Kinney v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 18-1522V

Filed: May 8, 2024

Special Master Horner

ERIN M. KINNEY,

Petitioner,

v.

SECRETARY OF HEALTH AND

HUMAN SERVICES,

Respondent.

Phyllis Widman, Widman Law Firm, LLC, Northfield, NJ, for petitioner.

Neil Bhargava, U.S. Department of Justice, Washington, DC, for respondent.

DECISION 1

On October 2, 2018, petitioner filed a petition under the National Childhood

Vaccine Injury Act, 42 U.S.C. § 300aa-10, et seq. (2012) (“Vaccine Act”). 2 (ECF No. 1.)

Petitioner initially alleged that she suffered a seizure disorder, postural orthostatic

tachycardia syndrome (“POTS”), and fibromyalgia following the administration of an

influenza (“flu”) vaccine on October 15, 2015, and a measles-mumps-rubella (“MMR”)

vaccine on October 21, 2015. (Id.) Petitioner later amended her petition to allege that

the flu and MMR vaccines caused her to suffer “a seizure disorder/epilepsy, periodic

paralysis, syncope, exacerbation of migraines, [POTS], cataplexy, narcolepsy,

fibromyalgia, focal postganglionic sudomotor impairment chronic fatigue, and severe

anxiety and depression.” (ECF No. 38.) For the reasons set forth below, I conclude

that petitioner is not entitled to compensation for her injuries.

1

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

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

Government Act of 2002. See 44 U.S.C. § 3501 note (2018) (Federal Management and Promotion of

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

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

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

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

will be redacted from public access.

2

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

300aa-10-34.

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I. Applicable Statutory Scheme

Under the National Vaccine Injury Compensation Program, compensation

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

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

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

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

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

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

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

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

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

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

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

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

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

was caused by some factor other than the vaccination. § 300aa-13(a)(1)(A); § 300 aa-

11(c)(1)(C)(i); § 300aa-14(a); § 300aa-13(a)(1)(B).

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

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

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

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

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

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

on the petitioner to introduce evidence demonstrating that the vaccination actually

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

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

1525 (Fed. Cir. 1991). Because petitioner’s injuries are not listed on the Vaccine Injury

Table, petitioner must satisfy this burden of proof.

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 of the injury or condition, but must

demonstrate that the vaccination was at least a “substantial factor” in causing the

condition, and was a “but for” cause. Shyface v. Sec’y of Health & Human Servs., 165

F.3d 1344, 1352 (Fed. Cir. 1999). Thus, the petitioner must supply “proof of a logical

sequence of cause and effect showing that the vaccination was the reason for the

injury;” the logical sequence must be supported by “reputable medical or scientific

explanation, i.e., evidence in the form of scientific studies or expert medical testimony.”

Althen, 418 F.3d at 1278; Grant v. Sec’y of Health & Human Servs., 956 F.2d 1144,

1148 (Fed. Cir. 1992). A petitioner may not receive a Vaccine Program award based

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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).

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

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

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

the vaccination brought about her injury by providing: (1) a medical theory

causally connecting the vaccination and the injury; (2) a logical sequence

of cause and effect showing that the vaccination was the reason for the

injury; and (3) a showing of proximate temporal relationship between

vaccination and injury. If Althen satisfies this burden, she is entitled to

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

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

vaccine.

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

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

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

expert. Id. at 1279-80. However, that expert’s opinion must be based upon “sound and

reliable” scientific explanation. Boatmon v. Sec’y of Health & Human Servs., 941 F.3d

1351, 1359 (Fed. Cir. 2019) (quoting Knudsen ex rel. Knudsen v. Sec’y of Health &

Human Servs., 35 F.3d 543, 548-49 (Fed. Cir. 1994)). The Althen court also indicated

that, in finding causation, a Program factfinder may rely upon “circumstantial evidence,”

which the court found to be consistent with the “system created by Congress, in which

close calls regarding causation are resolved in favor of injured claimants.” 418 F.3d at

1280.

II. Procedural History

This case was initially assigned to Special Master Moran. (ECF No. 4.)

Petitioner filed initial medical records as well as several witness affidavits in support of

her claim. (ECF Nos. 9, 12.) This case was reassigned to my docket on August 27,

2019. (ECF No. 25.) Petitioner then filed additional witness affidavits. (ECF No. 28.)

After reviewing petitioner’s filings, respondent filed his Rule 4(c) report recommending

against compensation on November 4, 2019. (ECF No. 31.) Subsequently, petitioner

filed additional medical records in November 2019 and January 2020. (ECF Nos. 32,

36.)

On January 7, 2020, petitioner filed her amended petition adding additional

conditions to her allegations. (ECF No. 38.) Petitioner then filed an expert report from

Yuval Shafrir, M.D., on April 4, 2020. (ECF No. 41; Ex. 25.) Petitioner also filed further

medical records in April and May of 2020. (ECF Nos. 49, 50.) On July 22, 2020,

petitioner filed a supplemental report from Dr. Shafrir incorporating a discussion of the

recently filed medical records. (ECF No. 52; Ex. 93.) Respondent subsequently filed a

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responsive expert report from M. Steven Evans, M.D., on November 3, 2020. (ECF No.

56; Ex. A.)

Petitioner again filed additional treatment records in December 2020 and

February 2021 (ECF Nos. 63, 65), followed by a second supplemental expert report

from Dr. Shafrir on May 27, 2021 (ECF No. 70; Ex. 98). Petitioner then filed additional

records on June 2, 2021. (ECF No. 72.) On August 30, 2021, the exchange of expert

reports concluded with respondent’s filing of a supplemental report from Dr. Evans.

(ECF No. 75; Ex. C.) Following the exchange of expert reports, petitioner requested

that this case be set for a hearing. (ECF No. 77.)

In anticipation of the hearing, petitioner filed additional evidence in January 2023,

including updated medical records and a supplemental affidavit. (ECF No. 89.) The

parties then filed a joint prehearing submission outlining the stipulated facts and facts in

dispute on January 24, 2023. (ECF No. 93.) On February 14, 2023, the parties filed

simultaneous prehearing briefs. (ECF Nos. 98, 99.) Respondent also filed a summary

of the medical literature contemporaneous with his prehearing brief. (ECF No. 99-1.)

Petitioner then filed a reply brief on February 22, 2023, followed by a summary of the

medical literature on February 28, 2023. (ECF Nos. 101, 104.)

An entitlement hearing was held on March 7, 2023. Petitioner, Dr. Shafrir, and

Dr. Evans, testified. (See Transcript “Tr.” at ECF No. 109.) At the close of the hearing,

both parties confirmed that post-hearing briefs were unnecessary. (Tr. 224.) This case

is now ripe for resolution.

III. Factual History

a. As Reflected in the Medical Records

Prior to vaccination, petitioner’s medical history was significant for migraines,

fibroadenoma of the breast, urinary tract infection, and pyelonephritis. (Ex. 6, pp. 13-19,

77, 92, 149-51; Ex. 91, pp. 12-14.) Petitioner received a flu vaccination on October 15,

2015, and an MMR vaccine on October 21, 2015. (Ex. 1; Ex. 2, ¶ 2; Ex. 6, pp. 142-43.)

On November 24, 2015, petitioner saw Dr. Jessica McCool who reported that

petitioner was experiencing dizzy spells, during which petitioner “experiences

tachycardia and feels like she can’t catch her breath.” (Ex. 95, p. 10.) Petitioner’s labs

from this visit came back as normal. (Ex. 6, p. 512.) Petitioner underwent a twenty-

four-hour Holter monitor for tachycardia on December 1, 2015. (Id. at 191-92.) The

monitor revealed sinus rhythm with low grade ventricular ectopy, brief early morning

ectopic atrial bradycardia, and no correlation of any specific rhythm disturbance or ST

changes with symptoms. (Id at 192.) Petitioner saw Dr. McCool again on December

17, 2015. (Ex. 95, p. 19.) Dr. McCool reported that petitioner’s sleep studies showed

“no abnormalities.” (Id.) Petitioner reported that “she has had [two] episodes where she

wakes up and cannot move her legs,” for about an hour. (Id.) Additionally, petitioner

reported falling asleep in the middle of doing something else. (Id.) Dr. McCool

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explained that “[b]ased on her current symptoms, [she] believe[d] that [petitioner] could

be suffering from narcolepsy with cataplexy.” (Id. at 20.)

On December 21, 2015, petitioner visited pulmonologist Jorge Alvarez, M.D. at

the Jennie Edmundson Hospital Sleep Disorder Center. (Ex. 6, p. 475.) Petitioner

indicated that “thinking, stress, outside noises, anything” made her unable to fall asleep,

and that this had been a problem for “4-5 years.” (Id. at 470.) Dr. Alvarez reported that,

based on petitioner’s sleep study, her “sleepy efficiency was normal,” however, her

“REM latency was slightly prolonged,” and she had a “diminished percent stage of total

REM sleep.” (Id. at 475.) On the same day, petitioner underwent a multiple sleep

latency test which showed a mean sleep latency of 7.9 minutes, evidence of three REM

sleep episodes, and was “consistent with and c[ould] help support a diagnosis of

narcolepsy.” (Id. at 476.) Dr. Alvarez ordered genetic testing on January 20, 2016,

which was negative for the HLA-DQB1*06:02 allele, a gene strongly associated with

narcolepsy. (Id. at 118-21.) On the same day, petitioner saw Dr. Alvarez for “excessive

daytime sleepiness, possible narcolepsy.” (Ex. 89, p. 7.) Dr. Alvarez reported that

petitioner “apparently had a [flu] vaccination this past year.” (Id.) Her symptoms

included “[e]xcessive daytime sleepiness intermittently throughout the day.” (Id.) Dr.

Alvarez recorded petitioner’s impression as narcolepsy with cataplexy and anxiety. (Id.

at 7-8.)

Petitioner’s next follow up appointment with Dr. Alvarez for possible narcolepsy

with cataplexy was on February 22, 2016. (Ex. 89, p. 5.) Petitioner reported sleeping

eight hours a night, however, not feeling rested. (Id.) She reported repetitive

movements, but no seizure activity. (Id.) Dr. Alvarez assessed petitioner with fear and

anxiety; repetitive words and movements, possible neurologic seizures; arthralgias; and

a working diagnosis of narcolepsy with cataplexy. (Id.) Petitioner was prescribed a low

dose of Xyrem. (Id. at 6.) On February 25, 2016, petitioner saw Dr. McCool for a follow

up appointment regarding her narcolepsy diagnosis. (Ex. 95, p. 13.) She complained of

the following symptoms: “word finding difficulty, worsening headaches, a problem with

her depth perception (no recent eye exam), episodes of confusion, muscle twitching,

joint pain distally (hands and feet, although no joint swelling), and her feet appearing

purplish in color at times.” (Id.) Petitioner reported feeling depressed about her

diagnosis. (Id.)

On March 15, 2016, petitioner had an appointment with Joseph F. Shehan, M.D

an internist. (Ex. 7, pp. 71-73.) Petitioner reported that around November 5, 2015, she

“started getting an unusual syndrome, which started with severe vertigo, nausea,

progressed to headaches, progressed to narcolepsy, which progressed to cataplexy

spells.” (Id. at 71.) Petitioner stated that she had now developed numbness and

tingling in her hands, arm weakness, and bilateral headaches that would start in the

back of the head. (Id.) She also noted that she had sustained numerous falls and has

woken up on the ground with no recollection of what happened. (Id.) Petitioner

informed Dr. Shehan that she had received flu and MMR vaccines in October 2015.

(Id.) Dr. Shehan noted that petitioner “has an unusual syndrome complex and this may

relate to immunizations.” (Id. at 73.) He added, “I am going to have to research [the

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vaccines] a little bit to see if there is anything that makes sense.” (Id.) Dr. Shehan

ordered a brain MRI, which petitioner underwent on March 19, 2016. (Ex. 4, pp. 167-

68.) The MRI showed mild scattered, punctate, nonspecific cerebral white matter signal

of unknown acute or ongoing significance, but no acute infarct, mass effect, or evidence

of acute intracranial hemorrhage. (Id. at 167.)

Petitioner presented to neurologist John Puente, M.D., on March 31, 2016. (Ex.

5, pp. 4-5.) Petitioner reported that she was in good health until around November

2015, when she “had an episode while at a convention where she thought she was food

poisoned” and “was bedridden and nauseous with vertigo for longer than a day.” (Id. at

4.) Petitioner further informed Dr. Puente that “she has had episodes of weakness, but

also falling episodes.” (Id.) Additionally, petitioner reported having “pain mostly in joints

and finally anxiousness.” (Id.) Petitioner also noted that she had symptoms of

intermittent weakness, worse on the right side; episodes of her legs “go[ing] out;” and

episodes of dizziness and vertigo followed by falling asleep or confusion. (Id.) Dr.

Puente noted that petitioner was diagnosed with narcolepsy following an abnormal

sleep study but that the bloodwork was inconclusive. (Id.) He further noted that

petitioner’s brain MRI revealed non-specific findings. (Id.) Dr. Puente ordered an EMG

to investigate weakness and an EEG to investigate potential seizures and

recommended petitioner consult a sleep specialist and pursue more aggressive

migraine therapy. (Id. at 5.) Later that day, petitioner followed up with Dr. Shehan and

reported feeling better. (Ex. 7, p. 68.) Petitioner stated that her general wellbeing had

improved with Lexapro. (Id.) Her neurologic examination was normal. (Id. at 69.) Dr.

Shehan noted that petitioner had received the MMR and flu shot in October of 2015,

and then developed severe vertigo on November 5, 2015, which was “[f]ollowed by

[n]arcolepsy progressing to [c]ataplexy.” (Id. at 70.) Petitioner was started on

proprandolol for her migraines. (Id.)

