Miller v. Secretary of Health and Human Services

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 11-852V
January 31, 2017
To be Published

***************************************
L.A.M., *
*
Petitioner, * Human papillomavirus (“HPV”) vaccine
* (“Gardasil”); migraines; postural
v. * orthostatic tachycardia syndrome
* (“POTS”); chronic fatigue syndrome;
SECRETARY OF HEALTH * conversion disorder; undifferentiated
AND HUMAN SERVICES, * connective tissue disease (“UCTD”);
* small fiber polyneuropathy.
Respondent. *
***************************************
Patricia A. Finn, Piermont, NY, for petitioner.
Debra A. Filteau Begley, Gordon Shemin, Lara A. Englund, Washington, DC, for respondent.

MILLMAN, Special Master

DECISION 1

On December 6, 2011, when petitioner was still a minor, her father 2 filed a petition pro se
under the National Childhood Vaccine Injury Act, 42 U.S.C. §§ 300aa-10–34 (2012), alleging
that human papillomavirus vaccine (“Gardasil”) administered on December 3, 2008 caused his

1
Vaccine Rule 18(b) states that special masters shall make all decisions available to the public unless the
decision contains trade secrets or commercial or financial information that is privileged and confidential,
or medical or similar information whose disclosure would constitute a clearly unwarranted invasion of
privacy. When a special master files a decision, a petitioner has 14 days to identify and move to redact
such information prior to the document’s disclosure. If the special master, upon review, agrees that the
identified material fits within the categories listed above, the special master shall redact such material
from public access. See also 42 U.S.C. § 300aa-12(d)(4)(B)(i) and (ii). Because petitioner requested the
court reporter at trial to redact her name to initials, being under the impression that the transcript would be
publicly available (which is not the case), the undersigned is cognizant that petitioner would want this
decision also to be redacted. Therefore, sua sponte, the undersigned redacts it without petitioner’s
motion.
2
Petitioner’s father is a thoracic and cardiac surgeon at the medical center where petitioner received most
of her medical care.
daughter severe and debilitating headaches, photophobia, 3 phonophobia, 4 extreme fatigue,
dizziness, and gait disturbances. Pet. Preamble & ¶ 2. His daughter having reached the age of
majority, on February 2, 2012, the original petitioner moved to substitute his daughter as
petitioner, which motion the undersigned granted. The current petitioner is the vaccinee.

From December 6, 2011 until June 25, 2012, petitioner’s father (at that time, he was
petitioner) did not file any medical records. On June 25, 2012, petitioner’s father advised the
undersigned during a telephonic status conference he attended with petitioner that petitioner had
retained the services of an attorney, Patricia A. Finn. On July 16, 2012, Ms. Finn moved to
substitute as attorney of record, which the undersigned granted. Ms. Finn said she would obtain
and file the medical records.

On October 19, 2012, petitioner filed a Certificate of Completion, stating that she had
filed a complete set of medical records.

On November 13, 2012, the undersigned issued an Order to Show Cause why the case
should not be dismissed based on the medical records showing that the same symptoms about
which petitioner complained Gardasil caused had occurred prior to vaccination on two occasions,
i.e., in May and June 2007, which her treating doctors attributed to a virus. The undersigned
suggested in the Order to Show Cause that if petitioner wanted to continue her petition, she
should amend her petition to allege significant aggravation. In addition, the undersigned noted in
the Order to Show Cause that the symptoms about which petitioner complained Gardasil caused
had occurred two months after her second Gardasil vaccination in the immediate aftermath of a
sore throat, fever, and swollen glands on February 15, 2009, suggesting that this diagnosed upper
respiratory viral infection triggered the resumption of her pre-vaccination symptoms.

On November 16, 2012, the undersigned held a telephonic status conference with counsel
during which petitioner’s counsel asked for 90 days to find an expert.

On February 25, 2013, the undersigned held another telephonic status conference with
counsel during which petitioner’s counsel said she had contacted Dr. Yehuda Shoenfeld, an
immunologist, who was willing to provide an opinion, which she expected in a month.

Four months later, on June 24, 2013, petitioner filed Dr. Shoenfeld’s response to the
questions the undersigned raised in her November 13, 2012 Order to Show Cause (Exhibit 24)
and also filed Dr. Shoenfeld’s expert report (Exhibit 38). In his response to the Order to Show
Cause, Dr. Shoenfeld attributed petitioner’s condition to aluminum adjuvant in Gardasil vaccine,
basing his analysis on a theory of autoimmune (auto-inflammatory) syndrome induced by
adjuvants (“ASIA”). Ex. 24, at 3 (the pages of the exhibit are unnumbered; the undersigned is

3
Photophobia is “abnormal visual intolerance to light.” Dorland’s Illustrated Medical Dictionary 1441
(32nd ed. 2012) (hereinafter, “Dorland’s”).
4
Phonophobia is “irrational fear of sounds or of speaking aloud.” Dorland’s at 1435.
2
using the CM-ECF numbering). In his expert report, Dr. Shoenfeld discusses the new ASIA
syndrome, which he first described in 2011. Ex. 38, at 2. He also opines that Gardasil caused
petitioner’s postural orthostatic tachycardia syndrome (“POTS”) and chronic fatigue syndrome
(“CFS”). Id. at 6. He notes that POTS and CFS are manifestations of ASIA syndrome. Id. at
10.

On July 19, 2013, respondent filed the expert report of Dr. J. Lindsay Whitton, an
immunologist, disputing the validity of Dr. Shoenfeld’s ASIA hypothesis. Ex. A. On the same
date, respondent filed the expert report of Dr. Edward W. Cetaruk, a toxicologist and specialist in
emergency medicine, also disputing the validity of Dr. Shoenfeld’s ASIA theory. Ex. VV.

On July 26, 2013, Dr. Shoenfeld responded to Dr. Cetaruk’s expert report, defending the
ASIA syndrome. Ex. 137. On August 8, 2013, Dr. Shoenfeld responded to Dr. Whitton’s expert
report, defending the ASIA syndrome. Ex. 249.

On December 6, 2013, respondent filed her Rule 4(c) Report, stating that petitioner did
not have a compensable case.

Together with her Rule 4(c) Report, respondent filed reports from the following three
experts:
(1) Dr. Carlos Rosé, a pediatric rheumatologist (Exhibit RRR);
(2) Dr. Max Wiznitzer, a pediatric neurologist (Exhibit BBBB); and
(3) Dr. Stephen McGeady, a pediatrician and immunologist (Exhibit MMMM).

On March 13, 2014, Dr. Shoenfeld responded to the expert reports of Dr. Rosé, Dr.
McGeady, and Dr. Wiznitzer. Exs. 471, 472, and 473.

On November 18, 2014, petitioner filed the affidavit of her father. Ex. 551. He states
that on or about February 15, 2009, petitioner developed a sore throat, fatigue, low grade
temperature, and swollen glands, which lasted about one week. Id. at ¶ 5. He also states that on
or about February 20, 2009, petitioner began to develop a headache and said it was about a 5 out
of 10 on the pain scale. Id. at ¶ 6. On February 21, 2009, petitioner’s headache worsened and
was about 9 out of 10 on the pain scale. Id. at ¶ 7. She began to experience nausea,
photophobia, and phonophobia, and she had no appetite and refused to eat or drink. She lay on a
couch in a dark, quiet room and did not move. Id. On February 26, 2009, petitioner’s primary
care physician, Dr. Kennette, diagnosed her with migraines and prescribed Lortab and Imitrex.
Id. at ¶ 8. Because the medications did not work, petitioner returned to Dr. Kennette on March 2,
2009. Id. at ¶ 9. Petitioner could not find her balance to walk, although she never had true
vertigo or nystagmus. Id. Petitioner would seem to collapse onto the floor, explaining that her
legs just went weak and she cried all day and night. Id. at ¶ 10. Petitioner was prescribed
Depakene and Antivert, which also did not work. Id. On March 6, 2009, petitioner went to the
Albany Medical Center Emergency Room and received Compazine, Toradol, and Benedryl. Id.
at ¶ 11. Dr. Nichter, a pediatric neurologist, evaluated petitioner and she received Depacon,
3
Reglan, and Compazine. Id. Conversations with Dr. Nichter resulted in an increase in the
dosage of Topamax and the beginning of multivitamins, vitamin B-2, melatonin for sleep, and
Maxalt-MLT. Id. at ¶ 12. He increased her dosage of Topamax three more times. Id. at ¶¶ 12,
14, 17. On April 6, 2009, petitioner saw Dr. Nichter who ordered a steroid pulse and prescribed
Dexamethasone. Id. at ¶ 16. On May 4, 2009, petitioner saw Dr. Magdi Sobeih, a pediatric
neurologist at Boston Children’s Hospital, who found nothing wrong with petitioner. Id. at ¶20.
When Dr. Sobeih suggested petitioner see a psychiatrist or psychologist, petitioner told Dr.
Sobeih her opinion of his diagnosis. Id. On May 21, 2009, petitioner saw Dr. Nichter who
prescribed Elavil and told her to wean off Topamax. Id. at ¶ 23. He increased the dosage of
Elavil three times. Id. at ¶¶ 24, 27, 30. He also prescribed Ativan. Id. at ¶ 30. Hypnosis failed
to resolved petitioner’s headaches. Id. at ¶ 31. On September 8, 2009, Dr. Nichter discontinued
Ativan and started petitioner on Cymbalta. Id. at ¶ 32. On September 16, 2009, petitioner tried
Reglan and Depakote, and a higher dosage of Inderal and Cymbalta. Id. at ¶ 34.

On October 6, 2009, petitioner saw Dr. Nichter because she was having syncopal
episodes: she would see black spots and fall to the floor. Id. at ¶ 35. He noted petitioner had
tachycardia, and weaned her off Inderal. Dr. Nichter said physical therapy was imperative. Id.
On October 21, 2009, petitioner took Ambien for sleep issues. Id. at ¶ 37. On November 6,
2009, petitioner saw Dr. Charles Rheeman, a neuro-ophthalmologist, because she complained of
difficulties with reading. Id. at ¶ 39. Dr. Rheeman examined petitioner and found her normal.
Id. at ¶ 40. Dr. Rheeman thought stressors caused petitioner’s difficulties with reading, which
infuriated petitioner. Id. On December 4, 2009, Dr. Petri suggested petitioner take Plaquenil.
Id. at ¶ 43. On December 17, 2009, petitioner took Midrodine for POTS. Id. at ¶ 44. On
January 14, 2010, petitioner took Florinef. Id. at ¶ 45. On February 11, 2010, petitioner stopped
taking Florinef and started taking Midrodine again, and the doctor increased the dosage March
11, 2010. Id. at ¶¶ 47, 49. On March 1, 2010, Neurontin was increased. Id. at ¶ 48. (The
undersigned counts 23 medications listed in this affidavit, most of them for headache.)

On December 19, 2014, the parties filed a stipulation of interim attorneys’ fees and costs.
The undersigned issued a decision on the same date, awarding interim attorneys’ fees and costs
based on the stipulation.

On May 14, 2015, respondent filed a supplemental expert report of Dr. Rosé. Ex.
AAAAAA.

On June 11, 2015, petitioner filed additional medical records. Exs. 552, 553.

On June 15, 2015, petitioner filed her affidavit. Ex. 554. Petitioner states that on
February 15, 2009, she developed a sore throat, fatigue, a low-grade temperature, and swollen
glands, which continued for about one week. Id. at ¶ 5. On February 20, 2009, she developed a
very painful headache. Id. at ¶ 6. On February 21, 2009, her headache worsened and felt like it
was 9 out of 10 on the pain scale. Id. at 7. She also had nausea, photophobia, and phonophobia.
She had no appetite and refused to eat or drink. She lay on the couch in a dark, quiet room and
4
did not move. Id. Petitioner saw her primary care physician, Dr. Kennette, on February 26,
2009. Id. at ¶ 8. Dr. Kennette diagnosed her with migraines and prescribed Lortabs and Imitrex.
Id. On May 4, 2009, petitioner saw Dr. Magdi Sobeih, a pediatric neurologist, who concluded
there was nothing wrong with petitioner and suggested petitioner see a psychiatrist or
psychologist, which petitioner stated was extremely upsetting to her and traumatized her. Id. at ¶
16. She saw Dr. Steven Sandler, a pediatric psychiatrist, at the end of summer 2009, who told
her he did not suspect her symptoms were psychosomatic, but his attempt to help her headaches
with hypnosis failed. Id. at ¶ 25. Once petitioner started school in September 2009, her
headaches worsened and her improvement in her ability to walk and her gait declined, resulting
in her not attending school. Id. at ¶ 27. On October 6, 2009, petitioner saw Dr. Nichter. At this
point, she was having dizzy episodes where she would see black spots and fall to the floor. Id. at
¶ 29. She also had tachycardia. Id. On October 21, 2009, she saw Dr. Sandler again 5 for
sleeping issues. Id. at ¶ 30. He prescribed Ambien, which resulted in her having severe
disorientation and hallucinations. Dr. Sandler then prescribed Trazadone, but she did not take it
for fear of side effects. Id. On November 6, 2009, she saw Dr. Charles Rheeman, a neuro-
ophthalmologist, for her difficulties in reading but he thought that stress was causing those
problems. She became very upset “because I knew I was suffering from something that was real
and the doctor’s opinion seemed to dismiss everything I had been going through.” Id. at ¶ 33.
On March 1, 2010, petitioner saw Dr. Nichter who questioned the diagnosis of POTS and
petitioner’s being treated with steroids. Id. at ¶ 41. Petitioner states she continues to have
difficulty reading. Id. at ¶¶ 50, 51.

On June 22, 2015, petitioner filed additional medical records. Exs. 573, 574. On that
same date, respondent filed the supplemental expert report of Dr. J. Lindsay Whitton, discussing
and disagreeing with Dr. Shoenfeld’s ASIA theory. Ex. BBBBBB.

On June 24, 2015, petitioner filed additional medical records. Ex. 575.

From July 13-15, 2015, the undersigned held a hearing in this case. Petitioner provided
additional exhibits in this case, which were marked as exhibits 577 and 578 with a color version
of exhibit 576.

On July 21, 2015, respondent filed Ex. AAAAAAA (or for easier reading, Ex. 7A),
consisting of a medical history, dated August 1, 2010, which petitioner’s father prepared and
from which he testified. Petitioner’s father notes that petitioner’s first post-vaccination headache
occurred on February 20, 2009, which was five days after she had a severe sore throat, fatigue, a
low-grade temperature, and swollen glands, but 11 weeks and two days after her second Gardasil
vaccination, administered on December 3, 2008. Ex. 7A, at 1. He dates her inability to walk to
March 2, 2009, or 12 weeks (three months) after her second Gardasil vaccination, describing her
inability as an inability to find balance to walk, although never any true vertigo or nystagmus.
She would just seem to collapse onto the floor. She would describe her legs as just going weak.

5
Petitioner has not filed the medical record reflecting her visit to Dr. Sandler for sleeping issues.
5
Her pain was now 10++ and she was crying throughout the day and night. Id. He notes that on
May 28, 2009, petitioner had increased lower extremity weakness and her headaches were still
problematic. Dr. Nichter described her gait as abasia/astasia. Id. at 2. Petitioner began physical
therapy with Adrian Fil on July 14, 2009. Id. at 3. Petitioner had brain MRIs on March 18, 2009
and June 9, 2009. Both were normal. Id. at 2, 3. She had an EMG nerve conduction study on
July 20, 2009, the results of which were normal. Id. at 3. Petitioner’s father notes that school
began on September 10, 2009. Petitioner tried to make it at school with assistance, but the
crowds, noise, and light became too much. Her headaches worsened even though she had
improved over the summer in her walking and gait. Id. Petitioner’s father notes that petitioner’s
passing out episodes became problematic. She said she saw black spots and then fell to the floor.
She had tachycardia. Physical therapy was deemed imperative. Id. Petitioner’s father notes that
petitioner saw Dr. Sandler for help with sleep problems, and he prescribed Ambien. Petitioner
had severe disorientation and hallucinations that night, including seeing the death of her brother.
Dr. Sandler then recommended Trazadone, but petitioner was reluctant to take it because of her
experience with Ambien. Id. at 4.

