P. v. Secretary of Health and Human Services ( 2021 )

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 16-1278V
Filed: April 26, 2021
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*
L.P., *
*
* TO BE PUBLISHED
Petitioner, *
*
v. *
* Influenza Vaccine; Postural Orthostatic
* Tachycardia Syndrome (POTS);
SECRETARY OF HEALTH AND * Dismissal Decision
HUMAN SERVICES, *
*
*
Respondent. *
*
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Andrew D. Downing, Van Cott & Talamante, PLLC, for Petitioner
Daniel A. Principato, U.S. Department of Justice, Washington, DC, for Respondent
DECISION ON ENTITLEMENT1
Oler, Special Master:
On October 5, 2016, L.P. (“Petitioner”) filed a petition for compensation under the National
Vaccine Injury Compensation Program, 42 U.S.C. § 300aa-10, et seq.2 (the “Vaccine Act” or
“Program”). The petition alleges that Petitioner developed postural orthostatic tachycardia
syndrome (“POTS”) as a result of the influenza (“flu”) vaccine she received on September 25,
2015. Pet. at 5-6, ECF No. 1.
1
This Decision will be posted on the United States Court of Federal Claims’ website, in accordance with
the E-Government Act of 2002, 44 U.S.C. § 3501 (2012). This means the Decision will be available to
anyone with access to the internet. As provided in 42 U.S.C. § 300aa-12(d)(4)(B), however, the parties
may object to the Decision’s inclusion of certain kinds of confidential information. To do so, each party
may, within 14 days, request redaction “of any information furnished by that party: (1) that is a trade secret
or commercial or financial in substance and is privileged or confidential; or (2) that includes medical files
or similar files, the disclosure of which would constitute a clearly unwarranted invasion of privacy.”
Vaccine Rule 18(b). Otherwise, this Decision will be available to the public in its present form. Id.
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).
1
Upon review of the evidence in this case, I find that Petitioner has failed to show that POTS
is her correct diagnosis or that the influenza vaccine she received on September 25, 2015 caused
her condition. The petition is accordingly dismissed.
I. Procedural History
On October 10, 2016, Petitioner filed her Petition. ECF No. 1. She filed medical records
and a statement of completion on December 19, 2016. ECF No. 14.
On January 17, 2017, Respondent filed a Rule 4(c) Report, presenting his analysis of
Petitioner’s claims and concluding this case is not appropriate for compensation under the terms
of the Vaccine Act. ECF No. 16.
On March 13, 2017, Petitioner filed an expert report from Dr. Jill Schofield as well as Dr.
Schofield’s curriculum vitae. ECF No. 18, Ex 30-31. On March 24, 2017, Petitioner filed the
medical literature associated with Dr. Schofield’s report. ECF Nos. 19-21, Exs. 32-49.
On October 5, 2017, Respondent filed an expert report from Dr. Thomas Leist, Dr. Leist’s
curriculum vitae, and the medical literature associated with his report. ECF No 28, Ex. A; Ex. A
Tabs 1-2.
On December 5, 2017, this case was assigned to my docket. ECF No. 32.
On August 13, 2018, Petitioner filed a supplemental expert report from Dr. Schofield. ECF
No. 36, Ex. 50. On April 29, 2020, and March 17, 2021, Petitioner filed additional medical
literature in support of Dr. Schofield’s reports. ECF No 53, Ex. 56; ECF No. 62, Ex. 57.
On October 15, 2018, Respondent filed a supplemental responsive expert report from Dr.
Leist, and the associated medical literature. ECF No. 37, Ex. B; Ex. B, Tab 1.
On August 20, 2019, Petitioner filed a Statement of Completion. ECF No. 48.
On December 20, 2019, Petitioner filed her Motion for Decision on the Record. ECF No.
49. On March 20, 2020, Respondent filed a Response. ECF No. 50. On April 29, 2020, Petitioner
filed a Reply brief. ECF No. 54.
On June 18, 2020, the parties filed a Status Report stating that the record in this matter was
complete. ECF No. 57. This matter is now ripe for adjudication.
II. Medical Records
A. Relevant Pre-Vaccination History
Prior to her vaccination on September 25, 2015, Petitioner had a history of heart
palpitations, exercise induced asthma, anxiety, scoliosis, allergic rhinitis, eustachian tube
dysfunction, premenstrual and menstrual irregularities, iron deficiency anemia, Vitamin D
2
deficiency, and a sensitivity to sunlight. She had suffered from allergic rhinitis since the age of
four, and she was diagnosed with exercise induced asthma in 2001. Ex. 10 at 17-19. In 2002,
Petitioner had a left breast biopsy. Ex. 5 at 1. In September 2012, an x-ray of Petitioner’s spine
revealed lumbar scoliosis measuring 20 degrees. Ex. 18 at 55.
In the two years leading up to Petitioner’s alleged vaccine injury, Petitioner regularly
visited various doctors with complaints of heart palpitations, back pain, allergy related symptoms,
and menstrual issues.
On February 27, 2013, Petitioner saw Dr. Yeash, her primary care physician, complaining
of irregular heartbeats occurring daily, sometimes at night, which seemed to trigger anxiety. Ex.
18 at 28. An EKG was non-diagnostic Id. at 29. Dr. Yeash assessed Petitioner with palpitations
and referred her to a cardiologist. Id. at 28.
On March 20, 2013, Petitioner saw Dr. Benedict, a cardiologist, complaining of heart
palpitations mostly when sleeping or sitting still, usually occurring one week before and during
her period and sometimes accompanied by a flushed or clammy feeling and lightheadedness. Ex.
5 at 8-9. Dr. Benedict ordered an EKG, an echocardiogram, and a Holter heart monitor. Id. at 8.
The results of the EKG and echocardiogram were non-diagnostic/normal. Id. at 11, 26.
On April 15, 2013, Petitioner saw Dr. Yeash for a medication check. Ex. 18 at 26. Her
bloodwork revealed low levels of Iron and Vitamin D. Dr. Yeash recommended supplements. Ex.
18 at 52.
On April 22, 2013, Dr. Benedict provided Petitioner with the results of her Holter monitor
test. Ex. 5 at 2. Seven total events of “fluttering in the chest” were recorded over a period of 30
days which did not correlate with premature atrial contractions (“PACs”)3. Id.
Petitioner visited Dr. Yeash on May 6, 2013 complaining of fatigue and constipation. Ex.
18 at 23. Dr. Yeash assessed Petitioner with anemia and premenstrual disorder and prescribed
0.5mg of Alprazolam every eight hours or as needed. Id. at 24.
Petitioner again visited Dr. Yeash on November 18, 2013 complaining of heavy periods,
trouble sleeping and tinnitus. Ex. 18 at 21. Dr. Yeah assessed Petitioner with an iron deficiency,
Vitamin D deficiency, metrorrhagia, tinnitus and insomnia. Id. He recommended that Petitioner
undergo an endometrial ablation to relieve her heavy periods and perhaps resolve her iron
deficiency. Id. Dr. Yeash recommended that Petitioner see an ENT for her tinnitus. Id.
3
Atrial Premature Complex is a single ectopic atrial beat arising prematurely, manifesting
electrocardiographically as an abnormally shaped premature P wave, usually with a slightly increased PR
interval. It occurs in normal hearts, sometimes associated with the use of stimulants, but may be associated
with structural heart disease. Dorland's Illustrated Medical Dictionary. (33 ed. 2019),
https://www.dorlandsonline.com/dorland/definition?id=66296 (last visited April 19, 2021) (hereinafter
“Dorland’s”).
3
On March 26, 2014, Petitioner saw Dr. Schkade, an ENT, complaining of allergies and
exercise induced asthma. Ex. 10 at 11. She reported an oral allergy to walnuts and tomatoes and
that Nasacort made her anxious. Id. at 12. Dr. Schkade noted a history of rhinoconjunctivitus,
pruritus and eustachian tube dysfunctions, which he indicted was probably secondary to her
allergic rhinitis. Id. at 12.
Petitioner returned to Dr. Schkade on April 12, 2014 for allergy testing and desensitization
injections. Ex. 10 at 13. Skin testing revealed that she was allergic to grass and Dr. Schkade
diagnosed her with chronic rhinitis due to non-allergenic symptoms in the winter. Id.
On April 24, 2014, Petitioner presented to Westside Women’s Clinic complaining of heavy
periods and insomnia due to having to get up at night to address her menstrual flow. Ex. 52 at 13.
Petitioner also reported a lack of libido. Id. She was assessed with dysmenorrhea. Id.
Petitioner saw Dr. Schkade on July 16, 2014 reporting a 50 percent improvement in her
allergic rhinitis since she started desensitization injections. Ex. 10 at 21. She reported that Flonase
changed her menstrual cycle and caused breast discomfort. Id. Dr. Schkade recommended
continued immunotherapy and both a nasal and ocular antihistamine. Id.
On October 15, 2014, Petitioner saw Dr. Schkade complaining of ear discomfort and a
pruritic skin rash in sun exposed areas. Ex 10 at 23. Dr. Schkade noted that Petitioner’s asthma
and allergic symptoms were under control and that her ear discomfort could be related to her
eustachian tube dysfunction. Id. at 24. He recommended that she see a dermatologist for possible
photosensitivity. Id.
Petitioner visited Dr. Maybach as a new patient on December 3, 2014. Ex. 18 at 19.
Petitioner reported having abnormal TSH levels but indicated she had never been on medication.
Id. She attributed her iron deficiency to her heavy periods and reported suffering from constipation
as a result of taking iron supplements. Id. Dr. Maybach assessed Petitioner with an iron deficiency
(chronic anemia), Vitamin D deficiency, and metrorrhagia. Id.
On February 11, 2015, Petitioner presented at Westside Women’s Care complaining of
pain on her left side and excessively heavy periods. Ex. 21 at 6. Petitioner reported having tried
every kind of birth control for her symptoms, but she reported they were either ineffective or
caused side effects. Id. Petitioner rejected trying an IUD because she was concerned about
hormone issues. Id. Her doctor found the pain on Petitioner’s left side to be consistent with
constipation. Id. An ultrasound showed a normal uterus with no abnormalities. Id.
Petitioner presented to Arvada Sports and Spine Group on April 8, 2015 complaining of
left side low back pain for the past three to four weeks possibly due to falling while walking her
dog. Ex. 11 at 1. Petitioner was also concerned that the pain might be related to her ovaries, internal
organs, or pre-menopausal hormone issues. Id. She also reported an irregular heartbeat and
constipation. Id. at 1-2. The therapist recommended a home exercise regime combined with
physical therapy once a week for six to eight weeks. Id. at 4. The therapist noted that Petitioner
“appeared to be anxious.” Id. at 2.
4
On April 10, 2015, Petitioner visited the Saint Anthony Hospital Emergency Department
complaining of a reddened sharp stabbing left lower quadrant abdominal pain over the past one
month as well as constipation. Ex. 25 at 5. The results of a pelvic ultrasound were normal. Id. at
7. The attending physician doubted diverticulitis and considered constipation to be likely. Id. at 7.
Petitioner presented to Hafner Chiropractic on April 14, 2015, complaining of sharp
burning stabbing pain and stiffness radiating down her left buttock that started after a workout one
month prior. Ex. 13 at 1. She reported having some anxiety and feeling hypermobile at times. Id.
Petitioner treated with Dr. Hafner from April 2014 through October of 2015. See generally, Ex.
13. Over the course of her treatment, she alternately reported her symptoms as either unchanged
or improved. Id.
On April 15, 2015, Petitioner retuned to Arvada Sports and Spine Group. Ex. 11 at 10. She
reported having gone to the ER concerned about a “burst ovarian cyst,” and that she was feeling
better after seeing a chiropractor yesterday. Id. at 10. An MRI revealed lumbar scoliosis and level
4-5 degeneration. Id. at 11. The therapist again noted that Petitioner “appeared anxious.” Id.
Petitioner treated with Arvada Sports and Spine Group from May 2015 through July 2015. See
generally, Ex. 11. Over the course of her treatment, Petitioner rated her pain as a 1/10 and noticed
that her pain seemed to coincide with her menstrual cycle. Id.
Petitioner visited Westside Women’s Care on April 17, 2015 complaining of severe
symptoms associated with premenstrual dysphoric disorder (“PMDD”), mainly anxiety, and stated
to her doctor: “I am losing my mind.” Ex. 21 at 5. Petitioner reported that she had been diagnosed
with PACs related to “hormones.” Id. Petitioner continued to resist any type of hormonal therapy
and reported that she had a bad reaction to SSRIs. Id. She eventually agreed to try a low dose of
Citalopram4 for her anxiety. Id.
On June 10, 2015, Petitioner saw Dr. Schkade and recounted an episode of pruritus while
on a trip to San Francisco. Id. at 27. She reported that a dermatologist told her she might have
polymorphous light eruption. Id. Petitioner felt that her current treatment was adequate and did not
feel the need to make any changes. Id.
Petitioner returned to Westside Women's Care on June 16, 2015 complaining of issues with
PMDD; that Citalopram made her more anxious and jittery; and that she thought she had a small
umbilical hernia from straining due to constipation. Ex. 21 at 3. Her doctor refilled a prescription
for Xanax; Petitioner refused to try 10 micrograms of birth control for PMDD. Id. Petitioner’s
blood work indicated that she had a vitamin D deficiency. Id.
On July 15, 2015, Petitioner saw Dr. Maino at Centura Health complaining of lower back
pain and an umbilical hernia. Ex. 22 at 1. Dr. Maino recommended an MRI for her back pain and
referred Petitioner to Dr. Brew. Id. at 3.
4
Citalopram hydrobromide is a selective serotonin reuptake inhibitor (SSRI), chemically unrelated to other
SSRIs and consisting of a racemic mixture of two stereoisomers (S- and R-, the S-isomer being
pharmaceutically active); used as an antidepressant, administered orally. Dorland's,
https://www.dorlandsonline.com/dorland/definition?id=9949) (last visited April 19, 2021).
5
Petitioner visited Dr. Brew at Surgical Specialists of Colorado on August 3, 2015
complaining of chronic constipation, palpitations and back pain. Ex. 15 at 1. Dr. Brew assessed
Petitioner with a very small asymptomatic umbilical hernia; he recommended observation and not
surgery. Id. at 3.
B. Post-Vaccination History
Petitioner received her flu vaccination at Costco in Westminster, Colorado on September
25, 2015. Ex. 2 at 1-4.
On October 6, 2015, Petitioner presented to Dr. Schkade and reporting having trouble with
her ears for the past week. Ex. 10 at 30. She stated she was hearing a new lower tone in her left
ear and it felt full like she couldn’t pop it. Id. Dr. Schkade noted increased post-nasal drainage and
some facial swelling which could indicate a low-grade viral infection. Id. at 30-31.
Petitioner presented to Taos Urgent Care on October 17, 2015 while in Taos, New Mexico.
She stated that she awoke in the middle of the night with her heart racing, pressure in her left ear
and tinnitus. Ex. 7 at 1. The results of her lab work and EKG were essentially normal, but she was
advised to follow up with her cardiologist. Id. at 5.
