Yalacki v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 14-278V

(Not to be published)

************************* Special Master Corcoran

MELANIE YALACKI, *

*

* Filed: January 31, 2019

Petitioner, *

* Entitlement; Hepatitis B

v. * Vaccine; Chronic Fatigue

* Syndrome (“CFS”); Postural

SECRETARY OF HEALTH AND * Orthostatic Tachycardia Syndrome

HUMAN SERVICES, * (“POTS”); Autoimmunity;

* Medically-Acceptable Timeframe.

Respondent. *

*

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

Richard Gage, Richard Gage, P.C., Cheyenne, WY, for Petitioner.

Sarah C. Duncan, U.S. Dep’t of Justice, Washington, DC, for Respondent.

DECISION DENYING ENTITLEMENT1

On April 10, 2014, Melanie Yalacki filed a Petition under the National Vaccine Injury

Compensation Program (the “Vaccine Program”2), alleging that the Hepatitis B (“Hep B”) vaccine

she received on June 2, 2011, caused her to suffer chronic fatigue syndrome (“CFS”) and/or

postural orthostatic tachycardia syndrome (“POTS”). Pet. at 1–2 (ECF No. 1).

1

Although this Decision has been formally designated “not to be published,” it will nevertheless be posted on the

United States Court of Federal Claims’ website in accordance with the E-Government Act of 2002, 44 U.S.C. § 3501

(2012). This means the Decision will be available to anyone with access to the internet. As provided by 42 U.S.C.

§ 300aa-12(d)(4)(B), however, the parties may object to the published Decision’s inclusion of certain kinds of

confidential information. Specifically, under Vaccine Rule 18(b), each party has fourteen (14) days within which to

request redaction “of any information furnished by that party: (1) that is a trade secret or commercial or financial in

substance and is privileged or confidential; or (2) that includes medical files or similar files, the disclosure of which

would constitute a clearly unwarranted invasion of privacy.” Vaccine Rule 18(b). Otherwise, the entire Decision will

be available to the public in its current form. Id.

2

The Vaccine Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660,

100 Stat. 3755 (codified as amended at 42 U.S.C. §§ 300aa-10–34 (2012)) (hereinafter “Vaccine Act” or “the Act”).

All subsequent references to sections of the Vaccine Act shall be to the pertinent subparagraph of 42 U.S.C. § 300aa.

A hearing in this matter was held on January 22–23, 2018. After consideration of the record

and testimony provided at hearing, I find that Petitioner is not entitled to a compensation award.

As discussed in more detail below, the Petitioner has not offered a reliable theory explaining how

the Hep B vaccine could cause either of her alleged injuries. In addition, there are legitimate

questions as to whether Petitioner actually suffered from CFS or POTS—but assuming that she

did, the medical record does not support the conclusion that the vaccine likely caused either injury.

The vaccination at issue was simply too remote in time from the record evidence most supportive

of either diagnosis, while the symptoms she points to that occurred closer in time to vaccination

either do not support her alleged injuries or can be explained by her pre-vaccination medical

history.

I. Factual Background

Pre-Vaccination History

Mrs. Yalacki’s medical history reflects numerous occasions on which she sought a

physician’s care. In the three years preceding the June 2011 vaccination in question, Petitioner

sought treatment for a wide variety of injuries that ranged from minor to serious. These include

(but are not limited to) muscle and joint pain, eye problems, dehydration, skin issues, and upper

respiratory infection (“URI”) symptoms.3 See generally Ex. 1, filed Apr. 11, 2014 (ECF No. 5-1).

Some of these doctor’s visits were objectively reasonable—for example, Petitioner sought care for

whiplash, a cervical sprain, and lumbar strain resulting from an April 30, 2010 car accident. Id. at

288. But overall, Mrs. Yalacki’s medical records reveal that she regularly obtained medical

assistance for general health concerns (some of which, in retrospect, do not appear to have merited

immediate attention).

The pre-vaccination medical record also establishes that the Petitioner intermittently

complained of symptoms very similar to those she allegedly experienced after receiving the Hep

3

See, e.g., Ex. 1 at 3–4 (ganglion cyst and wrist tendonitis due to hair twisting in May 2008); id. at 28 (bilateral hand

and finger pain in July 2008); id. at 55–56, 64–65, 68 (deep joint and muscle pain in the upper extremities and a scratch

on her eye from her fingernail in September 2008); id. at 80–82, 89–90 (bilateral hand and finger pain, tingling, and

burning, back pain and inflamed eyelid glands in October 2008); id. at 94–96, 102 (bilateral arm pain, hair pulling,

URI symptoms, and body aches in November 2008); id. at 104, 106–07, 110 (eye floaters, right eye “turning in,” and

feeling dehydrated after being in a sauna in December 2008); id. at 111–14 (severe body aches in January 2009); id.

at 145–46 (weeks of bilateral foot tingling and toe and calf cramps during exercise in February 2009); id. at 189–92,

197–99 (acne and neck strain in June 2009); id. at 238–39 (ankle injury in November 2009); id. at 247–49 (left knee

pain and metatarsalgia in February 2010); id. at 253, 270–73, 302–03 (acne; bilateral knee, foot, and ankle pain in

March 2010); id. at 282–83 (shin contusion in April 2010); id. at 288–92, 306–09, 321–23, 329–31, 420–21, 430–31

(car accident-related lower back and neck pain in May, June, and December 2010); id. at 316–17, 337–40, 343–45

(corneal dystrophy, dry eye syndrome, and groin pain after bike riding in June 2010); id. at 353–54, 359–60 (finger

injury and back pain in July 2010); id. at 404–05 (lower back pain in November 2010); id. at 454–58, 475–76 (allergic

reaction to bed covers, jaw pain, and lower back pain in February 2011); id. at 496–97, 500–01 (stomach ache and

lower back pain in March 2011); id. at 504–10, 523–34 (cough, shortness of breath, and lower back pain in April

2011); id. at 529–30, 539–40 (lower back pain and request for valium refill in May 2011).

2

B vaccine. For example, on June 24, 2008 (three years prior to the vaccination in question), Mrs.

Yalacki sought treatment for dizziness, nausea, shakiness, and near syncope after consuming

several doughnuts. Ex. 1 at 9–13. A few months later, on October 2, 2008, Petitioner complained

of fatigue, dizziness, nausea, and increased heart rate after taking Vicodin. Id. at 70. On four

occasions in January 2009, she reported fatigue, diffuse muscle aches, “burning in [her] chest,”

leg pain, and concern that she had lupus attributable to chemicals in her new car. Id. at 119–20,

126–27, 129–33. And two years later, on February 25, 2011, after being diagnosed with mild

anemia, Petitioner reported that she was “freaking out” and that she had “felt like passing out a

couple of times.” Id. at 482–83.4

Receipt of Hepatitis B Vaccine and Purported Immediate Reaction

On June 2, 2011, Mrs. Yalacki (then thirty-three years old) saw Laura Jarrell, M.D., at the

Kaiser Permanente5 facility in Lakewood, Colorado, to discuss treatment for chronic back pain.

Ex. 2 at 5–7, filed Apr. 11, 2014 (ECF No. 5-2). On the same date, Petitioner received her third

Hep B vaccine (the first two having been administered without incident on May 9, 2000, and

November 7, 2000). Id. at 6, 18, 39; Ex. 1 at 444.6

Almost immediately after, Mrs. Yalacki began reporting to treaters that she was

experiencing an adverse reaction. She phoned the Kaiser Permanente nurse advice line on the

afternoon of June 2, 2011, requesting a call back regarding body aches and fatigue. Ex. 2 at 16.

The nurse returned her call at 5:35 p.m., at which time Mrs. Yalacki stated that she was very tired

and had muscle aches, attributing her symptoms to the Hep B vaccine she had received earlier that

day. Id. Less than one hour later she called the advice line a second time, repeating her concern

that she “fe[lt] bad” after having received the Hep B vaccine. Id. at 17. She called a third time the

next morning, again expressing worries about a “vaccine reaction,” that she pinpointed as having

4

Besides seeking care for physical problems, the record reveals that in the years prior to vaccination, Petitioner also

discussed concerns regarding her mental health with treating physicians. See, e.g., Ex. 1 at 207–09 (July 15, 2009

report of depression and concern regarding short term memory loss and disorganized thoughts, which had begun years

before); id. at 367–69 (July 29, 2010 report of severe depression after stopping breastfeeding); id. at 380–81

(September 24, 2010 report of problems coping with anxiety and depression for many years, but declining

antidepressants or a mental health practitioner referral). However, Petitioner maintains that any such problems were

under control immediately prior to her receipt of the Hep B vaccine, and that she was in fact doing well mentally at

that time. Pet’r’s Post-Hr’g Br. at 2, filed Aug. 20, 2018 (ECF No. 96); Tr. at 237, 241, 392–93; see also Ex. 1 at 295

(“depression stable”), 360 (“depression stable”), 405 (anxiety stable with one dose of valium per week).

5

It appears from the medical record (which shows that Petitioner saw numerous different practitioners with the same

practice focus—for example, family medicine or cardiology) that Mrs. Yalacki did not regularly see a single primary

care physician. This may have been because her insurance was in the form of a health maintenance organization that

allowed her to see any professional available at the time.

6

It is unclear why eleven years elapsed between Petitioner’s second and third Hep B vaccinations. The Centers for

Disease Control and Prevention recommend a one-month gap between the first and second doses of Hep B, and a two-

month gap between the second and third. Immunization Schedules, Centers for Disease Control and Prevention

(Mar. 5, 2018), https://www.cdc.gov/vaccines/schedules/hcp/imz/adult.html.

3

begun within an hour and a half of the vaccine’s administration, and leaving her bed-ridden and

dizzy. Id. at 18. Based on such reports, the call log set forth an assessment of “reaction to

immunization.” Id.

Later in the day on June 3, 2011, Mrs. Yalacki returned to Dr. Jarrell based upon the alleged

reaction she had experienced the day before. Ex. 2 at 22–24. Her exam, however, was normal, with

no evidence of muscle weakness. Id. at 23. Dr. Jarrell’s diagnosis was fatigue as a possible side

effect of the vaccination, “though not compatible with allergic reaction,” adding that an unrelated

viral illness or Petitioner’s pre-vaccination anemia might be contributory factors to the symptoms

Petitioner reported. Id.

Despite Dr. Jarrell’s initial assessment, Petitioner continued to express concerns about an

ongoing reaction. Days after her appointment with Dr. Jarrell, Mrs. Yalacki called the nurse advice

line on June 6, 2011, with similar complaints about muscle weakness and fatigue that she reported

had lingered without improvement. Ex. 2 at 34. She reiterated her view that the Hep B vaccine was

the source of her symptoms. Id. That evening, a different physician, Li-Fen Lee, M.D., evaluated

Petitioner. Id. at 38. Noting that she was unable to keep her eyes open during the exam due to

fatigue, Dr. Lee ordered bloodwork. Id.

Based on Mrs. Yalacki’s demonstrated fatigue and her indications that she did not feel she

could adequately care for herself under the circumstances, Dr. Lee proposed that she go to Exempla

St. Joseph’s emergency room (“ER”). Ex. 2 at 39. There, Petitioner again reported five days of

marked fatigue since receiving the Hep B vaccine. Ex. 5 at 4, filed Apr. 11, 2014 (ECF No. 5-5).

Her exam was normal, however, and ER treaters did not propose that the vaccine was causal (or,

for that matter that any other “typical reaction to vaccine” was present). Id. at 5. Petitioner was

discharged that same evening with a diagnosis of fatigue. Id. at 5–7.

In the following days, Mrs. Yalacki continued to express alarm about her purported vaccine

reaction. Specifically, on June 7 and June 15, 2011, Petitioner again reported complaints to Dr.

Jarrell similar to what she had previously reported. See Ex. 2 at 47, 56–57. In response, Dr. Jarrell

contacted an infectious disease specialist, and reported to Petitioner that this specialist had

preliminarily stated that although mild fatigue could occur in association with vaccination,

Petitioner’s claimed symptoms were not consistent with what was ordinarily reported. Id. at 51.

Dr. Jarrell proposed additional bloodwork to check for evidence of an infection or inflammatory

disease. Id.

At her visit with Dr. Jarrell on June 15, 2011, Petitioner brought in “multiple web sites and

blog sites” for Dr. Jarrell to review about “stories of people who claim to be sick themselves or

know someone who has either been sick or died after receiving the hep B shot.” Ex. 2 at 56. Dr.

Jarrell, however, again expressed doubt that Petitioner’s symptoms had anything to do with the

4

vaccination, noting that Petitioner had received it before without incident, and that her blood tests

had raised no notable concerns. Id. at 57. She nevertheless referred Petitioner to an infectious

disease specialist for further evaluation. Id. at 57, 69. Prior to that visit, Petitioner saw Heather

Burton, M.D., on June 16, 2011. After recounting symptoms and a history much as before, Dr.

Burton proposed depression or anxiety as an explanation for Mrs. Yalacki’s condition, although

Petitioner declined to pursue mental health treatment. Id. at 87.

At. Dr. Jarrell’s referral, Mrs. Yalacki saw infectious disease specialist Miguel Mogyoros,

M.D., on June 20, 2011. Ex. 2 at 67–69. She recounted the same post-vaccination history and

symptoms as before, with Dr. Mogyoros noting that Petitioner had been “looking up vaccine side

effects in the internet and is convince[d] her symptoms are due to this vaccine.” Id. at 67.

Consistent with prior treaters, Dr. Mogyoros expressed the view that the Hep B vaccine was not

likely the source of Petitioner’s symptoms, and noted as well that bloodwork revealed no

identifiable other problems, but that Mrs. Yalacki was “not very interested” in his opinion and

seemed convinced the vaccine was causal of her alleged symptoms. Id. at 68. Any blood testing

Dr. Mogyoros performed was also negative. Id. at 72. He did, however, agree to report the claimed

reaction to the Vaccine Adverse Event Reporting System (“VAERS”). Id. at 68.

Although numerous treaters informed Petitioner in the same month she received the Hep

B vaccine that (a) they could not identify the source of her symptoms, and (b) they did not deem

it likely that the vaccine was causal of those symptoms, Mrs. Yalacki continued to seek treatment,7

including self-admission to two different hospital ERs where she informed providers of her

suspicions that the vaccine was related to her illness. See, e.g., Ex. 6 at 3–4, filed Apr. 11, 2014

(ECF No. 6-1) (June 16, 2011 visit at Porter Adventist Hospital ER; neurology work-up

recommended); Ex. 5 at 14–20 (June 18, 2011 visit to Exempla St. Joseph ER). Again, no etiology

was proposed for Petitioner’s symptoms, nor did treaters identify the Hep B vaccine as causal

(despite Petitioner’s assertions to the contrary).

After the second of these ER visits, Mrs. Yalacki received a more in-depth neurologic

work-up from Lynsee Lang, M.D., on June 22, 2011. Ex. 2 at 104–08. Around this time, Petitioner

also began to report experiencing multiple convulsion spells per day. Id. at 106. Dr. Lang noted,

however, that prior neurologic evaluations performed at ERs had discounted seizure as an

explanation for Petitioner’s condition, and an MRI produced normal results. Id. The exam was

7

Treaters also continued to propose to Mrs. Yalacki that her symptoms likely had a psychological component—an

assessment that she rejected. Thus, on June 30, 2011, Petitioner returned to Dr. Jarrell and admitted that she was

depressed, but did not want to be treated for fear of being “pigeon-holed,” and disputed the conclusion that she was

“unstable,” maintaining her belief (based on her own independent research) that the Hep B vaccine explained her

symptoms. Ex. 2 at 123–24. Dr. Jarrell nevertheless “strongly recommended” that Petitioner treat her depression

(based upon the opinion that doing so would ameliorate her symptoms), but Petitioner refused. Id. at 124. The

following month, another neurologic consult produced the opinion that Petitioner’s spells were pseudoseizures (which

are deemed psychological in origin rather than evidence of neurologic injury). Id. at 155–56; Dorland’s Illustrated

Medical Dictionary 1546 (32nd ed. 2012) (hereinafter “Dorland’s”).

5

otherwise unremarkable, as was an electroencephalogram Dr. Lang subsequently ordered. Id. at

107, 117. Dr. Lang concluded that Petitioner’s spells were unlikely true seizure activity “and could

be entirely unrelated to vaccination other than [as] a possible stressor that could have exposed this

phenomenon.” Id. at 108. Despite this work-up, Petitioner that same day requested additional

factors about her purported symptoms be added to the existing VAERS report, to “make sure other

people don’t get sick from this vaccine.” Id. at 79.

Defining Alleged Reaction as CFS or POTS

As Petitioner continued to seek medical guidance in the summer of 2011 for her alleged

vaccine-caused symptoms, she also began proposing her own characterizations of those symptoms

or exploring alternative explanations.

Thus, on July 8, 2011, Julie Cohen, M.D., consulted on Petitioner’s case. Ex. 2 at 136–37.

As before, Petitioner recounted a litany of post-vaccination symptoms, including several she had

not previously reported: cognitive delay, difficulty remembering basic words, and fainting. Id. at

136. Dr. Cohen proposed some repeated testing or seeking second opinions (for example, with

respect to the neurologic consult that Petitioner had received the month before but disputed). Id.

at 142. A few days later, however, on July 11, 2011, Mrs. Yalacki called Dr. Cohen’s office and

stated that she believed she was suffering from CFS. Id. at 146. The next day, she repeated this

assertion (although the record of her subsequent call uses the formal medical term “myalgic

encephalomyelitis” in lieu of CFS). Id. at 150.

