VICP Registry Case Source Bundle
Canonical URL: https://vicp-registry.org/case/USCOURTS-cofc-1_15-vv-00491
Package ID: USCOURTS-cofc-1_15-vv-00491
Petitioner: Cara Specks
Filed: 2015-05-13
Decided: 2023-04-14
Vaccine: influenza
Vaccination date: 2013-10-08
Condition: hyperadrenergic postural orthostatic tachycardia syndrome (“POTS”) with hypovolemia
Outcome: denied
Award amount USD: 

AI-assisted case summary:
Cara Specks filed a petition alleging that the influenza vaccine she received on October 8, 2013, caused her hyperadrenergic postural orthostatic tachycardia syndrome (POTS) with hypovolemia. The court reviewed extensive medical records and expert testimony from both sides. Petitioner's experts argued that POTS can have an autoimmune basis and that the flu vaccine could have triggered this autoimmune response through molecular mimicry. Respondent's expert contended that Petitioner's symptoms predated the vaccination and that deconditioning and dehydration were more likely causes, not the vaccine itself. The court found that while POTS can have an autoimmune etiology, Petitioner failed to demonstrate that the flu vaccine could trigger such a response or that her condition was not caused by factors unrelated to the vaccine. Crucially, the court noted significant evidence of pre-existing symptoms consistent with orthostatic intolerance, such as tachycardia, palpitations, and dizziness, dating back to 2011, which predated her vaccination. Despite opportunities to amend her claim to include significant aggravation, Petitioner did not do so. Ultimately, the court concluded that Petitioner failed to prove by a preponderance of the evidence that the flu vaccine was the cause-in-fact of her POTS and dismissed the claim.

Theory of causation field:
Off-Table

Public staged source text:

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DOCUMENT 1: USCOURTS-cofc-1_15-vv-00491-0
Date issued/filed: 2023-04-14
Pages: 57
Docket text: PUBLIC DECISION (Originally filed: 02/17/2023) regarding 88 DECISION of Special Master. Signed by Special Master Herbrina Sanders. (arm) Service on parties made.
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Case 1:15-vv-00491-UNJ Document 95 Filed 04/14/23 Page 1 of 57
In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
Filed: February 17, 2023
* * * * * * * * * * * * * * *
CARA SPECKS, * No. 15-491V
*
*
*
Petitioner, * Special Master Sanders
*
v. *
* Denial of Entitlement; Influenza
SECRETARY OF HEALTH * (“Flu”) Vaccine; Postural Orthostatic
AND HUMAN SERVICES, * Tachycardia Syndrome (“POTS”);
* Hypovolemia
Respondent. *
* * * * * * * * * * * * * * *
Edward Kraus, Kraus Law Group, LLC, Chicago, IL, for Petitioner.
Debra A. Filteau Begley, United States Department of Justice, Washington, DC, for Respondent.
ENTITLEMENT DECISION1
On May 13, 2015, Cara Specks (“Petitioner”) filed a petition for compensation pursuant to
the National Vaccine Injury Compensation Program.2 Pet. at 1, ECF No. 1; 42 U.S.C. §§ 300aa-1
to -34 (2012). Petitioner alleges that the influenza (“flu”) vaccine she received on October 8, 2013,
was the cause-in-fact of her “hyperadrenergic postural orthostatic tachycardia syndrome
(“POTS”)3 with hypovolemia[.]”4 Pet. at 1.
1 This Decision shall 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 note (2012) (Federal Management and Promotion of
Electronic Government Services). In accordance with Vaccine Rule 18(b), a party has 14 days to identify
and move to delete medical or other information that satisfies the criteria in § 300aa-12(d)(4)(B). Further,
consistent with the rule requirement, a motion for redaction must include a proposed redacted Decision. If,
upon review, I agree that the identified material fits within the requirements of that provision, such material
will be deleted from public access.
2 National Childhood Vaccine Injury Act of 1986, Pub L. No. 99-660, 100 Stat. 3755. Hereinafter, for ease
of citation, all “§” references to the Vaccine Act will be to the pertinent subparagraph of 42 U.S.C. § 300aa
(2012).
3 Postural orthostatic tachycardia syndrome (“POTS”) is “a group of symptoms (not including hypotension)
that sometimes occur when a person assumes an upright position, including tachycardia, tremulousness,
lightheadedness, sweating, and hyperventilation; this is seen more often in women than in men, and the
etiology is uncertain.” Dorland’s Illustrated Medical Dictionary 1, 1844 (32nd ed. 2012) [hereinafter
“Dorland’s”]. Hyperadrenergic refers to the “excessive activity of adrenergic nerve fibers with an increase
in the effects of adrenergic receptors.” Id. at 886.
4 Hypovolemia is “abnormally decreased volume of circulating blood in the body; the most common cause
is hemorrhage.” Dorland’s at 908.

Case 1:15-vv-00491-UNJ Document 95 Filed 04/14/23 Page 2 of 57
After carefully analyzing and weighing all the evidence and testimony presented in this
case in accordance with the applicable legal standards,5 I find that Petitioner has failed to provide
preponderant evidence that the flu vaccine she received on October 8, 2013, was the cause-in-fact
of her POTS and/or hypovolemia. Accordingly, Petitioner’s claim is hereby DISMISSED.
I. Procedural History
Petitioner filed her petition for compensation on May 13, 2015. Pet. at 1. On June 17, 2015,
Petitioner filed a notice of intent to file exhibits on a compact disc, including medical records,
Petitioner’s affidavit, and an expert report from David Axelrod, M.D.6 Pet’r’s Exs. 1–22, ECF No.
7. Petitioner filed a statement of completion on June 24, 2015. ECF No. 8. On September 29, 2015,
Petitioner submitted an outstanding medical record and an amended statement of completion.
Pet’r’s Ex. 23, ECF Nos. 15–16.
Respondent filed his Rule 4(c) report on January 19, 2016, recommending that
compensation be denied. Resp’t’s Report at 1, ECF No. 21. The same day, Respondent filed an
expert report and supporting medical literature from Phillip Low, M.D. Resp’t’s Exs. A, A Tabs
1–11, ECF No. 22. The presiding special master held a status conference with the parties on
January 28, 2016. Min. Entry, docketed Jan. 28, 2016. The presiding special master “articulated a
concern with the timing of onset . . . [and] that notations in some medical records . . . imply that
Petitioner’s symptoms may predate vaccination.” ECF No. 23 at 1 (citing Pet’r’s Ex. 4). Petitioner
“attempted to clarify which of the various symptoms, including shortness of breath [(“SOB”)] and
dizziness, were related to [her] alleged injury.” Id. She also indicated a desire to amend her petition
to include a claim of significant aggravation. Id. The presiding special master ordered Petitioner
to file an affidavit, supplemental expert report, and an amended petition. Id.
On March 3, 2016, Petitioner filed additional medical records. Pet’r’s Exs. 24–27, ECF
No. 24. The next day, Petitioner filed an affidavit. Pet’r’s Ex. 28, ECF No. 25. On March 4, 2016,
the presiding special master ordered Petitioner to file a supplemental expert report and an amended
petition, if necessary. ECF No. 26. On April 28, 2016, Petitioner filed a supplemental expert report
from Marcel Kinsbourne, M.D. Pet’r’s Exs. 29–30, ECF No. 27. The presiding special master held
a status conference with the parties on May 19, 2016, to discuss the ongoing dispute concerning
onset. ECF No. 28; see also Min. Entry, docketed May 19, 2016. The parties also addressed
Petitioner’s “assertion that the medical records misrepresented Petitioner’s medical history.” ECF
No. 28. The presiding special master ordered Petitioner to file a supplemental expert report from
Dr. Kinsbourne “addressing the symptoms documented in Petitioner’s medical history and their
5 While I have reviewed all of the information filed in this case, only those filings and records that are most
relevant to the decision will be discussed. Moriarty v. Sec'y of Health & Hum. Servs., 844 F.3d 1322, 1328
(Fed. Cir. 2016) (“[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); see also
Paterek v. Sec'y of Health & Hum. Servs., 527 F. App'x. 875, 884 (Fed. Cir. 2013) (“[f]inding certain
information not relevant does not lead to—and likely undermines—the conclusion that it was not
considered.”).
6 On June 29, 2015, Petitioner moved to strike Petitioner’s Exhibit 17, the expert report from Dr. Axelrod,
due to it containing an incorrect version of the document. See ECF No. 9. Petitioner refiled her expert report
the same day. Pet’r’s Ex. 17, ECF No. 10.
2

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relationship with orthostatic intolerance and POTS[.]” Id. Petitioner filed a supplemental expert
report from Dr. Kinsbourne on September 14, 2016. Pet’r’s Ex. 31, ECF No. 31.
This case was reassigned to me on January 11, 2017. ECF Nos. 33–34. On January 19,
2017, Respondent filed a supplemental expert report from Dr. Low and supporting medical
literature. Resp’t’s Exs. C, C Tabs 1–7, ECF No. 36. I held a status conference with the parties on
March 23, 2017. Min. Entry, docketed Mar. 23, 2017. Following the conference, I ordered
Petitioner to file a supplemental expert report addressing “whether [Petitioner] had any evidence
of autonomic neuropathy, in order to proceed on an immune-mediated causation theory.” ECF No.
37. I agreed with Petitioner’s suggestion for her expert to address a significant aggravation theory.
Id. On June 21, 2017, Petitioner filed a supplemental expert report and supporting medical
literature. Pet’r’s Exs. 32–39, ECF Nos. 39–40. Respondent submitted his supplemental expert
report and supporting medical literature on October 23, 2017. Resp’t’s Exs. D, D Tabs 1–6, ECF
No. 42. Petitioner filed additional medical records on December 21, 2017. Pet’r’s Exs. 40–42, ECF
No. 44. On March 13, 2018, Respondent filed a joint status report requesting that this case proceed
to an entitlement hearing. ECF No. 47.
I scheduled this matter for an entitlement hearing to take place on April 16–17, 2020.
Hearing Order, ECF No. 49. Petitioner filed additional medical records on January 31, 2020.
Pet’r’s Exs. 43–45, ECF No. 52. The same day, Petitioner filed a supplemental expert report from
Dr. Kinsbourne, along with supporting medical literature. Pet’r’s Exs. 46–61, ECF Nos. 53–56.
Petitioner also filed her pre-hearing brief on January 31, 2020. Pet’r’s Br., ECF No. 58. Respondent
filed his pre-hearing response brief and a supplemental expert report from Dr. Low on March 6,
2020. Resp’t’s Resp., ECF No. 60; Resp’t’s Ex. E, ECF No. 61.
I held a status conference with the parties on March 11, 2020, to discuss the implications
of the COVID-19 pandemic. See Min. Entry, docketed Mar. 18, 2020. On March 23, 2020, I
cancelled the entitlement hearing and ordered Respondent to submit any supporting medical
literature referenced in his last supplemental expert report. Non-PDF Order, docketed Mar. 23,
2020. Respondent filed medical literature on March 25, 2020. Resp’t’s Exs. E Tabs 1–18, ECF
No. 62.
I rescheduled the entitlement hearing to take place remotely on May 19–20, 2021. Hearing
Order, ECF No. 63. Petitioner filed an updated medical record on January 15, 2021. Pet’r’s Ex.
62, ECF No. 64. The hearing was held remotely as scheduled on May 19, 2021. Min. Entry,
docketed May 19, 2021. Following the entitlement hearing, Petitioner filed an outstanding medical
record. Pet’r’s Ex. 67, ECF No. 79.
Petitioner filed an opening post-hearing brief on August 24, 2021. Pet’r’s Br., ECF No. 84.
On September 8, 2021, Respondent filed his post-hearing response brief. Resp’t’s Resp., ECF No.
85. Petitioner filed her post-hearing reply brief on September 14, 2021. Pet’r’s Reply, ECF No.
86. This matter is now ripe for consideration.
II. Factual Background
A. Medical Records
3

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a. Pre-vaccination history
Petitioner’s pre-vaccination history is relevant for anxiety, depression, insomnia,
laryngopharyngeal reflux (“LPR”),7 and asthma. Pet’r’s Ex. 1 at 5. On January 12, 2011, Petitioner
presented to the emergency room (“ER”) for a two-day long anxiety attack. Pet’r’s Ex. 21 at 149.
The ER physician noted her history of anxiety and panic attacks. Id. She complained that it “fe[lt]
like [her] heart rate ke[pt] beating fast.” Id. at 150. Her EKG showed that she had sinus
tachycardia8 and that her heart rate was 114 beats per minute. Id. at 152. The ER physician gave
Petitioner Xanax, and her symptoms improved. Id. at 149.
Approximately one year later, on January 23, 2012, Petitioner presented to her primary
care physician (“PCP”) and reported a recent hospitalization for an abnormal EKG. Pet’r’s Ex. 13
at 1.9 Petitioner’s PCP referred her to a cardiologist10 for her palpitations and another specialist
for her “allergic rhinitis.”11 Id. Five days later, on January 28, 2012, Petitioner returned to her PCP
reporting that she “fe[lt] like [her] breathing [had] not improved[]” despite “[u]sing [an] inhaler
every [four] hours.” Id. at 3. Her PCP noted that Petitioner complained of increased respiratory
issues over the last two years. Id. Petitioner’s PCP also wrote that Petitioner quit smoking five
weeks ago. Id. Her PCP’s assessment of Petitioner included allergic rhinitis and asthma. Id.
On June 10, 2012, Petitioner called emergency personnel to her home after feeling
“lightheaded” and experiencing tachycardia. Pet’r’s Ex. 67 at 5.12 When personnel arrived, her
heart rate was measured in the 150s. Id. Petitioner was taken to the ER where a history of “feeling
‘lightheaded’ and tachy[cardia]” was noted. Id. Petitioner reported she thought she might be
anxious or dehydrated. Id. at 6. She also “said she smoked marijuana earlier” that she felt was
causing her heart rate to “go up[.]” Id. Petitioner’s physical examination was normal, and her
7 Laryngopharyngeal reflux (“LPR”) is “a complication of gastroesophageal reflux caused by reflux from
the esophagus into the pharynx, characterized by a variety of intermittent chronic symptoms, including
hoarseness, cough, throat clearing, globus pharyngeus, and dysphagia” (difficulty swallowing). Dorland’s
at 1616.
8 Sinus tachycardia is “tachycardia originating in the sinus node; it is normal during exercise or anxiety and
occurs abnormally associated with shock, hypotension, hypoxia, congestive heart failure, fever, and various
high output states.” Dorland’s at 1867. Tachycardia is “excessive rapidity in the action of the heart; the
term is usually applied to a heart rate above 100 beats per minute in an adult and is often qualified by the
locus of origin as well as by whether it is paroxysmal or nonparoxysmal.” Id.
9 Petitioner did not file medical records documenting a recent hospitalization at Northwest Community
Emergency Room as noted by her PCP. See Pet’r’s Ex. 13 at 1; Pet’r’s Ex. 31 at 1–20. The records from
Northwest Community Emergency Room are from Petitioner’s visit on June 10, 2012. See Pet’r’s Ex. 67
at 1–20.
10 Petitioner did not file records from a cardiologist for dates following this referral. She testified during the
hearing that she did not see a cardiologist following this visit. See Tr. 33:13–15.
11 Allergic rhinitis is “a general term used to denote any allergic reaction of the nasal mucosa; it may occur
perennially (annually) or seasonally[.]” Dorland’s at 1639.
12 Petitioner originally introduced this exhibit as Petitioner’s Exhibit 31, but she then realized that was an
error. Petitioner then re-introduced the exhibit as Petitioner’s Exhibit 67. See Tr. 38:17–19. This medical
record was not filed prior to the entitlement hearing in May of 2021. When it was ultimately filed, Petitioner
designated it as “Exhibit 31.” Since Petitioner’s Exhibit 31 is one of Dr. Kinsbourne’s expert reports, I will
refer to this exhibit as “Exhibit 67.”
4

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symptoms resolved with fluids while in the ER. Id. at 7. Petitioner received discharge instructions
for dizziness and palpitations. Id. at 11–12. The ER attending listed Petitioner’s diagnoses
including palpitations, anxiety disorder, and significant sinus tachycardia. Id. at 12.
Petitioner returned to her PCP on February 27, 2013.13 Pet’r’s Ex. 13 at 4. Petitioner
reported that had been seen three times for sinus pressure and pain and “then developed asthma.”
Id. Her PCP noted that Petitioner received oral steroids to treat her symptoms but that Petitioner
was worried that “steroids worsen her anxiety.” Id. On March 21, 2013, Petitioner presented to her
PCP reporting that she had SOB “off/on since Dec[ember].” Id. at 5. Petitioner also reported a pain
under her left ribcage and that she “c[ould not] finish her breaths.” Id.
On April 24, 2013, Petitioner returned to her PCP for “allergic rhinitis, asthma[,] and
symptoms.” Id. at 22. Petitioner reported that “about [one] week ago[,] she developed a headache
[] then . . . sinus pressure.” Id. Petitioner then “got a lot of fatigue . . . a sore throat and swollen
throat on the left . . . a very stuffy nose with clear discharge . . . sneez[ing] . . . [and t]hen her
asthma flared up[.]” Id. She reported she needed her inhaler every three hours and “was very low
energy.” Id. Petitioner noted that she “got prednisone 50 mg for [three] days until she was seen[,]”
which “worked right away for her.” Id. Her PCP noted that such treatment with prednisone
alleviated her symptoms. Id. at 27. Petitioner’s PCP also wrote that Petitioner was no longer
wheezing, but she “fe[lt] very short of breath and [] gets very winded.” Id. at 22. Upon
examination, Petitioner exhibited nasal congestion, pharyngitis, post-nasal drainage, dyspnea14
(occurring one to two times per day), and an irregular heartbeat/palpitations. Id. at 23. Her PCP
reiterated Petitioner’s diagnoses of asthma and allergic rhinitis. Id. at 25. Petitioner returned to her
PCP on June 24, 2013, reporting the same issues of SOB and related them to her asthma and
allergic rhinitis. Id. at 27.
b. Vaccination
Petitioner received the seasonal flu vaccine at issue on October 8, 2013. Pet’r’s Ex. 1 at 8.
Petitioner’s PCP noted Petitioner’s chronic conditions including “asthma [and] allergic rhinitis,
cause unspecified,” but indicated no other concerns during this visit. Id.
c. Post-vaccination history
On October 14, 2013, Petitioner reported to Jess Duyka, M.D., “with a greater than [six]
mo[nth] [history of] throat clearing, SOB, dry cough, nocturnal choking, globus sensation, [and]
hoarseness.” Pet’r’s Ex. 23 at 1, ECF No. 15-1. Upon examination, Dr. Duyka noted no concerns
except for inflammation of Petitioner’s larynx. Id. at 1–2. Dr. Duyka assessed Petitioner with a
cough, dyspnea, and LPR and she recommended a low acid diet. Id. at 2. Petitioner followed up
with Dr. Duyka on October 23, 2013, and reported no improvement since her last visit. Id. at 5.
Upon examination, Dr. Duyka noted that the inflammation in Petitioner’s larynx had resolved. Id.
13 The records from Lake County Health Department and Community Health Center Primary Care Services
are mostly handwritten. The records for this date are extremely illegible and difficult to read. See Pet’r’s
Ex. 13.
14 Dyspnea is “breathlessness or shortness of breath; difficult or labored respiration.” Dorland’s at 582.
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Dr. Duyka opined that “[t]his could be a laryngospasm brought on by transient reflux, but [Dr.
Duyka did not] see any signs of th[at] on [] exam.” Id.
Petitioner returned to her PCP on November 8, 2013, with complaints of a ten-day history
of abdominal pain, cramping, and severe diarrhea approximately ten times per day. Pet’r’s Ex. 1
at 3. She reported that she had experienced recent weight loss “due to [a decrease in] intake [and]
diarrhea.” Id. Petitioner underwent imaging and testing, including an abdominal X-ray, a fecal
stain, and labs to test for the presence of bacteria, including salmonella, parasites, and H. pylori,
which all yielded negative results. Id. at 11, 13–16. Petitioner’s PCP assessed her with abdominal
pain and diarrhea. Id. at 3.
Later the same day, November 8, 2013, Petitioner presented to the ER with the same
complaints of abdominal pain, cramping, and diarrhea plus light-headedness, nausea without
vomiting, chills, and weakness that “started yesterday.” Pet’r’s Ex. 4 at 155. She explained that
she “ke[pt] twitching” and “fe[lt] strange.” Id. at 169. Petitioner expressed that she thought her
diarrhea “might be related to Protonix,”15 which she took for her LPR. Id. at 155. She reported her
history of sinus tachycardia one year prior. Id. at 156, 165. Petitioner underwent an EKG, which
was normal. Id. at 169–70. The ER physician informed Petitioner that “she likely ha[d] a viral
syndrome[.]” Id. at 170. The impression included “malaise, weakness, diarrhea, dehydration, [and]
hypertension.” Id. The physician noted that Petitioner was “very difficult to reassure and want[ed]
an ‘answer[,]’ which [wa]s not likely forthcoming[,]” but the physician admitted Petitioner. Id.
During her hospital stay, Petitioner saw gastroenterologist Jeffrey Nathanson, M.D., on
November 9, 2013. Id. at 159. Petitioner reported that she had not been “feeling well” and had
intermittent SOB “for the last few months.” Id. Petitioner stated that she had seen an ENT specialist
prior to her hospitalization and flu vaccination and that the ENT suspected her symptoms “might
be due to LPR[,]” so she began taking Prilosec.16 Id. Petitioner reported that when she switched to
Protonix a month earlier, her SOB “somewhat improved.” Id. Dr. Nathanson noted that Petitioner
had not had diarrhea since her admission. Id. He also noted that Petitioner “fe[lt]” strongly [that
her] anxiety is not [the] cause of [her] symptoms but rather [is] secondary to the symptoms
themselves.” Id. Dr. Nathanson wrote that he “suspect[ed Petitioner’s] symptoms [were] functional
with a likely anxiety component . . . .” Id. at 161. He opined that it was “unclear if [Petitioner]
truly ha[d] reflux, as [there were] nonspecific findings on [her] laryngoscopy [that] often correlate
poorly with true acid reflux.” Id. Dr. Nathanson ordered lab work, including stool studies for
infectious etiologies, celiac serologies, and obstructive series, which were normal except for an
elevated thyroid stimulating hormone (“TSH”). Id. at 157–58, 161, 375–401.
Petitioner also presented to a physical therapist while hospitalized due to her complaints of
weakness. Id. at 162. Upon examination, Petitioner exhibited decreased balance, gait, functional
endurance, and functional strength. Id. at 163. The physical therapist noted that Petitioner
15 Protonix refers to the trademark preparations of pantoprazole sodium. Dorland’s at 1537. Pantoprazole
sodium is “a proton pump inhibitor . . . used in the treatment of . . . gastroesophageal reflux disease,
administered orally or intravenously[.]” Id. at 1371.
16 Prilosec is the trademark preparation of omeprazole. Dorland’s at 1514. Omeprazole is a “proton pump
inhibitor used in the treatment of dyspepsia, gastroesophageal reflux disease, and gastric hypersecretory
conditions[.]” Id. at 1319.
6

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“ambulate[d] very slowly[]” and that she “appear[ed] to be increasingly fatigued[.]” Id. at 162.
The physical therapist recommended that Petitioner receive physical therapy (“PT”) for “gait
training” once or twice more prior to discharge. Id. at 163.
On November 10, 2013, Petitioner was discharged from the hospital with diagnoses
including suspected functional irritable bowel syndrome (“IBS”),17 possible LPR, resolved
diarrhea, resolved abdominal pain, and elevated TSH. Id. at 158. The attending physician opined
that Petitioner’s light-headedness, generalized weakness, and diarrhea were “likely” related to viral
gastroenteritis.18 Id. at 156. The physician also noted that Petitioner could ambulate normally at
the time of discharge. Id.
Four days later, on November 14, 2013, Petitioner presented to internist Kimberly
Schaefer, M.D., for complaints of dizziness, diarrhea, nausea, vomiting, increased blood pressure
(“BP”), and tachycardia. Id. at 151. Petitioner reported that she had recently seen Dr. Nathanson,
who “felt her symptoms were [related to] autonomic dysfunction.” Id. Petitioner also reported that
she “fe[lt] her BP gets high when she stands up.” Id. Petitioner described feelings of flushing,
shaking, waves of nausea, headaches, and changes in temperature, and she stated that “[l]oud
noises and bright lights make her sick.” Id. Dr. Schaefer recorded Petitioner’s BP as 140/90 when
laying down and 128/88 when standing. Id. Dr. Schaefer noted Petitioner’s pulse was “too fast to
count.” Id. Dr. Schaefer wrote that Petitioner saw a psychiatrist during this visit who opined that
her symptoms were not psychiatric. Id. Dr. Schaefer also noted that Petitioner had a low appetite
and had lost twenty pounds over the last two months, some purposefully, but that her weight loss
became more “rapid over the last month.” Id. Petitioner’s family reported that Petitioner was
“starving herself,” and Dr. Schaefer encouraged her to eat and hydrate. Id. at 153.
On November 18, 2013, Petitioner returned to the ER with complaints including
palpitations, flushing, dizziness, diarrhea, nausea, vomiting, and sluggish speech. Id. at 146.
Petitioner reported her symptoms as “waxing and waning” for the past two months and that they
“were getting progressively worse.” Id. She also stated that she was under stress “as her family
th[ought] she [wa]s making up [her] symptoms.” Id. The ER physician admitted Petitioner for
further evaluation. Id. at 148–49.
During her hospital stay, on November 19, 2013, Petitioner saw cardiologist Jonathan
Gilbert, M.D., who noted that Petitioner’s BP and heart rate were elevated. Id. at 138. Dr. Gilbert
noted her BP as 170/101 and her heart rate as 134 beats per minute. Id. Dr. Gilbert wrote that
Petitioner reported her symptoms beginning on November 8, 2013. Id. Petitioner indicated that her
symptoms worsened when she was upright, she had an “unsteady gait,” and tingling and numbness
in her hands. Id. Dr. Gilbert opined that Petitioner suffered from sinus tachycardia and “possible
17 Irritable bowel syndrome (“IBS”) is “a common, chronic, noninflammatory condition characterized by
abdominal pain and altered bowel habits (diarrhea or constipation or both), but no detectable pathologic
change; there may be spasms of the intestinal muscles. A variant form is characterized by painless diarrhea.
It is usually due to a combination of psychologic and physiologic factors.” Dorland’s at 1835.
18 Gastroenteritis is “inflammation of the lining of the stomach and intestines, characterized by anorexia,
nausea, diarrhea, abdominal pain, and weakness. Causes include food poisoning . . . ; viral infections . . . ;
consumption of irritating food or drink; and sometimes psychological factors such as anger, stress, or fear.”
Dorland’s at 764.
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POTS-[a]utonomic [d]ysfunction.” Id. at 140. Dr. Gilbert noted that other etiologies for her
condition include “anxiety [and] bronchodilators[.]” Id. He prescribed beta-blockers. Id.