On October 20, 2015, Petitioner saw Dr. Hartemink, an ENT, reporting sudden hearing
loss and a sense of fullness in her left ear that began three or four days prior. Ex. 3 at 1. She
reported having a 20-year history of high frequency tinnitus in both ears but was hearing a new
low frequency thumping in her left ear that had since resolved. Id. An audiogram revealed mild
sensorineural low frequency hearing loss in the left ear. Id. at 2. Dr. Hartemink’s differential
diagnosis was sudden sensorineural hearing loss (SSHL), unilateral, verses atypical Ménière’s
disease. Id. at 1. Petitioner reported having issues with nasal steroid sprays, and Dr. Hartemink
decided on a low dose of prednisone - 20mg 2x a day for 7 days, then one tablet per day for 14
days. Id.
On October 28, 2015, Petitioner saw Dr. Kreutzer, another ENT, for a second opinion. Ex.
4 at 1. Petitioner reported having a 17-year history of high frequency tinnitus after suffering
whiplash in a car accident and occasional pressure in her left ear for over a decade. Id. She reported
a new low frequency sound in her left ear, fullness, and hyperacusis on October 1, 2015. Id. She
denied having vertigo but did feel "spacey." Id. An audiogram showed resolution of the low
frequency hearing loss, and Dr. Kreutzer’s differential diagnosis was either bilateral
endolymphatic hydrops or Ménière’s disease as opposed to bilateral autoimmune inner ear
disorder. Id. Dr. Kreutzer recommended a balance test, the results of which were unremarkable.
Id. at 5. “The caloric results indicated a unilateral weakness in the left ear” indicative of a left
peripheral pathology consistent with Ménière’s disease. Id.
Petitioner saw Dr. Yeash on November 2, 2015 reporting that she completed a course of
prednisone for ear issues and that she was having a lot of anxiety, elevated pulse, and mood swings.
Ex. 18 at 16. She also reported a history of PACs. Id. Dr. Yeash recommended that Petitioner
6
follow up with Dr. Benedict. Id. Dr. Yeash prescribed 0.5mg of Xanax and instructed her to take
either a half or whole tablet, every eight hours as needed. Id. at 17.
On November 4, 2015, Petitioner saw Dr. Hafner for pain in her left hip. Ex. 13. at 19. She
reported having increased panic attacks after being treated with steroids for an ear issue. Id.
Petitioner visited Dr. Benedict on November 6, 2015 recounting her episode in Toas, New
Mexico. Ex. 5 at 26, 38. Petitioner told Dr. Benedict that she had been treated with steroids for
possible Ménière’s and “went crazy on these.” Id. at 26. Dr. Benedict noted that the incident in
Taos occurred mid-cycle, and that Petitioner was still having periods and hot flashes. Id. Petitioner
was exercising and reported having no palpitations in the past two weeks. Id. at 38. An EKG
performed at Taos Urgent Care revealed a long QT which Dr. Benedict attributed to Petitioner
being on antihistamines at the time. Id. A subsequent EKG was normal. Id. at 37. Dr. Benedict
ordered a repeat Holter monitor. Ex. 5 at 36.
On November 10, 2015, Petitioner saw Dr. Yeash and informed him that two ENTs had
assessed her with possible Ménière’s disease. Ex. 18 at 14. Petitioner reported having dizziness
but no vertigo. Id. Dr. Yeash recommended that she continue seeing Dr. Benedict and prescribed
an anti-inflammatory for ongoing lower back pain. Id.
Petitioner returned to Dr. Hartemink on November 12, 2015 reporting that her hearing was
better and that the fullness was mostly gone. Ex. 3 at 5. She told him that the prednisone had caused
her severe anxiety and that she was experiencing mood swings, sleep issues and menstrual issues.
Id. Considering that Petitioner’s hearing issues had returned to normal after treatment with
prednisone, Dr. Hartemink’s differential diagnosis was sensorineural hearing loss, unilateral, or
Ménière’s disease. Id. at 6. Dr. Hartemink suggested a low salt diet and a prescription for dyazide.
Id. Petitioner declined the medication because her cardiologist told her that dyazide would make
her palpitations worse. Id.
On November 17, 2015, Petitioner saw a third ENT reporting that she developed a
humming sound in her left ear, hearing loss and hyperacusis four to six weeks prior. Ex. 17 at 4.
She informed the ENT that she completed treatment with steroids but was still having anxiety,
sleeping problems, unintentional weight loss, ringing in her ears/head noise, post-nasal drainage,
and an irregular/fast/pounding heartbeat. Id. The ENT assessed her with tinnitus, sensorineural
hearing loss, and labyrinth dysfunction. Id. at 6.
On November 19, 2015 Petitioner visited Swedish Medical Center ER complaining of
intermittent and worsening palpitations for the past month and an onset of paresthesia/tingling in
her fingers earlier that day. Ex. 23 at 42, 49. She reported that she was working at her desk and
couldn't get her heart to stop racing. Id. at 28. She informed the treating team that her cardiologist
prescribed propranolol but she could not take it due to her asthma. Id. at 48. She reported having
been recently treated with Prednisone which made her anxious. Id. at 42. She informed the treating
team that her cardiologist ordered a Holter monitor, but that was she could not complete the testing
due to an adverse reaction to the adhesive. Id. Her EKG and lab tests came back normal. Id. at 45.
The treating physician noted, “discussed lab results with patient. Patient improved spontaneously.
7
Tachycardia and tingling resolved.” Id. at 46. The attending physician suspected some component
of anxiety contributed to Petitioner’s symptoms and prescribed Diltiazem. Id.
Petitioner returned to Dr. Yeash to discuss her heart issues on November 30, 2015. Ex. 18
at 12. Dr. Yeash suspected that Petitioner’s palpitations were due to anxiety. Id. Nevertheless, he
recommended that Petitioner continue taking propranolol as needed. Id. He prescribed letrozole
for GE reflux, and recommended Pepcid at bedtime. Id.
On November 30, 2015, Dr. Benedict provided Petitioner with the results of her Holter
monitor testing. Ex. 5 at 51. The monitor recorded nine total events over the course of 14 days,
and that Petitioner was in sinus bradycardia (less than 60bpm) 24% of the time and sinus
tachycardia (greater than 100bpm) only 2% of the time. Id. at 52. Dr. Benedict concluded that her
symptoms were not associated with dysrhythmia and recommended that Petitioner continue taking
propranolol. Id.
Petitioner returned to Arvada Sports and Spine Group on December 3, 2015 reporting that
she had been feeling great until two or three months ago when she developed increased tinnitus,
low back pain, left hip pain, and tingling of the pubic symphysis. Ex. 11 at 23. She rated her pain
as a 1/10. Id. She also reported feeling constipated and that steroid treatment for possible Ménière’s
caused her to feel ill, lethargic, and weak. Id. The physical therapist noted that Petitioner "appeared
anxious." Id. at 23. She was referred to Dr. Sabin at Precision Orthopedics for evaluation of her
hip and low back pain. Id. at 24.
On December 4, 2015, Petitioner presented to Precision Orthopedics complaining of six
months of lower back pain, intermittent left hip pain, and numbness/tingling. Ex 8 at 1. She also
reported hearing loss, arrythmia, asthma, constipation, and anemia. Id. Dr. Sabin found no palpable
trigger points. Id. at 2. An x-ray of Petitioner’s left hip appeared normal with no evidence of
impingement or degeneration. Id. Dr. Sabin’s overall impression was “questionable hip
impingement, left side.” Id. at 5.
Petitioner returned to Arvada Sport and Spine Clinic on December 16, 2015 reporting
improvement in her left hip and groin pain since her previous visit. Ex. 11 at 26. Petitioner rated
her pain as 1/10. Id. She reported that she tested positive for hip joint dysfunction. Id. Her therapist
noted that she “appeared anxious.” Id.
On December 31, 2015, Petitioner returned to Arvada Sport and Spine Clinic and reported
improvement in her left hip pain over the past two weeks, possibly due to a new mattress. Ex. 11
at 28. She rated her pain as 1/10, was compliant with her home exercise regime, and noticed less
tingling in her pubic region. Id. Her therapist noted that she “appeared anxious.” Id.
Petitioner saw Dr. Yeash on January 15, 2016 reporting that she had not had a period for
the last few months. Ex. 18 at 10. Dr. Yeash noted that Petitioner had some signs and symptoms
of paroxysmal orthostatic tachycardia syndrome. Id. at 9. He noted that Petitioner was “fairly
anxious and that may be a cause of her palpitations as well.” Id. For the first time, the record states
that Petitioner’s history of palpitations was particularly related to standing. Id. at 10.
8
On January 20, 2016, Petitioner returned to Arvada Sport and Spine Clinic and reported:
“Overall, I've been feeling really good. My exercises have been getting easier and I haven't really
had too many symptoms so I was hoping to go through some new exercises in order to continue
with my strengthening to keep my pain at bay.” Ex. 11 at 30.
Petitioner met with a physician assistant at Dr. Yeash’s office on January 25, 2016 and
reported that she was still having palpitations, and that it was becoming difficult for her to work.
Ex. 18 at 7. Petitioner stated that she would like to see a cardiophysiologist and a neurologist, and
specifically requested a referral to Dr. Jill Schofield at University of Colorado Hospital. Id. The
PA noted that Petitioner remarked “on paper she looks good and physically she may look good,
but she says inside she does not feel good.” Id.
On January 26, 2016, Petitioner presented to Boulder Community Health ER complaining
of “epigastric abdominal pain and early satiety” beginning in November 2015. Ex. 12 at 2.
Petitioner’s husband reported that she began having abdominal pain and digestive issues after
completing a 10-day course of prednisone for a eustachian tube dysfunction in her left ear. Id. All
of her lab work came back normal and an examination revealed a benign abdomen, non-tender to
palpitation. Id. The attending physician referred her to a gastroenterologist. Id. His differential
diagnosis included gastritis, H. pylori, pancreatitis, peptic ulcer disease, celiac disease, and
depression. Id. at 4.
Petitioner saw Dr. Hartemink on February 2, 2016 complaining of dizziness and a
lightheaded “rocking motion.” Ex. 23 at 9. She requested that Dr. Hartemink re-check her for
vertigo. Id. She also reported the following new symptoms: heart palpitations, GI issues, bowel
movement issues, increased heart rate when standing up, increased car sickness, and intermittently
hearing her heartbeat in her left ear, especially when laying down at night. Id. Dr. Hartemink
assessed Petitioner with (1) sensorineural hearing loss, unilateral, and (2) inactive Ménière’s
disease. Id. at 10.
On February 4, 2016, Petitioner saw Dr. Mandagere, an endocrinologist, for concerns about
possible thyroid disease. Ex. 9 at 1. Petitioner reported having palpitations, alternating issues with
diarrhea and constipation, general weight loss, heat and cold intolerance, poor sleep, sore throat,
nausea, nighttime urination, diminished libido, abnormal periods, numbness/tingling and anxiety.
Id. at 2. Dr. Mandagere noted that Petitioner had “nonspecific complaints that are not thyroid
related.” Id. at 3. Petitioner’s TSH level was normal, “not even equivocal,” and Dr. Mandagere did
not find an endocrine cause for her palpitations. Id.
Petitioner visited Dr. Schkade to review her allergy and asthma treatment on February 9,
2016. Ex. 10 at 34. She reported having a rapid heart rate that increased when she stood up,
“although she did not appear to have any hypotensive symptoms.” Id. She reported that propranolol
caused her dyspnea due to her asthma, “although she had not used her inhaler for exercise induced
apnea in years.” Id. She also reported feeling flushed at times, having loose stools and headaches
associated with her rapid heart rate. Id. She did not want to resume her allergy injections. Id.
On February 10, 2016, Petitioner saw Dr. Moon, a neurologist, for a POTS evaluation. Ex.
15 at 16. Petitioner was concerned about a possible autoimmune disorder and reported that she
9
started having palpitations in September 2015. Id. She reported treatment with steroids for fullness
and hearing loss in her left ear in October 2015. Id. She reported that she then developed
tachycardia upon standing up first thing in the morning, anxiety, panic attacks, lightheadedness,
poor sleep, significant fatigue, indigestion, diarrhea, decreasing sweating, heat and cold
intolerance, low grade headache, nausea, decreased appetite, and phonophobia. Id. She reported
that tachycardia sometimes woke her up at night. Id. Dr. Moon assessed Petitioner with
dysautonomia, migraine headaches and anxiety. Id. Dr. Moon did not see any clear evidence of
POTS but recommended an MRI of the brain, a tilt table test, dysautonomia laboratory studies and
a repeat trial of propranolol. Id.
Petitioner saw a nurse practitioner at Rocky Mountain Gastroenterology on February 15,
2016 where she complained of intermittent stomach burning, heartburn, nausea, gas, constipation
and burping beginning after treatment with prednisone for possible Ménière’s disease. Ex. 6 at 1.
She reported losing ten pounds initially but had regained the weight. Id. She noted tomatoes,
onions, garlic, and fatty foods as triggers. Id. All of her lab work came back normal. Id. The NP
suspected that prednisone caused her some esophagitis, gastritis and possibly duodenitis. Id. at 4.
Petitioner elected conservative treatment with Zantac, Tums, H2 blocker and a restricted diet. Id.
On February 25, 2016, Petitioner underwent a tilt table test at Swedish Medical Center.
Ex. 23 at 19. The contemporaneous notes indicate that Petitioner showed no symptoms of POTS
when tilted 70% for 40 minutes, and no signs of syncope. Id. Her heart rate remained in the low
100s and her blood pressure was stable. Id.
Petitioner underwent an MRI at Touchstone Imaging on March 10, 2016 pursuant to Dr.
Moon’s orders. Ex. 3 at 12. The contemporaneous notes state that the results were normal with the
exception of one indication of a prior microhemorrhage in the right cerebrum. Id.
On March 15, 2016, Petitioner had a follow-up appointment with Dr. Moon regarding
dysautonomia. Ex. 16 at 13. Dr. Moon noted that autonomic laboratory testing and extensive
neuropathy laboratory testing were unremarkable; that the results of Petitioner’s tilt table test were
not conclusive; and that her MRI was normal with the exception of was one small area of possible
microhemorrhage in the right hemisphere. Id. Dr. Moon noted: “At this point we do not have
definitive POTS.” Id. Dr. Moon’s differential diagnosis was dysautonomia, migraine headache and
anxiety. Id. Dr. Moon recommended that Petitioner retry propranolol, explaining that a lower dose
should not interfere with her asthma, and that Petitioner should not expect to see results for
approximately one month. Id. Alternatively, Dr. Moon considered treating Petitioner for migraines
and anxiety, which he noted could either be co-morbidities to her autonomic complaints or the
actual primary problem. Id.
Petitioner saw Dr. Yeash on March 18, 2016 for dizziness, vertigo, poor concentration,
tachycardia when standing up, extreme fatigue, and weakness. Ex. 18 at 5. Petitioner requested
paperwork for short term disability. Id. Dr. Yeash’s notes state that Dr. Moon had diagnosed
Petitioner with dysautonomia and POTS. Id.
On April 12, 2016, Petitioner saw Dr. Foster, an ENT, at University of Colorado Hospital.
Dr. Foster noted that Petitioner had a history of low-grade dizziness with hearing loss, low pitched
10
tinnitus but no true vertigo, and premenstrual migraines. Ex. 24 at 20. Upon examination, Dr.