On July 28, 2011, Dr. Cohen evaluated Petitioner for syncopal episodes that she reported

had occurred every other day for a week. Ex. 2 at 192. Dr. Cohen’s examination of Mrs. Yalacki

was unremarkable, however, and she concluded that Petitioner did not have CFS, recommending

instead that Petitioner obtain a Holter monitor evaluation8 and echocardiogram to determine an

explanation for her syncopal episodes. Id. at 192–93. Subsequent testing over the next month for

Petitioner’s convulsion-like spells confirmed that they did not meet the clinical criteria for

seizures. Ex. 8 at 25–26, filed Apr. 11, 2014 (ECF No. 6-3). Mrs. Yalacki nevertheless “continued

to hold on to the idea that these [spells] occurred as a result of the HBV vaccination (which we

feel is not the case).” Id. at 23.

On September 8, 2011, Mrs. Yalacki saw cardiologist Joseph Abruzzo, M.D. Ex. 2 at 283–

84. Again she repeated her history since receiving the Hep B vaccine. Id. at 283. The Holter

monitor test revealed sinus rhythm with heart rate ranges between 50 and 140 beats per minute

(“BPM”), and the echocardiogram was normal. Id. Dr. Abruzzo’s initial evaluation, after review

of her file and the substantial testing she has already undergone (none of which had been positive

8

Holter monitors are attached to the body and measure a subject’s heart rate over twenty-four-hour periods. Tr. at 37.

6

for any understood etiology), was that Petitioner possibly was experiencing a “[s]yndrome of

autonomic neuropathy” that was at least temporally associated with the Hep B vaccine

administration. Id. at 284.9 To test this impression, Dr. Abruzzo proposed that Mrs. Yalacki treat

what could be an orthostatic condition with “aggressive water and salt intake,” and also scheduled

her for a tilt table test (in which an individual’s orthostatic readings are continuously taken while

the subject is secured to a flat table that is then tilted up)10—the test deemed most reliable for

diagnosing POTS (see Eduardo E. Bennaroch, Postural Tachycardia Syndrome: A Heterogeneous

and Multifactorial Disorder, 87 Mayo Clinic Proc. 1214, 1220 (2012), filed as Ex. H Tab 1, June

30, 2016 (ECF No. 42-8))—for later that month. Id. The tilt table test was performed on September

20, 2011, as scheduled, and although it was terminated after thirteen minutes due to leg pain, Dr.

Abruzzo (observing that “the HR [heart rate] and BP [blood pressure] did not vary in an important

way from baseline”) concluded that it revealed no evidence of autonomic dysfunction. Ex. 5

at 84.11 Petitioner’s heart rate increased by only ten BPM over the exam period. Id.

Treater Support for Petitioner’s CFS/POTS Diagnoses

Despite the aforementioned records (which are largely unsupportive of the conclusion that

Petitioner suffered from either CFS or POTS), Petitioner did later receive treater evaluations

supportive of some of these diagnoses—although it is not clear from the record how

comprehensive or reliable these diagnoses are.

On September 27, 2011, Petitioner presented to a new primary care physician (“PCP”),

Anisa Moore, M.D. Ex. 2 at 335–36. Dr. Moore’s examination of Mrs. Yalacki produced only

normal results, but based on the history she reported (and without any indication that Dr. Moore

had reviewed the expansive prior medical record), Dr. Moore diagnosed her with CFS. Id. at 335.

In so doing, Dr. Moore noted her view that, except for the temporal requirement, Mrs. Yalacki met

9

The record from this same time period memorializes a call Mrs. Yalacki made to the nurse line in which she

represented that Dr. Abruzzi had definitively informed her that her symptoms were attributable to the Hep B vaccine,

and asked that this be documented in her record. Ex. 2 at 291. The nurse taking the call reviewed the same record

referenced above, and on that basis responded that in fact all Dr. Abruzzo had stated was that there was a temporal

relationship with the vaccine. Id.

10

The standard tilt table test entails the patient remaining in a supine position for twenty minutes, followed by ten

minutes tilted upright, and that the heart rate and blood pressure should be measured minute by minute. Tr. at 265–

66. Preparation for the test begins the day before, to ensure that the patient has consumed sufficient fluids and has not

consumed alcohol or medications that might interfere with the results. Id. at 265.

11

Also in September of 2011, a rheumatologic work-up of Petitioner (intended to evaluate arthralgias that had been

allegedly present since the Hep B vaccination) found no evidence of any joint inflammation or damage, and no signs

to suggest inflammatory arthritis, connective tissue disorder or evidence of serum sickness-like disorder. Ex. 2 at 312–

13.

7

the Center for Disease Control’s (“CDC”) criteria for CFS.12 Id. Dr. Moore did not express an

opinion as to the causal role of the Hep B vaccine, although she forthrightly did not rule out the

possibility. Id.13 Dr. Moore subsequently urged Mrs. Yalacki to obtain treatment for CFS from a

specialist, but it is not evident from the record that Petitioner ever acted on this recommendation.

Id. at 359.

Another primary care physician Petitioner consulted in October 2011—Leslie Pearson,

M.D.—also concurred that Petitioner’s self-reported symptoms described CFS, although Dr.

Pearson added that a “MH [mental health] disorder” was likely contributing to Petitioner’s

symptoms. Ex. 2 at 402–03. Like Dr. Moore, moreover, Dr. Pearson stressed the importance of

obtaining proper specialized treatment for CFS (including cognitive therapy and graduated

exercise), and Dr. Pearson refused to sign short term disability paperwork for Petitioner without

Petitioner’s agreement to actively pursue such treatment. Id. at 402.

In January 2012, Petitioner saw yet another PCP, Andrea Fedele, M.D. (who, as discussed

below, also testified at hearing). Ex. 2 at 425–28. Based on Petitioner’s subjective symptoms and

a review of the CDC criteria, Dr. Fedele confirmed the CFS diagnosis, adding that “it is most

consistent by history as due to the vaccination received on 6/2/2011.” Id. at 428. As with Dr.

Moore’s diagnostic assessment, however, it does not appear from the January record of the visit to

Dr. Fedele that she reviewed or took into account Petitioner’s detailed prior history (although she

did purport to have reviewed prior testing results). See id. at 428.

Petitioner’s condition improved substantially beginning in early March of 2012, with fewer

body aches and less fatigue, as Dr. Fedele recognized. See Ex. 2 at 457–58. By June of that year,

12

The CDC states that a CFS diagnosis requires the following: 1) “clinically evaluated, unexplained persistent or

relapsing chronic fatigue that is of new or definite onset (i.e., not lifelong), is not the result of ongoing exertion, is not

substantially alleviated by rest, and results in substantial reducation [sic] in previous levels of occupational,

educational, social, or personal activities;” and 2) “concurrent occurrence of four or more of the following symptoms:

substantial impairment in short-term memory or concentration; sore throat; tender lymph nodes; muscle pain; multi-

joint pain without swelling or redness; headaches of a new type, pattern, or severity; unrefreshing sleep; and post-

exertional malaise lasting more than 24 hours,” all of which must persist or recur over six consecutive months and

may not have predated the fatigue. Ex. 125 at 1, filed Nov. 21, 2017 (ECF No. 75-2). The CDC also includes a list of

conditions that exclude a diagnosis of CFS, including major depressive disorders with psychotic or melancholic

features, among others. Id.

13

Later on, however, Petitioner took a more pointed approach in challenging Dr. Moore’s reluctance to link the Hep

B vaccine to her symptoms. On October 7, 2011, Mrs. Yalacki and her husband returned to Dr. Moore. Ex. 2 at 358–

59. The record from this visit reveals Dr. Moore’s recollection that Petitioner was “very invested in having the treating

physician and Kaiser Permanente as a corporation acknowledge that the hepatitis B vaccine caused p[atien]t’s

symptoms and condition,” but when Dr. Moore attempted to emphasize that she considered it more important to

provide good treatment to Petitioner than to identify the etiology of a condition that could not be “undone” (as the

vaccine’s damage, if any, occurred when it was administered the prior June), Petitioner and her husband became very

angry and accusatory, insisting that their own research revealed an association, and questioning Dr. Moore’s

competence to opine on the possibility of vaccine causation. Id. at 359.

8

Petitioner was able to do basic tasks such as getting groceries, and while she experienced some

fatigue, she noted that resting helped her feel better. Id. at 465. And then at a September 19th visit,

Petitioner reported that she was doing “much better” and was “far more functional.” Id. at 472.

She was able to resume teaching first grade that fall. Id.

Mere days after that September 19, 2012 visit, however, Petitioner’s health took a dramatic

turn for the worse. See Ex. 2 at 478. She called Kaiser Permanente on September 24th, complaining

of a headache, body aches, and fatigue. Id. Dr. Fedele followed up via telephone the following

day, at which time Mrs. Yalacki reported that she had experienced a “crash” four or five days prior.

Id. at 480. She again called the Kaiser Permanente line on September 28th, stating that she had

experienced exhaustion, body aches, headaches, and pain under her arms since receiving the Hep

B vaccine in June 2011. Id. at 484. However, Dr. Fedele did not perceive Petitioner’s condition to

be as bad as it had been the previous year upon returning her call later that afternoon. Id. at 485.

Subsequent visits to various physicians did not confirm the CFS diagnosis provided by

previous treaters. For example, in November 2012 Mrs. Yalacki saw another neurologist, Julie

Seibert, M.D. (a referral from Dr. Fedele) complaining of heart palpitations. Ex. 2 at 537–39. Dr.

Seibert did not believe that Petitioner had any neurologic problems, however, nor did she see

evidence of autonomic dysreflexia, although she proposed that Petitioner consult with a

cardiologist on the latter point. Id. at 538. Mrs. Yalacki saw Dr. Abruzzo again, in February 2013,

at which time he reviewed a newer echocardiogram and Holter monitor results, noting that both

were normal. Id. at 625. He reaffirmed that Petitioner’s September 2011 tilt table test had been

negative for any possible autonomic dysfunction. Id.

Petitioner nevertheless continued to seek referrals for new neurologists and cardiologists

(based in part on her own POTS and autonomic dysreflexia research) to obtain second and third

opinions. Ex. 2 at 630. To that end, on February 26, 2013, Mrs. Yalacki saw neurologist Karen

Rollins, M.D., who, noting Mrs. Yalacki’s normal neurologic testing results, felt she did not have

anything to add. Id. at 635–40. Dr. Rollins did, however, opine that (a) Petitioner did not have

POTS, (b) her symptoms were unrelated to her June 2011 vaccination, and (c) further medical

treatment was unnecessary. Id. at 636. Significantly (and in contrast to some treater records that

were more deferential to Petitioner’s claims, without independently verifying assertions made

about her history), Dr. Rollins’s treatment record includes a more expansive walkthrough of

Petitioner’s medical history post-vaccination, including her ER visits. Id. at 637–40.

The following month, on March 5, 2013, Mrs. Yalacki saw another cardiologist, Adam

Betkowski, M.D. Ex. 2 at 665–68. He took note of Petitioner’s negative tilt table test results, but

performed his own in-clinic check of blood pressure and heart rate, measuring both while sitting

and while standing. Id. at 667. He determined that her blood pressure and heart rate changes going

from one posture to the other were enough to “suggest possibly [POTS] with possibly borderline

9

orthostatic hypertension.” Id. Dr. Betkowski noted her heart rate as around 70 BPM during a seated

physical exam, which increased to 120 to 130 BPM when she stood up. Id. Dr. Betkowski

concluded that Petitioner “likely” had POTS, but recommended additional testing (including

another tilt table test) in order to confirm the supposition. Id. at 668. Later that same month,

Petitioner’s plasma norepinephrine levels were tested, but found to be well within the normal

range. Ex. 3 at 7, filed Apr. 11, 2014 (ECF No. 5-3).14

It does not appear from the record that a second tilt table test was ever performed despite

Dr. Betkowski’s recommendation. However, one year later (after Petitioner had moved to

California from Colorado), in March 2014 Mrs. Yalacki saw a new PCP, Rebecca Smith, M.D.

Ex. 12 at 1–3, filed June 18, 2014 (ECF No. 9-2). At her initial visit with Dr. Smith, Petitioner

reported that she had in fact been diagnosed with POTS based on a tilt table test, that she had CFS,

and that she had become “very ill” on June 2, 2011 after receiving a Hep B vaccine. Id.

One month later, Petitioner saw cardiovascular physician Brett Berman, M.D. Ex. 13 at 1–

3, filed June 27, 2014 (ECF No. 10-1). She reported that she had been diagnosed with POTS in

March 2013 (presumably relying on Dr. Betkowski’s assessment based solely on standing/sitting

measurements of heart rate and blood pressure). Id. at 1. She also informed him of the prior tilt

table test performed in 2011, although Dr. Berman deemed the results “unclear” based on

Petitioner’s recollections. Id. Dr. Berman’s examination revealed a regular heart rhythm with

mitral regurgitation, and an echocardiogram performed at this time revealed “sinus rhythm at 93

with increased voltage and possible left ventricular hypertrophy with T-wave changes possibly

secondary to repolarization abnormalities.” Id. Dr. Berman’s assessment was orthostatic

hypotension, unspecified chest pain, mitral valve insufficiency/aortic valve stenosis, and

nonspecific abnormal echocardiogram. Id.

In the spring of 2014, Petitioner visited Robert Gillespie, M.D., on two occasions. Ex. 12

at 5–7, 33–35. At her first visit with him on April 18th, she informed him that she had previously

been diagnosed with POTS. Id. at 5. Dr. Gillespie performed a sit-stand test, upon which Mrs.

Yalacki’s heart rate increased by twenty-eight BPM while her blood pressure remained unchanged.

Id. at 7. Based on her self-reported history and the sit-stand test results, Dr. Gillespie opined that

she had POTS. Id. Noting that she attributed her condition to receipt of the Hep B vaccine, he

remarked that he was unfamiliar with the idea that the vaccine could be causal. Id. At her second

visit with Dr. Gillespie on May 22, 2014, Petitioner’s heart rate increased from seventy-one to

eighty-eight BPM in a sit-stand test, with her blood pressure again remaining unchanged. Ex. 12

at 34. Dr. Gillespie reiterated his view that she had POTS at this time. Id.

14

It does not appear from the medical records filed in this case that Petitioner’s plasma norepinephrine levels were

tested at any time post-vaccination before March 24, 2013. As explained by Dr. Low at hearing, such results would

have been helpful in showing whether Petitioner had POTS earlier in time. See Tr. at 277–78.

10

At Dr. Gillespie’s referral, Petitioner went to yet another cardiologist, Elizabeth Noll,

M.D., on July 2, 2014. Ex. 15 at 1–4, filed Aug. 6, 2014 (ECF No. 12-2). After performing an

initial review of the records and an examination, Dr. Noll noted that “[a]lthough the diagnosis of

POTS has been questioned, the patient has also demonstrated significant increase in heart rate

during office exams when placed in an upright position.” Id. at 1. Dr. Noll’s assessment accepted

the prior POTS diagnosis (“currently carries a diagnosis of [POTS]”), but she acknowledged that

other testing (the Holter monitor, for example) did not support the diagnosis, and that the 2011

inconclusive tilt table test “reportedly did not demonstrate the typical heart rate increase seen

within the initial phase of upright tilt,” leading her to suggest that the test should be repeated. Id.

at 3.

No further records of Petitioner’s treatment since July 2014 have been filed. It also does

not appear that Petitioner ever underwent a second tilt table test.

II. Fact and Expert Witnesses

A. Petitioner’s Witnesses

1. Mrs. Melanie Yalacki

Petitioner testified both as part of her direct case and again in rebuttal. She maintained

(somewhat contrary to the record as discussed above, at least with regard to the years immediately

prior to vaccination) that before receipt of the third Hep B shot she was “very energetic” and had

a “zest for life.” Tr. at 236. She noted in particular that she had always been motivated in her work

as a teacher. Id. at 237–39. She also testified about her passions for exercise and spending time

with family. Id. at 240. She also recalled the enthusiasm and energy she had when planning a party

for her mother prior to vaccination. Id. at 241.

After the June 2011 vaccination, however, Petitioner began to feel weak and “really tired”

in a manner that she said was unusual. Tr. at 240. Her purported change in energy and overall

health status prevented her from pursuing her career. In particular, she recalled that by the summer

of 2012 (one year after the vaccination in question) she “started to feel a little better,” and was able

to obtain accommodations from her school administration to allow her to go back to work. Id. at

242. However, her health problems made it too hard to do so. Id. at 243.

In her rebuttal testimony, Mrs. Yalacki attempted to distinguish her pre-vaccination health

status from thereafter. Thus, she recalled that immediately before the June 2011 vaccination, she

was in the process of ending the school year (which, as a teacher, meant closing down her

classroom), preparing for and hosting her son’s seventh birthday party, and organizing the

11

aforementioned party for her mother. Tr. at 391–93. She exercised on the morning she received

the Hep B vaccination, and overall she characterized her health at that time as “stellar.” Id. at 394.

2. Dr. Andrea Fedele

Dr. Fedele was the first of two treating physicians to offer testimony on Petitioner’s behalf.

She also provided a one-page opinion letter. See Ex. 17, filed Apr. 7, 2015 (ECF No. 22-1). She

testified about the circumstances of her treatment of Mrs. Yalacki in 2012–13, and specifically the

bases for the CFS diagnosis she made.

Dr. Fedele practices family medicine in Colorado for Kaiser Permanente (in particular, the

KP Foundation Health Plan), the health provider from whom Petitioner received much of the

treatment at issue in this case. Tr. at 61–62, 104.15 She provided medical services to Mrs. Yalacki

between January 2012 and April 2013. Id. at 63.