The same day, Petitioner saw neurologist Janet Choi, M.D., for concerns of “autonomic
symptoms.” Id. at 140–41. Petitioner reported that she had “a bad cold and [SOB] that required
steroids . . . prior to the onset of all her problems.” Id. at 141. Dr. Choi wrote that Petitioner
experienced “spells consisting of multiple symptoms of anxiety, lightheadedness, slowing of
speech and cognition, clamminess and coldness of hands and feet, diaphoresis,19 palpitations,
flushing, [and] tinnitus[,]”20 but that Petitioner “denie[d] any associated mental anxiety.” Id. Dr.
Choi noted that Petitioner’s BP had been “variable upon standing, from as high as 175/83 to low .
. . [and that t]hese spells usually improve[d] upon laying back down.” Id. Petitioner underwent a
brain CT and an EEG, which were normal. Id. at 143. Dr. Choi noted that Petitioner’s use of
Coreg21 was helping to reduce her tachycardia. Id. at 134. Dr. Choi’s impression of Petitioner
included malaise and fatigue, nausea, and anorexia. Id. at 135. Dr. Choi opined that Petitioner
“could have [POTS], or some other autonomic dysfunction, such as an autoimmune etiology.” Id.
at 143. Dr. Choi recommended further testing. Id. Petitioner’s serum testing and labs on November
19, 2013, for autoimmune dysautonomia, paraneoplastic antibodies, cortisol levels, and Lyme
disease were all normal or negative. Id. at 352–54. These included tests for acetylcholine receptors
(“AChRs”) and ganglionic AChR antibodies. See id.
On November 20, 2013, Petitioner saw psychiatrist Susanna Kovari, M.D., to discuss her
anxiety. Id. at 135. Petitioner reported that “when [her] symptoms happen[,] she is not ‘mentally
anxious’ but her body feels like it is anxious.” Id. Dr. Kovari diagnosed Petitioner with an anxiety
disorder and recommended outpatient mental health treatment. Id. at 137. Petitioner was
discharged that day. Id.
The next day, November 21, 2013, Petitioner presented to cardiologist Manu Chander,
M.D., to follow up from her recent hospitalization. Id. at 129. Petitioner described her recent
symptoms and “insist[ed that] she does[ not] have anxiety and [that] the POTS [wa]s triggering
her [symptoms].” Id. Petitioner reported that her use of Coreg was making her “sedated and more
dizzy” but was helping her tachycardia. Id. Dr. Chander reduced Petitioner’s Coreg dosage and
recommended a tilt-table test. Id. Dr. Chander also gave Petitioner a psychiatric referral, which
Petitioner declined. Id. at 130.
Petitioner returned to Dr. Gilbert on November 23, 2013, for a follow-up. Id. at 126–29.
Dr. Gilbert reviewed Petitioner’s echocardiogram performed on November 19, 2013, and noted
that it was normal. Id. at 128. Dr. Gilbert indicated that Petitioner’s heart function was normal. Id.
19 Diaphoresis is “sweating, sometimes specifically that [was] induced artificially.” Dorland’s at 509.
20 Tinnitus is “a noise in the ears, such as ringing, buzzing, roaring, or clicking. It is usually subjective in
type[.]” Dorland’s at 1930.
21 Coreg is the trademark preparation of carvedilol. Dorland’s at 414. Carvedilol is “a beta-adrenergic
blocking agent used in the treatment of essential hypertension and as an adjunct in the treatment of mild or
moderate congestive heart failure[.]” Id. at 301.
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Dr. Gilbert assessed Petitioner with POTS, prescribed Midodrine,22 and referred her to a POTS
clinic. Id.
Petitioner underwent a tilt-table test on November 29, 2013. Id. at 177. Petitioner’s baseline
BP and heart rate were 127/78 and 87, respectively. Id. The testing revealed sinus tachycardia
beginning two minutes after Petitioner was placed in a head-up tilt, “with heart rates in the 113 to
140 beats per minute range.” Id. The technician noted that “[t]here was no concomitant significant
change in blood pressures. Specifically, there was no associated orthostatic hypotension.” Id.
Petitioner reported “multiple somatic complaints” during the head-up portion of the test, including
“hand shaking, lightheadedness, anxiousness, hyperventilation, lightheadedness, and nausea.” Id.
Petitioner indicated that such symptoms improved when she was placed in a supine position. Id.
The technician noted that “[i]mmediately prior” to being placed in a supine position, her BP was
125/83. Id. After two minutes in a supine position, Petitioner’s BP was 133/73, and her heart rate
was 94 beats per minute. Id. After five minutes, her BP decreased to 110/64. Id. Such findings
were “consistent with [POTS].” Id.
Petitioner followed up with Dr. Chander on December 2, 2013. Id. at 126. Dr. Chander
agreed that the tilt-table test was “suggestive of POTS.” Id. Petitioner reported feeling better on
Coreg and “especially since she started [M]idodrine.” Id. Dr. Chander encouraged Petitioner to
hydrate, eat well, wear pressure stockings, and continue taking her medications. Id.
On December 20, 2013, Petitioner returned to the ER complaining of ongoing POTS
symptoms, including that she had been “bed-ridden for the last month[]” and had left calf pain,
tingling in her left lower extremity, and dehydration. Id. at 123. The attending physician noted that
when Petitioner did not hydrate, her POTS symptoms worsened. Id. at 120. Petitioner received IV
fluids. Id. Petitioner returned to the ER on December 31, 2013, and January 2, 2014, reporting
“flare up[s]” of her POTS symptoms, including nausea, “generalized weakness, dizziness, and
‘feel[ing] like she will pass out[.]’” Id. at 116. Petitioner also reported that she was “unable to keep
up with [her two to three liter] hydration requirement.” Id. at 113, 116. Each time she presented
with these complaints Petitioner received IV fluids to successfully treat her symptoms. See id.
On January 6, 2014, Petitioner presented to neurologist Alexander Barboi, M.D., as he
specializes in autonomic disorders. Pet’r’s Ex. 6 at 8. He wrote that Petitioner “seem[ed] to have
long standing symptoms that were present for a while and then got better[,] such as intermittent
[SOB] after a bout of respiratory infection in December 2012, episodes of palpitations at night[,]
and dizzy spells in 2011[.]” Id. He also recorded a “more remote history of intermittent flushing[,]
abdominal pain[,] and diarrhea.” Id. Dr. Barboi noted that Petitioner’s “increased symptoms” of
“dizziness and presyncopal [sic] episodes[]” began in November of 2013. Id. He indicated that
since Petitioner’s November 2013 hospitalizations, she “has been quite restricted in her daily
activities with [an] inability to work and drive[.]” Id. Dr. Barboi’s impression of Petitioner was
“long-standing background autonomic dysfunction syndrome[,] acquired versus inherited.” Id. at
22 Midodrine hydrochloride is “a direct-acting sympathomimetic agent, that stimulates the a-adrenergic
receptors of the arteriolar and venous vasculature; used as a vasopressor in the treatment of orthostatic
hypotension.” Dorland’s at 1165.
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12. He also recorded his impression of possible “[s]icca syndrome”23 and “mastocyte activation
syndrome.”24 Id. Dr. Barboi wrote that there were “[u]nclear reasons for [Petitioner’s] worsening
[symptoms] in the past year.” Id. He recommended exercise, continued hydration, to take
Florinef25 instead of Coreg, and only to take Midodrine “sparingly.” Id.
Petitioner presented to the hospital for placement of a port-a-catheter to receive IV fluids
on January 17, 2014. Pet’r’s Ex. 4 at 88, 100. On January 20, 2014, Petitioner obtained approval
for home health services for IV fluids to treat her continued dehydration because she was
homebound as a result of her POTS and could not drive herself. Pet’r’s Ex. 3 at 50. Petitioner
received IV fluids every other day. See id.
On January 27, 2014, following Dr. Barboi’s suspicion, Petitioner underwent a lip biopsy
to rule out a possible Sjögren’s syndrome26 diagnosis. Pet’r’s Ex. 2 at 27. The clinical impression
of the biopsy indicated that the test “rule[d] out Sjögren’s.” Pet’r’s Ex. 4 at 57. Petitioner presented
to neurologist Hoyee Chan, M.D., on February 9, 2014. Id. at 65. Dr. Chan noted Petitioner’s lip
biopsy on January 27, 2014, and “[d]oubted [that] Sjögren’s [wa]s the cause of her POTS[.]”Id. at
67. Dr. Chan referred Petitioner to an endocrinologist to “[rule out] any adrenal insufficiency as
the cause of [her] POTS related symptoms.” Id.
Petitioner presented to endocrinologist Lisa Purdy, M.D., on February 11, 2014. Id. at 59.
Petitioner reported that she had been “homebound” for the past three months. Id. Petitioner
underwent cortisol testing, which did not suggest Addison’s disease,27 and her anti-Sjögren’s titer
was negative.28 Id. at 61, 276. Dr. Purdy wrote that Petitioner “has considerable anxiety associated
with her [POTS] condition, which exacerbates her other symptoms[,] including her BP.” Id. at 59.
23 Sicca syndrome is “keratoconjunctivitis and xerostomia without connective tissue disease[,]” also called
Sjögren’s syndrome. Dorland’s at 1848. Sjögren’s syndrome is “a symptom complex of unknown etiology,
usually occurring in middle-aged or older women, marked by the triad of keratoconjunctivitis sicca with or
without lacrimal gland enlargement, xerostomia with or without salivary gland enlargement, and the
presence of a connective tissue disease, usually rheumatoid arthritis but sometimes systemic lupus
erythematosus, scleroderma, or polymyositis. An abnormal immune response has been implicated.” Id.
24 Mastocyte activation syndrome or mastocytosis syndrome is “an episodic syndrome occurring in certain
patients with systemic mastocytosis, usually those with skin lesions, bone lesions, and hepatosplenomegaly,
presumably associated with histamine release from degranulation of mast cells, and characterized mainly
by intense pruritus, flushing, headache, tachycardia, hypotension, and syncope.” Dorland’s at 1838.
25 Florinef is the trademark preparation of fludrocortisone acetate. Dorland’s at 718. Fludrocortisone acetate
is “the acetate salt of a synthetic steroid with potent mineralocorticoid and high glucocorticoid activity,
used in replacement therapy for primary or secondary adrenocortical insufficiency in Addison disease and
for the treatment of salt-losing adrenogenital syndrome; administered orally.” Id. at 719.
26 See supra, note 23 (explaining that Sjögren’s syndrome is sicca syndrome).
27 Addison disease is “a chronic type of adrenocortical insufficiency, characterized by hypotension, weight
loss, anorexia, weakness, and a bronzelike hyperpigmentation of the skin. It is due to tuberculosis- or
autoimmune-induced destruction of the adrenal cortex, which results in deficiency of aldosterone and
cortisol and is fatal in the absence of replacement therapy[.]” Dorland’s at 528.
28 Petitioner’s medical records and filings contain several notations past this date that reflect she believed
she had Sjögren’s syndrome (based on Dr. Barboi’s impression) despite her negative lip biopsy and anti-
Sjögren’s titer. See, e.g., Tr. 30:6–12. Despite Petitioner and Dr. Barboi’s belief, the evidence fails to show
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On March 6, 2014, Petitioner consulted with rheumatologist Kenneth Crane, M.D. Id. at
34; Pet’r’s Ex. 2 at 9. Petitioner explained her medical history, including, among other things,
weight loss, weakness, fatigue, hoarseness and frequent sore throats, chest pain, rapid and sudden
changes in heartbeat, high BP, SOB, nausea, constipation, headaches, and dehydration. Pet’r’s Ex.
2 at 14–15. Dr. Crane assessed Petitioner with hyperadrenergic POTS. Id. at 13. Dr. Crane ordered
additional lab testing. Id.
On March 20, 2014, Petitioner underwent spirometry testing at the direction of
allergist/immunologist Paul Kentor, M.D. Pet’r’s Ex. 4 at 196. The spirometry test revealed no
evidence of asthma. Id. Petitioner also underwent a panel of tests, including an autoimmune
dysautonomia evaluation, on March 25, 2014. Id. at 227. This repeat test included serum testing
for AChR and g-AChR antibodies. Id. The results of this testing were normal. Id. On March 27,
2014, Petitioner presented for the additional lab work previously ordered by Dr. Crane. Pet’r’s Ex.
2 at 9. Petitioner’s lab results from this date revealed elevated C3 and C4 levels, SED rate, ANA
titer (of 1:160), and alpha-2 globulins. Id. at 17–35.
Petitioner followed up with Dr. Chan on March 28, 2014, to discuss her recent positive
ANA titer and Petitioner’s concern that this could be reflective of multiple sclerosis (“MS”).29 Id.
at 16. Dr. Chan wrote that Petitioner’s positive ANA was “very non-specific” and “could be [a]
false positive” in light of prior negative testing. Id. at 18. On April 25, 2014, Petitioner returned to
Dr. Chan reporting SOB with an “associated cough” and “burning” in her chest. Pet’r’s Ex. 7 at
73. On examination, Petitioner exhibited normal lung function. Id. at 76. Dr. Chan told Petitioner
that Petitioner’s symptoms were “most likely anxiety related.” Id. Petitioner underwent a
pulmonology consultation for her SOB and chest pain with Jeffrey Hamilton, M.D., on April 30,
2014. Id. at 64. Dr. Hamilton indicated that Petitioner’s physical exam was normal, and a chest CT
was “clear.” Id. at 68–69.
by a preponderant standard that Petitioner does, in fact, suffer from Sjögren’s. For example, when Petitioner
presented to rheumatologist Dr. Crane on March 6, 2014, she told Dr. Crane that she had been diagnosed
with Sjögren’s, confirmed by a lip biopsy. See Pet’r’s Ex. 2 at 9, 14–15. Based on Petitioner’s self-reported
history, Dr. Crane assessed her with Sjögren’s. Id. at 13. Petitioner also told Dr. Hamilton on April 30,
2014, that she had been diagnosed with Sjögren’s, which prompted him to make the same assessment and
to unsuccessfully look for an association between Petitioner’s POTS and Sjögren’s. Pet’r’s Ex. 7 at 64, 69.
Drs. Crane and Hamilton’s assessments do not provide support for a Sjögren’s syndrome diagnosis. In fact,
Petitioner’s reports to treaters are inconsistent with her laboratory testing that was non-diagnostic for
Sjögren’s. See, e.g., Pet’r’s Ex. 4 at 57. When rheumatologist Dr. Gan reviewed the results of Petitioner’s
lip biopsy first-hand on August 4, 2014, he, consistent with the original interpretation, determined the
results conclusively showed she did not have Sjögren’s. Pet’r’s Ex. 7 at 13–14. Additionally, other treaters
opined Petitioner did not have Sjögren’s. See, e.g., Pet’r’s Ex. 4 at 18, 67; Pet’r’s Ex. 7 at 73–74. Petitioner
Sjögren’s syndrome diagnosis is therefore not supported by a preponderance of the evidence, and I will not
credit Dr. Barboi’s unsubstantiated conclusion or discuss this issue further.
29 Multiple sclerosis is “a disease in which there are foci of demyelination throughout the white matter of
the central nervous system, sometimes extending into the gray matter; symptoms usually include weakness,
incoordination, paresthesias, speech disturbances, and visual complaints. The course of the disease is
usually prolonged, so that the term multiple also refers to remissions and relapses that occur over a period
of many years . . . . The etiology is unknown.” Dorland’s at 1680.
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Petitioner had a follow-up with Dr. Barboi on July 10, 2014. Id. at 159. Petitioner reported
“a chief complaint of [an] adrenergic flare” and that she was “in a constant [feeling of] fight or
flight.” Id. Petitioner explained that she was “unable to take care of herself” and that she “ha[d]
difficulty standing up for fear of passing out.” Id. at 159–60. Petitioner’s physical examination was
normal. Id. Dr. Barboi noted his impression as a “POTS flare.” Id. at 162–63. Dr. Barboi directed
Petitioner to the ER “for evaluation and admission, and medication titration.” Id. at 149. Petitioner
remained in the hospital from July 10 to July 13, 2014, and was treated with Ativan30 and IV fluids
until her symptoms resolved. Id. at 134.
On August 4, 2014, Petitioner returned to Dr. Chan with complaints of bleeding gums. Id.
at 21. The same day, Petitioner saw rheumatologist Justin Gan, M.D., to address her bleeding gums
and dry mouth. Id. at 10. Petitioner reported that her gums were also swollen and painful. Id. Dr.
Gan noted his impression that Petitioner’s dry mouth, dry eyes, and gum disease “may be related
to [her] POTS[.]” Id. at 14. The next day, on August 5, 2014, Petitioner returned to the ER with
complaints of nausea, fever, neck pain, bleeding gums, and dehydration and the need for IV fluids.
Id. at 164. Throughout 2015 and 2016, Petitioner presented to the ER on several occasions
reporting, among other things, SOB, joint pain, chest tightness, and difficulty swallowing. Pet’r’s
Ex. 12 at 17, 19–20, 26; Pet’r’s Ex. 11 at 7, 29, 31, 46, 55–56; Pet’r’s Ex. 24 at 50, 174, 183, ECF
No. 24-1. Petitioner was routinely treated with IV fluids. See id.
Petitioner had a follow-up with Dr. Barboi on June 14, 2016, during which he noted his
impression of hyperadrenergic POTS.31 Pet’r’s Ex. 42 at 174, ECF No. 44-3. Dr. Barboi did not
order further testing for autonomic nervous system dysfunction or opine that Petitioner’s POTS
was immune-mediated. Id. at 174–78. Petitioner underwent testing for anti-adrenergic antibodies
on July 14, 2020, which yielded negative or normal results. Pet’r’s Ex. 62 at 1, ECF No. 64-1.
Petitioner has not filed any additional medical records.
B. Petitioner’s Affidavits & Fact Testimony
Petitioner submitted two affidavits and testified at the entitlement hearing. See Pet’r’s Exs.
18, 28, ECF No. 25; see also Tr. 11–53. Petitioner wrote that she was “in good health” prior to her
October 8, 2013 vaccination. Pet’r’s Ex. 18 ¶ 2. Petitioner noted that she had received the flu
vaccine in the past “and never had a problem with it.” Id. ¶ 4; Tr. 17:12–17.
Petitioner attested that “[a]bout three weeks” post vaccination she developed symptoms,
including abdominal cramping, diarrhea, nausea, lightheadedness, tremors, and chills. Pet’r’s Ex.
18 ¶ 5. Petitioner was asked to further clarify when her gastrointestinal (“GI”) symptoms began.
She acknowledged that she presented to ENT Dr. Duyka on October 23, 2013, and testified that
she would have told Dr. Duyka of any “symptoms of gastrointestinal distress” if she had been
having them at that time, as Petitioner was “very thorough[.]” Tr. 18:6–14. Based on this
30 Ativan is the trademark preparation of lorazepam. Dorland’s at 173. Lorazepam is “a benzodiazepine
with anxiolytic and sedative effects . . . for the treatment of anxiety disorders and short-term relief of anxiety
symptoms[.]” Id. at 1074.
31 Dr. Barboi also noted his impression of sicca syndrome based on Petitioner’s lip biopsy, despite negative
serologies. Pet’r’s Ex. 42 at 174.
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discussion, Petitioner stated it would be fair to say her gastrointestinal symptoms began “sometime
after seeing Dr. Duyka in late October [of] 2013[.]” Tr. 18:15–18.
She continued that she had her “first hypertensive crisis” later, on November 8, 2013.
Pet’r’s Ex. 18 ¶ 5. Petitioner wrote that she returned to the ER for the second time that day “with
[an] extremely elevated [BP] and heart rate, slurred speech, and dizziness.” Id. She testified that
she was experiencing weakness and nausea without vomiting, which also began that day. Tr.
19:12–17. Petitioner explained that her symptoms of dizziness and weakness began while she was
sitting down, “relaxing” watching television. Tr. 19:18–22. She stated she then “suddenly[ had] a
sensation that [her] heart was racing[, and she i]mmediately[ began] to have palpitations.” Tr.
19:22–24. Petitioner indicated that “[s]ince that date,” she has had “chronic POTS symptoms[,]
including tachycardia, dizziness, flushing, tremors, and hypovolemia.” Pet’r’s Ex. 18 ¶ 5.
Petitioner later stated that when she reported symptoms of flushing, shaking, high BP, nausea,
jitteriness, and coldness to Dr. Schaefer on November 14, 2013, this was the first time she
experienced this “constellation of symptoms.” Tr. 22:22–23:1–4 (citing Pet’r’s Ex. 4 at 151).
Petitioner discussed several notations in her medical records that she asserted were
inaccurate. She addressed the November 9, 2013 note from Dr. Nathanson that indicated Petitioner
“had not been feeling well for the last few months.” Tr. 20:16–21 (citing Pet’r’s Ex. 4 at 159).
Petitioner testified that description “does[ not] sound accurate in its entirety.” Tr. 20:22. Petitioner
explained she was referring to her asthma and allergy symptoms in an attempt “to be thorough
with [Dr. Nathanson].” Tr. 21:2–5. But she was not referring to the symptoms of an elevated BP,
heart rate, dizziness, and weakness she experienced on November 8, 2013, which prompted her to
go to the hospital. Tr. 21:6–9.
Petitioner wrote that she is “aware that in the medical records from [her] hospitalization on
November 19, 2013, there is a notation that [she] had been having symptoms of ‘palpitations,
increased heart rate[,] flushing, diarrhea . . . for [the] past [two] months.’” Pet’r’s Ex. 28 ¶ 6 (citing
Pet’r’s Ex. 4 at 146). Petitioner attested that she “do[es] not specifically recall what [she] reported
at that time[] but that is not an accurate description of when [her] symptoms started.” Id. Instead,
she maintained her symptoms started “in very early November [of] 2013 and perhaps as early as
the very end of October 2013.” Id. Petitioner stated Dr. Choi’s November 19, 2013 note that
Petitioner reported a bad cold and SOB prior to the onset of her symptoms “is not accurate.” Tr.
24:4–11. Petitioner “believe[d Dr. Choi] was referring to [Petitioner’s] thorough explanation of
[her] previous medical issues . . . where [she] explained [she] had issues with asthma and then
separately explained to her that [she] had issues with allergies . . . sinuses and things of that nature.”
Tr. 24:12–21. Petitioner wrote that she “was never diagnosed with any viral illness during this
time.” Pet’r’s Ex. 18 ¶ 3; Pet’r’s Ex. 28 ¶ 3.
Petitioner discussed the visit notes from her January 6, 2014 encounter with Dr. Barboi.
Pet’r’s Ex. 28 ¶ 7 (citing Pet’r’s Ex. 6 at 8). Petitioner wrote that she does not “specifically recall”
what she said to Dr. Barboi on this occasion. Id. ¶ 8. She indicated that she “was having trouble
thinking clearly at that time” as she “had not yet started receiving proper treatment to enhance
proper profusion of blood to [her] brain.” Id. When confronted with the visit notes, she
acknowledged that the notation includes references to Petitioner’s “long standing symptoms” of
palpitations, dizzy spells, and SOB since 2011 and 2012, respectively. Id. ¶ 7 (citing Pet’r’s Ex. 6
at 8); Tr. 28:5–13. Petitioner attested that she was “sure” she told Dr. Barboi about “episodes of
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palpitations at night and dizzy spells” but that such symptoms did not begin until November of
2013. Pet’r’s Ex. 28 ¶ 8. She instead attributed her SOB complaints to her asthma and her
palpitations or dizziness to her anxiety “to make sure [she] was being thorough.” Tr. 28:17–22.
Petitioner attested that she “do[es] recall that in the summer of 2012,” she went to the ER
after feeling “ill” after being on an “airplane with no air conditioning for several hours.” Pet’r’s
Ex. 28 ¶ 9. Petitioner testified this occurred the same day she went to the ER, June 10, 2012. Tr.
30:17–25 (citing Pet’r’s Ex. 4 at 59; Pet’r’s Ex. 67). Petitioner described the circumstances that
caused her to go to the ER. She stated that after being in an airplane all day, she used cannabis at
night because she could not sleep. Tr. 39:16–22. She then had a coughing fit, her heart was racing,
and she was shaking. Tr. 39:23–24. Petitioner testified that her heartrate did not change depending
on her position during this time. Tr. 31:9–21. Instead, it was “consistent throughout.” Tr. 31:21–
23. She testified the ER doctors told her the cause of her symptoms was “probably dehydration[,]”
and she received fluids. Tr. 32:9–11, 39:21. She also clarified the circumstances surrounding her
January 12, 2011 ER visit. Tr. 41:23–42:1–25. She stated she presented with a high heart rate and
anxiety due to stress in her personal life. Tr. 42:2–17. Petitioner testified her heart rate was
“consistent no matter what position [she] was in[.]” Tr. 43:1–6. She stated that the attending
physician told her it was anxiety. Tr. 42:18–25.
She also acknowledged that Dr. Barboi recorded “a more remote history of intermittent
flushing[,] abdominal pain[,] and diarrhea.” Pet’r’s Ex. 28 ¶ 7 (citing Pet’r’s Ex. 6 at 8); Tr. 28:6–
13. She wrote that she “do[es] not know what [she] told Dr. Barboi about [her] intermittent
flushing” during this visit. Pet’r’s Ex. 28 ¶ 10. She indicated she “believe[s]” she told him that,
since childhood, she “occasionally experience[s] splotchiness on [her] chest and neck when [she
is] nervous.” Id. Petitioner recalled telling Dr. Barboi about her abdominal pain and diarrhea she
experienced before October of 2013, but she explained that she was “referring to the time period
when [she] was first diagnosed with laryngeal reflux[]” and was having a reaction to her
medications. Id. ¶ 11.
Petitioner described the difference between her pre- and post-vaccination anxiety
symptoms. Pet’r’s Ex. 18 ¶ 6. She explained that her pre-vaccination anxiety “was more a feeling
of worry” and “stress over [her] relationships.” Id. She noted that she “would feel shaky, have a
sense of . . . impending doom . . . [SOB,] and an elevated heart rate.” Id.; Pet’r’s Ex. 28 ¶ 4; Tr.
13:16–21. Petitioner testified that she was “able to discern” such symptoms were related to her
anxiety because they “would coincide with the emotions that [she] was feeling and anxious
thoughts.” Tr. 13:22–14:1. She wrote that her post-vaccination anxiety is “a constant feeling of
agitation and ‘fight or flight.’” Pet’r’s Ex. 18 ¶ 6; Pet’r’s Ex. 28 ¶ 4.
III. Experts
A. Expert Review
1. Petitioner’s Expert, David Axelrod, M.D.
Dr. Axelrod is a “[c]linical [i]mmunologist, trained at McGill University . . . and at the
National Institutes of Health [(“NIH”).]” Pet’r’s Ex. 17 at 1. He served as a principal investigator
at the Walter Reed Army Institute of Research, where his laboratory “participated in vaccine
development.” Id. Dr. Axelrod did not submit a curriculum vitae with his expert report. He
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authored one written report in support of Petitioner’s claim and did not testify at the entitlement
hearing. See id.