Foster did not find any abnormalities. Id. at 21. Dr. Foster’s diagnosis was probable progressive
vestibulopathy affecting the left inner ear. Id. Dr. Foster noted that the Petitioner’s migraines might
be associated with Ménière’s disease, and that her low frequency sensory neuro hearing loss
suggested hydrops5 but that recurrent spells were required to confirm. Id. She noted that
Petitioner’s dizzy spells were premenstrual and advised Petitioner to avoid migraine triggers. Id.
Petitioner saw Dr. Moon on April 13, 2016 and reported that she was feeling better;
however, she stopped taking the propranolol because it gave her nightmares. Ex. 16 at 12.
Petitioner indicated that she was taking riboflavin and magnesium and had found an exercise
regimen that seemed to help, but she was still having anxiety. Id. Dr. Moon assessed Petitioner
with dysautonomia and migraine headache. Id. In Dr. Moon’s opinion, the exercise regime would
improve Petitioner’s dysautonomia as well as her vertigo. Dr. Moon noted that Petitioner had
endolymphatic disease which can cause vertiginous dizziness separate from her dysautonomia
issues. Id.
On May 6, 2016, Dr. Yeash provided Petitioner with the results of blood work ordered on
March 24, 2016. Ex. 18 at 32. The results were normal, but Dr. Yeash recommended that Petitioner
continue taking an iron supplement. Id.
On May 13, 2016, Petitioner saw Dr. Yeash to obtain paperwork necessary for her to return
to work. Ex. 18 at 1. Dr. Yeash reported that Petitioner had no significant physical restrictions
other than those related with her balance issues due to Ménière’s and vestibular issues. Id. Dr.
Yeash noted that Petitioner’s POTS, Ménière’s, migraines and vertigo were all stable, and that she
was no longer taking Xanax for anxiety. Id.
Petitioner saw Dr. Schofield, on June 8, 2016. Dr. Schofield noted that Petitioner was
previously healthy with underlying joint hypermobility until an acute onset of quite severe postural
tachycardia syndrome, hearing loss and tinnitus one week following influenza vaccination. Ex. 24
at 35. Dr. Schofield indicated that “her clinical picture is very suspicious for an immune mediated
etiology possibly molecular mimicry secondary to influenza vaccination.” Id. Dr. Schofield’s
diagnosis included antiphospholipid syndrome (“APS”) with hearing loss, tinnitus and migraines.
Her differential diagnosis included celiac disease and autoimmune Ménière’s. Id. at 35. She noted
that Petitioner had joint hypermobility but no chronic joint pain or spontaneous joint dislocation
to suggest Ehlers-Danlos syndrome and thus did not refer Petitioner to a geneticist. Id.
On June 11, 2016, Petitioner visited Dr. Schkade to review her allergy treatment. Ex. 10 at
37. Petitioner did not want to continue her allergy shots. Id.
5
Ménière’s disease is a defined as hearing loss, tinnitus, and vertigo resulting from nonsuppurative disease
of the labyrinth with edema. It may also be referred to as endolymphatic hydrops, labyrinthine hydrops, and
recurrent aural vertigo. Dorland's, https://www.dorlandsonline.com/dorland/definition?id=70588 (last
visited April 19, 2021).
11
Petitioner presented to Westside Women's Clinic on July 28, 2016 complaining of
incapacitating menstrual migraines and vestibular migraines. Ex. 52 at 7. The doctor noted that her
symptoms were likely due to a sudden drop in her estrogen level. Id. Petitioner was prescribed
Prometrium for her menstrual symptoms. Id.
On September 12, 2016, Petitioner presented at Westside Women's Clinic reporting that
she noticed an improvement in her PMDD and PMS on the Prometrium. Ex 52. at 7.
Petitioner saw Dr. Yeash on September 16, 2016. He assessed Petitioner with (1) POTS,
(2) dysautonomia, (3) migraine with vertigo (4) Vitamin D deficiency, and (5) Vitamin B12
deficiency. Ex. 54 at 23. Dr. Yeash directed Petitioner to continue taking metoprolol and
prescribed 5mg Adderall to help with the neurovascular instability of POTS as well as 5mg Maxalt
for headache. Id. Petitioner reported that she was generally feeling a lot better and was able to
return to work. Id.
On October 14, 2016, Petitioner again saw Dr. Schofield. She complained of fatigue and
lack of focus. Ex. 28 at 4. Dr. Schofield recorded Petitioner as having a disorder of the autonomic
nervous system, unspecified. Id. at 3. Dr. Schofield noted that Petitioner was working full time,
and “possibly this is making her worse, but not nearly as severe as last year when she was trying.”
Id. Petitioner was using an exercise bike at home but was still experiencing migraines once a month
and oscillopsia6 when moving, but no dizziness or vertigo. Id. She tried taking aspirin but it did
not help and caused bruising and nosebleeds. Id. Dr. Schofield prescribed a daily Vitamin D
supplement and 10mg Vyvanse7 daily and suggested that Petitioner cut back from 40 hours per
week to 30. Id. Petitioner declined. Id. Dr. Schofield recommended repeat APS testing. Id.
Petitioner presented at Westside Women's Clinic on October 20, 2016 reporting that her
lab work for APS was negative, but that she was working on controlling her symptoms of
dysautonomia. Ex. 52 at 7.
On March 16, 2017, Petitioner saw Dr. Schkade reporting that when she eats eggs for
several days in a row it seems to cause some vestibular symptoms. Ex. 51 at 12.
On April 10, 2017, Petitioner presented to Westside Women's Clinic indicting that she
wanted to stop her Promethium because her specialist thought she had Ehlers-Danlos syndrome or
possibly Ménière’s disease. Ex 52 at 5. She reported that an echocardiogram done four years ago
6
Oscillopsia is a symptom in which objects appear to wiggle, jerk, or move back and forth; it sometimes
accompanies nystagmus, especially the downbeat type. Oscillopsia is also called oscillating vision.
Dorland’s, https://www.dorlandsonline.com/dorland/definition?id=35681&searchterm=oscillopsia (last
visited April 19, 2021).
7
Vyvanse is a central nervous system stimulant prescription medicine used to treat Attention-
Deficit/Hyperactivity Disorder (ADHD) and Binge Eating Disorder (BED). RxList - The Internet Drug
Index for Prescription Drugs, Medications, and Pill Identifier (2017), https://www.rxlist.com/vyvanse-
drug.htm (last visited April 19, 2021).
12
was abnormal, that she had extreme laxity in the ligaments in her arms, and severe joint and muscle
pain. Id. Petitioner reported that Prometrium made her symptoms worse. Id.
On May 31, 2018, Petitioner saw Dr. Yeash for a medication evaluation. Ex. 54 at 14. Dr.
Yeash assessed Petitioner with (1) anxiety (2) acid reflux disease (3) migraine with vertigo (4)
POTS (5) Ehlers-Danlos, hypermobile type (6) neutropenia and (7) iron deficiency anemia. Id. Dr.
Yeash noted Ménière’s disease had been ruled out. Petitioner felt that her vertigo was related to
her migraines. Id. Dr. Yeash remarked that Petitioner was managing her POTS very well. Id.
On July 19, 2018, Petitioner saw Dr. Yeah for a medication check. Ex. 54 at 11. Dr. Yeash
assessed Petitioner with (1) dysautonomia (2) Ehlers-Danlos, hypermobile type (3) concentration
deficit (4) acid reflux disease (5) decreased white blood cell count and (6) migraine with vertigo.
Id. Dr. Yeah prescribed 10mg Vyvanse for concentration deficit related to dysautonomia and
Ehlers-Danos syndrome. Petitioner tried Adderall and Concerta but reported that they were either
ineffective or caused side effects. Id.
Petitioner presented to Westside Women's Clinic on July 26, 2017 reporting that her
physician thought she had a variant of Ehlers-Danlos syndrome, not involving the cardiovascular
system, but causing laxity in her joints and ligaments. Ex. 52. at 6. She reported having no libido
but reported that Promethium was helping with her PMDD as well as her dysautonomia. Id.
Petitioner presented to Westside Women's Clinic for her annual visit on August 14, 2018.
Ex. 52 at 1. Her only complaint was having no libido. Id. Her periods were normal. She was taking
Vyvanse and a multivitamin and exercising on a regular basis. Id. She reported that she had been
diagnosed with Ménière’s disease, but that she was not having many symptoms at that time. Id.
On October 15, 2018, Petitioner saw Dr. Yeash for a medication check. Ex. 54 at 8. Dr.
Yeash assessed Petitioner with (1) concentration deficit (2) muscle contraction headache (3)
cervicogenic headache and (4) decreased white blood cell count. Id. Dr. Yeash noted that
Petitioner’s muscle contraction headaches were thought to be secondary to cervicogenic disc
disease. Id.
On April 15, 2019, Petitioner saw Dr. Yeash for a medication check. Ex. 54 at 4. Dr. Yeash
assessed Petitioner with (1) fatigue (2) concentration deficit (3) neutropenia (4) iron deficiency
anemia (5) subclinical hypothyroidism and (6) daytime somnolence. Id. Petitioner complained of
nonrestorative sleep, morning dry mouth, and excessive daytime somnolence. Id. Dr. Yeash
recommended that Petitioner be evaluated for sleep apnea. Id.
III. Petitioner’s Affidavit
Petitioner signed her affidavit on October 2, 2016. Ex. 1 at 4. In the affidavit, she stated
that she received her flu vaccine on September 25, 2015 and the following week, she began to
experience “a strange sensation” in her left ear. Id. at 1. She noted that the sensation was distinct
from the tinnitus she had previously experienced, in that she felt “a low hum, vibrating noise in
[her] left ear that would not go away.” Id.
13
Petitioner went on a trip to Taos soon thereafter, and during this trip, her feeling of fullness
in her left ear and tinnitus continued to worsen. Ex. 1 at 1. She also felt that her heart was beating
in an erratic manner and that it was racing. Id. at 2. She noted, “I had been diagnosed with PACs,
or extra heartbeats, years before, but this sensation felt very different and I was worried.” Id.
On October 19, 2015, Petitioner experienced hearing loss in her left ear and was diagnosed
with possible Meniere’s disease. Ex. 1 at 2. She was prescribed steroids and her hearing recovered.
Id.
In early November 2015, Petitioner began to notice that her heart was racing with a change
in position. Ex. 1 at 2. She indicated that her various symptoms impacted her work. Id. at 3.
Petitioner stated that she was able to work “sporadically through November and December of 2015
due to taking many vacation days, holidays, and a low number of clients.” Id. She further indicated
that her symptoms continued to worsen into January 2016. Id. On January 25, 2016, Petitioner
stated that she was forced to take a leave of absence from her job. Id.
Petitioner indicated that she experienced the following symptoms at the worst of her illness:
Orthostatic Tachycardia, palpitations or pounding heart, cold hands and feet,
inability to regulate body temperature, sweating irregularities, constipation,
diarrhea, loose stool, severe GERD, nausea, unexplained weight loss, nervousness,
anxiety, depression, flushing, heat intolerance, increased blood pressure, hair loss,
dry skin, adrenaline rushes, hearing loss, tinnitus, dizziness, motion intolerance,
extreme motion sickness, hyperacusis, brain fog/cognitive struggles, blurred vision,
tingling in my legs, feet, and face, exercise intolerance, fatigue, insomnia, and
reduced stress tolerance.
Ex. 1 at 3. Petitioner further stated that since the worst of her illness, she has seen some
improvement, but she continues to experience daily symptoms and to have flares. Id. at 3-4.
IV. Expert Opinions and Qualifications
A. Expert Qualifications
1. Dr. Schofield’s Qualifications
Dr Schofield graduated from the University of Colorado School of Medicine with Honors
in 1995 and completed her internship and residency in internal medicine at the Johns Hopkins
Hospital in Baltimore from 1995 to 1998. Ex. 31 at 2 (hereinafter “Schofield CV”). She worked
for 16 years as an attending physician at St. Joseph Hospital in Denver where she developed an
interest in autoimmune disease, specifically autonomic disorders in the antiphospholipid
syndrome. Schofield CV at 1. As there is currently no formally accredited fellowship training in
multi-specialty autoimmune disease, she designed a curriculum and completed training with
Professor Yehuda Shoenfeld at the University of Colorado from January 2015 to July 2016. Ex 30
at 1. She researches, publishes, and presents on the topics of autoimmune disease and
14
antiphospholipid syndrome. Schofield CV at 2-3. Of note, in 2014 she co-authored an article with
Professor Shoenfeld, and Dr. Graham Hughes entitled Postural tachycardia syndrome (POTS) and
other autonomic disorders in antiphospholipid (Hughes) syndrome (APS). 2014 LUPUS 23, 697-
702 (2014). Id. at 2. Dr. Schofield maintains a clinical practice in antiphospholipid syndrome
(“APS”) and the emerging area of autoimmune dysautonomia at the IMMUNOe Health and
Research Center in Denver, Colorado. Id. at 1. She is also a Clinical Assistant Professor of
Autoimmune Disease at the University of Colorado in the Department of Medicine. Id.
2. Dr. Leist’s Qualifications
Thomas P. Leist, MD, PhD, is Professor of Neurology, Chief of the Division of Clinical
Neuroimmunology, and Director of the Comprehensive Multiple Sclerosis Center at Jefferson
University in Philadelphia, PA. Ex. A, Tab 2 at 1 (hereinafter “Leist CV”). Dr. Leist also directs
the Jefferson Medical College fellowship program in clinical neuroimmunology. Leist CV at 2.
He earned a PhD from the University of Zurich in Switzerland and received his medical degree
from the University of Miami School of Medicine. Id. at 1. Dr Leist completed his residency at
Cornell Medical Center and Memorial Sloan-Kettering Medical Center in New York, and he
trained as a fellow at the National Institutes of Health in Bethesda, MD. Id. He conducts research
in multiple sclerosis and other autoimmune and infectious conditions of the CNS. He serves on the
editorial board for Practical Neurology and is an ad-hoc reviewer for several journals
including Neurology, Annals of Neurology, and Journal of Neuroimmunology. Id. He has been
published in a multitude of peer-reviewed publications and frequently presents on the topics of
multiple sclerosis and other autoimmune and infectious conditions of the CNS. Id. at 2-5, 6-11.
B. Expert Opinions
1. Dr. Schofield’s First Report
Dr. Schofield opined that Petitioner’s flu vaccination in September 2015 triggered an
autoimmune response that caused Petitioner to develop symptoms associated with an autoimmune
clotting disorder known as antiphospholipid syndrome (APS). See generally, First Schofield Rep.
According to Dr. Schofield, all of Petitioner’s clinical manifestations have been associated with
APS, and “[t]he clear temporal association of her illness with the influenza vaccination and the
time course of her antibody production and decrease in C4 level make it very likely that her illness
arose as a complication of the vaccination.” Id. at 8.