Petitioner presented to Jonathon Moravek, M.D., on April 18, 2016 for an EMG

and nerve conduction study (“NCS”) to evaluate her intermittent weakness and pain in

her ankles and wrists. (Ex. 5, pp. 6-9.) The EMG/NCS was normal. (Id. at 8-9.) Then,

petitioner presented to John Bertoni, M.D., on April 27, 2016, for a video EEG, which

was also normal. (Id. at 16-18.) On May 12, 2016, petitioner returned to Dr. Puente,

who noted that propranolol “seems to have helped” her migraine prophylaxis. (Id. at

10.) Dr. Puente recommended petitioner consult with a sleep specialist. (Id.)

Petitioner followed up with Dr. Shehan on June 7, 2016. (Ex. 7, pp. 65-67.) Dr.

Shehan noted that petitioner “presented today basically with a litany of different issues,”

including “increasing migraines, increasing spells which have been described as

cataplexy and narcolepsy,” and explained that the etiology of these conditions “remains

uncertain.” (Id.) Dr. Shehan documented two different types of spells petitioner was

experiencing, including “what is sort of an expressive aphasia.” (Id.) Dr. Shehan

referred petitioner to Barbara Clinkenbeard, APRN, for a second opinion. (Id. at 67.)

On July 11, 2016, petitioner returned to Dr. Shehan for continuing spells. (Ex. 7,

pp. 62-64.) Dr. Shehan prescribed Adderall and referred petitioner to pulmonary

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disease specialist John Shehan, M.D. 3, and neurologist Bernadette Hughes, M.D., for

evaluation for her spells. (Id. at 64.) Petitioner had an appointment with Dr. Hughes on

July 18, 2016, with a chief complaint of “dizziness and falling, migraines with nausea.”

(Ex. 23, p. 1.) Petitioner explained that she had experienced headaches since she was

14. (Id.) However, in November of 2015, those headaches increased, lasted two or

three days and she began to experience spells. (Id. at 1-2.) Petitioner was then

diagnosed with narcolepsy and cataplexy. (Id. at 2.) Petitioner reported that her

neurological tests had come back negative. (Id.) Dr. Hughes recommended seeing a

psychotherapist for cognitive behavior therapy. (Id. at 4.)

Petitioner presented to Nurse Clinkenbeard on July 20, 2016. (Ex. 7, pp. 60-61,

90-91.) She diagnosed petitioner with generalized anxiety disorder, panic attacks and

major depression. (Id. at 60.) Petitioner reported that she experienced her first

depressive episode in January 2016. (Id. at 90.) Nurse Clinkenbeard noted that

petitioner was easily overstimulated and angry, that she had an illogical thought process

at times, that she had thought blocking, that her abstract reasoning was impaired, and

that her judgment and insight were moderately impaired. (Id. at 90-91.) Petitioner told

Nurse Clinkenbeard that she had a three-day migraine in November 2015, followed by

an increased frequency of migraines and episodes of falling asleep and falling. (Id. at

91.) Nurse Clinkenbeard referred petitioner to therapist Jessica Winternheimer. (Id.)

On August 29, 2016, petitioner presented to Dr. Puente and reported that her

migraines were less severe but still frequent during the summer, which “limited her

activity level at times.” (Ex. 5, p. 12.) Petitioner noted that she was interested in

pursuing acupuncture and herbal and non-traditional therapies. (Id.) Dr. Puente

recommended petitioner try acupuncture, feverfew, magnesium, and a riboflavin

supplement. (Id.) Petitioner returned to Nurse Clinkenbeard on August 31, 2016. (Ex.

7, pp. 58-59, 92-93.) Nurse Clinkenbeard noted that petitioner was nonfunctional due to

her anxiety, and questioned whether petitioner had a somatization disorder. (Id. at 93.)

Petitioner reported blacking out in stressful situations. (Id.) Petitioner had a follow up

appointment with internist Dr. Shehan on September 3, 2016, and reported cataplexy

spells and periodic paralysis, “which may or may not be related to potassium.” (Id. at

53.) Dr. Shehan explained that petitioner “continues to have spells,” which he attributed

to anxiety. (Id.)

Petitioner’s next appointment was with Nurse Clinkenbeard on October 12, 2016.

(Ex. 7, pp. 51-52, 94-95.) Petitioner reported that her mood fluctuates “more than [one

to two] times per day.” (Id. at 95.) Petitioner then underwent cognitive behavior therapy

with Jessica Winternheimer between October 13, 2016, and December 22, 2016. (Ex.

19.) Petitioner reported that, “in October 2015 she began experience[ing] dizziness,

‘seizures,’ phantom pains and dropping things.” (Id. at 3.) Because of these

experiences, she developed anxiety. (Id.) Petitioner was diagnosed with generalized

anxiety disorder. (Id. at 4.)

3

Petitioner saw two Dr. Shehans during the course of her treatment: Dr. Joseph Shehan, an internist, and

Dr. John Shehan, a pulmonologist.

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On November 28, 2016, petitioner had an appointment with Dr. Puente, during

which she reported that her migraines remained the same, and that she experienced a

stutter, odor sensitivity, confusion after blackouts, bowel pain, and nausea. (Ex. 5, p.

14.) Dr. Puente ordered an MRI and recommended that petitioner consider going to

acupuncture. (Id. at 15.) Petitioner had a follow up appointment with Nurse

Clinkenbeard on December 12, 2016. (Ex. 7, pp. 49-50, 96-97.) Petitioner reported to

internist Dr. Shehan the next day. (Id. at 44-48.) Dr. Shehan opined that he was

“somewhat reluctant to believe these are pseudoseizures as she has lost urine

incontinence [sic].” (Id. at 44.) He referred her to another neurologist, Deepak

Madhavan, M.D. (Id. at 47.)

Petitioner presented to internist Dr. Shehan again on January 23, 2017. (Ex. 7,

pp. 38-40.) During the exam, petitioner “laps[ed] into a stupor off and on,” and it

became “somewhat difficult to communicate with her.” (Id. at 38.) He reported that

petitioner was “fatigued, weak, and c[ould not] seem to stay on task.” (Id.) Petitioner

underwent two psychological evaluations performed by Aveva Shukert, Ph.D; one on

January 30, 2017 and the second on February 6, 2017. (Ex. 17.) Petitioner “reported

cataplexy-like episodes which began in November 2015.” (Id. at 5.) She stated that it

occurred after she received two vaccinations on the same day, one for MMR and one

for flu vaccine.” (Id.) Petitioner had been diagnosed with narcolepsy, however, did not

agree that that diagnosis was appropriate. (Id.) Petitioner explained that her episodes

were “triggered by sudden loud noises or stressful days.” (Id.) Additionally, petitioner

noted that she “had a history of migraines.” (Id.) Petitioner’s boyfriend explained that

“he can predict when she is about to have one because she has hand tremors and

stops doing the activity in which she had been engaged.” (Id.) Dr. Shukert reported

that “[t]he present evaluation was scheduled to evaluate both cognitive issues and

emotional and personality issues that might have an impact on [petitioner’s] episodes.”

(Id.) The first cognitive test showed that petitioner’s Processing Speed Index score was

below average, and she “had trouble with immediate short-term memory for visual

material and building speed on this timed test.” (Id. at 6.) Petitioner’s second

evaluation revealed “various negative emotional experiences and [that she] tends to be

quite self-critical and guilt prone.” (Id.) Dr. Shukert reported that petitioner reported

feeling “overwhelmed by life,” and that she was “prone to suicidal ideation.” (Id. at 7.)

Dr. Shukert cautioned that petitioner had been sitting with her boyfriend while

completing this second exam, and that petitioner “was cautioned repeatedly not to

consult him when choosing her answers.” (Id. at 6.) Dr. Shukert’s diagnostic

considerations included anxiety related disorders and she recommended psychotherapy

and antidepressant/antianxiety medication. (Id. at 7.)

On February 8, 2017, petitioner saw John C. Goldner, M.D. (Ex. 24, p. 14-16.)

Dr. Goldner noted that petitioner had been diagnosed with multiple issues including,

narcolepsy, weakness in her left arm of uncertain etiology, and migraines. (Id. at 14.)

Dr. Goldner recounted how petitioner had a history of migraines that got worse after

November 2015. (Id. at 14-15.) Additionally, petitioner described spells where she

loses consciousness. (Id.) Dr. Goldner explained that these spells sounded like

“hypnagogic hallucinations.” (Id. at 15.) Petitioner also explained that “her wrists and

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hands started to hurt, and she had trouble grasping things.” (Id.) Dr. Goldner ordered a

nerve condition study which petitioner underwent on April 6, 2017; the results of which

were normal. (Id. at 5.)

Petitioner had an appointment with neurologist John M. Hannam, M.D. on April

11, 2017. (Ex. 4, pp. 148-51.) Petitioner reported that she had experienced migraines

since she was 13 years old. (Id. at 148.) She explained that her migraines got worse

after she developed “a flu-like illness” in November of 2015. (Id.) At the same time,

petitioner also began to have “spells where she would suddenly collapse.” (Id.) Before

petitioner’s spells, she experiences tremors which sometimes continue after she has

collapsed, however, “[s]he has never had a convulsive seizure.” (Id.) Sometimes,

petitioner loses control of her bladder during these spells. (Id.) These spells increased

when petitioner was experiencing stress or feeling depressed. (Id.) Dr. Hannam

reported that petitioner’s studies had come back as normal, except for petitioner’s sleep

study, which showed narcolepsy. (Id. at 148-49.) Dr. Hannam summarized that one of

petitioner’s practitioners from psychiatry suspected pseudoseizures, however, Dr.

Shehan believed she could have epilepsy because she lost control of her bladder. (Id.

at 149.) Petitioner’s next follow up appointment was with internist Dr. Shehan on April

24, 2017. (Ex. 7, p. 33-35.) Dr. Shehan reported that he continued petitioner on her

current course of treatment. (Id. at 35.) On July 18, 2017, petitioner saw internist Dr.

Shehan again for migraine management. (Id. at 29-32.) Additionally, petitioner

reported continuing to have spells. (Id.)

Petitioner had an initial consultation at an epilepsy clinic on September 28, 2017,

with Dr. Madhavan and Erin L. Smith, M.D. (Ex. 4, pp. 151-57.) Petitioner reported that

her history included migraines, narcolepsy, anxiety, and depression. (Id. at 152.) She

again explained that her symptoms began after a flu-like illness in November of 2015.

(Id.) Petitioner explained that she has three types of spells. (Id.) During one type of

spell, she “seems to suddenly fall asleep and then collapse[s] to the ground.” (Id.)

During these spells, she sometimes loses incontinence. (Id.) Dr. Madhavan and Dr.

Smith explained that these spells are consistent with narcolepsy for which she is being

treated. (Id.) During the second type of spell, petitioner “suddenly collapse[s] to the

ground, however, her eyes remain open and she appears to maintain consciousness.”

(Id.) This spell depends on petitioner’s stress levels. (Id.) Additionally, after these

spells, petitioner feels fearful and speaks like a toddler. (Id.) During the final type of

spell, petitioner “will suddenly have a blank stare and will be able to speak, however,

she requires repeated instruction and guidance to be able to function.” (Id.) Petitioner’s

triggers include bright lights, reflections, and stress. (Id.) Dr. Madhavan and Dr. Smith

scheduled petitioner for an EEG. (Id. at 156.)

Petitioner saw internist Dr. Shehan two more times before the end of the year,

once on October 12, 2017, and then again on December 12, 2017. (Ex. 7, pp. 19-28.)

On October 12, 2017, Dr. Shehan explained that some of petitioner’s symptoms could

be related to “a conversion disorder.” (Id. at 24.) Dr. Shehan reported that they were

waiting on the results of petitioner’s EEG. (Id.) Petitioner reported feeling depressed.

(Id.) Dr. Shehan prescribed cognitive therapy. (Id. at 27.) On December 12, 2017,

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petitioner reported that her symptoms continued. (Id. at 19.) Dr. Shehan considered

whether petitioner might have fibromyalgia. (Id. at 22.)

In January 2018, petitioner began seeing rheumatologist Harry Klein, M.D. (Ex.

7, pp. 14-18.) Petitioner’s presenting symptoms included joint pain in her hands,

ankles, and muscles, along with anxiety. (Id. at 14.) Petitioner explained that nine days

after she received both the flu and MMR vaccines, petitioner developed flu like

symptoms, her joint pain began, and her “feet also started turning purple.” (Id.)

Additionally, petitioner reported her narcolepsy diagnosis, and that her genetic testing

revealed no genetic mutation for this. (Id.) Petitioner also reports vertigo, nausea, and

headaches. (Id.) Dr. Klein notes that petitioner “attributes this to having had a flu shot

and MMR at that time,” however, he explained that after reviewing her labs he does not

believe that her condition suggests an inflammatory or autoimmune process. (Id. at 17.)

Instead, he attributes her headaches, IBS issues, and the joint pain to fibromyalgia.

(Id.) Petitioner had a follow up appointment with internist Dr. Shehan on January 23,

2018, during which she reported that she was unable to get out of bed because of her

fatigue and headaches. (Id. at 10.) Dr. Shehan suggested that petitioner undergo a tilt

table to test for an autonomic issue like POTS. (Id.)