Petitioner’s father notes that petitioner saw Dr. Charles Rheeman a neuro-
ophthalmologist because of her difficulty reading. Petitioner’s father notes that the office was
tiny with people and staff everywhere. Dr. Rheeman found petitioner normal after examination
and suggested that stressors were the root of her problem. Petitioner’s father writes that
petitioner promptly told Dr. Rheeman off. Id. Petitioner’s father notes that, from late March to
late April 2010, petitioner had a period of gradual good improvement. Id. at 5. Her headaches
were 3/10. Her school time increased to several hours each morning. She began to play the flute
again. She had been released from physical therapy, but stamina and fatigue were still
problematic. She enjoyed herself on a cruise during Easter break, but had times of needing to
crash. Id. Petitioner’s father notes that, beginning in late April 2010 through May, she had
severe worsening with headaches of “40”/10, according to petitioner. Id. On May 5 and 6, 2010,
petitioner’s father e-mailed petitioner’s story to Dr. Julian Stewart, a pediatric
electrophysiologist at Westchester Medical Center. He replied that petitioner’s blood pressure
that low while supine was not part of POTS at all. He said that even hypotension while upright
is not part of POTs, although late during a tilt-table test, there are gradual vasodepressor
responses. Dr. Stewart inquired whether petitioner had been checked for Addison’s and for any
other symptoms of autonomic failure. Id. (Dr. Stewart’s e-mail response is not part of the
record.) Petitioner’s father notes that, on July 29, 2010, after a consultation with Dr. Jill
Abelseth, an endocrinologist, a Cortrosyn 6 stimulation test for adrenocorticotropic hormone
(“ACTH”) was done, and the result was normal. Id. at 6. Petitioner’s father notes that petitioner
saw Dr. Peter Rowe, a pediatrician, at Johns Hopkins, who felt petitioner had chronic fatigue

6
Cortrosyn is “trademark for a preparation of cosyntropin.” Dorland’s at 422. Cosyntropin is “a
synthetic polypeptide identical with the first 24 amino acids of corticotropin, having the corticotropic
activity of corticotropin but lacking its allergenicity; used in the diagnosis of adrenal insufficiency by
plasma corticol response following subcutaneous, intramuscular, or intravenous injection.” Dorland’s at
424.
6
syndrome. Id. Petitioner’s father notes that from September 2010 to June 2011, petitioner was
back to school full time and missed only two weeks in total. He states she easily fatigued and
always had a headache. Her school absences were related to fatigue or headache worsening. Id.
Petitioner’s father’s chronology ends after June 2011.

On October 28, 2015, petitioner filed her posthearing brief.

On February 1 29, 2016, respondent filed her posthearing brief.

FACTS

Pre-vaccination Records

Petitioner was born on February 2, 1994.

On April 5, 2004, petitioner went to her pediatrician, Dr. Karen M. Kennette at Pondview
Pediatrics, complaining of having a cold for two and one-half weeks. Med. recs. Ex. 575, at 1.
She still had a low-grade fever and was sleeping nonstop. Her father was worried because she
had been sleeping a lot since she had a strep throat possibly in December. Id. On physical
examination, petitioner’s tympanic membranes were congested, her nose had copious drainage,
and her throat was beefy red with a thick post-nasal drip. Her nasal mucosa were inflamed with
the left nostril completely occluded. Id. A quick strep test was negative. Dr. Kennette
diagnosed petitioner with pharyngitis/sinusitis and prescribed Flonase, albuterol inhaler, and
Zithromax. Id.

Also on April 5, 2004, petitioner’s Epstein-Barr virus (“EBV”) nuclear antigen 7 was
weakly positive at 1:10. Med. recs. Ex. 8, at 16.

On March 14, 2005, petitioner saw Dr. Richard L. Uhl, an orthopedist, for a fracture to
her left ring finger. Med. recs. Ex. 14, at 1.

On April 4, 2005, petitioner returned to Dr. Uhl, complaining her ring finger was still
tender and painful. Id. at 2.

On April 29, 2005, petitioner returned to Dr. Uhl. Her finger fracture completely healed.
Id. at 3.

On October 24, 2005, petitioner went to Dr. Uhl with a right heel injury. The x-rays did
not show any abnormalities. Id. at 4.

7
Nuclear antigens are “the components of cell nuclei with which antinuclear antibodies [ANA] . . . react.”
Dorland’s at 105. “Antinuclear” is destructive to or reactive with components of the cell nucleus, as
antinuclear antibody.” Id. at 108.
7
 On April 6, 2006, petitioner went to Dr. Uhl, complaining of a right ankle injury, which
he diagnosed as a fracture. He recommended a short leg cast. Id. at 5.

On April 17, 2006, Dr. Uhl switched petitioner into an equalizer boot. The x-rays
showed no displacement. Id. at 6.

On April 25, 2006, petitioner saw Dr. Uhl on an urgent basis because of a new injury to
her right lower extremity. Id. at 7. She gave a history that her leg fell through a beach chair and
she hit her ankle. She had increased pain in her foot, ankle, and knee. She said her knee was
bruised. Dr. Uhl evaluated petitioner’s knee and found it was not particularly bruised or tender.
The ankle was slightly tender. X-rays showed absolutely no displacement from the initial films.
Dr. Uhl suspected this was a contusion. Id.

On May 6, 2006, petitioner saw Dr. Uhl, complaining of pain in her foot, which was
slowly improving. Id. at 8.

On June 26, 2006, petitioner saw Dr. John A. DiPreta, another orthopedist with the same
group as Dr. Uhl. Id. at 9. He said petitioner had a history of recurrent ankle injuries. Petitioner
and her mother felt she had not really gotten any better and the ankle was not quite right. She
had pain in various parts of her ankle since her injury. Petitioner had another injury on June 25,
2006 after getting out of the pool when her ankle gave out. She had sharp, shooting pains.
Petitioner and her mother were quite frustrated because they felt this interfered with petitioner’s
ability to participate in activities. On physical examination, her sensory exam was normal. The
range of motion of her ankle, hindfoot, and midfoot were within normal limits. Strength
measured 4+/5. X-rays were unremarkable. Dr. DiPreta’s impression was petitioner had right
ankle pain. He questioned whether petitioner had some sort of deconditioning and would benefit
from physical therapy. Id.

On March 30, 2007, petitioner saw Dr. Uhl for pain to the end of her right thumb. Id. at
10. X-rays were negative for fracture and the thumb did not droop. Id.

On June 6, 2007, when petitioner was 13 years old, she went to Pond View Pediatrics,
complaining that, for the prior six days, she had had severe headaches, great sensitivity to light,
and dizziness. Med. recs. Ex. 12, at 16 (same record at Ex. 574, at 3). She said she felt as if she
were on a boat. Id. She was afebrile and did not have cold symptoms. Id. When she stood up,
she felt very dizzy. Id. Dr. Kennette examined petitioner in a dark room where petitioner was
wearing dark sunglasses. Id. Petitioner’s gait was slightly slow secondary to her headaches. Id.
The doctor’s differential diagnosis was migraine, 8 Lyme disease, and viral meningitis. Id.

8
Migraine is “an often familial symptom complex of periodic attacks of vascular headache, usually
temporal and unilateral in onset, commonly associated with irritability, nausea, vomiting, constipation or
diarrhea, and often photophobia. Attacks are preceded by constriction of the cranial arteries, often with
8
 On June 7, 2007, petitioner’s father called Dr. Kennette to say that petitioner still had a
severe headache. Med. rec. Ex. 12, at 17 (same record at Ex. 574, at 6). On June 7, 2007,
because of petitioner’s headaches, she underwent a brain MRI. Med. recs. Ex. 552, at 46 (same
record at Ex. 574, at 1). It was normal. Id.

On June 8, 2007, petitioner’s mother called the pediatrician to say that petitioner was still
complaining of a headache. Med. recs. Ex. 12, at 18. It was absolutely no better. Petitioner was
taking her medicines and resting. She had to lie in a dark room. The mother said petitioner’s
brain MRI was negative and she wanted to know what else could be done. Petitioner’s mother
was very upset. Id. The pediatrician’s staff telephoned petitioner’s mother to take petitioner to
Albany Medical Center emergency room since her pain was no better. Id. Petitioner could get a
neurologist to check her there and obtain IVIG medications. Id.

On June 8, 2007, petitioner went to Albany Medical Center Emergency Department at the
suggestion of her pediatrician. Med. recs. Ex. 1, at 1. Dr. Noah White examined her and took a
history that she had an episode three weeks earlier while refereeing a children’s soccer match in
which she felt as if her head were spinning, and she had some headache associated with that
feeling. Id. She had had to sit down. Id. This episode resolved within 24 hours. Id. Petitioner
said she had been fine until about one week previously when she again developed a headache
similar to the previous headache. Id. It was bilateral and frontal. Id. She had only a mild
amount of dizziness. Id. She also had photophobia, phonophobia, and associated nausea. Id.
She saw her primary care physician, who recommended she have a neurology consult. Id. She
had some associated nausea, but no vomiting. Id. In addition, petitioner had been at the
Emergency Department on June 7, 2007 for the same problem, during which she participated in
tests, including a brain MRI. The test results were normal, except for a complete blood count,
which had an elevated white count of 10,600. Id. On physical examination, petitioner was
sitting in a darkened room and appeared to have a mild amount of discomfort. Id. Dr. White
diagnosed petitioner with migrainous headache, prescribed Compazine, and recommended she
have a neurologic consultation. Id. at 2. The neurologist on call was Dr. Jerome Haller, a
pediatric neurologist, who saw petitioner and agreed she had migrainous-type headache. Id. Dr.
Haller believed her history suggested she had a basilar migraine three weeks earlier, and
prescribed Imitrex with a follow up with a neurologist in six to eight weeks. Id. After the
administration of Compazine and Benadryl, petitioner said her headache had significantly
improved to a 2/10 from a prior 6/10. Id. The final diagnosis was migraine. Id. Dr. White also
discussed the case with Dr. Chame Blackburn, an emergency medicine physician. Id. at 2, 3.

On June 20, 2007, petitioner saw Dr. Uhl, complaining of reinjuring her right ankle.
Med. recs. Ex. 14, at 11. X-rays were normal. Id.

resultant prodromal sensory (especially ocular) symptoms . . .; the migraines themselves commence with
the vasodilation that follows. Two primary types are distinguished [migraines with aura and migraines
without aura]; the variety without an aura is more common.” Dorland’s at 1166.
9
 On August 14, 2007, petitioner complained to her pediatrician of being tired when she
was walking while on a trip with her family. It was unclear what was the etiology for her fatigue
when she was walking. Dr. Kennette told her to keep a log. Med. recs. Ex. 12, at 11 (same
record at Ex. 574, at 2.)

On December 10, 2007, petitioner saw Dr. Uhl, complaining of injuring her right ankle
again. Med. recs. Ex. 14, at 12. Dr. Uhl suspected a ligament sprain. Id.

On January 9, 2008, petitioner saw Dr. Uhl, who noted she was improving following her
sixth ankle sprain. Id. at 13. She needed to go to physical therapy. Id.

On March 14, 2008, petitioner saw Dr. Uhl with an injured left thumb. Id. at 14. This
appeared to be a sesamoid fracture. Id.

On March 25, 2008, petitioner returned to Dr. Uhl, complaining that the cast was
bothering her and that she had pain in her thumb. Id. at 15. Dr. Uhl removed the cast. New x-
rays showed the alignment maintained. All splints tried on petitioner were uncomfortable. They
settled on a particular splint. Id.

On March 26, 2008, petitioner’s mother called Dr. Uhl and said petitioner’s thumb was
discolored and quite cool. Id. at 16. They came in and Dr. Uhl removed the splint. He made a
new splint molded around the thumb, which she seemed to tolerate much better. He discussed
the possibility of a regional pain syndrome. Id.

On April 2, 2008, petitioner returned to Dr. Uhl with her left thumb looking better. Id. at
17. However, petitioner complained that her pain persisted and she held her hand in a flexed
position. Dr. Uhl recommended petitioner start Neurontin 100 mg. in the evening for nerve-
related pain. Id. Petitioner complained of numbness and tingling throughout the thumb. Id.

On April 14, 2008, petitioner returned to Dr. Uhl saying she was no better, but her thumb
in fact looked better. Id. at 18. Her hand was moving better. Dr. Uhl wanted to increase her
Neurontin to twice a day. Id.

On May 5, 2008, petitioner returned to Dr. Uhl, looking somewhat better. Id. at 19.

On June 9, 2008, petitioner returned to Dr. Uhl, having made minimal progress. Id. at 20.
She was unable to move her thumb particularly well. She had spasms when attempting to do so.
Her hand was not particularly swollen. Dr. Uhl suspected petitioner had a complex regional pain
syndrome in addition to her microtrabecular fractures. Id.

10
 On June 30, 2008, petitioner returned to Dr. Uhl, having reinjured her left thumb. Id. at
22. X-rays were negative. Id. He thought she should look for other causes of her discomfort.
Id.

Post-vaccination Records

On August 26, 2008, petitioner received her first Gardasil vaccination. Med. recs. Ex.
13, at 3.

On September 2, 2008, petitioner returned to Dr. Uhl with an injury to her left ankle.
Med. recs. Ex. 14, at 23. X-rays showed a non-displaced fracture. Her left thumb was doing
much better. Id.

On September 8, 2008, petitioner saw Dr. Uhl for a left distal fibula fracture. Id. at 25.
She was having problems with the cast rubbing her big toe. Dr. Uhl did not even see a fracture
on x-ray. But he thought she did have one. Id.

On September 22, 2008, petitioner returned to Dr. Uhl. Her left ankle fracture was
healing slowly. Id. at 24.

On October 8, 2008, petitioner saw Dr. Uhl, having reinjured her left ankle. Id. at 26. X-
rays did not show any specific abnormalities. Id.

On December 3, 2008, petitioner received her second Gardasil vaccination. Med. recs.
Ex. 13, at 3.

On February 26, 2009, two and three-quarters months after vaccination, petitioner went
to Pond View Pediatrics to see her pediatrician Dr. Kennette, complaining of a bad headache she
had since February 21, 2009, of feeling not good, and having weak pain, cold symptoms, nausea,
fever, dizziness, and photophobia. Med. recs. Ex. 12, at 26. That morning, she took two Advil
and drank ginger ale without any change in her headache. Id. She had been on Cipro 9 since the
prior Thursday. Id. Her father, a physician, wrote the prescription for Cipro for presumed
sinusitis. Id. The pediatrician diagnosed petitioner with photophobia, bitemporal squeezing
9
Cipro is the trademark name “for preparations of ciprofloxacin hydrochloride.” Dorland’s at 362.
Ciprofloxacin is “a fluoroquinolone antibacterial effective against many gram-positive and gram-negative
bacteria. . . .” Id. Some of the possible side effects of Cipro are: headache with chest pain and severe
dizziness; fainting; fast or pounding heartbeats; muscle pain or weakness; being more sensitive to
temperature, light touch, or the sense of body position; changes in mood or behavior, including
depression, confusion, hallucinations, paranoia, tremors, feeling restless or anxious, unusual thoughts or
behavior, insomnia, and nightmares; increased pressure inside the skull, including severe headaches,
ringing in the ears, vision problems, and pain behind the eyes; severe skin reaction, including a red or
purple skin rash that spreads; and nausea, vomiting, and diarrhea.
https://www.drugs.com/ciprofloxacin.html (last visited: January 7, 2017).
11
pain, and migraine. Id. Petitioner walked out of the doctor’s office holding onto her mother’s
arm. Id. The physician presumed petitioner had sinusitis. Id.

On March 1, 2009, at 8:30 p.m., the pediatrician’s office notes a telephone call regarding
petitioner. Id. at 27. Petitioner had had a headache for one week and saw Dr. Kennette, who
gave her Lortab and Imitrex and petitioner got some relief, but she was crying in pain and
nauseated. Id. She did not vomit, but had photophobia. Id. Petitioner was advised to try two
tablets of Lortab and see if they helped. Id. If petitioner did not have relief, she was told to go to
the emergency room. Id.