2. Petitioner’s Expert, Marcel Kinsbourne, M.D.
Dr. Kinsbourne received his medical degree from Guy’s Hospital in London, England in
1955. Tr. 56:11–13; Pet’r’s Ex. 30, ECF No. 27-2. He did “nine years of post-graduate training in
neurology, pediatrics, and pediatric neurology.” Tr. 56:13–15. Dr. Kinsbourne spent three
additional years “working and teaching on comprehensive neuroscience” at Oxford University. Tr.
56:15–17. He came to the United States in 1967 to be a professor of neurology and pediatrics and
later the director of pediatric neurology at Duke University Medical Center. Tr. 56:18–21; Pet’r’s
Ex. 30 at 2. Dr. Kinsbourne served as a professor of pediatric neurology and psychology at the
University of Toronto from approximately 1979–1985. Pet’r’s Ex. 30 at 2. He was the director of
the behavioral neurology department at the Eunice Kennedy Shriver Center from 1980–1991. Id.
He served as a lecturer in neurology at Harvard Medical School and as a clinical associate in
neurology at Massachusetts General Hospital from 1981–1991. Id. Dr. Kinsbourne joined the
faculty at the New School in New York in 1995, which “is not a medical school” but instead he
was “working in the effort to teach psychology, the essentials of neuroscience.” Tr. 57:5–9. He
testified he has been studying neuroscience for “all of [his] adult life.” Tr. 57:14–16.
Dr. Kinsbourne has received numerous honors and awards, has served on advisory
committees and editorial boards, and holds memberships in scientific societies. Pet’r’s Ex. 30 at
3–6. His curriculum vitae includes over four-hundred peer-reviewed articles, book chapters, and
books of which he is a listed author. See id. at 7–40. Dr. Kinsbourne testified that he is retired from
treating patients but stays up to date by reading “everything pertinent to his interests” in
neuroscience and by participating in the Vaccine Program. Tr. 59:8–19. He noted that he still
participates in peer reviewing for medical journals. Tr. 59:23–25. Dr. Kinsbourne submitted four
expert reports and testified at the entitlement hearing. See Pet’r’s Exs. 29, 31, 32, 46; Tr. 56–153.
Petitioner offered Dr. Kinsbourne as an expert in neurology without objection, and I recognized
him as such. Tr. 60:12–21.
However, during his testimony, Dr. Kinsbourne discussed principles of immunology, to
which Respondent noted a continuous objection. See Tr. 62–73. Respondent argued Dr.
Kinsbourne had no specific training or expertise in neuroimmunology that allows him to testify as
an expert in that field. Tr. 66:17–21. Under voir dire, Dr. Kinsbourne testified that “[y]ou could[
not] do neurology in some way where you are ignorant of such basically related sciences as
neuroimmunology.” Tr. 63:19–21. Dr. Kinsbourne stated that “at the level which [he is] discussing
[immunology], any qualified neurologist would be perfectly capable of doing it.” Tr. 66:14–15.
He noted that throughout his career as a neurologist, he has “frequently” treated patients with
autoimmune neurological conditions. Tr. 68:10–13. Dr. Kinsbourne testified that he has only
assessed a patient with POTS as part of his participation in the Vaccine Program. Tr. 118:11–13.
Based on Dr. Kinsbourne’s representations during voir dire, I allowed Dr. Kinsbourne to testify to
matters related to immunology. See Tr. 72–73. Respondent agreed it would be proper to admit the
full testimony of Dr. Kinsbourne and for me to assign appropriate weight, rather than to strike
portions of his testimony. See Tr. 229–30. The hearing continued under that premise.
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3. Respondent’s Expert, Phillip Low, M.D.
Dr. Low received his medical degree from the University of Sydney in Sydney, Australia
in 1965. Resp’t’s Ex. B, ECF No. 22-13. His relevant post-graduate training includes residencies
in neurology at the Royal Prince Alfred Hospital in Australia and the Mayo Clinic in Rochester,
Minnesota in 1973 and 1980, respectively. Id. at 1–2. Dr. Low also completed a research
fellowship in neurology at the Mayo Clinic in 1977. Id. at 2. Dr. Low has held numerous
appointments at the Mayo Clinic. See id. at 2–4. Dr. Low served as an assistant and then associate
professor of neurology from 1978–1982 and 1982–1984, respectively. Id. at 2–3. Dr. Low trained
physicians in the field of autonomic neuropathy, including several of the authors of the submitted
literature. Tr. 157:18–20. From 1989–2004, Dr. Low was the Chairman of the Division of Clinical
Neurophysiology. Resp’t’s Ex. B at 3. He is board certified in “psychiatry and neurology” and
neurology with a subspeciality in clinical neurophysiology. Id. He explained that his certification
in clinical neurophysiology includes a specialization in autonomic disorders. Tr. 161:8–17. Dr.
Low has received numerous honors and awards, holds memberships in honorary societies and
committees, and serves on editorial boards. Resp’t’s Ex. B at 3–5. His curriculum vitae includes
approximately four-hundred peer-reviewed articles, and hundreds of edited textbooks, book
chapters, studies, and editorials of which he is a listed author. See id. at 5–101.
Dr. Low founded the Autonomic Reflex Laboratory at the Mayo Clinic in 1982. Id. at 3.
He stated that in this lab, he discovered the test that is used to “assess patients with autonomic
conditions” called the “QSART.” Tr. 155:8–16. He was also involved in the development of the
tilt-table test. Tr. 155:17–19. He served as the head of the Peripheral Nerve Center from 1994–
2002. Resp’t’s Ex. B at 3. Dr. Low testified that this is “a center that focuses on autonomic
disorders.” Tr. 155:4–7. He also headed an “NIH-funded program project . . . that was aimed at
autoimmune disorders.” Tr. 156:13–19. Dr. Low testified that he has evaluated “thousands” of
patients with autonomic disorders and “thousands” with POTS throughout his career. Tr. 159:8–
15. He has treated patients with “autoimmune disorders related to the autonomic nervous system.”
Tr. 159:17–20. Dr. Low noted that he is one of many who has and is currently investigating
whether there is an autoimmune basis for POTS and that he was the first to “identify the presence
of an antibody in POTS.” Tr. 160:20–23. He noted that he later determined that the antibody,
AChR, is a “bystander antibody” and that it “does nothing.” Tr. 161:1–6. He indicated he currently
devotes half of his clinical practice to research and the other half to treating patients. Tr. 158:13–
25. Dr. Low submitted four expert reports and testified at the entitlement hearing. Resp’t’s Exs.
A, C, D, E; Tr. 153–229. Respondent offered Dr. Low as an expert in neurology, neurophysiology,
and autonomic neuropathies without objection, and I recognized him as such. Tr. 162:6–11.
B. Expert Reports and Testimony
1. Petitioner’s Expert, Dr. Axelrod
Dr. Axelrod submitted one written report early in this case, without medical literature, and
did not testify at the entitlement hearing. See Pet’r’s Ex. 17. Dr. Axelrod noted that Petitioner’s
medical records reflect that she experienced symptoms consistent with POTS within twenty-one
days of her October 8, 2013 flu vaccination. Id. at 1. Such symptoms included Petitioner’s diarrhea,
abdominal cramping, anorexia, LPR, chest pressure, hypertension, tachycardia, slurred speech,
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profound weakness, and weight loss. Id. Dr. Axelrod opined that the twenty-one-day period
between Petitioner’s flu vaccination and the development of her POTS establishes a causal
relationship. Id. at 3.
He proposed a biological mechanism and argued that after Petitioner received the flu
vaccine, “she experienced [] an innate immune response to the vaccine, which included the release
of cytokines that would have allowed her adaptive peripheral immune response to the vaccine to
enter the central nervous system through a more permeable blood brain barrier,” and to cause her
POTS with autonomic neuropathy. Id. at 4. Dr. Axelrod noted that generally “vaccination results
in elevated levels of Interleukin-1ß, Interleukin-6, Tumor Necrosis Factor-ɑ [(“TNFɑ”),] and G-
CSF.” Id. at 3. He continued that “TNFɑ and Interleukin 6 result in disruption of the blood brain
barrier through down regulation of interendothelial adherens and tight junction proteins, leading
to elevation of paracellular permeability.” Id. at 3–4. He cited articles to support these claims but
did not provide them for consideration along with his report. He continued that “[t]his permeability
allows blood borne chemicals, such as cytokines, and cells produced in the peripheral circulation,
to enter the environment of the brain, and to act upon cells within the brain . . . [and] central
nervous system.” Id. at 4.
Dr. Axelrod relied on the concept of molecular mimicry and argued that there are “lipid
structures on the influenza vaccine that are homologous to lipids on nervous tissues.” Id. He
referred to the P2 protein, syntaxin, and hemagglutinin specific immune cells as the potential
homologous structures between the influenza vaccine and nerve tissues. Id. He continued that
“[g]anglioside GM1b on nerve tissues may act as an influenza receptor, to which the influenza
vaccine products can attach.” Id. Once this happens, the immune response to the flu vaccine could
result in damage to nerve tissues. Id. Dr. Axelrod also referred to the concept of “epitope
spreading” and argued that the damage to Petitioner’s nervous system triggered by her immune
response to the vaccine “expose[d] other structures of the nervous tissues[.]” Id. This continued to
cause damage to the nervous system “even after the vaccine products [] disappeared from [her]
body[.]” Id.
2. Petitioner’s Expert, Dr. Kinsbourne
Dr. Kinsbourne summarized Petitioner’s clinical history consistent with her medical
records and Petitioner’s corrections. See Pet’r’s Ex. 29 at 1–3; Pet’r’s Exs. 18, 28. Dr. Kinsbourne
wrote that Petitioner’s POTS diagnosis “is not in question.” Pet’r’s Ex. 29 at 3. He opined that
Petitioner’s POTS was caused by her October 8, 2013 flu vaccine “to a reasonable degree of
medical probability.” Id. at 8.
In support of his conclusion, Dr. Kinsbourne endorsed Dr. Axelrod’s proposed biological
mechanism. Id. at 6. Dr. Kinsbourne acknowledged that “[i]t is certainly the case that scientific
certainty on the specifics of vaccine causation of [an] immune-mediated nerve injury is currently
out of reach.” Id. However, he maintained that Dr. Axelrod’s proposed theory involving a
“peripheral nerve injury via neuroinflammation and possible molecular mimicry is quite specific
enough for purposes of formulating a medically reasonable mechanism of injury[.]” Id. Dr.
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Kinsbourne cited a study by Blitshteyn et al.,32 which found that molecular mimicry is a “possible
pathogenesis” of the new onset of POTS post vaccination due to the “formation of cross-reacting
autoantibodies to the potential targets of the autonomic ganglia, neurons, cardiac proteins or
vascular receptors.” Pet’r’s Ex. 39 at 2, ECF No. 67-6.
Dr. Kinsbourne expanded on Dr. Axelrod’s theory of causation. Dr. Kinsbourne testified
that there is currently a consensus in the medical community that POTS can be an immune-
mediated condition. Tr. 80:10–12. Dr. Kinsbourne cited medical literature to show that “many
investigators [] regard POTS as immune mediated.” Pet’r’s Ex. 29 at 5 (citing Pet’r’s Ex. 39;
Pet’r’s Ex. 66, ECF No. 70-5).33 He cited a year 2000 study by Vernino et al.34 and argued that it
showed “a direct demonstration of autoimmunity among patients with POTS.” Id. (citing Pet’r’s
Ex. 52, ECF No. 68-4). In that study, Vernino et al. tested serum from 157 patients with varying
types of dysautonomia, including POTS. Pet’r’s Ex. 52 at 1. The authors found ganglionic
acetylcholine receptor (“gAChRs”) antibodies in 6 out of 67 patients with either POTS, idiopathic
gastrointestinal dysmotility, or diabetic autonomic neuropathy for a total of 9%. Id. at 1, 3. Based
on their study, the authors determined that “[s]eropositivity for antibodies that bind to or block
ganglionic acetylcholine receptors identifie[d] patients with various forms of autoimmune
autonomic neuropathy[.]” Id. at 1. They continued that “[t]he positive correlation between high
levels of ganglionic-receptor antibodies and the severity of autonomic dysfunction suggests that
the antibodies have a pathogenic role in these types of neuropathy [sic].” Id. The authors concluded
that autonomic neuropathy has “a presumed autoimmune basis.” Id. Dr. Kinsbourne opined that
Petitioner suffered from autonomic neuropathy in addition to POTS. Pet’r’s Ex. 29 at 4. However,
on cross-examination, Dr. Kinsbourne abandoned his reliance on AChRs. He testified that
acetylcholine receptor antibodies are no longer relevant to his theory of vaccine causation. Tr.
120:10–14. Instead, Dr. Kinsbourne explained that his theory is focused on autoantibodies to G
protein coupled receptors (“GPCRs”), including particular adrenergic antibodies. Tr. 120:14–19.
Dr. Kinsbourne explained that autoantibodies against GPCRs are “receptor surfaces which
the autonomic nervous system uses to implement its commands . . . .” Tr. 95:11–14. They “are on
the surface of the cell and they conduct the stimulus given [to] them by the antibody to the internal
part of the cell.” Tr. 95:16–18. He continued that the “antibody either enhances the function
involved of that cell or inhibits it, in both cases, causing disease.” Tr. 95:18–20. He testified that
a “POTS population has a higher incidence of anti-A-adrenergic receptor antibodies and anti-B2
receptor surfaces.” Tr. 97:6–9. Dr. Kinsbourne explained that an adrenergic receptor antibody is a
type of G-protein antibody. See Tr. 120.
Dr. Kinsbourne argued that as autoantibodies to GPCRs are frequently seen in patients with
POTS, this supports his assertion that POTS has an autoimmune trigger. See, e.g., Pet’r’s Ex. 46
at 2. He testified that GPCRs have been associated with autonomic function or disease, such as
autoimmune autonomic disorders. Tr. 95:25–96:12. Dr. Kinsbourne noted that “in cardiovascular
32 S. Blitshteyn, Postural tachycardia syndrome following human papillomavirus vaccination, 21 EUR. J.
NEUROL. 135–39 (2014).
33 S. Blitshteyn, supra, note 32; M. Thieben et al., Postural Orthostatic Tachycardia Syndrome: The Mayo
Clinic Experience, 82(3) MAYO CLIN. PROC. 308–13 (2007).
34 S. Vernino et al., Autoantibodies to Ganglionic Acetylcholine Receptors in Autoimmune Autonomic
Neuropathies, 343 N. ENG. J. MED. 847–55 (2000).
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disorders other than POTS[,]” these autoantibodies against GPCRs “have been associated with
disorders of autonomic dysfunction such as inappropriate sinus tachycardia and orthostatic
hypotension.” Pet’r’s Ex. 46 at 2 (citing Pet’r’s Ex. 56 at 1, ECF No. 68-8).35 The authors of the
Chiale et al. study analyzed patients with inappropriate sinus tachycardia (an arrythmia) and
healthy controls and found that “no anti-autonomic receptor antibodies were detected in healthy
controls[,]” but “[i]n marked contrast, anti-ß adrenergic receptor antibodies were found in 11 of
21 patients affected by the arrhythmia.” Pet’r’s Ex. 56 at 3. They concluded that there is a link
between inappropriate sinus tachycardia and circulating anti-ß adrenergic receptor antibodies. Id.
at 1.
Dr. Kinsbourne cited articles showing that such antibodies to adrenergic alpha-1
adrenergic, beta-adrenergic, muscarinic receptors, and cardiac lipid raft-associated proteins have
also been identified in POTS patients. Pet’r’s Ex. 46 at 2 (citing Pet’r’s Ex. 47 at 1, ECF No. 67-
8; Pet’r’s Ex. 49, ECF No. 68-1; Pet’r’s Ex. 57 at 3, ECF No. 68-9).36 For example, in 2019, the
Gunning et al. study “looked at [] whether th[ere] were elevated, G protein coupled adrenergic
antibodies [in POTS] and they found them.” Tr. 102:8–10 (citing Pet’r’s Ex. 47). The Gunning et
al. study examined 55 patients with POTS and found elevated serum levels of autoantibodies
against alpha-1 adrenergic receptors and muscarinic cholinergic receptors in 89% and 51% of
patients, respectively. Pet’r’s Ex. 47 at 5. Dr. Kinsbourne testified that the Gunning et al. study
noted that a “well documented association with vaccination preceding the development of POTS
is known.” Tr. 102:12–15 (citing Pet’r’s Ex. 47 at 8). The 2019 Hineno et al. study cited by Dr.
Kinsbourne sought to investigate the presence of autoantibodies against G protein coupled
receptors in Japanese girls who complained of symptoms including orthostatic dysregulation
following receipt of the HPV vaccine. Pet’r’s Ex. 57 at 1. The authors found that serum levels of
autoantibodies against various adrenergic receptors and muscarinic acetylcholine receptors were
elevated in girls who had received the HPV vaccine compared to those who did not receive the
vaccine. Id. Hineno et al. determined that the “serum levels of these autoantibodies tended to
decrease with the time course of the illness,” however, “there was no statistically meaningful
association between the clinical symptoms and elevated serum levels of these autoantibodies.” Id.
The authors concluded that this study provided evidence that “post-vaccination abnormal
autoimmunity plays an important role in the development of unique symptoms after HPV
vaccination.” Id. Dr. Kinsbourne argued these adrenergic receptors documented in such studies are
the same GPCRs that affect the regulation of the immune system and may increase inflammatory
responses. Pet’r’s Ex. 46 at 2. Dr. Kinsbourne cited the 2016 study by Fedorowski et al.,37 which
examined 17 POTS patients and found 47% had alpha-1 receptor antibodies, 65% had beta-1
receptor antibodies, and 71% had beta-2 receptor autoantibodies. Pet’r’s Ex. 51 at 7, ECF No. 68-
3. The authors concluded that based on the percentage of POTS patients with autoantibodies, there
35 P. Chiale et al., Inappropriate sinus tachycardia may be related to an immunologic disorder involving
cardiac ß andrenergic receptors, 3 HEART RHYTHM 1182–86 (2006).
36 W. Gunning et al., Postural Orthostatic Tachycardia Syndrome is Associated with Elevated G-Protein
Coupled Receptor Autoantibodies, X J. AM. HEART ASSOC. 1–10 (2019); H. Li et al., Autoimmune Basis
for Postural Tachycardia Syndrome, X J. AM. HEART ASSOC. 1–10 (2014); A. Hineno et al., Autoantibodies
against Autonomic Nerve Receptors in Adolescent Japanese Girls after Immunization with Human
Papillomavirus Vaccine, 2(2) ANN. ARTHRITIS CLIN. RHEUMATOL. 1014–20 (2019).
37 A. Fedorowski et al., Antiadrenergic autoimmunity in postural tachycardia syndrome, 19 EUR. SOC.
CARDIOL. 1211–19 (2017).
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is “an apparent autoimmune diathesis that supports the concept that these autoantibodies play a
role in the pathophysiology of this entity.” Id.
Dr. Kinsbourne also relied on the 2014 Li et al.38 study that used a bioassay and “measured
blood levels of various adrenergic receptor autoantibodies in 14 POTS patients.” Pet’r’s Ex. 46 at
2 (citing Pet’r’s Ex. 49 at 1). The authors found 50% of patients had alpha-1 adrenergic receptor
antibodies, 50% had beta-2 adrenergic receptor antibodies, and all patients had beta-1
autoantibodies. Pet’r’s Ex. 49 at 7. Li et al. explained that this finding supported their hypothesis
that POTS patients manifest “autoantibodies to the pressor [alpha-1 adrenergic receptor] and could
partially block the effectiveness of the normal [alpha-1 adrenergic receptor] endogenous ligand
norepinephrine central to the homeostatic response to upright posture.” Id. at 2. Doing so impairs
vasoconstriction, thereby increasing baroreceptor activation and sympathetic nervous system
activity. Id. The authors determined that the beta-1 adrenergic receptors “would respond to this
increased sympathoneural output and circulating norepinephrine with an exaggerated
tachycardia[,]” resulting in POTS. Id. In other words, their findings supported the relationship
between such antibodies and POTS because alpha-1 adrenergic antibodies “act by rendering these
receptors partially inactive” causing peripheral blood vessels to be “unable to fully constrict on
standing, producing a postural tachycardia.” Id. The authors indicated that beta-1 and beta-2
adrenergic receptor autoantibodies increase the severity of the tachycardia. See id.
In another animal model by Li et al.39 published in 2019, the authors immunized rabbits
with alpha-1 and beta-1 adrenergic receptor peptides. Pet’r’s Ex. 48 at 1, ECF No. 67-9. The
authors found that they were able to induce an exaggerated postural tachycardia (measured using
a tilt-table test) with such receptors. Id. at 2–3. They also found that they were able to block the
alpha-1 and beta-1 autoantibodies from interacting with the receptors, and this caused the heart
rates of the rabbits to return to normal. Id. at 3. Dr. Kinsbourne argued this was “no coincidence”
because “if you then get rid of the autoantibodies, then the effect is reversed.” Tr. 104:7–9. The
authors concluded that their study “supports the concept that cardiovascular autoantibodies play
an important role in POTS pathophysiology.” Pet’r’s Ex. 48 at 8; Tr. 99:18–20. Dr. Kinsbourne
was asked how this study supported his theory that a flu vaccine can cause POTS, and he stated it
is because “vaccines stimulate antibodies.” Tr. 104:2. He continued that in the Li et al. animal
model, “we see that if the antibody that[ is] stimulated happens to be of the two kinds mentioned[],
then even in animals, you get a tilt[-]test result [indicative of POTS] very similar to [that] in
humans.” Tr. 104:3–6.
Dr. Kinsbourne noted that a 2015 study by Blitshteyn et al.40 documents a report of 31 out
of 100 POTS patients who had “one or more markers of autoimmunity.” Pet’r’s Ex. 46 at 2 (citing
Pet’r’s Ex. 33 at 1, ECF No. 67-2). Such markers primarily consisted of elevated ANA titers.
Pet’r’s Ex. 33 at 2–3. The authors wrote that “the question of whether POTS itself is an
autoimmune disorder needs to be answered.” Id. at 6. They confirmed that “adrenergic
38 H. Li et al., Autoimmune Basis for Postural Tachycardia Syndrome, X J. AM. HEART ASSOC. 1–10
(2014).
39 H. Li et al., Adrenergic Autoantibody-Induced Postural Tachycardia Syndrome in Rabbits, X J. AM.
HEART ASSOC. 1–9 (2019).
40 S. Blitshteyn, Autoimmune markers and autoimmune disorders in patients with postural tachycardia
syndrome (POTS), 24 LUPUS 1364–69 (2015).
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autoantibodies . . . appear to be good candidates mechanistically, in that these antibodies may
explain the lack of proper vasoconstriction and increased resting and postural tachycardia in
patients with POTS.” Id. However, on cross-examination, Dr. Kinsbourne admitted that “we do
not know if G protein antibodies are causative of a disease process or induced by the disease.” Tr.
135:18–21.
Dr. Kinsbourne testified regarding the Kharraziha et al.41 article. Tr. 106:3–6 (citing Pet’r’s
Ex. 64, ECF No. 70-3). He explained this article was published recently in 2020 and that the
authors “looked at the receptor surfaces for the POTS relevant adrenergic receptors.” Tr. 106:19–
20. Kharraziha et al. examined 48 patients with POTS, and 25 healthy individuals, using a
“commercial cell-based assay.” Pet’r’s Ex. 64 at 1. The authors found that sera from POTS patients
contained adrenergic receptor antibodies “to a higher degree compared with controls.” Id. Based
on this finding, the authors concluded that “[s]erum-mediated activation of these receptors has
high predictive value for POTS.” Id. The authors found that “these receptor surfaces had been
activated[.]” Tr. 106:20–21. Dr. Kinsbourne explained that this is “what you would expect if there
had been autoantibodies attacking them.” Tr. 106:22–24. Dr. Kinsbourne testified that the authors
“direct[ly] demonstrate[ed]” that the “degree of activation of the adrenergic A receptor was
associated with the severity of orthostatic symptoms in POTS.” Tr. 107:3–7. The authors posited
that their findings “provide new insights in the pathophysiology of POTS and pondered further
research on a possible autoimmune involvement in POTS.” Tr. 107:18–20 (citing Pet’r’s Ex. 64 at
2). Dr. Kinsbourne opined that while the medical literature does not provide scientific certainty for
POTS being immune-mediated, it provides “a very high probability” that it is. Tr. 108:4–6.
On cross-examination, Respondent confronted Dr. Kinsbourne with the 2018 article by
Vernino and Stiles.42 Tr. 132:6–13 (citing Pet’r’s Ex. 53 at 4, ECF No. 68-5). Vernino and Stiles
proposed that an autoimmune basis for POTS “has been suggested based on . . . the occasional
association of POTS with . . . autoimmune disorders.” Pet’r’s Ex. 53 at 1–2. They cited a study of
3,300 POTS patients, which found only 16% had a comorbid autoimmune disease. Id. at 2. They
summarized the “current state of knowledge on the role of autoimmunity in POTS[.]” Id. at 1. The
authors indicated that “[t]he presence of GPCR or low titers of g-AChR autoantibodies alone are
insufficient proof of an autoimmune cause for POTS based on the current research.” Id. at 4. They
also noted that “[a]t this time, adrenergic, muscarinic, and angiotensin receptor antibodies have
not been proven to be causative or useful in confirming a POTS diagnosis.” Id. at 3. Vernino and
Stiles concluded that “[f]urther research is needed to understand the pathological significance, if
any, of GPCR autoantibodies in POTS.” Id. Dr. Kinsbourne read the authors’ conclusion which
indicated that “the evidence for an autoimmune cause is insufficient at this time . . . .” Tr. 132:14–
19 (citing Pet’r’s Ex. 53 at 4). Dr. Kinsbourne maintained the article showed support for an
autoimmune etiology for POTS. Tr. 132:6–13. He eventually agreed that while some studies have
shown antibodies have been found in patients with POTS, such “evidence is not sufficient to
declare POTS an autoimmune disease[.]” Tr. 132:21–25.
41 I. Kharraziha et al., Serum Activity Against G Protein-Coupled Receptors and Severity of Orthostatic
Symptoms in Postural Orthostatic Tachycardia Syndrome, 9 J. AM. HEART ASSOC. 1–17 (2020).
42 S. Vernino & L. Stiles, Autoimmunity in postural orthostatic tachycardia syndrome: current
understanding, 215 AUTONOMIC NEURO. BASIC & CLIN. 78–82 (2018).
