature was recorded as

normal (Id. at 7, 18); and first reported taking ibuprofen prior to onset during a

rheumatology appointment approximately three months later (Ex. 5, p. 150).

Dr. Ahmed also suggests that a fever could have been masked by the

presumably cold river petitioner was swimming in just prior to onset. (Ex. 42, p. 7; Ex.

46, p. 5.) While this potentially has an attractive logic, it is not sufficiently substantiated.

Paramedics noted that petitioner’s skin was “cool” and “dry,” her temperature was

recorded as 98.9˚ Fahrenheit upon admission to the hospital, and there was no

observation of fever of chills at any point. (Ex. 4, pp. 5, 23.) Dr. Ahmed opines that

petitioner’s recorded temperature was “surprisingly warm” given the circumstances, but

he does not go so far as to opine that petitioner actually had a fever when she arrived at

the hospital. (Ex. 42, p. 7.) He instead asserts that “a slight temperature of 98.9

degrees F when measured 43 minutes later . . . is more likely than not a reflection of a

higher temperature prior to swimming that was lowered to 98.9 degrees F after

swimming in a cold river.”20 (Ex. 46, pp. 5-6.) However, Dr. Ahmed does not explain

why this would not have been accounted for by the treating physicians, given that they

were aware of her EMS history and that she had been swimming. (See Ex. 4, p. 23-28.)

20

Of note, Dr. Ahmed appears to have identified the wrong river. Dr. Ahmed cites the USGS Data

Grapher website for the Tualatin River, which he suggests “is a way to know exactly what the temperature

of the river was that day.” (Ex. 46, pp. 5-6 (citing USGS Data Grapher, U.S. DEP’T INTERIOR: U.S.

GEOLOGICAL SURVEY, https://or.water.usgs.gov/cgi-

bin/grapher/graph_setup.pl?basin_id+tualatin&site_id=14207200 (last modified July 6, 2024); Data from

U.S. Geological Survey (Water Temperature (˚C) graph): Tualatin River at Oswego Diversion Dam (2021)

(Ex. 47)).) He reasons that the Legacy Meridian Park Medical Center is in Tualatin, Oregon, and

therefore, the river that petitioner “would have swam in is the Tualatin River,” which had a water

temperature of 69.9˚ Fahrenheit on August 12, 2016. (Ex. 46, pp. 5-6.) However, there is no mention of

the Tualatin River in the medical records. Instead, a triage nurse noted on intake that petitioner was

actually swimming in the Willamette River. (Ex. 4, p. 7.)

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Finally, Dr. Ahmed suggests that petitioner could have simply overlooked the

fever or forgotten to mention a fever to her treaters. (Ex. 42, p. 7.) However, accepting

this explanation requires overlooking that treaters took petitioner’s temperature within

an hour of onset and found it to be normal. (Ex. 4, p. 5.) Additionally, although

paramedics initially noted that petitioner was “unable to answer any questions” and was

“not acting normally,” she was eventually more responsive once her facial paralysis

subsided. (Id. at 23.) There is no evidence that calls into question petitioner’s ability to

relay subjective symptoms or medical history to her treaters, especially in light of the

fact that she contemporaneously reported other symptoms, such as headache and a

recent history of hypertension. (Id. at 6-7, 23.) The notion that petitioner was simply

oblivious to her own bodily symptoms is obviously speculation.

Petitioner may also satisfy her burden under Althen prong two through

presentation of medical opinion as contained within her medical records. Andreu, 569

F.3d at 1375-76; Capizzano, 440 F.3d at 1326 (noting that “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’” (alteration in original)

(quoting Althen, 418 F.3d at 1280)); but see § 300aa-13(b) (providing that “[a]ny such

diagnosis, conclusion, judgment, test result, report, or summary shall not be binding on

the special master or court”); Snyder, 88 Fed. Cl. at 745 n.67 (“[T]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.”). In the instant case, however, the

opinions of petitioner’s medical providers are not otherwise helpful in clarifying the

cause of her condition. In the only notation addressing the possibility of vaccine

causation, petitioner’s neurologist suggested that RCVS could have resulted from either

Zoloft or the vaccine. (Ex. 6, p. 4.) Her working diagnoses remained RCVS or drug-

induced lupus secondary to Zoloft only until focal cerebral arteriopathy was advanced

as the primary diagnosis in 2020. (Compare Ex. 10, p. 87; Ex. 12, p. 323; Ex. 15, pp.