On March 2, 2009, at 10:40 a.m., the pediatrician’s office notes a telephone call
regarding petitioner. Id. Petitioner did not go to the emergency room. She took the Lortab and
in six to seven hours after she used ice, she seemed a little better. Id. Petitioner just woke up
about 20 minutes earlier. She still had a headache but it was not as bad. She had no other
symptoms and was not ill. Id. Petitioner could move her head and neck fine. Her mother would
watch her that day. If she got worse, she was to call back for an appointment that day. If she
woke on the following morning and still had a headache, she should call for an appointment that
day. Id.

On March 3, 2009, petitioner’s EBV nuclear antigen was weakly positive at 1:10. 10 Med.
recs. Ex. 8, at 16.

On March 6, 2009, petitioner went to the Albany Medical Center Emergency Department
where she saw Dr. Joshua J. Hurwitz, who admitted her as an in-patient. Med. recs. Ex. 1, at 4.
Petitioner said she had two and one-half weeks of migraine headache pain (putting onset in the
third week of February 2009, or two and three-quarters months after the second Gardasil
vaccination.) Id. She complained of alternating symptoms of pressure, stabbing, multilocational
pain, bitemporal pressure, vertigo, nausea and vomiting with low-grade fever. Id. She stated she
had had one previous episode like this in July 2008 (one month before her first Gardasil
vaccination) when she had a couple of weeks of headache pain, which the doctors diagnosed as
migraine after a normal brain MRI. Id. One new symptom was retro-orbital pressure and ataxia.
Id. She felt as if the room were spinning. Id. Her pediatrician was Dr. Karen Kennette. Id.
Over the prior couple of weeks, she had tried Percocet, Imitrex, NSAIDs, Benadryl, Compazine,
Depakene, and Antivert. Id. None of these medications addressed her pain. Id. On physical
examination, petitioner had a negative Romberg sign 11 yet she appeared to overcorrect with loss
of balance. Id. at 5. Her gait was narrow-based, but ataxic with petitioner requiring assistance in
order to ambulate without falling. Id.

10
This was the same result as on April 5, 2004 (pre-vaccination). Med. recs. Ex. 8, at 16.
11
The Romberg sign is “swaying of the body or falling when standing with the feet close together and the
eyes closed; the result of loss of joint position sense, seen in tabes dorsalis and other diseases affecting the
posterior columns.” Dorland’s at 1715.
12
 On March 6, 2009, on recommendation from Dr. Hurwitz, petitioner saw Dr. Charles
Nichter, a pediatric neurologist. Id. at 7. He took a history from petitioner and her parents. Id.
Unlike the history petitioner gave Dr. Hurwitz in the Emergency Department, petitioner told Dr.
Nichter that there was no clear nausea or vomiting with her headaches. Id. She also told him
that, two years previously (2007), she had a similar event, which was brief. Id. Petitioner’s
family history was positive for multiple sclerosis. Id. On physical examination, petitioner had a
normal gait. Id. at 8. She did tandem gait with “an ever so slight wobble.” Id. She hopped on
one foot and two feet. Id. She squatted without difficulty. Id. Dr. Nichter assessed petitioner as
having headaches and dizziness. Id. He felt she did not have concerning ataxia or vertigo. Id.
She also did not have nystagmus. Id. He felt her variety of medications might have been
exacerbating her headaches. Id. Dr. Nichter prescribed Reglan and then Depacon. Id. In future,
he would decide whether to prescribe Depakote or Topamax. Id.

On March 8, 2009, petitioner’s father telephoned the staff physician to report that
petitioner had a good day March 7, 2009, but on March 8, 2009, she had a headache of 9/10 and
difficulty sleeping the prior night. Id. at 11. She could walk with a little assistance. Id.

On March 13, 2009, Dr. Kennette wrote a letter to petitioner’s high school, explaining
that petitioner had been unable to attend school for the prior two to three weeks due to severe
daily headaches. Petitioner had been unable to sit, stand, or concentrate long enough to attend
classes. Id. at 33.

On March 16, 2009, petitioner’s mother telephoned Dr. Nichter to say that petitioner was
a little better, had less headache, and functioned better. Med. recs. Ex. 1, at 12. Petitioner went
walking for half a block the day before. Id. She had some dizziness and a sense of spinning. Id.
She was able to get out of bed and went to school for half a day the prior week. Id. Dr. Nichter
advised increasing petitioner’s vitamin B2 and continuing on multivitamins with B complexes
and magnesium. Id. She was to continue on Topamax. Id.

On March 18, 2009, petitioner underwent a brain MRI because of her migraine
headaches. Med. recs. Ex. 552, at 45. The MRI was normal. Id.

On March 26, 2009, Dr. Nichter saw petitioner with her parents as a follow up visit to his
initial visit with her in the Emergency Room on March 6, 2009 for migraines. Med. recs. Ex.
553, at 115. Petitioner gave Dr. Nichter a history that she had a sore throat after receiving
Gardasil vaccine, and then, a week or two afterwards, had significant migraine headaches. Id. at
116. Since the emergency room visit, petitioner’s mother states petitioner was better. Id. Her
headaches started at 2-3/10 in the morning. Id. By the afternoon, they might increase to 4-5/10,
and by evening, 8/10. Id. She did not have stabbing, sharp pains. Id. The headaches were more
throbbing and pressure-like. Id. She had significant photophobia and significant vertigo. Id.
Overall she was minimally to mildly better. Id. Petitioner’s headaches, vertigo, and photophobia
made her dysfunctional even when she wore sunglasses. Id. Petitioner did not have frank
weakness, but rather just unsteadiness. She did not have marked lethargy or unresponsiveness.
13
She did not have any activity to suggest seizures. There was a family history of multiple
sclerosis, but no headaches. Her brain MRI, MRA, and MRV were unremarkable. Id. On
physical examination, she had no focal weakness. She could hop on one foot and two feet, but
required support from a table or a chair. Id. at 117. She could walk 10 feet, but often sought her
mother’s support. Id. Dr. Nichter’s assessment was that her significant migraine might relate to
Gardasil, “although there is no clear literature to support that.” Id. His plan was to increase
petitioner’s vitamin B2 and her Topamax dosage. Id. He considered steroids (Decadron or
prednisone) in the future. Id.

On March 31, 2009, Dr. Kennette’s office received a telephone call from petitioner’s
mother. Med. recs. Ex. 12, at 35. Petitioner’s mother wanted the lot number of the Gardasil that
petitioner had received. She said that petitioner’s headaches had been ongoing since petitioner
received Gardasil. In addition, a friend had received the same lot number of Gardasil and she
had the same problem as petitioner. Id.

Also on March 31, 2009, Dr. Kennette filled out a VAERS (Vaccine Adverse Event
Reporting System) form, writing that petitioner received Gardasil on December 3, 2008 and the
onset of her vaccine reaction on February 21, 2009 or eleven weeks and three days later. Med.
recs. Ex. 12, at 34. The only adverse event Dr. Kennette described was protracted headache. Id.
Dr. Kennette states on the VAERS form that petitioner recovered. Id.

On April 6, 2009, petitioner and her parents saw Dr. Nichter again. Med. recs. Ex. 1, at
16. She had slight improvement, but on Thursday night and Friday, she was working on a school
project and sleep was difficult. Id. On Friday, her headaches were 9/10 to 10/10, bitemporal,
and crushing, associated with photophobia, and phonophobia. Id. She did not vomit, but her
appetite had significantly decreased, and she had lost four pounds. Id. She swayed from side to
side and, sometimes, her legs felt like jello with her knees about to give out. Id. Sometimes, the
fragrance of foods nauseated her. Id. On physical examination, petitioner could sit but tended to
lean. Id. at 17. When she walked, she leaned along furniture without frank ataxia, but with a
leaning on objects kind of gait. Id. She could not stand independently. Id. Dr. Nichter assessed
petitioner as having minimally improved migraine, and a wobbly gait although not formally
vertigo (she said nothing was spinning or tilting), and no clear ataxia. Id.

Also on April 6, 2009, petitioner’s ANA was 1:640 with an atypical discrete speckled
pattern. Med. recs. Ex. 1, at 19.

On April 13, 2009, petitioner and her parents saw Dr. Nichter again. Med. recs. Ex. 1, at
19. She had significant photophobia, but her blurred vision resolved. Id. She had a slight
improvement in appetite. Id. Besides her headaches, her gait was of concern. Id. Her legs
seemed to her as if they were going to give in. Id. At times, she had more of a slither to the
ground than a frank direct fall from a standing position. Id. She had a little left neck tenderness
that appeared mild. Id. After a physical examination, Dr. Nichter wrote her migraines had

14
improved, petitioner had minimal to no vertigo and minimal to no ataxia. Id. at 20. She had a
wobbly gait, without evidence of posterior column dysfunction. Id.

On April 22, 2009, Dr. Kennette’s office called petitioner’s mother. Med. recs. Ex. 12, at
37. Petitioner still had daily headaches, which were worse at night, and felt that her legs were
not part of her body. She was unable to walk without holding onto objects. She had been unable
to attend school for the past month. There was a lot of stress at home since petitioner’s maternal
grandmother died on March 22, 2009 and petitioner’s father had surgery during the past month.
Id. Petitioner’s father was meeting with Dr. Sarah Elmendorf and would like Dr. Kennette to
call him. Id. Dr. Kennette’s office notes on April 23, 2009 that there were telephone calls over
the prior 24 hours with petitioner’s mother, father, and Dr. Elmendorf. Id. at 39. Petitioner was
not improving at all. She had headaches, weakness, poor appetite, and had lost some weight. Id.

On April 23, 2009, petitioner’s mother phoned Dr. Kennette’s office. Id. at 38. She
wanted the vaccination dates and lot numbers for the Gardasil petitioner received and the name
of who administered the vaccination. This information had been previously sent to petitioner’s
mother, but she misplaced it and needed it immediately because she, her husband, and petitioner
were going to Boston and putting together a log of events. In addition, she wanted the dates of
petitioner’s visits for headaches. Dr. Kennette’s assistant started with June 2007. Id.

On April 24, 2009, petitioner’s father called, concerned that petitioner now complained
of muscle pains and had Theraband for home exercises. Id. at 40. There was a question whether
her symptoms represented a myositis syndrome or if she had conversion syndrome because of
astasia-abasia. Id.

On April 28, 2009, petitioner’s mother called Dr. Kennette’s office. Id. at 41. Petitioner
was getting worse. Dr. Kennette was supposed to be setting up a visit to a doctor in Boston.
Petitioner’s father wanted to speak to Dr. Kennette. Id.

On May 1, 2009, petitioner visited Dr. Kennette for a reevaluation of her “weakness”
(which Dr. Kennette put in quotation marks) and headaches. Id. at 42. Petitioner had not been in
school for two months and was unable to walk or stand from a sitting position without assistance.
Her feet felt cold and she weighed 116.5 that day. Petitioner walked down the hall hugging the
wall. She sat in a dark room with sunglasses on. When she sat on the examination table, she
leaned against the wall. Her muscle tone had decreased. The strength in her lower extremities
seemed to be 4+ to 5 out of a maximum of 5. Her deep tendon reflexes in her lower extremities
were difficult to elicit. Petitioner’s mood was depressed but her orientation normal. She felt
tired, sad, and frustrated. She had normal skin temperature and color over her feet and hands.
She was wearing a T-shirt, sweatshirt, and heavy sweat pants. The outside temperature was
about 65 degrees. Petitioner had protracted inability to walk without support, a persistent
“migraine”-like headache (Dr. Kennette put “migraine” in quotation marks), mild anorexia, an
eight-pound weight loss over 8-10 months, and mild depression. She questioned whether
petitioner had an undiagnosed neuromuscular condition. Id.
15
 On May 4, 2009, petitioner saw Dr. Magdi Sobeih, a behavioral neurologist, at Children’s
Hospital in Boston. Med. recs. Ex. 2, at 1. Dr. Sobeih saw petitioner to evaluate her headache
and walking difficulties. “After a thorough evaluation I have concluded that there are no
neurobiological abnormalities or neuropathological concerns to [petitioner]’s complaints.” Id.
Dr. Sobeith recommended petitioner participate in therapy and take Elavil. He did not
recommend that she have any further neurological workup but follow up with her primary
physician. The history petitioner’s parents gave was that during February break, petitioner
complained of a sore throat and was ill for one week. On Monday, she went to school but the
school sent her home because she was feeling ill. On Tuesday, she went back to school and
complained of headaches with a stabbing type of pain all around, more on the right side. She
described it as vise-like, which then progressed to a pressure-like headache. She stated it felt as
if someone were dropping an anvil on it. She described pressure all around her head. None of
the therapeutic interventions made any difference. Loud noise or attempts to read made her
headaches worse. Her appetite decreased and she lost ten pounds. Certain smells bothered her.
She complained of dizziness. She felt unsteady and needed to lean on a wall. This resulted in
her inability to ambulate effectively. She tended to slide along a wall. “There has been some
suggestion of temporal association according to the family with [petitioner] having received the
HPV vaccine and then subsequently had the sore throat and a week later having headaches.” Id.
Because of her headaches, her doctor started her on Topamax, vitamin B2, magnesium, a
multivitamin, and Ibuprofen. None made any difference to her headache in any way. Id. at 2.
The most recent symptoms had been difficulty in ambulation. She felt as if she were swaying
from side to side and her legs and knees were going to give out. She had to lean on a wall in
order to get up or to walk. She also wore dark glasses because light bothered her eyes. She was
unable to attend school for many weeks and had a home tutor. All of petitioner’s lab work was
negative. She had negative Lyme titers, negative Epstein-Barr virus titers, and a normal C-
reactive protein of 0.2. Dr. Sobeih believed petitioner’s antinuclear antibody of 1:640 with an
atypical discrete speckled pattern was probably a false positive. Her sedimentation rate was
eight, which is normal. Id. Her DNA antibody was negative for double-stranded DNA. Id. at 2-
3. Her brain MRI, MRA, and MRV were normal. Id. at 3. On physical examination, petitioner
could not bear weight on her legs and walk. She complained of photophobia and covered her
eyes. On gait testing, petitioner had a significant amount of astasia-abasia. 12 She had a

12
Abasia-astasia or astasia-abasia is “motor incoordination with an inability to stand or walk despite
normal ability to move the lower limbs when sitting or lying down, a form of hysterical ataxia.”
Dorland’s at 167. Hysterical ataxia is “ataxia that is part of a conversion disorder.” Id. at 171. Ataxia is
“failure of muscular coordination; irregularity of muscular action.” Id. at 170. Conversion disorder is “a
mental disorder characterized by conversion symptoms (loss or alteration of voluntary motor or sensory
functioning suggesting physical illness, such as seizures, paralysis, dyskinesia, anesthesia, blindness, or
aphonia) having no demonstrable physiological basis and whose psychological basis is suggested by (1)
exacerbation of symptoms at times of psychological stress, (2) relief from tension or inner conflicts
(primary gain) provided by the symptoms, or (3) secondary gains (support, attention, avoidance of
unpleasant responsibilities) provided by the symptoms. . . . [H]istrionic personality traits are also
common. Symptoms are neither intentionally produced nor feigned. . . .” Id. at 549. “Histrionic” is
16
completely functional 13 gait without weakness. Sensory examination and coordination were
normal. She did not have dysmetria or ataxia. Dr. Sobeih wrote:

I had a long discussion with the parents that there is no
neuropathological finding. There is no focality on neurological
exam; there is no neurological cause for [petitioner]’s symptoms.
This did present as a functional gait disturbance.

Id. Dr. Sobeih recommended that petitioner have ongoing counseling. He stated, “I do not feel
there is any association between the Gardasil HPV vaccine and the onset of these symptoms.”
Id. He continued:

I discussed this at length with the parents. I discussed that this is
presenting as a mood disorder that needs appropriate care. . . . It
would be very important to[o] that [petitioner] continue under the
care of appropriate psychological or psychiatric services and
someone to monitor her response to any medications such as
amitriptyline. However I do not feel there is any need for any
further neurological workup or followup. I discussed this with the
parents and with [petitioner] and I counseled further mental health
care should be provided.