Although Dr. Fedele has seen patients with CFS in her time as a physician, treatment of

the condition is not a regular feature of her medical practice, and she admittedly lacks specialized

expertise with it. Tr. at 104. She also has no specialized training in immunology, and Mrs. Yalacki

was not her patient at the time of the 2011 vaccination at issue. Id. at 105–06.

At hearing, Dr. Fedele was questioned about her treatment of Mrs. Yalacki. Tr. at 63–83.

She confirmed that she had diagnosed Petitioner with CFS slightly more than six months after Mrs.

Yalacki received the Hep B vaccine. Id. at 63. Overall, she emphasized that her personal

examination of Mrs. Yalacki revealed (or confirmed, based on Petitioner’s self-reporting) fatigue,

post-exertional malaise, unrefreshing sleep, cognitive impairment, and orthostatic symptoms—all

of which are clinical indicia of CFS. Id. at 64, 81–84.16 She obtained those indicia, however, from

computer diagnostic information maintained by Kaiser Permanente, as opposed to her own

individual expertise in treating others with CFS. Id. at 65, 105. She also noted that, although at

certain points in 2012 Mrs. Yalacki appeared to be recovering from her CFS symptoms, these

15

Dr. Fedele’s curriculum vitae was not filed in this case.

16

On cross examination, Respondent took issue with the record evidence purported to support certain of Dr. Fedele’s

findings with respect to CFS. Thus, Dr. Fedele allowed that shortness of breath was not equivalent to post-exertional

fatigue (something Petitioner reported experiencing). Tr. at 93. She was also asked several questions about the strength

of evidence supporting the conclusion that Petitioner was experiencing “unrefreshing sleep,” acknowledging that

although Petitioner reported being bed-ridden, this was more consistent with generalized fatigue. Id. at 97. In another

instance, Dr. Fedele seemed to interpret being bed-ridden as proof of unrefreshing sleep. Id. at 74 (discussing October

22, 2012 record). Ultimately, however, because CFS can be diagnosed based on multiple criteria, I do not find that

the evidentiary strength of the CFS diagnosis turns on whether in fact Petitioner actually experienced “unrefreshing

sleep.”

12

symptoms soon returned in a way that Dr. Fedele found to be consistent with CFS. Id. at 71–72

(discussing records pertaining to successive visits to Dr. Fedele in September 2012).

Dr. Fedele’s testimony featured a review of all medical records documenting her treatment

of Petitioner throughout the relevant time period. See generally Tr. at 63–83. She frequently read

her notations in particular records aloud without additional comment. See, e.g., id. at 68, 72, 73,

75–79. However, in some instances she provided context for her notes. For example, Dr. Fedele

recalled that as of her first visit with Petitioner (on January 10, 2012), she did not have the benefit

of a complete set of Petitioner’s prior medical records. Id. at 103, 106; see also Ex. 2 at 425.

Although Dr. Fedele stressed that her own examinations of Petitioner revealed symptoms of CFS,

she admitted that records establishing similar symptoms before vaccination would have been

relevant to the accuracy of her diagnosis. Tr. at 96. Her diagnosis was also in some respects based

on Petitioner’s self-reported symptoms; she accepted Petitioner’s reported pain rather than

verifying its sources in her examination. Id. at 94.

Dr. Fedele also addressed the issue of Petitioner’s mental condition, which she conceded

could have explained some of her symptoms such as fatigue. Tr. at 99–100. She acknowledged

that she had not confirmed whether an underlying psychological problem could have contributed

to Mrs. Yalacki’s symptoms, noting that she relied on Petitioner’s denial that she was experiencing

depression or any related condition at the time Dr. Fedele was treating her. Id. at 99. She was,

however, aware of Mrs. Yalacki’s prior treatment for depression and other mental health problems,

and allowed that evidence suggesting prior treaters had associated such underlying health mental

issues with Petitioner’s symptoms was relevant to the CFS diagnosis. Id. at 101–02.

In addition to her testimony (and despite her admitted lack of immunologic expertise), Dr.

Fedele also offered a written letter supporting vaccine causation. See Ex. 17. At trial, however, she

admitted that, although her letter assumed vaccine causation based on the onset of Petitioner’s

symptoms shortly after receiving the Hep B vaccine, she could not establish causality from a

medical or scientific standpoint. Tr. at 83, 92–93, 106–07. In addition, although Dr. Fedele noted

that symptoms experienced by Petitioner before vaccination might be distinguishable from those

she experienced came after, she agreed that the Hep B vaccine could not logically be deemed

causal of any pre-vaccination symptoms. Id. at 108, 109.

3. Dr. Robert Gillespie

Dr. Gillespie was one of the treating cardiologists Petitioner saw in 2014, after she moved

to California. He did not provide a written report, but testified at hearing in support of the

contention that Petitioner was accurately diagnosed with POTS. Tr. at 167–68.

Dr. Gillespie received his B.S. from the University of California-Los Angeles (“UCLA”)

and his M.D. from the University of Chicago, then completed a residency at Loyola University

Medical Center in Maywood, Illinois, followed by a fellowship in cardiovascular medicine at

13

UCLA. Ex. 132 at 1–2, filed Dec. 22, 2017 (ECF No. 80-1). He specializes in cardiovascular

disease, and his practice is based in San Diego, California. Tr. at 165–66. He acknowledged that

he lacks specialized expertise in POTS, although he has diagnosed it and felt that his overall

experience with heart issues made him competent to render an opinion in this case as to its

applicability to Petitioner. Id. at 179.

Dr. Gillespie only saw Mrs. Yalacki on two occasions, both in 2014, and he recalled having

her as a patient. Tr. at 167, 170–71. During the first visit in April 2014, Petitioner informed Dr.

Gillespie that she had previously been diagnosed with POTS. Id. at 169. As he did not possess all

of her prior medical records at the time of this initial visit, Dr. Gillespie attempted to confirm the

diagnosis, and therefore sought to perform a sit-stand test to measure orthostatic hypotension (a

drop in blood pressure) and any heart rate increase when Petitioner stood up (in comparison to

readings obtained while she was seated). Tr. at 169–70; Ex. 12 at 6–7. The orthostatic readings

revealed no substantive change in blood pressure, but Petitioner did display a heart rate increase

of twenty-eight BPM and became symptomatic—that is, she felt so faint upon standing that she

had to lie down. Tr. at 170, 179–80. In Dr. Gillespie’s view, these results were consistent with a

POTS diagnosis, although he allowed that the heart rate increase was just under the thirty BPM

requirement for the diagnosis, and that his records from that visit did not corroborate his

recollection of Petitioner being symptomatic after standing. Id. at 179–80.

Dr. Gillespie next saw Petitioner in May 2014. Tr. at 171. She provided him with her past

medical records at this visit, which he reviewed briefly in in conjunction with his examination of

her. Id. At this visit, Petitioner showed a heart rate increase on standing of only eighteen beats per

minute. Id. at 182; Ex. 12 at 33 (showing heart rate increase from seventy-one BPM when seated

to eighty-eight BPM when standing). Dr. Gillespie nonetheless found this increase sufficient to

seek further testing, so he referred Petitioner to Dr. Noll, an electrophysiologist, for formal

confirmation. Tr. at 172–74, 182. He did not recall, however, whether Petitioner was again

symptomatic after standing, although he surmised she likely was (as the record suggested that he

terminated the sit-stand test prematurely). Id. at 171–72, 180.

On cross examination, Dr. Gillespie was asked about the appropriateness of relying on

orthostatic readings taken from a sit-stand test as opposed to a tilt table test. He acknowledged that

the tilt table test was preferable for diagnosing POTS, but argued nevertheless that a sit-stand test

was an adequate alternative, especially when dealing with a patient like Petitioner, whose

symptoms had previously prevented her from completing her first such test in 2011. Tr. at 178–

79. He also allowed that Petitioner’s medical history allowed for the “understandable concern”

that her post-vaccination symptoms were connected to her pre-vaccination state (and in particular

admitted that deconditioning could exacerbate orthostatic intolerance symptoms), but otherwise

felt it unlikely that anxiety explained Petitioner’s overall condition. Id. at 174, 176. Overall, Dr.

14

Gillespie emphasized that his POTS diagnosis was derived from Petitioner’s actual presentation at

his two visits with her in 2014 (almost three years after vaccination). Id. at 177.

4. Dr. Yehuda Shoenfeld

Dr. Shoenfeld was the sole non-treating medical expert who testified on Petitioner’s behalf

in this case. He offered a theory explaining how the Hep B vaccine could cause POTS and CFS,

as well as an explanation of how the vaccine specifically caused Mrs. Yalacki’s claimed illnesses.

Besides his oral testimony, Dr. Shoenfeld provided a total of five reports on behalf of

Petitioner, modifying his causation theory over time in response to my preliminary determinations

about the theory’s credibility. See generally Ex. 18, filed Dec. 22, 2015 (ECF No. 29-1)

(“Shoenfeld First Rep.”); Ex. 111, filed Mar. 28, 2016 (ECF No. 33-1) (“Shoenfeld Second Rep.”);

Ex. 116, filed Jan. 30, 2017 (ECF No. 53-1); Ex. 117, filed Aug. 31, 2017 (ECF No. 57-1)

(“Shoenfeld Fourth Rep.”); Ex. 127, filed Nov. 29, 2017 (ECF No. 76-1) (“Shoenfeld Fifth

Rep.”).17 In particular, although Dr. Shoenfeld initially proposed a theory he has embraced in other

cases termed “autoimmune/inflammatory syndrome induced by adjuvants” (“ASIA”) to explain

causation, he largely abandoned it in response to my expressed skepticism of its reliability (as

discussed below). Compare Shoenfeld First Rep. at 12–13 (discussing applicability of ASIA

theory to Petitioner’s case) with Shoenfeld Fourth Rep. at 13–14 (explaining theory of causation

based solely on mechanism of molecular mimicry and with no discussion of ASIA).

Dr. Shoenfeld, an internist and clinical immunologist, identifies himself as the head of the

Center for Autoimmune Diseases, which he founded at the Sheba Medical Center in Israel.

Shoenfeld First Rep. at 1; Tr. at 9. He holds the Laura Schwarz–Kipp Chair for Research of

Autoimmune Diseases at Tel Aviv University and has published numerous peer-reviewed articles

and books, primarily in the field of autoimmune and rheumatic diseases. Shoenfeld First Rep. at 1;

Tr. at 9. He serves on the editorial board of thirty-two journals in the field of autoimmunity, and

regularly speaks at conferences centered on autoimmune issues. Shoenfeld First Rep. at 1.18

17

Petitioner also offered a sixth expert report from Dr. Shoenfeld in November 2018, ten months after the conclusion

of the hearing, and three months after both sides had filed post-trial briefs. See Ex. 134, filed Nov. 19, 2018 (ECF No.

97-1). I struck the report from the record because it was (a) untimely, (b) not filed with my permission or at my request,

and (c) was not based on newly-discovered or published literature that could itself not have been filed in a timely

fashion. Order at 2–3, dated Dec. 7, 2018 (ECF No. 101). However, even if I had allowed the report into evidence, it

would not have appreciably aided Petitioner in meeting her burden of proof. The untimely report addresses a single

issue: cross-reactivity between the Hep B vaccine and CFS/POTS based upon possible homology based on a six-

amino acid chain rather than five. Ex. 134 at 1. However, the reliability and plausibility of Petitioner’s causation theory

writ large does not turn on this point in the slightest; for even if accepted as true, it does not make it more likely than

not that any components of the Hep B vaccine could initiate any autoimmune or otherwise aberrant immune response

sufficient to cause CFS or POTS, for the numerous reasons discussed below.

18

On cross-examination, Respondent devoted many questions to undermining Dr. Shoenfeld’s credentials, reported

titles, and research topics and practices. See Tr. at 148–64. For example, Respondent sought Dr. Shoenfeld’s

acknowledgement that he is not actually employed at Sheba Hospital in Tel Aviv (id. at 148–50), that a paper he wrote

15

However, Dr. Shoenfeld does not have specialized expertise in the study or treatment of either

POTS or chronic fatigue, although he did assert that he had published articles on both. Tr. at 9.

At hearing, Dr. Shoenfeld testified about Petitioner’s claimed diagnoses of POTS and CFS,

as well as about possible causal connections between the Hep B vaccine and the two conditions.

Although the opinions he offered differed slightly when discussing each diagnosis, in either case

he opined that the Hep B vaccine could (and in this case did) cause the relevant illness via some

kind of autoimmune process. Dr. Shoenfeld explicitly termed POTS a “classic autoimmune

disease” that could be vaccine-caused. Tr. at 13. CFS, by contrast, only “smell[s] of

autoimmunity,” given the lack of direct scientific support for the position that it is autoimmune,

although he nevertheless proposed it was “probably” autoimmune in origin as well. Id. at 133–35,

208.

Dr. Shoenfeld began his testimony with a discussion of POTS, characterizing it as featuring

a rapidly increased heart rate when a person stands due to a rush of blood to the head. Tr. at 12–

13. He explained further that POTS reflects the working of the autonomic nervous system, which

controls body functions automatically, without will or knowledge on the part of the individual at

issue. Id. at 13. Several different triggers can bring about POTS, including viruses, bacteria, or

vaccines containing adjuvants. Id. at 17–18. The primary diagnostic criteria for POTS, in Dr.

Shoenfeld’s view, is an increased heart rate of at least thirty BPM upon moving from a seated or

recumbent position to standing. Id. at 25. He added, however, that some individuals may

experience a heart rate increase just shy of thirty BPM but still warrant the POTS diagnosis,

especially if the heart rate increase is accompanied by presyncope.19 Id. at 29.

Dr. Shoenfeld also briefly discussed his understanding of the two methods of diagnosing

POTS: the tilt table test and the sit-stand test. Tr. at 25–26. He characterized the tilt table test as

on the ASIA theory’s applicability to the HPV vaccine was later retracted (id. at 162–64), that he appears to serve on

the advisory board of an anti-vaccination group (the group’s website lists him as a board member) (id. at 154–56), and

that the same anti-vaccination group appears to have funded some of his research (id. at 156–62).

These attacks were somewhat successful. Because Dr. Shoenfeld’s medical expertise on immunological matters has

been demonstrated in numerous prior Vaccine Program cases (including cases I have heard personally), evidence of

personal bias or misrepresentations in his CV established by such questioning in this case (which were not established

to be intentional per se) is not enough for me to find him unqualified to testify. Nevertheless, Dr. Shoenfeld’s

combative response to this questioning, coupled with outright evasiveness in responding to certain questions regarding

his background, did reduce his overall credibility as a truthful witness.

In any event, my ultimate decision in this case turns less on Dr. Shoenfeld’s personal credibility and more on the

overall unreliability of the scientific theory he offered when weighed against the strength of Respondent’s expert

evidence. Dr. Shoenfeld is advised, however, to correct any errors in his CV of this nature if he wishes to maintain his

professional credibility as a Vaccine Program expert in future proceedings.

19

Presyncope is a feeling of faintness or lightheadedness. Balance Problems, Mayo Clinic (May 17, 2018),

https://www.mayoclinic.org/diseases-conditions/balance-problems/symptoms-causes/syc-20350474.

16

“elegant,” but deemed the sit-stand test “much more effective” and “more accurate.” Id. at 25–26,

205. In his view, a positive sit-stand test result (revealing a heart rate increase of thirty BPM or

more) would strongly confirm a POTS diagnosis, but a negative result would not rule out a POTS

diagnosis. Id. at 28. He went so far as to disparage the tilt table test, saying, “[w]hat is a tilt test? I

mean, it has a name, and it may impress lay people who are not in the medical field.” Id. at 234.

In Dr. Shoenfeld’s opinion, POTS is an autoimmune disease, a viewpoint he stated is

supported by “several papers.” Tr. at 14–15. Indeed, when questioned as to whether it was always

autoimmune in origin, he proposed that “most if not all POTS . . . cases are autoimmune [in] origin

until proven otherwise.” Id. at 227. Autoimmune disease, he explained, “is a condition in which

the immune system . . . turns toward our own body constituents.” Id. at 11. Such diseases are a

downside to an otherwise evolutionarily advantageous “aggressive immune system,” and he noted

that, as women have more aggressive immune systems than men, autoimmune diseases affect

women at a rate almost ten times higher than they do men. Id. at 11–12. Dr. Shoenfeld explained

that an antibody generated in reaction to a foreign antigen (whether presented by a live virus or

vaccine component) may be identified as pathogenic if it is directed at and affects a “functional

epitope,” or self protein structure in the body, resulting in harm or dysfunction. Id. at 15–16. The

best way to identify a pathogenic autoantibody, in his view, is to inject it into a healthy specimen

to see whether it causes disease, though he also noted that pathogenic autoantibodies can be

identified via in utero transfer from pregnant women to their children. Id. at 16.

Based on review of the record in this case, Dr. Shoenfeld opined that Petitioner in fact

suffered from POTS. Tr. at 57. In support, he referenced the results of her various sit-stand tests,

concluding that her heart rate increase of twenty-eight BPM, though admittedly below the

diagnostic criteria of thirty BPM, was nonetheless indicative of POTS. Id. at 27. This was so even

though some of Mrs. Yalacki’s testing was not completed, since the records (for example, from

Dr. Gillespie’s examination) revealed that testing was halted out of concern that Mrs. Yalacki

might faint. Id. at 51, 54. He also cited POTS diagnoses by three treating cardiologists, the fact

that Petitioner lost consciousness several times in the months following vaccination, and a high

recorded heart rate in a Holter monitor test as a basis for his opinion. Id. at 36–37, 57. By contrast,

he found her initial, negative tilt table test from 2011 to be insignificant, despite the fact that it was

performed closer in time to her receipt of the Hep B vaccine. See id. at 40.