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Dr. Kinsbourne further relied on the Vernino and Stiles article’s extensive list of
autoimmune disorders that are, according to the authors, “comorbid with POTS[,]” including,
among others, inflammatory bowel diseases such as Crohn’s43 and ulcerative colitis,44 MS,
Sjögren’s syndrome, rheumatoid arthritis (“RA”),45 and connective tissue disease,46 to argue that
“POTS too is autoimmune[.]” See Pet’r’s Ex. 46 at 1 (citing Pet’r’s Ex. 53 at 2). Dr. Kinsbourne
wrote that this “impl[ies]” that POTS has “underlying mechanisms that overlap with” such
autoimmune diseases. Id. Dr. Kinsbourne wrote that “patients with POTS have a higher prevalence
of autoimmune markers and co-morbid autoimmune disorders than the general population.” Id. at
3. He noted that Petitioner did too, as she “had a positive ANA blood test.” Id.
Dr. Kinsbourne cited several case reports, which he argued support Petitioner’s theory of
vaccine causation. Pet’r’s Ex. 29 at 7. Several reports contain evidence of patients who experienced
the abrupt onset of POTS or orthostatic hypotension/intolerance following the receipt of a HPV
vaccine. Id. (citing Pet’r’s Ex. 34, ECF No. 67-3; Pet’r’s Ex. 39; Pet’r’s Ex. 55, ECF No. 68-7;
Pet’r’s Ex. 57).47 He also cited a case report by Tsai et al.,48 which documented a single case of a
patient who developed POTS after receiving an influenza (H1N1) vaccination. Id. (citing Pet’r’s
Ex. 14, ECF No. 67-1). Dr. Kinsbourne attacked Respondent’s expert Dr. Low’s assertion that
such data has “little scientific merit” since it was not developed in large epidemiologic studies. Id.
Dr. Kinsbourne wrote it “would indeed be convenient to be able to refer to large[,] controlled
studies for corroboration of vaccine causation in POTS cases.” Id. However, he acknowledged that
no epidemiological studies related to POTS onset post flu vaccination, “or any vaccination,” have
been published. Id. Dr. Kinsbourne could not point to evidence that showed that the flu vaccine
43 Crohn disease is “one of the principal forms of inflammatory bowel disease, a chronic granulomatous
disease of the gastrointestinal tract of unknown etiology; it can involve any part of the tract, but most often
is found in the terminal ileum. Characteristics include scarring and thickening of the bowel wall that
frequently leads to intestinal obstruction, abscesses, and fistula formation. There is a high rate of recurrence
after treatment.” Dorland’s at 531.
44 Ulcerative colitis is “one of the principal types of inflammatory bowel disease, consisting of chronic,
recurrent ulceration in the colon, chiefly of the mucosa and submucosa, having an unknown cause. It is
manifested clinically by cramping abdominal pain, rectal bleeding, and loose discharges of blood, pus, and
mucus with scanty fecal particles. Complications include hemorrhoids, abscesses, fistulas, perforation of
the colon, pseudopolyps, and carcinoma.” Dorland’s at 384.
45 Rheumatoid arthritis is “a chronic systemic disease primarily of the joints, usually polyarticular, marked
by inflammatory changes in the synovial membranes and articular structures and by muscle atrophy and
rarefaction of the bones. In late stages, deformity and ankylosis develop. The cause is unknown, but
autoimmune mechanisms and virus infection have been postulated.” Dorland’s at 157.
46 Connective tissue disease or mixed connective tissue disease is “a disorder combining features of
scleroderma, myositis, systemic lupus erythematosus, and rheumatoid arthritis, and marked serologically
by the presence of antibody against extractable nuclear antigen.” Dorland’s at 539.
47 S. Dahan et al., Postural Orthostatic Tachycardia Syndrome (POTS) – A novel member of the
autoimmune family, 0 LUPUS 1–4 (2016); S. Blitshteyn, Postural tachycardia syndrome following human
papillomavirus vaccination, 21 EUR. J. NEUROL. 135–39 (2014); L. Brinth, Orthostatic intolerance and
postural tachycardia syndrome as suspected adverse effects of vaccination against human papillomavirus,
33 VACCINE 2602–05 (2015); A. Hineno et al., Autoantibodies against Autonomic Nerve Receptors in
Adolescent Japanese Girls after Immunization with Human Papillomavirus Vaccine, 2(2) ANN. ARTHRITIS
CLIN. RHEUMATOL. 1014–20 (2019).
48 C. Tsai et al., Novel H1N1 Influenza Vaccine the Cause of Postural Orthostatic, 31(2) J. MED. SCI. 91–
93 (2011).
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could trigger the G protein antibodies implicated in his proposed biological mechanism. Tr.
136:22–137:17. Instead, he stated he was “sure” that he did not “file[] evidence specifically that
the flu vaccine can trigger G protein antibodies.” Tr. 137:15–17, 138:2–139:2.
Nonetheless, he argued Petitioner’s POTS was more likely than not immune-mediated. Tr.
92:18–20. He based this opinion, in part, on the fact that “there is no alternative reasonable
alternative explanation[.]” Tr. 93:5–6. Specifically, Dr. Kinsbourne opined that Petitioner’s
October 8, 2013 flu vaccine “stimulated an immune response . . . which gave rise to antibodies
that happened, in her case, to attack certain regulatory mechanisms of autonomic function . . . that
regulate the sympathetic [immune] system’s response to certain challenges and stressors.” Tr.
64:3–9. He explained that Petitioner’s immune response caused two things. Tr. 64:10–11. First, it
disrupted the regulation of her blood flow so that when she stood up, she lacked a “hydrostatic
gradient” wherein blood drains from the brain and settles in the abdominal organs and legs. Tr.
64:11–16. Her autonomic system failed to counteract that by contracting her blood vessels and
keeping the blood from draining into her legs away from the brain. Tr. 64:16–19, 80:3–9. He
explained that “there are receptors in the sympathetic nervous system which cause the distal
contractions which keep the blood flowing to the brain.” Tr. 64:20–22. But if an antibody blocks
the receptor sites, blood pools in the legs and abdomen away from the brain, and “results in the
person feeling faint and losing consciousness.” Tr. 64:23–65:2. Such stress stimulates the
sympathetic nervous system and “causes the heart rate to accelerate.” Tr. 65:3–4, 79:10–14.
Dr. Kinsbourne indicated that Petitioner’s medical records do not contain procedures “that
could verify tissue injury” as Dr. Low required to validate Petitioner’s medical theory of
autoimmunity. Pet’r’s Ex. 32 at 3. Dr. Kinsbourne argued that adrenergic autoantibodies
“modulate the function of [GPCRs], regardless of whether they produce tissue injury.” Pet’r’s Ex.
46 at 4. He testified that electrodiagnosis, such as EMGs, are capable of reaching and reading large
fibers. Tr. 109:8–22. However, “autonomic nerve fibers are very different. They are thin. They are
either unmyelinated or very likely myelinated. And in them, the EMG . . . is negative.” Tr. 109:22–
25. He therefore argued that electrodiagnosis cannot determine whether autonomic nerves are
damaged or not. Tr. 109:25–110:2. He also noted that one cannot biopsy the autonomic nerves like
they can in cases of small fiber neuropathy, because to do so one would have to delve “deep in the
body[,]” which standard hospitals do not do. Tr. 110:3–17. On cross-examination, Dr. Kinsbourne
testified that Petitioner’s clinical testing, both post vaccination and more recently in 2020, did not
show evidence of G protein antibodies. Tr. 133:17–23. He argued this is not surprising as
antibodies “tend to fade away over time.” Tr. 134:9–135:3 (citing Pet’r’s Ex. 57). He cited the
Hineno et al.49 article, which noted that autoantibodies dwindle over time, as support. Tr. 105:10–
25 (citing Pet’r’s Ex. 57 at 4); see also Pet’r’s Ex. 62. Aside from the presence of antibodies, Dr.
Kinsbourne testified that B and T cells can also be responsible for autoimmune damage. Tr.
144:23–145:2. He argued that even though antibodies “may fade away[,]” the T cells specifically
“may continue to do damage.” Tr. 145:3–4. He sees POTS as a condition where “there is an attack
which causes the damage and the agent may go away, but the damage remains.” Tr. 143:2–7. Dr.
Kinsbourne opined that the T cells were therefore responsible for Petitioner’s active injury seven
years post vaccination. Tr. 145:8–10. However, he stated that the understanding of such cellular
49 A. Hineno et al., Autoantibodies against Autonomic Nerve Receptors in Adolescent Japanese Girls after
Immunization with Human Papillomavirus Vaccine, 2(2) ANN. ARTHRITIS CLIN. RHEUMATOL. 1014–20
(2019).
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immunity “is a work in progress[]” and there has not been “much written about it at this time.” Tr.
145:11–15. Dr. Kinsbourne argued that “[i]n view of her clear-cut diagnosis of POTS and the
extensive and still growing support for an autoimmune mechanism [] in POTS in the medical
literature,” Petitioner’s POTS was caused by an autoimmune reaction to her October 8, 2013 flu
vaccine. Pet’r’s Ex. 32 at 4.
He was asked which subtype of POTS Petitioner suffers from. Dr. Kinsbourne argued that
Petitioner suffers from hyperadrenergic POTS. Tr. 120:23–25. He stated that “there[ is] only one
subtype of POTS[,] and it[ is] hyperadrenergic POTS.” Tr. 123:3–124:17. Dr. Kinsbourne
indicated that he does not think that there are other subtypes or classifications of POTS but rather
that “they overlap or are the same.” Tr. 121:16–19, 122:2–3. On cross-examination, Dr.
Kinsbourne was asked if he knew about POTS associated with hypovolemia, and he testified,
“[w]ell, hypovolemia is one of the – is one of the many – one of the parts of the mechanisms of
causing the disability. Hypovolemia is[ not] a particular type of POTS which by itself causes the
condition.” Tr. 122:4–9. He was also asked if any of Petitioner’s submitted literature discusses
hypovolemic POTS, and he testified that he “d[id not] think there was occasion to discuss it
because there[ is] no evidence that [Petitioner] was hypovolemic at the onset[,]” only
“subsequently.” Tr. 122:11–18. Dr. Kinsbourne stated that if there is hypovolemia with POTS,
“you correct it, [but] you have[ not] cured the POTS.” Tr. 124:5–14. As an example, he testified
that Petitioner had “been hypovolemic many times and had infusions to correct that.” Tr. 125:12–
15.
Regarding timing for the onset of an autoimmune disease post vaccination, Dr. Kinsbourne
testified that “within an accepted time margin of less than 42 days, [Petitioner] began to show
symptoms compatible with POTS[.]” Tr. 111:22–24. He indicated that “it[ is] generally accepted
that when vaccines cause . . . the onset of autoimmune disease, that the onset of clinical
manifestations occurs within the framework of six weeks[.]” Tr. 113:5–8. Dr. Kinsbourne argued
that Petitioner’s onset of symptoms is “well within that framework.” Tr. 113:8–9.
As support, he attributed Petitioner’s nausea, diarrhea, and abdominal pain symptoms
beginning around October 29, 2013, to “part of the presentation of [her] POTS.” Pet’r’s Ex. 29 at
4; Tr. 80:19–25. Dr. Kinsbourne noted that vomiting and diarrhea are “themselves symptoms of
POTS and may precede complaints of orthostatic instability.” Pet’r’s Ex. 32 at 2. He relied on an
article by Parsaik et al.,50 which indicates that the clinical presentation of POTS can include
“orthostatic, nonorthostatic (i.e.[,] nausea, vomiting, diarrhea, constipation, bladder and pupillary
dysfunction), and generalized (fatigue and sleep disturbances) symptoms.” Pet’r’s Ex. 29 at 4
(citing Pet’r’s Ex. 61, ECF No. 69-3). The authors noted that nausea occurs in 59% of patients
with orthostatic intolerance; abdominal pain in 24%; and diarrhea in 32%. See id. Dr. Kinsbourne
cited an abstract of a study by Sullivan et al.,51 which documented that the most common
presenting gastrointestinal symptoms associated with the onset of POTS were abdominal pain,
nausea, and vomiting. Pet’r’s Ex. 32 at 2 (citing Pet’r’s Ex. 38 at 1, ECF No. 40-6). Dr. Kinsbourne
50 A. Parsaik et al., Deconditioning in patients with orthostatic intolerance, 79 NEUROL. 1435–40 (2012).
51 S. Sullivan et al., Gastrointestinal Symptoms Associated with Orthostatic Intolerance, 40(4) J. PED.
GASTRO. & NUTRITION 1–2 (2005).
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also relied on one of the case studies by Blitshteyn et al.,52 documenting six patients with POTS
triggered by the HPV vaccine. Id. (citing Pet’r’s Ex. 39). Patient 2 in the study experienced the
onset of diarrhea, nausea, and weight loss two months following receipt of the third HPV vaccine.
Pet’r’s Ex. 39 at 2. The authors summarized that the six patients “developed new onset of POTS 6
days to 2 months following” receipt of the HPV vaccine. Id. at 1. Dr. Kinsbourne opined that
Petitioner’s diarrhea and GI issues around this time could also be related to Petitioner’s
medications used to treat her LPR. Pet’r’s Ex. 29 at 4. He did not argue such symptoms were
caused by a viral illness, and he noted that Petitioner’s testing did not support that conclusion. Id.
Dr. Kinsbourne addressed Dr. Low’s contention that Petitioner’s POTS began prior to her
October 8, 2013 flu vaccine. Id. Dr. Kinsbourne called Dr. Low’s claim “untenable[.]” Pet’r’s Ex.
32 at 1. He argued Petitioner was not suffering from symptoms of POTS prior to late October of
2013, when her GI issues began. Id.; Tr. 86:9–13. Dr. Kinsbourne discussed the clinical
significance of Petitioner’s symptoms and “their relationship with orthostatic intolerance and
POTS.” Pet’r’s Ex. 31 at 1. He did not agree with Dr. Low’s argument that some of her symptoms
“retrospectively meet the diagnostic criteria for POTS[.]” Id. at 1–2. Dr. Kinsbourne maintained
that any symptoms she experienced pre vaccination did “not at all amount to POTS as defined in
medical literature.” Id. at 2. As support, he cited the Arnold et al.53 article, which defined POTS
as an increased heart rate of “≥30 [beats per minute] within 10 minutes of assuming an upright
posture and in the absence of orthostatic hypotension.” Id. (citing Pet’r’s Ex. 58 at 2, ECF No. 69-
1). The authors wrote that orthostatic intolerance symptoms must last for ≥6 months. See id.; see
also Tr. 77–78. Dr. Kinsbourne defined orthostatic hypotension as “where a person may stand up
and faint.” Tr. 75:18–20. But he described POTS “different[ly] from that because when a POTS
person stands up, they do[ not] immediately . . . experience a problem.” Tr. 76:1–3. Instead, over
five or ten minutes, the “heart rate gets faster and faster and faster and the point is reached when
the pulse rate is so quick that the emptying of the heart into the aorta and the supplying of blood
is insufficient[.]” Tr. 76:3–9. Such patients have to sit down to avoid passing out. Tr. 76:9–12. Dr.
Kinsbourne “scrutinize[d]” Petitioner’s pre-vaccination medical records to determine if they
showed evidence of symptoms consistent with that definition. Pet’r’s Ex. 31 at 2. He argued
“[t]here is no evidence in contemporaneous medical records of POTS prior to the influenza
vaccination.” Id. at 4. Dr. Kinsbourne also indicated that Petitioner had never been diagnosed with
POTS pre vaccination. Id. at 1.
Dr. Kinsbourne opined that by the time Petitioner’s POTS diagnosis was confirmed with
her tilt-table test on November 29, 2013, she had been experiencing symptoms of orthostatic
intolerance for “about four weeks.” Tr. 81:6–9. However, he maintained that the fact that she did
not have symptoms of orthostatic intolerance for six months or more does not detract from the
validity of her POTS diagnosis. Tr. 81:10–12. Instead, he testified that “strictly speaking,” her
diagnosis on November 29, 2013, would more appropriately be “presumptive POTS to be
confirmed on a timescale[]” once such symptoms had been present for six months as required for
the diagnosis of POTS. Tr. 81:15–19.
52 S. Blitshteyn, Postural tachycardia syndrome following human papillomavirus vaccination, 21 EUR. J.
NEUROL. 135–39 (2014).
53 A. Arnold et al., Postural tachycardia syndrome – Diagnosis, physiology, and prognosis, 215
AUTONOMIC NEURO. BASIC & CLIN. 3–11 (2018).
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He attacked Dr. Low’s reliance on Dr. Barboi’s notation reflecting “long-standing”
autonomic symptoms, including flushing, abdominal pain, palpitations, dizzy spells, and SOB to
say her condition preceded her vaccination. Pet’r’s Ex. 29 at 4. He addressed each symptom in
turn. Dr. Kinsbourne wrote that “flushing and abdominal pain are not remotely diagnostic of
POTS[.]” Id. Dr. Kinsbourne attributed Petitioner’s SOB to her asthma. Id. Dr. Kinsbourne
maintained that he had no reason to doubt Petitioner’s asthma diagnosis. Tr. 126:10–23. However,
without specifically referring to the results of Petitioner’s March 20, 2014 spirometry testing, he
testified that if Petitioner had undergone spirometry testing that contradicted an asthma diagnosis,
then he would agree with such results. Tr. 127:10–16. Following that course of questioning, Dr.
Kinsbourne opined that if Petitioner did not have asthma, her pre-vaccination SOB “could well
[have] be[en] part of a panic attack.” Tr. 129:2–7. He generally attributed Petitioner’s SOB
reported from December 2012 to March 2013 to her asthma “playing up” and noted that asthma
“can be precipitated by anxiety.” Tr. 130:14–25 (citing Pet’r’s Ex. 13 at 5). Dr. Kinsbourne
testified that reflux can also cause SOB. Tr. 151:3–6.
Dr. Kinsbourne addressed Petitioner’s remaining symptoms of palpitations and dizzy spells
and wrote they can “have many causes[.]” Pet’r’s Ex. 29 at 4. He argued that “[o]ne cannot base a
diagnosis on such scant and non-specific information.” Id.; Tr. 142:9–14. Dr. Kinsbourne opined
that Petitioner’s history of symptoms from 2011 noted by Dr. Barboi “have no apparent relevance
to [the] onset of [Petitioner’s] POTS” because they are non-specific symptoms. Pet’r’s Ex. 32 at
1. He wrote that “Dr. Barboi made a clear distinction between these non-specific episodes and the
acute onset of [her] POTS” by noting that “in November of 2013[, Petitioner] started having
increased symptoms of dizziness and presyncopal episodes.” Pet’r’s Ex. 29 at 4. Dr. Kinsbourne
argued that Dr. Barboi’s notation therefore does not show that Petitioner’s POTS began before
November of 2013. Id.
Dr. Kinsbourne admitted, however, that Dr. Barboi’s notation reflected long-standing
symptoms of autonomic dysfunction, just not long-standing POTS. Pet’r’s Ex. 31 at 3. Dr.
Kinsbourne maintained that there is no evidence that Petitioner suffered from dysautonomia prior
to late October of 2013. Tr. 86:14–18, 89:13–15. He testified that dysautonomia “is ongoing” and
that Petitioner’s “medical records would have recorded such a state if it were the case.” Tr. 88:20–
21. Dr. Kinsbourne explicitly stated that “[i]f there had been a prior dysautonomia[,] one would
invoke very significant aggravation of that prior condition, but prior POTS is not in evidence.”
Pet’r’s Ex. 32 at 2.
Dr. Kinsbourne continued his discussion of Petitioner’s medical records seeking evidence
to disprove a pre-vaccination dysautonomia. He discussed Petitioner’s pre-vaccination episodes of
tachycardia in detail to differentiate such symptoms from her post-vaccination POTS. See, e.g.,
Tr. 73–74, 86:19–20 (citing Pet’r’s Ex. 21 at 149–50). Dr. Kinsbourne described Petitioner’s
history of supraventricular tachycardia and noted that while her heartbeat was rapid, it was overall
regular and was not affected by orthostasis, or whether she was sitting, standing, or lying down.
Tr. 74:17–22. Dr. Kinsbourne testified that “this happens in people who have anxiety disorders”
and it is not specifically related to POTS. Tr. 74:22–25. Dr. Kinsbourne stated that Petitioner’s
pre-vaccination history of panic attacks and anxiety could both in themselves aggravate POTS. Tr.
126:3–9. Regarding her 2011 visit to the ER, Dr. Kinsbourne described Petitioner’s condition as
“a typical panic attack in a person who has anxiety.” Tr. 87:6–10. He agreed with Petitioner’s
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treaters’ assessment of anxiety during that visit. Tr. 87:13–17. He stated he would not have been
concerned about dysautonomia in 2011 because “there[ is] no statement that [her symptoms] came
on when she stood up from lying down.” Tr. 87:18–22. Dr. Kinsbourne also addressed Petitioner’s
June 10, 2012 ER visit following being in a hot airplane and smoking marijuana. Tr. 87:25–88:21
(citing Pet’r’s Ex. 67 at 5). Dr. Kinsbourne stated that marijuana can cause tachycardia. Tr. 88:8–
9. He testified that her medical records show no evidence of dysautonomia because her condition
was not dependent on her posture and this “was an isolated attack.” Tr. 88:10–17. Rather, “[t]hese
were occasional, brief attacks of anxiety or panic.” Tr. 88:18.
He also relied on Petitioner’s extensive visits with treaters for her pre-vaccination
conditions, such as asthma, to opine that if Petitioner were having orthostatic intolerance or
syncope, these complaints would not have “escaped [her treater’s] attention.” Pet’r’s Ex. 31 at 2–
3. He applied the same logic to Petitioner’s October of 2013 visits with Dr. Duyka that occurred
post vaccination, but before the onset of her POTS. Dr. Kinsbourne noted that Dr. Duyka also did
not include complaints of POTS or orthostatic intolerance. Id. (citing Pet’r’s Ex. 23 at 1–7).
Specifically, he testified regarding Petitioner’s October 23, 2013 visit with Dr. Duyka and noted
that under history of present illness, it indicated “intermittent episodes of [SOB] associated with
changes in her voice, episodes of coughing, waking up at night with a salty, bitter taste in her
mouth.” Tr. 90:10–13 (citing Pet’r’s Ex. 22 at 9). Dr. Kinsbourne stated that was “clearly reflux.”
Tr. 90:15. He also stated that Dr. Duyka was “very specific” and noted no cardiovascular
symptoms, including chest pain, palpitations, lightheadedness, or syncope. Tr. 90:19–21.
Dr. Kinsbourne addressed Dr. Low’s contention that dehydration and deconditioning
caused Petitioner’s POTS. Dr. Kinsbourne wrote that the “ingredients” for Dr. Low’s theory are
“dehydration and deconditioning secondary to diarrheas and hypervolemia.”54 Pet’r’s Ex. 29 at 8.
Dr. Kinsbourne argued that “[t]hese handicaps are indeed consequences of POTS, but hardly
explain it.” Id. He stated that deconditioning and hypovolemia are secondary aggravating factors
of POTS, but in themselves are “not sufficient to cause POTS.” Tr. 122:21–25. He relied on
medical literature to argue such conditions would not cause POTS. Pet’r’s Ex. 29 at 8 (citing Pet’r’s
Ex. 66; Pet’r’s Ex. 54, ECF No. 68-6). Thieben et al.55 indicated that neuropathic or autoimmune
bases exist for a substantial percentage of POTS cases. Pet’r’s Ex. 66. However, “hyperadrenergic
and hypovolemic correlates are likely compensatory or exacerbating.” See id. Benarroch56 noted
that “there is evidence that bed rest or deconditioning do not primarily affect the reflex control of
muscle sympathetic activity.” Pet’r’s Ex. 54. Dr. Kinsbourne relied on a study by Figueroa et al.57
that studied exercise capacity in POTS patients and concluded that “not all patients with POTS are
deconditioned,” which “raises the possibility that varying degrees of deconditioning may result
54 Dr. Kinsbourne referred to hypervolemia, but it is not clear why when the petition alleges POTS with
hypovolemia. Hypervolemia is an “abnormal increase in the volume of circulating blood plasma[,]”
whereas hypovolemia is the inverse. See Dorland’s at 898, 908; see also supra, note 4 (defining
hypovolemia).
55 M. Thieben et al., Postural Orthostatic Tachycardia Syndrome: The Mayo Clinic Experience, 82(3)
MAYO CLIN. PROC. 308–13 (2007).
56 E. Benarroch, Postural Tachycardia Syndrome: A Heterogeneous and Multifactorial Disorder, 87(12)
MAYO CLIN. PROC. 1214–25 (2012).
57 R. Figueroa et al., Acute volume loading and exercise capacity in postural tachycardia syndrome, 117(6)
J. APPL. PHYSIOL. 663–68 (2014).
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secondary to orthostatic tachycardia, rather than as a primary pathophysiological phenomenon.”
Pet’r’s Ex. 32 at 2 (citing Pet’r’s Ex. 35, ECF No. 40-3). Figueroa et al. also noted that “[m]any
patients with POTS exhibit hypovolemia coupled with cardiac atrophy[.]” Pet’r’s Ex. 35 at 2.
Instead, Dr. Kinsbourne maintained that Blitshteyn and Fries58 showed that deconditioning “as a
sufficient cause for the new onset of POTS has itself been called into serious question.” Pet’r’s Ex.
32 at 2 (citing Pet’r’s Ex. 40, ECF No. 44-1). The authors noted that “[d]econditioning can occur
secondary to prolonged bed rest and chronic inactivity in patients with POTS, but it does not appear
to be a primary underlying mechanism.” Pet’r’s Ex. 40 at 1. Dr. Kinsbourne opined that
deconditioning is a “big factor in the secondary effects of orthostatic intolerance.” Tr. 97:20–21
(citing Pet’r’s Ex. 61).59
He argued that deconditioning “cannot be a preponderant theory of causation[]” in
Petitioner’s case. Pet’r’s Ex. 32 at 2. Dr. Kinsbourne posited that prior to November 8, 2013, there
was no evidence of deconditioning because there was no evidence that Petitioner “was
immobilized to be deconditioned.” Tr. 108:18–21. He testified that Petitioner was functioning
normally prior to this time and was able to work. Tr. 83:21–25. Dr. Kinsbourne noted that she
“was only in [the] hospital for two days (November 8–10, 2013).” Pet’r’s Ex. 32 at 2. This, Dr.
Kinsbourne maintained, “falls well short of” Dr. Low’s proposed timeframe of two to four weeks
bedrest “sufficient to induce deconditioning.” Id. at 3. Dr. Kinsbourne posited that dehydration or
deconditioning would not “themselves bring [POTS] about[.]” Pet’r’s Ex. 29 at 8. He argued that
“Dr. Low’s hypothesis of alternative causation cannot succeed based on dehydration and
deconditioning alone, but requires an antecedent diagnosis of POTS, which is not in evidence.” Id.
Dr. Kinsbourne acknowledged other triggers for POTS. Id. at 6. He cited an article by
Grubb,60 which documents a case study of a 34-year-old woman with POTS following a febrile
illness. Id. (citing Pet’r’s Ex. 15 at 1). Dr. Kinsbourne cited the Parsaik et al.61 study, wherein the
authors noted that 30% of patients with POTS “identified a preceding event as [a] possible trigger
for their symptoms, with viral illness being the most common.” Id. (citing Pet’r’s Ex. 61). Dr.
Kinsbourne addressed Dr. Low’s assertion that Petitioner’s viral illness was the cause of her POTS.