On February 5, 2018, petitioner was admitted for a long-term video EEG. (Ex. 4,

p. 10.) The overnight results of this study were normal; therefore, the EEG was

continued into the next day. (Id. at 17.) Petitioner “had one brief seizure (lasted about

20 seconds),” during the second day of her study. (Id. at 19.) Petitioner was

discharged on February 8, 2018. (Id. at 20.) In the discharge summary, Dr. Madhavan

reported that petitioner had a “history of migraines, narcolepsy, anxiety, depression, and

of spells.” (Id. at 21.) Dr. Madhavan reported that the “EEG monitoring study is

consistent with the presence of mild to moderate diffuse cerebral dysfunction with

frequent bursts of sharply contoured slowing noted diffusely.” (Id. at 26.) Additionally,

petitioner “did show onset of rhythmic activity in the fronto-central head region which

appeared to be consistent with seizure.” (Id.) One week later, petitioner had an

appointment with Antonio P. Reyes, M.D. for lightheadedness. (Ex. 3, p. 3.) Petitioner

reported that over the past two years she “would get sudden tachycardia” while “sitting

on her couch or doing mild activities.” (Id.) “Based on her orthostatic BP check,” Dr.

Reyes diagnosed petitioner with POTS and recommended increasing her fluid and salt

intake and losing weight. (Id. at 6.) Additionally, petitioner was scheduled for an

echocardiogram and a stress test. (Id.)

Petitioner had a follow up appointment with internist Dr. Shehan on May 7, 2018.

(Ex. 7, pp. 7-9.) Dr. Shehan reported that petitioner’s ongoing issues included a skin

rash, fibromyalgia, unconfirmed POTS, and tachycardia. (Id. at 7.) Petitioner described

fewer spells since increasing her potassium. (Id.) Petitioner was referred to another

cardiologist to confirm her POTS diagnosis. (Id. at 9.) Petitioner reported an

improvement in her symptoms to Dr. Madhavan on July 2, 2018. (Ex. 4, pp. 157-62.)

On October 2, 2018, petitioner had another follow up appointment with internist Dr.

Shehan. (Ex. 7, pp. 3-6.) Petitioner reported feeling much better. (Id. at 3.) In addition

10

to her current symptoms, petitioner reported a gluten intolerance and that she continues

to follow a gluten free diet. (Id. at 6.)

In May of 2019, petitioner had her first appointment with neurologist and

epileptologist Aditya Vuppala, M.B.B.S at an epilepsy clinic. (Ex. 22, pp. 162-67.) Dr.

Vuppala reported that petitioner’s history included migraines, narcolepsy, anxiety,

depression, and seizures. (Id. at 162.) Petitioner explained episodes where she loses

awareness once or twice a week, however, these episodes had decreased in frequency.

(Id. at 163.) Additionally, petitioner reported falling due to her narcolepsy zero to four

times a week. (Id.) Dr. Vuppala determined that it was possible that petitioner’s

episodes were epileptic seizures, however, she also notes a differential diagnosis of

autonomic dysfunction. (Id. at 166-67.) Dr. Vuppala encouraged petitioner undergo

POTS testing. (Id. at 167.) Petitioner had a follow up appointment for her fibromyalgia

with Dr. Klein on September 27, 2019. (Ex. 90, pp. 34-37.) Petitioner reported that she

underwent POTS testing. (Id. at 34.) Dr. Klein considered Ehlers Danlos syndrome 4 as

a potential diagnosis for petitioner. (Id. at 37.) Later that year, on December 24, 2019,

petitioner had another appointment with Dr. Klein for fibromyalgia. (Ex. 94, pp. 37-40.)

Petitioner had a follow up appointment with Dr. Vuppala on January 16, 2020.

(Ex. 96, pp. 3-8.) Dr. Vuppala recounted petitioner’s history, and then noted that her

POTS screening “did not show any evidence of autonomic dysfunction.” (Id. at 3-4.)

Petitioner reported that her episodes continued. (Id. at 3.) On April 7, 2020, petitioner

had a follow up appointment with Dr. Klein regarding her fibromyalgia. (Ex. 90, pp. 8-

11.) Petitioner began seeing Michael Summers, M.D., a sleep medicine specialist, on

May 13, 2020. (Ex. 96, pp. 14-18.) Dr. Summer’s impression of petitioner included

hypersomnolence, “out of proportion to what one would expect given the amount of

sleep she gets,” and seizure disorder. (Id. at 15.) Petitioner reported, again, that she

had been healthy until 2015 when, 15 days after she received the MMR vaccine, she

began to suffer from falls. (Id. at 16.) Petitioner reported that her symptoms improved

when she was on seizure medication but not when she was on narcolepsy medication.

(Id.) Dr. Summers explained that he wanted to confirm her diagnosis before

progressing petitioner’s treatment. (Id.) Finally, on December 1, 2020, petitioner was

evaluated by Carey Ann Ronspies, M.D. for “features of a genetic disorder of connective

tissue and common co-morbidities.” (Id. at 19.) Dr. Ronspies also noted that petitioner

has a history of recurrent falls, seizure disorder, narcolepsy and cataplexy, anxiety and

depression, fibromyalgia, and hypokalemia. (Id.) Dr. Ronspies explained that

petitioner’s symptoms are not typical of hereditary Ehlers Danlos syndrome and

recommended genetic testing to confirm a diagnosis given her complex history. (Id. at

19-20.)

4

Ehlers Danlos Syndrome is defined as “a group of inherited disorders of connective tissue.” Ehlers-

Danlos syndrome, DORLAND’S MEDICAL DICTIONARY ONLINE,

https://www.dorlandsonline.com/dorland/definition?id=110561 (last visited April 12, 2024). Symptoms

include “hyperextensible skin and joints, easy bruisability, and friability of tissues with bleeding and poor

wound healing.” (Id.)

11

On March 3, 2021, petitioner had an appointment with Nurse Practitioner Kiley J.

Meyer for lightheadedness. (Ex. 106, pp. 7-9.) Ms. Meyer explained that petitioner

“may have POTS.” (Id. at 7.) She noted that petitioner had not undergone testing to

confirm this diagnosis, but she had increased her fluid and salt intake, mitigating her

symptoms. (Id.) Petitioner’s care for Ehlers Danlos syndrome, periodic paralysis,

seizures, POTS, narcolepsy, and other conditions continued throughout 2022. (Ex.

105.)

b. As Reflected in Affidavits and Testimony

i. Petitioner’s affidavits and testimony

Petitioner submitted two affidavits in this case, one on November 29, 2018 and

the second on January 24, 2023, and testified at the entitlement hearing. (Exs. 2, 107;

Tr. 4-50, 221-25.) Before her vaccination, petitioner reported that she was “an active

person in [her] community.” (Ex. 2, ¶ 3.) She “worked at [her] local YMCA in the toddler

room as the staff lead . . . overs[eeing] 12-16 children age [two to four],” and as a

waitress. (Id. ¶¶ 4, 8.) Additionally, she volunteered at the human society, Susan G.

Komen for the Cute, Nebraska Children’s Home, among other organizations, and

“worked as a character actress for a party planning company. (Id. ¶¶ 5-7.) Petitioner

also cared for her two dogs. (Id. ¶ 10.) She spent time sewing, reading, and organizing

local comic book conventions. (Id. ¶¶ 12-14.)

Petitioner testified that she received a flu vaccine on October 15, 2015, and an

MMR vaccine on October 21, 2015. (Ex. 2, ¶ 2; Tr. 11.) She explained that she did not

experience an adverse reaction after her flu vaccine, however, about one week after

receiving the MMR vaccine, she noticed that she “started to feel extremely tired,

extremely fatigued, and irritable.” (Tr. 12.) At first, she attributed this to being

overworked and stressed. (Id.) She explained that her first memorable experience

began when she attended a conference. (Id. at 12-13.) She explained that, after

checking into her hotel room, she got dizzy while unpacking and vomited. (Id. at 13-14.)

Over the next three days, she continued to feel awful and experience vertigo. (Id. at

14.) She described how pain “radiat[ed] down [her] neck and spine, out to . . . her

fingers and hands.” (Id.) Petitioner was unable to attend any of the conference. (Id. at

14-15.) She stated that she remembered feeling betrayed by her body. (Id.) She

called her primary care physician and the on call nurse diagnosed her with the flu and

instructed her to drink fluids and rest. (Ex. 2, ¶ 21.)

The day after petitioner got home from the conference, petitioner testified that

she “stood up to go to the restroom and then [she] woke up on the floor having urinated

[her]self.” (Tr. 15-16; Ex. 2 ¶ 23.) She explained that she believes she experienced “a

partial seizure of the memory loss and the fear.” (Tr. 16.) She called her primary care

physician again, and again was told she had the flu. (Ex. 2, ¶ 25.) Petitioner booked

the next available appointment with her primary care physician. (Tr. 16.) She explained

that going to the emergency room was cost prohibitive at the time. (Id.) Two days after

that, on November 11, 2015, petitioner also began to experience pain in her hands,

12

wrists, hips, and ankles. (Id. at 18; Ex. 2, ¶ 26.) Petitioner explained that at that time

she was also experiencing symptoms of cataplexy due to extreme stress. (Tr. 18-19.)

Additionally, she described having night terrors and falling asleep during the day. (Id. at

19.)

Her symptoms became chronic overtime and she explained that she began to

see specialist physicians in the hope of getting a better idea of what was going on with

her. (Tr. 19-20.) Petitioner explained that she underwent an MSLT at a sleep clinic and

was diagnosed with narcolepsy. (Id. at 21.) She has not received a study since

because she would have to go off her medications and fears the impact on her life if she

stopped taking her medications. (Id. at 21-22.) Petitioner was diagnosed with Complex

Partial Seizures, which “cause [her] to enter a state of impaired consciousness or to

lose consciousness altogether.” (Ex. 2, ¶ 28.) Additionally, she has been diagnosed

with POTS, which causes “dizziness, blurred vision, nausea and vomiting, brain fog,

chest pain, blood pooling in [her] hands or feet, headaches, neck pain, insomnia, and

shaking.” (Id. ¶ 32.) Petitioner has also been diagnosed with fibromyalgia, causing

“severe joint and muscle pain;” chronic fatigue syndrome, causing constant fatigue and

mental fog; headaches; and numbness in her hands and feet. (Id. ¶ 36; Tr. 24-28.)

Petitioner also suffers from migraines, but it is unknown whether this is a symptom of

her other conditions. (Ex. 2, ¶ 38.) She explained that her current medications cause

gastrointestinal issues, and she has trouble regulating her emotions. (Id. at ¶¶ 8-11; Tr.

at 32-33.)

Petitioner testified that she was 22 years old when her symptoms began and that

her life had changed significantly since her diagnoses. (Tr. 9.) She explained that, to

have a good day, she cannot do anything physically exerting or stressful. (Id. at 9-10.)

She sleeps for about 10 hours for her narcolepsy and has increased her water and

sodium intake to keep her blood pressure in check. (Id. at 10.) She has to plan three to

four days ahead to ensure her narcolepsy and her POTS are not triggered. (Id. at 10-

11.) Petitioner testified that before she developed narcolepsy, she did experience some

sleep issues, however, she explained that these were normally experiences and she felt

like her narcolepsy symptoms were not normal. (Id. at 40-43.) Additionally, petitioner

explained that she had always experienced some pain in her hands and wrists,

however, the pain was different after she had been vaccinated. (Id. at 44.) After

petitioner’s diagnoses, she lost her job and was unable to volunteer, or work as a

seamstress. (Ex. 2, ¶ 16.) Petitioner moved back in with her parents and has been

unable to drive. (Id. ¶¶ 17, 19.) Her quality of life has been reduced greatly and she

must use a wheelchair and avoid large gatherings altogether. (Id. ¶¶ 39-40.) Petitioner

testified that she initially did not believe her condition was related to her vaccines. (Tr.

29.) However, after about six months, she read the labels on the vaccines and began to

believe her vaccines had caused her conditions. (Id. at 29-30.)

Petitioner described how her condition has impacted her family, especially her

grandparents, which has contributed to her feelings of anxiety, guilt, and depression.

(Ex. 2, ¶¶ 12-13, 17.) Additionally, petitioner explained that her condition has led to

increased financial strain on both her and her family. (Id. ¶¶ 13, 15-16.) She has a

13

service dog, however, “obtaining, training, and caring” for the dog has also created

additional financial strain. (Id. ¶ 14.) Petitioner explained that her “injury has forever

changed [her] on the inside and outside.” (Id. ¶ 18.)

ii. Other witness statements

Petitioner has submitted eight witness statements in this case provided by family

members and friends. (Exs. 9-16.) All of these affidavits explain that petitioner’s

condition has greatly impacted her life and that onset of her condition followed her

vaccinations. (Id.) I have reviewed and considered all of these statements; however,

none of the specific recollections contained in these statements effect the causal

analysis below.

IV. Expert Opinions

a. Petitioner’s Expert, Yuval Shafrir, M.D. 5

Dr. Shafrir’s opinion offers a very broad scope, discussing numerous conditions

that he opines may help explain petitioner’s overall clinical presentation. However, his

theory of causation is comparatively narrow. Therefore, I have relied on extensive

footnoting within this summary to address these many conditions while also maintaining

focus on the operative aspects of Dr. Shafir’s theory. However, the analysis that follows

does, at points, incorporate these footnotes by reference.