Turning to the question of whether Petitioner’s alleged case of POTS resulted from an

autoimmune process, Dr. Shoenfeld simply (and in a somewhat circular fashion) stated that the

fact that she had the disease was strong evidence of its autoimmune nature. Tr. at 233. Because he

believes that POTS is an autoimmune disease, it follows that it has an autoimmune etiology. Id.

He did, however, cite certain literature filed in this case as supporting his contention that POTS

could be autoimmune. Shoenfeld First Rep. at 8 (citing M. Thieben, et al., Postural Orthostatic

Tachycardia Syndrome: The Mayo Clinic Experience, 82 Mayo Clinic Proc. 308 (2007), filed as

17

Ex. 43, Mar. 31, 2016 (ECF No. 34) (“Thieben”)). Thieben was a retrospective study of 152 POTS

patients seen at the Mayo Clinic over eleven years, and considered the data and test results obtained

during treatment. Thieben hypothesized that a particular autoantibody (the ganglionic

acetylcholine receptor) was associated with neuropathic cases of POTS, although by its own terms

the article does not propose or embrace Dr. Shoenfeld’s contention that POTS is in all cases an

autoimmune disease. Thieben at 308.

Consistent with the above discussion of autoantibodies, Dr. Shoenfeld proposed that the

Hep B vaccine could cause POTS through the mechanism of molecular mimicry. Tr. at 19–20. As

he explained, because of sequential/structural similarities between peptide amino acid sequences

within the viral protein components of vaccines and self protein structures in the human body,

antibodies produced in response to a vaccine might also mistakenly attack the self structures,

thereby turning the antibodies into autoantibodies and causing harm in the form of an autoimmune

disease. Id. at 20. He emphasized the role of the alum adjuvant in vaccines in aiding this process,

as it can drastically increase the production of autoantibodies. Id. at 21.20 In this case, Dr.

Shoenfeld maintained that a particular peptide sequence in the Hep B vaccine—LLLCL—has

homology with “myelin sheets of nerves,” and could therefore result in an autoantibody response

triggered by the vaccine. Id. at 23, 213–18.21 CFS, he later noted, could also be vaccine-caused

through the same mechanism. Id. at 142, 209.

Despite the above, Dr. Shoenfeld acknowledged limitations to his assertions that

Petitioner’s POTS was autoimmune in nature. Thus, he conceded that Mrs. Yalacki was never

tested for the specific autoantibodies known to be associated with POTS. Tr. at 231–32. In

addition, Dr. Shoenfeld maintained that Mrs. Yalacki had undergone plasmapheresis,22 a treatment

directed at autoimmune diseases and which purportedly brought one autoimmune POTS patient

into remission as identified in a scientific study. Id. at 17; Shoenfeld Fifth Rep. at 4 (citing J.

Hendrickson, et al., Complex Regional Pain Syndrome and Dysautonomia in a 14-Year-Old Girl

Responsive to Therapeutic Plasma Exchange, 31 J. Clinical Apheresis 368 (2016), filed as Ex. 128,

Nov. 30, 2017 (ECF No. 77-1)). But he could not point to any medical records establishing that

20

Dr. Shoenfeld did, however, attempt to maintain in so arguing that he was not re-introducing his ASIA theory

through a back door. See Tr. at 122–24.

21

Tangential to his main theory, Dr. Shoenfeld also referenced the condition of small fiber neuropathy—an illness he

acknowledged Petitioner has not been diagnosed with—as nevertheless relevant, given that it purportedly proceeds by

the same molecular mimicry mechanism proposed in this case. Shoenfeld First Rep. at 22; Tr. at 209–11. He did,

however, maintain that it is common for individuals suffering from small fiber neuropathy also to have CFS. Tr. at 212

(discussing M. Martinez-Lavín, Hypothesis: Human Papillomavirus Vaccination Syndrome—Small Fiber Neuropathy

and Dysautonomia Could Be its Underlying Pathogenesis, 34 Clinical Rheumatology 1165 (2015), filed as Ex. 86,

Mar. 31, 2016 (ECF No. 34)).

22

The process of drawing blood, removing the plasma therefrom, and replacing it with another substance, such as

albumin or type-specific fresh frozen plasma. Dorland’s at 1456.

18

Petitioner in fact received plasmapheresis, and I have found in the medical record no evidence that

such treatment occurred. Tr. at 17, 203–04. When faced with the absence of such evidence, Dr.

Shoenfeld again resorted to the same “heads I win, tails you lose” logic that he embraced when

asked about the significance of negative orthostatic testing results in Petitioner’s history, stating

that “[i]f it happened, it supports; if it didn’t happen, it does not exclude.” Id. at 204.

Another deficiency in Dr. Shoenfeld’s contentions concerning the autoimmune character

of POTS was highlighted by his attempt to explain precisely how autoantibodies allegedly

produced in response to the Hep B vaccine would cause POTS. Dr. Shoenfeld pointed to an item

of literature establishing that the gene that codes for norepinephrine transport plays a role “in

regulating the orthostatic reaction,” with the antibodies presumably interfering in some way with

the norepinephrine transporter, affecting its function and resulting in POTS. Tr. at 223, 230

(discussing J. Shannon, et al., Orthostatic Intolerance and Tachycardia Associated with

Norepinephrine-Transporter Deficiency, 342 New England J. Med. 541 (2000), filed as Ex. S, Jan.

17, 2018 (ECF No. 83-1) (“Shannon”)). Shannon compared findings between an individual known

to have orthostatic intolerance and her twin. Shannon at 541. But Dr. Shoenfeld acknowledged

that Shannon does not establish that this same transporter is harmed in the manner alleged, nor

does the article speak about the relevant autoantibodies. Tr. at 223, 225. Indeed, he expressed doubt

that the target of the autoantibody attack could even be identified (id. at 229 (“you can never know

where it might affect”)), and ultimately relied on the reflexive logic of the existence of Petitioner’s

alleged POTS as evidence that the autoimmune process he proposed had in fact occurred. Id. at

221.

Dr. Shoenfeld also maintained that, based upon his review of the medical records,

Petitioner had CFS.23 He began with review of the CDC diagnostic criteria for CFS, noting that

the condition is associated with orthostatic intolerance. Tr. at 129–30. In his view, however, some

criteria (like fatigue) are more significant to the diagnosis than others (such as memory loss). Id.

at 144. He acknowledged as well that depression can overlap with CFS, although he disputed that

the existence of depression is an exclusionary factor, and in fact maintained that a person with

depression would be susceptible to CFS, especially after vaccination. Id. at 116, 117, 131.

In his discussion of CFS, Dr. Shoenfeld conceded that the disease is not widely considered

to be autoimmune, but insisted that it “has an autoimmune flavor.” Tr. at 135. He also admitted

that no pathogenic autoantibodies have been identified in relation to CFS, but argued that it is his

expectation that such autoantibodies will likely be discovered eventually, given CFS’s “association

with other autoimmune diseases,” its “close overlap” with POTS, and the unique prevalence of

23

It is somewhat unclear whether Petitioner maintains that she suffers from both conditions or merely pleads them as

alternative injuries equally supported by the record. In her post-hearing brief, Petitioner states that she suffered from

“CFS and/or POTS.” Pet’r’s Post-Hr’g Br. at 5. Regardless, Dr. Shoenfeld expressed the opinion that both could have

a similar autoimmune character, as well as a similar vaccine-induced origin. Tr. at 142.

19

CFS among women (similar to other autoimmune diseases). Id. at 134–35. He also noted that, as

with other autoimmune diseases, CFS patents can be subject to relapse and remission. Id. at 132.

Part of Dr. Shoenfeld’s testimony involved a chronological review of Mrs. Yalacki’s post-

vaccination medical history, allowing him to point out times and occurrences that he maintained

were consistent with his causation theory. First, looking to early June 2011, he opined that onset

of POTS or CFS did not occur within ninety minutes after vaccination, contrary to Petitioner’s

statements to treaters. Rather, he characterized Petitioner’s state on June 2nd and 3rd as reflective

of a post-vaccination malaise common to any individual who receives a vaccine. Tr. at 117–18

(noting that vaccine package insert anticipates some malaise after vaccination), 120, 124–25.

Not long thereafter, however, Petitioner experienced onset of CFS and/or POTS—although

Dr. Shoenfeld equivocated greatly as to the precise date of onset. Thus, he seemed to identify

June 6, 2011—four days post-vaccination—as the date Petitioner’s CFS began, based on medical

record evidence of a significant worsening of her fatigue that he distinguished from her

immediately-reported reaction. Tr. at 136–37, 141–42, 198. He deemed such a four-day timeframe

medically acceptable, given that this was third Hep B dose Petitioner had received, prompting a

“challenge-rechallenge” effect24 more rapid (in generating antibodies responsive to vaccination)

than an individual would experience if the vaccine were being administered for the first time. Id.

at 59, 60. Subsequently, the medical record revealed ongoing progression of Petitioner’s fatigue

that Dr. Shoenfeld deemed corroborative of her later CFS diagnoses in the following year and

thereafter. Id. at 40, 138, 139.

In some of his prior written reports, however, Dr. Shoenfeld embraced Petitioner’s

immediate malaise reaction (within two hours of vaccination) as a medically acceptable timeframe

for onset of her POTS and/or CFS. Shoenfeld First Rep. at 14; Shoenfeld Fourth Rep. at 13. When

confronted with this discrepancy, Dr. Shoenfeld countered that his understanding of the case had

evolved after closer study. Tr. at 185, 199. At the same time, he maintained that Petitioner’s onset

may have begun within ninety minutes after vaccination (as the records indicate she reported to

treaters), emphasizing that the only important consideration was the fact that onset post-dated

vaccination. Id. at 191 (“[t]he start might have been immediately after the vaccine, the start might

have been several days after the vaccine, the start might have been also several weeks after the

vaccine . . . we cannot know. None of us can know. We can only assume that the vaccine caused

it”), 192, 202 (agreeing with Respondent that “no objective evidence” existed establishing when

Petitioner’s nonspecific vaccine-induced malaise ended and her CFS and/or POTS began).

24

A “challenge-rechallenge” effect occurs “when a patient who had an adverse reaction to a vaccine suffers worsened

symptoms from an additional injection of the vaccine.” Capizzano v. Sec’y of Health & Human Servs., 440 F.3d 1317,

1322 (Fed. Cir. 2006). In this case, of course, the eleven-year gap between when Mrs. Yalacki last received the Hep

B vaccine and her June 2011 dose is simply too long to give consideration to this argument (which Dr. Shoenfeld

otherwise did not linger on in his testimony).

20

With regard to onset of Petitioner’s POTS, Dr. Shoenfeld stressed that evidence of

dizziness was more probative than fatigue (although because CFS and POTS had some

symptomatic overlap, fatigue could be a POTS symptom). Tr. at 190, 194. However, he was

reluctant to attribute reports of dizziness the day after vaccination as onset of Petitioner’s POTS.

Id. at 194–96. Rather, Dr. Shoenfeld seemed more comfortable referencing symptoms that

Petitioner displayed a little more than one month later (beginning July 8, 2011) as “classically”

proof of orthostatic intolerance, with a fainting incident reported by Mrs. Yalacki to treaters on

July 28, 2011 as further evidence of her POTS. Id. at 32–33. In August and September of that year,

Petitioner’s orthostatic problems became even more evident, and were subsequently confirmed by

heart rate monitor testing. Id. at 34–36, 38–39 (deeming significant Dr. Abruzzo’s statement from

September 2011 that Petitioner might have an “autonomic neuropathy”).25

Dr. Shoenfeld disputed the existence of reasonable alternative explanations for Petitioner’s

symptoms. He noted that treaters had early on excluded the possibility of a viral infection, ongoing

inflammation, or some similar cause for her reaction and fatigue. Tr. at 126–28. However, he was

more conclusory when discussing Petitioner’s overall history, including the ample evidence of

Petitioner’s preexisting symptoms, which included not only fatigue but considerable mental health

issues that could have related to her post-vaccination condition. See, e.g., id. at 38–39 (“[t]here is

only one time, I believe, that in that file [Petitioner’s medical record] the word ‘tired’ was

mentioned before the hepatitis B”), 140 (maintaining that there is “no comparison” between

Petitioner’s pre- and post-vaccination symptoms relevant to her purported CFS or POTS

diagnoses).

B. Respondent’s Witnesses

1. Dr. Philip Low

Dr. Low filed two reports in this case and also testified at hearing. See Ex. H, filed June

30, 2016 (ECF No. 42-7); Ex. N, filed Oct. 16, 2017 (ECF No. 64-6). Dr. Low offered the opinion

that Mrs. Yalacki suffers from “severe debilitating deconditioning,” and that any associated mild

orthostatic intolerance she has experienced was solely the product of that deconditioning (which

in turn stemmed from her demonstrated anxiety). Tr. at 259, 299.

As noted in his curriculum vitae (“CV”), Dr. Low received his medical and research

doctorate degrees from the University of Sydney in Australia. Ex. I at 1, filed June 30, 2016, ECF

No. 43-7 (“Low CV”); Tr. at 249. He completed a fellowship in internal medicine with the Royal

Australian College of Physicians, as well as a neurology residency at the Mayo Clinic in Rochester,

25

Dr. Shoenfeld also attempted to diminish record proof that undermined or contradicted a POTS diagnosis. Thus,

when asked about determinations in February 2013 by Dr. Rollins that Petitioner did not likely have POTS given the

orthostatic readings she obtained, Dr. Shoenfeld demurred, arguing (as before in his testimony) that while positive

results confirmed his preferred diagnosis, negative tests did not necessarily exclude it. Tr. at 207–08.

21

Minnesota. Low CV at 1–2. Currently, Dr. Low serves as a Professor of Neurology at the Mayo

Clinic Medical School. Id. at 3. During his time at Mayo, Dr. Low has served in various

departmental and academic capacities, including as Director of the Neuroscience Laboratory,

Director of the Autonomic Reflex Laboratory (which he founded), and Chairman of the Division

of Clinical Neurophysiology. Low CV at 3–4; Tr. at 254. Dr. Low has co-authored over four

hundred items of literature in the field of autoimmunity, including many articles on POTS,

antibody-mediated autoimmune neuropathy, and orthostatic intolerance. Low CV at 9–50; Tr.

at 258. Indeed, he is a senior author or author in roughly half of the articles on POTS referenced

in Dr. Shoenfeld’s reports and filed by Petitioner. Tr. at 271. He has served on the editorial boards

of multiple journals centered on autonomic and nervous system research. Low CV at 4.

Over the past forty years, Dr. Low’s time has been divided evenly between patient practice

and research. Tr. at 255–56. During his clinical practice, which is focused on autonomic disorders,

Dr. Low estimates that he sees twenty to thirty patients per week. Id. at 256. He has treated many

patients with POTS, small fiber neuropathy, orthostatic intolerance, CFS, autoimmune disorders,

and autoimmune neuropathies. Id. at 256–57.

At hearing, Dr. Low provided extensive background information on the autonomic nervous

system. As he explained, the autonomic system controls the heart rate and blood pressure,

stabilizing both without conscious effort as people move between different postures and positions.

Tr. at 260. He defined terms relevant to autonomic nervous system dysfunction, including

autonomic neuropathy (“neuropathy due to structural damage of autonomic fibers,” with many

apparent and readily-identified symptoms). Id. at 261. Tests exist to assess possible damage to the

autonomic system, which Dr. Low himself has helped to develop. Id. at 264. He was dismissive of

the term dysautonomia, however, calling it an “almost useless term” that is frequently employed

as a catch-all when a treater “can’t think of something better” to precisely explain the source of an

orthostatic problem. Id. at 261.

Orthostatic intolerance, Dr. Low explained, is an umbrella term for conditions in which

“when you stand up, you feel bad, and if you sit down or lay down, you no longer feel bad.” Tr.

at 262–63. He distinguished between three subcategories of orthostatic intolerance: orthostatic

hypotension, in which an individual’s blood pressure drops when she stands up, unaccompanied

by a significant change in heart rate; POTS, in which the heart rate increases but blood pressure

remains unchanged when an individual stands up; and syncope, in which both the heart rate and

blood pressure undergo a delayed and sudden drop, often leading to fainting. Id. at 263. POTS, Dr.

Low stated, is not usually caused by damage to the autonomic nervous system. Id. at 270. CFS can

be associated with POTS, he noted, though the existence of chronic fatigue is not integral to a

POTS diagnosis. Id.

22

Dr. Low also provided a detailed explanation of deconditioning and its relationship to

orthostatic intolerance and POTS. He deemed it very common for POTS (and other forms of

orthostatic intolerance) to be the result of physical deconditioning,26 whether due to inactivity or

environmental demands. Tr. at 280–81. He described a study of his own, in which he found that

ninety percent of a set of POTS patients had “laboratory-proven” deconditioning. Id.; see also A.

Parsaik, et al., Deconditioning in Patients with Orthostatic Intolerance, 79 Neurology 1435 (2012),

filed as Ex. H Tab 7, June 30, 2016 (ECF No. 43-2) (Dr. Low as co-author). He also referenced

studies involving astronauts upon their return to earth as confirming the effects of the

deconditioning they experienced after spending long amounts of time in space. Tr. at 281.

Accordingly, in Dr. Low’s view, deconditioning can cause POTS (although it more commonly

leads to a “lesser degree” of orthostatic tachycardia). Id. at 281–82. He estimated that the negative

effects of deconditioning could manifest after just two weeks of physical inactivity. Id. at 282.