Id. Dr. Kinsbourne agreed that infection is a possible cause of POTS. Tr. 91:25. However, while
he opined that Dr. Low’s list of potential causes of POTS, including trauma, surgery, childbirth,
infections, and immunizations, is “indeed diverse[,]” Petitioner “did not experience trauma, did
not have surgery, did not give birth, was not shown to be infected, not stressed out of the ordinary,
but she was indeed immunized.” Pet’r’s Ex. 29 at 6.
Under my questioning, Dr. Kinsbourne testified that it “could be the case” that Petitioner’s
POTS was “relapsing because it [wa]s exacerbated by her other conditions, specifically her asthma
and her anxiety[.]” Tr. 145:16–20. He further opined that “one should[ not] forget” the fact that
58 S. Blitshteyn & D. Fries, Postural tachycardia syndrome is not caused by deconditioning, 6(3) PUL.
VASC. RES. INST. 401 (2016).
59 A. Parsaik et al., Deconditioning in patients with orthostatic intolerance, 79 NEUROL. 1435–40 (2012).
60 B. Grubb, Postural Tachycardia Syndrome, 117 CLIN. UPDATE 2814–17 (2008).
61 A. Parsaik et al., Deconditioning in patients with orthostatic intolerance, 79 NEUROL. 1435–40 (2012).
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Petitioner “seems to have Sjögren’s syndrome[,]”62 which made her “vulnerable to POTS.” Tr.
145:21–23. He stated that such a vulnerability is “not a question of what ought to trigger [POTS,]”
because one can have a vulnerability that does not lead to POTS. Tr. 145:23–25. Dr. Kinsbourne
continued that a vulnerability could still “trigger the actual POTS, which is [his] theory in this
case.” Tr. 145:25–146:2. He clarified that his theory is that Petitioner had a “latent” vulnerability
to POTS, and he argued that the trigger was her flu vaccine. Tr. 145:25–146:10. He maintained
that he was not incorporating a rechallenge theory into his argument. Tr. 149:19–21.
3. Respondent’s Expert, Dr. Low
Dr. Low did not dispute Petitioner’s post-vaccination POTS diagnosis. Resp’t’s Ex. A at
4. Rather, he testified that Petitioner’s October 8, 2013 flu vaccine did not cause her POTS. Tr.
196:1–2. Dr. Low opined that “the likely sequence of events” is that Petitioner “had orthostatic
intolerance and some autonomic instability for a significant duration before her vaccination.”
Resp’t’s Ex. A at 5. Dr. Low testified that in 2013, Petitioner experienced a “presumed viral illness
with gastroenteritis, . . . and about that time, she had dehydration and that exacerbated . . . both the
hypovolemia, as well as her anxiety.” Tr. 184:13–18. He noted that diarrhea could also lead to
dehydration. Tr. 178:22–25. Dr. Low continued that Petitioner then became less active leading to
her deconditioning, which impacted her POTS symptoms. Tr. 184:19–24. Dr. Low opined that
Petitioner’s November 8, 2013 hospitalization resulting in her being bedridden contributed to the
manifestation of her POTS. Tr. 185:17–22. Dr. Low argued both deconditioning and dehydration
“magnif[ied]” Petitioner’s POTS symptoms. Resp’t’s Ex. A at 5. Dr. Low argued that he sees “no
obvious linkage” between the worsening of Petitioner’s condition and the receipt of her flu
vaccine. Tr. 195:18–22. Dr. Low indicated that he has seen “many” patients who presented like
Petitioner. Tr. 185:24–25.
Dr. Low opined that Dr. Kinsbourne “has a very limited and distorted understanding of
POTS.” Tr. 164:20–21. Dr. Low discussed relevant information to the “condition” of POTS based
on his expertise as an autonomic specialist. Resp’t’s Ex. A at 2–3. He defined POTS as “a
syndrome in which – where patients have symptoms of orthostatic intolerance, coupled with
orthostatic tachycardia.” Tr. 163:2–4. He explained that POTS is “characterized by an increase in
heart rate of >30 beats per minute associated with symptoms of orthostatic intolerance, when the
person stands up, and clears when the person sits back down.” Resp’t’s Ex. A at 3. He described
orthostatic intolerance as “symptoms of reduced cerebral perfusion,” including lightheadedness,
dimming of vision, and cognitive difficulties. Id. Orthostatic intolerance also includes symptoms
of sympathetic activation such as palpitations, tremulousness, nausea, and diaphoresis. Id. He
described POTS as the “classic example of orthostatic intolerance.” Id. (citing Resp’t’s Ex. A, Tab
1, ECF No. 73-1; Resp’t’s Ex. E, Tab 13, ECF No. 74-11).63 Dr. Low testified that a POTS
patient’s sympathetic nervous system is overactive upon standing and that POTS symptoms, such
62 See supra, note 28 (explaining that the record does not contain preponderant evidence that Petitioner
suffers from Sjögren’s syndrome). Further, Dr. Kinsbourne did not otherwise make a connection between
the autoimmune mechanism of Sjögren’s or explain how it could act as an autoimmune comorbidity or
vulnerability in the development of POTS.
63 E. Benarroch, Postural Tachycardia Syndrome: A Heterogeneous and Multifactorial Disorder, 87(12)
MAYO CLIN. PROC. 1214–25 (2012); M. Thieben et al., Postural Orthostatic Tachycardia Syndrome: The
Mayo Clinic Experience, 82(3) MAYO CLIN. PROC. 308–13 (2007).
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as dizziness, occur when the person stands, not when they are seated. Tr. 165:1–2, 178:6–15. Dr.
Low noted that this is because BP and heart rate increase during sympathetic activation. Resp’t’s
Ex. A at 3. Dr. Low also wrote that POTS patients have “more than just orthostatic intolerance[,]”
including chronic fatigue, pain, and headaches, GI complaints, insomnia, and somatic
hypervigilance. See id. at 4.
He disagreed with Dr. Kinsbourne’s assertion that the diagnosis of POTS requires six
months of sustained orthostatic intolerance. See Tr. 200. Instead, even when confronted with
medical literature that indicates the six-month severity requirement, he maintained that POTS
requires “the presences of symptoms for six months, of which it does[ not] all have to be orthostatic
intolerance.” Tr. 201:7–9; see also Pet’r’s Ex. 58 at 2. As an example, he noted that the astronauts
in one of his studies had POTS without sustained orthostatic intolerance for more than six months.
Tr. 207:23–22. He explained that the six-month severity requirement in Petitioner’s purported
definition of POTS is not the main diagnostic criterion since treaters “do[ not] wait six months
before [] mak[ing] the diagnosis. You take into consideration all of the symptoms that they have
had for the previous duration and that[ is] where the six months comes in.” Tr. 183:8–12. Dr. Low
characterized Dr. Kinsbourne’s claim that a POTS diagnosis requires a six-month history of
orthostatic intolerance as “surprising[]” because if one were to “strictly follow[] the guidelines that
[Dr. Kinsbourne] claims, then [Petitioner] does not have POTS, the primary claim that [Dr.
Kinsbourne] makes.” Resp’t’s Ex. D at 2.
Dr. Low acknowledged that there is a difference between a symptom of dysautonomia and
POTS. Tr. 201:19–22. He wrote that the term dysautonomia refers to abnormal function of the
autonomic nervous system. Resp’t’s Ex. D at 1. He defined dysautonomia as “an imbalance of the
autonomic nervous system” wherein “the sympathetic [nervous system] rears its ugly head and
causes symptoms.” Tr. 163:10–18. Dr. Low explained that such an imbalance is “not necessarily”
a damaged autonomic nervous system, “[i]t[ is] just a lack of control.” Tr. 163:19–22.
Next, Dr. Low described the subtypes of POTS. He stated that neuropathic POTS is
classified as “regular POTS” and is an example of when POTS can occur as a result of damage to
the autonomic nervous system. Tr. 165:10–13, 166:13–15. He defined neuropathic POTS as when
“someone has a limited autonomic neuropathy where the nerves to the extremities are partly
damaged.” Tr. 165:14–15. He continued, “because of that [damage], [the patient’s] blood pressure
would try to drop, but [because of] sympathetic overactivity . . . [it is] prevent[ed] from
dropping[,]” causing tachycardia. Tr. 165:15–18. Dr. Low stated that blood pressure drops
approximately five milliliters in cases of neuropathic POTS. Tr. 166:13–18. Dr. Low then
described hyperadrenergic POTS and noted that to meet such classification of POTS, the patient
must have “a plasma norepinephrine that[ is] excessive when they stand up.” Tr. 167:2–4. Dr. Low
wrote that a hyperadrenergic state can result from “increased sympathetic activity that can be
caused by POTS and hypovolemia” but it can also be caused by anxiety/panic attacks. Resp’t’s
Ex. A at 4. Dr. Low acknowledged that someone can have a “hyperadrenergic event[,]” such as
anxiety or panic that causes tachycardia, separate from POTS. Tr. 167:18–22. He stated the “clue”
for this occurrence is “that that person will have a tachycardia when they[ are] sitting down” in
addition to upon standing, and elevated blood pressure. Tr. 167:20–168:5. In hyperadrenergic
POTS, the surge in blood pressure “goes up quite a bit . . . 10, 15, 20, milliliters[s].” Tr. 166:15–
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18. Dr. Low testified that two other subtypes of POTS include “constitutional or POTS associated
with deconditioning[,]” and POTS associated with anxiety panic. Tr. 166:22–167:10.
He addressed the results of Petitioner’s tilt-table test consistent with his criteria for the
classifications of POTS. Dr. Low opined that Petitioner’s tilt-table test showed “regular POTS, not
hyperadrenergic POTS.” Tr. 166:21–22. In light of this determination, he disagreed with Dr.
Barboi’s diagnosis of hyperadrenergic POTS. Tr. 204:4–9 (citing Pet’r’s Ex. 44 at 146). Dr. Low
testified that he understood why Dr. Barboi made such a diagnosis because Petitioner had episodes
of hypertension. Tr. 204:21–23. He said that this is “reasonable[,]” but it does not “make him right.
He actually made a mistake.” Tr. 204:23–24. Dr. Low posited that there is no debate surrounding
the categorizations of POTS and instead, “Dr. Barboi was just a bit sloppy here.” Tr. 205:9–14.
Dr. Low was confronted with the Arnold et al.64 article which indicated that subtypes of POTS
“are not mutually exclusive of each other and many patients have features consistent with more
than one subtype.” Tr. 205:15–206:8 (citing Pet’r’s Ex. 58 at 2). He testified that he had “no
problem with that” statement. Tr. 206:9. Dr. Low argued that, to him, since Petitioner’s clinical
testing did not support a diagnosis of hyperadrenergic POTS, he “found a better way to explain
her episodic symptoms[]” and opined that Petitioner had POTS with anxiety-panic. Tr. 204:14–
19.
Dr. Low put forth multiple potential causes of POTS, including primary overactivity of the
sympathetic nervous system due to deconditioning, reduced plasma volume associated with
hypovolemia, and venous pooling. Tr. 165:3–9; Resp’t’s Ex. A at 3. He argued that deconditioning
is “the prime cause of POTS[,]” including each subtype. Tr. 209:21–210:9. He explained this is
the case because patients improve with reconditioning. Tr. 210:10–11. Dr. Low disagreed with Dr.
Kinsbourne’s assertion that deconditioning has not been described as a cause of POTS. Resp’t’s
Ex. D at 2. Dr. Low acknowledged that “the focus” of Petitioner’s cited literature “might have
been restricted to another mechanism, such as hypovolemia or neuropathy, but not to the exclusion
of deconditioning.” Id. Dr. Low did not cite to specific literature filed by Petitioner. See id. He
supported his argument with the fact that he was the “lead/senior author in the majority of the
publications that [Dr. Kinsbourne] cites.” Id. For example, he explained that early on, he tried to
divide the mechanisms into groups, including deconditioning, neuropathic, and hyperadrenergic.
Id. (citing Resp’t’s Ex. D, Tab 2, ECF No. 74-2).65 Then, he tried to “quantify how often
deconditioning was the underlying mechanism in POTS.” Id. (citing Resp’t’s Ex. A, Tab 7, ECF
No. 73-6).66 To quantify this, authors, including Dr. Low, conducted a study of 184 patients with
POTS who underwent exercise testing to show evidence of deconditioning. Resp’t’s Ex. A, Tab 7
at 3. They found that 95% of the patients exhibited deconditioning and that it “may play a central
role in pathophysiology.” Id. at 1. They also noted that the patients’ deconditioning improved and
was reversed with exercise. Id. Dr. Low eventually agreed that deconditioning can also be a
secondary effect of POTS. Tr. 211:13–19.
64 A. Arnold et al., Postural tachycardia syndrome – Diagnosis, physiology, and prognosis, 215
AUTONOMIC NEURO. BASIC & CLIN. 3–11 (2018).
65 P. Low et al., Postural Tachycardia Syndrome (POTS), 20 J. CARDIOVASC. ELECTROPHYSIOL. 352–58
(2009).
66 A. Parsaik et al., Deconditioning in patients with orthostatic intolerance, 79 NEUROL. 1435–43 (2012).
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In support of his theory on causation, Dr. Low argued that “[t]ypical of [POTS],” Petitioner
became physically inactive post vaccination and “bec[ame] deconditioned[,] further aggravating
her POTS and expanding her symptoms . . . .” Resp’t’s Ex. A at 5 (citing Resp’t’s Ex. A, Tab 7).
Dr. Low cited the Parsaik et al.67 article, which indicated that a two-week period of non-
continuous bedrest could induce deconditioning. Id.; Resp’t’s Ex. D at 3 (citing Resp’t’s Ex. A,
Tab 7). Dr. Low wrote that the two-week period is a minimum timeframe. See id. Dr. Low relied
on Petitioner’s “reported prolonged periods of being bedridden and unable to even care for
herself[]” to highlight evidence of deconditioning. Resp’t’s Ex. A at 5 (citing Pet’r’s Ex. 4 at 60,
124). However, on cross-examination, he stated there was no “good evidence” and that he
“honestly d[id not] know” if Petitioner was suffering from deconditioning prior to November 8,
2013. Tr. 206:10–207:2. Dr. Low further relied on two studies showing that when healthy people,
without preexisting symptoms of orthostatic intolerance, remain bedridden for as little as two to
four weeks, they develop symptoms consistent with POTS. Resp’t’s Ex. C at 1 (citing Resp’t’s
Exs. C, Tabs 5–6, ECF Nos. 73-13–73-14).68 However, the study by Miller et al. involved male
subjects, ages 17 to 23, who “had just completed 8 weeks of basic training in the United States Air
Force.” Resp’t’s Ex. C, Tab 5 at 1. The subjects in the Schlegel et al. study had just returned from
space. Resp’t’s Ex. C, Tab 6 at 1.
Dr. Low also discussed dehydration as a cause of POTS and opined that Petitioner’s
dehydration, experienced as a result of her diarrhea, contributed to her worsening POTS. He
explained the process through which dehydration could cause POTS. Tr. 179:2–4. Dr. Low stated
that dehydration causes hypovolemia, which is when “the [blood] volume is reduced when you
stand up, because of the shift of fluid in the lower half of your body, not enough goes to the brain
and that triggers an increase in sympathetic activity.” Tr. 179:5–10 (citing Resp’t’s Exs. C, Tabs
1, 3, ECF Nos. 73-9, 73-11).69 He wrote that “[h]ypovolemia (low plasma volume) will regularly
cause orthostatic intolerance and orthostatic tachycardia[,]” which improve with fluids in
hypovolemic POTS patients. Resp’t’s Ex. C at 1 (citing Resp’t’s Exs. C, Tabs 1, 3). In support of
his position, Dr. Low emphasized that Petitioner reported “drinking little water around the time
her symptoms worsened[.]” Resp’t’s Ex. A at 5 (citing Pet’r’s Ex. 4 at 152, 170).
Dr. Low’s main argument is that Petitioner’s autonomic disorder predated her vaccination.
See Resp’t’s Ex. C at 2. Dr. Low argued that Petitioner’s POTS “began a long time ago . . .
[p]robably 2011 . . . but it[ is] hard to put a specific beginning date.” Tr. 183:18–23. He testified
that Petitioner “had some dysautonomia for years and then for a couple of months before the
vaccine, she started getting worse[.]” Tr. 177:6–12. He continued that Petitioner then had a more
acute illness about three weeks after . . . characterized by gastroenteritis. And by the time she
presented to the hospital [on November 8, 2013,] she had a hyperadrenergic response of some
sort.” Tr. 177:9–12. He opined that Petitioner’s November 8, 2013 diagnosis of viral gastroenteritis
“could be the correct diagnosis” since it was tested for. Tr. 176:16–177:2. Dr. Low therefore
opined that Petitioner’s “POTS began with dysautonomia and orthostatic intolerance . . . when
67 See id.
68 P. Miller et al., Modification of the effects of two weeks of bed rest upon circulatory functions in man, 35
AEROSP. MED. 931–39 (1964); T. Schlegel et al., Cardiovascular and Valsalva responses during parabolic
flight, 85(5) J. APPL. PHYSIOL. 1957–65 (1998).
69 F. Fouad et al., Idiopathic Hypovolemia, 104 ANN. INT. MED. 298–303 (1986); G. Jacob et al., Relation
of blood volume and blood pressure in orthostatic intolerance, 315(2) AM. J. MED. SCI. 95–100 (1998).
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[she] developed vomiting and diarrhea, she developed florid POTS, and this became chronic
because of severe deconditioning.” Resp’t’s Ex. C at 3. He argued this progression was all part of
“the same condition” of POTS that predated her flu vaccine. Id. Dr. Low indicated that preexisting
dysautonomia is important because “there is a linked spectrum of autonomic symptoms from
dysfunction to POTS.” Resp’t’s Ex. D at 1. He testified that POTS symptoms can wax and wane,
and patients experience periods of remission. Tr. 184:2–8.
As support for his contention that Petitioner’s POTS predated her vaccination, he relied on
Dr. Barboi’s January 6, 2014 notation indicating Petitioner had “long-standing” autonomic
symptoms, such as palpitations and dizziness/lightheadedness. Resp’t’s Ex. C at 2 (citing Pet’r’s
Ex. 6 at 8); Tr. 199:8–10. Dr. Low also relied on Petitioner’s two ER visits in 2011 and 2012 for
palpitations and dizzy spells, and SOB, respectively, to add context to Dr. Barboi’s notation.
Resp’t’s Ex. A at 4. He noted that during Petitioner’s January 12, 2011 ER visit, she had feelings
that her “heart ke[pt] beating fast” and that her pulse was 114. Tr. 168:13–169:3 (citing Pet’r’s Ex.
21 at 146, 150). Dr. Low testified that Petitioner “clearly ha[d] dysautonomia” at this time, which
was triggered by anxiety-panic. Tr. 169:9–11. He based this assessment on the fact that her pulse
was 114 while sitting down, indicating tachycardia. See Tr. 169:14–21. Dr. Low discussed
Petitioner’s June 10, 2012 ER visit that also showed evidence of tachycardia. Tr. 170:14, 198:7–
12 (citing Pet’r’s Ex. 67 at 5–12). He opined that Petitioner “clearly had a sympathetic
overactivity” on this occasion, as evidenced by her feelings of lightheadedness and tachycardia “in
the 150s.” Tr. 170:20–25. Dr. Low argued this occasion was “more autonomic and not just anxiety”
related. Tr. 171:10–11. He based this opinion also on the fact that she improved with IV fluids. Tr.
171:16–19, 199:15–17. However, Dr. Low admitted that there was “not too much evidence of
orthostatic intolerance” recorded in the visit notes from this date. Tr. 199:6–8. He conceded the
marijuana Petitioner used on June 10, 2012, “could [have] contribute[d] to the lightheadedness[.]”
Tr. 199:18–21.
Dr. Low addressed Petitioner’s SOB from early to mid-2013. Tr. 171:20–172:5. He
testified that SOB “is a very common symptom of dysautonomia[.]” Tr. 172:1–2. He argued that
Petitioner’s breathing issues could be explained by her pre-vaccination dysautonomia. Tr. 174:1–
7. Dr. Low argued that the “clue” that Petitioner was experiencing dysautonomia instead of another
pulmonary condition, like asthma, was that “she had full respiratory function test[ing] showing
that she had no evidence of lung disease or of obstructive airway disease and nothing to suggest
asthma.” Tr. 172:2–5 (citing Pet’r’s Ex. 4 at 196). In support of his conclusion that Petitioner did
not have asthma, Dr. Low testified regarding Petitioner’s March 20, 2014 spirometry testing and
stated that it did not show evidence of “much” asthma. Tr. 172:20–173:11 (citing Pet’r’s Ex. 4 at
196). Dr. Low argued it is not true that a spirometry test would only show evidence of asthma if
the patient was having an asthma attack because “[g]enerally, there are some changes even
between attacks.” Tr. 173:1–4. Despite the spirometry test results, Dr. Low testified that Petitioner
“could have” some degree of asthma. Tr. 202:1–3. He opined that Petitioner “has asthma, but not
very bad, and a lot of the difficulty with breathing had to do not with asthma but with anxiety and
dysautonomia.” Tr. 202:17–20. Dr. Low further opined that Petitioner’s SOB was not related to
her preexisting allergies because she had an allergy test that yielded negative results. Tr. 173:12–
16 (citing Pet’r’s Ex. 13 at 44–46).
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He stated that Petitioner’s preexisting anxiety and panic attacks “[we]re [also]
manifestations of [her] dysautonomia.” Tr. 203:1–2. He explained that anxiety “is dysautonomia,
but it is triggered by emotional factors.” Tr. 169:11–13, 203:2–3. Dr. Low testified that “[p]anic
is an excellent example of an autonomic stall. The sympathetic[ nervous system has] gone haywire
during the [attack]. But it is driven by an emotional trigger.” Tr. 203:6–8. Dr. Low addressed
Petitioner’s June 13, 2013 medical record, indicating that she recently discontinued Celexa that
she was taking for her anxiety. Tr. 175:18–25 (citing Pet’r’s Ex. 13 at 22–25). Dr. Low stated that
if patients “stop [taking Celexa] suddenly, it could make the[ir] anxiety worse.” Tr. 176:1–2. Dr.
Low admitted that a patient can have anxiety symptoms that are unrelated to dysautonomia. Tr.
203:9–11.
Dr. Low wrote that while Dr. Kinsbourne is correct that Petitioner’s treaters posited
alternative explanations for her pre-vaccination symptoms, such as asthma and anxiety, “this [] is
the usual scenario since autonomic disorders are frequently misdiagnosed.” Resp’t’s Ex. C at 2.
Dr. Low indicated that it may be hard for a patient with autonomic dysfunction to get a proper
diagnosis until they are seen by an autonomic specialist. Tr. 183:1–4. Dr. Low argued that if he,
as an autonomic specialist, had seen Petitioner present with a history of dizziness, difficulties
breathing, a fast heart rate, and alterations in BP, he would have determined that “combination of
symptoms” to “fit into an autonomic diagnosis of dysautonomia . . . .” Resp’t’s Ex. C at 2. Dr.
Low opined that such preexisting symptoms “def[y] any of the alternative diagnoses.” Id. He
opined that “in terms of mechanism, . . . one could speculate that [Petitioner] had – her anxiety
became worse[.]” Tr. 177:15–17. Dr. Low wrote that Dr. Kinsbourne “does not seem to challenge
that [Petitioner] had dysautonomia prior to her current illness.” Resp’t’s Ex. D at 1. What Dr.
Kinsbourne does challenge, according to Dr. Low, is whether Petitioner specifically had POTS pre
vaccination. Id. Dr. Low highlighted that Petitioner did not have autonomic testing “so she
obviously could not have been diagnosed as having POTS previously.” Id.
He cited the articles by Thieben et al. and Benarroch to note that 50% of POTS patients
experience “an antecedent event” that can be “quite diverse and non-specific.” Resp’t’s Ex. A at 5
(citing Resp’t’s Ex. A, Tab 1; Resp’t’s Ex. E, Tab 13).70 These events include trauma, “an illness
like [P]etitioner had,” surgery, childbirth, infections, stress, and immunizations. Id. Dr. Low noted
that many POTS patients have “prior symptoms of dysautonomia.” Resp’t’s Ex. C at 3. He argued
this “makes the point that although the[ patients] might relate onset to some event, such as an
infection, surgery, vaccination, stress, childbirth, etc.[,] the onset is not truly acute but dependent
in significant part on a predisposition to develop POTS.” Id. Dr. Low posited that “the diverse
nature of the presumed inciting event would argue against the event as the cause of POTS” and in
this case that is Petitioner’s October 8, 2013 flu vaccine. Id.
On cross-examination, Dr. Low was asked to clarify when he believed Petitioner’s POTS
began. Tr. 197:22–23. In response, Dr. Low stated he “was deliberately a little vague on that simply
because dysautonomia [he thinks] began a long time ago.” Tr. 197:24–198:1. He continued, “[a]s
far as the actual orthostatic intolerance of POTS, that was clearly closer to the vaccine date, and
sometime in the previous year . . . when she started getting episodes of tachycardia, et cetera.” Tr.
70 M. Thieben et al., Postural Orthostatic Tachycardia Syndrome: The Mayo Clinic Experience, 82(3)
MAYO CLIN. PROC. 308–13 (2007); E. Benarroch, Postural Tachycardia Syndrome: A Heterogeneous and
Multifactorial Disorder, 87(12) MAYO CLIN. PROC. 1214–25 (2012).
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195:13–17, 198:1–5. He argued that Petitioner “was deteriorating” during the two months prior to
her October 8, 2013 flu vaccine. Tr. 176:10–11. By three weeks post vaccination, “things really
went downhill” with her diarrhea and tachycardia. Tr. 176:11–15. Dr. Low addressed Dr.
Kinsbourne’s contention that Petitioner’s diarrhea beginning in late October of 2013 was the onset
of Petitioner’s POTS. Dr. Low testified that diarrhea as the first symptom of POTS “would be
most unusual” and he has never heard of POTS manifesting that way. Tr. 177:18–21, 178:3–4. He
admitted that GI issues are common in POTS patients. Tr. 203:12–14. Dr. Low testified that
Petitioner’s gastroenteritis was associated with her POTS but was not a manifestation. Tr. 178:1–
3.
Dr. Low attacked Petitioner’s proposed biological mechanism and stated that Dr. Axelrod’s
“vague cytokine/molecular mimicry type attribution . . . is quite nonspecific [and] is not a reliable
theory in this instance.” Resp’t’s Ex. A at 5. Dr. Low posited that while “loose attribution” is
“often made” to cytokines and molecular mimicry or secondary immune responses, such
references “are dogged by [a] lack of specificity.” Id. Dr. Low argued that, to him, molecular
mimicry is “next to meaningless . . . because it[ is] so nonspecific.” Tr. 186:9–16. He opined that
single case reports like those authored by Tsai et al. or Blitshteyn, “have little scientific merit[]”
and are “suspect” because they do not have control data. Resp’t’s Ex. A at 5 (citing Pet’r’s Exs.