Id. at 3-4.

On May 5, 2009, petitioner’s mother called Dr. Kennette. Med. recs. Ex. 12, at 44. The
consultant in Boston felt petitioner had nothing neurologically wrong with her, that she never
had migraines, and was depressed. Id.

Also on May 5, 2009, Dr. Kennette filled out a child and adolescent psychiatric telephone
consultation request to Four Winds Foundation, asking if a psychiatrist would see petitioner for
conversion syndrome. Id. at 48. Petitioner had been seen in Boston where she received an
assessment of “no neurological disease” and a question arose concerning whether petitioner were
depressed and should have a trial antidepressant and therapeutic counseling. Id. The
recommendation was to have petitioner’s parents call for an appointment.

“excessively dramatic or emotional; of or relating to the behavioral characteristics of histrionic
personality disorder.” Id. at 864. Histrionic personality disorder is “a personality disorder marked by
excessive emotionality and attention-seeking behavior.” Id. at 550.
13
A functional disorder is “a disorder of physiological function having no known organic basis. . . . [T]he
term is often used in psychiatry as roughly equivalent to ‘psychogenic disorder’ . . . .” Dorland’s at 550.
17
 On May 6, 2009, petitioner’s mother called Dr. Kennette. Id. at 45. Petitioner was going
back to school. The school needed a note stating she could return and limit herself to part-time
attendance. Petitioner would be in a wheelchair. Id.

On May 7, 2009, Dr. Kennette called petitioner’s father to discuss where to go from
there. Id.

On May 8, 2009, a nurse’s note from Dr. Kennette’s office states that petitioner was
concerned because Boston doctors suggested a psychiatrist assess her. Id. at 47. Petitioner
requested a meeting with Dr. Kennette to discuss this. In addition, when petitioner’s mother
brought the doctor’s note to school, indicating petitioner would be coming back to school part-
time, the mother ran into petitioner’s former coach and gym teachers. While discussing
petitioner, the coaches indicated that a lot of girl athletes seemed to be “sick” (the nurse used
quotation marks around “sick”) now and were unable to do sports. Petitioner’s mother was
obtaining a list of the girls’ names from the teachers and coaches and was having the parents call
her to see if these girls’ sicknesses were associated with Gardasil. Id.

On May 8, 2009, Dr. Kennette met first with petitioner’s parents and spoke to them for
20 minutes. Id. at 46. Then, Dr. Kennette met with petitioner and spoke to her for about an hour
alone. They discussed how petitioner felt, what had and had not helped, the need for her to go
back to school, strategies for coping with food, sound and light sensitivity, dealing with parental
and friends’ expectations, etc. Dr. Kennette emphasized that petitioner needed to go back to
school, with or without a wheelchair, on a full-time basis. She needed to work with the gym and
music teachers for alternative work, e.g., physical therapy sessions instead of gym, composition
instead of playing in music class. Petitioner needed to check with her neurologist regarding her
use of Topamax since it was not helping. Perhaps she should start a new medicine such as Elavil
for headache and mood. She needed a positive outlook on improvement. Id.

On May 12, 2009, petitioner saw Dr. Jason Mouzakes, an ear, nose, and throat specialist,
for a vestibular evaluation. Med. recs. Ex. 4, at 1. Petitioner was taking melatonin,
multivitamins, Topamax, and Vitamin B-12. She complained of an eating disorder, migraine
headaches, and vertigo. Petitioner gave a history that, over the prior three months, she had
episodes of debilitating headache and dizziness, as well as photophobia, nausea, and
phonophobia. She had tried several medications including Antivert and Depakene without
improvement. She had a normal head MRI. All lab work, including Lyme titer, was normal. Id.
Dr. Mouzakes wrote that petitioner’s physical examination was reassuring. Id. at 2. He ordered
that petitioner have an ENG study for further evaluation of her inner ear balance system. He also
ordered an audiogram to evaluate her middle and inner ear findings. Since petitioner had missed
more than three months of school, he would expedite the ENG testing. Id.

On May 13, 2009, petitioner had audiologic testing at the hearing center at Albany
Medical Center Hospital. Id. at 3. Under “Complaint” is the note that onset of symptoms of
dizziness and hypersensitivity to sounds and light was in February 2009 “correspond[ing] with
18
the administration of Gardasil vaccine” (although the vaccine was administered December 3,
2008). Id. Petitioner’s hearing test results were normal bilaterally. She had normal middle ear
function and normal outer hair cell function in the cochlea. Id.

On May 14, 2009, petitioner and her parents saw Dr. Nichter. Med. recs. Ex. 1, at 22.
Since her last visit to Dr. Nichter, she had seen a pediatric neurologist in Boston who thought
petitioner had a major psychological or psychiatric component to an ill-defined headache
syndrome. Id. The Boston doctor was not convinced petitioner even had migraines. Id.
Petitioner’s mother said petitioner’s headaches were better since Dr. Nichter first saw petitioner
in the ER, but they were quite variable. Id. On May 13, 2009, petitioner underwent vestibular
testing and she had a significant headache. Id. But, at other times, her headaches were better.
Id. She still had photophobia and phonophobia. Id. Normal sounds were extremely loud and
regular lights created major photophobia. Id. What Dr. Nichter found most pronounced was
petitioner’s abasia-astasia type gait (consistent with Dr. Sobeih’s diagnosis). Id. She would
lurch onto an arm or side of a chair or a wall. Id. At night, she would fall to the floor and sort of
get up to go to the bathroom. Id. She stated it was difficult for her to concentrate even with a
homebound school program for a few hours. Id. She was unable to walk, and had decreased
appetite. Id. Smell or fragrance of food was problematic. Id. at 22-23. On physical
examination, she bore weight but had swaying when she tried to walk. Id. at 23. However,
when Dr. Nichter swayed in the opposite direction while walking with petitioner, petitioner
seemed to adjust her swaying and, when he moved her arm in a different way, she also adjusted
accordingly. Id. When Dr. Nichter tested her sensation, petitioner said “sharp” when he placed a
dull object on her leg. Id. However, she was not consistent when he placed sharp and dull
objects on the same area. Id. Dr. Nichter prescribed Elavil and suggested decreasing Topamax.
Id.

On May 18, 2009, Dr. Kennette wrote a letter to petitioner’s high school, requesting
permission for petitioner to return to school on a graduated basis. Med. recs. Ex. 12, at 49.
Petitioner was trying to regain strength and ambulation, but might need to use a wheelchair
between classes and asked for accommodation for her to do so. In addition, Dr. Kennette asked
the school to work with petitioner’s family in obtaining any necessary academic support to make
up work she missed, including tutoring. Id.

On May 22, 2009, Jamie Steck, a pediatric physical therapist, evaluated petitioner. Med.
recs. Ex. 11, at 1. Petitioners’ parents and neurologist, Dr. Nichter, referred petitioner for
physical therapy because of parental ongoing concerns regarding her inability to walk
independently, unstable standing balance, weakness, and decondition noted since she had a sore
throat about three months earlier just prior to February School Vacation week. Id. A few days
after the sore throat, she complained of headaches. On Friday of that vacation week, petitioner
had significant sensitivity to light and sound, was exhausted, and complained of severe headache.
She was given migraine medication, but had no change. She subsequently went to Albany
Medical Center emergency room for severe headaches and was given a migraine cocktail
combination, but reacted to the medicine. She had frantic, anxious behavior, which led to her
19
being seen by a neurologist. Dr. Nichter prescribed a multivitamin, Topomax, and Elavil. She
continued to complain of headaches that were band-like on the lateral side of her head. Her
headache symptoms increased with neck hyperextension and rotation motions. Boston
Children’s Hospital neurology also evaluated petitioner and petitioner’s mother reported that the
hospital thought her symptoms were psychological. Petitioner had a very limited diet due to
sensitivity to smell and taste. She had lost 20 pounds since becoming ill. She had progressively
greater difficulty with balance and standing and got weaker as time passed.

Petitioner also said she could not make her legs do what she wanted them to do and they
felt as if they were going to give out on her. P-T Steck was concerned about petitioner’s
severely limited standing balance, inability to walk independently, decreased coordination, speed
of her limb motion noted more in the left leg than in the right, and decreased positional sense of
her left lower extremity. Dr. Mouzakes evaluated petitioner for vestibular problems, and ruled
out vertigo. She had a negative MRI and a normal EEG. Previous neurological examinations
did not reveal any neurologic involvement despite her inability to sustain balance independently
or to coordinate independent gait. Petitioner’s mother reported she had been “clutsy” as a child
and often injured herself playing soccer. She fractured her left ankle in August 2008.
Petitioner’s mother wondered if petitioner’s second Gardasil vaccination in December 2008
affected petitioner’s current status. Petitioner’s mother reported petitioner currently attended
school two hours a day while sitting in a wheel chair, and was exhausted upon return home.
Petitioner had been an A student and now had extreme difficulty reading and attending at school.
Petitioner reported that, while reading, things became blurry and words moved on the page. She
continued to have light sensitivity and her eyelids drooped over half of her eye throughout the
evaluation. Petitioner presented with a low affect and tended to look in a downward gaze with
her neck held in a forward flexed position with a slight rotation to the left. Despite being given
verbal prompts to encourage eye contact or hold her head up, she continued to posture her neck
down. During gross visual testing, petitioner was able to move her eyes in all directions, and P-T
Steck noted petitioner’s eyelid motion, but, at rest in sitting, her eyelids were lowered covering
half of her eyes. Id. Petitioner reported having a very difficult time keeping up with her school
work, and falling a lot at home. Id. Petitioner showed a decrease in the rate of her language
output and a slow reaction time in answering questions. Id. at 2.

Petitioner had muscle tone on the low end of normal throughout her trunk and
extremities. Id. When supported with maximum assistance in standing, petitioner laterally
glided and pushed her weight dangerously toward the right in dystonic motion. She presented
with ataxic arm and leg motions, especially in the left leg. During assisted standing, petitioner
held her left leg abducted and externally rotated at her hip, with the knee in hyperextension.
While attempting assisted steps, petitioner circumducted her left leg (circled her leg from the hip
to generate swing phase), showed plantar flexion (foot drop), and then hyperextended her knee
upon weight bearing with a flat foot placement that maintained her left ankle in a plantar flexed
position. Id. Petitioner had generalized muscle weakness throughout her trunk and extremities
due to deconditioning. During manual muscle testing, she had strength within functional limits
through her trunk and extremities at a good minus grade with the exception of left ankle eversion
20
and supination control, which was fair. Petitioner was able to lie down and sit up on her own,
but her movement showed decomposition, which was slow and mechanical like a puppet. She
showed incoordination in all functional movement. Her grip strength was weak, but her writing
skills remained intact. Id. P-T Steck recommended physical therapy three times a week. Id. at
4. She spoke with petitioner’s neurologist and pediatrician, and her neurologist would see her
again. Her symptoms and movement pattern were typical for cerebellar involvement. In
addition, her limited diet and nutrition had an effect on her symptoms. P-T Steck recommended
an ophthalmologist examine petitioner considering her visual concerns. She recommended home
exercises.

On May 28, 2009, petitioner and her parents saw Dr. Nichter on an urgent basis for
petitioner’s weakness, gait disturbance, and migraine. Med. recs. Ex. 1, at 25. A physical
therapist thought she had weakness in her left leg and foot drop. Petitioner’s mother stated she
did see a circumduction of petitioner’s left leg at times although there was no catch at the left
foot or stumbling. Petitioner would turn her left foot in at times. This was noticeable when
petitioner had significant activity or a stressful day. There was no new weakness in her arm or
weakness in her face. It was not clearly related to the severity of her migraines. There was no
new ataxia. If there were a social event where music played, petitioner’s headache would be
quite severe. She used sunglasses a bit less now than previously. She had stopped Topamax and
vitamin B2. Id. She was taking magnesium, multivitamins, and Elavil. Id. at 25-26. Physical
examination showed full strength in her arms, but occasional give-away weakness in the
quadriceps and hamstrings. Id. at 26. She had variable responses to position sense, but she was
correct at least 75 to 85 percent of the time. Id. Vibratory sense was normal. Id. When
petitioner walked, she still lurched to one side or the other. Id. At times, she would invert her
left foot, but there was never a foot drop. Id. The foot inversion was intermittent, i.e.,
inconsistent. Id. Dr. Nichter assessed petitioner’s migraines and photophobia as a little bit
better. Id. Her gait remained in the abasia-astasia category. Id.

On June 7, 2009, petitioner had a brain MRI done because of her headaches. Med. recs.
Ex. 574. Her brain MRI was negative. Id.

On June 25, 2009, petitioner saw Dr. Hilaire J. Meuwissen, an allergist and
immunologist. Med. recs. Ex. 573, at 1. Petitioner’s illness began approximately February 15,
2009 with a severe sore throat and fatigue, low-grade temperature, and swollen glands for about
a week, about two months after she received her second Gardasil vaccination. Id. No doctor
made a definite diagnosis after migraine therapy failed. Petitioner told Dr. Meuwissen that
concentration was difficult and reading not easy because words moved back and forth and
became larger and smaller haphazardly. Id. Petitioner walked close to the wall with support
from the wall and reported she had many bruises from bumps and almost falling. Id. at 2. She
looked pale and distressed and wore sunglasses because of extreme sensitivity to light. She was
very sensitive on percussion of her frontal and maxillary sinus. Dr. Meuwissen’s assessment was
that petitioner might have a neurologic condition that her upper respiratory infection in February
caused. Id. There was a remote possibility she might have a variant form of Guillain-Barré
21
syndrome secondary to Gardasil vaccination although the interval between vaccination and onset
was long. Id.

On June 30, 2009, petitioner’s antinuclear antibody (“ANA”) was 1:640 in an atypical
discrete speckled pattern. Med. recs. Ex. 8, at 17.

On July 6, 2009, petitioner and her parents saw Dr. Nichter. Med. recs. Ex. 1, at 28.
Petitioner had undergone a brain MRI and MRA, both of which were normal. Her family said
petitioner was 30 to 40 percent better. Her headaches were fewer, lasting an entire day or a few
hours. She was able to walk more upright, although she still needed support. She could tolerate
sunlight and her appetite was better. Her mood and disposition were better. She complained of
belly pain twice a week. Id. On physical examination, her strength was 5/5 with occasional
giveaway weakness. Id. at 29. She had less lurching gait. She took two to three steps on her
own without leaning as much. There was no foot drop or involuntary movement. Dr. Nichter’s
assessment was that petitioner’s migraines and abasia-astasia were both improving. Muscle
strength testing was quite variable as she had giveaway weakness but sometimes she generated
more force. Id.

On July 14, 2009, petitioner started physical therapy with Adrienne Fil at Sunnyview
Rehabilitation Hospital. Med. recs. Ex. 11, at 6. According to Ms. Fil’s record of August 13,
2009, after 14 P-T sessions, petitioner’s “physical presentation with mobility continues to be
incongruent with objective measurements.” Id. at 8. Ms. Fil questioned the possibility of
petitioner having a conversion disorder. Id. When Ms. Fil drew less focus to petitioner’s
impairments, petitioner had spontaneous improvement in her lower extremity function. Id. at 8-
9. Petitioner’s mother became concerned about petitioner continually blacking out and
collapsing. Id. at 9. During the P-T session, petitioner was standing for at least 50 minutes of
the hour-long session without difficulty while doing activities. Id. Ms. Fil was aware that
petitioner was referred for a psych intervention earlier in her diagnosis and petitioner became
physically worse. “Perhaps with her physically improving now she may be more open to
counseling. . . .” Id. Ms. Fil mentioned this to petitioner’s parents, but not to petitioner directly.
Id.

On July 20, 2009, petitioner had a nerve conduction study (“NCS”), electromyography
(“EMG”), and F Wave test done to determine if she had inflammatory neuropathy. Med. recs.
Ex. 9, at 6. Dr. Matthew J. Murnane concluded the tests were normal without evidence of a
peripheral neuropathy. Id. at 7.