Dr. Schofield reported that prior to 2015, Petitioner “had enjoyed good health her whole
life;” but that dramatically changed when she received her flu vaccination. First Schofield Rep. at
3. Dr. Schofield’s review of Petitioner’s medical records revealed that one week after her
vaccination, Petitioner began to experience tinnitus and hearing loss in her left ear which was
diagnosed in late October 2015 as suspected Ménière’s disease. Id. In April of 2106, Dr. Schofield
noted that another ENT diagnosed Petitioner with possible Ménière’s disease as well as
progressive vestibular disorder. Id.
Dr. Schofield observed that Petitioner developed a number of other systemic symptoms “at
the same time” including vestibular migraines, cognitive dysfunction, tachycardia, heart rate
15
lability, adrenaline surges at night, insomnia, severe fatigue, flushing, heat intolerance, difficulty
regulating her temperature, polyuria, nausea, paresthesia in her legs, orthostatic tachycardia and
POTS. First Schofield Rep. at 3-4. Dr. Schofield noted that symptoms of dysautonomia such as
migraine headaches, cognitive issues, sensorineural hearing loss and Ménière’s disease “may all
occur in association with APS.” Id. at 5.
Upon examination, Dr. Schofield discovered that Petitioner had other symptoms related to
APS including reduced tear production, Livedo reticularis, joint hypermobility, abdominal bruit,
and POTS. First Schofield Rep. at 5. Dr. Schofield referred to four articles, one of which she
authored herself and another which she co-authored, in support of the theory that many of
Petitioner’s symptoms are common in patients with APS. See Schofield, et al., Postural
tachycardia syndrome (POTS) and other autonomic disorders in antiphospholipid (Hughes)
syndrome (APS), 23 LUPUS 7, 697-702 (2014) (filed as Ex. 45, Ref. No 14) (hereinafter “Schofield-
1); JR Schofield, Autonomic neuropathy—in its many guises—as the initial manifestation of the
antiphospholipid syndrome, IMMUNOL RES. (2017) (filed as Ex. 46, Ref. No. 15) (hereinafter
“Schofield-2”); DA Mouadeb & MJ Ruckenstein, Antiphospholipid inner ear syndrome, 115
LARYNGOSCOPE 5, 879-83 (2005) (filed as Ex. 47, Ref. No. 16) (hereinafter “Mouadeb &
Ruckenstein”); GRV Hughes, Heparin, antiphospholipid antibodies and the brain, 21 LUPUS 10,
1039-40 (2012).
When Dr. Schofield first evaluated Petitioner in June of 2016, she noticed “a clear temporal
relationship to the onset of her symptoms and the influenza vaccine she received.” First Schofield
Rep. at 4. Suspicious of an immune-mediated mechanism triggered by the vaccination, Dr.
Schofield ran a number of tests to determine the cause of Petitioner’s POTS. Id. Initially, she found
Petitioner to be “indeterminate or low positive at 18 MPL” for anticardiolipin IgM antibody, one
of the antibodies associated with APS. Id. However, repeated testing came back negative. Id. at 6.
Dr. Schofield observed that APS is also associated with a low C4 level and testing revealed
that Petitioner had a low C4 level on three serial occasions, “suggestive of either active
autoimmunity or a genetic predisposition to autoimmunity.” First Schofield Rep. at 6. By January
of 2017, Petitioner’s C4 level had normalized, indicating that her autoimmunity was transient as
opposed to genetic. Id. at 6-7. Dr. Schofield referred to several articles suggesting that “transient
production of anticardiolipin antibodies and clinical manifestations of APS (including stroke) as
occurred in [Petitioner’s] case has [sic] been reported in more than one publication.” Id. at 8; see
also, Perdan-Pirkmajer, et al., Autoimmune response following influenza vaccination in patients
with autoimmune inflammatory rheumatic disease, 21 LUPUS 2, 175-83 (2012) (filed as Ex. 34,
Ref No. 3) (hereinafter “Perdan-Pirkmajer”); Agmon-Levin, et al., Influenza vaccine and
autoimmunity, 11 ISR MED ASSOC J. 3, 183-5 (2009);11(3):183-85 (filed as Ex. 41, Ref. No. 10)
(hereinafter “Agmon-Levin”); Toplak, et al., Autoimmune response following annual influenza
vaccination in 92 apparently healthy adults, 8 AUTOIMMUN Rev. 2 134-38 (2008) (filed as Ex. 42,
Ref. No. 11) (hereinafter “Toplak”).
Dr. Schofield claimed that “it is well recognized that APS may be triggered by vaccination
and infection.” Id. at 4. In support of that statement, Dr. Schofield referred to the Cruz-Tapias
article, but offered no explanation or discussion of that article’s findings. See Cruz-Tapias, et al.,
Infections and vaccines in the etiology of antiphospholipid syndrome, 24 CURR OPIN RHEUMATOL
16
4, 389-93 (2012) (filed as Ex. 49, Ref. No. 18) (hereinafter “Cruz-Tapias”). Dr. Schofield stated
that the “most widely recognized mechanism by which infections or vaccines may trigger
autoimmunity is that of molecular mimicry;” she further stated that there are “surprisingly few
examples by which molecular mimicry has been demonstrated and the reality is that infection or
vaccination-induced autoimmunity is likely much more complex in most instances.” Id. at 9. Dr.
Schofield suggested other proposed mechanisms by which a vaccine may trigger autoimmunity
such as cell damage that causes an infection, revealing antigens to the immune system that were
previously hidden, as well as alteration of a host antigen such that it becomes recognized as foreign.
Id. at 10.
In summary, Dr. Schofield reported that “everything about [Petitioner’s] case is consistent
with transient antiphospholipid antibody production and resultant complement activation
secondary to the influenza vaccination, including the close temporal relationship of her symptom
onset to the vaccination, the nature of her symptoms and the documented autonomic, hearing and
vestibular dysfunction.” Id. at 10.
2. Dr. Leist’s First Report
Dr. Leist’s first report challenged Dr. Schofield’s finding of a close temporal relationship
between Petitioner’s flu vaccination and the onset of her symptoms; Dr. Schofield’s statement that
Petitioner was officially diagnosed with POTS in February 2016; and Dr. Schofield’s contention
that a borderline positive anticardiolipin IgM titer is indicative of APS. Id. at 11-12.
Dr. Leist did not find any notations in Petitioner’s medical records of any immediate or
delayed side effects in the hours and days following her flu vaccination. First Leist Rep. at 11. Dr.
Leist remarked that Petitioner had a long history of palpitations, eustachian tube dysfunctions,
tinnitus, intermittent pressure/fullness in her left ear, asthma, significant premenstrual symptoms
and irregularities, as well as an even longer history of back pain, hip pain, and joint hypermobility
for which she sought care prior to and after the administration of her influenza vaccine on
September 25, 2015. Id. at 14-15.
Dr. Leist went on to observe that the contemporaneous records were not consistent with
Dr. Schofield’s claim that Petitioner was “eventually officially diagnosed with POTS in February,
2016 by tilt table testing done at Swedish Medical Center in Denver.” First Leist Rep. at 14. To
the contrary, Dr. Leist noted that after receiving the results of Petitioner’s tilt table test, Dr. Moon
specifically recorded: “At this point we don’t have definitive POTS.” Id.
Using the National Institutes of Health’s diagnostic criteria, Dr. Leist also found that the
results of Petitioner’s tilt table test did not warrant a diagnosis of POTS. First Leist Rep. at 13. To
diagnose a patient with POTS, the National Institutes of Health requires “lightheadedness or
fainting accompanied by a rapid increase in heartbeat of more than 30 beats per minute, or a heart
rate that exceeds 120 beats per minute, within 10 minutes of rising.” Id. Prior to the start of the tilt
test, [Petitioner]’s heart rate was measured while she was laying down, sitting, and standing. Id.
Her heart rate did not increase by 30 beats per minute” Id. Dr. Leist observed that Petitioner
remained asymptomatic during her test. Id at 14. “There was no significant change of the heart rate
17
between the start of the tilt table test (13:35, test minute 0; heart rate 102) and the subsequent time
points (e.g., 13:45; test minute 10; heart rate 94). Id.
Dr. Leist noted that Petitioner had twice undergone Holter monitor testing for palpitations
that she reported as occurring at night, when sitting still, and during the week prior to and during
her period. First Leist Rep. at 12. In 2013, after wearing a Holter monitor for 30 days, Petitioner’s
cardiologist did not find any correlation with the seven events recorded by the monitor and
Petitioner’s subjective feelings of “fluttering in the chest”. Id. In November 2015, after wearing a
Holter monitor for 14 days, the results revealed that Petitioner’s baseline heart rate was 54 to 67
bpm and that she remained in sinus rhythm throughout the monitoring period. Id. at 13. The Holter
monitor test results, according to Dr. Leist, are further evidence that Petitioner did not fulfill the
diagnostic criteria for POTS. Id.
Finally, Dr. Leist took issue with Dr. Schofield’s reliance on the presence of
antiphospholipid antibodies in support of the claim that vaccines can induce antiphospholipid
syndrome, “which appears to be central to Dr. Schofield’s theory of how influenza vaccine could
have caused [L.P.’s] condition.” First Leist Rep. at 14. Dr. Leist observed that Petitioner’s first
test for anticardiolipin IgM on June 8, 2016, was negative. Id. at 11. (Exhibit 24 at 66). The second
test on September 28, 2016, was also negative, and on October 14, 2016, a third test (performed
on a specimen obtained in June 2016) came back borderline positive. Id. Dr. Leist pointed out that
a borderline positive anticardiolipin IgM titer, by itself, is not clinically significant or indicative of
APS. Id. at 12. Moreover, Petitioner’s anticardiolipin IgM titer “could have been elevated for many
reasons other than, as alleged by Dr. Schofield, influenza vaccine given 9 months earlier.” Id. at
11-12.
Upon reviewing Dr Schofield’s medical literature, Dr. Leist found little to no relevant
evidence supporting her opinions. For example, many of Dr. Schofield’s cited articles merely
provided evidence of a temporal association between flu vaccination and other unrelated diseases
such as various demyelinating disorders of the central nervous system, giant cell arteritis,
autoimmune inflammatory rheumatic disease, polymyalgia rheumatica, subacute thyroiditis and
dyserythropoiesis, Chug-Strauss syndrome, narcolepsy, and Guillain-Barré syndrome. Id. at 7; see
also Exs. 32-38, 40, 44. Dr. Leist noted that the Jeffs article concerned variants of a flu vaccine
other than Afluria, the vaccine that Petitioner received. Id. at 8; see also Jeffs, et al., Viral RNA in
the influenza vaccine may have contributed to the development of ANCA-associated vasculitis in
a patient following immunization, 35 CLIN RHEUMATOL 4, 943-51 (2016) (filed as Ex. 39, Ref No.
8). Dr. Leist noted that the Agmon-Levin article discussed an increase in antinuclear
antibodies and antiphospholipid antibodies in 92 healthy individuals up to six months after
influenza vaccination; however, there is no evidence that Petitioner had antinuclear antibodies or
antiphospholipid antibodies above the normal limit. Id. at 8; see also Ex. 41. The Toplak article
also discussed an increase in antinuclear antibodies and antiphospholipid antibodies in 92 healthy
individuals; however, Dr. Leist observed that none of the individuals studied was “reported to have
developed clinical symptoms and the authors did not study fluctuation of the antibody markers
over time in unvaccinated controls.” Id. at 8, quoting Ex. 42. The Abu-Shakra article found that
influenza vaccination was safe for patients with lupus; although it may trigger the generation of
autoantibodies, the effect was usually short lived and not associated with clinical significance. Id.
at 8, see also Abu-Shakra, et al., Influenza vaccination of patients with systemic lupus
18
erythematosus: safety and immunogenicity issues, 6 AUTOIMMUN REV. 8, 543-46 (2007) (filed as
Ex. 43, Ref No. 12). The Schofield-1, Schofield-2, and Mouadeb & Ruckenstein articles relating
APS with other disorders such as POTS and Ménière’s did not include any mention of the flu
vaccine. Id. at 8; see also Exs. 45, 46, 47, 48.
Having reviewed Petitioner’s medical records, Dr. Leist opined “that Petitioner did not
incur an injury due to influenza vaccine she received on September 25, 2015.” First Leist Rep. at
15.
3. Dr. Schofield’s Supplemental Report
In response to Dr. Leist’s report, Dr. Schofield argued that Dr. Leist was not qualified to
assess whether Petitioner has POTS or APS. Dr. Schofield’s review of Petitioner’s pre-vaccination
medical history indicated that Petitioner may have been predisposed to autoimmunity, and Dr.
Schofield refuted Dr. Leist’s argument that a low positive anticardiolipin IgM level is clinically
insignificant.
Dr. Schofield noted that while Dr. Leist may have great expertise in multiple sclerosis, he
has no documented experience with autonomic disorders, APS, and vaccine induced immunity.
Second Schofield Rep. at 1. In Dr. Schofield’s personal experience, physicians who specialize in
multiple sclerosis have limited knowledge of the emerging field of dysautonomia “for which there
is not currently a formal training program.” Id. Furthermore, Dr. Schofield stated that Dr. Leist’s
first report demonstrates that he has limited knowledge of the diagnostic criteria for POTS and
does not know how to interpret a tilt table test. Id.
With respect to Petitioner’s tilt table test, Dr. Leist referred to the National Institutes of
Health’s current diagnostic criteria for POTS; however, Dr. Schofield reported that “most
specialists in the field use the 2015 Heath Rhythm Society Expert Consensus Statement on the
Diagnosis and Treatment of POTS.” Second Schofield Rep. at 1; see also Sheldon, et al., 2015
Heart Rhythm Society Expert and Consensus Statement on the Diagnosis and Treatment of
Postural Tachycardia Syndrome, Inappropriate Sinus Tachycardia, and Vasovagal Syncope, 12
HEART RHYTHM 6, 41-63 (2015) (filed as Ex. 57) (hereinafter “Consensus Statement”). The
Consensus Statement, in part, characterizes POTS as “an increase in heart rate of >30 beats per
minute (bpm) when moving from a recumbent to a standing position.” Id. Dr. Schofield’s review
of the record revealed that Petitioner’s heart rate when laying and sitting at 1300 and 1302,
respectively, was 68 bpm. Id. at 2. When she was titled upright at 1305, her hear rate quickly rose
to 94 bpm and by the end of the test was 101, 107, 108 and 111 at the last four time points. Id. at
2. “Thus, her HR rose from 68 to 111 – a 43 point increase” which Dr. Schofield claimed easily
meets the criteria for POTS. Id. Regardless, Petitioner’s inability to “do her job, drive, etc. with a
constellation of symptoms typical of that seen in POTS and lasting more than 3-6 months . . . is
what makes the unequivocal diagnosis of POTS in the context of her abnormal tilt table test” Id.
at 2.
With respect to Petitioner’s pre-vaccination medical history, Dr. Schofield admitted that
she did not originally review Petitioner’s prior records because Petitioner reported to Dr. Schofield
“that she ‘was completely healthy’, i.e., any prior medical history did not seem significant enough
to her to warrant spending time on it.” Second Schofield Rep. at 2. Nevertheless, having reviewed
19
Dr. Leist’s summary of the pre-vaccination medical records, Dr. Schofield did not find them to be
inconsistent with the opinions set forth in her first report. Id. According to Dr. Schofield,
Petitioner’s history indicates that she likely had mild underlying mast cell activation syndrome
(MCAS),8 which is characterized by symptoms occurring in “two or more organ systems that are
of a generally allergic and/or inflammatory theme.” Id. Dr. Schofield claimed that Petitioner’s
problems with “allergies, asthma, anxiety, flushing, hives, rashes and palpitations are very
characteristic of MCAS.” Id.