All three of Dr. Shafrir’s reports include an extensive discussion of petitioner’s

medical history interwoven with editorialization. (Ex. 25, pp. 1-41; Ex. 93; Ex. 98, pp. 3-

17.) Ultimately, he concludes that there is “decisive evidence” that petitioner was in

5

Dr. Shafrir provided three reports (Exs. 25, 93, and 98) and also testified during the entitlement hearing

(Tr. 51-141, 212-224). During the hearing, he was proffered without objection as an expert in neurology

and epileptology. (Id. at 56.) Petitioner additionally sought to present Dr. Shafrir as an expert in

neuroimmune disorders, but respondent objected, arguing that Dr. Shafrir had not demonstrated any

specialized experience with neuroimmune disorders beyond what would be seen by a practicing

neurologist. (Id.) Upon later cross-examination, Dr. Shafrir confirmed that he had no training in

immunology subsequent to medical school. (Id. at 105.) Dr. Shafrir received his medical degree from the

Sackler School of Medicine at Tel Aviv University in 1982. (Ex. 26, p. 1.) Between 1983 and 1988, he

completed a residency in pediatrics at Kaplan Hospital in Rehovot, Israel, Beilinson Medical Center in

Petah Tikvah, Israel, and North Shore University Hospital in Manhasset, New York. (Id. at 1-2.) He then

completed a pediatric neurology residency and fellowship at the Washington University Medical Center in

St. Louis, Missouri. (Id. at 2.) In 1992, Dr. Shafrir completed his pediatric neurophysiology and

epileptology fellowship at Miami Children’s Hospital. (Id.) He is board certified in pediatrics as well as in

neurology, with a special qualification in child neurology, and clinical neurophysiology. (Id.) Dr. Shafrir’s

clinical career has been dedicated to pediatric neurology. (Id. at 2-4.) Since 2019, Dr. Shafrir has

conducted a private practice in which he sees about 10 patients a week and also works one to two weeks

per month at various hospitals locum tenens. (Tr. 53.) He primarily sees patients with neuroimmune

disorders, including PANDAS, PANS, chronic fatigue syndrome, and POTS. (Id.) Dr. Shafrir has co-

authored several publications in various neurology journals, including publications addressing seizures

and epilepsy, but not any relating to the other conditions at issue in this case. (Ex. 26, pp. 4-5.)

Considering all of this, and the record as a whole, Dr. Shafrir is accepted for purposes of this decision as

an expert in neurology and epileptology, but not neuroimmune disorders in particular.

14

good health and with normal function prior to vaccination and then experienced an

abrupt and dramatic decline in function beginning about two weeks after vaccination.

(Ex. 25, pp. 42-43.) Dr. Shafrir indicates that petitioner’s multiple diagnoses are a

“major problem” in analyzing petitioner’s case. (Id. at 43.) He does not fault petitioner

as “doctor shopping,” but suggests that many of her doctors failed to address her

presentation holistically. (Id.) He finds Dr. Joseph Shehan’s assessment to have been

the most reliable. (Id. at 43-44.) He is critical of the fact that several medical entries

stress petitioner’s “flu-like illness” at the time of onset without acknowledging her prior

vaccinations. (Id.)

Dr. Shafrir opines that petitioner presented with a “progressive symptom

complex” that included “identifiable components” of:

- Narcolepsy with possible cataplexy

- Presumed partial complex seizures

- Possible hypokalemic periodic paralysis

- Muscle spasms

- Generalized weakness, in particular weakness of upper extremities

- Fatigue

- Postural Orthostatic Tachycardia Syndrome (POTS)

- An onset of relatively severe psychiatric disorder with depression and

incapacitating anxiety

- Nausea and vomiting

- Polyarthralgia

- Pain in her hands and also in the feet

(Id. at 44.) Given these features, he opines that petitioner’s clinical picture “fit[s] very

well” with the criteria for myalgic encephalomyelitis, otherwise known as chronic fatigue

syndrome. (Id. at 44-45 (citing IOM (Institute of Medicine), Beyond Myalgic

Encephalomyelitis/Chronic Fatigue Syndrome, NAT. ACAD. PRESS 1 (2015) (Ex. 27)).)

Dr. Shafrir explains that, though common, this condition is a syndrome “the etiology of

which has not been yet clarified.” (Id. at 45.) However, he opines that autoimmunity “is

probably the most common biologic explanation.” (Id. (citing Jonas Bloomberg et al.,

Infection Elicited Autoimmunity and Myalgic Encephalomyelitis/Chronic Fatigue

Syndrome: An Explanatory Model, 9 FRONTIERS IMMUNOLOGY 1 (2018) (Ex. 28);

Franziska Sotzny et al., Myalgic Encephalomyelitis/Chronic Fatigue Syndrome –

Evidence for an Autoimmune Disease, 17 AUTOIMMUNITY REVS. 601 (2018) (Ex. 29)) 6.)

6

It is important to stress, as Dr. Shafrir acknowledges in his report, that these two papers do not establish

that chronic fatigue syndrome is autoimmune, they merely hypothesize that it may be. For example,

Blomberg, et al, specifically explain that “much work remains before the autoimmune nature of ME/CFS

can be considered established” and further explain that evidence suggesting a metabolic etiology for the

condition does not fit well into the proposed model. (Bloomberg et al., supra, at Ex. 28, p. 11.) During the

hearing, Dr. Shafrir cited a finding from Sotzny, et al., that 20% of patients had symptom relief with

Rituximab as “decisive proof” that chronic fatigue syndrome is autoimmune. (Tr. 89-91.) However,

Sotzny, et al, indicate that, while there is “convincing evidence” of autoimmunity in at least a subset of

chronic fatigue syndrome cases, the pathomechanism is incompletely understood and likely involves a

combination of dysregulation within the immune, autonomic, and metabolic systems. (Sotzny et al.,

supra, at Ex. 29, pp. 1-2.) I am aware of one prior decision by a different special master finding a

15

He also notes that chronic fatigue can be a feature of patients with other rheumatologic

and autoimmune conditions. (Id. (citing Mark R. Zielinski et al., Fatigue, Sleep and

Autoimmune and Related Disorders, 10 FRONTIERS IMMUNOLOGY 1 (2019) (Ex. 30);

Gerwyn Morris et al., Central Pathways Causing Fatigue in Neuro-Inflammatory and

Autoimmune Illnesses, 13 BIOMED CENT. MED. 1 (2015) (Ex. 31). 7) Dr. Shafrir cites a

single paper hypothesizing that chronic fatigue syndrome and fibromyalgia can be

vaccine caused. (Id. (citing Jacob N. Ablin & Dan Buskila, Fibromyalgia, Chronic

Fatigue, Functional Disorders, and Vaccination: Where Do We Stand?, in VACCINES &

AUTOIMMUNITY 331 (Yehuda Shoenfeld et al. ed., 2015) (Ex. 32). 8) He further cites two

petitioner entitled to compensation for chronic fatigue syndrome caused by the flu vaccine. Bryan v.

Sec’y of Health & Human Servs., No. 14-898V, 2020 WL 7089841 (Fed Cl. Spec. Mstr. Oct. 9, 2020).

However, the Bryan case was decided on a very different record and, in particular, based on a theory that

has not been presented in this case. On this record, Dr. Shafrir has not preponderantly established that

chronic fatigue syndrome is autoimmune.

7

These two papers observe that fatigue occurs commonly in patients with a number of different

autoimmune conditions. The authors propose neuroimmune and metabolic pathways that could explain

how fatigue could be a consequence of otherwise established autoimmune conditions. However, fatigue

remains a non-specific finding. (Zielinski et al., supra, at Ex. 30, p. 1 (explaining that “[f]atigue is multi-

faceted and broadly defined, which makes understanding the cause of its manifestations especially

difficult in conditions with diverse pathology including autoimmune diseases.”); Morris et al., supra, at Ex.

31, p. 14 (stating that “[w]hen viewed as a whole these observations also support the view that severe

intractable fatigue results from processes which are not disease specific but involved in disease

pathogenesis.”)) Dr. Shafrir additionally cites the package insert for the Fluzone vaccine as reporting

fatigue within its post-marketing experience. (Ex. 25, p. 46 (citing Fluzone Prescribing Information

[hereinafter Fluzone Package Insert], Ex. 35).) Again, however, this reference to fatigue does nothing to

dispel the notion of fatigue as a non-specific symptom. Moreover, post-marketing experience generally

represents unverified passive surveillance, which is not typically considered persuasive. Specifically, the

package insert explains that the disclosed adverse events were “spontaneously reported” and “[b]ecause

these events are reported voluntarily from a population of uncertain size, it is not always possible to

reliably estimate their frequency or establish a causal relationship to vaccine exposure.” (Fluzone

Package Insert, supra, at Ex. 35, p. 10.) The fact that fatigue can be seen in autoimmune conditions

does not add significant support to Dr. Shafrir’s assertion that chronic fatigue syndrome is autoimmune.

8

This paper relies in substantial part on the assertion that another fatiguing illness, Gulf War Syndrome,

is a vaccine-caused entity as well as a broader concept known as Autoimmune Syndrome Induced by

Adjuvants or “ASIA,” which purports to link vaccines to autoimmunity broadly. (Ablin & Buskila, supra, at

Ex. 32.) I have addressed both of these concepts in greater detail in prior decisions, including discussion

of many of the same papers cited by Ablin and Buskila. As explained in those decisions, these materials

do not provide meaningful evidence supporting vaccine causation. Skinner-Smith v. Sec’y of Health &

Human Servs., No. 14-1212V, 2022 WL 4116896, at *31-35 (Fed. Cl. Spec. Mstr. Aug. 15, 2022) (finding

that literature relating to Gulf War Syndrome did not support petitioner’s theory that the Tdap vaccine can

cause chronic fatigue syndrome); J.F. v. Sec’y of Health & Human Servs., No. 13-799V, 2022 WL

5434214, at *29-32, n. 34 (Fed. Cl. Spec. Mstr. Sept. 9, 2022) (explaining that “petitioner is unpersuasive

in advancing ASIA as sound and reliable for any purpose and my conclusion is that ASIA fails as a

concept fundamentally and in toto.”) These prior decisions, and others subsequently discussed below,

are not binding and do not dictate the outcome of this case. Boatmon v. Sec’y of Health & Human Servs.,

941 F.3d 1351, 1358 (Fed. Cir. 2019). However, special masters are meant to apply their accumulated

experience. Hodges v. Sec’y of Health & Human Servs., 9 F.3d 958, 961 (Fed. Cir. 1993) (explaining that

“Congress assigned to a group of specialists, the Special Masters within the Court of Federal Claims, the

unenviable job of sorting through these painful cases and, based upon their accumulated expertise in the

field, judging the merits of the individuals claims.”) Though these prior decisions provide more detailed

discussion, I find the Ablin and Buskila paper unpersuasive on this record in any event. Even if Dr.

16

case reports of post flu vaccine chronic fatigue syndrome 9 and a study examining

fatigue following rubella vaccination. 10 (Id. at 45-46.)

Despite identifying chronic fatigue syndrome as fitting “very well” with petitioner’s

clinical syndrome, he further opines that “[a] multisystemic autoimmune condition” may

explain these very unusual associations” in petitioner’s case. (Ex. 25, p. 46.)

Therefore, his report cites several additional conditions, each of which he asserts is also

an autoimmune condition, as including symptoms relevant to petitioner’s history. (Id.)

During the hearing, Dr. Shafrir ultimately opined that in addition to chronic fatigue

Shafrir had been successful in demonstrating that chronic fatigue syndrome is autoimmune, he still would

not have preponderantly established that it can be caused or triggered by vaccination. Accord Skinner-

Smith, 2022 WL 4116896.

9

The two case reports are presented in a single paper. (Sean P, J. Lynch et al., Should Influenza

Vaccination be Mandatory for Healthcare Workers?, 347 BRIT. MED. J. 1 (2013) (Ex. 33).) The authors

disclaim the assertion of any causal relationship, explaining that “[a] definite causal relationship between

vaccination and chronic fatigue syndrome is not claimed here, all that has been established is a possible

temporal relationship.” (Id. at 4.) Case reports are not wholly without evidentiary value; however, as

anecdotal reports, they are considered an especially weak form of evidence. See, e.g. Crutchfield v.

Sec’y of Health & Human Servs., No. 09-0039V, 2014 WL 1665227, at *19 (Fed. Cl. Spec. Mstr. Apr. 7,

2014) (“single case reports of Disease X occurring after Factor Y . . . do not offer strong evidence that the

temporal relationship is a causal one—the temporal relationship could be pure random chance”), aff’d,

125 Fed. Cl. 251 (2014); but see Paluck ex rel. Paluck v. Sec’y of Health & Human Servs., 104 Fed. Cl.

457, 475 (2012) (noting that “the fact that case reports can by their nature only present indicia of

causation does not deprive them of all evidentiary weight.”) Dr. Shafrir has not preponderantly

established that the flu vaccine in particular can cause chronic fatigue syndrome.

10

(Michal Morag et al., Psychological Variables as Predictors of Rubella Antibody Titers and Fatigue – A

Prospective, Double Blind Study, 33 J. PSYCHIATRIC RSCH 389 (1999) (Ex. 34).) Dr. Shafrir characterizes

this study as one reporting post-vaccination chronic fatigue syndrome. (Ex. 25, p. 45-46.) However, this

is not accurate. While fatigue-related symptoms were examined 10 weeks post-vaccination, the aim of

the study was to assess whether personality and other psychologic variables can predict antibody titers

and then, by extension, whether psychological variables can then be used to predict post-vaccination

fatigue. (Morag et al., supra, at Ex. 34, p. 1.) The study examined a cohort of subjects previously

vaccinated for rubella and a cohort that had not previously been vaccinated. (Id.) Subjects were

provided a questionnaire both before and after vaccination and antibody titers were measured at the time

of the second questionnaire. (Id. at 2-3.) Subjects provided subjective reports of fatigue-related

symptoms based on questions relating to Post Viral Fatigue Syndrome as defined by the CDC, but were

not diagnostically screened for chronic fatigue syndrome. (Id.) The authors suggest that their findings

show that subjects deemed to have higher-self-esteem (which they relate to lower stress) saw a better

immune response to vaccination whereas those deemed more neurotic (which they relate to depression)

had a less effective immune response. (Id. at 5.) Regarding reports of fatigue, the authors posited that

their results were consistent with factors of psychologic outlook as driving the subjects’ degree of

sensitivity to symptoms of fatigue. (Id. at 5-6.) The authors conclude that “[t]he findings of the present

study underscore the importance of distinguishing between variables that influence general biases in

symptom-complaining, and variables that help in predicting specific infection-induced effects.” (Id. at 6.)