36, 70-71; Ex. 16, pp. 35, 51; Ex. 32, p. 109, with Ex. 34, p. 7.) However, there is no

treater opinion causally linking petitioner’s focal cerebral arteriopathy to her Menactra

vaccination as she alleges.

Accordingly, petitioner has not preponderantly shown that the vaccine did cause

her injury under Althen prong two.

c. Proximate temporal relationship between vaccination and significant

aggravation (Althen prong three)

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

between the vaccination and the injury alleged. Althen, 418 F.3d at 1278. A petitioner

must offer “preponderant proof that the onset of symptoms occurred within a timeframe

for which, given the medical understanding of the disorders etiology, it is medically

acceptable to infer causation-in-fact.” de Bazan v. Sec’y of Health & Human Servs.,

539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for what is a medically

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acceptable timeframe must coincide with the theory of how the relevant vaccine can

cause an injury (Althen prong one’s requirement). Id.; Shapiro v. Sec’y of Health &

Human Servs., 101 Fed. Cl. 532, 542 (2011), mot. for recons. den’d after remand, 105

Fed. Cl. 353 (2012), aff’d, 503 F. App’x 952 (Fed. Cir. 2013); Koehn ex rel. Koehn v.

Sec’y of Health & Human Servs., No. 11-355V, 2013 WL 3214877, at *26 (Fed. Cl.

Spec. Mstr. May 30, 2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).

In the instant case, petitioner received the subject Menactra vaccine at

approximately 4:00 p.m. on August 11, 2016. (Ex. 1, pp. 5, 7.) At around 7:30 p.m. on

August 12, 2016, paramedics were dispatched in response to a 911 call related to

petitioner’s stroke. (Ex. 4, p. 22.) Thus, onset of petitioner’s stroke was around 26-27

hours post-vaccination. Dr. Felling notes increased risk of brain infarction within one

week following infectious or inflammatory syndromes. (Ex. 21, p. 4 (citing Macko et al.,

supra, at Ex. 27; Fullerton et al., supra at Ex. A, Tab 6).) He further notes that that

onset of petitioner’s focal cerebral arteriopathy within 24 hours of vaccination is

consistent with a post-vaccination inflammatory response as fever commonly occurs

within 24 hours post-vaccination. (Id.) Dr. Ahmed agrees that onset of petitioner’s

stroke was medically acceptable, reasoning that petitioner’s onset aligns with the

McDonald study’s finding that cytokine elevations plateau at around 24 hours. (Ex. 42,

pp. 6, 7-8 (citing McDonald et al., supra, at Ex. 37).)

Although respondent’s experts do not meaningfully dispute petitioner’s contention

that onset of stroke approximately 26-27 hours post-vaccination is a medically

acceptable timeframe for inferring causation in this case, petitioner cannot carry her

overall burden of proof based on third Althen prong. Specifically, under Althen prong

one, petitioner did not preponderantly demonstrate that the Menacta vaccine can

produce an inflammatory response that could be implicated as a trigger of focal cerebral

arteriopathy or stroke. Additionally, petitioner did not present preponderant clinical

evidence of the theorized inflammatory response under Althen prong two. Accordingly,

while the timing of onset may be consistent with the inflammatory mechanism proposed

in this case, a temporal association between vaccination and injury onset is by itself

insufficient to prove vaccine causation. Grant, 956 F.2d at 1148.

VI. Conclusion

Petitioner has clearly suffered a serious injury, and for that she has my

sympathy. However, for all of the reasons described above, there is not preponderant

evidence that petitioner’s focal cerebral arteriopathy or stroke was caused-in-fact by her

Menactra vaccination. Therefore, this case is dismissed.21

21

In the absence of a timely-filed motion for review of this Decision, the Clerk of the Court shall enter

judgment accordingly.

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IT IS SO ORDERED.

s/Daniel T. Horner

Daniel T. Horner

Special Master

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