Dr. Schofield performed further testing on Petitioner, and although Petitioner tested
negative for MCAS, Dr. Schofield’s “clinical suspicion for this diagnosis remains high.” Id. at 3.
Dr. Schofield explained that diagnosis can be difficult given that it “requires capturing chemical
mediators that are released from overactive mast cells and these mediators begin to break down at
room temperature within 1-2 minutes.” Id. at 3.
Dr. Schofield went on to propose that “the presence of MCAS (suspected as the cause for
the milder issues in [Petitioner]’s background), a disorder of the primitive immune system, may
predispose to autoimmunity as the primitive and acquired arms of the immune system interact
significantly.” Second Schofield Rep. at 6. Dr. Schofield reported that MCAS is often a
comorbidity of dysautonomia, and that many of Dr. Schofield’s patients have both MCAS and
autoimmunity. Id. at 2-3. Also, in Dr. Schofield’s experience, “many patients who develop severe
autoimmune dysautonomia have much milder underlying symptoms suggesting orthostatic
intolerance and/or immune dysregulations just as [Petitioner]’s history suggests.” Id. Those
symptoms do not become severe until they are triggered by an event that activates the immune
system, for example, a vaccination. Id. at 3. It is Dr. Schofield’s opinion that Petitioner likely had
MCAS which predisposed her to developing an autoimmune disorder that was triggered by her flu
vaccination given that “one week following her vaccination her symptoms became so severe that
she struggled to function.” Id. at 3.
Dr. Schofield stressed that even low positive/indeterminate anticardiolipin IgM levels can
be significant, and “must be interpreted in the context of the patient’s clinical phenotype to
determine whether they are important.” Id. at 3-4. A patient with a high titer but no signs or
symptoms would only require observation; however, in a patient like Petitioner, with reported
8
Dr. Schofield raised the potential diagnosis of MCAS in her second report. Respondent filed the Akin
article, which delineates the proposed criteria for mast cell activation syndrome: 1. Episodic multisystem
symptoms consistent with mast cell activation; 2. Appropriate response to medications targeting mast cell
activation; and 3. Documented increase in validated markers of mast cell activation systemically (i.e., either
in serum or urine) during a symptomatic period compared with the patient’s baseline values. Akin C., Mast
cell activation syndromes, 140 J ALLERGY CLIN IMMUNOL 2, 349-55 (2017) (filed as Ex. B, Tab
1) (hereinafter “Akin”). Dr. Schofield conceded that Petitioner’s “first round of testing was negative” for
MCAS. Second Schofield Rep. at 2. Dr. Schofield additionally described the interplay between MCAS and
vaccination as follows: “MCAS--a disorder of the innate immune system--may theoretically predispose
patients to a vaccine injury. As an emerging syndrome, there has not yet been a lot of research on many
aspects of MCAS, so this remains a hypothesis…” Id. at 3. Dr. Leist did not find any support in Petitioner’s
medical records for a diagnosis of MCAS. Ultimately, I find that Petitioner did not present preponderant
evidence that she had MCAS and further that her purported underlying MCAS predisposed her to a vaccine
injury.
20
autonomic and vestibular dysfunctions, even a low level of antiphospholipid antibodies becomes
relevant, especially considering that Petitioner’s symptoms improved with antiphospholipid
seroconversion. Id. at 4. The temporal relationship between the presence of those antibodies to
Petitioner’s flu vaccination suggests that they were triggered by the vaccination. Id.
Dr. Schofield stated that Petitioner’s clinical manifestation of Ménière’s disease was
further evidence of the clinical significance of her anticardiolipin IgM levels. Second Schofield
Rep. at 5. Dr. Schofield discussed the Mouadeb & Ruckenstein article which studied 168 adult
patients suffering from progressive hearing loss with or without vertigo. Id. at 5; see also Mouadeb
& Ruckenstein. The authors reported that “[f]orty-two patients (25%) had at least one elevated
antiphospholipid antibody marker. . . [and of] the 42 patients, 64% (n = 27) met the diagnostic
criteria for Ménière's disease.” Id. at 5, quoting Mouadeb & Ruckenstein. The authors of the study
concluded that the “data support the hypothesis that antiphospholipid antibodies are involved in
the pathogenesis of some forms of inner ear dysfunction . . .” Id. Dr. Schofield reports that “while
we have a lot to learn about the mechanisms by which both inner ear disease and autonomic
dysfunction may occur in the context of APS, the most likely mechanism is sludging or
microthrombosis of the smallest blood vessels including those that perfuse the tiny small fiber
autonomic nerves and the inner ear.” Id. at 7.
With respect to Dr. Leist’s criticisms of her medical literature, Dr. Schofield responded
that the purpose of the literature she cited “was to illustrate that multiple different autoimmune
disorders--both neurological and non-neurological--may arise in the post vaccination period and
were presumed to be triggered by the vaccination in those cases.” Id. at 6. According to Dr.
Schofield, the literature evidences that most experts in the field use a period of 30 days to define
temporal association. Id.
In summary, Dr. Schofield opined as follows: “Based on the clear temporal relationship of
the severe decline in [Petitioner]’s health to the influenza vaccination given in September 2015,
the transient positivity of both antiphospholipid antibodies and the low C4 level (both seen in
antiphospholipid syndrome) as well as the presence of clinical manifestations of antiphospholipid
syndrome (autonomic dysfunction and inner ear disease), I believe that this represents a vaccine
injury.” Second Schofield Rep. at 7.
4. Dr. Leist’s Supplemental Report
In his second report, Dr. Leist challenged Dr. Schofield’s opinions on the grounds that Dr.
Schofield failed to demonstrate that Petitioner has POTS; failed to demonstrate that Petitioner has
MCAS; failed to demonstrate that Petitioner has APS; and failed to establish that there is any
mechanistic link between the influenza vaccine and sensorineural hearing loss.
First, Dr. Leist refuted Dr. Schofield’s interpretation of Petitioner’s tilt table test. Second
Leist Rep. at 3. Dr. Leist stated that the contemporaneous medical records do not support Dr.
Schofield’s findings, and he agreed with the contemporaneous assessment. Id. Dr. Leist suggested
that Dr. Schofield incorrectly combined Petitioner’s heart rate readings taken prior to the tilt table
test with her heat rate readings taken after the tilt test had begun. Id. Dr. Leist noted that prior to
the start of the tilt test, between 13:00 and 13:05, Petitioner’s heart rate was measured while laying
21
down, sitting and standing. Id. In Dr. Leist’s interpretation of the record, Petitioner’s heart rate
increased from 68bpm to 94bpm from lying down to standing up – a change of 26bpm – which
does not satisfy the criteria set forth in the Consensus Statement, Dr. Schofield’s preferred
diagnostic reference. Id.; see also Ex. 57.
Dr. Leist highlighted that the tilt table test did not start until 13:35, as clearly noted on the
contemporaneous chart used to record Petitioner’s symptoms. Second Leist Rep. at 4. When the
table was in the horizontal position, Petitioner’s heart rate was 102bpm. Id. As the table was raised
to 70 degrees, Petitioner’s heart rate was measured every five minutes for 40 minutes. Id. Dr. Leist
noted that Petitioner’s heart rate fluctuated between 89 and 111; again, not meeting the criterion
set forth in the Consensus Statement. Id. at 3; Ex. 57.
Dr. Leist noted that according to the Consensus Statement, the standing (or orthostatic)
heart rate for individuals with POTS is often 120bpm or higher. Second Leist Rep. at 5; Ex. 57.
Dr. Leist observed that Petitioner’s heart rate never elevated to 120 bpm, either before or during
the tilt table test. Id. Additionally, Dr. Leist reiterated that the results of Petitioner’s Holter monitor
test, obtained approximately 39-59 days after vaccination, were not indicative of POTS. Id. at 4.
The results revealed that Petitioner had an average heart rate of 64 bpm, and that Petitioner’s heart
rate was below 60 bpm 24% of the time and above 100bpm only 2% of the time. Id. According to
Dr. Leist, the Holter monitor results are “also not supportive of a diagnosis of [POTS].” Id. at 5.
Second, Dr. Leist stated that Dr. Schofield provided no discussion of the specific findings
on which she based her diagnosis of Petitioner’s MCAS, and no discussion of how MCAS could
be caused by the influenza vaccine. Second Leist Rep. at 5.
Third, Dr. Leist stated that Dr. Schofield failed to demonstrate that Petitioner has APS. Id.
at 1. He doubted Dr. Schofield’s theory that a borderline positive anticardiolipin level is clinically
relevant based on the fact that she “appears to apply personal discretionary standard when
entertaining diagnosis of anticardiolipin syndrome in [Petitioner]’ case. Id. at 2. He questioned her
personal decision to no longer send samples to the University of Colorado Hospital laboratory for
testing, and her criticisms of the Hospital’s laboratory practices, especially considering that the
University of Colorado Hospital is accredited by all the relevant federal agencies, and is certified
by the Colorado Department of Public Health which has an interest in ensuring the quality of
laboratory testing. Id. at 1-2. It is Dr. Leist’s opinion that, “In absence of positive anticardiolipin
antibodies it is unlikely that [L.P.] suffered from an anticardiolipin antibody related condition.” Id.
at 5. Even assuming that a borderline test result is clinically significant, Dr. Leist noted that that
Dr. Schofield failed to explain how a transient borderline anticardiolipin antibody level would be
related to an influenza vaccination eight months earlier as opposed to some other intervening event.
Id. at 1.
Finally, Dr. Leist stated that Dr. Schofield failed to propose a mechanism by which
“transient low level anticardiolipin antibodies can cause a clot forming, thrombotic condition of
the inner ear.” Id. at 2. “Dr. Schofield neither provides evidence that this actually occurred in
[Petitioner]’s case nor does she provide information that this is actually known to occur as a
consequence of non-live influenza vaccine.” Id. at 2. Dr. Leist discounted Dr. Schofield’s reference
to the Mouadeb & Ruckstein article on the grounds that the “article does not go beyond the
22
description that 42 of a series of 168 patients with sensorineural hearing loss had a least one
antiphospholipid marker.” Id. According to Dr. Leist, the article does not report any association
between sensorineural hearing loss and the influenza vaccine. Id. “It is not known that influenza
vaccine causes induction anticardiolipin antibodies that in turn can cause clinical disease;” thus,
Dr. Leist found Dr. Schofield’s theory to be nothing more than speculation. Id. at 5.
In conclusion, Dr. Leist observed that [Petitioner] had conditions related to her heart, ears,
balance, and lungs before September 25, 2015, and continued to suffer from those conditions after
September 25, 2015. Second Leist Rep. at 5. Dr. Leist reiterated: “It is my opinion that [Petitioner]
did not incur an injury due to [the] influenza vaccine she received on September 25, 2015 whether
listed in the Vaccine Injury Table or not.” Id.
V. Applicable Law
A. Petitioner’s Burden in Vaccine Program Cases
Under the Vaccine Act, when a petitioner suffers an alleged injury that is not listed in the
Vaccine Injury Table, a petitioner may demonstrate that she suffered an “off-Table” injury.
§ 11(c)(1)(C)(ii).
In attempting to establish entitlement to a Vaccine Program award of compensation for a
off-Table claim, a petitioner must satisfy all three of the elements established by the Federal Circuit
in Althen v. Sec’y of Health & Hum. Servs., 418 F.3d 1274 (Fed. Cir. 2005). Althen requires that
petitioner establish by preponderant evidence that the vaccination she received caused her injury
“by providing: (1) a medical theory causally connecting the vaccination and the injury; (2) a logical
sequence of cause and effect showing that the vaccination was the reason for the injury; and (3) a
showing of a proximate temporal relationship between vaccination and injury.” Id. at 1278.
Under the first prong of Althen, petitioners must provide a “reputable medical theory,”
demonstrating that the vaccine received can cause the type of injury alleged. Pafford, 451 F.3d at
1355-56 (citations omitted). To satisfy this prong, a petitioner’s theory must be based on a “sound
and reliable medical or scientific explanation.” Knudsen v. Sec’y of Health & Hum. Servs., 35 F.3d
543, 548 (Fed. Cir. 1994). Proof that the proffered medical theory is reasonable, plausible, or
possible does not satisfy a petitioner’s burden. Boatmon v. Sec’y of Health & Hum. Servs., 941
F.3d 1351, 1359-60 (Fed. Cir. 2019).
Petitioners may satisfy the first Althen prong without resort to medical literature,
epidemiological studies, demonstration of a specific mechanism, or a generally accepted medical
theory. Andreu v. Sec’y of Health & Hum. Servs., 569 F.3d 1367, 1378-79 (Fed. Cir. 2009) (citing
Capizzano, 440 F.3d at 1325-26). However, special masters are “entitled to require some indicia
of reliability to support the assertion of the expert witness.” Boatmon, 941 F.3d at 1360, quoting
Moberly, 592 F.3d at 1324. Special Masters, despite their expertise, are not empowered by statute
to conclusively resolve what are complex scientific and medical questions, and thus scientific
evidence offered to establish Althen prong one is viewed “not through the lens of the laboratorian,
but instead from the vantage point of the Vaccine Act’s preponderant evidence standard.” Id. at
1380. Accordingly, special masters must take care not to increase the burden placed on petitioners
23
in offering a scientific theory linking vaccine to injury. Contreras v. Sec’y of Health & Hum.
Servs., 121 Fed. Cl. 230, 245 (2015), vacated on other grounds, 844 F.3d 1363 (Fed. Cir. 2017);
see also Hock v. Sec’y of Health & Hum. Servs., No. 17-168V, 2020 U.S. Claims LEXIS 2202 at
*52 (Fed. Cl. Spec. Mstr. Sept. 30, 2020).
The second Althen prong requires proof of a logical sequence of cause and effect, usually
supported by facts derived from a petitioner’s medical records. Althen, 418 F.3d at 1278; Andreu,
569 F.3d at 1375-77; Capizzano, 440 F.3d at 1326 (“medical records and medical opinion
testimony are favored in vaccine cases, as treating physicians are likely to be in the best position
to determine whether a ‘logical sequence of cause-and-effect show[s] that the vaccination was the
reason for the injury’”) (quoting Althen, 418 F.3d at 1280). Medical records are generally viewed
as particularly trustworthy evidence, since they are created contemporaneously with the treatment
of the patient. Cucuras v. Sec’y of Health & Hum. Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993).
However, medical records and/or statements of a treating physician’s views do not per se
bind the special master to adopt the conclusions of such an individual, even if they must be
considered and carefully evaluated. Section 13(b)(1) (providing that “[a]ny such diagnosis,
conclusion, judgment, test result, report, or summary shall not be binding on the special master or
court”). As with expert testimony offered to establish a theory of causation, the opinions or
diagnoses of treating physicians are only as trustworthy as the reasonableness of their suppositions
or bases. The views of treating physicians should also be weighed against other, contrary evidence
also present in the record. Hibbard v. Sec’y of Health & Hum. Servs., 100 Fed. Cl. 742, 749 (2011),
aff’d, 698 F.3d 1355 (Fed. Cir. 2012); Caves v. Sec’y of Health & Hum. Servs., No. 06-522V, 2011
WL 1935813, at *17 (Fed. Cl. Spec. Mstr. Apr. 29, 2011), mot. for review den’d, 100 Fed. Cl. 344,
356 (2011), aff’d without opinion, 475 Fed. App’x 765 (Fed. Cir. 2012).