14, 39);71 see also Resp’t’s Ex. C at 4. He therefore classified the findings from these articles
regarding vaccine causation “into the category of possible but unlikely.” Resp’t’s Ex. A at 5. Dr.
Low argued that large, epidemiological studies are more reliable and do not support vaccine
causation. Id. As an example, Dr. Low cited a study by Zhou et al.,72 which showed no relationship
between vaccinations and the development of POTS. Id. (citing Resp’t’s Ex. A, Tab 10, ECF No.
22-11). The Zhou et al. study analyzed VAERS reports for vaccines generally from 1991 to 2001
and determined that the most reported post-vaccination adverse events included fever, injection-
site hypersensitivity, rash, injection-site edema, and vasodilation. Resp’t’s Ex. A, Tab 10 at 2.
Dr. Low argued that POTS is not known to be an autoimmune condition. Tr. 188:4–5. He
said there is “an interest” in G proteins as being implicated in the autoimmunity of the condition
but such evidence is not conclusive because such antibodies can be found in normal people and/or
are present in other disorders besides POTS. Tr. 188:18–189:20 (citing Resp’t’s Ex. E, Tab 17,
ECF No. 74-14).73 He testified that G protein antibodies have not been found to be causative of
any condition, instead they are secondary or reactive. Tr. 190:9–25. Dr. Low stated that currently
there are no causative antibodies in POTS. Tr. 191:1–3.
He discussed the progression of studies regarding the relevant antibodies found in POTS.
Dr. Low noted that the scientific community defines the method “by which an autoantibody-
mediated autonomic disorder” develops differently than Dr. Kinsbourne proposes. Resp’t’s Ex. E
at 1. To make a “designation[,]” that an antibody is the cause of an autoimmune disorder, Dr. Low
71 C. Tsai et al., Novel H1N1 Influenza Vaccine the Cause of Postural Orthostatic, 31(2) J. MED. SCI. 91–
93 (2011); S. Blitshteyn, Postural tachycardia syndrome following human papillomavirus vaccination, 21
EUR. J. NEUROL. 135–39 (2014).
72 W. Zhou et al., Surveillance for Safety After Immunization: Vaccine Adverse Event Reporting System
(VAERS) – United States, 1991–2001, 52 SURVEILL. SUMM. 1–28 (2003).
73 S. Vernino & L. Stiles, Autoimmunity in postural orthostatic tachycardia syndrome: current
understanding, 215 AUTONOMIC NEURO. BASIC & CLIN. 78–82 (2018).
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wrote that several steps must occur. Id. He noted that first, a high titer is necessary “because . . .
low antibody titers are often shown to be clinically insignificant.” Id. Then, “one must demonstrate
that there is a linear relationship between [the] antibody titer and disease severity, which is done
by showing that a higher titer is associated with more severe disease.” Id. Dr. Low continued that
the next step is to show that the disease can be passively transferred. Id. He explained this is
accomplished through an “animal experiment where the relevant and purified antibody is infused,
and the infusion produces the relevant disease in the experimental animal.” Id. Dr. Low indicated
that the last step “is to characterize the antibody and demonstrate that you can immunize the
experimental animal with [the] purified antibody to reproduce the disease.” Id. at 1–2. He cited the
Thieben et al.74 study, which showed that “15% of POTS patients had low titer ganglionic antibody
(“AChR”).” Resp’t’s Ex. D at 2–3 (citing Resp’t’s Ex. E, Tab 13). Dr. Low argued that “these are
secondary, nonspecific [antibodies that] do not cause tissue injury, and [are] not causally related
to POTS.” Id. at 3. Dr. Low cited a case by Cutsforth-Gregory et al.75 that likewise found that high
titer antibodies were associated with autonomic impairment. Resp’t’s Ex. E at 3 (citing Resp’t’s
Ex. E, Tab 6, ECF No. 74-4). Dr. Low posited that “[t]here is wide consensus in the medical
community that we no longer attempt to measure this [AChR] antibody.” Resp’t’s Ex. D at 3.
As support, Dr. Low relied on the series of studies by Vernino et al.,76 which focused on
autoimmune autonomic disorders, including autoimmune autonomic ganglionopathy (“AAG”).77
Resp’t’s Ex. E at 1–2 (citing Resp’t’s Ex. D, Tab 6, ECF No. 42-7). He used these studies and
AAG “as an example of how one goes about demonstrating that an antibody is the cause of an
autoimmune disorder.” Id. at 1. Vernino et al. demonstrated that patients with AAG had high titers
of ganglionic antibodies (AChRs). Id. at 2 (citing Resp’t’s Ex. D, Tab 6). The authors also
demonstrated a linear relationship between the ganglionic antibody titer and disease severity. See
id. They noted that “higher levels of [the ganglionic] antibody were significantly associated with
greater severity of autonomic dysfunction.” Resp’t’s Ex. D, Tab 6 at 7. Another study by Vernino
et al.78 found that the passive transfer of the antibody reproduced AAG in an experimental animal
model of mice. Resp’t’s Ex. E, Tab 16 at 1, ECF No. 74-13. In that study, mice were injected with
IgG containing ganglionic AChR antibodies and developed symptoms of autonomic dysfunction,
including GI issues, urinary retention, dilated pupils, reduced heart rate variability, and impaired
responses to stress. Id. Using the “fully characterized pure antibody,” Vernino et al.79 was able to
“immunize the experimental animal to reproduce [autonomic neuropathy].” Resp’t’s Ex. E at 2
(citing Resp’t’s Ex. E, Tab 15, ECF No. 74-12).
74 M. Thieben et al., Postural Orthostatic Tachycardia Syndrome: The Mayo Clinic Experience, 82(3)
MAYO CLIN. PROC. 308–13 (2007).
75 J. Cutsforth-Gregory et al., Ganglionic Antibody Level as a Predictor of Severity of Autonomic Failure,
93(10) MAYO CLIN. PROC. 1440–47 (2018).
76 S. Vernino et al., Autoantibodies to Ganglionic Acetylcholine Receptors in Autoimmune Autonomic
Neuropathies, 343 N. ENG. J. MED. 847–55 (2000).
77 Autoimmune autonomic ganglionopathy is “an antibody-mediated disease that classically manifests with
widespread autonomic failure [] involving sympathetic, parasympathetic, and enteric functions[.]” See J.
Cutsforth-Gregory et al., Ganglionic Antibody Level as a Predictor of Severity of Autonomic Failure, 93(10)
MAYO CLIN. PROC. 1440 (2018).
78 S. Vernino et al., Passive Transfer of Autoimmune Autonomic Neuropathy to Mice, 24(32) J. NEURO.
7037–42 (2004).
79 S. Vernino et al., Experimental Autoimmune Autonomic Neuropathy, 90 J. NEUROPHYSIOL. 2053–59
(2003).
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However, Dr. Low noted that later studies did not show any correlation between antibody
titer and disease severity in POTS patients. Id. at 3 (citing Resp’t’s Ex. E, Tab 13; Resp’t’s Ex. E,
Tab 17; Resp’t’s Ex. E, Tab 10, ECF No. 74-8; Resp’t’s Ex. E, Tab 8, ECF No. 74-6).80 Dr. Low
argued that “evidence suggesting that POTS is autoimmune has not even demonstrated the first
step – showing that antibodies are seen in high titers . . . .” Id. Based on the discrepancy between
earlier and later studies, he wrote that the Mayo Laboratory re-evaluated the relationship between
“antibody titer to autonomic impairment.” Id. Dr. Low noted that “[e]ven in a condition that has
an established association with these antibodies, [autoimmune autonomic neuropathy], . . . low
titers are of no clinical significance.” Id. Dr. Low addressed the 2018 Vernino and Stiles article
which stated that there is evidence of dysregulation of the immune system, including the “presence
of autoantibodies directed against targets in the autonomic system.” Tr. 214:21–215:11 (citing
Resp’t’s Ex. E, Tab 17 at 4). Dr. Low did not agree that this meant the authors found such
autoantibodies had a causative impact. Tr. 215:6–11. He maintained that the research is still
developing and as it presently stands, such autoantibodies are bystander antibodies that have no
significance. Tr. 215:15–216:6.
Dr. Low was equivocal when asked whether autoantibodies to GPCRs are currently being
considered as potentially pathologic in POTS. Tr. 217:2–5. He stated it is true “in that all the
evidence we have – we do[ not] know if you can measure it accurately.” Tr. 217:5–7. He continued
that “if it does – if it really exists, then it probably is a reactive or secondary antibody and not a
causative antibody[.]” Tr. 217:7–9. As an example, Dr. Low opined that the adrenergic antibody
identified in the Li et al.81 study as being associated with POTS “has never been identified nor
characterized” consistent with the methodology described above for determining whether an
antibody is causative of an autoimmune disease. Resp’t’s Ex. E at 3 (citing Pet’r’s Ex. 48); Tr.
193:22–23. Dr. Low continued that the Li et al. study did not show any evidence of passive transfer
or evidence of tissue injury. See Resp’t’s Ex. E at 3. Thus, the animal model does not establish
“that [an] antibody can cause a disease process.” See id. Dr. Low noted that if there is an
autoimmune attack on the sympathetic nervous system, “you expect to see pathology[,]” such as
in autoimmune autonomic ganglionopathy, but Li et al. did not show this. Tr. 193:23–194:3. Dr.
Low opined that the Li et al. study therefore did not “really provide any insights into the
pathogenesis of POTS.” Tr. 207:3–9 (citing Pet’r’s Ex. 48 at 6).
Dr. Low argued that instead, the methodology used in that study is “seriously flawed.”
Resp’t’s Ex. E at 3; Tr. 191:18–21 (citing Pet’r’s Ex. 48). As support for this opinion, Dr. Low
noted that the animals in that study did not have orthostatic symptoms required for a POTS
diagnosis. Resp’t’s Ex. E at 3. He additionally stated that rabbits are not a good model for studying
orthostatic intolerance or hypertension because they are “too short to have significant orthostatic
stress.” Tr. 191:22–192:3. He also noted “[m]ost importantly” that there was no control group,
80 M. Thieben et al., Postural Orthostatic Tachycardia Syndrome: The Mayo Clinic Experience, 82(3)
MAYO CLIN. PROC. 308–13 (2007); S. Vernino & L. Stiles, Autoimmunity in postural orthostatic
tachycardia syndrome: current understanding, 215 AUTONOMIC NEURO. BASIC & CLIN. 78–82 (2018); A.
McKeon et al., Ganglionic Acetylcholine Receptor Autoantibody, 66(6) ARCH. NEUROL. 735–41 (2009);
Y. Li et al., Clinical Experience of Seropositive Ganglionic Acetylcholine Receptor Antibody in a Tertiary
Neurology Referral Center, 52 MUSCLE NERVE 386–91 (2015).
81 H. Li et al., Adrenergic Autoantibody-Induced Postural Tachycardia Syndrome in Rabbits, X J. AM.
HEART ASSOC. 1–9 (2019).
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“consisting of animals that were not immunized” that could have shown “possible intervening
events, apart from immunization, that could result in the modest” symptoms the rabbits
experienced, such as dehydration, discomfort, and stress. Resp’t’s Ex. E at 3; Tr. 193:3–19. Dr.
Low admitted that the authors were able to show that immunizing rabbits with particular peptides
results in altered vasoreactivity. Tr. 192:12–18. However, he said this was not surprising and “has
nothing to do with POTS.” Tr. 192:18–19. He therefore disagreed with the authors’ assertion that
vasoreactivity is related to POTS. Tr. 192:20–22. Instead, Dr. Low stated that “what [the authors
are] saying is that the fact that these peptides do something and when you change – when – the
fact that you immunize them, you must be doing something to their receptors.” Tr. 192:23–193:1.
Dr. Low thought the authors “could be right[,]” in that assessment, but that still “has nothing to do
with POTS.” Tr. 193:1–2. Dr. Low argued that Dr. Kinsbourne “at best” has provided evidence
that research regarding an autoimmune basis for POTS is “ongoing.” Resp’t’s Ex. E at 4.
He addressed the Gunning et al.82 article, which used the ELISA test to detect
autoantibodies against GPCRs, and called the kit “terrible.” Tr. 212:14–213:6 (citing Pet’r’s Ex.
47). He stated that the ELISA test does not work for large surface antibodies and that GPCRs are
large proteins. Tr. 214:1–2. Rather, ELISA tests are used for small protein antibodies. Tr. 213:6–
23. On cross-examination, Dr. Low was confronted with the article’s mention that “these kits have
been validated by the manufacturer and used successfully in a [separate] recent report identifying
autoantibodies to beta-adrenergic and muscarinic cholinergic receptors in chronic fatigue
syndrome, of which many symptoms overlap with POTS.” Tr. 212:20–25. Dr. Low was
“surprised” to be asked about this statement because “these experiments [] do[ not] mean very
much because . . . many G protein antibodies are increased in many diseases, including chronic
fatigue [syndrome.]” Tr. 213:10–14. Dr. Low further argued that “[n]o one has been able to
validate the test . . .” or reproduce it, “including Vernino.” Tr. 213:6–10. Dr. Low took issue with
this study’s use of a research company that is “selling directly to patients[,]” rather than getting
validation or certification from other studies. Tr. 213:15–17.
Dr. Low also addressed the Kharraziha et al.83 article. Tr. 214:15–18, 218:15–219:18
(citing Pet’r’s Ex. 64). Dr. Low opined that the bioassay used in this study was likewise not an
adequate test. Tr. 218:3–5. He argued that this is a lesser test than the ELISA and explained that it
is “pre-lab type testing where . . . you look at the cremasteric muscle of the rat.” Tr. 218:10–15.
He admitted that this study was “a little more sophisticated, looking at tissue.” Tr. 218:15–16.
However, he argued “you need to get beyond that to get serious.” Tr. 218:17. He was confronted
with Kharraziha et al.’s conclusion that the serum of patients with POTS “demonstrate activity
against cardiovascular and nociceptive G protein coupled receptors[,] and such activation is highly
predictive of POTS diagnosis.” Tr. 218:18–22. Dr. Low maintained that because the methodology
was questionable, “the clinical correlation was not that convincing and to claim it[ is] a predictive
test . . . is just not correct.” Tr. 219:1–4.
Dr. Low opined that Dr. Kinsbourne “has offered no reliable evidence that a flu vaccine
can cause, or does cause, POTS.” Resp’t’s Ex. E at 4. Dr. Low explicitly stated that there is no
82 W. Gunning et al., Postural Orthostatic Tachycardia Syndrome is Associated with Elevated G-Protein
Coupled Receptor Autoantibodies, X J. AM. HEART ASSOC. 1–10 (2019).
83 I. Kharraziha et al., Serum Activity Against G Protein-Coupled Receptors and Severity of Orthostatic
Symptoms in Postural Orthostatic Tachycardia Syndrome, 9 J. AM. HEART ASSOC. 1–17 (2020).
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evidence that the flu vaccine could induce the antibodies posited by Dr. Kinsbourne, and that fact
has “been totally skimmed over.” Tr. 194:17–20. Dr. Low testified that “[t]here is no antibody that
has produced POTS[.]” Tr. 196:8–9. Dr. Low therefore argued that there is no direct evidence to
show that Petitioner’s flu vaccine “ha[d] anything to do with [her] POTS[.]” Resp’t’s Ex. A at 4;
Resp’t’s Ex. E at 1.
He wrote that Petitioner’s preexisting orthostatic intolerance “coupled with [her] lack of
tissue injury” to show evidence of molecular mimicry, weakens Petitioner’s argument for vaccine
causation. Resp’t’s Ex. C at 3–4. In support of this conclusion, Dr. Low testified that “[i]f POTS
is autoimmune, because the autoimmune process is so predictable, that [he] would expect to see
pathologic change.” Tr. 220:21–24. He argued that “all significant autoimmune autonomic
neuropathies” cause tissue injury. Resp’t’s Ex. C at 1–2. Dr. Low maintained that “all proven cases
of vaccine injury have resulted in tissue damage[,]” as exemplified by “the beautiful pathology”
seen in cases of vaccine-caused Guillain-Barré syndrome.84 Resp’t’s Ex. D at 2. He continued,
“[e]very case where there is an autoimmune primary injury to the autonomic nervous system has
resulted in tissue injury.” Id. He explained that “[o]ne reason for this reasonable requirement is
that, in many chronic conditions, there are secondary nonspecific, usually minor abnormalities,
often described as minor nonspecific abnormalities.” Id. Dr. Low argued that evidence of tissue
injury is important for “differentiating primary causative mechanism[s] for secondary non-specific
abnormalities.” Id. at 3. Dr. Low wrote that “low levels of antibodies generally have no linear
connection with disease severity. Thus, the antibodies identified by Dr. Kinsbourne fall into the
category of minor nonspecific abnormalities.” Resp’t’s Ex. E at 3. He argued that “research has
demonstrated that no clinical significance can be placed on such minor abnormalities.” Id.
Dr. Low wrote that Petitioner’s “extensive studies” showed no damage to her autonomic
nerves, and, in his review of Petitioner’s medical records, he saw “no symptoms or test results that
provide any evidence of significant autonomic neuropathy.” Resp’t’s Ex. A at 4. He argued that
evidence of damage to autonomic nerves, “such as [that] occurring in [] autoimmune autonomic
neuropathies,” would produce “easily identifiable clinical deficits[,] such as orthostatic
hypotension, pupillary abnormalities . . . gastroparesis, [and] bladder or bowel failure.” Id. (citing
Resp’t’s Ex. A, Tab 9, ECF No. 73-8).85 Dr. Low wrote that Petitioner “had none of these
manifestations[]” to suggest an autonomic injury. Id.; Resp’t’s Ex. E at 4. He continued that “one
would not expect vaccine injury to cause just POTS without other manifestations of injury to the
sympathetic nervous system.” Resp’t’s Ex. E at 4.
84 Guillain-Barré syndrome is “rapidly progressive ascending motor neuron paralysis of unknown etiology,
frequently seen after an enteric or respiratory infection. An autoimmune mechanism following viral
infection has been postulated. It begins with paresthesias of the feet, followed by flaccid paralysis of the
entire lower limbs, ascending to the trunk, upper limbs, and face; other characteristics include slight fever,
bulbar palsy, absent or lessened tendon reflexes, and increased protein in the cerebrospinal fluid without a
corresponding increase in cells. Variant forms include acute autonomic neuropathy, Miller-Fisher
syndrome, acute motor axonal neuropathy, and acute motor-sensory axonal neuropathy.” Dorland’s at
1832.
85 S. Vernino et al., Autoantibodies to Ganglionic Acetylcholine Receptors in Autoimmune Autonomic
Neuropathies, 343 N. ENG. J. MED. 847–55 (2000).
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Dr. Low maintained that “if you cannot show tissue injury, you do not have a specific
immune-mediated complication.” Resp’t’s Ex. C at 2. Dr. Low opined that Petitioner had “quite
aggressive treatment and testing[,]” and that if evidence of autoimmunity existed, it would have
appeared in her testing, including her norepinephrine testing. Tr. 223:17–224:10, 227:9–14 (citing
Pet’r’s Ex. 21 at 46). Dr. Low argued that the reason that an autoimmune etiology was not revealed
by Petitioner’s testing is because POTS is “not necessarily autoimmune,” so there is no test that
could show that. Tr. 224:11–17. Regarding Petitioner’s July 2020 antibody testing, Dr. Low
explained that autoantibodies would fade over time in monophasic illnesses, but POTS is not
monophasic so antibodies would not be expected to fade. Tr. 214:8–14. Rather, “POTS is a
persistent condition,” so one would expect antibodies to persist. Tr. 191:11–12. Dr. Low argued
that “if you look at the testing in the papers that have been presented” by Petitioner, it references
the presence of such adrenergic antibodies in POTS patients. Tr. 191:13–16. Such testing was
conducted and gathered from the patients at different durations, many of whom “had POTS for
many years[.]” See id. He did not cite specific articles when making this statement. See id. Dr.
Low maintained that Dr. Kinsbourne’s “idea that [antibodies] came and then [] disappeared does[
not] make any sense.” Tr. 191:15–17. He therefore did not believe Petitioner’s medical records
showed any evidence of autoimmunity. See id. Dr. Low “fully agree[d]” with Dr. Kinsbourne’s
argument that “there need not be tissue injury for POTS to occur.” Resp’t’s Ex. C at 1. Dr. Low
argued that this is true because “POTS is a condition and not a disease[]” and there are mechanisms
for POTS, such as deconditioning, medications, hypovolemia, or stress, that do not produce an
immune response at all, which is what happened in Petitioner’s case. Id.; see also Tr. 225:3–5.
Dr. Low discussed the relationship between POTS and other autoimmune disorders. He
testified that secondary POTS can occur in patients that are already suffering from an autoimmune
disorder. Tr. 165:19–25. He was careful in saying this does not “mean POTS is autoimmune . . .
the POTS was purely as a result of damage, clearly secondary.” Tr. 165:25–166:3. He explicitly
stated that hyperadrenergic POTS is “definitely not” presumed to be autoimmune-based. Tr.
167:13–15. He indicated he does not “know of any cases of hyperadrenergic POTS that[ were] due
to [an] autoimmune disorder.” Tr. 167:15–17.
IV. Applicable Legal Standards
To receive compensation under the Vaccine Act, a petitioner must demonstrate either that:
(1) the petitioner suffered a “Table injury” by receiving a covered vaccine and subsequently
developing a listed injury within the time frame prescribed by the Vaccine Injury Table set forth
at 42 U.S.C. § 300aa-14, as amended by 42 C.F.R. § 100.3; or (2) the petitioner suffered an “off-
Table injury,” one not listed on the Table, as a result of his receiving a covered vaccine. See 42
U.S.C. §§ 300aa-11(c)(1)(C); Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1321
(Fed. Cir. 2010); Capizzano v. Sec’y of Health & Hum. Servs., 440 F.3d 1317, 1319–20 (Fed. Cir.
2006). Petitioner does not allege a Table injury in this case; thus, she must prove that her injury
was caused-in-fact by a Table vaccine.
To establish causation-in-fact, a petitioner must demonstrate by a preponderance of the
evidence that the vaccine was the cause of the injury. 42 U.S.C. § 300aa-13(a)(1)(A). A petitioner
is required to prove that the vaccine was “not only a but-for cause of the injury but also a substantial
factor in bringing about the injury.” Moberly, 592 F.3d at 1321–22 (quoting Shyface v. Sec’y of
Health & Hum. Servs., 165 F.3d 1344, 1352–53 (Fed. Cir. 1999)).
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In the seminal case of Althen v. Sec’y of the Dept. of Health & Hum. Servs., the Federal
Circuit set forth a three-pronged test used to determine whether a petitioner has established a causal
link between a vaccine and the claimed injury. See 418 F.3d 1274, 1278–79 (Fed. Cir. 2005). The
Althen test requires petitioners to set forth: “(1) a medical theory causally connecting the
vaccination and the injury; (2) a logical sequence of cause and effect showing that the vaccination
was the reason for the injury; and (3) a showing of a proximate temporal relationship between
vaccination and injury.” Id. at 1278. To establish entitlement to compensation under the Program,
a petitioner is required to establish each of the three prongs of Althen by a preponderance of the
evidence. Id. “[C]lose calls regarding causation are resolved in favor of injured claimants.” Id. at
1280. Further, evidence used to satisfy one prong of the test may overlap to satisfy another prong.
Capizzano, 440 F.3d at 1326.
A petitioner who satisfies all three prongs of the Althen test has established a prima facie
showing of causation. Hammitt v. Sec’y of Health & Hum. Servs., 98 Fed. Cl. 719, 726 (2011). A
petitioner who demonstrates by a preponderance of the evidence that he suffered an injury caused
by vaccination is entitled to compensation unless the respondent can demonstrate by a
preponderance of the evidence that the injury was caused by factors unrelated to the vaccination.
See Althen, 418 F.3d at 1278; Knudsen v. Sec’y of Health & Hum. Servs., 35 F.3d 543, 547 (Fed.
Cir. 1994). In such a case, the government must not merely prove the existence of an alternative
cause, but that such an alternative actually caused the injury. Knudsen, 35 F.3d at 549.
Additionally, a factor unrelated “may not include ‘any idiopathic, unexplained, unknown,
hypothetical, or undocumentable cause, factor, injury, illness or condition.’” 42 U.S.C. § 300aa-
13(a)(2); see also Doe v. Sec’y of Health & Hum. Servs., 601 F.3d 1349 (Fed. Cir. 2010)
(explaining that an idiopathic diagnosis cannot be a “factor unrelated,” as it is idiopathic).
In considering the reliability of a petitioner’s evidence of a prima facie case, the special
master may consider alternative causes for a petitioner’s condition that are reasonably raised in the
record, even if the respondent does not pursue a formal alternative cause argument. Doe, 601 F.3d
at 1358. Thus, in weighing a petitioner’s case-in-chief, a special master may consider evidence
that the petitioner’s alleged injury could have been caused by alternative causes. Id.
V. Discussion
A. Experts86
Although special masters have the discretion to be informed by past rulings and
experiences, case-specific filings and testimony are the most helpful types of evidence, given the
fact-specific nature of each decision. See Doe v. Sec’y of Health & Hum. Servs., 76 Fed. Cl. 328,
338–39 (2007). To that end, experts are an essential piece of a petitioner’s claim and Respondent’s
defense. Where both sides offer expert testimony, a special master’s decision may be “based on
the credibility of the experts and the relative persuasiveness of their competing theories.”
Broekelschen v. Sec’y of Health & Hum. Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (citing
Lampe v. Sec’y of Health & Hum. Servs., 219 F.3d 1357, 1361 (Fed. Cir. 2000)). However, nothing
86 As Dr. Axelrod only submitted one brief expert report and did not testify at the entitlement hearing, I am
not relying on his opinions in this Decision, except to the extent that Dr. Kinsbourne adopts or expands
upon the basic principles put forth in his report.
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requires the acceptance of an expert's conclusion “connected to existing data only by the ipse dixit
of the expert,” especially if “there is simply too great an analytical gap between the data and the
opinion proffered.” Snyder v. Sec’y of Health & Hum. Servs., 88 Fed. Cl. 706, 743 (2009) (quoting
Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997)); see also Isaac v. Sec'y of Health & Hum.
Servs., No. 08–601V, 2012 WL 3609993, at *17 (Fed. Cl. Spec. Mstr. July 30, 2012), mot. for
review den'd, 108 Fed. Cl. 743 (2013), aff'd, 540 F. App’x. 999 (Fed. Cir. 2013). Weighing the
relative persuasiveness of competing expert testimony, based on a particular expert's credibility,
is part of the overall reliability analysis to which special masters must subject expert testimony in
Vaccine Program cases. Moberly, 592 F.3d at 1325–26 (“[a]ssessments as to the reliability of
expert testimony often turn on credibility determinations”); see also Porter v. Sec'y of Health &
Hum. Servs., 663 F.3d 1242, 1250 (Fed. Cir. 2011) (“[T]his court has unambiguously explained
that special masters are expected to consider the credibility of expert witnesses in evaluating
petitions for compensation under the Vaccine Act.”).