On August 10, 2009, petitioner’s father wrote Dr. David Cornbluth, stating that petitioner
in February 2009 developed what seemed to be a viral illness two months after a Gardasil
immunization. Med. recs. Ex. 3, at 3. This rapidly progressed to severe headaches, photophobia,
phonophobia, complete loss of appetite, and a balance/gait disturbance. A multitude of testing
was unrevealing. She had been out of school since February with home tutoring since then. She
would sit in a dark, quiet room, unable to tolerate playing her flute, with no stamina for any
22
activity, although previously she had been an avid flute player and on the soccer and track teams.
Standard migraine prescriptions were not helpful, including IV Depakote. Previously, petitioner
was wheelchair-bound or wall walking only. Now she did some walking on her own.
Petitioner’s father asked if Dr. Cornbluth would be willing to see petitioner. Id.

On August 12, 2009, Dr. Kennette recorded petitioner’s 15 year and six month old visit.
Med. recs. Ex. 12, at 50. Petitioner was doing physical therapy at Sunnyview with Adrienne Fil
at least three times a week since the end of June. Petitioner’s nerve conduction and EMG studies
were normal. Id. Petitioner’s sensation was stronger on her right. She was currently taking
Periactin, multivitamins, and Elavil. She had gained two pounds. Her blood pressure was
108/64. She weighed 113 and ¼ pounds. Her height was 5’5 and ¼ inches. Her BMI was 18,
which put her in the 10-25% group. She was wearing sunglasses. She had cool, bluish feet. Her
left calf was smaller than her right calf. Her proximate strength was 4+/5. Petitioner had
ongoing issues with gait, headaches, photophobia, hyperacusis, 14 change in taste, and food
aversion for five to six months. Id. There was no specific diagnosis made up to that date.
Petitioner’s parents were considering consulting with Dr. David Cornbluth in Baltimore. There
was a follow up with the neurologist the following week. Perhaps petitioner should have a
lumbar puncture. Id.

On August 17, 2009, petitioner and her parents saw Dr. Nichter. Med. recs. Ex. 1, at 31.
Petitioner underwent EMG and nerve conduction studies, which were normal. Since Dr. Nichter
last saw petitioner on July 6, 2009, she had had “enormous variability.” Id. She could walk on a
board, walk independently, and, on one occasion, walk a few miles. The headaches were
variable, from mild to so severe she was weeping. She had photophobia and phonophobia. She
had a significant decrease in appetite. Petitioner’s father was researching vaccine-related
individuals. Id. On physical examination, petitioner could walk and move from chair to
standing. Id. at 32. She took several steps walking on her own and leaned on the side of the wall
as she moved from the clinic to the checkout area. She did not have footdrop. There was an
occasional inturning of her left foot. Id. Dr. Nichter’s assessment was that petitioner was
improving and her gait was significantly better. She was down to one severe headache a week.
He increased her Elavil. He also recommended she do five sit-ups a day and continue physical
therapy three times a week, one of which times was aquatherapy. Id.

On August 25, 2009, petitioner’s parents met with Dr. Steven Sandler, 15 a pediatrician
and psychiatrist at Albany Medical College, to find out if petitioner’s multiple physical

14
Hyperacusis is “exceptionally acute hearing; the hearing threshold being unusually low. It may or may
not be accompanied by pain.” Dorland’s at 886.
15
Dr. Steven Bruce Sandler was board-certified in psychiatry on October 30, 1990. This board
certification is valid indefinitely. He was board-certified in child and adolescent psychiatry on November
11, 2000 through December 31, 2010, but his status as of January 23, 2017 was not board-certified in
child and adolescent psychiatry. https://application.abpn.com/verifycert/verifyCert.asp?a=1&u=1# (last
visited: Jan. 23, 2017).
23
symptoms were psychological in origin. Petitioner was not with her parents at this first
conference with Dr. Sandler. Med. recs. Ex. 7, at 1. Petitioner’s parents were concerned that
Gardasil vaccination in December 2008 may have caused her whole problem. In February 2009,
petitioner developed a viral illness with headache and malaise. She also developed photophobia,
phonophobia, and annoyance with smells. After two or three weeks, she had a gait problem. A
number of physicians saw her. Her strength and physical examinations were normal. Her testing
was normal except for an elevated antinuclear antibody (“ANA”). A presumptive diagnosis was
migraines. Petitioner became so incapacitated that she had been in a wheelchair and out of
school since February. Petitioner seemed to be depressed and had lost weight, mostly because
the smell, taste, and consistency of food troubled her. Id. A child neurologist at Boston
Children’s Hospital felt the cause might be psychological. A physical therapist, Adrian Fil, at
Sunnyview Hospital, noted petitioner’s sensitivity to sound and light as well as her gait had
improved slightly, but Ms. Fil pointed out to petitioner’s parents that petitioner’s examination
was inconsistent from one day to the next. Id. Petitioner was a high honors student, and
remained a high honors student even while at home and studying with a home tutor. She had
trouble reading and had to isolate one line at a time with an index card. Nevertheless, she read
three books on her own in the summer. Id. Petitioner told her parents she did not want to go
back to her high school because of the students and their reaction to her illness. Id. Petitioner
took Imitrex, hydrocodone, Benadryl, intravenous Depakene, Maxalt, Compazine, and B
vitamins for migraine headaches. She was currently on Amitriptyline, Periactin, and
multivamins. Id. Petitioner had an older brother and a younger sister. Id. at 2.

On September 1, 2009, petitioner saw Dr. Sandler. Id. at 3. He notes: “She says it all
began with a sore throat in February. Then, she developed flu symptoms, a headache,
wobbliness, and a sense that the halls were spinning at school. The headache has persisted ever
since. It is mostly bitemporal but sometimes she feels it at the back of her head too.” The
quality of the headache varied. Sometimes it felt like a knife, but at other times it pulsed or
throbbed or felt like pressure. It never went away and varied from 2/10 to 10/10. She said she
wanted to go back to school (the opposite of what petitioner’s parents told Dr. Sandler on August
25, 2009). Id. at 3. Petitioner also had photophobia and phonophobia. Id. Petitioner told Dr.
Sandler that she had a headache for a week in the seventh grade, which was diagnosed as a
migraine and which resolved completely. Id. She also told Dr. Sandler that she was quite happy
in February 2009 and had no particular stressors. Id. Besides her headache, and the annoyance
of loud or high-pitched sounds and of light, petitioner said food tasted weird to her, being either
too salty or too bitter. Id. Her appetite had declined and she had lost weight. Petitioner said she
and her mother were best friends, but she had not seen much of her father growing up because he
worked long hours as a physician. Petitioner denied depression (the opposite of what petitioner’s
parents told Dr. Sandler on August 25, 2009). She said she woke up a lot at night. Id.

Dr. Sandler noted that petitioner came to the office with the assistance of her mother
because she was unstable walking on her own. However, she did walk unassisted as she left Dr.
Sandler’s office, but walked very slowly and not steadily. He noted she was alert, oriented, very
cooperative with the interview, and made good eye contact. Her speech was clear and normal in
24
flow and volume. Her thought process was entirely normal and she appeared alert and oriented
with normal intellectual capacities. Dr. Sandler summarized his impression. Petitioner’s parents
believed her symptoms since February 2009 were due to a Gardasil immunization. She sounded
quite eager to go back to school and join her friends and activities. Dr. Sandler had “no
suspicion that she is malingering 16 or trying to play a sick role.” Id. He did not suspect her
symptoms were psychosomatic. 17 She read several books that summer with great effort. Id. He
offered her a session of hypnosis to alleviate her headache pain and she agreed to come back in a
week to do that. Id. at 4. He concluded that petitioner did not seem to be suffering from
significant anxiety or depression that might exacerbate her symptoms or worsen her perception
of physical pain. Id.

What is noticeable about Dr. Sandler’s opinion is he has no notation that he ever read
petitioner’s medical records including the physical examinations that other physicians performed
on petitioner, or performed his own physical examination of her. (He could not have seen
petitioner’s father’s summary of petitioner’s medical records because petitioner’s father did not
create it until a year after this visit.18) Moreover, he never comments about the discrepancy
between petitioner’s parents’ statements and petitioner’s own statements. For example,
petitioner’s parents told Dr. Sandler on August 25, 2009 that petitioner was depressed. Petitioner
denied depression when she saw Dr. Sandler on September 1, 2009. Petitioner’s parents told Dr.
Sandler on August 25, 2009 that petitioner did not want to go back to school because of her
classmates’ reaction to her illness. On September 1, 2009, petitioner conveyed the impression
that she was quite eager to return to school, rejoin her friends, and resume activities. These
discrepancies passed without Dr. Sandler’s comment.

On September 8, 2009, petitioner and her parents saw Dr. Nichter. Med. recs. Ex. 1, at
34. Using Ativan gave her a paradoxical reaction where she was seeing bugs and it did not
assuage her headache. Id. Her headaches occurred at least three times a week and Elavil was not
helpful. Excedrin Migraine with caffeine seemed to wire her up as well. Therapy was going
well. She could walk more independently and consistently. Her left leg seemed to turn in. She
saw Dr. Sandler who did not think petitioner was having a conversion reaction. He was going to
try hypnosis on her. Id. On physical examination, she had variable results in her legs. Id. at 35.
Sometimes she had giveaway weakness. At other times, the left foot would turn in. There was
no ataxia. Dr. Nichter’s assessment was that petitioner continued to improve slowly. She had
16
Malingering is “the willful, deliberate, and fraudulent feigning or exaggeration of the symptoms of
illness or injury, done for the purpose of a consciously desired end.” Dorland’s at 1099.
17
Psychosomatic disorder is “a disorder in which the physical symptoms are caused or exacerbated by
psychological factors, such as migraine headache, lower back pain, or irritable bowel syndrome. The
synonym psychophysiologic disorders, used in previous official nomenclatures and defined as ‘physical
disorders of presumably psychogenic origin,’ has been replaced in DSM-IV by the more neutral phrase
psychological factors affecting physical condition, which may be applied to any physical condition
judged to be adversely affected by one or more psychological or behavioral factors, and is subtyped on
the basis of the specific factors involved.” Dorland’s at 552.
18
See Exhibit AAAAAAA, medical history dated August 1, 2010 prepared by petitioner’s father.
25
some dizziness upon standing which was separate from headache. Dr. Nichter prescribed
hypnosis with the psychiatrist. Petitioner’s parents were not interested in acupuncture. Id.

Also, on September 8, 2009, petitioner again saw Dr. Sandler. Med. recs. Ex. 7, at 5.
Her headaches persisted and were currently 4-5/10 in severity. Dr. Sandler diagnosed petitioner
with mood euthymia. 19 He used hypnosis, guided imagery, and Thought Field Therapy.
Petitioner had some relief (her headache was then 4/10) with guided imagery. His plan was that
petitioner would have no further visits unless needed and she would practice at home. Id.

On September 16, 2009, Dr. Nichter wrote a Transfer Summary for the pediatric
Emergency Room. Med. recs. Ex. 1, at 38. The history he wrote was that petitioner developed
severe migraine in February 2009 after a sore throat. Id. In light of some mild depression, she
saw Dr. Sandler who tried hypnosis with minimal or no success. Id. Petitioner recently went to
school and was able to persist until around 1:00 p.m. but not on the subsequent day. Id. She had
severe headaches and on the prior night, which were associated with phonophobia and
photophobia. Id. There had been a question of numbness and tingling in the left leg. Id. When
the headache was less, her leg was nearly normal. Id. She did reasonably well in school. Id.
For petitioner’s physical examination, petitioner was in a dark room with her parents. Id. Dr.
Nichter’s assessment was that petitioner had migraines that might be related to Gardasil
administered one or two months before the onset of her migraines. Id.

On September 16, 2009, at 1:30 p.m., petitioner went to the Albany Medical Center
Emergency Room where she saw Dr. Cha Pranati. Id. at 40. Petitioner’s history was gait
disturbance and migraine-like headaches. Dr. Pranati writes, “[I]t was thought that these
complaints might have been secondary to her Gardasil vaccine, which was given in December
2008. She started with gait disturbance in February 2009. According to mom, she was not able
to walk without significant support February 2009 to July 2009.” Id. Petitioner’s headache was
persistent accompanied by photophobia and phonophobia. Id. Medical staff performed multiple
investigations, including MRI and MRA, and everything was normal. Id. Her ANA was high at
1:640, but her ds-DNA 20 was normal. Id. Petitioner came to the ER with more severe headache
since school opened. While her appetite had decreased, her photophobia and phonophobia were
more pronounced. Petitioner’s mother said they had tried many different medications for
migraine and nothing worked very well for petitioner. Petitioner reported her pain was 9-10/10.
Petitioner also complained of an abnormal sensation in her left leg, but she was able to walk
without support. Petitioner had a history of two ankle fractures in the past. Id. Petitioner was on
Elavil, Periactin, and Endural. Id. at 40-41. On physical examination, she was lying in bed with
the lights switched off. Id. at 41. Petitioner had full strength and no sensory deficit. Her
aggravated migraine-like headache had persisted for four to five days. All her investigations had
been negative. Dr. Dorothy T. Damore, a pediatric neurologist assisting in the Emergency

19
Euthymia is “a state of mental tranquility and well-being; neither depressed nor manic.” Dorland’s at
655.
20
“Ds-DNA” is double-stranded DNA. Dorland’s at 568.
26
Department, recommended doing a lumbar puncture to rule out pseudotumor cerebri. Petitioner
received 5 mg of Reglan IV and 1000 mg of Depacon and the lumbar puncture was performed.
One hour after receiving Reglan, petitioner reported minimal improvement. Id. Dr. Pranati
diagnosed petitioner with headache, likely migraine. Id. at 42. Dr. Pranati did a physical
examination which showed petitioner had 5/5 strength in her arms and legs and no sensory
deficit. Med. recs. Ex. 553, at 56. Dr. Nichter, in a note to the pediatric emergency department,
dated September 16, 2009, commented that the stress of school might have brought out the worst
again in petitioner’s migraines. Id. at 59.

On September 30, 2009, the physical therapist Adrienne Fil at Sunnyview Rehabilitation
Hospital noted that petitioner had had 29 P-T sessions and had shown functional gains, but had a
recent setback after a significant increase in her headaches resulting in her going to the
emergency room September 16, 2009. Med. recs. Ex. 11, at 10. Petitioner’s mother said
petitioner had a bad reaction to pain medications with no relief in her pain. Petitioner’s lower
extremity function, gait quality, and balance declined. Id. Ms. Fil noted that petitioner had low
tone with functional mobility with a floppy upper body and left lower extremity despite having
strength on muscle testing. Id. at 12. Petitioner had depression in her earlier treatments,
frequently reporting she was unable to sleep and had no appetite. Id. As her function improved,
she was more social and had better endurance. But with the recent setback, she appeared more
depressed. She continued to be unable to attend a full day of school due to headaches and had an
aide for safety while negotiating between classes. Id.

On October 6, 2009, Dr. Nichter wrote petitioner’s pediatrician, Dr. Kennette, stating he
saw petitioner and her parents for petitioner’s migraines and gait disturbance. Med. recs. Ex. 1,
at 44. The history he recounts is that petitioner developed a sore throat and afterward a profound
migraine at the end of February 2009 and went to the emergency room in early March 2009. She
had received a Gardasil vaccination a few weeks earlier. Testing included nerve conduction and
EMG to rule out Guillain-Barré syndrome. She also had MRI, MRA, and lumbar puncture, the
results of which were also unremarkable. Ativan was unsuccessful and she continued to have
headaches, which were diffuse, ranging from 4/10 to 8/10. There were no clear precipitators.
Elavil was discontinued and she was on Periactin, Propranolol, and Cymbalta. Cymbalta had not
affected the severity of the headaches. Dr. Nichter was seeing petitioner now for syncopal
episodes occurring at least five to seven times a week during which she would stand up and walk
toward the kitchen or another location, have black spots, and be on the floor. She was a bit
tachycardic after the event. With the introduction of the Propranolol, these events significantly
increased. Her gait was not as efficient after the lumbar puncture as before it, but she was
improving. The lumbar puncture was benign and the opening pressure was 16. Dr. Sandler did
not see any pathologic or psychological issues. Id. During her physical examination, petitioner
wore sunglasses and lay her head on her mother’s lap during most of the visit. Id. at 45.
Petitioner was able to jump on two feet. She balanced on one foot for about ten seconds. Her
gait was slow, but not lurching. Dr. Nichter’s assessment was that petitioner’s gait continued to
improve. Propranolol may have exacerbated her syncope. Id. There was no clear successful
intervention in her headaches. Id. at 46. His plan was to decrease the Propranolol and stop at
27
three- to four- day intervals, continue Cymbalta and Periactin, and to make an appointment with
Dr. Argoff to facilitate any new or different pain management such as Botox or acupuncture. Id.