The third Althen prong requires establishing a “proximate temporal relationship” between
the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been equated to
the phrase “medically-acceptable temporal relationship.” Id. A petitioner must offer “preponderant
proof that the onset of symptoms occurred within a timeframe which, given the medical
understanding of the disorder’s etiology, it is medically acceptable to infer causation.” de Bazan
v. Sec’y of Health & Hum. Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for what
is a medically acceptable timeframe must also coincide with the theory of how the relevant vaccine
can cause an injury (Althen prong one’s requirement). Id. at 1352; Shapiro v. Sec’y of Health &
Hum. Servs., 101 Fed. Cl. 532, 542 (2011), recons. den’d after remand, 105 Fed. Cl. 353 (2012),
aff’d mem., 503 F. App’x 952 (Fed. Cir. 2013); Koehn v. Sec’y of Health & Hum. Servs., No. 11-
355V, 2013 WL 3214877 (Fed. Cl. Spec. Mstr. May 30, 2013), mot. for review den’d (Fed. Cl.
Dec. 3, 2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).
B. Law Governing Analysis of Fact Evidence
The parties agree that there are no medical facts in dispute with respect to Petitioner’s
medical records and Petitioner’s timeline of symptoms. Joint Submission at 8, ECF No. 83; see
also Ex. 11 (Petitioner Timeline of Symptoms). Accordingly, Petitioner’s medical records are
presumed to accurate and complete and are afforded substantial weight. Cucuras, 993 F.2d at 1528;
24
Doe/70 v. Sec’y of Health & Hum. Servs., 95 Fed. Cl. 598, 608 (2010); Lowrie v. Sec’y of Health
& Hum. Servs., No. 03-1585V, 2005 WL 6117475, at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005).
C. Analysis of Expert Testimony
Establishing a sound and reliable medical theory connecting the vaccine to the injury often
requires a petitioner to present expert testimony in support of her claim. Lampe v. Sec’y of Health
& Hum. Servs., 219 F.3d 1357, 1361 (Fed. Cir. 2000). Vaccine Program expert testimony is usually
evaluated according to the factors for analyzing scientific reliability set forth in Daubert v. Merrell
Dow Pharm., Inc., 509 U.S. 579, 594-96 (1993). See Cedillo v. Sec’y of Health & Hum. Servs.,
617 F.3d 1328, 1339 (Fed. Cir. 2010) (citing Terran v. Sec’y of Health & Hum. Servs., 195 F.3d
1302, 1316 (Fed. Cir. 1999). “The Daubert factors for analyzing the reliability of testimony are:
(1) whether a theory or technique can be (and has been) tested; (2) whether the theory or technique
has been subjected to peer review and publication; (3) whether there is a known or potential rate
of error and whether there are standards for controlling the error; and (4) whether the theory or
technique enjoys general acceptance within a relevant scientific community.” Terran, 195 F.3d at1316 n.2 (citing Daubert, 509 U.S. at 592-95).
The Daubert factors play a slightly different role in Vaccine Program cases than they do
when applied in other federal judicial fora. Daubert factors are employed by judges to exclude
evidence that is unreliable and potentially confusing to a jury. In Vaccine Program cases, these
factors are used in the weighing of the reliability of scientific evidence. Davis v. Sec’y of Health
& Hum. Servs., 94 Fed. Cl. 53, 66-67 (2010) (“uniquely in this Circuit, the Daubert factors have
been employed also as an acceptable evidentiary-gauging tool with respect to persuasiveness of
expert testimony already admitted”).
Respondent frequently offers one or more experts of his own in order to rebut a petitioner’s
case. Where both sides offer expert testimony, a special master’s decision may be “based on the
credibility of the experts and the relative persuasiveness of their competing theories.”
Broekelschen v. Sec’y of Health & Hum. Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (citing
Lampe, 219 F.3d at 1362). However, nothing requires the acceptance of an expert’s conclusion
“connected to existing data only by the ipse dixit of the expert,” especially if “there is simply too
great an analytical gap between the data and the opinion proffered.” Snyder, 88 Fed. Cl. at 743
(quoting Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997)). A “special master is entitled to
require some indicia of reliability to support the assertion of the expert witness.” Moberly, 592
F.3d at 1324. Weighing the relative persuasiveness of competing expert testimony, based on a
particular expert’s credibility, is part of the overall reliability analysis to which special masters
must subject expert testimony in Vaccine Program cases. Id. at 1325-26 (“[a]ssessments as to the
reliability of expert testimony often turn on credibility determinations”).
D. Consideration of Medical Literature
Although this decision discusses some but not all of the medical literature in detail, I
reviewed and considered all of the medical records and literature submitted in this matter. See
Moriarty v. Sec’y of Health & Hum. Servs., 844 F.3d 1322, 1328 (Fed. Cir. 2016) (“We generally
presume that a special master considered the relevant record evidence even though [s]he does not
25
explicitly reference such evidence in h[er] decision.”); Simanski v. Sec’y of Health & Hum. Servs.,
115 Fed. Cl. 407, 436 (2014) (“[A] Special Master is ‘not required to discuss every piece of
evidence or testimony in her decision.’” (citation omitted)), aff’d, 601 F. App’x 982 (Fed. Cir.
2015).
VI. Analysis
Because Petitioner does not allege an injury listed on the Vaccine Injury Table, her claim
is classified as “off-Table.” As noted above, to prevail on an “off-Table” claim, Petitioner must
prove by preponderant evidence that she suffered an injury and that this injury was caused by the
vaccination at issue. See Capizzano, 440 F.3d at 1320.
In certain cases, the appropriate first step is to determine the precise nature of a petitioner's
injury before engaging in the Althen analysis. Broekelschen, 618 F.3d at 1346. An injury which
predates vaccination can defeat a Vaccine Program claim entirely. Shalala v. Whitecotton, 514
U.S. 268, 274-75 (1995) (Vaccine Act claimant who demonstrates she experienced symptoms of
injury after receipt of vaccination does not succeed in her claim if the evidence indicates that she
had symptoms of injury before her vaccination); Locane v. Sec'y of Health & Hum. Servs., 99 Fed.
Cl. 715, 727 (2011), aff'd, 685 F.3d 1375 (Fed. Cir. 2012) (finding that petitioner's Crohn's disease
began prior to her vaccinations and therefore vaccine causation could not be established).
A. The Expert Opinion Evidence
In weighing the persuasiveness of opinion testimony, special masters may consider the
background of the expert who is offering an opinion. See Snyder v. Sec'y of Health & Hum. Servs.,
553 F. App'x 994, 1000–02 (Fed. Cir. 2014) (special master's finding that respondent's experts
were more persuasive due in part to their current practice in neurology compared to petitioner's
expert who had no recent practice was not arbitrary or capricious); see also Locane, 99 Fed. Cl.
727. This flows naturally from a special master's duty to evaluate expert credibility in the process
of weighing the evidence. Porter v. Sec'y of Health & Hum. Servs., 663 F.3d 1242, 1250 (Fed. Cir.
2011) (“[t]he Federal Circuit has unambiguously explained that special masters are expected to
consider the credibility of expert witnesses in evaluating petitions for compensation under the
Vaccine Act”). I have evaluated the opinions of both experts in this case and find that Dr. Leist is
the more persuasive of the two.
Dr. Leist is a board-certified neurologist with a Ph.D. in biochemistry. See Leist CV at 1.
He is a professor of Neurology at Thomas Jefferson University and has been on faculty at that
institution for more than 20 years. Id. Among other positions, he currently serves as the Chief of
the clinical neuroimmunology division.
Dr. Schofield is a physician who is board certified in internal medicine. See Schofield CV
at 3. During her time as an attending physician at St. Joseph Hospital in Denver, Dr. Schofield
stated that she developed an interest in autoimmune disease. First Schofield Rep. at 1. Based on
this interest, Dr. Schofield completed an informal (not accredited) fellowship training program in
multi-specialty autoimmune disease from January 2015 through July 2016. Id. at 1-2. During this
time, she also started her own clinic involving dysautonomia and antiphospholipid syndrome
26
(hereinafter “APS”). Id. at 2. She currently works as a staff physician at the IMMUNOe Health
and Research Center where she performs clinical work in APS and autoimmune dysautonomia. Id.
Although Dr. Schofield has experience in the field of dysautonomia, she is not a
neurologist. On the other hand, Dr. Leist has extensive medical training, including a three-year
neurology residency at the Cornell Medical Center and the Sloan Kettering Memorial Cancer
Center. Leist CV at 1. This three years of formal training, in addition to his 20 plus years of work
as a neurologist, and his board certification in neurology all render him the more persuasive of the
two experts, especially as his opinion relates to a condition that falls in the field of neurology as
opposed to internal medicine.
B. There is not Preponderant Evidence that Petitioner Suffers from POTS9
The first question to be addressed is whether petitioner’s medical history supports a finding
that she suffered from POTS. For the reasons discussed below, I find that it does not.
Sheldon, et al. defined POTS as follows:
POTS is a clinical syndrome usually characterized by (1) frequent symptoms that
occur with standing, such as light-headedness, palpitations, tremor, generalized
weakness, blurred vision, exercise intolerance, and fatigue; (2) an increase in heart
rate of ≥30 beats per minute (bpm) when moving from a recumbent to a standing
position…; and (3) the absence of orthostatic hypotension (>20 mm Hg drop in
systolic blood pressure).
9
I will note at the outset that the precise nature of Petitioner’s injury as alleged throughout this case is
unclear. The petition repeatedly uses the term “adverse reaction” to describe Petitioner’s injury. See Pet. at
1, 7. The petition also states that
At the worst of her illness, [L.P.] experienced the following symptoms: Orthostatic
Tachycardia, palpitations or pounding heart, cold hands and feet, inability to regulate body
temperature, sweating irregularities, constipation, diarrhea, loose stool, severe GERD,
nausea, unexplained weight loss, nervousness, anxiety, depression, flushing, heat
intolerance, increased blood pressure, hair loss, dry skin, adrenaline rushes, hearing loss,
tinnitus, dizziness, motion intolerance, extreme motion sickness, hyperacusis, brain
fog/cognitive struggles, blurred vision, tingling in her legs, feet, and face, exercise
intolerance, fatigue, insomnia, and reduced stress tolerance.
Id. at 6. This list of conditions is reiterated in Petitioner’s affidavit and in her Motion for a Decision on the
Record. See Ex. 1 at 3; Pet. Motion at 18. However, in her Reply Brief, Petitioner argues that she has met
Althen prong one and has shown that vaccination can cause POTS (stating “the growing body of medical
literature since this case was filed in 2016 increasingly suggests an autoimmune basis for POTS.”). See
Reply at 7-8. Further, Dr. Schofield opined as follows: “During my initial evaluation, there was a clear
temporal relationship to the onset of her symptoms and the influenza vaccine she received and I was
suspicious of an immune-mediated mechanism for her dysautonomia triggered by the vaccination. I ordered
serological testing for autoimmune and non-autoimmune causes for her POTS…” First Schofield Rep. at
4. Accordingly, I have evaluated whether Petitioner suffered from POTS in conducting my analysis in this
case.
27
Sheldon, et al., 2015 Heart Rhythm Society Expert Consensus Statement on the Diagnosis and
Treatment of Postural Tachycardia Syndrome, Inappropriate Sinus Tachycardia, and Vasovagal
Syncope, 12 HEART RHYTHM at 3 (2017) (filed as Ex. 57) (hereinafter “Sheldon”). Sheldon goes
on to note that “[t]he standing (or orthostatic) heart rate of individuals with POTS is often ≥120
bpm.” Id.
1. Tilt Table Testing
Petitioner visited the Swedish Medical Center for tilt table testing on February 25, 2016.
Ex. 23 at 18-25. Dr. Schofield contends that Petitioner was “officially diagnosed with POTS in
February, 2016 by tilt table testing done at Swedish Medical Center in Denver.” First Schofield
Rep. at 4. However, Petitioner’s treating neurologist, Dr. Moon, noted that Petitioner’s tilt table
test was “not conclusive”. Ex. 16 at 13. In the assessment portion of the March 15, 2016 record,
Dr. Moon further noted that “[a]t this point, we don’t have definitive POTS.” Id. Respondent’s
expert, Dr. Leist, provided an opinion consistent with that of Dr. Moon stating that “[t]he records
do … not support a diagnosis of postural orthostatic tachycardia syndrome.” First Leist Rep. at 14.
The results of Petitioner’s tilt table test are documented in the following chart:
Ex. 23 at 20. Dr. Leist noted that the first three entries were taken when Petitioner was laying
down, sitting up, and standing, and that these entries took place prior to the start of the test. See
First Leist Rep. at 13; Second Leist Rep. at 3. This interpretation is supported by the above chart
which indicates “pre tilt table” when describing the entries at 1300 and 1305. Ex. 23 at 20.
According to Dr. Leist, the actual tilt table test was conducted between 1335 and 1415.
Second Leist Rep. at 3. Once the test began at 1335, Petitioner’s heart rate was recorded at 102
bpm. Ex. 23 at 20. At the conclusion of the test, her heart rate was 111 bpm. Id. This change in
28
heart rate does not meet the criterion outlined by Sheldon which requires an increase in heart rate
of ≥30 beats per minute. Sheldon at 3. I also note that Petitioner’s heart rate never exceeded 120
bpm, which is inconsistent with a POTS diagnosis; Sheldon noted that “[t]he standing (or
orthostatic) heart rate of individuals with POTS is often ≥120 bpm.” Id.
In addition, I note that Petitioner did not experience symptoms during the test, which
further suggests that she does not have POTS. Dr. Schofield addressed this point in her second
report. She stated,
Dr. Leist also makes note that [L.P.] did not have any symptoms during the study.
That portion of the report is usually done by a technician, many of whom do not
even ask the patient if they have symptoms. All patients with POTS have numerous
symptoms all the time and learn to not complain, so unless someone is specifically
asking the patient if they are having symptoms, patients will almost never report
them. In my experience, it is common for this to be the case on formal tilt table
reports.
Second Schofield Rep. at 2. This point would be more compelling if there were an absence of
symptom discussion by the technician during the test. The fact that “Ø symptoms” is repeatedly
annotated in the records indicates that the technician asked whether Petitioner was experiencing
symptoms and contemporaneously recorded that she was not.
Dr. Schofield contends that Petitioner’s tilt table test was diagnostic of POTS and that she
“very clearly … met the formal criteria for POTS.” Second Schofield Rep. at 2. She stated, “A tilt
table test demonstrated a rise in heart rate from 68 to the 100’s without a drop in her blood pressure
consistent with postural tachycardia syndrome.” First Schofield Rep. at 5. Dr. Schofield combined
the results from the pretest and the test to arrive at this conclusion. Although no literature was filed
which directly addresses the point as to whether these initial readings should be considered in
assessing the test results, several points indicate that they should not. First, the fact that the readings
are classified as “pre tilt table” suggests that they are not to be used as part of the formal test.