In determining whether a particular expert's testimony was reliable or credible, a special
master may consider whether the expert is offering an opinion that exceeds the expert's training or
competence. Walton v. Sec'y of Health & Hum. Servs., No. 04–503V, 2007 WL 1467307, at *17–
18 (Fed. Cl. Spec. Mstr. Apr. 30, 2007) (concluding that an otolaryngologist was not well suited
to testify about disciplines other than her own specialty). While all testimony of the experts offered
at the entitlement hearing was heard and considered, a special master may properly evaluate, and
give appropriate weight to, whether certain testimony is beyond a particular expert's purview. See,
e.g., King v. Sec'y of Health & Hum. Servs., No. 03-584V, 2010 WL 892296, at *78–79 (Fed. Cl.
Spec. Mstr. Mar. 12, 2010) (determining that a petitioner's expert was far less qualified to offer
opinion on general causation issues pertaining to autism than specific issues pertaining to the
petitioner's actual medical history, given the nature of the expert's qualifications). This case
ultimately turns not only on Petitioner’s medical history, but also the persuasiveness of the written
reports, supporting documentation, and expert testimony. I therefore must assess each expert’s
knowledge in relation to the facts of Petitioner’s case and assign weight accordingly. This
assessment will inform my analysis pursuant to each prong of Althen.
Petitioner’s expert, Dr. Kinsbourne, is now retired and has been for over 20 years. He spent
his career focusing on neurology, and much of his practice dealt specifically with pediatric and
behavioral neurology. See Pet’r’s Ex. 30; Tr. 56–72. It is true that Dr. Kinsbourne has treated
patients with autoimmune conditions generally, but he admitted that any POTS diagnosis he has
made has been limited to those within the Vaccine Program. See Tr. 68:10–13, 118:11–13.
Moreover, although Dr. Kinsbourne’s curriculum vitae reflects that he has an extensive publication
history, it is unrevealing of any body of publications directly relevant to the condition of POTS.
Conversely, Dr. Low, in addition to a background in neurology, is among the leading autonomic
specialists in the medical community and focuses primarily on autonomic conditions, including
POTS. See Resp’t’s Ex. B; Tr. 155–62. Dr. Low has treated and diagnosed thousands of POTS
patients or those suffering from autonomic disorders. See Tr. 159:8–15. I must note that I am not
accepting the opinion of Dr. Low carte blanche, as cautioned against by Petitioner. See Pet’r’s
Post-Hrg. Br. at 2. However, I base this Decision, in part, on Dr. Low’s credentials and expertise
in autonomic conditions, including POTS specifically, as compared to Dr. Kinsbourne’s specialty
in pediatric neurology.
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Petitioner’s medical theory is predicated on POTS having an autoimmune basis. Dr.
Kinsbourne is not an expert in immunology. However, I agree with Dr. Kinsbourne that on the
level he discussed the immune response to vaccinations, any neurologist would be able to elicit a
general understanding of such principles. See Tr. 66:14–15. Alternatively, Dr. Low’s role in the
investigation of an autoimmune etiology for POTS enhances the credibility of his testimony
regarding the same. Respondent contemplated but ultimately decided not to move to strike Dr.
Kinsbourne’s hearing testimony pertaining to immunology.87 I will recognize Respondent’s
request for me to “assign proper weight” to such testimony in accordance with Dr. Kinsbourne’s
subject-matter expertise. See Tr. 62–73, 229–30.
The limitations of Dr. Kinsbourne’s knowledge on the subject are evinced by the fact that
he authored his expert reports under the premise that AChR autoantibodies are associated with
POTS. On the stand, he then completely abandoned his reliance on such antibodies when he
presumably realized they are no longer thought to be associated with POTS. I cannot ignore Dr.
Kinsbourne’s reversal. Furthermore, Dr. Kinsbourne failed to acknowledge that POTS has several
subtypes, albeit not mutually exclusive. In Dr. Kinsbourne’s opinion, POTS has only one subtype,
hyperadrenergic POTS. See Tr. 123:3–124:17.
Dr. Kinsbourne is an extremely qualified expert in his field. He has a history of providing
useful testimony and persuasive explanations in cases before me, as well as other special masters
in the Program. Several special masters have also previously been critical of Dr. Kinsbourne for
opining beyond his area of expertise and into the field of immunology. See, e.g., Kottenstette v.
Sec'y of Health & Hum. Servs., No. 15-1016V, 2020 WL 4197301, at *13–14 (Fed. Cl. Spec. Mstr.
June 2, 2020), mot. for review den’d, No. 15-1016V, 2020 WL 4592590 (Fed. Cl. 2020), rev'd on
other grounds, 861 F. App’x. 433 (Fed. Cir. 2021). In this case, Dr. Kinsbourne’s reliance on a
seemingly outdated understanding of POTS and his lack of any clinical experience relative to the
syndrome is consistent with Respondent’s criticism and therefore affects the weight of his
testimony. It is also the case that key elements of Dr. Kinsbourne’s mechanistic theory are
grounded in immunology, a subject that he admits is beyond his area of expertise. Ultimately, his
opinion was delivered with less persuasive support and specificity than that of Respondent’s
expert, Dr. Low. See Broekelschen, 618 F.3d at 1347 (citing Lampe, 219 F.3d at 1362) (finding
that 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[]”).
B. Althen Prong One
Under the first prong of Althen, a petitioner must offer a scientific or medical theory that
answers in the affirmative the question: “can the vaccine[] at issue cause the type of injury
alleged?” See Pafford v. Sec’y of Health & Hum. Servs., No. 01-0165V, 2004 WL 1717359, at *4
(Fed. Cl. Spec. Mstr. July 16, 2004), mot. for review den’d, 64 Fed. Cl. 19 (2005), aff’d, 451 F.3d
1352 (Fed. Cir. 2006). To satisfy this prong, a petitioner’s theory must be based on a “sound and
reliable medical or scientific explanation.” Knudsen, 35 F.3d at 548. Such a theory must only be
“legally probable, not medically or scientifically certain.” Id. at 548–49. A petitioner is not
required to identify “specific biological mechanisms” to establish causation, nor are they required
87 Motions to strike expert testimony are rarely granted pursuant the relaxed interpretation of the Federal
Rules of Civil Procedure in the Program.
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to present “epidemiologic studies, rechallenge[] the presence of pathological markers or genetic
disposition, or general acceptance in the scientific or medical communities.” Capizzano, 440 F.3d
at 1325 (quoting Althen, 418 F.3d at 1280). Scientific and “objective confirmation” of the medical
theory with additional medical documentation is unnecessary. Althen, 418 F.3d at 1278–81; see
also Moberly, 592 F.3d at 1322. However, as the Federal Circuit has made clear, “simply
identifying a ‘plausible’ theory of causation is insufficient for a petitioner to meet her burden of
proof.” LaLonde v. Sec’y of Health & Hum. Servs., 746 F.3d 1334, 1339 (Fed. Cir. 2014) (citing
Moberly, 592 F.3d at 1322). Rather, “[a] petitioner must provide a reputable medical or scientific
explanation that pertains specifically to the petitioner’s case.” Moberly, 592 F.3d at 1322. In
general, “the statutory standard of preponderance of the evidence requires a petitioner to
demonstrate that the vaccine more likely than not caused the condition alleged.” LaLonde, 746
F.3d at 1339.
Furthermore, establishing a sound and reliable medical theory connecting the vaccine to
the injury often requires a petitioner to present expert testimony in support of her claim. Lampe,
219 F.3d at 1361. The Supreme Court’s opinion in Daubert v. Merrell Dow Pharmaceuticals, Inc.,
509 U.S. 579 (1993), requires that courts determine the reliability of an expert opinion before it
may be considered as evidence. “In short, the requirement that an expert’s testimony pertain to
‘scientific knowledge’ establishes a standard of evidentiary reliability.” Id. at 590 (citation
omitted). Thus, for Vaccine Act claims, a “special master is entitled to require some indicia of
reliability to support the assertion of the expert witness.” Moberly, 592 F.3d at 1324. The Daubert
factors are used in the weighing of the reliability of scientific evidence proffered. Davis v. Sec’y
of Health & Hum. Servs., 94 Fed. Cl. 53, 66–67 (2010) (“[U]niquely in this Circuit, the Daubert
factors have been employed also as an acceptable evidentiary-gauging tool with respect to
persuasiveness of expert testimony already admitted[.]”).
Petitioner has failed to meet her burden under Althen prong one. Petitioner posited a theory
of the flu vaccine’s role in the development of POTS via molecular mimicry.88 As discussed in
more detail below, this biological mechanism is only minimally supported by the submitted
evidence because while Petitioner has shown that POTS can have an autoimmune etiology, she
has failed to show that the flu vaccine can trigger an immune-mediated response resulting in POTS.
a. Autoimmune Etiology of POTS
For Petitioner to satisfy her burden as to her proposed biological mechanism, she must
establish that POTS has an autoimmune etiology. Petitioner argued that GPCR autoantibodies are
found in patients with POTS, which supports an autoimmune “trigger” for the condition.
Historically in the Program, petitioners have been unsuccessful in establishing an autoimmune
etiology for POTS based on the presence of certain autoantibodies. See, e.g., L.P. v. Sec’y of Health
& Hum. Servs., No. 16-1278V, 2021 WL 2373863, at *29 (Fed. Cl. Spec. Mstr. Apr. 26, 2021)
(rejecting the petitioner’s claim that the flu vaccine can cause POTS via the induction of
88 Petitioner alleged that her flu vaccination caused POTS with hypovolemia. Pet. at 1. However, Petitioner
did not provide testimony or evidence regarding the biological mechanism connecting the flu vaccine to
hypovolemia. Instead, Dr. Kinsbourne testified that “[w]ell, hypovolemia is one of the – is one of the many
– one of the parts of the mechanisms of causing the disability.” Tr. 122:4–9.
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antiphospholipid antibodies).89 However, we are now confronted with a growing number of studies
that place an importance on the role of adrenergic receptor autoantibodies in the development of
POTS. This shift in the medical community’s understanding of the potential autoimmune etiology
of POTS signals that such autoantibodies could be causative of an autoimmune process resulting
in POTS.
Indeed, older studies support Petitioner’s argument that autoantibodies to adrenergic
receptors, including alpha-1 and beta-1 and beta-2 adrenergic receptors, have been found in POTS
patients. However, such earlier studies are not determinative, as subsequent studies still questioned
the role of autoimmunity in the development of POTS. For example, the 2014 study by Li et al.
found at least one subset of adrenergic autoantibodies in each of the study’s 14 POTS patients.
Pet’r’s Ex. 49 at 1, 4, 7. A 2015 study by Blitshteyn et al. determined that 31 out of 100 POTS
patients had “markers of autoimmunity.” Pet’r’s Ex. 33 at 1. While they indicated that adrenergic
autoantibodies “appear to be good candidates mechanistically,” they concluded at that time that
the question of whether POTS is an autoimmune disorder still needed to be answered. Id. at 6.
By 2017, the role of such adrenergic autoantibodies was revisited, and small-scale studies
showed that such autoantibodies are involved in the pathophysiology of POTS, providing an
autoimmune basis for the condition. See Pet’r’s Ex. 51 at 7. In 2018, Vernino and Stiles undertook
efforts to catalog the body of prior research investigating an autoimmune basis for POTS. See
Pet’r’s Ex. 53. While the authors, relying on previously cited studies, admitted that GPCR
autoantibodies have been documented in POTS patients, they noted the current literature in 2018
revealed that adrenergic and muscarinic antibodies may have not been causative of POTS in larger
studies. Id. at 3. Part of the reason for this discrepancy is because GPCR autoantibodies have been
found in normal, healthy people. See id.; Tr. 189:16–18. Vernino and Stiles concluded that further
research is needed in larger cohorts to determine the pathological significance of GPCR
autoantibodies in POTS. Pet’r’s Ex. 53 at 3.
Notwithstanding Vernino and Stiles’ conclusion, the Program does not require evidence
from large epidemiological studies for a petitioner’s claim under Althen prong one to be successful.
See Capizzano, 440 F.3d at 1325 (quoting Althen, 418 F.3d at 1280) (indicating that to satisfy
prong one, a petitioner is not required to present “epidemiologic studies, rechallenge[] the presence
of pathological markers or genetic disposition, or general acceptance in the scientific or medical
communities.”). Indeed, subsequent literature, including an animal model, further supports the role
of adrenergic autoantibodies in the development of POTS, thus providing preponderant evidence
89 See also Yalacki v. Sec’y of Health & Hum. Servs., No. 14-278V, 2019 WL 1061429, at *34 (Fed. Cl.
Spec. Mstr. Jan. 31, 2019), mot. for review den’d, 146 Fed. Cl. 80 (2019) (finding that the evidence
presented to show POTS is autoimmune was thin and that the petitioner failed to show a HPV vaccine likely
causes “the production of antibodies associated with autonomic damage or interference sufficient to cause
POTS”); Johnson v. Sec’y of Health & Hum. Servs., No. 14-254V, 2018 WL 2051760, at *1 (Fed. Cl. Spec.
Mstr. Mar. 23, 2018) (ruling against the petitioner in a case alleging that the HPV vaccine caused POTS
and noting that the medical literature suggesting that POTS “might be autoimmune appears [to be]
extremely limited”); L.A.M. v. Sec’y of Health & Hum. Servs., No. 11-852V, 2017 WL 527576, at *63 (Fed.
Cl. Spec. Mstr. Jan. 31, 2017) (finding that most cases of POTS do not have an autoimmune etiology and
that the petitioner’s claim that the HPV vaccine caused POTS must fail because she did not provide
corroborating evidence of an autoimmune process).
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of an autoimmune etiology for the condition. See, e.g., Pet’r’s Exs. 47–48. By 2019, autonomic
specialists continued to investigate an autoimmune basis for POTS. Gunning et al. used an ELISA
test and found elevated titers of alpha-1 adrenergic autoantibodies and M4 muscarinic
acetylcholine receptor antibodies in POTS patients. See Pet’r’s Ex. 47 at 1. I am not persuaded by
Dr. Low’s attacks on the methodology used in this study. Specifically, he took issue with the
authors’ use of the ELISA test. He argued it is used for the detection of small proteins but since G
proteins are large proteins, the test’s ability to measure the presence of such antibodies is unlikely.
See Tr. 189:4–6, 212–14. Dr. Low demonstrated an outright refusal to acknowledge the authors’
findings of adrenergic autoantibodies in POTS patients. Further, Dr. Low seemed to classify
Gunning et al.’s findings as isolated and posited that the authors’ findings have not been validated
or reproduced in subsequent studies, “including [by] Vernino.” See Tr. 213:6–10. He did not offer
evidence in support of his argument, nor did he identify how many times researchers have
unsuccessfully attempted to reproduce Gunning et al.’s results. In fact, his reference to the work
of Dr. Vernino here cuts against his argument because the submitted research by Vernino was
conducted and published prior to the 2019 Gunning et al. study. See, e.g., Pet’r’s Ex. 52 (published
in 2000); Resp’t’s Ex. E, Tab 15 (published in 2003); Resp’t’s Ex. E, Tab 16 (published in 2004);
Pet’r’s Ex. 53 (published in 2018). Based on the submitted evidence, it does not appear that
Vernino et al. sought to reproduce Gunning et al.’s findings. I am therefore unpersuaded by Dr.
Low’s arguments regarding the significance of the Gunning et al. study.
Also in 2019, Li et al. purported to show the first animal model of POTS with an
autoimmune etiology by immunizing rabbits with alpha-1 and beta-1 adrenergic receptor
autoantibodies. The researchers observed that the rabbits then experienced a postural tachycardic
response measured on a tilt-table test. See Pet’r’s Ex. 48 at 3. The authors’ determination that they
were able to block the adrenergic autoantibodies from interacting with receptors in the rabbits,
making their heart rates return to baseline, appears to support their conclusion that such
autoantibodies play a causative role in the development of POTS. This finding further supports
their claim that POTS is autoimmune. In fact, Dr. Low agreed that these authors sought to, and
showed, that immunizing rabbits with these particular antibodies results in changes to their
receptors and vasoreactivity. Tr. 192:12–19. Dr. Low then opined that vasoreactivity “has nothing
to do with POTS.” Tr. 192:19. When asked how that is, Dr. Low could not explain why
vasoreactivity had nothing to do with POTS, instead stating that the authors “could be right” that
immunizing the rabbits with such autoantibodies “must be doing something to their receptors.” Tr.
192:20–193:1. He argued, however, that if Petitioner’s theory were true, and that antibodies could
alter the receptors, he would expect to see “some pathology.” Tr. 194:4–8. Dr. Low attacked the
authors’ failure to look for evidence of pathology in the rabbits because “[e]very case where there
is an autoimmune primary injury to the autonomic nervous system has resulted in tissue injury.”
Resp’t’s Ex. D at 2. He expanded on that argument and maintained that in an autoimmune attack
on the nervous system triggered by a vaccine, “you expect to see pathology[,]” such as the
“beautiful pathology” visible through clinical testing seen in autoimmune autonomic
ganglionopathy or Guillain-Barré syndrome. Tr. 193:23–194:3; Resp’t’s Ex. D at 2. He did not
further elaborate on this argument or provide any supporting evidence in the form of medical
literature or otherwise. See, e.g., Resp’t’s Ex. D at 2. Dr. Low’s exacting requirement of clinical
evidence of pathologic change and/or tissue injury to show autoimmunity is inconsistent with the
Program’s standards. See Capizzano, 440 F.3d at 1325 (quoting Althen, 418 F.3d at 1280)
(indicating that to satisfy prong one, a petitioner is not required to identify “specific biological
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mechanisms” to establish causation, nor are they required to present “epidemiologic studies,
rechallenge[] the presence of pathological markers or genetic disposition, or general acceptance in
the scientific or medical communities.”). Therefore, I will not require such of Petitioner.
More recent studies corroborate earlier studies that show POTS can have an autoimmune
etiology based on the presence of adrenergic autoantibodies. As recently as 2020, Kharraziha et
al. used a cell-based assay and determined that sera from POTS patients contained adrenergic
receptor antibodies “to a higher degree compared with [healthy] controls.” Pet’r’s Ex. 64 at 1. The
authors found this supported the “predictive value” of the role of such autoantibodies as a cause of
POTS. See id. Respondent’s expert Dr. Low took issue with the predictive value that these
receptors have in causing POTS, primarily because the authors used a bioassay, a lesser test than
the ELISA. I do not find Dr. Low’s argument convincing, as he again demonstrated the same
blanket refusal to acknowledge the authors’ findings as credible. While Petitioner’s own expert
admitted “we do not know if G protein antibodies are causative of a disease process or induced by
disease[,]” Tr. 135:18–21, Petitioner’s introduction of a recent study that bolsters earlier findings
and the role of such autoantibodies provides support for the autoimmune etiology of POTS. It is
true that Dr. Kinsbourne agreed that while some studies have shown antibodies have been found
in patients with POTS, such evidence is “not sufficient to declare” POTS an autoimmune disease.
Tr. 132:21–25. However, I agree with his statement that while the medical literature does not
provide scientific certainty for POTS being immune-mediated, it provides “a very high
probability” that it could be. Tr. 108:4–6.
b. Flu Vaccine as Trigger of POTS via Molecular Mimicry
While I have determined that autoimmunity can explain the pathogenesis of POTS, the
evidence does not explain how the flu vaccine can trigger such a response. Petitioner relied on a
cross-reaction between vaccine-generated autoantibodies and antibodies associated with GPCRs,
adrenergic receptor antibodies. This theory is based on the structural similarities between amino
acid sequences within the viral protein components of the flu vaccine and the self-protein
sympathetic nervous system receptors that might mistakenly get attacked by such autoantibodies
triggered by the vaccine. Indeed, Petitioner’s medical literature and expert testimony does not
address or explain how the flu vaccine could trigger such autoantibodies and cause POTS. In fact,
Petitioner’s own expert provided the best evidence against his theory of vaccine causation. Dr.
Kinsbourne could not cite to any evidence that supported his position that the flu vaccine could
induce GPCR antibodies. Instead, he stated he was “sure” he did not submit evidence that
establishes the flu vaccine can trigger these antibodies. See Tr. 137:15–17, 138:2–139:2. He also
conceded that no studies have been done that relate to POTS post flu “or any vaccination[.]” Pet’r’s
Ex. 29 at 7. While exact certainty and epidemiological studies are not required in the Program,
Petitioner was unable to cite to any evidence that suggests a reason to find it likely that the
proposed autoimmune cross-reaction triggered by the flu vaccine does, in fact, occur. See Knudsen,
35 F.3d at 548–49; Capizzano, 440 F.3d at 1325 (quoting Althen, 418 F.3d at 1280–81) (finding a
petitioner does not need to identify specific biological mechanisms or scientific and “objective
confirmation” of the medical theory with medical documentation).
The Gunning et al. study notes an association between vaccination generally and POTS.
Pet’r’s Ex. 47 at 8. The authors indicated that a number of studies have reported molecular mimicry
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associated with autoimmune diseases, and that POTS is such a condition based on the presence of
several antibodies in patients. See id. Likewise, a case report by Tsai et al. documented a patient
who developed POTS following receipt of the H1N1 influenza vaccination. Pet’r’s Ex. 14 at 2.
The authors concluded that the mechanism of the flu vaccine causing neurological complications
is not clear, but they documented the presence of an “unidentified antibody” as the proposed cause
of POTS. Id. at 3. While such reports reflect the fact that molecular mimicry has been proposed as
a potential mechanism in the post vaccination onset of POTS, this conclusion is not applicable to
the seasonal flu vaccine at issue here without explanation. The Tsai et al. study documented an
association between a type of flu vaccine and POTS, but the authors did not set forth a medical
theory casually connecting the vaccine to the development of POTS.
Petitioner’s main support was found in case reports that documented an association
between the HPV vaccine and POTS via molecular mimicry. See, e.g., Pet’r’s Ex. 16. However,
Petitioner did not receive the HPV vaccine. While such comparisons can be helpful in certain
circumstances, Petitioner’s expert did not sufficiently explain the basis for his comparison between
the flu and HPV vaccines. Petitioner has therefore failed to show that her proposed theory of
molecular mimicry applies to the flu vaccine and POTS. See W.C. v. Sec’y of Health & Hum.
Servs., 704 F.3d 1352, 1360 (2013) (finding that a petitioner cannot prevail by simply invoking
the term ‘molecular mimicry,’ or by showing that molecular mimicry is a valid theory to explain
how other triggers may have induced other diseases and determining that a petitioner must produce
additional evidence that molecular mimicry can cause the flu vaccine to cause POTS). If I accepted
Petitioner’s assertion that molecular mimicry could be used to demonstrate an association between
any combination of antigens and autoimmune injuries, Althen prong one “would be rendered
meaningless.” See Caves v. Sec’y of Health & Hum. Servs., 100 Fed. Cl. 119, 135 (2011), aff’d,
463 F. App’x. 932 (2012); see also McKown v. Sec’y of Health & Hum. Servs., No. 15-1451, 2019
WL 4072113, *50 (Fed. Cl. Spec. Mstr. July 15, 2019) (“[M]erely chanting the words ‘molecular
mimicry’ in a Vaccine Act case does not render a causation theory scientifically reliable, absent
additional evidence specifically tying the mechanism to the injury and/or the vaccine in
question.”).
Lastly, I cannot ignore the fact that to date, no claim has succeeded in the Program that
alleged vaccine-caused POTS. Indeed, that pertains to all covered vaccines in the Program. See,
e.g., Hibbard v. Sec’y of Health & Hum. Servs., 698 F.3d 1355 (Fed. Cir. 2012) (affirming the
special master’s dismissal of a case alleging that the flu vaccine caused POTS); America v. Sec’y
of Health & Hum. Servs., No. 17-542V, 2022 WL 278151, at *27 (Fed. Cl. Spec. Mstr. Jan. 4,
2022) (ruling against the petitioner’s argument that the HPV vaccine can interfere with the nervous
system sufficient to cause POTS, autonomic dysfunction or generalized dysautonomia, or
vasovagal syncope); Hughes v. Sec’y of Health & Hum. Servs., No. 16-930V, 2021 WL 839092,
at *30 (Fed. Cl. Spec. Mstr. Jan. 4, 2021) (denying compensation for a claim involving the HPV
vaccine and POTS); E.S. v. Sec’y of Health & Hum. Servs., No. 17-480V, 2020 WL 9076620, at
*49–51 (Fed. Cl. Spec. Mstr. Nov. 13, 2020); Balasco v. Sec’y of Health & Hum. Servs., No. 17-
215V, 2020 WL 1240917, at *33–34 (Fed. Cl. Spec. Mstr. Feb. 14, 2020); Combs v. Sec’y of
Health & Hum. Servs., No. 14-878V, 2018 WL 1581672 (Fed. Cl. Spec. Mstr. Jan. 31, 2017);
Turkopolis v. Sec’y of Health & Hum. Servs., No. 10-351V, 2014 WL 2872215 (Fed. Cl. Spec.
Mstr. May 30, 2014). This is not to say that a future case alleging vaccine-caused POTS cannot
and will not succeed in the Program based on the evolving understanding of the post vaccination
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pathogenesis of the condition. However, Petitioner’s claim is not one of those cases. Therefore,
Petitioner has failed to satisfy the first prong of Althen by a preponderance of the evidence.
C. Althen Prongs Two and Three
Under the second prong of Althen, a petitioner must prove that the vaccine actually did
cause the alleged injury in a particular case. See Pafford, 2004 WL 1717359, at *4; Althen, 418
F.3d at 1279. The second Althen prong requires proof of a logical sequence of cause and effect,
usually supported by facts derived from a petitioner’s medical records. Althen, 418 F.3d at 1278;
Capizzano, 440 F.3d at 1326; Grant v. Sec’y of Health & Hum. Servs., 956 F.2d 1144, 1148 (Fed.
Cir. 1992). A petitioner does not meet this obligation by showing only a temporal association
between the vaccination and the injury; instead, the petitioner “must explain how and why the
injury occurred.” Pafford, 2004 WL 1717359, at *4 (emphasis in original). The special master in
Pafford noted petitioners “must prove [] both that [their] vaccinations were a substantial factor in
causing the illness . . . and that the harm would not have occurred in the absence of the
vaccination.” 2004 WL 1717359, at *4 (citing Shyface, 165 F.3d at 1352). A reputable medical or
scientific explanation must support this logical sequence of cause and effect. Hodges v. Sec’y of
Health & Hum. Servs., 9 F.3d 958, 961 (Fed Cir. 1993) (citation omitted). Nevertheless,
“[r]equiring epidemiologic studies . . . or general acceptance in the scientific or medical
communities . . . impermissibly raises a claimant’s burden under the Vaccine Act and hinders the
system created by Congress . . . .” Capizzano, 440 F.3d at 1325–26. “[C]lose calls regarding
causation are resolved in favor of injured claimants.” Althen, 418 F.3d at 1280. The record often
includes “evidence of possible sources of injury” that can show alternate causes for the alleged
vaccine-related injury. See Stone v. Sec’y of Health & Hum. Servs., 676 F.3d 1373, 1379 (Fed. Cir.