Dr. Low emphatically contested Dr. Shoenfeld’s view that POTS is predominantly

autoimmune in nature, supporting his position with experiences from his own research at Mayo.

Tr. at 271. Dr. Low agreed that there does exist a form of autonomic neuropathy involving a single

type of ganglionopathy-associated autoantibody, and that Thieben had observed that six of forty-

two studied subjects (or approximately fourteen percent) tested positive for this antibody. Id. at

271–72; Thieben at 311, 313. This kind of neuropathy involves structural damage to the autonomic

nervous system, resulting in POTS-like symptoms as well as many other symptoms not present in

this case (or in most POTS cases for that matter). Tr. at 272, 303–04 (listing loss of blood pressure

control, loss of bladder control, loss of ability to breathe, and tissue injury as other clinical indicia

of existence of autoimmune-mediated autonomic neuropathy). It would also be characterized by

high levels of the relevant autoantibody. Id. at 272.

But Dr. Low indicated that his own extensive research into POTS and the autonomic

nervous system had led him to question the prevalence of autoimmune-caused autonomic

neuropathy. As he explained, his study and treatment of POTS patients had generally revealed

“multiple antibodies at low titers.” Tr. at 272. In addition, Dr. Low noted that since Thieben’s

publication over ten years ago, researchers at Mayo had looked more closely into the correlation

between the autoantibodies it first observed and POTS but found “zero relationship of titer to

autoimmune failure.” Id. As a result, Dr. Low today does not routinely test POTS patients for

particular autoantibodies, “because we have not been able to demonstrate any causative antibody.”

Id. at 274. He also added that, unlike diseases widely understood to be autoimmune (for example,

Guillain-Barré syndrome), POTS cannot be effectively treated with immunosupressants or other

immune-mediating therapies like plasmapheresis. Id. at 274–75.

26

Deconditioning is “a change in cardiovascular function after prolonged periods of weightlessness.” Dorland’s

at 475.

23

There are certain clinical procedures widely recognized as appropriate for diagnosing

POTS. Tr. at 264–66. Contrary to Dr. Shoenfeld, Dr. Low opined that the tilt table test is “essential

for the diagnosis of POTS,” and that a consensus view exists in the medical community that this

is the case. Id. at 265, 297–98, 307. He deemed the sit-stand test, by contrast, “totally inadequate”

to make a formal diagnosis of POTS, although he allowed that it was a reasonable tool for treaters

to use in assessing if a potential POTS diagnosis was worthy of further investigation. Id. at 305–

06. The sit-stand test is unstandardized, and necessarily requires a patient to contract her muscles

(thereby affecting the heart rate reading), which the tilt table test largely avoids. Id. at 266–67,

305. He conceded that the tilt table test is not perfect, however, and that more accurate results

could be obtained by performing a “parachute tilt,” which entails the use of a harness. Id. at 267.

He also noted that a Holter monitor is not a useful diagnostic for POTS, as it simply measures

heart rate over time and does not discount the natural surges in heart rate that many people

experience intermittently, especially when they suffer from anxiety. Id. at 270. Besides the tilt

table test, Dr. Low routinely measures autonomic function to test for POTS, and also measures

plasma norepinephrine levels in the patient’s blood, both while sitting and standing. Id. at 269,

296–70.

Dr. Low reiterated that a measured heart rate increase of at least thirty BPM in a

standardized tilt table test is a critical diagnostic feature of POTS. Tr. at 301. He added, however,

that this is a “very low bar,” and that in addition to the sharp increase in heart rate, a POTS patient

would typically present with a high absolute heart rate as well—typically above 120 BPM. Id.

at 302. This type of heart rate increase and high absolute heart rate would be consistent over

multiple readings for a POTS patient, he noted. Id. at 301.

Based on the above, his own personal knowledge, and his review of the medical records,

Dr. Low opined that Petitioner did not likely have POTS in 2011 or 2012. Tr. at 283. Her tilt table

test (performed in September 2011) lasted for thirteen minutes, longer than the standard ten, but

her heart rate increased by only ten BPM. Id. (discussing Ex. 5 at 84). Records from that same visit

also did not reflect other symptoms of orthostatic intolerance essential for a POTS diagnosis. Id.

at 283–84. Otherwise, throughout Petitioner’s medical records over the relevant time period, there

were “too many normal type recordings” of her heart rate to substantiate a POTS diagnosis. Id.

at 301. In addition, and although not measured until 2013, Mrs. Yalacki’s plasma norepinephrine

levels also tested at normal levels. Id. at 278. At most, she experienced intermittent mild orthostatic

intolerance attributable to deconditioning. Id. at 293–94, 301. He also noted that the many heart

rate increase readings seen in the medical record and cited to as proof of POTS could equally be

attributed to Petitioner’s demonstrated long-standing anxiety. Id. at 296.

To substantiate his conclusions, Dr. Low highlighted numerous aspects of Petitioner’s

medical record. In the years before receiving the Hep B vaccine, Petitioner showed signs of an

overactive sympathetic nervous system (dizziness, nausea, etc.) on several occasions, indicating

24

possible anxiety. Tr. at 279–80 (discussing Ex. 1 at 9, 70 (June and October 2008 records)). He

deemed it common in “patients who have significant deconditioning” to display such symptoms.

Id. at 280. Dr. Low went on to characterize Petitioner’s post-vaccination symptoms beginning June

2011 as a continuation of such prior symptoms. Id. And he took particular note of some of the

neurologic evaluations Petitioner received in 2012 and 2013. Thus, Dr. Seibert deemed it unlikely

in November 2012 that Mrs. Yalacki was suffering from “autonomic dysreflexia” (which Dr. Low

characterized as featuring “storms” in which the autonomic nervous system “goes crazy”). Id. at

293 (discussing Ex. 2 at 537). Dr. Rollins similarly doubted that the existing test results and record

at the time (winter 2013) supported a POTS diagnosis. Tr. at 293 (discussing Ex. 2 at 636).

Dr. Low also reviewed some of the cardiologic exams and associated orthostatic testing

Petitioner underwent in the years after her receipt of the Hep B vaccine, concluding from these

records that there was not strong evidence supporting a POTS diagnosis. For example, he noted

that during Petitioner’s visits to Dr. Betkowski in March 2013 (almost two years after receiving

the Hep B vaccine), testing revealed a blood pressure drop on the sit-stand test—a determination

inconsistent with a POTS diagnosis, even if Petitioner’s heart rate did increase (which could, in

Dr. Low’s view, simply reveal a “healthy heart”). Tr. at 268–69, 286 (discussing Ex. 2 at 667). He

was similarly dismissive of the orthostatic readings obtained at an April 2013 visit with Dr.

Betkowski, noting that while tests revealed a “generous heart rate response,” they similarly showed

a drop in blood pressure that would not be consistent with POTS. Id. at 286–87 (discussing Ex. 2

at 702).

Dr. Gillespie’s examinations of Petitioner in 2014 (which, as noted above, Dr. Gillespie

discussed at hearing) were no more persuasive to Dr. Low of the accuracy of the POTS diagnosis.

He characterized the heart rate increase that Dr. Gillespie measured via a sit-stand test during

Petitioner’s April 2014 exam (from seventy-one to eighty-eight BPM) as “unimpressive,” and

otherwise “very typical of the changes one sees with deconditioning.” Tr. at 288–89 (discussing

Ex. 12 at 6). Indeed, the fact that Petitioner had been able to stand for a lengthy period of time

during this exam to remeasure her standing blood pressure was evidence that she was in fact

“orthostatically tolerant” as of that time. Id. at 288. Dr. Gillespie’s findings at Petitioner’s May

2014 visit were also in Dr. Low’s view unsupportive of a POTS diagnosis, as she experienced a

fairly normal heart rate increase. Id. at 298 (discussing Ex. 12 at 33–34). And at another treater’s

visit in July 2014, Petitioner displayed a modest standing absolute heart rate of 106 BPM, which

Dr. Low deemed insufficient to suggest POTS. Id. at 290 (discussing Ex. 15 at 203). At best, the

heart rate increase Petitioner displayed at this time indicated the need for a repeat of the negative

tilt table test she had received in 2011. Id. at 290–91.

Besides noting the deficiencies in the medical record for a POTS diagnosis, Dr. Low

testified that he saw no evidence in that same record supporting the conclusion that Petitioner

suffered from an autoimmune-mediated autonomic neuropathy that could have caused her POTS

25

symptoms. The medical record, he opined, did not suggest that Mrs. Yalacki had ever suffered any

injury to autonomic structures, nor did she display the secondary symptoms (in addition to

orthostatic intolerance suggestive of POTS) that would reveal the existence of such damage, such

as loss of bladder control or breathing difficulties. Tr. at 294. There is also no evidence in the

record that Petitioner tested positive for the autoantibody discussed in Thieben (and although

Petitioner may not have undergone such testing, Dr. Low suggested that this was likely due to the

fact that treaters saw no need to do so). Id. at 295.

Finally, Dr. Low addressed some specific components of Petitioner’s causation theory. In

his understanding of Dr. Shoenfeld’s testimony, Dr. Shoenfeld had proposed that an “adrenergic

antibody,” presumably produced in response to the Hep B vaccine, was the most likely mechanistic

causal element in triggering POTS. Tr. at 272. But literature offered to support this contention did

not involve an actual measurement of the antibody in question in humans. Id. (discussing H. Li, et

al., Autoimmune Basis for Postural Tachycardia Syndrome, J. Am. Heart Ass’n 1 (2014), filed as

Ex. 58, Mar. 31, 2016 (ECF No. 34) (“Li”)). Rather, the Li study evaluated the effect of an injection

of blood serum from fourteen POTS patients into animals on arteriole contractibility, concluding

that POTS could have an autoimmune pathology. Tr. at 272–73; Li at 9. Dr. Low did not accept

this finding, however, interpreting Li to be observing merely “a secondary phenomenon that occurs

in people who have sympathetic activity, either because of the disease, or because of treatment,”

not that the antibody itself was associated with causing POTS. Tr. at 273–74.

Dr. Low also criticized Dr. Shoenfeld’s reliance on Shannon, which, as noted above,

looked at the norepinephrine transporter responsible for uptake and management of adrenaline in

the blood based on a single-patient evaluation, and which Dr. Shoenfeld argued was evidence of a

plausible antigenic target for his theorized autoimmune attack. Tr. at 275–76 (discussing generally

Shannon). Normally, when a person stands, the sympathetic nerve is activated, causing the release

of norepinephrine (a kind of adrenaline specific to blood vessels), with some norepinephrine

interacting with a receptor while the rest is taken back up by the transporter. Id. at 276. Shannon

considered a single individual who experienced dysfunction of the transporter (likely due to

genetic mutation) in comparison to her healthy twin, concluding that the excess norepinephrine

that was not taken back up due to transporter failure resulted in tachycardia. Id. (discussing

Shannon at 542–44). But Dr. Low questioned the significance of Shannon, noting first that it

involved a single individual, and second that Mrs. Yalacki’s own blood norepinephrine levels were

tested in March 2013 and found to be normal, rendering Shannon’s findings immaterial. Tr. at

276–77 (discussing Ex. 3 at 7), 278 (characterizing the norepinephrine amounts measured in

Petitioner as “not the value you would expect in someone with norepinephrine transporter

blockage”).

26

2. Dr. Peter Donofrio

Peter Donofrio, M.D., provided two written reports on Respondent’s behalf and testified at

hearing. See Ex. A, filed July 27, 2015 (ECF No. 25-1); Ex. O, filed Oct. 16, 2017 (ECF No. 64-

9). Dr. Donofrio offered the opinion that Mrs. Yalacki did not have CFS, and that any post-

vaccination symptoms she did experience were most likely attributable to her prior documented

mental health problems and anxiety.

As reflected in his CV, Dr. Donofrio received his B.S. at the University of Notre Dame in

Indiana, followed by his M.D. at Ohio State University in Columbus. Ex. B at 1, filed July 27,

2015 (ECF No. 25-8) (“Donofrio CV”). He completed a three-year internal medicine residency at

Good Samaritan Hospital in Cincinnati, Ohio, followed by a three-year neurology residency at the

University of Michigan. Id. at 2. He also completed a neuromuscular fellowship at the University

of Michigan. Id. Dr. Donofrio holds board certifications in neurology, nerve conduction studies,

electromyography, and neuromuscular disorders. Tr. at 309. He currently serves as a professor of

neurology at Vanderbilt University School of Medicine in Nashville, Tennessee, and previously

worked as a professor of neurology at Wake Forest University and the University of Michigan.

Donofrio CV at 2–3. In addition to his teaching and research as a professor, he has a clinical

practice as well that takes up half of his time, seeing thirty to forty patients per week with a wide

variety of neurologic illnesses, including peripheral neuropathies, myasthenia gravis, and CFS. Tr.

at 310, 311, 314. He acknowledged, however, that he only encounters CFS a handful of times per

year. Id. at 339.

Dr. Donofrio began his testimony with a discussion of CFS. In his experience, CFS is

reasonably considered as a possible explanation for generalized symptoms of weakness and fatigue

that cannot otherwise be attributed to an identifiable neurologic or muscular problem. Tr. at 314.

Dr. Donofrio disputed that CFS has an autoimmune basis, however, maintaining that (a) no

autoantibody had ever been identified as associated with CFS, and (b) nothing was yet understood

about the “passive physiology” of the condition’s course (meaning how an autoantibody would

interfere with some body process to cause CFS from a pathological perspective). Id. at 332–33.

In analyzing whether Petitioner’s history suggested CFS as a proper diagnosis, Dr.

Donofrio discussed and elaborated upon the same CDC criteria27 reviewed by Dr. Fedele when

she diagnosed Petitioner, adding that their application also required consideration of a patient’s

27

Dr. Donofrio also briefly addressed the proposed CFS criteria articulated by the Institute of Medicine (the “IOM”),

which were released in 2015 and somewhat narrow the relevant criteria, focusing on two (post-exertional malaise and

unrefreshing sleep) over other CFS factors listed in the CDC criteria, and adding additional symptoms to the list of

relevant criteria. Tr. at 329–30 (discussing Ex. A Tab 1, filed July 27, 2015 (ECF No. 25-2)). Dr. Donofrio’s testimony

focused far more on the CDC criteria, and he opined that the IOM criteria are easier to meet, although he said he did

not discount them altogether simply for that reason. Id. at 335.

27

medical history, a physical and mental health status exam, and lab tests. Tr. at 314–15. He

emphasized that these criteria require a new onset of unexplained, persistent or relapsing fatigue

that cannot be attributed to exertion, is not alleviated by rest, and which produces deficits in the

patient’s ability to engage in her life and occupation. Id. at 315 (discussing Ex. 125 at 1). He also

underscored that included as an exclusionary criterion is evidence of “any past or current diagnosis

of major depressive disorder.” Id. at 316–17 (quoting Ex. 125 at 1).

Based upon the above, Dr. Donofrio reviewed Petitioner’s medical record at hearing in an

effort to demonstrate the basis for his opinion that she could not properly be diagnosed with CFS.

He readily admitted that the records displayed many instances in which Petitioner reported

debilitating fatigue. Tr. at 317. He questioned, however, whether any “impairment of memory”

was evident in the medical record, especially since Petitioner was very proactive in seeking

treatment and was otherwise never tested for mental deficits (procedures Dr. Donofrio deemed

easy to perform) when her fatigue was evaluated by treaters. Id. at 317–19. He also noted a lack

of evidence that Petitioner had a sore throat or swollen lymph nodes. Id. at 319. And he opined

that there was a lack of medical record evidence that Petitioner was experiencing unrefreshing

sleep. Id. at 323–24, 331. Dr. Donofrio distinguished this from mere fatigue or experiencing a

“bad” sleep occasionally, adding that differentiating fatigue from persistent unrefreshing sleep

would require careful treater inquiry. Id. at 324.

Dr. Donofrio took particular exception to the conclusion that Mrs. Yalacki demonstrated

muscle pain, noting that there was ample pre-vaccination evidence of similar symptoms that also

predated her 2011 claims of fatigue, reviewing medical records from as far back as 2008 and 2009

to support this contention. Tr. at 319–22 (discussing Ex. 1 at 56, 80, 125, 127). When asked on

cross-examination about the relevance of evidence of symptoms so long before vaccination, he

responded that the CDC criteria provide that such evidence bore on whether the aches or pain were

in fact new, and thus would be proper to consider. Id. at 334–35 (discussing Ex. 125 at 1 (CDC

criteria requires that muscle pain did not predate onset of fatigue in order to constitute a symptom

of CFS)).

Dr. Donofrio also placed emphasis on one particular exclusionary criterion: the existence

of a depressive disorder or other mental health condition. Tr. at 325.28 Thus, he observed that

28

After Respondent inquired of Dr. Donofrio’s credentials and expertise, Petitioner’s counsel objected to Dr. Donofrio

being deemed or qualified as an expert on psychiatric matters, solely based on his neurologic training and background.

Tr. at 312. I noted the reasonableness of the objection, and do not give great weight to testimony by Dr. Donofrio

intending to offer a mental health diagnosis of Mrs. Yalacki. Id. at 312–13. However, because preexisting mental

health issues bear on the appropriateness of a CFS diagnosis, and because Petitioner’s record is replete with references

to a variety of mental health problems, many of which predated vaccination, I give some consideration to such

evidence, and whether (as a treater familiar with CFS) a practitioner like Dr. Donofrio would take such matters into

account. See id. at 325 (Dr. Donofrio confirming a mental health diagnosis was not part of his opinion, even though

he considered record evidence of Petitioner’s reported mental health status in reaching his opinion as to the

appropriateness of a CFS diagnosis).