Second, Petitioner’s treating neurologist, Dr. Moon, noted that “We did see that her heart rate did
fluctuate significantly prior to the tilt table.” Ex. 16 at 13. This statement also supports the
distinction between the pre-test numbers and the rest of the testing. Finally, a second neurologist,
Dr. Leist, has opined that the testing did not begin until 1335. Second Leist Rep. at 3. Ultimately,
I credit the opinions of the two board certified neurologists over that of Dr. Schofield. In so doing,
I find that Petitioner’s tilt table test was not diagnostic of POTS.
2. Other Factors
Dr. Leist opined that other evidence in Petitioner’s medical records also suggests that she
does not have POTS. Dr. Leist pointed out that Petitioner wore an event recorder between
November 6 and November 20, 2015. During this time, Petitioner’s average heart rate was 63 bpm
29
and she was in sinus bradycardia10 of less than 60 bpm for 24% of the time. Second Leist Rep. at
4. In addition, Petitioner’s heart rate was greater than 100 bpm during only 2% of this time period.
Id. Dr. Leist opined that these factors indicate that Petitioner does not have POTS.11 Id. Dr. Leist
further remarked about this time period as follows: “[L.P.] marked a total of 9 events when she
felt symptoms between November 6 and November 12, 2015, 4 of these occurred before 6 am, and
it could be argued that they occurred while she was in bed. She marked no events between
November 13 and November 20.” Id.
In addition to the November 6 through November 20 time period, Dr. Leist noted that
“[c]ardiac monitor data obtained between about 39 and 59 days after [L.P.] had received influenza
vaccine on September 25, 2015 are not supportive of a diagnosis of Postural Tachycardia
Syndrome. The data do however support that [L.P.] has spontaneous, unprovoked fluctuations of
the heart rate and that she is at times bradycardic.” Second Leist Rep. at 4.
The tilt table test as well as the other evidence from Petitioner’s medical records
demonstrates that she does not meet the diagnostic criteria for POTS.
3. Treating Physicians
Petitioner visited Dr. Yeash (her PCP) on March 18, 2016 for dizziness, vertigo, poor
concentration, tachycardia when standing up, extreme fatigue, and weakness. Ex. 18 at 5.
Petitioner requested paperwork for short term disability. Id. In the HPI, Dr. Yeash’s notes indicate
that her neurologist had diagnosed her with dysautonomia and POTS. Id. In fact, during
Petitioner’s March 15, 2016 follow-up appointment with Dr Moon, he noted that “At this point we
do not have definitive POTS.” Ex. 16 at 13.
At each subsequent visit from March 18, 2016 through May 31, 2018, Dr. Yeash assessed
Petitioner with POTS. See Ex. 18 at 1, 5; Ex. 54 at 14, 23. These assessments were based on
inaccurate information; specifically, that Dr. Moon had assessed Petitioner with POTS. As such, I
do not find it to be persuasive evidence that POTS is Petitioner’s correct diagnosis.
None of Petitioner’s other treating physicians (other than Dr. Schofield) diagnosed
Petitioner with POTS or linked Petitioner’s condition to her flu vaccine. Accordingly, based on
the results of the tilt table test, the other factors described above, and the opinion of Petitioner’s
treating neurologist as well as the opinion of Dr. Leist, I conclude that there is not preponderant
evidence that Petitioner suffers from POTS.
C. There is not Preponderant Evidence that Petitioner Suffers from APS
10
Bradycardia is a slowness of the heartbeat, as evidenced by slowing of the pulse rate to less than 60.
Dorland's, https://www.dorlandsonline.com/dorland/definition?id=6816&searchterm=bradycardia (last
visited April 9, 2021).
11
In Balasco v. Sec’y of Health & Hum. Servs., 2020 WL 1240917, the special master noted that some of
the medical literature filed in that case indicates that extended Holter monitors are not useful in detecting
POTS. See Balasco, n32. The literature referenced in that decision was not filed in the present case.
30
Dr. Schofield repeatedly discussed APS in her expert reports. Although she did not
definitively state that Petitioner had APS, she discussed the condition enough that it is appropriate
to provide some background. I note that it is unclear whether Dr. Schofield is contending that
Petitioner developed APS as a result of her flu vaccine. Certainly, Dr. Leist believed that to be her
contention. (“Dr. Schofield’s theory appears to be that influenza vaccine induced antiphospholipid
syndrome which in turn induced an inner ear condition [L.P.’s] case.”) Second Leist Rep. at 1.
Based on this ambiguity, I have included a brief analysis concerning whether there is preponderant
evidence that Petitioner suffers from APS and whether the flu vaccine can cause APS.
Cruz-Tapias described APS as
an autoimmune multisystemic disease associated with recurrent fetal loss,
thromboembolic phenomena, thrombocytopenia as well as neurological, cardiac
and dermatological involvement. APS is characterized by the presence of
antiphospholipid antibodies which bind negatively charged phospholipids, mainly
through b2-glycoprotein I (b2-GPI). The factors causing production of anti-b2-GPI
antibodies remain undefined, but there is evidence that molecular mimicry is one
of the mechanisms by which experimental APS can occur in association with
pathogens.
Cruz-Tapias at 390.
Throughout her two reports, Dr. Schofield noted that a number of Petitioner’s clinical signs
and symptoms were consistent with APS. She described these consistencies without ever giving
Petitioner an APS diagnosis. See e.g., First Schofield Rep. at 4 (“Autonomic dysfunction, migraine
headaches, cognitive issues, sensorineural hearing loss and Meniere’s like syndrome may all
[occur] in association with APS”); First Schofield Rep. at 8 (“In addition, all the clinical
manifestations she experienced have been well described in association with the antiphospholipid
syndrome, including migraines and cognitive dysfunction, hearing and vestibular issues and
autonomic nervous system dysfunction.”); Second Schofield Rep. at 4. (“Anticardiolipin
antibodies are often present in individuals with the antiphospholipid antibody syndrome”).
As discussed later in this Decision, Petitioner had three tests for antiphospholipid
antibodies, none of which were positive. Dr. Leist opined that “…low levels of antiphospholipid
IgM antibodies are not diagnostic antiphospholipid syndrome. Negative antiphospholipid IgM,
IgG, and IgA antibody tests are not consistent with the diagnosis of antiphospholipid syndrome…”
First Leist Rep. at 14. In Schofield-1, Dr. Schofield stated:
The diagnosis of APS was determined by the presence of at least one
antiphospholipid antibody (lupus anticoagulant, anticardiolipin immunoglobulin
IgG or IgM, or beta 2 microglobulin I IgG or IgM) on more than one occasion at
least 12 weeks apart as well as one or more clinical manifestations of the syndrome.
Not all patients met the revised Sapporo classification criteria for definite APS,
which requires thrombosis or specific pregnancy morbidity and medium to high
titer antibody levels. The classification criteria were designed for rigorous clinical
research studies not for diagnosis, and patients with low titer antibody positivity
31
were included as were patients without a history of thrombosis who had well-
described nonthrombotic manifestations of the syndrome.
Schofield-1 at 698. Additionally, in Schofield-2, Dr. Schofield noted, “The diagnosis of APS was
determined by the presence of one or more antiphospholipid antibodies on more than one occasion
at least 12 weeks apart as well as one or more clinical manifestations of the syndrome.” Schofield-
2 at 3. Although Petitioner did not file the diagnostic criteria for APS, I note that she did not test
positive for antiphospholipid antibodies on more than one occasion at least 12 weeks apart. Based
on Dr. Leist’s opinion, and Dr. Schofield’s lack of a clear diagnosis, I conclude that Petitioner has
not presented preponderant evidence that she suffered from APS.
Based upon the findings that Petitioner has not established through preponderant evidence
that she suffered from either POTS or APS, Petitioner may not receive compensation. Lombardi
v. Sec'y of Health & Hum. Servs., 656 F.3d 1343 (Fed. Cir. 2011). However, for the sake of
completeness, I will review the other elements of her claim.
D. Petitioner Has Not Carried Her Burden of Proof regarding Causation
1. Althen Prong 1
In the context of the Program, “to establish causation, the standard of proof is
preponderance of evidence, not scientific certainty.” Langland v. Sec’y of Health & Hum. Serv.,
109 Fed. Cl. 421, 441 (2013). Petitioner’s burden under Althen’s first prong is to provide a medical
theory causally connecting the vaccination and the injury. Id. This theory must be sound and
reliable. Boatmon, 941 F.3d at 1359.
Before discussing Petitioner’s prong one theory in this case, I will briefly address whether
Petitioner has presented preponderant evidence that the flu vaccine can cause APS.
a. Antiphospholipid Syndrome
In her first report, Dr. Schofield opined that “It is well recognized that APS may be
triggered by vaccination and infection.” First Schofield Rep. at 4. Dr. Schofield cited to Cruz-
Tapias in support of this proposition. Cruz-Tapias noted that the infections most frequently
associated with APS include parvovirus B19, cytomegalovirus (CMV), toxoplasma, rubella virus,
varicella-zoster virus, HIV, streptococcal and staphylococcal infections, gram-negative bacteria
and Mycoplasma pneumoniae. Cruz-Tapias at 389. With respect to vaccination, Cruz-Tapias
discussed an association between APS and tetanus toxoid vaccines and noted that individuals
immunized with tetanus toxoid vaccines developed anti-b2-GPI/antitetanus toxoid cross-reactive
antibodies via molecular mimicry. Id. at 390. While this article provides some support for a
connection between APS and tetanus toxoid vaccines, it does not discuss the flu vaccine.
In Schofield-1, Dr. Schofield noted that “[o]ne patient (#13) developed APS, POTS, and
NCS two months after human papillomavirus (HPV) vaccination…” Schofield-1 at 698. The
article did not elaborate on how the HPV vaccine caused APS (or POTS). The article did not
discuss the flu vaccine.
32
Dr. Leist opined that “Dr. Schofield’s claim that influenza vaccine caused antiphospholipid
syndrome as root cause for a host of symptoms in L.P.’s case is not supported by the records.”
First Leist Rep. at 12.
Two articles which discuss APS following different vaccines (not the vaccine at issue in
this case) along with Dr. Schofield’s opinion that “It is well recognized that APS may be triggered
by vaccination...” is not sufficient for Petitioner to preponderantly establish that the flu vaccine
can cause APS.
b. POTS
Petitioner’s prong one theory is that the influenza vaccination caused Petitioner to develop
a transient upregulation of antiphospholipid antibodies which in turn caused damage to Petitioner’s
inner ear and vestibular system and resulted in Petitioner developing POTS. This theory can be
broken down into two discrete questions: 1) Can the influenza vaccine cause the development of
transient antiphospholipid antibodies; and 2) can a transient upregulation in antiphospholipid
antibodies cause POTS.
i. Can the Influenza Vaccine Induce Transient Upregulation in
Antiphospholipid Antibodies?
Dr. Schofield stated that “Transient production of anticardiolipin antibodies and clinical
manifestations of APS (including stroke) as occurred in [L.P.’s] case has been reported in more
than one publication … in association with the influenza vaccine.” First Schofield Rep. at 8. As
support for this proposition, Dr. Schofield cited to several articles. See Perdan-Pirkmajer, et al.,
Autoimmune response following influenza vaccination in patients with autoimmune inflammatory
rheumatic disease, 21 LUPUS 175-83 (2012) (filed as Ex. 34) (hereinafter “Perdan-Pirkmajer”);
Agmon-Levin; and Toplak.
Perdan-Pirkmajer studied 218 patients with autoimmune inflammatory rheumatic disease
(AIRD). In this study, 50 patients were vaccinated against seasonal influenza, six against H1N1,
104 against both, and there were 58 non-vaccinated controls. Perdan-Pirkmajer at 175. Blood
samples were taken and screened for autoantibodies before vaccination, one month after
vaccination, and six months after vaccination. Id. The study concluded that “Although no
convincing differences between the seasonal and H1N1 vaccines were observed, our results imply
that there might be a slight tendency of the H1N1 vaccine towards aCL [anticardiolipin antibodies]
induction.” Id. The authors noted “the potential of both vaccines to induce de novo aCL IgG/IgM
in susceptible subjects. Nevertheless, although a transient increase in aCL IgG after either
vaccination was often observed, the long-term effect of vaccination resulted in lower aCL IgG in
most patients.” Id. at 181. This study seems to tell us that patients with AIRD may experience a
transient increase in anticardiolipin antibodies after vaccination with seasonal influenza/H1N1.
Because Petitioner does not have AIRD, it is unclear how this study is relevant to her case.
Dr. Schofield cited to the Toplak paper as support for her theory that flu vaccination can
cause an increase in anticardiolipin antibodies and/or APS. Toplak evaluated the possibility of
33
autoimmune responses following flu vaccination by measuring specific autoantibodies in 92
healthy adults before vaccination, one month after vaccination, and six months after vaccination.
Toplak at 134. Toplak found that “There were no statistically significant differences in the
percentage of positive ANA, aCL, anti-β2-GPI, LA and anti-ENA before,1 month and 6 months
after the vaccination.” Id. However, while the study found that influenza vaccination did not alter
the percentage of healthy adults with positive autoantibodies, an “[i]ncreased level of
autoantibodies or appearance of new autoantibodies was observed 1 month after the vaccination
in 15% and 6 months after the vaccination in 13% of participants, suggesting de novo induction of
autoantibodies after the influenza vaccination in selected individuals.” Id. at 137. Toplak did note
changes in anticardiolipin antibodies in some study participants. Topak at 138. Ultimately, Topak
provides some support for the proposition that flu vaccine can result in an increase in
anticardiolipin antibodies.12 Of note, the Topak paper specifically found that no participant
developed clinical signs of autoimmune disease within six months of vaccination. Id. at 136.
The Agmon-Levin article is an opinion piece that presents a broad discussion of vaccines
and autoimmunity. The authors note that “the latency period between vaccination and
autoimmunity ranges from days to years.” Agmon-Levin at 648. They cite to Toplak as one study
that supports this proposition (noting that “Toplak et al. reported the production of autoantibodies
(such as antinuclear and antiphospholipid antibodies) in 92 healthy medical workers up to 6
months after influenza vaccination.”). This article provides no further discussion of anticardiolipin
antibodies or APS.
In summary, the above-mentioned literature, specifically the Toplak article does provide
some evidence that the flu vaccine can result in the transient upregulation of anticardiolipin
antibodies.
ii. Can the Transient Upregulation of Antiphospholipid Antibodies
Cause POTS?
Petitioner filed a one-page abstract which described patients with hearing loss. See
Mouadeb & Ruckstein. The abstract described a study cohort which included 168 patients referred
for diagnosis and treatment of progressive hearing loss. Mouadeb & Ruckstein at 879. All patients
had blood tests for autoimmune and infectious diseases, including testing for anticardiolipin
antibodies, anti-B2 glycoprotein, and lupus anticoagulant. Id. The results of the study indicated
that 42 patients (25%) had at least one elevated antiphospholipid antibody marker. Id. The study
concluded that “These data support the hypothesis that antiphospholipid antibodies are involved
in the pathogenesis of some forms of inner ear dysfunction, presumably by causing microthrombus
formation in the labyrinthine vasculature.” Id. The abstract went on to note that “Basic science
studies are required to better understand the mechanisms by which antiphospholipid antibodies
mediate inner ear dysfunction. Clinical studies to evaluate the efficacy of anticoagulation in this
group of patients are also required.” Id.