2012).
In Program cases, contemporaneous medical records and the opinions of treating
physicians are favored. Capizzano, 440 F.3d at 1326 (citing Althen, 418 F.3d at 1280). Indeed,
when reviewing the record, a special master must consider the opinions of treating physicians. Id.
This is because “treating physicians are likely to be in the best position to determine whether ‘a
logical sequence of cause and effect show[s] that the vaccination was the reason for the injury.’”
Id. In addition, “[m]edical records, in general, warrant consideration as trustworthy evidence. The
records contain information supplied to or by health professionals to facilitate diagnosis and
treatment of medical conditions. With proper treatment hanging in the balance, accuracy has an
extra premium. These records are also generally contemporaneous to the medical events.” Cucuras
v. Sec’y of Health & Hum. Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993). While a special master
must consider these opinions and records, they are not “binding on the special master or court.” 42
U.S.C. § 300aa-13(b)(1). Rather, when “evaluating the weight to be afforded to any such . . .
[evidence], the special master . . . shall consider the entire record . . . .” Id. There is no presumption
that medical records are accurate and complete as to all the patient’s physical conditions. Kirby v.
Sec’y of Health & Hum. Servs., 997 F.3d 1378, 1383 (Fed. Cir. 2021) (finding that “[b]ecause a
reasonable fact finder could conclude that [the petitioner’s] testimony [wa]s not inconsistent with
her medical records . . . it was not arbitrary and capricious for the special master to credit [the
petitioner’s] testimony” over her medical records). Where there are inconsistencies, special
masters are within their discretion to award contemporaneous medical records greater weight than
later conflicting testimony. See Cucuras, 993 F.2d at 1528 (holding that the special master’s
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reliance on contemporaneous medical records over conflicting oral testimony given after the fact
was not arbitrary or capricious); see also Burns v. Sec’y of Health & Hum. Servs., 3 F.3d 415, 417
(Fed. Cir. 1993) (holding that the decision of whether to accord greater weight to contemporaneous
medical records or later given testimony is “uniquely within the purview of the special master”).
Indeed, the Court of Federal Claims has outlined four potential explanations for inconsistencies
between contemporaneously created medical records and later testimony: (1) a person’s failure to
recount to the medical professional everything that happened during the relevant time period; (2)
the medical professional’s failure to document everything reported to her or him; (3) a person’s
faulty recollection of the events when presenting testimony; or (4) a person’s purposeful
recounting of symptoms that did not exist. LaLonde v. Sec’y of Health & Hum. Servs., 110 Fed.
Cl. 184, 203–04 (2013), aff’d, 746 F.3d 1334 (Fed. Cir. 2014).
Under the third prong of Althen, a petitioner must show that the timing of the injury fits
with the causal theory. See Althen, 418 F.3d at 1278. For example, if a petitioner’s theory involves
a process that takes several days to develop after vaccination, an injury that occurred within a day
of vaccination would not be temporally consistent with that theory. Conversely, if the theory is
one that anticipates a rapid development of a reaction post-vaccination, the development of the
alleged injury weeks or months post vaccination would not be consistent with that theory. See de
Bazan v. Sec’y of Health & Hum. Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). Causation-in-fact
cannot be inferred from temporal proximity alone. See Grant, 956 F.2d at 1148; Thibaudeau v.
Sec’y of Health & Hum. Servs., 24 Cl. Ct. 400, 403–04 (1991); see also Hasler v. United States,
718 F.2d 202, 205 (6th Cir. 1983) (“Without more, [a] proximate temporal relationship will not
support a finding of causation.”).
a. Petitioner’s Preexisting Symptoms
Petitioner has failed to establish by preponderant evidence a logical sequence of cause and
effect showing that her October 8, 2013 flu vaccination was the reason for her development of
POTS pursuant to Althen prong two. Specifically, the evidence does not establish it more likely
than not that Petitioner’s condition began after her vaccination. A petitioner cannot succeed on a
claim of causation-in-fact where the alleged condition preexisted the vaccination. See W.C., 704
F.3d at 1354–55 (affirming the special master’s denial of compensation of a claim of causation-
in-fact because “[i]f a petitioner has a disorder before being vaccinated, the vaccine logically
cannot have caused the disorder[]”). Therefore, I must begin my analysis of Althen prong two with
a discussion of Petitioner’s preexisting symptoms.
From the start of the case, Petitioner’s medical records revealed that she was suffering from
symptoms prior to her flu vaccination that were similar to her post-vaccination symptoms. In light
of this, I (and the special master to whom this case was assigned before me), explicitly afforded
Petitioner multiple opportunities to propose a significant aggravation theory. See ECF Nos. 23, 26,
37. Despite such opportunities, Petitioner’s expert Dr. Kinsbourne explicitly stated that “[i]f there
had been a prior dysautonomia one would invoke very significant aggravation of that prior
condition, but prior POTS is not in evidence.” Pet’r’s Ex. 32 at 2. Although Petitioner indicated
during a status conference held on January 28, 2016, her intention to amend her claim and include
a significant aggravation cause of action, she ultimately did not do so. See ECF No. 23 at 1.
Furthermore, Petitioner has not offered evidence of a biological mechanism consistent with
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significant aggravation. As such, a significant aggravation claim is not before me to consider. See
Hirmiz v. Sec’y of Health & Hum. Servs., 119 Fed. Cl. 209, 220 (2014) (rejecting the petitioners’
attempt to raise a significant aggravation claim after a special master issued an entitlement decision
because the evidence “cited by petitioners that would support a significant-aggravation theory . . .
was submitted in support of separate and distinct theories of causation[] . . . [that involved]
neurological dysfunction beginning after the administration of the influenza vaccine[]”) (emphasis
in original).
Petitioner’s medical record shows by preponderant evidence that for approximately two
years prior to her October 8, 2013 flu vaccination, she exhibited symptoms of orthostatic
intolerance; and she was subsequently diagnosed with POTS, an orthostatic disorder. Her
symptoms of orthostatic intolerance included tachycardia, palpitations, and
dizziness/lightheadedness. For example, on January 12, 2011, Petitioner presented to the ER with
complaints of palpitations and tachycardia. See Pet’r’s Ex. 21 at 49, 150. Petitioner described the
sensation as a feeling that her “heart rate kept beating fast.” Id. at 150. The next year, on January
23, 2012, Petitioner complained of palpitations to her PCP, for which she received a referral to a
cardiologist. See Pet’r’s Ex. 13 at 1. On June 10, 2012, Petitioner experienced another episode of
tachycardia requiring her to go to the ER. See Pet’r’s Ex. 67. Petitioner’s medical records,
affidavits, and testimony collectively reflect that she reported palpitations, shaking, dizziness, and
lightheadedness on this occasion. See id. at 5, 11; Tr. 13:16–21; Pet’r’s Ex. 28 ¶ 4. During a visit
on April 24, 2013, Petitioner’s PCP noted that Petitioner exhibited an irregular
heartbeat/palpitations on exam. Pet’r’s Ex. 13 at 23.
Post vaccination, Petitioner reported similar complaints of tachycardia and dizziness on
several dates during November of 2013, including on November 4, 18, and 19, 2013. See Pet’r’s
Ex. 4 at 151, 146, 140. In fact, when Petitioner complained of tachycardia and dizziness on
November 18, 2013, she indicated that she had been experiencing increased palpitations for the
past two months. See id. at 146. Petitioner addressed this notation in an affidavit drafted on
February 23, 2016, approximately three years after this visit. She merely stated that while she is
aware her records reflect such symptoms as persisting for two months, “that is not an accurate
description of when [her] symptoms started.” Pet’r’s Ex. 28 ¶ 6. However, Petitioner could not
support her assertion that such records were incorrect and wrote that she “d[id] not specifically
recall what [she] reported [to treaters] at that time[.]” Id.
While there is no presumption that medical records are accurate, in order for Petitioner to
overcome the statements in her medical records, she must offer evidence that does not conflict
with such statements. See Kirby, 997 F.3d at 1383–84 (rejecting the presumption that medical
records are accurate and complete as to all the patient’s physical conditions and noting that in the
absence of this presumption, the reasonable fact finder was within his discretion to consider the
medical and testimonial record to conclude that the petitioner’s medical records did not conflict
with later testimony, and to credit such later testimony). Indeed, when witness testimony is offered
to overcome the weight of contemporaneous medical records, such testimony must be “consistent,
clear, cogent, and compelling.” Matthews v. Sec’y of Health & Hum. Servs., No. 19-414V, 2021
WL 4190265, at *5 (Fed. Cl. Spec. Mstr. Aug. 19, 2021), mot. for review den’d, 157 Fed. Cl. 777
(citing Blutstein v. Sec’y of Health & Hum. Servs., No. 90-2808V, 1998 WL 408611, at *5 (Fed.
Cl. Spec. Mstr. June 30, 1998)). Further, the Court of Federal Claims has acknowledged that “the
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absence of a reference to a condition or circumstance [in contemporaneous medical records] is
much less significant than a reference which negates the existence of the condition or
circumstance.” See id. (citing Shapiro v. Sec’y of Health & Hum. Servs., 101 Fed. Cl. 532, 541
(2011); Murphy v. Sec’y of Health & Hum. Servs., 23 Cl. Ct. 726, 733 (Fed. Cl. 1991), aff’d, 968
F.2d 1226 (Fed. Cir. 1992)).
As noted, Petitioner’s medical record from November 18, 2013, indicates that she told
treaters her tachycardia, dizziness, and palpitation symptoms had been present for two months.
Pet’r’s Ex. 4 at 146. It was only years later, during her written testimony, that she said that is not
when her symptoms began. Testimony offered after the events in question is less reliable than
contemporaneous reports when the motivation for accurate explication of symptoms is more
immediate. See Reusser v. Sec’y of Health & Hum. Servs., 28 Fed. Cl. 516, 523 (1993) (“[W]ritten
documentation recorded by a disinterested person at or soon after the event at issue is generally
more reliable than the recollection of a party to a lawsuit many years later.”). Petitioner’s medical
record therefore directly negates and contradicts her assertion that she was not experiencing such
symptoms around or before November 18, 2013. See Matthews, 2021 WL 4190265, at *5 (citing
Shapiro, 101 Fed. Cl. at 541).
More importantly, Petitioner’s reasoning for the discrepancy between her medical record
and later testimony is not consistent, clear, cogent, or compelling in as much as she could not
explain why such records would incorrectly reflect that her symptoms persisted for two months.
See Matthews, 2021 WL 4190265, at *5. Instead, she admitted that she does not “specifically recall
what [she] reported at that time[.]” Pet’r’s Ex. 28 ¶ 6. It is difficult to credit Petitioner’s statement
made in an affidavit authored approximately three years after the date of the visit, especially in
light of her admitted inability to remember what she told treaters. See Reusser, 28 Fed. Cl. at 523.
I must also acknowledge that there is a tendency in human nature to remember things in a way that
best fits within the narrator’s perspective of what happened. See LaLonde, 110 Fed. Cl. at 203.
More so, the Program has long recognized that when witness testimony conflicts with
contemporaneous medical records, the Court may accord such testimony lesser weight. Cucuras,
993 F.2d at 1528; Rickett v. Sec’y of Health & Hum. Servs., 468 F. App’x. 952, 958 (Fed. Cir.
2011) (holding that when medical records and testimony are “inconsistent, a special master may
give greater weight to the medical records”). As a result, I find preponderant evidence that
Petitioner’s medical record shows preexisting symptoms of tachycardia, dizziness, and
palpitations.
Petitioner’s preexisting symptoms also included SOB. Petitioner experienced numerous
episodes of SOB throughout 2012 and pre vaccination in 2013. Petitioner reported increased
respiratory issues for the last two years on January 28, 2012, which indicates her respiratory
problems began in January of 2010. Pet’r’s Ex. 13 at 3. On March 21, 2013, Petitioner reported
SOB and indicated that it had been “off/on since Dec[ember of 2012].” Id. at 5. She complained
of SOB again on April 24 and June 24, 2013. See id. at 22–23, 27. She experienced the same SOB
post vaccination in October and November 2013, and even reported that it had been occurring for
several months prior. For instance, on October 14, 2013, less than one week post vaccination,
Petitioner reported that she had been experiencing SOB for the last six months. Pet’r’s Ex. 23 at
1. On November 19, 2013, Petitioner reiterated that she had been having SOB for the “last few
months.” Pet’r’s Ex. 4 at 159. While Petitioner argued her history of SOB could be explained by
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her asthma diagnosis, her explanation is not sufficiently supported by the record. Indeed, Dr. Low
relied on the results of Petitioner’s March 20, 2014 spirometry testing to highlight the lack of
evidence of asthma. In fact, Petitioner’s spirometry testing showed full respiratory function. See
id. at 196; see also Tr. 172. Without diagnostic evidence of asthma, I find Dr. Low’s position that
Petitioner’s SOB symptoms were instead related to her dysautonomia, to be persuasive.
Petitioner’s medical records therefore demonstrate that she experienced several symptoms
prior to October 8, 2013, that were similar in nature to the symptoms she experienced post
vaccination and are consistent with autonomic dysfunction/dysautonomia and POTS. They also
show that she repeatedly reported such symptoms pre vaccination. While Petitioner maintained
that her pre vaccination episodes were entirely unrelated to her POTS, her assertions are
unavailing. Indeed, Petitioner did not successfully differentiate her pre and post vaccination
symptoms of palpitations/tachycardia, dizziness, and SOB in terms of nature or severity, she
merely argued her pre vaccination symptoms were caused by factors other than her POTS, such as
anxiety and dehydration.
Petitioner attempted to support her position that her POTS began post vaccination with the
fact that she was never diagnosed with POTS prior to her October 8, 2013 flu vaccination.
Petitioner’s date of diagnosis provides no insight into her condition onset, without the context of
her medical record. See W.C., 704 F.3d at 1358. In fact, Dr. Low asserted that he, as one of the
leading autonomic specialists, likewise would not have diagnosed Petitioner formally with POTS
in 2011 because such a “laboratory” diagnosis of the condition can only be confirmed with a tilt-
table test. See Resp’t’s Ex. C at 3; Tr. 183:1–4. However, Dr. Low’s description of POTS as
requiring only orthostatic intolerance associated with tachycardia is persuasive and consistent with
the Dorland’s definition of POTS (noting that POTS refers to a “group of symptoms . . . that
sometimes occur when a person assumes an upright position, including tachycardia,
tremulousness, [and] lightheadedness . . . .”).90 As Petitioner did not undergo a tilt-table test until
late November of 2013 and did not present to an autonomic specialist until 2014, I do not find it
more likely than not that she would have received a diagnosis of POTS pre vaccination despite the
presence of autonomic symptoms.
Petitioner’s claim likewise fails under Althen prong three because if a condition began
before vaccination, it would be logically impossible to infer that Petitioner’s injury occurred
“within a timeframe for which . . . it is medically acceptable to infer causation-in-fact.” W.C., 704
F.3d at 1358. As I have already determined that Petitioner has not presented preponderant evidence
that her condition began post vaccination, and she has failed to establish a biological mechanism
within which to assess the onset of her condition, it is impossible for me to analyze or for Petitioner
to satisfy her claim under prong three. Therefore, a more thorough discussion of Althen prong three
is inapplicable.
b. Petitioner’s Post-vaccination POTS Manifestations
Petitioner cannot establish a logical sequence of cause and effect connecting her
vaccination with her development of POTS, as there is preponderant evidence that her POTS
predated her vaccination. Additionally, the submitted evidence, including medical literature and
90 See supra, note 3 (defining POTS).
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credible expert testimony, establishes by preponderant evidence that dehydration,
deconditioning,91 and anxiety are all potential causes of the manifestation of Petitioner’s
orthostatic intolerance and POTS post vaccination. See Resp’t’s Exs. C, Tabs 1, 3, 5–6; Resp’t’s
Ex. A, Tab 7 at 1, 3; Resp’t’s Ex. A, Tab 1 at 3–4, 6; see also Tr. 165:3–9, 179:2–10, 203, 209–
10. I will not go so far as to determine whether either or all of these conditions are alternative
cause(s) for Petitioner’s POTS. Such a determination is unnecessary pursuant to prong two of
Althen. Petitioner did not meet her burden with respect to any Althen prong and cannot make a
prima facie case for entitlement. Therefore, Respondent is under no obligation to establish an
alternative cause. I will, however, discuss alternative causation as part of my analysis of
Petitioner’s medical records and her causation claim. Proof of a “logical sequence of cause and
effect” will eliminate potential likely alternatives. Walther v. Sec’y of Health & Hum. Servs., 485
F.3d 1146, 1151 (Fed. Cir. 2007).
When Petitioner presented to the ER on November 8, 2013, she had been experiencing
diarrhea ten times per day for the past ten days.92 See Pet’r’s Ex. 1 at 3. Her treater’s impression
record noted dehydration. See, e.g., Pet’r’s Ex. 4 at 170. The record also reflects that Petitioner
was experiencing heightened anxiety around this time. See id. Petitioner’s worsening symptoms
on November 8, 2013, caused her to remain in the ER until November 10, 2013. Following this
hospitalization, Petitioner then became inactive and eventually homebound and bedridden. In fact,
Petitioner repeatedly related this time period as the beginning of her diminished activity and
capabilities. For instance, on December 20, 2013, Petitioner reported being bedridden for the past
month, roughly since her November 2013 hospitalization. Pet’r’s Ex. 4 at 123. By January of 2014,
Petitioner received approval for home health services for IV fluids because she was homebound
as a result of her POTS symptoms. Pet’r’s Ex. 3 at 50. On February 11, 2014, she indicated that
she had been homebound for the previous three months. Pet’r’s Ex. 4 at 59. The medical literature
by Parsaik et al. submitted by Respondent provides preponderant evidence that a one to three
month period of discontinuous bedrest is sufficient deconditioning to trigger POTS symptoms.
See, e.g., Resp’t’s Ex. A, Tab 7 (indicating that a two-week, non-continuous period is enough to
produce effects of deconditioning).
I do, however, need to delve deeper into Petitioner’s arguments on dehydration. Petitioner
alleged in her petition that her flu vaccine caused hyperadrenergic POTS with hypovolemia. Pet.
at 1. Yet, Petitioner has put forth very limited evidence regarding her hypovolemia. Based on Dr.
Kinsbourne’s limited testimony, it is not clear to me whether he is referring to hypovolemia
interchangeably with dehydration. For example, he testified that Petitioner had “been hypovolemic
many times and had infusions to correct that.” Tr. 125:14–15. This statement appears to allude to
Petitioner’s treatment with IV fluids to correct her dehydration caused by her POTS “flare ups.”
91 I must note that some medical literature claims deconditioning in particular to be a secondary factor of
POTS, rather than a primary mechanism. See Pet’r’s Exs. 35, 40.
92 Petitioner’s treaters indicated that her diarrhea was “likely [caused by a] a viral syndrome” or viral
gastroenteritis. Pet’r’s Ex. 4 at 156, 170. Petitioner’s labs neither confirmed nor denied this assessment.
However, Petitioner’s treaters’ impressions attributable to a specific, albeit ambiguous, cause is consistent
with Dr. Low’s testimony that POTS would not present for the first time with GI symptoms. Even though
the evidence shows GI symptoms are commonly seen in patients with POTS, Dr. Low’s testimony that he
has never seen POTS present that way among his “thousands” of POTS patients is convincing evidence
that Petitioner’s POTS likewise did not present that way.
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See, e.g., Pet’r’s Ex. 4 at 113–16 (noting that Petitioner was unable to keep up with her hydration
requirement and that her POTS manifestations improved with IV fluids and hydration). I will not
speculate as to Dr. Kinsbourne’s understanding of hypovolemia,93 or what he was referring to
during such testimony, but I will point out that dehydration carries a different meaning. While
dehydration is due to insufficient fluid intake or loss of body water, hypovolemia is defined as an
“abnormally decreased volume of circulating blood in the body,” with the most common cause
being a hemorrhage. Dorland’s at 481, 908. The two terms are therefore not synonymous. Further,
when asked on cross-examination about POTS associated with hypovolemia, Dr. Kinsbourne
admitted that none of the literature he filed discusses hypovolemic POTS because he did not “think
there was occasion to discuss it because there[ is] not evidence that [Petitioner] was hypovolemic
at the onset[,]” only subsequently. Tr. 122:11–15. Again, I do not know if Dr. Kinsbourne was
referring to true hypovolemia or if he meant dehydration. It appears that the issue of hypovolemia
was essentially glossed over by Petitioner’s expert. Without arguments from Petitioner regarding
a biological mechanism connecting the flu vaccine to POTS with hypovolemia, I cannot analyze
her hypovolemia claim under any prong of Althen. Indeed, in light of Petitioner’s expert’s
ambiguous testimony, I must afford Dr. Low’s consistent and cohesive argument that dehydration
and hypovolemia are separate causes of POTS more weight. See Tr. 179:5–10.
In addition to Petitioner’s dehydration and deconditioning, which could themselves both
have caused her worsening symptoms consistent with POTS, I asked Petitioner’s expert Dr.
Kinsbourne to tell me if he saw Petitioner’s POTS “as relapsing because it [was] exacerbated by
her other conditions, specifically her asthma and anxiety[.]” Tr. 145:16–18. He agreed that it
“could be the case[]” that such factors were “working together[.]” Tr. 145:18–20.94 Indeed, during
Petitioner’s November 9, 2013 hospitalization, for what she considered to be the onset of her
POTS, Petitioner’s treaters thought strongly that her constellation of symptoms was anxiety-
related. See Pet’r’s Ex. 4 at 161. Cardiologist Dr. Gilbert noted on November 19, 2013, that anxiety
was a possible cause of Petitioner’s symptoms. See id. at 140. Even after she received her formal
POTS diagnosis and throughout her treatment, Petitioner’s treaters maintained that her symptoms
were caused by her anxiety. On February 11, 2014, endocrinologist Dr. Purdy opined that anxiety
was the cause of her symptoms. Id. at 59. Likewise, Petitioner’s neurologist Dr. Chan implicated
Petitioner’s anxiety as the cause of her continued symptoms on April 25, 2014. Pet’r’s Ex. 7 at 76.
Notably, none of Petitioner’s treaters attributed her autonomic symptoms and POTS diagnosis to
her October 8, 2013 flu vaccination.
93 Dr. Kinsbourne’s testimony is minimally supported by Respondent’s expert Dr. Low. Dr. Low also
testified that symptoms of hypovolemia (orthostatic intolerance and orthostatic tachycardia) can improve
with fluids in patients with hypovolemic POTS. Resp’t’s Ex. C at 1 (citing Resp’t’s Exs. C, Tabs 1, 3).
94 I must reiterate that Petitioner and her expert were afforded several opportunities to present and opine as
to any arguments that her October 8, 2013 flu vaccine significantly aggravated her prior condition. In fact,
the presiding special master to whom this case was assigned before me explicitly told Petitioner to file an
amended petition including a significant aggravation claim, and she did not. ECF No. 23 at 1. I also ordered
Petitioner’s expert to address a significant aggravation claim through a written report. ECF No. 37. Dr.
Kinsbourne did so, but he directly opined against the possibility or viability of a significant aggravation
claim and vehemently maintained that Petitioner’s POTS began post vaccination. See Pet’r’s Ex. 29 at 8;
Pet’r’s Ex. 31 at 1, 4; Pet’r’s Ex. 32 at 2. Most notably, Dr. Kinsbourne wrote that “[i]f there had been a
prior dysautonomia[,] one would invoke very significant aggravation of that prior condition, but prior POTS
is not in evidence.” Pet’r’s Ex. 32 at 2. Petitioner has not presented a significant aggravation claim for me
to consider, and significant aggravation is therefore not at issue.
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c. Autoimmune Response in Petitioner
Petitioner has failed to show that the flu vaccine can cause POTS via autoantibodies to
GPCRs pursuant to Althen prong one. Additionally, Petitioner is unable to show evidence of an
inflammatory or otherwise, immune-mediated response to establish that an autoimmune process
occurred in her case pursuant to Althen prong two. Evidence of autoimmunity cannot be
established merely with symptoms of POTS. Petitioner underwent extensive testing and a complete
autoimmune workup on November 19, 2013, which yielded negative results. See Pet’r’s Ex. 4 at
352–54; Tr. 223–24, 227. Petitioner also underwent additional testing in July of 2020 for the exact
GPCR autoantibodies asserted to be causative in this case. Such results were likewise negative.
See Pet’r’s Ex. 62; see also Tr. 133:17–23. To show that she experienced an immune-mediated
response, Petitioner’s expert Dr. Kinsbourne seemingly relied only on the fact that “there is no
alternative reasonable alternative explanation[]” for Petitioner’s POTS, other than an autoimmune
etiology. See Tr. 92:18–20, 93:5–6. Such arguments do not provide persuasive support for
evidence of an immune-mediated response following Petitioner’s October 8, 2013 flu vaccination.
Likewise, Dr. Kinsbourne’s argument that antibodies fade over time so the lack of
antibodies in Petitioner’s July 2020 tests was not surprising is irreconcilable with Petitioner’s
current condition. Dr. Kinsbourne was asked to explain how Petitioner’s condition continued if
her body was not actively engaged in an immune response seen with the presence of
autoantibodies. Tr. 142:18–143:1. He stated that POTS is a condition wherein “there is an attack
which causes damage and the agent may go away, but the damage remains.” Tr. 143:5–6. Dr.
Kinsbourne implicated humoral and cellular immunity but was otherwise unable to explain how
Petitioner’s POTS continued if her antibodies were negative in July of 2020. See Tr. 145:2. In fact,
he admitted that “it[ is] unlikely that the antibodies were still actively injuring [Petitioner]” seven
years later. Tr. 145:8–10. At best, he implicated T cells as responsible for continuing the damage,
but he could not say so with any confidence and admitted that “[w]hat the cellular immunity does[,
he] do[es not] know because there is[ not] much written about it at this time.” Tr. 145:11–12.
Alternatively, Dr. Low credibly explained consistent with principles of autoimmunity, that if an
antibody is actually the cause of a condition, then the antibody would continue to be present for
the duration of the disease. He explicitly stated that “POTS is a persistent condition,” and therefore
he would expect to see the antibodies persist. See Tr. 191:4–12. Petitioner’s argument that
antibodies to GPCRs were present post vaccination and then disappeared throughout the course of
her disease is not supported by preponderant evidence. Petitioner has failed to satisfy her burden
pursuant to Althen prong two.
VI. Conclusion
After a careful review of the record, Petitioner has failed to prove by preponderant evidence
that her POTS with hypovolemia were caused-in-fact by her October 8, 2013 flu vaccination.
Accordingly, Petitioner’s claim is hereby DENIED and her petition is DISMISSED.95
IT IS SO ORDERED.
95 Pursuant to Vaccine Rule 11(a), entry of judgment is expedited by the parties’ joint filing of a notice
renouncing the right to seek review.
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s/Herbrina D. Sanders
Herbrina D. Sanders
Special Master
57