On October 21, 2009, petitioner’s mother called Dr. Kennette’s office to complain that
petitioner had fever, chest pain from coughing, and a migraine-like headache. Med. recs. Ex. 12,
at 54. Petiitoner’s mother was concerned because petitioner’s headaches were getting worse.
She wanted to speak with Dr. Kennette. Petitioner’s fever the day before was 100.4 degrees.
That day it was over 101 degrees. She had a sore throat and cough for over two days, upper
chest pain, severe headache with the cough, and “faints” (the notetaker put “faints” in quotation
marks) when she tried to stand up. Her heart rate ranged from the 90s to 144 with blood pressure
90s/70s. Dr. Kennette instructed the mother to seek emergency room care. Id.

On October 23, 2009, petitioner and her parents saw Dr. Joel M. Kremer, a
rheumatologist. Med. recs. Ex. 10, at 1. They gave a history of a six-week interval between
petitioner’s second Gardasil and the onset of her symptoms of sore throat and headache. Id.
Petitioner’s mother has Raynaud’s. 21 Id. at 2. Dr. Kremer noted that the etiology of petitioner’s
severe headaches and various neurologic deficits was obscure at that time. He noted a five-page
summary from VAERS (Vaccine Adverse Events Reporting System) comparing events
following Gardasil vaccination vs. Menactra vaccination through November 30, 2008. The
summary seemed to indicate that there was an increased incidence of general reactions to
Gardasil compared to Menactra, specifically pain, paralysis, syncope, vasculitis, and lupus.
There were 28 cases of lupus reported following Gardasil compared to six lupus cases reported
following Menactra. Dr. Kremer gave this VAERS summary to petitioner’s parents. He
scheduled further tests: a repeat ANA, CH50, DNA antibody, C3, C4, FSH, LH, cardiolipin
antibody, lupus anticoagulant, and cryoglobulins together with a metabolic panel and routine
urine. Id.

Also on October 23, 2009, in the evening, petitioner went with her parents to Albany
Medical Center Emergency Department, complaining of difficulty breathing at home. Med. recs.
Ex. 553, at 52. Over the last three days, she had some increasing congestion, including bringing
up a productive sputum. That day, however, she began having a fever and started Tamiflu.
However, her cough persisted, similar to a croup cough, and she had stridorous respirations to
the point she was having difficulty breathing. Upon arrival in the Emergency Department, her
breathing improved significantly and her parents stated that she had significant improvement on
the way to the Emergency Department. Id. Dr. John Burton did a physical examination and
found some mild tonsillar hypertrophy to the oropharynx, but no exudate or erythema. Id. at 53.
Oxygen saturation was normal. She did not have any stridor or retractions. Her lungs were clear
without wheezes or rales. Dr. Burton diagnosed petitioner with viral syndrome and tracheitis.

21
Raynaud’s phenomenon is “intermittent bilateral ischemia of the fingers, toes, and sometimes ears and
nose, with severe pallor and often paresthesias and pain, usually brought on by cold or emotional stimuli
and relieved by heat; it is usually due to an underlying disease or anatomical abnormality. When it is
idiopathic or primary it is called Raynaud disease.” Dorland’s at 1430.
28
He states in the medical record, “In the Emergency Department, the etiology of this patient’s
difficulty breathing over the last 2 days and particularly this evening was somewhat unclear,
although this seems to be consistent with a history of a viral tracheitis.” Id. A chest x-ray was
normal and she had a normal epiglottis and normal retropharyngeal tissues. Id.

On October 27, 2009, petitioner’s hexagonal phospholipid was 7.3 whereas less than 6.2
was negative and greater than 6.2 was positive. Med. recs. Ex. 8, at 5. On the same date,
petitioner had an abnormal lupus anticoagulant panel. Id. Petitioner’s ANA was 1:1280 with a
speckled pattern. Id. at 17.

On November 5, 2009, Dr. Charles E. Argoff, a neurologist with special qualifications in
pain management, wrote a progress note. Id. at 47. The history was that petitioner was in her
usual state of health until the end of February 2009 when she began to experience a daily
headache. “This appeared to be in association with her use of Gardasil. . . .” Id. [Dr. Argoff’s
record does not reflect that the end of February is nearly three months after December 8th when
petitioner received Gardasil.] Testing included lumbar puncture, MRI, MRA, and
“electrophysiological studies because she was at times unable to walk.” Id. Dr. Argoff writes he
spent over 45 minutes in face to face contact with petitioner in the presence of her parents. To
date, all diagnostic studies were negative. Petitioner currently complained of daily headaches
with photophobia, severe pounding, sharp and stabbing type of headache across her entire head,
and inability to function as well as to attend school. In addition, when she took certain
medication, she had difficulty walking and had a dystonic reaction to Reglan when the ER at
Albany Medical Center gave it to her. More recently, she was prescribed Ambien to help her
sleep and she had a similar reaction. Today, petitioner had difficulty walking in Dr. Argoff’s
office and her parents told him this difficulty occurred frequently. She had been treated with a
variety of agents including Cymbalta, Topamax, amitriptyline, Aleve, Periactin, Ativan,
Propranolol, magnesium, multivitamins, and vitamin B2 and nothing had helped her. Petitioner
complained of words not appearing as words when she looked at them, but she had not seen her
ophthalmologist recently. She had not seen a neuro-ophthalmologist either. A pediatric
neurologist at Boston Children’s Hospital told her that her complaints were somatic, but did not
perform any diagnostic studies. Dr. Sandler, a psychiatrist at Albany Medical Center, saw her
but did not feel she had any significant psychiatric issues. Id. Petitioner had headaches daily.
Id. at 48. On physical examination, petitioner was able to walk normally, but unable to perform
tandem heel and toe gait comfortably because she felt unsteady. However, the Romberg sign
was negative. Dr. Argoff’s impression was that petitioner had chronic neurological symptoms of
uncertain etiology. She appeared to have apraxic 22 difficulties from the motor function point of
view, but her difficulty with gait was difficult to diagnose. He recommended that petitioner see
Dr. Changizi, one of his movement disorder colleagues, for evaluation of any movement
disorder. He also recommended that petitioner see Dr. Rheeman, a neuro-ophthalmologist,
because of petitioner’s difficulty reading words. Petitioner was already scheduled to see Dr.

22
Motor apraxia is “impairment of skilled movements that is greater than or different in form from that
caused by weakness of the affected parts; the patient appears clumsy rather than weak.” Dorland’s at 121.
29
David Cornblath at Johns Hopkins University because of his involvement with the Merck
Gardasil studies. Dr. Argoff thought petitioner’s headaches might be better controlled with the
use of botulinum toxin chemosurgical therapy or specific Botox injections. But he deferred this
recommendation. Id.

On November 8, 2009, petitioner saw Dr. Charles Rheeman, a neuro-ophthalmologist, to
evaluate petitioner for difficulty in reading. Med. recs. Ex. 15, at 2. She gave a history that she
developed numerous symptoms in February 2009. Id. She received two doses of Gardasil, the
second in December 2008. Id. Since February 2009, she had had daily severe headaches
associated with photophobia and phonophobia. Id. She also developed problems with walking
and was undergoing physical therapy. Id. Her main visual complaint was difficulty reading
because the words “float.” Id. She used a paper for alignment in order to read. Id. She also had
trouble sleeping and eating, having lost about thirty pounds. Id. She reportedly had a negative
MRI and negative lumbar puncture. Id. She had taken numerous migraine headache medicines
without relief. Id. Dr. Rheeman stated that petitioner’s entire eye examination was normal. Id.
He wrote in a letter to Dr. Charles Argoff:

I do not have a good explanation for why she is having trouble
reading. At this point, I could not entirely rule out a non-organic
cause. For example, as far as her difficulty ambulating is
concerned, you told me you did not find any weakness or
numbness on exam. She could barely walk without her mother’s
assistance today. However, the patient’s mom told me [petitioner]
was able to walk about two miles trick or treating on Halloween
night.

Id.

On November 10, 2009, petitioner and her parents went to Johns Hopkins University to
see Dr. David Reid Cornblath, a neurologist, about petitioner’s headaches because he consulted
with Merck regarding Gardasil. Med. recs. Ex. 3, at 7. Petitioner’s father sent in advance a 100-
page notebook to Dr. Cornblath on Gardasil adverse reactions. Id. Dr. Cornblath recounted
petitioner’s short series of headaches in 2007 after a soccer game. The headaches were mild and
resolved, and she had a negative head MRI. Petitioner received two Gardasil vaccinations, the
first on August 26, 2008, and the second on December 3, 2008. She was well until about
February 15, 2009 when she developed a sore throat, fatigue, low-grade fever, and swollen
glands, lasting a week. Id. After that, she had headaches, which worsened and were associated
with nausea, photophobia, phonophobia, and loss of appetite. Id. Her pediatrician Dr. Kennette
diagnosed her on February 26, 2009 with migraine and prescribed Lortab and Imitrex. Id.
Symptoms continued and, by March 2009, petitioner developed a profound inability to maintain
balance in order to walk, although never having true vertigo or nystagmus. Id. Symptoms
continued with severe unremitting headaches for nine months. Id. Over that time, she had
extensive testing including MRI and spinal tap, both of which were normal. She saw a number
30
of physicians, none of whom was able to find her abnormal neurologically. Id. Her grades were
excellent (high 80s to 90s except for math where she had a 99), whether home-schooled or back
at school. Id.

Petitioner’s laboratory studies were normal for the following tests: CBC, cryoglobulins,
PT, PTT, hexagonal phospholipids, Russell viper venom, CSF (0 cells, glucose 56, protein 22),
CMP, CK, iron, homocysteine, quantitative immunoglobulins, CRP, serum immunofixation,
FSH, LH T4, TSH, antithyroglobulin antibodies, thyroid peroxidase antibodies, vitamin D, Lyme
C6, EBV, cardiolipin, double-stranded DNA, C3, C4, T-cell subsets, and total complement. Id.
Her ANA on October 27, 2009 was 1:1280. On April 6, 2009 and June 30, 2009, her ANA was
1:640. MRA done on June 9, 2009 was normal. MRA of the neck done on October 13, 2009
was normal. MRV done on March 18, 2009 was normal. Brain MRIs done on March 18, 2009
and June 9, 2009 were normal. A nerve conduction study of July 20, 2009 was normal. Id. at 8.

Petitioner filled out a new-patient questionnaire for Dr. Cornblath. Petitioner listed the
following symptoms: (1) altered taste and smell; (2) change in appetite; (3) weight loss; (4)
difficulty sleeping; (5) fatigue; (6) neck pain; (7) joint pain; (8) difficulty concentrating; (9)
dizziness; (10) headaches; (11) lethargy; (12) balance problem; (13) blurred vision; (14) double
vision; (15) trouble concentrating; (16) numbness in legs; (17) poor balance; (18) poor
coordination; (19) trouble walking; (20) weakness in legs, left more than right; (21) fainting; (22)
abdominal pain; (23) hoarseness; (24) shooting pains; (25) fainting spells; and (26) trouble with
smell. Id.

Her medications included: Topamax (no effect), Amitriptyline (no effect), Propranolol
(no benefit but petitioner developed presyncope); dexamethasone (no effect), Cymbalta (no
effect), Ambien (violent hallucinations), and Reglan (created intense anxiety). Id.

On physical examination, Dr. Cornblath found petitioner’s gait striking. Id. at 9. When
she walked with her mother, petitioner held on quite tightly and appeared as though she were
going to fall. Id. But when petitioner walked with Dr. Cornblath, she hardly required any real
assistance. Id. She could rise from a chair without the use of her hands. Id. Dr. Cornblath’s
assessment was that, after a viral infection in mid-February, petitioner developed what became
incapacitating daily headaches. Id. Dr. Cornblath stated that he discussed Gardasil with
petitioner and her parents:

I have explained to the family why I do not believe her current
symptoms can be related to the Gardasil vaccine. We have gone
over the concepts of biological possibility and the kinds of events
of a neuroimmune nature that are known to occur following
vaccines at a low incidence. Her symptoms began two months
after vaccination and were closely in time follow[ing] some sort of
viral infection. Thus, I do not believe there is any relationship

31
 between her current symptoms and her receipt of the Gardasil
vaccine.

Id. Dr. Cornblath wrote that the cause of petitioner’s headache remained unknown. He
pondered whether the dosages of petitioner’s various medications had been high enough to work.
He suggested that petitioner talk with her physicians about returning to those medications and
raising their dosage. Dr. Cornblath spoke with Dr. Nichter who told him that, in treatment of
pediatric migraine, low dosage is standard practice. Id.

Dr. Cornblath wrote:

There is no clear neurological explanation for her gait dysfunction.
This has been noted multiple times in her past records where her
gait has been called “astasia-abasia.”

At the end of the interview, [petitioner] asked me if I thought she
was crazy. I told her that she had a serious set of symptoms for
which the doctors had been unable to find the cause. However, in
most people of her age who have a normal neurologic examination
and extensive normal neurological testing, she has an excellent
prognosis for her recovery. I explained . . . however that a
recovery of her medical condition requires close cooperation with
her [doctors] and a positive attitude on her part.

Id. Dr. Cornblath recommended biofeedback as a possible help in a conversation with Dr.
Nichter. Dr. Cornblath noted that petitioner’s parents were still convinced that Gardasil caused
petitioner’s problems. Id.

On November 13, 2009, Dr. Kremer, the rheumatologist, spoke with petitioner’s mother
and then petitioner’s father. Med. recs. Ex. 10, at 3. Petitioner had a positive ANA of 1:1280
speckled and a weakly positive hexagonal phospholipid neutralization test with a norm INR,
negative anti-cardiolipin antibody, and negative beta 2 glycoprotein 1. Dr. Kremer told both
parents that he found it difficult to connect these lab test results with petitioner’s clinical picture
given the multiple negative imaging studies she had. He recommended they see Dr. Michelle
Petrie at Johns Hopkins Medical Center in Baltimore. They mentioned they had just returned
from Johns Hopkins after seeing Dr. Cornblath, a neurologist, who suggested increasing
petitioner’s dosage of Topamax. Dr. Kremer said he would e-mail Dr. Petrie to see if she would
consider seeing petitioner as an additional consultant. Id.

On November 17, 2009, petitioner and her parents visited Dr. Nichter. Med. recs. Ex. 1,
at 50. Among petitioner’s other tests, her sedimentation rate and C-reactive protein were normal.
Petitioner and her parents met Dr. Cornblath in Baltimore, and he did not feel that Gardasil was
related to her present clinical condition. In a personal phone call Dr. Cornbluth made to Dr.
32
Nichter, “he stated he thought most of the findings were not physiologic.” Id. Petitioner also
saw a neuro-ophthalmologist who found her entire eye examination was benign. He raised
questions as to stressors in petitioner’s life. Petitioner and her parents met with Dr. Sandler who
felt she did not have any major psychologic or psychiatric dysfunction, and recommended
trazadone for sleep. But after taking Ambien once and having almost a hallucinatory response in
terms of seeing death in her brother, petitioner was quite agitated and confused. Petitioner and
her parents saw Dr. Argoff who recommended Botox injections but also recommended they see a
movement disorder specialist, Dr. Changizi, “but the family did not wish to go that route.” Id.
Petitioner’s headaches waxed and waned. At times, she did well. For example, she walked most
likely five miles during a Halloween event. She seemed fatigued, but still walked over three to
five miles. After her experience with Ambien, she had a severe headache. Id. Of note, Periactin
did not result in significant improvement. Id. at 50-51. Propranolol resulted in a syncopal-like
process. Id. at 52. Cymbalta made no difference. On physical examination, petitioner’s
weakness seemed quite variable. At times, she was weaker on the left than on the right, but it
was inconsistent. “She could barely walk during the examination, and yet when coming in, she
walked from the parking lot to the sitting room without any assistance.” Id. She could not jump
on two feet without some assistance. Id. at 51-52. There was some decrease in vibratory sense
at the left toe, but it was very inconsistent. Id. at 52. Dr. Nichter’s assessment was that
petitioner’s gait overall was much improved compared to three to four months previously, but
there was a dip approximately two months ago. Headache continued to be quite a serious
problem. Syncopal events had subsided. Id. Petitioner was not on any medicines and Dr.
Nichter did not recommend that she go on any medicines. In light of petitioner’s hair falling out,
he recommended that she take a good multivitamin with minerals including selenium. He
recommended that petitioner and her parents discuss with Dr. Kennette, petitioner’s pediatrician,
a psychiatric evaluation and specifically any medications that would be a mild mood elevator.
Id.