12
This point does not necessarily support the proposition that flu vaccine can cause APS. The fact that
anticardiolipin antibodies are often present in individuals with APS does not mean that an increase in
anticardiolipin antibodies leads to APS.
34
Dr. Leist did not find the one page abstract persuasive and remarked that the Mouadeb &
Ruckstein article “does not go beyond the description that 42 of a series of 168 patients with
sensorineural hearing [loss] had a least one antiphospholipid marker.” Second Leist Rep. at 5. He
further stated that “the authors speculate how anticardiolipin antibodies could potentially cause
hearing issues.” Id.
This one-page abstract provides some minimal evidence that hearing loss can be associated
with antiphospholipid antibodies. However, it does not provide any connection to POTS. Dr.
Schofield stated that “Autonomic dysfunction, migraine headaches, cognitive issues, sensorineural
hearing loss and Meniere’s like syndrome may all occur in association with APS.” First Schofield
Rep. at 4. Similar to the one page abstract, this statement does not include any analysis of whether
or how a “Ménière’s like syndrome” can lead to POTS.
Further, in Schofield-1, the authors wrote: “we do not know what the frequency of
autonomic dysfunction may be in the overall APS patient population, nor how often
antiphospholipid antibodies may be present in patients with various autonomic disorders.”
Schofield-1 at 700-01. The fact that it is unclear to Dr. Schofield whether antiphospholipid
antibodies are even present in patients with autonomic disorders suggests that there is not
preponderant evidence that the upregulation of antiphospholipid antibodies can cause POTS.
Ultimately, for the reasons discussed above, I find that Petitioner has not presented
preponderant evidence in the form of a reputable medical theory which demonstrates that the flu
vaccine can cause either APS or POTS.
2. Althen Prong 2
Under Althen’s second prong, a petitioner must “prove a logical sequence of cause and
effect showing that the vaccination was the reason for the injury.” Althen, 418 F.3d at 1278. The
sequence of cause and effect must be “'logical' and legally probable, not medically or scientifically
certain.” Id. A petitioner is not required to show “epidemiologic studies, rechallenge, the presence
of pathological markers or genetic disposition, or general acceptance in the scientific or medical
communities to establish a logical sequence of cause and effect.” Id. (omitting internal citations).
Capizzano v. Sec'y of Health & Hum. Servs., 440 F.3d 1317, 1325 (Fed. Cir. 2006). Instead,
circumstantial evidence and reliable medical opinions may be sufficient to satisfy the second
Althen prong. Isaac v. Sec’y of Health & Hum. Servs., No. 08-601V, 2012 U.S. Claims LEXIS
1023 at *75 (Fed. Cl. Spec. Mstr. July 30, 2012), aff’d 108 Fed. Cl. 743 (Fed. Cl. 2013).
a. Petitioner’s Pre-Existing Symptoms
A petitioner cannot succeed on a claim of causation-in-fact where the alleged condition
preexisted the vaccination. See W.C. v. Sec'y of Health & Hum. Servs., 704 F.3d 1352, 1354–55
(Fed. Cir. 2013) (affirming the special master’s denial of compensation on claim of causation-in-
fact because “[i]f a petitioner has a disorder before being vaccinated, the vaccine logically cannot
have caused the disorder”). In this case, the medical records demonstrate that Petitioner was
suffering from a host of symptoms prior to her flu vaccination that were similar to her symptoms
post vaccination. For at least two years prior to September 25, 2015, Petitioner frequently
35
Polymorphous Light Eruption/ 10-15-14: ENT history of pruritic erythema, possible photosensitivity Ex. 10 at 24
Rash due to Sun Exposure 06-10-15: possible polymorphous light eruption Ex. 10 at 27
Hypermobility 04-14-14: Petitioner reported feeling “hypermobile at times” Ex. 13 at 1
Petitioner’s medical records demonstrate that she had a number of medical concerns prior
to September 25, 2015 that were similar in nature to her symptoms after vaccination. Petitioner
contends that her symptoms after vaccination were different in both their nature and severity.
Although Petitioner states that “there is not a single pre-vaccination record of
dysautonomia or POTS” (Pet’r’s Reply at 3), this contention is not supported by the medical
records cited above, which demonstrate that Petitioner repeatedly complained of heart palpitations
in the years before she received her flu vaccination.
Petitioner additionally differentiated between a low frequency “thumping” sound that she
experienced after vaccination (Ex. 3 at 1) and her tinnitus documented pre-vaccination. In her
affidavit, Petitioner stated that “[a]lthough I had experienced a high-pitched tinnitus in both ears
before, this sensation was different, as I began to experience a low hum, vibrating noise in my left
ear that would not go away.” Ex. 1, ¶ 3. Dr. Leist opined that that Petitioner had a history of
Eustachian tube dysfunction and tinnitus. He remarked in his report “Dr. Kreutzer recorded an at
least 10-year history of tinnitus, intermittent ear pressure, and fullness of the left ear (Exhibit 4 at
1; Exhibit 13 at 2).” First Leist Rep. at 14. He further opined that “[L.P.] had tinnitus and pressure
and fullness before and after administration of influenza vaccine on September 25, 2015.” Id.While the specific symptoms that Petitioner experienced after vaccination are somewhat different
than her pre-vaccination complaints, they appear to be substantially similar. Ultimately, the
medical records establish that Petitioner experienced symptoms of dysautonomia and tinnitus prior
to her September 25, 2015 vaccination.
In her second expert report, Dr. Schofield stated, “many patients who develop severe
autoimmune dysautonomia have much milder underlying symptoms suggesting mild orthostatic
intolerance and/or immune dysregulation just as [L.P.’s] history suggests.” Second Schofield Rep.
at 3. Dr. Schofield did not provide any further discussion concerning this point. She did not
elaborate as to how Petitioner’s pre-existing symptoms supported her theory that the flu vaccine
did cause Petitioner’s condition.
b. Anticardiolipin Antibodies
Aside from a temporal correlation between Petitioner’s symptoms and her vaccination, Dr.
Schofield points to two main tests in support of her position that the flu vaccine did cause
Petitioner’s illness: Petitioner’s aCL IgM and her low C4 level. I will address each of these in turn.
Dr. Schofield ordered tests for anticardiolipin antibodies on June 8, 2016. These results are
depicted below:
37
Ex. 24 at 66-67. The lab assessed both tests as negative. In her first expert report, Dr. Schofield
described the test results as follows: “I ordered serological testing for autoimmune and non-
autoimmune causes for her POTS which was notable for a positive anticardiolipin IgM antibody-
-one of the antibodies associated with the autoimmune clotting disorder antiphospholipid
syndrome (APS).” First Schofield Rep. at 4. In her second report, Dr. Schofield clarified this point
and noted that Petitioner’s anticardiolipin antibody test came back as “indeterminate” or “low
positive.”
Her anticardiolipin IgM level during my initial evaluation (one full year after the
vaccination) was actually indeterminate or low positive at 18 MPL (indeterminate
or low positive is 12.5 to 20 MPL), not negative. The University of Colorado
Rheumatology laboratory has elected not to report the low positive/indeterminate
anticardiolipin antibody results based on the formal 2006 revised Sapporo Criteria
for a diagnosis of antiphospholipid syndrome (APS). … The University of
Colorado laboratory is the only laboratory I know of that does this and when I was
practicing there, I met with the head of the Rheumatology laboratory requesting
they report the low/indeterminate positive results as they were clearly clinically
important in some of my patients. They preferred to report the low/indeterminate
titer results to me directly rather than reporting them in the chart.
Second Schofield Rep. at 3. Dr. Schofield pasted an example of the way other laboratories report
anticardiolipin antibodies into her report.
38
Ex. 28 at 8. It is not clear why Dr. Schofield sent these results to a different lab. With respect to
this testing, she stated, “Repeat testing for antiphospholipid antibodies … many months later
showed this testing had normalized, suggesting the autoimmunity was transient…” First Schofield
Rep. at 7.
Dr. Leist opined as follows: “Absence of anticardiolipin antibodies renders anticardiolipin
syndrome or for that matter an anticardiolipin antibody related condition unlikely.” Second Leist
Rep. at 1. He further stated that “Laboratory tests in [L.P.] do not fulfill laboratory criteria of the
“The International consensus statement on an update of the classification criteria for definite
antiphospholipid syndrome (APS)” [antiphospholipid antibodies include anticardiolipin, beta-2
glycoprotein I, and lupus anticoagulant antibodies].” Id. at 2.
It is unclear how an indeterminate level aCL taken more than eight months after
vaccination demonstrates that Petitioner’s flu vaccination did cause her condition. Although Dr.
Schofield stated, “I suspect it would have been higher if it were tested closer to the time of the
illness onset” (Second Schofield Rep. at 7), this statement is entirely speculative. Further, it is also
unclear how Petitioner’s negative test from June 2016 compares with her negative test from the
same lab in September 2016, as Dr. Schofield included the indeterminate test value of 18 in her
report, but did not indicate what the value was for the September test. In short, I do not find Dr.
Schofield’s opinion concerning this matter to be persuasive.
c. Complement Component 4 (C4)
Dr. Schofield also opined that Petitioner’s low C4 is indicative of autoimmunity and thus
supports her position that the flu vaccine did cause Petitioner’s condition. Dr. Schofield stated:
“There was also a persistently low C4 level on three serial occasions (the first being done Sept
2016) suggestive of either active autoimmunity or a genetic predisposition to autoimmunity.
Repeat testing in January 2018 showed this level had normalized consistent with active
autoimmunity rather than a genetically low level.” Second Schofield Rep. at 7.
Petitioner’s testing does indicate that her C4 level was low on three occasions. On June 8,
2016, Petitioner’s C4 level was 13.7 (reference range 19.0-52.0 mg/dL). Ex. 24 at 56. On
September 28, 2016, Petitioner’s C4 was 13.3 (reference range 19.0-52.0 mg/dL). Ex. 29 at 16.
On October 14, 2016, Petitioner’s C4 was 12 (reference range 14-44). Ex. 28 at 6. Dr. Schofield
did not spend time in her reports discussing the meaning of C4 levels. Other than to state that these
40
levels are indicative of persistent autoimmunity, Dr. Schofield did not explain or describe how a
low C4 level eight plus months after vaccination is significant to this case. Further, it is unclear
why Petitioner’s aCL level normalized and her C4 did not and how this supports Petitioner’s theory
that her flu vaccine did cause her condition. Dr. Leist did not discuss Petitioner’s C4 levels in his
report. Ultimately, while Petitioner’s C4 level was low on three occasions, the significance of these
levels has not been explained in any meaningful way that connects these results to vaccination,
which occurred between eight and twelve plus months prior.
d. Petitioner’s Treating Physicians
In weighing evidence, special masters are expected to consider the views of treating
doctors. Cappizano v. Sec’y of Health & Human Servs., 440 F.3d 1317, 1326 (Fed. Cir. 2006).
The views of treating doctors about the appropriate diagnosis are often persuasive because the
doctors have direct experience with the patient whom they are diagnosing. See McCulloch v. Sec’y
of Health & Human Servs., No. 09-293V, 2015 WL 3640610, at *20 (Fed. Cl. Spec. Mstr. May
22, 2015).
I have considered the fact that Dr. Schofield was one of Petitioner’s treating physicians in
arriving at my determination in this case. I also note that none of Petitioner’s other treating doctors
connected any of her symptoms with her flu vaccination.
For the reasons articulated above, I find that Petitioner has failed to preponderantly
demonstrate that her flu vaccination “did cause” any of her medical problems and has thus not
established the second prong of Althen.
3. Althen Prong 3
The timing prong contains two parts. First, a petitioner must establish the “timeframe for
which it is medically acceptable to infer causation” and second, she must demonstrate that the
onset of the disease occurred in this period. Shapiro v. Secʼy of Health & Hum. Servs., 101 Fed.
Cl. 532, 542-43 (2011), recons. denied after remand on other grounds, 105 Fed. Cl. 353 (2012),
aff’d without op., 503 F. App’x 952 (Fed. Cir. 2013).
Petitioner failed to establish a timeframe for which it is medically acceptable to infer
causation. In Dr. Schofield’s first report, she stated that “The mean time to post-vaccination
symptom onset is two weeks, but it may range from a few days to a few months.” In her second
report, Dr. Schofield claimed that “it is generally accepted by most experts in the field of
autoimmune disease that vaccinations are one of the environmental triggers of autoimmune disease
and a period of 30 days has been usually used to define temporal association.” Second Schofield
Rep. at 6. Dr. Schofield did not provide a specific opinion on the appropriate window between flu
vaccine and onset of POTS or APS. Further, she did not cite to any medical literature specifically
establishing a temporal association between the flu vaccine and POTS or APS. Painting with such
a broad brush in discussing the appropriate onset interval between vaccinations generally and
autoimmune diseases generally is not persuasive.
41
Additionally, even assuming 30 days is an acceptable timeframe to infer causation,
Petitioner failed to establish that the onset of her alleged injury occurred during this window. Dr.
Schofield reported that there was “a clear temporal relationship to the onset of [Petitioner’s]
symptoms and the influenza vaccine she received and [Dr. Schofield] was suspicious of an
immune-mediated mechanism for her dysautonomia triggered by the vaccination.” First Schofield
Rep. at 4. However, in drafting her first report, Dr. Schofield failed to review Petitioner’s prior
medical history and instead chose to rely on Petitioner’s statement that she “was completely
healthy” prior to her vaccination. Second Schofield Rep. at 2. Dr. Schofield failed to distinguish
Petitioner’s pre-vaccination symptoms from her post-vaccination symptoms, and thus failed
establish the onset of Petitioner’s alleged injury.13 Petitioner has not presented preponderant proof
with respect to the third Althen prong.
VII. Conclusion
Upon careful evaluation of all the evidence submitted in this matter, including the medical
records, the affidavit, as well as the experts’ opinions and medical literature, I conclude that
Petitioner has not shown by preponderant evidence that she is entitled to compensation under the
Vaccine Act. Her petition is therefore DISMISSED. The clerk shall enter judgment
accordingly.14
IT IS SO ORDERED.
s/ Katherine E. Oler
Katherine E. Oler
Special Master
13
In her second report, Dr. Schofield pivoted from her position that Petitioner was completely healthy
before vaccination and opined that “many patients who develop severe autoimmune dysautonomia have
much milder underlying symptoms suggesting mild orthostatic intolerance and/or immune dysregulation
just as [L.P.’s] history suggests.” Second Schofield Rep. at 3. Dr. Schofield did not elucidate how
vaccination as a trigger for Petitioner’s underlying symptoms fits into the 30-day temporal window
discussed above.
14
Pursuant to Vaccine Rule 11(a), the parties may expedite entry of judgment by each filing (either jointly
or separately) a notice renouncing their right to seek review.
42