Nothing in the study purports to establish that the rubella vaccine is a cause of chronic fatigue syndrome.

Dr. Shafrir has not preponderantly established that the MMR vaccine can cause chronic fatigue

syndrome.

17

syndrome petitioner should carry diagnoses of narcolepsy, 11 POTS, 12 epilepsy, 13 and,

fibromyalgia. 14 (Tr. 58-59, 79.) He characterized depression and anxiety as “possible,”

11

In his report and throughout much of his testimony, Dr. Shafrir did not distinguish between type one and

type two narcolepsy (Ex. 25, p. 46), though some of his cited literature does. The distinction is important

because respondent’s expert, Dr. Evans, opines that only type one narcolepsy can be considered

autoimmune. (Tr. 156-58.) During the hearing, Dr. Shafrir acknowledged that type one narcolepsy is

associated with a particular HLA antigen (see also n. 21, infra), but asserted that the presence of that

antigen is not a diagnostic requirement. (Id. at 68.) Thus, he testified that “by definition, [you] can have

narcolepsy without this HLA.” (Id. at 72.) But this testimony did not specifically resolve the distinction

between type one and type two narcolepsy. It was not until he returned for rebuttal testimony that Dr.

Shafrir specifically confirmed he is opining that petitioner suffered type one narcolepsy. (Id. at 214.)

According to the literature Dr. Shafrir has provided, type one narcolepsy is characterized by either the

presence of cataplexy and a positive multiple sleep latency test or hypocretin deficiency. (Sagarika Nallu

& Selim R. Benbadis, Narcolepsy, MEDSCAPE (last updated Aug. 3, 2020) (Ex. 99, p. 3).) Dr. Shafrir has

not preponderantly established that all forms of narcolepsy are autoimmune or that any type of

narcolepsy beyond type one narcolepsy is autoimmune. The experts’ disagreement as to whether

petitioner suffered type one narcolepsy in particular turns on two issues, their disagreement as to the

diagnostic significance of the HLA allele and their disagreement as to whether petitioner suffered

cataplexy. As discussed under Althen prong two, below, I do not find it necessary to resolve the

diagnostic question because I conclude that the HLA allele is critical to Dr. Shafrir’s theory of causation

regardless of whether it is diagnostic of type one narcolepsy.

12

POTS is a condition affecting the autonomic nervous system resulting in tachycardia and orthostatic

symptoms. Although Dr. Shafrir’s opinion is premised on each of the conditions he has identified being

autoimmune, he has acknowledged that POTS is a syndrome that has many causes. (Ex. 25, p. 47.) He

includes two citations for the proposition that at least a subset of cases may be autoimmune. (Id. (citing

Steven Vernino & Lauren E. Stiles, Autoimmunity in Postural Orthostatic Tachycardia Syndrome: Current

Understanding, 215 AUTONOMIC NEUROSCIENCE: BASIC & CLINICAL 78 (2018) (Ex. 59); S. Dahan et al.,

Postural Orthostatic Tachycardia Syndrome (POTS) – A Novel Member of the Autoimmune Family, 25

LUPUS 339 (2016) (Ex. 60)).) I discussed extensively in a prior decision why there is not strong evidence

supporting POTS as an autoimmune condition. C.F. v. Sec’y of Health & Human Servs., No. 15-731V,

2023 WL 2198809, at *31-36 (Fed. Cl. Spec. Mstr. Jan. 20, 2023). Even on a record that was far more

developed on this issue than what has been presented in this case, I concluded that the petitioner had

only demonstrated that it is “plausible, but yet to be established” that POTS has any autoimmune basis.

Id. at 31. Based on my review of the Vernino and Stiles, and Dahen et al. papers cited in this case, their

discussion of the autoimmune hypothesis of POTS is consistent with my discussion and conclusion in

C.F. Dr. Shafrir has not preponderantly established on this record that POTS is either autoimmune or

vaccine caused.

13

Dr. Shafrir cites the following articles to support his assertion that epilepsy can be autoimmune: Mei-

Sing Ong et al., Population-Level Evidence for an Autoimmune Etiology of Epilepsy, 71 J. AM. MED. ASS’N

NEUROLOGY 569 (2014) (Ex. 64); Antonio Greco et al., Autoimmune Epilepsy, 15 AUTOIMMUNITY REVS. 221

(2016) (Ex. 65); M. Toledano et al., Utility of an Immunotherapy Trial in Evaluating Patients with

Presumed Autoimmune Epilepsy, 82 NEUROLOGY 1578 (2014) (Ex. 66); Andrew McKeon, Antibody

Prevalence in Epilepsy (APE) Score—Evolution in Autoimmune Epilepsy Practice, 74 J. AM. MED. ASS’N

NEUROLOGY 384 (2017) (Ex. 67); James B. Lilleker et al., VGKC Complex Antibodies in Epilepsy:

Diagnostic Yield and Therapeutic Implications, 22 SEIZURE 776 (2013) (Ex. 68); Eoin P. Flanagan et al.,

Basal Ganglia T1 Hyperintensity in LGI1-Autoantibody Faciobrachial Dystonic Seizures, 2 NEUROLOGY

NEUROIMMUNOLOGY & NEUROINFLAMMATION 1 (2015) (Ex. 69); Claude Steriade et al., Electroclinical

Features of Seizures Associated with Autoimmune Encephalitis, 60 SEIZURE: EUR. J. EPILEPSY 198 (2018)

(Ex. 70). Dr. Evans indicates that autoimmune epilepsy occurs specifically within the context of

autoimmune encephalitis, which he asserts has a distinct clinical presentation. (Ex. A, p. 13.) Upon my

review, I do not see where any of the literature cited by Dr. Shafrir would necessarily contradict that

explanation, though two of the papers do otherwise discuss epilepsy as being comorbid to several other

18

but “much more difficult to relate it to a particular autoimmune attack.” (Id. at 58.)

Although petitioner has also asserted that she had a preexisting migraine disorder that

was significantly aggravated as part of her alleged vaccine injury (ECF No. 98, p. 10.),

Dr. Shafrir indicated during the hearing that he did not believe petitioner’s migraines

were implicated as part of her alleged post-vaccination condition. 15 (Tr. 63.)

In summarizing his medical theory, Dr. Shafrir reiterates that the clinical picture

fits chronic fatigue syndrome but concludes that given its other unusual features “I

cannot think of any better unifying diagnosis beside an autoimmune process.” (Ex. 25,

p. 49.) Dr. Shafrir includes a number of citations for the general proposition that both

the flu and MMR vaccines have been associated with autoimmune phenomenon

types of autoimmune disorders. (Ong et al., supra, at Ex. 64; Greco et al., supra at Ex. 65.) Dr. Shafrir

has not opined that petitioner suffered an autoimmune encephalitis. (Tr. 94-95.) Dr. Shafrir has not

preponderantly established on this record that any form of autoimmune epilepsy is implicated. In fact, he

acknowledged during the hearing that he felt this was a less well established diagnosis for petitioner as

compared to the other conditions he advanced. (Id.)

14

Dr. Shafrir provides two citations to explain the etiology of fibromyalgia. (Ex. 25, p. 47 (citing Camillo

Giacomelli et al., The Interaction Between Autoimmune Diseases and Fibromyalgia: Risk, Disease

Course and Management, 9 EXPERT REV. CLINICAL IMMUNOLOGY 1069 (2013) (Ex. 61); Dan Buskila et al.,

Etiology of Fibromyalgia: The Possible Role of Infection and Vaccination, 8 AUTOIMMUNITY REVS. 41

(2008) (Ex. 62)).) They do not support the conclusion that it is either autoimmune or vaccine-caused.

Giacomelli, et al, state that “Fibromyalgia (FM) is a common non-autoimmune rheumatologic disease with

a wide range of symptoms that worsen the clinical status of patients. Several authors have tried to

identify a putative autoimmune biomarker, but unfortunately, without positive results.” (Giacomelli et al.,

supra, at Ex. 61, p. 1.) Buskila, et al., indicate that fibromyalgia is often seen in patients with autoimmune

disease, and it may itself involve immunological aberration, but stop short of concluding it is itself

autoimmune. (Buskila et al., supra, at Ex. 62, pp. 1-2.) They further explain that current evidence linking

fibromyalgia to vaccination is only “anecdotal” and that any role for vaccination in precipitating

fibromyalgia “still remains to be established.” (Id. at 3.) Dr. Shafrir provided a third citation to a study by

Klein, et al., for the proposition that chronic pain has been described as a manifestation of potassium

channel autoimmunity, which he also otherwise implicates within his theory. (Ex. 25, p. 47 (citing

Christopher J. Klein et al., Chronic Pain as a Manifestation of Potassium Channel-Complex Autoimmunity,

79 NEUROLOGY 1136 (2012) (Ex. 63)).) However, the Klein study was specifically accounted for by

Giocomelli, et al., in their assessment of fibromyalgia etiology. (Giacomelli et al., supra, at Ex. 61, p. 3.)

They concluded that the proposed antibodies have not been validated as a useful biomarker for

fibromyalgia. (Id.) Thus, on this record Dr. Shafrir has not preponderantly established that fibromyalgia is

either autoimmune or vaccine caused.

15

In his report, Dr. Shafrir also referenced hypokalemic periodic paralysis and acquired neuromyotonia as

additional conditions implicated by petitioner’s medical records. (Ex. 25, p. 46.) However, he stopped

short of asserting petitioner actually suffered these conditions. (Id.)

19

generally and that molecular mimicry, 16 epitope spreading, 17 and bystander activation 18

and have been proposed as potential explanations. 19 Ultimately, however, he indicates

that “[o]ther than a few rare cases, the exact mechanisms by which infections or

vaccinations can induce autoimmune disease has not been fully clarified.” (Id.)

More specifically, Dr. Shafrir asserts that molecular mimicry has specifically been

demonstrated in the context of narcolepsy caused by the flu vaccine. 20 (Ex. 25, p. 49.)

This ultimately represents the crux of Dr. Shafrir’s theory. However, he acknowledged

that “even in the case of narcolepsy and influenza vaccination we are far from

understanding the full mechanism. For example, only a tiny minority of the patients who

carry the major risk factor of HLA DQB1*06:02/DQA1*01:02[21] and received the H1N1

16

According to the literature cited by Dr. Shafrir, “molecular mimicry” occurs when “[c]ross-reactivity

between a foreign antigen (such as a microorganism’s peptides) and self antigens induces a break of self

tolerance and leads to autoimmunity.” (Nancy Agmon-Levin et al., Vaccines and Autoimmunity, 5 NATURE

REVS. RHEUMATOLOGY 648, 650 (2009) (Ex. 84, p. 3 (Box 2)).)

17

Dr. Shafrir’s reference defines “epitope spreading” as “[b]roadening or diversification of the initial

immune response from the dominant epitope to subdominant (cryptic) epitopes. Thus, the response to a

single peptide spread to several responses directed at different epitopes either within the same antigen

(intramolecular spreading) or in other antigens (intermolecular spreading).” (Agmon-Levin et al., supra, at

Ex. 84, p. 3 (Box 2).)

18

Dr. Shafrir’s reference defines “bystander activation” as occurring when “[t]he initial immune response

to an antigen might induce tissue damage and the release of sequestered antigens. These newly

exposed antigens activate autoreactive lymphocytes (that is, T cells) that were not directly involved in the

initial response. In addition, antigen-presenting cells activated by the initial antigen are capable of further

activating macrophages, which perturb preprimed autoreactive T cells in a bystander manner.” (Agmon-

Levin et al., supra, at Ex. 84, p. 3 (Box 2).)

19

In his report Dr. Shafrir also referenced polyclonal activation, but during the hearing indicated he does

not believe that concept is implicated in this case. (Ex. 25, p. 49; Tr. 99.)

20

The following articles pertaining to allegedly vaccine-caused narcolepsy have been filed in this case:

Guo Luo et al., Autoimmunity to Hypocretin and Molecular Mimicry to Flu in Type 1 Narcolepsy, 115

PROC. NAT’L ACAD. SCI. E12323 (2018) (Ex. 37); Syed Sohail Ahmed et al., Antibodies to Influenza

Nucleoprotein Cross-React with Human Hypocretin Receptor 2, 7 SCI. TRANSLATIONAL MED. 1 (2015) (Ex.

38); Markku Partinen et al., Increased Incidence and Clinical Picture of Childhood Narcolepsy Following

the 2009 H1N1 Pandemic Vaccination Campaign in Finland, PUB. LIBR. SCI. ONE e33723 (2012) (Ex. 39)

(also filed as Ex. A, Tab 14); Richard E. Rosch et al., Narcolepsy Following Yellow Fever Vaccination: A

Case Report, 7 FRONTIERS NEUROLOGY 1 (2016) (Ex. 40); Sebjorg Elizabeth Hesla Nordstrand et al.,

Psychiatric Symptoms in Patients with Post-H1N1 Narcolepsy Type 1 in Norway, 42 J. SLEEP 1 (2019)

(Ex. 41); Anna-Helena Saariaho et al., Autoantibodies Against Ganglioside GM3 are Associated with

Narcolepsy-Cataplexy Developing After Pandemrix Vaccination Against 2009 Pandemic H1N1 Type

Influenza Virus, 63 J. AUTOIMMUNITY 68 (2015) (Ex. 42); Segal & Shoenfeld, supra, at Ex. 85.