28

records from before vaccination (and even the same month thereof) to more than one year after

mentioned Petitioner’s long-standing struggles with depression and anxiety. Id. at 325–26

(discussing Ex. 2 at 550 (November 2012 record)), 326–27 (discussing Ex. 1 at 327 (September

2010 record)), 327–28 (discussing Ex. 2 at 123–24 (June 30, 2011 record where treater “strongly

recommended” depression treatment, which Petitioner refused)). He deemed the June 2011 record

especially significant, as it reflected the fact that within a month of vaccination Petitioner was

aware of the possibility that the actual source of her symptoms had nothing to do with the Hep B

vaccine. Id. at 328–29.

The fact that Petitioner also experienced intermittent improvement, as reflected in her

medical history, was further evidence to Dr. Donofrio that the CFS diagnosis was inaccurate. His

read of the medical records suggested that Mrs. Yalacki was not experiencing fatigue or other such

symptoms for approximately six months, from March until September 2012. Tr. at 331. In Dr.

Donofrio’s experience, it was unheard of for patients with CFS to experience “spontaneous six-

month remissions.” Id. at 331, 338. He did, however, admit that the severity of CFS symptoms

could wax and wane from day to day, although an intercurrent infection (a URI, for example)

might also make it mistakenly appear to an individual that her CFS had worsened. Id. at 332, 337–

38.29

3. Dr. J. Lindsay Whitton

Dr. Whitton, an immunologist, was Respondent’s third expert, offering two written reports

in addition to his hearing testimony. See Ex. E, filed June 30, 2016 (ECF No. 38-1); Ex. M, filed

Oct. 16, 2017 (ECF No. 64-1). He opined that Dr. Shoenfeld’s view that the Hep B could cause

CFS or POTS was scientifically unreliable. Tr. at 351.

As shown in his CV, Dr. Whitton received his medical degree, as well as a Ph.D. in

molecular biology, from the University of Glasgow in Scotland. Ex. G at 1, filed June 30, 2016

(ECF No. 42-6) (“Whitton CV”). He currently works as a professor at Scripps Research Institute

in La Jolla, California, where he both teaches and does research on the topics of virology and

immunology. Id.; Tr. at 343–44. His research focuses on immunologic responses to viruses,

making him very familiar with the innate and adaptive immune systems. Tr. at 347–48, 350. He

serves on the editorial board of several reputable medical journals. Whitton CV at 1–2. Although

not licensed as a medical doctor in the United States, Dr. Whitton maintained that the education

and training he had received abroad was sufficient to meet those standards had he sought licensure.

Tr. at 345–46.

29

On cross examination, Dr. Donofrio allowed that such an intercurrent infection would constitute an “immune

challenge,” raising the possibility (to the extent that a person’s existing CFS was worsened by the infection) that CFS

itself is immune-mediated. Tr. at 335–36. However, Dr. Donofrio emphasized that the impact of such an infection

would be felt by any person independent of their preexisting CFS. Id. at 336.

29

Dr. Whitton initially provided a series of definitions relevant to his opinion. He defined

“antigen” as something (usually a protein) that triggers an adaptive immune response, whether in

the form of the production of antibodies or a T cell response. Tr. at 353. Proteins are made up of

chain of amino acids, of which there total twenty standard to the human body. Id. at 353–54. A

chain of amino acids is called a peptide, and molecular mimicry can occur when a peptide in an

antigenic protein shares “homology,” or identity, with a self protein in the body, making both look

the same to any immune response (antibodies or T cells) generated in reaction to the antigen. Id.

at 355. Autoimmune disease will occur if that immune response mistakenly attacks the self protein

or structure. Id. Dr. Whitton added that the term “molecular mimicry” applies only cases actually

resulting in disease, and cautioned that it is incorrect to assume that homology between antigen

components and a self protein will invariably result in harm. Id.

With the above as backdrop, Dr. Whitton turned to Petitioner’s invocation of molecular

mimicry as a mechanism by which the Hep B vaccine could cause an autoimmune response of

some kind resulting in disease. He characterized Dr. Shoenfeld’s argument as holding that a surface

antigen of the vaccine included an amino acid peptide sequence that had homology with

components of the norepinephrine transporter, and that the unusual nature of this homology

resulted in a cross-attack by antibodies produced in response to the vaccine and causing autonomic

dysfunction sufficient to result in CFS or POTS. Tr. at 352. He noted that Dr. Shoenfeld proposed

a pentamer, or five amino acid chain sequence, was sufficient for homology to exist—but in Dr.

Whitton’s view, homology on that scale was wide-spread in the human body, and thus not rare at

all. Id. at 356–58.

In support of this view, he referenced literature confirming that homology was

“commonplace,” and the reasonable result of the fact that human proteins were comprised of a

finite set of amino acids. Tr. at 362–64 (discussing A. Silvanovich, et al., The Value of Short Amino

Acid Sequence Matches for Prediction of Protein Allergenicity, 90 Toxicological Sciences 252

(2006), filed as Ex. E Tab 5, June 30, 2016 (ECF No. 38-6)). In fact, Dr. Whitton noted, if a mere

match between a five-amino acid peptide component of an antigen and a self protein component

were enough to result in molecular mimicry, “we would be dead” from all the autoimmune cross-

reactivity that would result. Id. at 366, 377. Dr. Whitton therefore maintained that the homologous

sequences identified by Dr. Shoenfeld were “cherry picked for this case,” and amounted to

selection bias rather than verified and reliable scientific evidence of a pathologic cross-reaction

spurred by molecular mimicry. Id. at 361.

Dr. Whitton next attacked the bases for Petitioner’s argument that the norepinephrine

transporter is the target antigen for the alleged autoimmune cross-reactive process. Tr. at 366–67.

He opined that Petitioner’s normal plasma norepinephrine test result from 2013 reflected that she

does not have a defect in that protein. Id. at 367. Further, with regard to Petitioner’s argument

30

about homology between the Hep B vaccine and a specific target antigen, Dr. Whitton argued that

Petitioner had mistakenly referenced homologous epitopes from the Hep C rather than Hep B virus,

and that those that were derived from the Hep B virus were actually limited to a single homologous

epitope. Id. at 371–72. And he proposed that the homologous self-epitopes in question are not

“antibody epitopes” that would (mistakenly) recognize antibodies produced in response to the

vaccine, but T cell epitopes, meaning that they were inconsistent with Dr. Shoenfeld’s entire

theory. Id. at 373.

Dr. Whitton also spoke to the purported timeframe in which Petitioner alleges to have

experienced a vaccine reaction. Although he allowed that certain severe and immediate reactions

by the adaptive immune system to vaccination are possible in a short timeframe (for example,

anaphylaxis), he disputed that the record in this case revealed such a clear reaction. Tr. at 378. He

more definitively rejected the notion that Petitioner’s onset occurred within two hours of

vaccination, noting that even Dr. Shoenfeld allowed for the fact that post-vaccine “malaise” might

last for up to twenty-four hours. Id. at 379. In his understanding, the best models for how molecular

mimicry leads to autoimmune cross-reactions have shown that it can take six to ten days for the

antibody upregulation to occur, far longer than the short timeframes argued for by Petitioner. Id.

at 379–81. He added that he would also expect some evidence of nonspecific indicators of an

autoimmune process (such as proof of ongoing inflammation) to exist if Petitioner’s timeframe for

onset were accurate, although he admitted that such speculation on his part went beyond his

expertise in this case as an immunologist and virologist. Id. at 390.

In addition to offering an opinion specific to components of Petitioner’s causation theory,

Dr. Whitton commented on the persuasiveness of that theory in light of the evidence offered in its

support. He maintained that Petitioner had not offered broadly reliable evidence associating the

Hep B vaccine with POTS or CFS. Tr. at 382. When challenged by Petitioner to enumerate what

such evidence would look like, Dr. Whitton responded that he would need to see proof of (a) the

relevant autoantibody, (b) evidence of Mrs. Yalacki’s norepinephrine transporter protein

dysfunction, or (c) some kind of experimental study or model establishing that the Hep B vaccine

had been associated with the injuries alleged. Id. at 383–85. He also attacked Dr. Shoenfeld’s

questioning the possibility that an unidentified wild virus could have caused Petitioner’s POTS or

CFS, noting that in his view a viral infection was generally more likely to trigger disease or an

aberrant immune response than a vaccine. Id. at 387–89.

III. Procedural History

As noted above, this case was initiated in April 2014. Petitioner subsequently filed relevant

medical records, concluding the process on August 6, 2014, with the Statement of Completion

31

(ECF No. 13). Respondent’s Rule 4(c) Report was thereafter filed on October 6th (ECF No. 14),

in which Respondent challenged the appropriateness of an entitlement award.

Petitioner filed Dr. Shoenfeld’s first expert report on December 22, 2015. Noting that Dr.

Shoenfeld relied on his ASIA theory to explain vaccine causation in her case, I stated during a

status conference that other special masters have repeatedly found this theory to be unpersuasive

and scientifically unreliable. See Order, dated Jan. 5, 2016 (ECF No. 30).30 After Petitioner filed

an additional report from Dr. Shoenfeld that largely reiterated his prior statements invoking ASIA,

I again expressed my concerns to Petitioner that reliance on this theory would be inadvisable. See

Order, dated July 19, 2016 (ECF No. 47).

Petitioner subsequently filed additional expert reports from Dr. Shoenfeld that did not raise

ASIA and supporting medical literature, as well as a written evaluation from Jack Kleid, M.D.31

Respondent filed reports and literature from Drs. Low, Donofrio, and Whitton. Petitioner amended

her claim on August 31, 2017, the same day she filed her prehearing brief, arguing in the alternative

in both documents that the Hep B vaccine significantly aggravated a preexisting condition. See

Am. Pet. at 2, filed Aug. 31, 2017 (ECF No. 56); Pet’r’s Pre-Hr’g Br. at 7–14, filed Aug. 31, 2017

(ECF No. 58). Respondent submitted his prehearing brief in October of 2017, and a two-day

entitlement hearing took place on January 22–23, 2018. The parties submitted post-hearing briefs

on August 20, 2018. This case is now ripe for decision.

IV. Applicable Legal Standards

A. Claimant’s Burden in Vaccine Program Cases

To receive compensation in the Vaccine Program, a petitioner must prove either: (1) that

he suffered a “Table Injury”—i.e., an injury falling within the Vaccine Injury Table, corresponding

to one of the vaccinations in question and also occurring within a statutorily-prescribed period of

30

In my Order, I directed Petitioner’s attention to the following Vaccine Program cases in which special masters did

not accept the ASIA theory as a scientifically-reliable explanation for vaccine-caused injuries: Rowan v. Sec’y of

Health & Human Servs., No. 10-272V, 2014 WL 7465661 (Fed. Cl. Spec. Mstr. Dec. 8, 2014), mot. for review denied,

2015 WL 3562409 (Fed. Cl. June 9, 2015); D’Angiolini v. Sec’y of Health & Human Servs., No. 99-578V, 2014 WL

1678145 (Fed. Cl. Spec. Mstr. Mar. 27, 2014), mot. for review denied, 122 Fed. Cl. 86 (2015).

31

Although Dr. Kleid’s CV was not filed in this case, his report indicates that he works as an associate professor of

cardiology at the University of California San Diego. Ex. 115 at 15, filed Nov. 17, 2016 (ECF No. 50-1). Dr. Kleid’s

report contains a review of Mrs. Yalacki’s medical record, as well as a discussion of his evaluation of her. See

generally id. He conducted a form of video surveillance over three- and six-day periods in February, April, and

September of 2016. Id. at 2, 12. He proposed other diagnostic tests, including a treadmill stress test, which Petitioner

declined to undergo. Id. at 12. Based on his review of the records and the video surveillance of Mrs. Yalacki, Dr. Kleid

concluded that she suffers from POTS and CFS. Id. at 13. However, because his opinion bears only on her 2016

condition—five years after the vaccination at issue—and because he was not called to testify, I give his written opinion

very little weight.

32

time—or, in the alternative, (2) that his illnesses were actually caused by a vaccine (a “Non-Table

Injury”). See Sections 13(a)(1)(A), 11(c)(1), and 14(a), as amended by 42 C.F.R. § 100.3; see also

Shalala v. Whitecotton, 514 U.S. 268, 270 (1995) (quoting 42 U.S.C. § 11(c)(1)(C)(i)); Moberly

v. Sec’y of Health & Human Servs., 592 F.3d 1315, 1321 (Fed. Cir. 2010); Capizzano v. Sec’y of

Health & Human Servs., 440 F.3d 1317, 1320 (Fed. Cir. 2006).32 Petitioner in this case asserts

only a non-Table claim.

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

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

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

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

existence.” Moberly, 592 F.3d at 1322 n.2; see also Snowbank Enter. v. United States, 6 Cl. Ct.

476, 486 (1984) (mere conjecture or speculation is insufficient under a preponderance standard).

A petitioner may not receive a Vaccine Program award based solely on his assertions; rather, the

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

Section 13(a)(1).

When a Table Injury claim is successfully established, causation is presumed. 42 C.F.R.

§ 100.3. Table claims must satisfy with evidence the specific elements of the relevant claim,

including the definitions of terms set in the Qualifications and Aids to Interpretation (the “QAI”).

Section 14(b). Case law underscores that, to obtain the benefit of the presumption of causation

associated with a Table claim, the claim’s requirements must be strictly construed. Miller v. Sec’y

of Health & Human Servs., No. 02-235V, 2015 WL 5456093, at *24 (Fed. Cl. Spec. Mstr. Aug.

18, 2015) (requiring petitioner to satisfy the “strict Table definition” of encephalopathy).

For a non-Table claim, proof of medical certainty is not required. Bunting v. Sec’y of Health

& Human Servs., 931 F.2d 867, 873 (Fed. Cir. 1991). In such circumstances, a petitioner must

demonstrate that the vaccine was “not only [the] but-for cause of the injury but also a substantial

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

& Human Servs., 165 F.3d 1344, 1352–53 (Fed. Cir. 1999)); Pafford v. Sec’y of Health & Human

Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006). A petitioner asserting a non-Table claim must satisfy

all three of the elements established by the Federal Circuit in Althen v. Secretary of Health &

Human Services: “(1) a medical theory causally connecting the vaccination and the injury; (2) a

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

and (3) a showing of a proximate temporal relationship between vaccination and injury.” 418 F.3d

1274, 1278 (Fed. Cir. 2005).

32

Decisions of special masters (some of which I reference in this ruling) constitute persuasive but not binding

authority. Hanlon v. Sec’y of Health & Human Servs., 40 Fed. Cl. 625, 630 (1998). By contrast, Federal Circuit rulings

concerning legal issues are binding on special masters. Guillory v. Sec’y of Health & Human Servs., 59 Fed. Cl. 121,

124 (2003), aff’d, 104 F. App’x 712 (Fed. Cir. 2004); see also Spooner v. Sec’y of Health & Human Servs., No. 13-

159V, 2014 WL 504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014).

33

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

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

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

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

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

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

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

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

theory. Andreu v. Sec’y of Health & Human Servs., 569 F.3d 1367, 1378–79 (Fed. Cir. 2009)

(citing Capizzano, 440 F.3d at 1325–26). Special masters, despite their expertise, are not

empowered by statute to conclusively resolve what are essentially thorny scientific and medical

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

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

evidence standard.” Id. at 1380. Accordingly, special masters must take care not to increase the

burden placed on petitioners in offering a scientific theory linking vaccine to injury. Contreras v.

Sec’y of Health & Human Servs., 121 Fed. Cl. 230, 245 (2015), vacated on other grounds, 844

F.3d 1363 (Fed. Cir. 2017).

In discussing the evidentiary standard applicable to the first Althen prong, many decisions

of the Court of Federal Claims and Federal Circuit have emphasized that petitioners need only

establish a causation theory’s biologic plausibility (and thus need not do so with preponderant

proof). Tarsell v. United States, 133 Fed. Cl. 782, 792–93 (2017) (special master committed legal

error by requiring petitioner to establish first Althen prong by preponderance; that standard applied

only to second prong and petitioner’s overall burden); Contreras, 121 Fed. Cl. at 245

(“[p]lausibility . . . in many cases may be enough to satisfy Althen prong one” (emphasis in

original)); see also Andreu, 569 F.3d at 1375. At the same time, there is contrary authority from

the Federal Circuit suggesting that the preponderance standard applied when evaluating a

claimant’s overall success in a Vaccine Act claim also bears on the first Althen prong. See, e.g.,

Broekelschen v. Sec’y of Health & Human Servs., 618 F.3d 1339, 1350 (Fed. Cir. 2010) (affirming

special master’s determination that expert “had not provided a ‘reliable medical or scientific

explanation’ sufficient to prove by a preponderance of the evidence a medical theory linking the

[relevant vaccine to relevant injury]”) (emphasis added). Regardless, one thing remains: petitioners

always have the burden of establishing their Vaccine Act claim overall with preponderant

evidence. W.C. v. Sec’y of Health & Human Servs., 704 F.3d 1352, 1356 (Fed. Cir. 2013) (citations

omitted); Tarsell, 133 Fed. Cl. at 793 (noting that Moberly “addresses the petitioner’s overall

burden of proving causation-in-fact under the Vaccine Act” by a preponderance).