On December 4, 2009, petitioner went to Dr. Michelle A. Petri and Dr. Saru Sachdeva at
Johns Hopkins University for a second opinion regarding her headaches and positive ANA.
Med. recs. Ex. 5, at 1. Petitioner told Dr. Petri that she had a short series of headaches in 2007
and, on February 15, 2009, she developed a sore throat, low-grade fever, and swollen lymph
nodes, lasting for about one week. Id. She also had mild headaches at that time. Id. One week
later, on February 21, 2009, her headaches worsened. Id. She was diagnosed with migraine. Id.
Her symptoms continued until March. Id. She also developed an inability to maintain balance in
order to walk. She did not have vertigo or nystagmus. Id. Her headaches worsened. Id. She
began various medications, including multivitamins and melatonin. Id. She had lower extremity
weakness and, on June 30, 2009, testing showed she had an elevated ANA. Id. at 1, 2. On
November 11, 2009, she saw Dr. Cornblath at Johns Hopkins, who did not feel that Gardasil
caused her symptoms. Id. at 2. He evaluated her and did not find any objective evidence of
neurological deficits. Id. On October 23, 2009, petitioner had a positive ANA at a titer of
1:1280 and a borderline low hematocrit. Her hexagonal phospholipid was positive. She had a
normal Russell viper venom time. Her anti-cardiolipin antibodies were negative. Her iron
studies, serum immunoglobulin, and thyroid studies were normal. Her 25-hydroxyvitamin D
33
was mildly low at 33.6. Petitioner complained of headaches, bluish discoloration of her toes,
photophobia, and phonophobia. She was wearing sunglasses. Her mother had possible
rheumatoid arthritis although the family is uncertain about this. On review of systems, the
pertinent positives were excessive hair loss and bluish discoloration of the toes. She stated she
felt dizzy upon getting up from a supine position and felt weakness and numbness in her left
lower extremity. She stated her right knee was painful because of over compensation as she used
her right leg more. Id.

On physical examination, Dr. Petri did not find any alopecia (hair loss). Id. at 3.
Petitioner had livedo 23 around both knees and forearms. There was cyanosis 24 in the toes. On
neurological exam, petitioner did not have any objective evidence of sensory or motor deficits.
Her Romberg’s test was negative. Dr. Petri diagnosed petitioner with undifferentiated
connective tissue disease (“UCTD”) based on petitioner’s positive ANA, Raynaud’s disease,
livedo, and lupus anticoagulant. Id. She recommended petitioner take Plaquenil. In answer to
petitioner’s parents’ concern that Gardasil caused petitioner’s headaches, Dr. Petri wrote that
symptom onset was six weeks post-vaccination. (Actually, it was 10 weeks post-vaccination.)
Id. Dr. Petri engaged in a detailed discussion with the family. She said there is a mean of three
to four years between positive serologies and clinical onset of symptoms in systemic lupus
erythematosus (“SLE”). Plaquenil would delay the progression of UCTD to SLE. Ten percent
of UCTD progressed to SLE. Petitioner needed to avoid sunlight, garlic, G-CSF, echinacea,
melatonin, Bactrim, and alfalfa sprouts. Dr. Petri gave petitioner a headache prevention diet and
recommended nortriptyline. Petitioner was advised to take 2.5 mg. of amlodipine for her
Raynaud’s syndrome. If her lupus anticoagulant remained positive, she should consider starting
aspirin. She should stop taking melatonin as this worsened SLE. Dr. Petri recommended
petitioner take a tilt table test to rule out neutrally mediated hypotension. Id. Dr. Petri noted that
she could not connect petitioner’s UCTD to Gardasil. Id.

On December 16, 2009, Dr. Nichter called Dr. Kennette to discuss the apparent lack of
effective treatment offered to petitioner as of that date and what, if anything could be considered
next. Med. recs. Ex. 12, at 57. Dr. Kennette suggested petitioner’s returning to see Dr. Sandler,
the psychiatrist, was in her best interests. Id.

On December 17, 2009, Dr. Kennette called Dr. Sandler who said he was ready to see
petitioner whenever she was ready to return. Id.

Also on December 17, 2009, petitioner underwent a transthoracic echo, which was
abnormal, showing a trace mitral regurgitation, tricuspid regurgitation, and aortic insufficiency. 25
Med. recs. Ex. 13, at 3. She had normal left ventricular function. Id.

23
Livedo is “a discolored spot or patch on the skin.” Dorland’s at 1067.
24
Cyanosis is “a bluish discoloration.” Dorland’s at 452.
25
Mitral regurgitation is “the backflow of blood from the left ventricle into the left atrium, owing to
mitral valve insufficiency; it may be acute or chronic, and is usually due to mitral valve prolapse,
34
 On January 6, 2010, petitioner wore a Holter monitor, which showed occasional
tachycardia of 160 beats per minute at 1:34 a.m., dizziness reported with normal sinus rhythm
and a heart rate of 70 beats per minute, and rare PACs. 26 Id. at 4.

On January 14, 2010, petitioner saw Dr. James O’Brien, a cardiologist, for syncope and
palpitations. Id. at 5. He reviewed her January 14, 2010 EKG which showed sinus rhythm with
an incomplete right bundle branch block, 27 as well as the results of her January 6, 2010 Holter
monitor. Id. Dr. O’Brien attributed petitioner’s near syncope to vasovagal 28 intolerance. Id. at
6.

On January 19, 2010, petitioner saw Dr. Nichter. Med. recs. Ex. 18, at 1. The cardiology
department at the Children’s Hospital at Albany Medical Center felt she met the criteria for
POTS. Id.

Also on January 19, 2010, petitioner’s hexagonal phospholipid was now 6.2 which was
borderline since negative was below 6.2 and positive was above 6.2. Med. recs. Ex. 8, at 5. She
again had an abnormal lupus anticoagulant panel. Id. Her ANA was 1:640 with an atypical
discrete speckled pattern. Id. at 17.

On February 11, 2010, petitioner saw Dr. O’Brien for an evaluation of her syncope and
palpitations. Med. recs. Ex. 13, at 8. An EKG done on February 11, 2010 showed sinus rhythm

rheumatic heart disease, or a complication of cardiac dilatation.” Dorland’s at 1621. Tricuspid
regurgitation is “the backflow of blood from the right ventricle into the right atrium, owing to tricuspid
valve insufficiency.” Id. Aortic insufficiency is “defective functioning of the aortic valve, with
incomplete closure resulting in aortic regurgitation.” Id. at 945.
26
PAC stands for “premature atrial complex.” Dorland’s at 1359. Atrial premature complex is “a single
ectopic atrial beat arising prematurely, manifest 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.” Id. at 395.
The P wave is “in the electrocardiogram, the initial deflection of the cardiac cycle, representing excitation
of the atria.” Id. at 2077. The PR interval is “the portion of the electrocardiogram between the onset of
the P wave (atrial depolarization) and the onset of the QRS complex (ventricular depolarization), lasting
approximately 0.12 to 0.20 second in the adult. It is the time taken for an impulse to traverse the
atrioventricular node, bundle of His, and bundle branches.” Id. at 951.
27
A bundle branch block is an “interruption of conduction in one of the main bundle branches, left or
right; the sequence of ventricular depolarization is altered since the impulse reaches one ventricle and
then travels to the other.” Dorland’s at 226.
28
Vasovagal syncope is a “transient vascular and neurogenic reaction marked by pallor, nausea, sweating,
bradycardia, and rapid fall in arterial blood pressure which, when below a critical level, results in loss of
consciousness and characteristic electroencephalographic changes. It is most often evoked by emotional
stress associated with fear or pain.” Dorland’s at 1818.
35
with normal intervals. Id. Dr. O’Brien felt the best diagnosis was vasovagal intolerance. Id. at
9.

On March 1, 2010, Dr. Nichter noted that petitioner’s ANA went from 1:1280 to 1:640.
Med. recs. at Ex. 18.2, at 1. Her cardiolipin was minimally elevated or basically within normal
limits. Id. Her gait had significantly improved and she could almost run. Id. More recently,
petitioner developed POTS. Id. She had a vesicular rash on her skin occasionally and a reddish
hue on her cheeks, but that did not meet the criteria for a butterfly rash of systemic lupus
erythematosus. Id. at 2. Dr. Nichter queried whether there was any relationship between POTS
and rheumatological disorders. Id.

On May 20, 2010, Dr. Nichter noted that petitioner had headache with major visual
complaints and abnormal autonomic function, although other aspects of autonomic dysfunction,
such as sweating, bowel, bladder, and gastric emptying, had been completely normal. Med. recs.
Ex. 18.3, at 2-3. Her tests for Hashimoto’s encephalopathy and thyroid peroxidases were
completely normal. Id. Dr. Nichter stated, “One cannot cogently bring all components to her
history into a single story.” Id. He said autonomic dysfunction was a consideration. Id.

On July 20, 2010, petitioner saw Dr. Jill M. Abelseth, an endocrinologist. Med. recs. Ex.
17, at 1. Petitioner had normal adrenal and thyroid function studies. Id. at 2.

On July 29, 2010, petitioner had the same borderline 6.2 for hexagonal phospholipid as
she had on January 19, 2010. Med. recs. Ex. 8, at 5. Her lupus anticoagulant panel had become
borderline whereas, previously, it was abnormal. Id. Testing for AChReceptor 29 (“AChR”)
(muscle) binding antibody was negative. Id. at 21. Testing for N type calcium channel antibody
was negative. Id. Testing for P/Q type calcium channel antibody was negative. Id. at 22.
Testing for AChR ganglionic neuronal antibody was negative. Id. Testing for neuronal voltage-
gated potassium channel antibody was negative. Id. Petitioner’s ANA was 1:1280 with an
atypical discrete speckled pattern. Id. at 17.

On August 6, 2010, petitioner saw Dr. Kennette for her 16-year, five-month check-up.
Med. recs. Ex. 12, at 60. She had headaches 24/7, which were on a 6/10 scale that day. She had
taken a Caribbean cruise in April and was going to Disney World during the New Year. She had
low blood pressure attacks and fell down. Her blood pressure was very low and her heart rate
dropped usually with body position changes. She was taking Aleve and Tylenol PM. She did
minimal walking of less than one mile when tolerated. Her periods were irregular for four

29
ACh stands for “acetylcholine.” Dorland’s at 14. Acetylcholine is “a reversible acetic ester of choline;
it is a cholinergic agonist and serves as a neurotransmitter at the myoneural junctions of striated muscles,
at autonomic effector cells innervated by parasympathetic nerves, at the preganglionic synapses of the
sympathetic and parasympathetic nervous systems, and at various sites in the central nervous system.” Id.
at 12. “Myoneural” pertains “to both muscle and nerve; said of the nerve terminations in muscles.” Id. at
1224.
36
months, ranging from three to eight weeks. She weighed 120 pounds. Her BMI was 19. She
seemed sullen and upset. Her heart rate was 68-72. She had a one and one-half year history of
daily headaches ranging from 3/10 to “40”/10 (Dr. Kennette used quotation marks), which were
unresponsive to myriad interventions. Petitioner’s previous episodes of abnormal gait were now
resolved. Now she had episodes of syncope secondary to lower blood pressure and abnormal
pulse. Her ANA was between 640 and 1280 for the past year. She had Raynaud’s disease.
Petitioner did not wish to discuss guidance or counseling that day, but desired to keep in regular
contact with Dr. Kennette by telephone for “emotional support” (Dr. Kennette used quotation
marks). Id. at 60-61. The total time Dr. Kennette spent with petitioner and her parents was one
hour and 45 minutes. Id. at 61.

In an addendum to her August 6, 2010 visit notes, Dr. Kennette recorded that petitioner’s
father brought an extensive set of medical records which included reviews of information that
Dr. Kennette had not received, e.g., from Dr. O’Brien, the cardiologist, an update from Dr. Sarah
Elmendorf, 30 an infectious disease expert, and information from an upcoming visit to Johns
Hopkins Hospital. Id. at 62. Dr. Kennette reviewed the various medication trials, e.g., Florinef
(petitioner did not tolerate it), and Midodrine (petitioner did not feel it was helpful). She
reviewed laboratory data not previously provided, e.g., EKG, Holter monitor, echocardiogram,
and basic metabolic profile, all of which were normal. She reviewed Dr. O’Brien’s provisional
diagnoses of tachycardia and dysautonomia. Dr. Kennette had an extensive one-on-one
interview with petitioner alone to update her on her condition and discuss her current status at
home and her impression of how she felt. Plus Dr. Kennette reviewed with petitioner current
strategies for school limitations based on her physical abilities. Id. Dr. Kennette discovered
after reviewing all of the reports given to her that day by petitioner’s family that petitioner had
not received the Western blot examination of blood for Lyme disease or empiric treatment for
Lyme disease. Id. at 63. Dr. Kennette was going to add a request for the Western blot test to be
done on July 29, 2010. After speaking to petitioner’s father, Dr. Kennette wanted to empirically
treat petitioner for Lyme disease with Doxycycline 200 mg. daily for two to four months and
reassess her symptoms. Id.

On August 9, 2010, Dr. Kennette telephoned petitioner’s mother. Id. Petitioner had not
yet started taking Doxycycline because she was “not feeling well enough to eat much” (Dr.
Kennette used quotation marks) over the weekend. Petitioner was going to seek an opinion at
Johns Hopkings with Dr. Rowe, a pediatric diagnostic clinician, and might try Doxycycline at a
lower dose when she and her parents returned, perhaps 300 mg/day instead of 400 mg/day. Id.

30
Petitioner did not file any medical records from Dr. Sarah Elmendorf. Petitioner’s father testified that
he has known Dr. Elmendorf since medical school, they were both on the overgoverning board of the
hospital for well over ten years, they have sat on many committees together, and they live six blocks
apart. Tr. at 168. He used Dr. Elmendorf as a sounding board to discuss petitioner’s condition and
treatment, and any avenues petitioner and her parents could pursue for diagnosis and treatment. Id. at
169.
37
 On August 11, 2010, petitioner saw Dr. Peter C. Rowe at Johns Hopkins University for
further evaluation of her orthostatic intolerance, fatigue, and other problems. Med. recs. Ex. 6, at
4. She was quite flexible as a child and could put her leg behind her head, had a positive Gorlin
sign, 31 and could make a clover-like configuration with her tongue. She had a number of
fractures. At age 8, she fell on her wrist and fractured it. She sprained her left ankle soon
afterwards, requiring a cast and then a walking boot. At age 11, she fractured her left fourth
finger when someone stepped on her hand. At age 12, petitioner had a fracture at the epiphysis
of the right ankle while playing soccer and was in a cast and a boot for a total of seven weeks.
She underwent nuclear medicine scanning at that time because of persistent pain and concern
about complex regional pain syndrome. At age 14, she fractured several bones in the left hand
after hyperextending her thumb in volleyball. Also at age 14, she fractured her left fibular in
soccer and refractured this bone when she fell walking up stairs. She had some headaches in
2007 that resolved. Id.