21

“HLA” refers to “human leukocyte antigens,” which are histocompatibility antigens governed by genes

of the HLA complex, a chromosome region containing multiple alleles – i.e. genetic variants at different

loci. Human leukocyte antigens, DORLAND’S MEDICAL DICTIONARY ONLINE,

https://www.dorlandsonline.com/dorland/definition?id=56923 (last visited April 12, 2024). The letters “DQ”

identify the location of the allele at issue and “B1” and “A1” identify the specific allele. Id. The alleles are

in turn associated with antigens that are typed by their serologic reactions. Id. DQB1*0602 is a class II

HLA molecule that “initiate[s] the adaptive immune response by presenting short, pathogen-derived

peptides to T cells.” If a self-peptide is presented, this can lead to autoimmune disease. (See Nathaniel

20

vaccine with the offensive adjuvant actually developed narcolepsy.” (Id. at 49-50.)

Thus, he opines that petitioner’s influenza vaccine “produced an initial autoimmune

response against multiple components of multiple systems in her body” and “[a]

reasonable candidate is an initial process that produces antibodies against components

of the potassium channel and against the hypocretin receptor” as seen in narcolepsy.

(Id. at 50.)

During the hearing, Dr. Shafrir further explained his theory as follows: “[W]e have

several conditions that are presumably autoimmune and I explain why, and then in one

of them we have a good explanation so I make the assumption that it’s the same

process in the other, where the mechanism is not known.” (Tr. 107-08.) Specifically, he

testified that:

[O]ne of the conditions she has is narcolepsy, and in contrast to most other

vaccine-related injury, in narcolepsy we have some, not full in any way, but

some understanding of the mechanism. So we know that in narcolepsy they

demonstrated actually molecular mimicry as the mechanism, and the

production of antibodies affecting both – in this particular case, the influenza

vaccine, and the hypocretin receptor and the hypocretin molecule itself.

(Id. at 97.) He asserts that epitope spreading and bystander activation can explain how

the autoimmune reaction leading to narcolepsy can lead to further attack on other

targets that were not attacked in the initial autoimmune reaction. (Id. at 98; Ex. 25, p.

50 (citing Agmon-Levin et al., supra, at Ex. 84); Yahel Segal & Yehuda Shoenfeld,

Vaccine-Induced Autoimmunity: The Role of Molecular Mimicry and Immune

Crossreaction, 15 CELLULAR & MOLECULAR IMMUNOLOGY 586 (2018) (Ex. 85)).)

Dr. Shafrir asserts that all of the conditions he identified as present in petitioner’s

case arose simultaneously on November 6, 2015, at the time of the abrupt illness she

described in her testimony. (Tr. 135-36.) He opines that this timing is appropriate to

infer vaccine-causation. (Id. at 99-100.)

F. Watson et al., Does Narcolepsy Symptom Severity Vary According to HLA-DQB1*0602 Allele Status?,

33 Sleep 29 (2010) (Ex. 101); see also Rama J. Wahab et al., Celiac Disease Autoimmunity and

Emotional and Behavioral Problems in Childhood, 144 Pediatrics 1 (2019) (Ex. 73); Takashi Kanbayashi

et al., Symptomatic Narcolepsy in Patients with Neuromyelitis Opticia and Multiple Sclerosis, 66 Archives

Neurology 1563 (2009) (Ex. 46); but see M. Vitiello et al., Type on Narcolepsy in Anti-Hu Antibodies

Mediated Encephalitis: A Case Report, 47 Congresso Nazionale 1 (2017) (Ex. 44) (narcolepsy patients

negative for HLA DQB1*0602 alleles).) In particular, “[h]igher levels of surface expression of HLA

DQB1*0602 on antigen-presenting cells […] could increase the likelihood that hypocretin producing cell

autoantigens” are presented to T cells. (Watson et al., supra, at Ex. 101, p. 5.) Thus, DQB1*0602 has

been specifically implicated as having “direct involvement” in susceptibility to narcolepsy. (Id. at

1.) References to “DQB1*0602” can relate to either allele status or the resulting histocompatibility

antigen.

21

b. Respondent’s Expert, M. Steven Evans, M.D. 22

Dr. Evans agrees that petitioner had a complicated medical history without any

definitive diagnosis. (Ex. A, p. 7.) He particularly stressed Dr. Shehan’s summary that

petitioner’s “litany of different issues” represented “one of the most complicated patients

I take care of” with increasing spells that are “very unusual.” (Id. (quoting Ex. 90, p.

107).) Dr. Evans notes that many diagnoses were considered despite only having weak

support and that many of her diagnoses are for very different types of conditions that

typically do not co-occur. (Id.) Because petitioner suffered episodes of sudden loss or

alteration of consciousness, he finds it reasonable that narcolepsy and epilepsy were

the two most prominently considered conditions. (Id. at 8.) However, he opines there is

ultimately inadequate evidence to support either diagnosis. (Id. at 7-10.) Based on his

review of the subsequently filed medical records, Dr. Evans confirmed in a second

report that his opinion did not change. (Ex. C, p. 5.) Dr. Evans provided extensive

discussion of the diagnostic considerations at issue; however, in light of the analysis

that follows, it is not necessary to detail the points he raised.

Dr. Evans acknowledges that there are some pieces of literature, largely case

reports, hypothesizing that conditions such as chronic fatigue syndrome, POTS, and

fibromyalgia, are autoimmune; however, he characterizes that evidence as very weak

and does not agree that any of the conditions are autoimmune. (Tr. 205-07.)

Regarding narcolepsy, Dr. Evans explains that only type one narcolepsy is thought to

be autoimmune. (Id. at 156-58.) Whereas type two narcolepsy involves the loss of

orexin-containing neurons, type one narcolepsy involves the loss of hypocretin neurons.

(Id.) Type one narcolepsy is associated with a specific allele (HLA-DQB1*06:02). (Id.;

Ex. A, p. 8.) However, Dr. Evans does not agree that the flu vaccine (even including the

Pandemrix vaccine) has been established via molecular mimicry as a cause of type one

narcolepsy. (Tr. 176.)

In this case, Dr. Evans notes that petitioner was specifically tested for the HLA-

DQB1*06:02 allele and the test was negative; therefore, he opines that this finding

weighs “strongly” against any diagnosis of narcolepsy at all, leaving the diagnosis

“speculative” in petitioner’s case. (Ex. A, p. 8.) However, to the extent it does not

22

Dr. Evans submitted two reports and also testified at the hearing. (Exs. A, C; Tr. 141-210.) He was

proffered without objection as an expert in neurology and epileptology. (Tr. 144.) He graduated with his

bachelors’ degree from the University of Kentucky and his medical degree and a Masters in Physiology

from the University of Louisville School of Medicine. (Ex. B, p. 1.) He completed an internship, his

residency in neurology, and a postdoctoral fellowship in neuropharmacology at Barnes

Hospital/Washington University School of Medicine. (Id.) He is board certified by the American Board of

Psychiatry and Neurology in clinical neurophysiology and epilepsy and by the National Board of Medical

Examiners. (Id. at 4.) He currently works as a professor in the Department of Neurology at the University

of Louisville and sees patients as the University of Louisville Hospital, Jewish Hospital in Louisville

Kentucky, and Owensboro Health Regional Hospital. (Id. at 1-2.) At the time he submitted his CV to the

court, he had written five book chapters and reviews, 42 peer-reviewed articles, and 72 abstracts. (Id. at

8-15.) Dr. Evan’s inpatient practice included general neurology practice and a stroke program, and his

outpatient practice focused primarily on epilepsy. (Tr. 143.) Dr. Evans also has a background in

electroencephalopathy. (Id. at 144.)

22

definitively rule out any type of narcolepsy, it would be far more likely that petitioner

would have type two narcolepsy. (Tr. 156-58.) Although this allele can be found in

people who do not have narcolepsy, it is found in 98% of patients with type one

narcolepsy. 23 (Id.; see also Hanna M. Ollila et al., HLA-DPB1 and HLA Class I Confer

Risk of and Protection from Narcolepsy, 96 AM. J. HUM. GENETICS 136, 136 (2015) (Ex.

A, Tab 13, p. 1).)

V. Discussion

Petitioner obviously has a complicated medical history and, as Dr. Shafrir

explained, her medical history reflects a prolonged, and no doubt frustrating, search for

a satisfactory explanation for her condition. That diagnostic uncertainty continues to be

reflected in the competing expert opinions in this case. Dr. Shafrir opines that petitioner

suffered simultaneous onset of the following conditions: narcolepsy, epilepsy, chronic

fatigue syndrome, fibromyalgia, and POTS. (Ex. 25, p. 44.) Further, Dr. Shafrir opines

that each of these conditions is autoimmune and that they can therefore be viewed

collectively as a unified syndrome of autoimmunity. (Id. at 46, 49.) Dr. Evans largely

disagrees on respondent’s behalf. (Tr. 205-07, 156-58.) However, the purpose of this

decision is not to resolve petitioner’s search for a medical explanation. Instead, the

purpose of this decision is to determine whether petitioner has met her own burden of

proof with respect to whether her condition, either in whole or in part, was caused by the

vaccine(s) at issue. Accord Orgel-Olsen v. Sec’y of Health & Human Servs., 15-285V,

2022 WL 1598143, at *36 (Fed. Cl. Spec. Mstr. Mar. 11, 2022) (explaining in conclusion

that “[p]erhaps unsurprisingly, however, this legal Program cannot achieve for petitioner

the clarify that eluded his many treating physicians.”)

Based on the theory petitioner has presented, it is not ultimately necessary to

definitively catalog and categorize her symptoms. Dr. Shafrir is very clear in presenting

petitioner’s alleged narcolepsy as the linchpin of his theory of causation. Specifically,

he opines that, of all the conditions he has discussed, he can locate good evidence only

for his contention that narcolepsy can be caused by the flu vaccination. (Ex. 25, pp. 49-

50; Tr. 97.) He opines only by extension from that condition that it is reasonable to

conclude that the entirety of petitioner’s presentation was also vaccine-caused. (Tr.

107-08.) Thus, regardless of whether petitioner would qualify for any of the other

diagnoses, my conclusion that Dr. Shafrir has not preponderantly supported any

vaccine-caused narcolepsy is dispositive. Therefore, the Althen analysis below focuses

primarily on petitioner’s alleged narcolepsy.

a. 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 v.

Sec’y of Health & Human Servs., 451 F.3d 1352, 1355-56 (Fed. Cir. 2006) (quoting

23

Dr. Shafrir disagrees with specifically placing the prevalence at 98%. (Tr. 71-72.) While he

acknowledges this figure is included in some of the literature, he indicates that other literature has

identified lower percentages. (Id.)

23

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, 35 F.3d at 548-49. 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, 1378-79

(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

Knudsen, 35 F.3d at 548-49).

Apart from narcolepsy, Dr. Shafrir has provided little to no direct evidence

supporting the opinion that any of the conditions allegedly at issue can be caused by

either of the vaccines at issue. Moreover, absent his reliance on autoimmune

narcolepsy (see n. 11, 21, supra), Dr. Shafrir has not otherwise offered any other clearly

articulated theory that would point to either vaccine as a cause of petitioner’s condition.

In particular, the evidence of record is insufficient to preponderantly establish a stand-

alone causal theory for chronic fatigue syndrome, POTS, epilepsy, fibromyalgia,

hypokalemic periodic paralysis or acquired neuromyotonia, or migraines. (See n. 6-10

(CFS), n. 12 (POTS), n. 13 (epilepsy), n. 14 (fibromyalgia), n. 15 (hypokalemic periodic

paralysis/acquired neuromytonia) supra; Tr. 63.)

Instead, Dr. Shafrir premises his theory on the idea that there is sufficient

evidence from which to conclude that the flu and/or MMR vaccines can cause type one

narcolepsy via molecular mimicry. (Ex. 25, pp. 49-50; Tr. 97.) From that starting

premise, he further opines that the specific concepts of epitope spreading and

bystander activation permit the conclusion that the cause of one autoimmune condition

can also be the cause of additional autoimmune conditions affecting other body

systems. (Ex. 25, p.50; Tr. 98.) He therefore concludes that, because appropriate

medical thinking seeks a unifying diagnosis, if one of petitioner’s conditions is implicated

as a vaccine-caused autoimmune condition, i.e. narcolepsy, then it is reasonable to also

assume that her entire constellation of syndromes is likewise due to the same

underlying cause. (Ex. 25, p. 46.) Upon my review of the record as a whole, none of

these premises is well supported and Dr. Shafrir’s theory is not sound and reliable.

The fact that type one narcolepsy is autoimmune does not automatically mean

that any vaccine can cause the condition via molecular mimicry. Molecular mimicry is a

hypothesis whereby a specific foreign antigen may have sufficient similarity to bodily

tissue that the immune system is triggered to “cross-react” against the bodily tissue, i.e.

to attack the body itself when activated to clear the foreign antigen. (See Segal &

Shoenfeld, supra, at Ex. 85, p. 1.) Molecular mimicry “is a generally accepted scientific

principle, [but] mere invocation of the scientific term does not carry a petitioner’s burden

in a Program case.” Deshler v. Sec'y of Health & Human Servs., No. 16-1070V, 2020

WL 4593162, at *20 (Fed. Cl. Spec. Mstr. July 1, 2020) (citing Forrest v. Sec’y of Health

& Human Servs., No. 14-1046V, 2019 WL 925495, at *3 (Fed. Cl. Spec. Mstr. Jan. 18,

24

2019)). During the hearing, Dr. Shafrir agreed, noting that “[i]t’s not enough that you

say that you think it's molecular mimicry,” and explaining that asserting causation via

molecular mimicry requires demonstration that mimicry between portions of the vaccine

and components of the bodily tissue actually exists. 24 (Tr. 130-31.)