34

The second Althen prong requires proof of a logical sequence of cause and effect, usually

supported by facts derived from a petitioner’s medical records. Althen, 418 F.3d at 1278; Andreu,

569 F.3d at 1375–77; Capizzano, 440 F.3d at 1326; Grant v. Sec’y of Health & Human Servs., 956

F.2d 1144, 1148 (Fed. Cir. 1992). In establishing that a vaccine “did cause” injury, the opinions

and views of the injured party’s treating physicians are entitled to some weight. Andreu, 569 F.3d

at 1367; Capizzano, 440 F.3d at 1326 (“medical records and medical opinion testimony are favored

in vaccine cases, as treating physicians are likely to be in the best position to determine whether a

‘logical sequence of cause and effect show[s] that the vaccination was the reason for the injury’”)

(quoting Althen, 418 F.3d at 1280). Medical records are generally viewed as particularly

trustworthy evidence, since they are created contemporaneously with the treatment of the patient.

Cucuras v. Sec’y of Health & Human Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993).

However, medical records and/or statements of a treating physician’s views do not per se

bind the special master to adopt the conclusions of such an individual, even if they must be

considered and carefully evaluated. Section 13(b)(1) (providing that “[a]ny such diagnosis,

conclusion, judgment, test result, report, or summary shall not be binding on the special master or

court”); Snyder v. Sec’y of Health & Human Servs., 88 Fed. Cl. 706, 746 n.67 (2009) (“there is

nothing . . . that mandates that the testimony of a treating physician is sacrosanct—that it must be

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

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

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

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

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

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

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

Human Servs., 100 Fed. Cl. 119, 136 (2011), aff’d, 463 F. App’x 932 (Fed. Cir. 2012); Veryzer v.

Sec’y of Health & Human Servs., No. 06-522V, 2011 WL 1935813, at *17 (Fed. Cl. Spec. Mstr.

Apr. 29, 2011), mot. for review denied, 100 Fed. Cl. 344, 356 (2011), aff’d without opinion, 475

F. App’x 765 (Fed. Cir. 2012).

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

the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been equated to the

phrase “medically-acceptable temporal relationship.” Id. A petitioner must offer “preponderant

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

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

Sec’y of Health & Human Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for what

is a medically acceptable timeframe must also coincide with the theory of how the relevant vaccine

can cause an injury (Althen prong one’s requirement). Id. at 1352; Shapiro v. Sec’y of Health &

Human Servs., 101 Fed. Cl. 532, 542 (2011), recons. denied after remand, 105 Fed. Cl. 353 (2012),

aff’d mem., 2013 WL 1896173 (Fed. Cir. 2013); Koehn v. Sec’y of Health & Human Servs., No.

35

11-355V, 2013 WL 3214877 (Fed. Cl. Spec. Mstr. May 30, 2013), mot. for review denied (Fed.

Cl. Dec. 3, 2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).

B. Law Governing Factual Determinations

The process for making determinations in Vaccine Program cases regarding factual issues

begins with consideration of the medical records. Section 11(c)(2). The special master is required

to consider “all [] relevant medical and scientific evidence contained in the record,” including “any

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

record regarding the nature, causation, and aggravation of the petitioner’s illness, disability, injury,

condition, or death,” as well as “the results of any diagnostic or evaluative test which are contained

in the record and the summaries and conclusions.” Section 13(b)(1)(A). The special master is then

required to weigh the evidence presented, including contemporaneous medical records and

testimony. See Burns v. Sec’y of Health & Human Servs., 3 F.3d 415, 417 (Fed. Cir. 1993) (it is

within the special master’s discretion to determine whether to afford greater weight to

contemporaneous medical records than to other evidence, such as oral testimony surrounding the

events in question that was given at a later date, provided that such a determination is evidenced

by a rational determination).

Medical records that are created contemporaneously with the events they describe are

presumed to be accurate and “complete” (i.e., presenting all relevant information on a patient’s

health problems). Cucuras, 993 F.2d at 1528; Doe/70 v. Sec’y of Health & Human Servs., 95 Fed.

Cl. 598, 608 (2010) (“[g]iven the inconsistencies between petitioner’s testimony and his

contemporaneous medical records, the special master’s decision to rely on petitioner’s medical

records was rational and consistent with applicable law”); Rickett v. Sec’y of Health & Human

Servs., 468 F. App’x 952 (Fed. Cir. 2011) (non-precedential opinion). This presumption is based

on the linked propositions that (i) sick people visit medical professionals; (ii) sick people honestly

report their health problems to those professionals; and (iii) medical professionals record what they

are told or observe when examining their patients in as accurate a manner as possible, so that they

are aware of enough relevant facts to make appropriate treatment decisions. Sanchez v. Sec’y of

Health & Human Servs., No. 11-685V, 2013 WL 1880825, at *2 (Fed. Cl. Spec. Mstr. Apr. 10,

2013); Cucuras v. Sec’y of Health & Human Servs., 26 Cl. Ct. 537, 543 (1992), aff’d, 993 F.2d

1525 (Fed. Cir. 1993) (“[i]t strains reason to conclude that petitioners would fail to accurately

report the onset of their daughter’s symptoms. It is equally unlikely that pediatric neurologists,

who are trained in taking medical histories concerning the onset of neurologically significant

symptoms, would consistently but erroneously report the onset of seizures a week after they in fact

occurred”).

Accordingly, if the medical records are clear, consistent, and complete, then they should

be afforded substantial weight. Lowrie v. Sec’y of Health & Human Servs., No. 03-1585V, 2005

36

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

records are generally found to be deserving of greater evidentiary weight than oral testimony—

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

see also Murphy v. Sec’y of Health & Human Servs., 23 Cl. Ct. 726, 733 (1991), aff’d, 968 F.2d

1226 (Fed. Cir.), cert. denied sub nom. Murphy v. Sullivan, 506 U.S. 974 (1992) (citing United

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

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

weight”)).

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

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

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

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

the factual predicates for its application are weak or lacking”); Lowrie, 2005 WL 6117475, at *19

(“[w]ritten records which are, themselves, inconsistent, should be accorded less deference than

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

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

testimony should be afforded. Andreu, 569 F.3d at 1379; Bradley v. Sec’y of Health & Human

Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).

When witness testimony is offered to overcome the presumption of accuracy afforded to

contemporaneous medical records, such testimony must be “consistent, clear, cogent, and

compelling.” Sanchez, 2013 WL 1880825, at *3 (citing Blutstein v. Sec’y of Health & Human

Servs., No. 90-2808V, 1998 WL 408611, at *5 (Fed. Cl. Spec. Mstr. June 30, 1998)). In

determining the accuracy and completeness of medical records, the Court of Federal Claims has

listed four possible explanations for inconsistencies between contemporaneously created medical

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

that happened during the relevant time period; (2) the medical professional’s failure to document

everything reported to her or him; (3) a person’s faulty recollection of the events when presenting

testimony; or (4) a person’s purposeful recounting of symptoms that did not exist. La Londe v.

Sec’y Health & Human Servs., 110 Fed. Cl. 184, 203–04 (2013), aff’d, 746 F.3d 1334 (Fed. Cir.

2014). In making a determination regarding whether to afford greater weight to contemporaneous

medical records over contrary testimony, there must be evidence that this decision was the result

of a rational determination. Burns, 3 F.3d at 417.

C. Analysis of Expert Testimony

Establishing a sound and reliable medical theory often requires a petitioner to present

expert testimony in support of his claim. Lampe v. Sec’y of Health & Human Servs., 219 F.3d

1357, 1361 (Fed. Cir. 2000). Vaccine Program expert testimony is usually evaluated according to

37

the factors for analyzing scientific reliability set forth in Daubert v. Merrell Dow Pharmaceuticals,

Inc., 509 U.S. 579, 594–96 (1993). See Cedillo v. Sec’y of Health & Human Servs., 617 F.3d 1328,

1339 (Fed. Cir. 2010) (citing Terran v. Sec’y of Health & Human Servs., 195 F.3d 1302, 1316

(Fed. Cir. 1999)). “The Daubert factors for analyzing the reliability of testimony are: (1) whether

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

subjected to peer review and publication; (3) whether there is a known or potential rate of error

and whether there are standards for controlling the error; and (4) whether the theory or technique

enjoys general acceptance within a relevant scientific community.” Terran, 195 F.3d at 1316 n.2

(citing Daubert, 509 U.S. at 592–95).

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

when applied in other federal judicial fora (such as the district courts). Daubert factors are usually

employed by judges (in the performance of their evidentiary gatekeeper roles) to exclude evidence

that is unreliable and/or could confuse a jury. In Vaccine Program cases, by contrast, these factors

are used in the weighing of the reliability of scientific evidence proffered. Davis v. Sec’y of Health

& Human Servs., 94 Fed. Cl. 53, 66–67 (2010) (“uniquely in this Circuit, the Daubert factors have

been employed also as an acceptable evidentiary-gauging tool with respect to persuasiveness of

expert testimony already admitted”). The flexible use of the Daubert factors to evaluate the

persuasiveness and reliability of expert testimony has routinely been upheld. See, e.g., Snyder, 88

Fed. Cl. at 742–45. In this matter (as in numerous other Vaccine Program cases), Daubert has not

been employed at the threshold, to determine what evidence should be admitted, but instead to

determine whether expert testimony offered is reliable and/or persuasive.

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

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

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

Broekelschen, 618 F.3d at 1347 (citing Lampe, 219 F.3d at 1362). However, nothing requires the

acceptance of an expert’s conclusion “connected to existing data only by the ipse dixit of the

expert,” especially if “there is simply too great an analytical gap between the data and the opinion

proffered.” Snyder, 88 Fed. Cl. at 743 (quoting Gen. Elec. Co. v. Joiner, 522 U.S. 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 review denied, 108 Fed. Cl. 743 (2013), aff’d, 540 F. App’x

999 (Fed. Cir. 2013) (citing Cedillo, 617 F.3d at 1339).

D. Consideration of Medical Literature

Both parties relied on significant amounts of medical and scientific literature to support

their respective positions. I have reviewed all of the medical literature submitted in this case,

although my decision does not discuss each filed article in detail (nor would it be reasonable to

require a special master to do so—especially in a case like this, where far more literature than was

38

necessary has been filed).33 Moriarty v. Sec’y of Health & Human Servs., 844 F.3d 1322, 1328

(Fed. Cir. 2016) (“[w]e generally presume that a special master considered the relevant record

evidence even though he does not explicitly reference such evidence in his decision”) (citation

omitted).

ANALYSIS

I. Overview of Medical Terms and Relevant Prior Decisions

A. POTS

The experts testifying at hearing defined POTS correctly for the most part, although a few

additional points should be made about it. POTS is unquestionably a subset of orthostatic

intolerance, not a wholly separate clinical entity. See R. Freeman, et al., Consensus Statement on

the Definition of Orthostatic Hypotension, Neurally Mediated Syncope and the Postural

Tachycardia Syndrome, 21 Clinical Autonomic Res. 69, 69 (2011), filed as Ex. A Tab 4, July 27,

2015 (ECF No. 25-5) (“Freeman”). It is marked by an increase in heart rate, or tachycardia, caused

by a change in body position from the supine position to the upright position, without an

accompanying increase in blood pressure. See Freeman at 71; B. Grubb, et al., The Postural

Tachycardia Syndrome: A Concise Guide to Diagnosis and Management, 17 J. Cardiovascular

Electrophysiology 1, 1 (2006), filed as Ex. 35, Mar. 31, 2016 (ECF No. 34); P. Low, et al., Postural

Tachycardia Syndrome (POTS), 20 J. Cardiovascular Electrophysiology 352, 352–53 (2008), filed

as Ex. 59, Mar. 31, 2016 (ECF No. 34) (“Low”).

In POTS, an individual’s inability to make a “prompt physiological adaptation to gravity”

results in feelings of dizziness and lightheadedness, as well as fatigue, headache, and exercise

intolerance. S. Raj, The Postural Tachycardia Syndrome (POTS): Pathophysiology, Diagnosis &

Management, 6 Indian Pacing & Electrophysiology J. 84, 84 (2006), filed as Ex. 39, Mar. 31, 2016

(ECF No. 34) (“Raj”). Thus, a claimant alleging a vaccine injury of POTS is arguing that the

relevant vaccine has done something to the autonomic system sufficient to cause a chronic aberrant

response to orthostatic change.

There are several POTS variants with different possible etiologies, although research has

not conclusively established any one particular explanation for most POTS cases. Freeman at 72.

33

This case unquestionably stands as an example of the over-filing of literature by a petitioner. By my informal

account, Petitioner filed more than one hundred articles in support of her claim. Although admittedly a large number

of them involve the abandoned ASIA theory, this still seems excessive, especially in light of the fact that both experts

only directly addressed a fraction of these articles in their hearing testimony. Indeed, Petitioner filed so many

individual articles in the course of supplementing Dr. Shoenfeld’s opinions that she ended up mistakenly refiling the

same articles several times over. See, e.g., Exs. 35 and 72 (same article), Exs. 37 and 69 (same article), Exs. 47 and

62 (same article), and Exs. 67 and 99 (former an abstract of the latter).

39

Two proposed etiologies for POTS are a hyperadrenergic state (meaning elevated norepinephrine

concentrations) leading to tachycardia, or a neuropathic variant resulting from autonomic nerve

fiber damage. Thieben at 308, 313; Freeman at 72; see also K. Kimpinski, et al., A Prospective, 1-

Year Follow-up Study of Postural Tachycardia Syndrome, 87 Mayo Clinic Proc. 746, 746 (2012),

filed as Ex. 37, Mar. 31, 2016 (ECF No. 34) (“Kimpinski”). But POTS can also be the secondary

result of other conditions—lower limb blood pooling, hypovolemia (meaning decreased blood

plasma), or deconditioning due to inactivity (as Dr. Low explained). Kimpinski at 746; Thieben at

308. POTS is more commonly experienced by women. Freeman at 72; Raj at 86.

There is reliable literature exploring the possibility (as emphasized by Petitioner) that some

cases of POTS could be autoimmune-mediated. See, e.g., Thieben at 311, 313 (noting that six of

forty-two patients tested positive for a particular ganglionic antibody); X. Wang, et al.,

Autoimmunoreactive IgGs Against Cardiac Lipid Raft-Associated Proteins in Patients with POTS,

162 Translational Res. 1, 34, 34–35 (2013), filed as Ex. 99, Mar. 31, 2016 (ECF No. 34) (study

finding presence of autoantibodies against cardiac membranes in POTS patients; Dr. Low as co-

author). The neuropathic form of POTS in particular was previously speculated to be autoimmune

in origin. Low at 354. However, at hearing Dr. Low testified that after studying the matter for some

time, he personally had moved away from autoimmunity as the most likely explanation for POTS

in the majority of individuals, and even Thieben allows that autoimmune-implicated POTS would

not be the most common way in which it occurs—and if it did, would be accompanied by evidence

of “sympathetic denervation.” Thieben at 312–13; Low at 354 (noting that neuropathic POTS is

evidenced by axon reflex tests or sweat tests that reveal “sudomotor denervation to the foot and

toes”).34 At a minimum, an individual suffering from an autonomic neuropathy mediated by

autoimmunity would have a number of presenting symptoms, in addition to orthostatic

tachycardia, revealing harm to the autonomic nervous system.

I have twice had the opportunity to consider whether certain forms of orthostatic

intolerance can be vaccine-caused, albeit in the context of a different vaccine, the human papilloma

virus (“HPV”) vaccine. See generally Johnson v. Sec’y of Health & Human Servs., No. 14-254V,

2018 WL 2051760 (Fed. Cl. Spec. Mstr. Mar. 23, 2018); Combs v. Sec’y of Health & Human

Servs., No. 14-878V, 2018 WL 1581672 (Fed. Cl. Spec. Mstr. Feb. 15, 2018). In both cases, I

found the petitioner had not met the burden of proof.

34

In addition, Dr. Low in his own writing has moved away from finding significant the fact that some individuals with

POTS reported experiencing a viral infection prior to their symptoms, further diminishing the likelihood that most

cases of POTS would be autoimmune in nature (since viral infection would be in most cases the likely start for a

pathogenic autoimmune cross-reaction). Compare Thieben at 310 (90.5% of studied patients had experienced an

antecedent infection) with Low at 353 (noting that “recent experience” has suggested an antecedent infection is less

common in POTS patients than previously proposed). Low was published only two years after Thieben, and both

articles are now at least ten years old.

40

Johnson is more on point with the present case. There, a young woman alleged that the

HPV vaccine caused POTS diagnosed several years after vaccination, relying (as here) on the

testimony of Dr. Shoenfeld (whose initial intent to offer ASIA as an explanation was rejected by

me in advance in that case as well, and for the same reasons). Johnson, 2018 WL 2051760, at *7

n.11, *26 n.35. In determining that the petitioner had not established a reliable medical causation

theory, I found that she failed to demonstrate that POTS is generally autoimmune in origin. Id.

at *24–25. I also determined that the petitioner’s overall disease course, measured from the date

of the alleged causal vaccination to the time her symptoms were thought to possibly reflect POTS,

was simply too meandering and lengthy to deem it a medically reasonable timeframe. Id. at *22–

25.

Combs, by contrast, only involved a claim that a young woman developed syncope well

after receipt of the HPV vaccine. Combs, 2018 WL 1581672, at *1. But Respondent, as here, called

upon Dr. Low, who provided extensive testimony about the autonomic nervous system and

discussed the same kind of orthostatic intolerance issues raised in this case. After a hearing and

full consideration of the evidence and expert testimony, I found that the petitioner had not

established that her condition arose from damage to the autonomic nervous system (as there was

no such evidence to support that contention), nor that her syncope was likely vaccine-caused. Id.

Such decisions do not dictate the outcome of this case. However, they do demonstrate the

existing lack of persuasive scientific evidence associating vaccination to significant orthostatic

intolerance (beyond recognized, close-in-time reactions like syncope, which is itself a Table claim

for certain vaccines including Hep B (42 C.F.R. § 100.3 VIII(C) (2018)), as well as the kind of

hurdles a petitioner faces in attempting to obtain an entitlement award based on such a theory.