Incidences of type one narcolepsy have been shown to have increased following

the H1N1 pandemic. (Fang Han et al., Narcolepsy Onset is Seasonal and Increased

Following the 2009 H1N1 Pandemic in China, 70 ANNALS NEUROLOGY 410 (2011) (Ex. A,

Tab 8).) Further, the record evidence includes several studies associating type one

narcolepsy to a specific formulation of H1N1 pandemic strain flu vaccination called

Pandemrix. (Partinen et al., supra, at Ex. 39; Nordstrand et al., supra, at Ex. 41;

Saariaho et al., supra, at Ex. 42.) Additionally, Dr. Shafrir cited a study by Luo, et al.,

that proposed molecular mimicry between hemagglutinin within the Pandemrix vaccine

and hypocretin peptides. (Luo et al., supra, at Ex. 37.) On cross-examination, however,

he acknowledged that this study fell short of proving causality with respect to the

autoantibodies it identified. (Tr. 108-09). A later study by Vuorela, et al., filed by

respondent, also showed a pathogenic, cross-reactive role for influenza virus-specific T

cells from the Pandemrix vaccine in causing type one narcolepsy. (A. Vuorela et al.,

Enhanced Influenza A H1N1 T Cell Epitope Recognition and Cross-Reactivity to

Protein-O-Mannosyltransferase 1 in Pandemrix-Associated Narcolepsy Type 1, 12

NATURE COMMC’N 1 (2021) (Ex. C, Tab 6).) However, Vuorela, et al., implicated a

different autoantigen (protein-O-mannosyltransferase 1) for the first time. The Vuorela

authors otherwise noted Luo, et al, cited by Dr. Shafrir, to be among a body of

conflicting literature regarding the cross-reactive potential of certain hypocretin epitopes.

(Vuorela et al., supra, at Ex. C, Tab 6, p. 9.) Thus, even despite submitting the Vuorela,

et al., study, Dr. Evans opines that the available evidence falls short of demonstrating

molecular mimicry as a cause of Pandemrix-related type one narcolepsy, especially

because an autoantigen has not been clearly identified. (Tr. 176.)

But in any event, safety reviews examining a number of different H1N1 pandemic

flu vaccines confirmed that the elevated risk of narcolepsy was specific to the

Pandemrix formulation. (Tomi O. Sarkanen et al., Incidence of Narcolepsy After H1N1

Influenza and Vaccinations: Systematic Review and Meta-Analysis, 38 SLEEP MED.

REVS. 177 (2018) (Ex. A, Tab 16); Claudia Maria Trombetta et al., Influenza Vaccines:

24

In point of fact, prior caselaw in this program persuasively establishes that identifying a mimic (i.e.

homology) alone is not sufficient to meet a petitioner’s burden of proof. Specifically, “the finding of

sequence homology does not necessarily mean the similarity has significance to the immune system.”

Tullio v. Sec'y of Health & Human Servs., No. 15-51V, 2019 WL 7580149, at *15 (Fed. Cl. Spec. Mstr.

Dec. 19, 2019), aff’d, 149 Fed. Cl. 448 (2020); see also Caredio ex re. D.C. v. Sec'y of Health & Human

Servs., No. 17-0079V, 2021 WL 4100294, at *31 (Fed. Cl. Spec. Mstr. July 30, 2021) (“demonstration of

homology alone is not enough to establish a preponderant causation theory”) (emphasis in original) (citing

Schultz v. Sec'y of Health & Human Servs., No. 16-539V, 2020 WL 1039161, at *22 n. 24 (Fed. Cl. Spec.

Mstr. Jan. 24, 2020), mot. for rev. denied, 2021 WL 6058835 (Fed. Cl. Dec. 3, 2021). Nonetheless,

petitioners in this program are not required to prove their theories to the level of scientific certainty. Prior

cases have expressed with regard to the application of molecular mimicry that “[t]he line must be drawn

somewhere between speculation and certainty.” Brayboy v. Sec'y of Health & Human Servs., No. 15-

183V, 2021 WL 4453146, at *19 (Fed. Cl. Spec. Mstr. Aug. 30, 2021).

25

Evaluation of the Safety Profile, 14 HUM. VACCINES & IMMUNOTHERAPEUTICS 657 (2018)

(Ex. A, Tab 19).) One possible explanation for this is that the Pandemrix vaccine was

unique with respect to the adjuvant it used. (See Partinen et al., supra, at Ex. 39, p. 7-

8.) In that regard, the material Dr. Shafrir relies upon regarding molecular mimicry

stresses the possible role of adjuvants in explaining autoimmunity. (Agmon-Levin et al.,

supra, at Ex. 84.) Thus, Dr. Shafrir does specifically opine that only the minority of

vaccinees who received “the offensive adjuvant” actually developed narcolepsy. (Ex.

24, pp. 49-50.) Dr. Sharir also suggested that the Pandemrix vaccine may have had a

higher dose of antigen as compared to other pandemic vaccines. (Tr. 114.)

In light of all this, there is no basis on this record for suggesting that the evidence

pertaining to Pandemrix-caused narcolepsy is in any way generalizable to other

vaccines, even other formulations of the flu vaccine. Petitioner’s own expert opines that

the causal relationship at issue is likely due to the specific formulation of the Pandemrix

vaccine, which is not the vaccine petitioner received. (Ex. 25, pp. 49-50.) Nor, based

on the expert testimony available in this case, is it even necessarily clear that the

above-discussed literature establishes that molecular mimicry is the actual explanation

for Pandemrix-caused narcolepsy. While both Vuorela, et al., and Luo, et al., provide

some evidence supporting a molecular mimicry theory, the two studies are in tension in

that each study identifies a different pathway. Ultimately, neither expert suggests the

mechanism of causation is understood. (Vuorela et al., supra, at Ex. C, Tab 6; Luo et

al., supra, at Ex. 37; Ex. 25, p. 49; Tr. 176.) In fact, while petitioner is not obligated to

prove a mechanism, it is worth nothing that Dr. Shafrir’s own characterization is that we

are “far” from understanding the full mechanism of Pandemrix-caused narcolepsy. (Ex.

25, p. 49.) And, in any event, both the Vuorela and Luo studies were specific to the

Pandemrix formulation of the H1N1 vaccine. (Vuorela et al., supra, at Ex. C, Tab 6; Luo

et al., supra, at Ex. 37.)

Accordingly, for all these reasons, Dr. Shafrir has not presented a sound and

reliable opinion theorizing that either the seasonal flu or MMR vaccines (as opposed to

the Pandemrix vaccine) can cause narcolepsy. 25 This is a threshold issue that is fatal to

Dr. Shafrir’s theory, because he very clearly acknowledges that of all the conditions he

has discussed, narcolepsy has the strongest supporting evidence and that it is only or

25

Several prior decisions have similarly held that petitioners failed to preponderantly establish a theory of

causation implicating the seasonal flu vaccine as a cause of narcolepsy. D’Tiole v. Sec’y of Health &

Human Servs., No. 15-85V, 2016 WL 7664475 (Fed Cl. Spec. Mstr. Nov. 28, 2016), mot. rev. den’d, 132

Fed Cl. 421 (2017), aff’d 726 Fed.Appx. 809 (Fed. Cir. 2018); McCollum v. Sec’y of Health & Human

Servs., No. 14-790V, 2017 WL 5386613 (Fed Cl. Spec. Mstr. Sept. 15, 2017), mot. rev. den’d 135 Fed.

Cl. 735, aff’d 760 Fed.Appx. 1003 (Fed. Cir. 2019); Dougherty v. Sec’y of Health & Human Servs., No.

15-1333V, 2018 WL 3989519 (Fed. Cl. Spec. Mstr. July 5, 2018), mot. rev. den’d 141 Fed. Cl. 223

(2018); but see Henkel ex rel. V.H. v. Sec’y of Health & Human Servs., No. 15-1048V, 2022 WL

16557979 (Fed. Cl. Spec. Mstr. Aug. 31, 2022), mot. rev. den’d 165 Fed. Cl. 153 (2023). In the one prior

case in which a petitioner did preponderantly establish a theory of causation linking the flu vaccine to

narcolepsy, the petitioner’s expert provided a substantially more detailed showing of molecular mimicry

than what is available on this record, including specific demonstration of a proposed homology. Henkel,

2022 WL 16557979, at *35-43. Dr. Shafrir’s theory in this case, while involving the same basic assertion,

is not supported to anything close to the same degree.

26

primarily his ability to identify vaccine-caused narcolepsy that permits him to theorize

that the remainder of petitioner’s alleged conditions were also vaccine-caused. (Tr. 58-

59, 97-99.)

Even assuming arguendo that Dr. Shafrir had been persuasive in contending that

the vaccine(s) at issue can cause narcolepsy, his second premise – that epitope

spreading and bystander activation can explain how one autoimmune process can

cause all of the other autoimmune conditions alleged – is likewise entirely unsupported

on this record. As with molecular mimicry, there is no debate that these are valid

scientific principles in the abstract. Dr. Evans agrees that it is “possible but not proven”

that these concepts could explain the presence of the multiple autoimmune conditions

allegedly at issue. (Tr. 176.) However, Dr. Shafrir has not presented any support for

the notion that either bystander activation or epitope spreading have been shown to be

possible causes of any of the specific conditions at issue in this case, either alone or in

combination. 26 Moreover, the specific papers Dr. Shafrir cites when invoking bystander

activation and epitope spreading do not assert, let alone substantiate, that these

concepts would work synergistically to cause a constellation of otherwise distinct

autoimmune conditions in the manner Dr. Shafrir proposes. (Ex. 25, p. 50 (citing

Agmon-Levin et al., supra, at Ex. 84; Segal & Shoenfeld, supra, at Ex. 85).) Rather,

these papers reflect discussion of these mechanisms as various possible mechanisms

that may or may not separately explain individual autoimmune conditions. (Agmon-

Levin et al., supra, at Ex. 84; Segal & Shoenfeld, supra, at Ex. 85.) On the whole, they

reflect that autoimmune conditions are influenced by many factors that are not well

understood. The fact that a person may be prone to autoimmunity or experience

multiple autoimmune conditions does not automatically lead to the conclusion that the

one autoimmune condition is causally related the other(s).

In that regard, Dr. Shafrir’s third premise reveals the speculative nature of his

theory overall. In effect, Dr. Shafrir opines that the presence of one autoimmune

condition in itself simply raises a suspicion that the same autoimmune process also

explains any other condition or symptoms petitioner may have. (Ex. 25, p. 46.) Dr.

Shafrir suggests that autoimmune diseases can be widespread, have broad diagnostic

criteria, and “we have absolutely no idea why certain autoimmune diseases affect one

place and not another place.” (Tr. 61.) Thus, Dr. Shafrir testified that

this is practically a basis tenet in medical thinking, medical reasoning, that

you try to explain an entire syndrome with a unified diagnosis. So looking

at this unified diagnosis, and knowing that at least one of her diagnoses,

narcolepsy, is an autoimmune disease, and . . . we do not have any other

explanation for this, you have to assume that autoimmune process was a

cause of her other – the other component of her syndrome.

26

By way of counter example, although the above-discussed Pandemrix vaccine has been shown to

cause narcolepsy, Dr. Harris cited a largescale epidemiologic study that nonetheless found no increased

risk of epileptic seizures following that vaccine. (Lisen Arnheim Dahlstrom et al., Risk of Presentation to

Hospital with Epileptic Seizures After Vaccination with Monovalent AS03 Adjuvanted Pandemic A/H1N1

2009 Influenza Vaccine (Pandemrix): Self Controlled Case Series Study, 345 BRIT. MED. J. 1 (2012) (Ex.

A, Tab 1).)

27

(Tr. 59.)

Dr. Shafrir’s opinion on this point is self-contradictory. Dr. Shafrir’s reasoning is

based on the idea that a unifying diagnosis is preferred; however, he is clear in opining

that petitioner does not have any unifying diagnosis that he can identify. Instead, he

explicitly invokes several distinct diagnoses to explain her clinical presentation. 27 As

discussed separately above, for most of the conditions at issue there is not

preponderant evidence that they are autoimmune and the reasons for suspecting an

autoimmune process are different in each instance. (See n. 6-10 (chronic fatigue

syndrome), n. 12 (POTS, n. 13 (epilepsy), and n. 14 (fibromyalgia), supra.) Once Dr.

Shafrir resorts to invoking multiple diagnoses to explain the overall clinical presentation,

he has provided no scientific or medical explanation that would justify setting aside the

finer etiologic understanding of each separate condition in favor of a unified syndrome

for which no diagnosis exists. During the hearing, Dr. Shafrir acknowledged he is

effectively proposing a novel syndrome that has never been described in literature or

even identified by a single case report as vaccine caused. (Tr. 133-34.) To the extent

Dr. Shafrir suggested that chronic fatigue syndrome could be a likely, if incomplete,

unifying diagnosis, he has not preponderantly established that it is in itself an

autoimmune condition or, even if it were, that it can be caused by vaccination. (See n.

6-10, supra.) When none of the conditions singularly have any strong suspicion of

vaccine-causation there is no basis for then contending that they should somehow in

combination support a different or stronger conclusion.

Dr. Shafrir’s explicit testimony is that he is merely “assum[ing]” that if one

identified condition has a known mechanism, then that mechanism must also explain

petitioner’s entire picture of health. (Tr. 58-59.) On cross-examination, he specifically

testified that “we have several conditions that are presumably autoimmune and I explain

why, and then in one of them we have a good explanation so I make the assumption

that it’s the same process in the other, where the mechanism is not known.” (Tr. 107-

08.) Even accounting for the fact that petitioner is not obligated to specifically prove an

underlying mechanism, this is clearly speculative. Dr. Shafrir is seeking to leverage the

shortcomings of our understanding of these conditions as affirmative evidence of a

single underlying cause. However, this is simply not credible. The limits of our

understanding of these conditions are the limits of our understanding, not evidence

supporting some other hypothesis. As Dr. Shafrir himself puts it, “we have absolutely

no idea why certain autoimmune diseases affect one place and not another place.” (Tr.