These hurdles bear especially on the present case, as discussed below.

B. CFS

The primary characteristic of CFS is “severe disabling fatigue,” which is accompanied by

other symptoms including memory and concentration impairment, muscle pain, and impaired

sleep. See K. Fukuda, et al., The Chronic Fatigue Syndrome: A Comprehensive Approach to Its

Definition and Study, 121 Annals of Internal Med. 953, 953 (1994), filed as Ex. Q, Oct. 16, 2017

(ECF No. 65-2). CFS is, to some extent, a diagnosis of exclusion, as a patient can only properly

be diagnosed with it once other potential causes have been ruled out. See id. Many CFS patients

also suffer from POTS, and the conditions are considered to overlap. R. Sheldon, et al., 2015 Heart

Rhythm Society Expert Consensus Statement on the Diagnosis and Treatment of Postural

Tachycardia Syndrome, Inappropriate Sinus Tachycardia, and Vasovagal Syndrome, 12 Heart

Rhythm e41, e43 (2015), filed as Ex. N Tab 2, Oct. 16, 2017 (ECF No. 64-8) (“Sheldon”).

41

Petitioners alleging a CFS injury resulting from the Hep B vaccine have been successful in

two reasoned Vaccine Program decisions,35 but both are facially distinguishable because in each

the petitioner’s vaccine was demonstrated to have contributed to an existing documented disease

process. In Doe/68 v. Secretary of Health & Human Services, No. [redacted], 2010 WL 2300592

(Fed. Cl. Spec. Mstr. May 24, 2010), the petitioner already suffered from chronic inflammation as

a result of “decades of urinary tract and allergic conditions, and chronic leakage from silicone

capsules [breast implants]” prior to receiving the Hep B vaccine. Doe/68, 2010 WL 2300592, at

*35. The special master found that the Hep B vaccine was thus a substantial factor that combined

with her preexisting and demonstrated chronic inflammation to cause chronic fatigue. Id.

Similarly, in Doe/52 v. Secretary of Health & Human Services, No. [redacted], 2009 WL 2506199

(Fed. Cl. Spec. Mstr. Dec. 15, 2009), a petitioner alleged that the Hep B vaccine reactivated the

latent Epstein-Barr virus she had contracted prior to vaccination, which also played a substantial

factor in generation of her CFS. Doe/52, 2009 WL 2506199, at *14. Mrs. Yalacki, by contrast,

alleges no such combination of factors or reactivation of a prior condition.

II. Petitioner Has Not Established Grounds for Entitlement Based on Her POTS Claim

with Sufficient Preponderant Evidence

A. Petitioner Has Not Established a Plausible Causation Theory

Having heard the experts and reviewed each side’s medical literature and reports, I find

that Petitioner has not presented a plausible theory, supported by sufficient reliable evidence, that

the Hep B vaccine can cause POTS.36

35

An unsuccessful Hep B/CFS petitioner’s case was initially reversed by the Court of Federal Claims on appeal in

Dobrydnev v. Sec’y of Health & Human Servs., 98 Fed. Cl. 190 (2011). However, the Federal Circuit subsequently

reinstated the special master’s decision denying entitlement. 566 F. App’x 976 (Fed. Cir. 2014). In another case, a

petitioner who fell ill after receiving his second Hep B shot claimed a wide variety of symptoms, including some

characteristic of CFS. Dunbar v. Sec’y of Health & Human Servs., No. 98-627V, 2007 WL 2844826, at *14, *18 (Fed.

Cl. Spec. Mstr. Sept. 14, 2007). The special master ruled in the petitioner’s favor, but did not expressly find that the

petitioner had CFS. See id. at *27–28.

36

In her Amended Petition and Prehearing Brief, Petitioner also alleged (in the alternative) that the Hep B vaccine

significantly aggravated her preexisting POTS and/or CFS. Am. Pet. at 2; Pet’r’s Pre-Hr’g Br. at 7–14. Petitioner

briefly reiterated this argument in her Post-Hearing Brief as well. See Pet’r’s Post-Hr’g Br. at 12 n.1. She did not,

however, attempt to substantiate this claim with expert testimony at hearing, focusing instead on her post-vaccination

symptoms, and with Dr. Shoenfeld only addressing the capacity for the vaccine to cause directly either alleged injury—

not make the conditions qualitatively worse.

Regardless, even if Petitioner had more robustly sought to defend her halfheartedly-alleged significant aggravation

claim, such a claim could not be preponderantly established on this record. Among other things, a significant

aggravation claim must establish a worsening of a petitioner’s condition beyond what would be expected absent

vaccination, which is not apparent here. Loving v. Sec’y of Health & Human Servs., 86 Fed. Cl. 135, 137 (2009). The

record does not establish that the vaccine caused an immediate reaction (despite Petitioner's claims to the contrary),

and treater evaluations in fact did not support CFS or POTS in the first two months after vaccination—precisely when

worsening should have been evident. Her overall course also does not seem to follow a trajectory of worsening (and

indeed her CFS symptoms even abated for a period in 2012). In addition, as Loving recognizes, a significant

aggravation claim must meet all of the underlying Althen prongs—but as set forth in §§II(A–B) and §III(A) of this

42

Before discussing specific deficiencies in Petitioner’s theory, it is appropriate at the outset

to note the competence and qualifications gap separating both sides’ experts.37 Respondent offered

two experts (putting aside Dr. Donofrio, who focused on CFS), one of whom happens to be one of

the foremost authorities on the autonomic nervous system—in the United States if not the world.

Petitioner, by contrast, utilized a single causation expert, Dr. Shoenfeld, who has previously

testified unpersuasively before me on the same topic, and whose expertise on the immune system

and autoimmunity in general was not accompanied by comparable expertise in treating or studying

POTS and CFS (beyond addressing it as another possible autoimmune disease likely explained by

his ASIA theory). See Johnson, 2018 WL 2051760, at *7–12, *23.

Dr. Shoenfeld’s deficiencies as an expert in this case go beyond his comparative lack of

competence on POTS or the autonomic nervous system, however. For time and again, when

testifying in Vaccine Program cases, Dr. Shoenfeld has readily voiced his belief about the

prevalence of autoimmunity and its unerring connection to vaccination—a view so deeply

entrenched and unshakable that it often defies the very legal standards I am called to apply

(especially when he is asked about the timeframe over which such autoimmunity might germinate).

See, e.g., Garner v. Sec’y of Health & Human Servs., No. 15–063V, 2017 WL 1713184, at *16–

17 (Fed. Cl. Spec. Mstr. Mar. 24, 2017), mot. for review denied, 133 Fed. Cl. 140 (2017);

Crutchfield v. Sec’y of Health & Human Servs., No. 09-0039V, 2014 WL 1665227, at *11–13

(Fed. Cl. Spec. Mstr. Apr. 7, 2014); Hennessey v. Sec’y of Health & Human Servs., 91 Fed. Cl.

126, 142 (2010) (rejecting Dr. Shoenfeld’s attempt to satisfy the third Althen prong by positing

that any timeframe is appropriate). Such blanket assertions harm his overall credibility.

Dr. Shoenfeld was generally qualified to give an opinion in this case, and I have considered

that opinion carefully. But he is comparatively lacking in expertise with the autonomic nervous

system or POTS, and that, in addition to his other demonstrated biases and deficiencies (not to

mention the apparent misrepresentations on his CV pointed out at hearing by Respondent),38 leads

me to give less weight overall to his pronouncements about POTS and its causes than to the

testimony of Respondent’s experts, who together provided a comprehensive and more persuasive

picture of the condition at issue and the low likelihood that a vaccine could instigate it.39

decision, Petitioner has not carried her preponderant burden of proof on direct causation, a failure that undermines a

significant aggravation claim a well.

37

I do not include the treating physicians who testified on Petitioner’s behalf in this calculation, since they did not

offer opinions on causation.

38

See supra note 18.

39

Of course, a different presentation by Petitioner (if supported by experts who matched Respondent’s experts’

qualifications to opine on the autonomic nervous system or vaccine interaction with the same) might lead to a different

outcome. But it is within my discretion to evaluate expert credibility (a function of the expert’s competence to testify

43

But even if I had found Dr. Shoenfeld more credible or persuasive as an expert, I would

still find significant deficiencies in Petitioner’s causation theory with respect to POTS. Petitioner

proposed that POTS is usually an autoimmune disease, mediated by autoantibodies produced in

response to the Hep B vaccine that cross-react with norepinephrine transporter proteins, interfering

with the autonomic nervous system to cause orthostatic imbalance. But Respondent effectively

rebutted that assumption. Admittedly, there is literature support (such as Thieben) for the idea that

a particular form of autonomic neuropathy might be associated with a particular autoantibody,

thereby suggesting autoimmunity as the pathologic mechanism. But Dr. Low (whose direct

experience studying the etiology of POTS far outweighed Dr. Shoenfeld’s) persuasively

established that an autoimmune explanation for POTS is far less accepted today than when first

written about in Thieben (an article he co-authored) ten years ago; he does not test for the presence

of autoantibodies in POTS patients in most cases, and POTS is not treated with immune system

suppression methods like plasmapheresis. The remaining scientific evidence offered by Petitioner

suggesting the POTS is typically autoimmune was thin, relying on single case reports (Shannon),

a kind of evidence not given significant weight in Program cases,40 or only indirectly supported a

connection between autoimmunity and conditions such as POTS (see, e.g., Li). And Dr. Shoenfeld

in no way undercut Dr. Low’s testimony (corroborated by several items of literature) that there are

other POTS variants that clearly are not autoimmune in etiology, such as hyperadrenergic POTS

or POTS due to deconditioning, or that these are more common explanations for the condition. See

Low at 354–56.

Next, even if it is granted that some rare forms of POTS are autoimmune in origin, there

remain substantial deficiencies in Petitioner’s theory that the Hep B vaccine could trigger a

pathogenic process resulting in such an autoimmune attack leading to POTS. As I have noted

before, it is not enough for a claimant to invoke the concept of molecular mimicry along with some

identified homology between an amino acid sequence and a target antigen in order to carry her

burden. Johnson, 2018 WL 2051760, at *26. Rather, a petitioner needs to cite to evidence,

circumstantial or otherwise, suggesting reason to find it plausible that the proposed autoimmune

cross-reaction triggered by the relevant vaccine does occur. But Petitioner offered nothing reliable

to support the contentions that (a) the Hep B vaccine likely does cause the production of antibodies

associated with autonomic damage or interference sufficient to cause POTS (as opposed to

different diseases known to be predominantly autoimmune), and (b) that those same antibodies do

lead to such a pathogenic process.

Such points were also effectively undermined by Dr. Whitton’s testimony on immunologic

topics relevant to Althen prong one. Dr. Whitton was broadly persuasive in his points about the

on a topic, but also a matter that is impacted by a given expert’s honesty, clarity, and overall persuasiveness) in

determining if a petitioner has carried her burden of proof. See Broekelschen, 618 F.3d at 1347.

40

See, e.g., Crutchfield, 2014 WL 1665227, at *19.

44

limited conclusions that one could draw from evidence of amino acid sequence homology

(especially where, as here, it appears to have been cherry-picked to bulwark a theory, rather than

discovered in studying POTS and its pathogenesis). He similarly established convincingly that the

evidence that the norepinephrine transporter protein is the target antigen for autonomic nervous

system interference sufficient to result in POTS is undeveloped, as is the front-end component of

Petitioner’s theory proposing that some specific components of the Hep B vaccine can mimic a

target antigen epitope on the transporter protein that would be the subject of an autoimmune attack.

Because Petitioner could not point to any studies linking the Hep B vaccine to POTS or

autonomic neuropathy of any kind,41 she had to rely on the little existing circumstantial evidence

that suggests it could be autoimmune, and theorize how that process might work, or the association

of the Hep B vaccine with other, distinguishable autoimmune diseases. But the evidence she

offered connecting the Hep B vaccine to POTS was speculative, limited, or rebutted, and she could

not breathe life into it with Dr. Shoenfeld’s ipse dixit pronouncements on topics about which he

knew demonstrably less than Dr. Low. Petitioner has therefore not established a plausible

causation theory connecting the Hep B vaccine to POTS.

B. Even if Petitioner Had POTS, the Record Does Not Establish That

It Was Caused by the Hepatitis B Vaccine

The record is not in agreement as to whether Mrs. Yalacki actually ever had (or today has)

POTS. There are ample points in the medical record where Petitioner demonstrated clinical indicia

of POTS, such as dizziness and fatigue. But she experienced such symptoms both before and after

the vaccination at issue, making it difficult to give more significance to her symptoms in the

summer of 2011 than to her pre-vaccination history and the many congruent complaints recorded

therein.42

41

My observation that Petitioner has not offered direct evidence associating the Hep B vaccine with POTS is not

equivalent to requiring such evidence. As I have already noted above in my discussion of the legal standards applicable

to Program cases, there is no particular category of evidence a petitioner must file to prevail on her claim, and claimants

can unquestionably offer reliable circumstantial proof to support their theory (and do so successfully all the time). To

give but one possible example, a petitioner is not required to offer epidemiologic evidence establishing the incidence

of injury X after receipt of vaccine Y—and so the fact that a petitioner cannot cite an epidemiologic study establishing

such an association is not grounds for a claim’s summary dismissal (in the same way it would be, by comparison, if a

petitioner could not prove the fact of vaccination). But (as the Federal Circuit recently reiterated) consideration by a

special master of epidemiologic evidence that exists and that is unhelpful to a petitioner’s claim is not tantamount to

requiring that such evidence be submitted. D’Tiole v. Sec’y of Health & Human Servs., 726 F. App’x 809, 811–12

(Fed. Cir. 2018). Thus, as part of the evidentiary weighing process, I may take into account the nature of the evidence

offered, and doing so does not mean I am elevating Petitioner’s burden.

42

Because POTS is understood to be difficult to diagnose, symptoms can long precede a formal treater determination

designating POTS as the best descriptor for a patient’s symptoms. See Sheldon at e44. This means that, just as a

symptom in 2011 could be related to a POTS diagnosis Ms Yalacki received in 2012 or 2013, symptoms she

experienced before the vaccination could equally be associated with such later diagnoses.

45

Treater support for the diagnosis is also inconclusive. Some treaters (Drs. Gillespie and

Betkowski, for example) seem to have either leaned in favor of a POTS diagnosis or outright

proposed it, although they based their determinations on a sit-stand test or Petitioner’s own

recitation of her medical history as having been diagnosed with POTS in the past, without

corroborating the diagnosis with follow-up testing, and recommended further testing as well to

confirm the diagnosis’s accuracy. Dr. Gillespie was certainly a credible witness, giving his

diagnosis some heft, but it is self-evident that his testimony was based solely on two encounters

with Petitioner that occurred almost three years after her receipt of the Hep B vaccine. And as Dr.

Low explained, some of the sit-stand orthostatic readings upon which these treaters relied were

less supportive of the diagnosis than they believed. E.g., Ex. 2 at 667, 702 (Petitioner’s blood

pressure dropped during March 2013 and April 2013 sit-stand tests with Dr. Betkowski, which

would be inconsistent with POTS diagnosis); Ex. 12 at 34 (Dr. Gillespie finding a sit-stand test

result of heart rate increase from seventy-one BPM to eighty-eight BPM to support a POTS

diagnosis despite diagnostic criteria of thirty BPM increase or greater).

On the other hand, an equal number of treaters ruled out POTS or doubted its diagnostic

veracity—and they did so on the basis of better testing evidence. Dr. Abruzzo, for example,

appears to be the first cardiologist Petitioner saw in 2011 who hypothesized her symptoms could

be the product of autonomic neuropathy, but he also is the only treater to have performed a tilt

table test, and the results of that test did not confirm POTS, causing him to abandon his initial

speculation as to the source of her symptoms. Ex 5 at 84. Another cardiologist, Dr. Noll,

acknowledged the contrary diagnostic evidence unsupportive of the diagnosis. And two other

treaters (neurologists Drs. Rollins and Seibert) did not accept the diagnosis at all. Furthermore, I

find that the tilt table test is in fact the accepted best clinical test for POTS, and reject Dr.

Shoenfeld’s conclusory assertions embracing the sit-stand test over it as wholly unpersuasive. The

result of the single tilt table test Petitioner received—as well as the fact that she has never had a

follow-up test—makes it extremely difficult to accept the POTS diagnosis given the overall

inconclusiveness of this record.

However, even if I assume (consistent with the remedial nature of the Vaccine Program,

and the concurrent admonition that special masters decide close issues in a petitioner’s favor

(Capizzano, 1440 F.3d at 1327)) that Petitioner did have POTS, the record strongly contradicts

Petitioner’s argument that it could have been caused by her June 2011 Hep B vaccine.

Fundamentally, the record does not reflect the causation theory proposed by Dr. Shoenfeld

as having occurred in “real time.” Petitioner posits that the Hep B vaccine initiated an autoimmune

reaction mediated by autoantibodies that would have been produced not long after the June 2, 2011

vaccination. But there is no evidence the Petitioner even had these antibodies, and no evidence

that she was experiencing an autoimmune process at all. This could be corroborated, for example,

by lab tests suggesting the presence of inflammation, or contemporaneous treater speculation about

46

the character of her symptoms—and yet the work-ups Petitioner received in the summer of 2011

did not so find. In addition, Petitioner’s theory proposes the autoantibodies interfering with the

norepinephrine transporter protein—but there is no corroborative evidence of other symptoms that

this transporter was malfuncti

This text is long and has been trimmed here. Open the source document for the complete record.