61 (emphasis added).) The fact that petitioner’s clinical presentation otherwise remains

27

Petitioner explicitly confirmed this understanding in her prehearing reply brief. Respondent had argued

that Dr. Shafrir’s failure to identify a diagnosed beyond an “autoimmune process” broadly meant that no

Althen analysis was necessary in this case due to the lack of an identified injury. (ECF No. 99, pp. 23-25

(citing Ex. 25, p. 49).) In reply, petitioner argued that “both Dr. Shafrir and Petitioner’s treating doctors

have in fact provided Petitioner with clear diagnoses.” (ECF No. 101, p., 3 (emphasis added).) Note the

plural. Petitioner continued, “Dr. Shafrir’s statement regarding an ‘autoimmune process’ was not meant to

be the be-all end-all diagnosis in his opinion, but rather just a statement made in trying to create a

‘unifying’ or umbrella term to demonstrate his opinion that all of Petitioner’s issues were derived from the

vaccination events.” (Id.)

28

enigmatic does not mean that Dr. Shafrir’s proffered explanation is either sound or

reliable. Nothing requires the acceptance of an expert’s conclusion “connected to

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

an analytical gap between the data and the opinion proffered.” Snyder ex. rel Snyder v.

Sec’y of Health & Human Servs., 88 Fed. Cl. 706, 743 (2009) (quoting Gen. Elec. Co. v.

Joiner, 522 U.S. 136, 146 (1997)); see also Isaac v. Sec’y of Health & Human Servs.,

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

rev. denied, 108 Fed. Cl. 743 (2013), aff’d, 540 F. Appx. 999 (Fed. Cir. 2013).

For all these reasons, Dr. Shafrir fails to preponderantly establish not only that

the vaccines at issue can cause narcolepsy, but also that autoimmune narcolepsy, if

present, can in itself help to explain petitioner’s broader constellation of symptoms.

Accordingly, petitioner has not met her burden of proof under Althen prong one. And,

importantly, this analysis stands regardless of whether Dr. Shafrir can separately

establish that petitioner actually suffers any of the specific conditions he asserts.

b. 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 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. 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, 88 Fed. Cl. at

746 n. 67 (“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.”) 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 v. Sec’y of Health & Human Servs., 88 F.4th 958, 963 (Fed. Cir.

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

As discussed under Althen prong one, the crux of petitioner’s theory is that she

can demonstrate her entire clinical presentation to be vaccine-caused because, among

her various conditions, she suffers autoimmune narcolepsy for which the Pandemrix flu

vaccine has been implicated as a cause. However, even without resolving the experts’

differences regarding whether petitioner can actually be diagnosed with type one

narcolepsy specifically, petitioner’s negative test for the DQB1*0602 allele is highly

relevant and virtually fatal in itself to petitioner’s claim.

Dr. Evans cited literature supporting the idea that the DQB1*0602 allele is

present in an overwhelming proportion of type one narcolepsy patients, about 98%.

(Ex. A, p. 8; Tr. 156-58; Ollila et al., supra, at Ex. A, Tab 13.) Dr. Shafrir acknowledged

29

that some literature does reflect the 98% prevalence of the HLA cited by Dr. Evans, but

suggested the specific figure varies in different studies. (Tr. 71.) This is largely due to

the strictness with which cataplexy may be defined among different studies. (Watson et

al., supra, at 101, p. 5.) Thus, Dr. Shafrir countered that the allele is not necessary for

diagnosis. (Tr. 70-72.) For example, he discussed a study by Watson, et al., that found

that 58 out of 158 narcolepsy subjects did not have the particular HLA. (Id. at 71

(discussing Watson et al., supra, at 101).) Conversely, as Dr. Evans acknowledged, not

everyone who has the allele suffers type one narcolepsy even as it remains highly

prevalent among type one narcoleptics. (Id. at 156-58.)

Importantly, however, the Watson, et al., study cited by Dr. Shafrir concluded that

there is a dose response relationship between allele status and disease severity.

(Watson et al., supra, at Ex. 101, p. 4.) Thus, the study demonstrated that the

DQB1*0602 allele is not merely associated with type one narcolepsy, it is disease

modifying. (Id.) The authors therefore concluded that “[r]egardless of the diagnostic

utility of HLA genotyping, the presence of HLA-DQB1*0602 likely identified an

etiologically distinct and symptomatically more severe narcolepsy phenotype.” (Id. at 6.)

In that regard, Dr. Shafrir’s own citations reflect that genetic susceptibility is a “chief

pillar” of autoimmunity. (Segal & Shoenfeld, supra, at Ex. 85, p. 2; Agmon-Levin et al.,

supra, at Ex. 84, p. 1.) Moreover, Dr. Shafrir agreed during cross-examination that his

theory of causation depends specifically on cross-reaction between influenza and

hypocretin and that the primary studies he relies upon with respect to that showing were

all dependent upon the subjects having the DQB1*0602 allele. (Tr. 108, 130-31; see

also Luo et al., supra, at Ex. 37.) Accordingly, even if HLA-DQB1*0602-positive

narcolepsy is not coextensive with type one narcolepsy as Dr. Shafrir asserts (Tr. 215-

16), the evidence strongly suggests that it is a distinct etiologic phenotype. Further, on

this record, the Pandemrix vaccine has been implicated as a cause of only that specific

phenotype. (See Vuorela et al., supra, at Ex. C, Tab 6.)

This understanding is consistent with Dr. Shafrir’s own articulation of the science.

Dr. Shafrir specifically stated in his expert report that

One of the rare cases in which molecular mimicry was demonstrated is in

narcolepsy caused by influenza vaccine . . . However, even in the case of

narcolepsy and influenza vaccination we are far from understanding the

full mechanism. For example, only a tiny minority of the patients who

carry the major risk factor of HLA DQB1*06:02/DQA1*01:02 and received

the H1N1 vaccine with the offensive adjuvant actually developed

narcolepsy.

(Ex. 25, pp. 49-50.)

Regardless of her clinical diagnosis, petitioner’s HLA test specifically confirms

she is not within that HLA-DQB1*0602-positive phenotype of narcolepsy. Therefore,

even if Dr. Shafrir’s theory vis-à-vis narcolepsy was accepted, the fact that petitioner

tested negative for HLA-DQB1*0602 dramatically undercuts any application of Dr.

30

Shafrir’s theory of causation to petitioner’s own specific case regardless of whether it is

dispositive of diagnosis.

Further to this threshold issue, petitioner’s medical records do not support her

claim that her condition is vaccine caused. On the whole, they reflect a complicated

medical history that fails to establish any clear explanation for petitioner’s condition.

While Dr. Shafrir has many criticisms of petitioner’s treating physicians and the

healthcare system more broadly, that does not change the nature of the records the

treating physicians created or what those records actually evidence. 28 Nonetheless,

petitioner argues that her “treating physicians have hypothesized that her conditions are

directly related to her October 2105 vaccinations as there is seemingly no logical

explanation otherwise.” (ECF No. 98, p. 9 (citing Ex. 7, pp. 71, 73).) On this point

petitioner cites to Dr. Shehan’s record from March 16, 2016. Petitioner is quite right to

characterize this as merely hypothesis. Specifically, Dr. Shehan wrote of petitioner:

“She has an unusual symptom complex and this may relate to the immunizations. I am

going to have to research them a little bit to see if there is anything that makes sense.”

(Ex. 7, p. 73.) This is the only treating physician notation petitioner presents as

providing any support for vaccine causation and it is clearly inadequate to support her

burden of proof.

Another special master has previously explained that medical records may

include notations where a physician “may well be indicating a question in the physician’s

mind whether there is a causal relationship, or a suspicion that there might be a causal

relationship. However, that is quite different from an indication that such physician has

reached a conclusion concerning a causal relationship.” Stapleford v. Sec’y of Health

and Human Servs., No. 03-234V, 2009 WL 1456441, at *17 n.24 (Fed. Cl. Spec. Mstr.

May 1, 2009) (emphasis in original), aff’d, 89 Fed. Cl. 456 (2009). In this case, the fact

that Dr. Shehan had not reached a conclusion regarding vaccine causation is explicitly

confirmed by his statement that he needed to conduct further research “to see if

anything makes sense.” (Ex. 7, p. 73.) Moreover, 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). Thus, “[a] treating physician’s

recognition of a temporal relationship does not advance the analysis of causation.”

Isaac v. Sec’y of Health and Human Servs., 2012 WL 3609993, at *26. Here, even

assuming that Dr. Shehan recorded an unequivocal opinion that petitioner’s condition

was vaccine-related, his opinion as stated would still at best represent recognition that

petitioner began experiencing unusual symptoms after her vaccinations.

28

For example, Dr. Shafrir indicated that he felt petitioner should have been treated with immunotherapy

for her chronic fatigue syndrome (Tr 77-79); however, when pressed on cross-examination as to whether

that was the standard of care for chronic fatigue syndrome, Dr. Shafrir engaged in extended discussion of

what he felt the standard of care should be without ever grappling with what the standard of care actually

is for chronic fatigue syndrome. (Id. at 116-20.) It should also be noted that Dr. Shafrir’s qualification is

as a neurologist, which reduces his credibility with respect to his attempts to re-diagnose petitioner with

conditions that are not within his area of expertise. (E.g. Id. at 120-21.)

31

Petitioner otherwise relies primarily on Dr. Shafrir’s separate diagnostic opinion

to make sense of petitioner’s clinical history. In that regard, petitioner notes that while

Dr. Shafrir has identified several specific diagnoses, he also expressed that petitioner’s

symptoms “fit very well” the diagnostic criteria for chronic fatigue syndrome. (ECF No.

101, pp. 2-3.) In fact, the viability of this one diagnosis is not disputed by respondent’s

expert. (Tr. 166.) However, the presence of chronic fatigue syndrome does not help

support any logical sequence of cause-and-effect implicating petitioner’s vaccinations

as a cause of her condition(s). For the reasons discussed above, there is not

preponderant evidence either that (a) chronic fatigue syndrome is autoimmune or (b)

that, even if so, it is vaccine-triggered. (See n.6-10, supra.)

Dr. Shafrir also makes much of the idea that petitioner’s initial flu-like

presentation is causally meaningful. (Ex. 25, p. 51.) He opines this episode is better

understood as a systemic vaccine reaction and as part of petitioner’s autoimmune

process rather than an actual flu-like illness. (Id.) However, the literature he cites also

makes clear that chronic fatigue syndrome itself often begins with a presentation of flu-

like symptoms. (See IOM, supra, at Ex. 27, p. 15.) Therefore, if petitioner is properly

diagnosed with chronic fatigue syndrome as Dr. Shafrir suggests, then this is

explanation enough for the abrupt flu-like episode petitioner experienced, implicating

neither autoimmunity nor petitioner’s vaccinations.

It is also worth noting that Dr. Shafrir stressed during the hearing that his opinion

is based at least in part on the onset of all of petitioner’s conditions having been

simultaneous, characterizing it as “the main basis of my entire argument.” (Tr. 131-32.)

However, he provided no discussion whatsoever regarding whether it is actually

reasonable to opine that molecular mimicry, bystander activation, and epitope spreading

would all generate different diseases that would all manifest at the same time.

For all these reasons, petitioner has not preponderantly demonstrated any logical

sequence of cause and effect implicating either of her vaccinations as a cause of her

condition.

c. 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 disorder's etiology, it is medically

acceptable to infer causation.” Bazan v. Sec'y of Health & Human Servs., 539 F.3d

1347, 1352 (Fed. Cir. 2008). The explanation for what is a medically acceptable

timeframe must coincide with the theory of how the relevant vaccine can cause an injury

(Althen prong one's requirement). Id. at 1352; Shapiro v. Sec’y of Health & Human

Servs., 101 Fed. Cl. 532, 542 (2011), mot. for recons. den’d after remand, 105 Fed. Cl.

353 (2012), aff’d, 503 Fed. Appx. 952 (Fed. Cir. 2013); 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).

32

Here, for all the reasons discussed in the preceding sections, this case turns on

Althen prongs one and two and it is therefore not necessary to separately address

Althen prong three. Because Althen prong three coincides with Althen prong one,

petitioner’s inability to meet her burden under prong one effectively precludes her from

being able to meet her burden under Althen prong three. However, even assuming the

timing of petitioner’s flu-like episode is generally consistent with molecular mimicry

leading to autoimmune injury, it is far from clear that Dr. Shafrir is credible in stressing

the simultaneous onset of all of the conditions he has identified for the reasons

discussed under Althen prong two, above. But in any event, if petitioner did satisfy

Althen prong three, that alone would not satisfy her overall burden of proof. Veryzer v.

Sec’y of Health & Human Servs., 100 Fed. Cl. 344, 356 (2011) (explaining that a

“temporal relationship alone will not demonstrate the requisite causal link and that

petitioner must posit a medical theory causally connecting the vaccine and injury”);

Hibbard v. Sec’y of Health & Human Servs., 698 F.3d 1355, 1364-65 (Fed. Cir. 2012)

(holding the special master did not err in resolving the case pursuant to prong two when

respondent conceded that petitioner met prong three).

VI. Conclusion

Petitioner has clearly suffered and for that she has my sympathy. The fact that

this decision effectively leaves her condition unexplained is in no way meant to minimize

her condition or the impact it has had on her life. However, for all the reasons

discussed above, petitioner has not met her burden of proof with specific respect to

demonstrating that her condition (in whole or in part) was vaccine caused. Accordingly,

this case is dismissed. 29

IT IS SO ORDERED.

s/Daniel T. Horner

Daniel T. Horner

Special Master

29

In the absence of a timely-filed motion for review of this Decision, the Clerk of the Court shall enter

judgment accordingly.

33