Dr. Rowe noted that petitioner did not have an immediate reaction to either of her two
Gardasil vaccinations, the first on August 26, 2008 and the second on December 3, 2008. Id.
Her main problems began on February 15, 2009, when she suddenly developed a sore throat,
fatigue, and swollen glands that lasted a week, followed within five days by a headache, which
became progressively worse, associated with photophobia, phonophobia, and diminished
appetite. Id. She had not been well since the onset of this illness. By early March 2009,
petitioner was collapsing, weak, unable to walk, and spent much of the day reclining. She did
not walk much until August 2009. Although Dr. Petrie diagnosed petitioner with UCTD and had
recommended Plaquenil, petitioner had not started Plaquenil. Id.

Petitioner had seen cardiologist, Dr. James O’Brien, on December 17, 2009, who felt she
had vasovagal syncope and an associated POTS. Id. at 5. Trials of Florinef and midodrine were

31
The Gorlin sign is “the ability to touch the tip of the nose with the tongue, frequently a sign of Ehlers-
Danlos syndrome.” Dorland’s at 1711. Ehlers-Danlos syndrome is “a group of inherited disorders of the
connective tissue; they were formerly classified into ten types, but more recently only six types are
distinguished, varying widely in severity. The major manifestations include hyperextensible skin and
joints, easy bruisability, friability of tissues with bleeding and poor wound healing, calcified
subcutaneous spheroids, and pseudotumors. The hypermobility type (formerly type III) is autosomal
dominant and most common type; mitral valve prolapse accompanies the skin and joint anomalies. The
classical type (formerly types I and II) has both autosomal dominant and autosomal recessive subtypes; it
includes mitral valve prolapse as well as fibrous growths on pressure areas such as the knees and elbows.
The vascular type (formerly type IV) is autosomal dominant and is characterized by fragile blood vessels
and organs that may rupture, as well as distinctive facial features such as protruding eyes and thin nose
and lips. The kyphoscoliosis type (formerly type VI) is a rare, autosomal recessive type characterized by
kyphoscoliosis and eye fragility accompanying bone and joint anomalies. The arthrochalasis type
(formerly types VIIA and VIIB) is a rare, autosomal dominant type in which joints are particularly loose
and prone to dislocation; patients also suffer from arthritis and bone loss. The dermatosparaxis type
(formerly type VIIC) is an autosomal recessive type characterized by particularly fragile and sagging
skin. Most types are related to defects in procollagen . . . .” Id. at 1828-29.
38
ineffective. Petitioner increased her intake of salt and fluids. Nevertheless, her systolic
pressures have been in the 60-80 range. On electrocardiogram, she had normal left ventricular
function, a normal aortic root of 2.5 cm, and echocardiographic evidence of trace mitral
regurgitation, tricuspid regurgitation, and aortic insufficiency, but no murmur.

Currently, petitioner reported headaches, lightheadedness, syncope, fatigue, cognitive
problems, photophobia, phonophobia, gastrointestinal symptoms, some hair loss, problems
regulating temperature, cold feet and hands, numbness in an ulnar distribution which awakened
her every other night, insomnia, racing of her heart, occasional shortness of breath, acne, and
increased thirst. Petitioner reported a constant headache that never resolved, but also clusters of
more intense worsened headaches. Sometimes, the headaches felt like a vise, exerting pressure
within her head, and stabbing, causing downward pressure on the top of her head. Loud noises
and bright lights aggravated the intensity of her headache, although lately the photophobia had
not been as bad. She slept with earplugs. She often skipped breakfast. She stated she never had
a problem with lightheadedness and syncope until her illness in February 2009. Her legs would
give out in March 2009 and her heart raced. She had a poorly coordinated gait that may have
been related to weakness and deconditioning. Lightheadedness and syncope were more clearly
reported in April or May 2009 whenever she would move from sitting to standing after she had a
month or more of almost total inactivity. Her Holter monitor average heart rate was 76 beats per
minute with a range of 52-160 beats. She had a true loss of consciousness with syncope about 12
times over the course of the illness, but syncope was less frequent in recent months. She still had
some lightheadedness with dimming of her vision when she stood up, but tended to hold on
tightly to something and resolved the lightheadedness fairly promptly. She had a number of
orthostatic intolerance postures, such as sitting with her knees to her chest frequently. Fatigue
occurred daily, although she had occasional spurts of better energy. Activity and sleeping too
much or too little worsened her fatigue. After a syncopal episode, her fatigue was often worse.
It was also worse after shopping. Id. Hot weather also worsened her fatigue. Id. at 6. She could
force herself to attend a special event or have a special day, but then her malaise increased for
one to two days afterward. She had a variable attention span and concentration. Her
understanding tended to flag when she was more tired. However, her grades had been good. She
was still quite sensitive to sounds within her house although her photophobia and phonophobia
were slightly better. Her gastrointestinal symptoms included a sense of tightness in the
epigastric area and a feeling that she could not breathe. This occurred less than five days a week
and lasted a couple of hours when present. She had reflux one to three times a week and early
satiety but no aphthous ulcers. She lost 20 pounds early in her illness, but regained about 10
pounds over the last year. Going off milk for a month did not improve her. She said she had lots
of hair in her brushes and in the drains, but she did not have any complete patches of alopecia on
examination. Petitioner preferred the temperature in her room to be about 67 degrees and often
felt quite hot. Her temperature regulation problems varied substantially. Her parents
occasionally found her lying on the hot driveway in the summer sun with winter clothing on,
trying to get warm. Her Lyme test, Ehrlichia test, and Babesia test were negative. The family
history is notable for allergies in her father and a paternal aunt. Id.

39
 On physical examination, Dr. Rowe detected petitioner had blue sclerae, 32 a positive
Gorlin sign, and subluxation/clicking of the temporomandibular joint (“TMJ”) with mouth
opening. She could place her palms flat on the floor. Since her Beighton score was only 1, she
did not meet the full criteria for joint hypermobility. She had diffuse acrocyanosis. 33 He did not
see evidence of Raynaud’s phenomenon during this visit. Romberg sign was negative. She was
a bit unsteady with tandem gait. She had hypermobility on straight leg raise, with stretch elicited
at 70 degrees bilaterally, with end-range 120 degrees on the right and 110 degrees on the left, far
greater than normal. Dr. Rowe performed a standing test to evaluate petitioner’s orthostatic
tolerance. Her lowest resting heart rate supine was 47 beats per minute with a blood pressure of
103/56. On standing, she had an immediate increase to 82 beats per minute and continued to
increase gradually to a maximum of 98 beats per minute after nine minutes. Id. Petitioner had
an initial increase in her lightheadedness with standing that improved after about a minute, but
her fatigue level and lightheadedness increased modestly over the 10 minutes of standing. Id. at
7.

Dr. Rowe’s assessment was that petitioner had a post-viral fatigue illness that now met
the criteria for chronic fatigue syndrome since she had fatigue for more than six months, post-
exertional worsening of malaise, new-onset headaches, myalgias, cognitive problems, and
unrefreshing sleep. Id. at 7. Petitioner had resting hypotension without formal tilt testing and
had recurrent syncope that was consistent with neutrally-mediated hypotension. Her standing
test that day was entirely consistent with POTS. She had a 51-beat per minute increase in heart
rate within 10 minutes of standing, essentially doubling her heart rate associated with some
modest increases in fatigue and lightheadedness. Her heart rate changed despite taking high salt
and fluid. Petitioner had a lot in the way of allergies or asthma, some mild acne, and
deconditioning. She had a number of phenotypic features usually seen in association with
connective tissue laxity, but did not meet the full Beighton score criteria for hypermobility, but
had a number of other features, such as blue sclerae, the Gorlin sign, and extreme hypermobility
at the hips. Dr. Rowe said, “I suspect the connective tissue phenotype is allowing excessive
vascular compliance in the dependent circulation, and is a factor contributing to her orthostatic
intolerance, along with the deconditioning, which in turn causes a loss of plasma volume.” Id.
He suggested petitioner increase her exercise and improve her conditioning status with physical
therapy. Id. For the orthostatic intolerance, Dr. Rowe suggested she raise the head of her bed
and wear compression garments. She could use postural counter-maneuvers such as clenching

32
Sclera is “the tough white outer coat of the eyeball.” Dorland’s at 1678. Blue sclerae is “a prominent
feature of osteogenesis imperfecta, and is seen in certain other abnormalities.” Id. at 1679. Osteogenesis
imperfecta is “a group of inherited connective tissue disorders characterized by brittle, easily fractured
bones and sometimes other manifestations, including blue sclerae, wormian bones, shortened limbs and
limb deformities, fragile skin, muscle weakness, lax joints, bleeding and easy bruising, hearing loss,
dyspnea, and dentinogenesis imperfecta.” Id. at 1346.
33
Acrocyanosis is “symmetrical cyanosis of the extremities, with persistent, uneven blue or red
discoloration of the skin of the digits, wrists, and ankles accompanied by profuse sweating and coldness
of the digits. Called also Raynaud sign.” Dorland’s at 19.
40
her fists when she began to stand or when she felt lightheaded. He also suggested petitioner
receive two-liter infusions of normal saline over one to two hours to modulate autonomic tone.
Id.

On November 2, 2010, petitioner returned to Dr. Rowe much improved after adopting his
suggestions, such as raising the head of her bed, increasing her salt intake, and using postural
maneuvers. Id. at 9. Her school grades were in the 90s and she was taking up the flute and the
drama club. Id.

On January 23, 2011, petitioner saw Dr. Uhl, the orthopedist, with an injured right knee
while climbing on a snow bank. Med. recs. Ex. 14, at 28. Dr. Uhl suspected medial collateral
ligament injury, but he could not explain her complaint of some numbness. He noted that “in the
past the patient has had altered sensations and may be predisposed to RSD [reflex sympathetic
dystrophy also known as complex regional pain syndrome 34].” Id. He also noted that petitioner
had a prolonged period of thumb pain “with no specific explanation.” Id.

On February 11, 2011, petitioner and her parents saw Dr. Nichter. Med. recs. Ex. 18.4, at
1 . Since her last visit, petitioner had made significant progress. Id. Her gait was basically
normal. Id. Her vertigo was much improved. Id. She continued to have headaches. Id. She
still had fatigue and some elements of POTS. Id. Fluids and salt had been helpful. Id. She did
quite well academically, having an over 90 percent average. Id.

On September 9, 2011, petitioner saw Dr. Kennette, complaining of a sore throat for three
days. Med. recs. Ex. 12, at 65. She had a very busy summer and felt good. She was alert,
active, and chatty. She was not wearing sunglasses. Dr. Kennette diagnosed petitioner with
pharyngitis and tonsillitis. She prescribed penicillin as a “rescue” prescription, but on September
12, 2011, petitioner’s throat culture was negative. Id.

On September 12, 2011, petitioner’s rheumatoid factor was 22, which is higher than
normal, which is below 20. Med. recs. Ex. 8, at 17. Her ANA was 1:640 in an atypical discrete
speckled pattern. The normal result should be below 1:320. Id. Her EBV IgG was positive at
1:10 and weakly positive at 1:640. Id. at 16. Her EBV IgM was also positive. Id.

On September 16, 2011, petitioner saw Dr. Kennette for her 17-year, seven-month visit.
Med. recs. Ex. 12, at 66. Her monospot test 35 was positive and she had a slight elevation in her
white blood cells. Petitioner was in school all day. She had been on penicillin for seven days.
She was occasionally on a treadmill. She had normal gait and strength. Petitioner was much
improved concerning non-specific chronic headaches, decreased blood pressure with irregular

Dorland’s at 585, 1826.
34

The mononucleosis spot test or monospot test is “a type of heterophile antibody test for infectious
35

mononucleosis. . . .” Dorland’s at 1894.
41
heart rate, and fatigue. She had a recent diagnosis of mono. She had acne, for which Dr.
Kennette prescribed Clindamycin. 36

On September 19, 2011, Dr. Kennette wrote a letter to petitioner’s high school, stating
petitioner was clearly much improved from the prior year. Id. at 67. However, at times,
petitioner might need a modified school environment and/or time frames for assignments and
tests. She frequently had headaches, but they were not usually as severe as the ones she had in
the past. But she might need access to large print books or books on tape and must be allowed
access to frequent water breaks throughout the day. Id.

On October 12, 2012, petitioner saw Dr. David Palat, a pulmonologist, for bronchitis,
chest pain, and cough. Med. recs. Ex. 21, at 1. In his review of systems, Dr. Palat notes
petitioner had no vision problems. Id. He also notes petitioner did not have palpitations, her
heart rate was not fast, and her hands and feet were not cold. Id. at 2. He notes that petitioner
did not feel weak. She did not have finger pain or blanching with cold. She did not have
arthritis. She did not have localized joint pain or localized joint stiffness. She did not have
dizziness, sleep disturbances, or insomnia. Id. Dr. Palat measured petitioner’s blood pressure. It
was 112/80. Her pulse rate was 84 beats per minute. Id. She weighed 133 pounds and was five
feet 7 inches tall. Id. Petitioner’s gait and stance were normal. Id. at 3. Dr. Palat’s assessment
was bronchitis. Id.

On November 21, 2012, petitioner and her mother saw Dr. Jennifer Lindstrom, a
pediatrician and internal medicine specialist, for the first time (to replace Dr. Kennette). Med.
recs. Ex. 552, at 23. Petitioner’s mother believed that Gardasil caused all her medical problems,
including gait instability, severe headaches, an elevated ANA, and orthostatic hypotension. Id.
Petitioner had been on multiple headache medications without success. Hypnosis failed to help
her. Petitioner refused to follow up with neurology again. Petitioner saw a rheumatologist about
her elevated ANA and she diagnosed petitioner with undifferentiated connective tissue disease.
Petitioner had not followed up on this. Dr. O’Brien recommended petitioner take midodrine and
Florinef for her orthostatic hypotension, but petitioner was no longer taking them. She instead
tried to follow a high sodium diet. Id. Petitioner was drinking four to eight alcoholic drinks on
the weekend, which qualified as binge drinking. Id. at 24. Petitioner’s headaches failed to
respond to Topamax, Imitrex, Lortab, Cymbalta, Toradol, Compazine, and Benadryl. Id. at 25.
Dr. Lindstrom counseled petitioner that four to eight drinks on the weekend qualified as binge
drinking. Id. at 24. Petitioner said she would cut back. Id. at 25.

On March 7, 2013, petitioner with her parents saw Dr. Nichter, complaining of a
significant exacerbation of her migraines. Med. recs. Ex. 552, at 20. The prior week she had a
lot of pain and told her father to cut her head off. The headaches were frontal, temporal, and
sometimes extending to the back. They could be 10/10 and petitioner was crying at times. She
had photophobia. Id. Petitioner had academic stresses and social stresses with her roommate at

36
Clindamycin is an antibiotic “effective primarily against gram-positive bacteria.” Dorland’s at 372.
42
college. Id. Lortab, Imitrex, Ativan, and Reglan did not improve her headaches, with the latter
two causing negative adverse reactions. Benadryl had given her “a buzz” and was not sedative.
Id. at 21. Petitioner’s physical examination was normal. Petitioner had been in good health.
She did not have joint swelling or decline in vision or hearing. Petitioner was “alert and
interactive with a wonderful fund of knowledge. She was quite articulate in explaining why she
understands playing the role of another person i[s] understanding herself.” Id. Dr. Nichter’s
assessment was that the cause of petitioner’s migraines was most likely multifactorial in that
stressors had accumulated and exacerbated her migraines. Dr. Nichter discussed with petitioner
and her parents going to the emergency room to have a combination of Toradol, Benadryl, and
Reglan administered, but they decided not to do that. Id. Dr. Nichter provided the name and
telephone number of an acupuncturist. Id.

On March 28, 2013, Dr. Nichter wrote a letter to the campus center of the college
petitioner attended, requesting a single dormitory room for her because her living arrangement
with a roommate exacerbated petitioner’s headaches. Sleeping continued to be a challenging
problem for her. Id. at 19.

On January 23, 2014, petitioner saw Dr. Laura El Hage for her annual examination. Id. at
15. Petitioner had chronic daily headache but they did not worsen when she began oral
contraceptives. She did not have any abnormal neurologic symptoms such as numbness or
weakness during her headaches. Id. Petitioner occasionally used EtOH (ethyl alcohol). 37
Petitioner said she did not binge. She denied any other illicit drug use. She said she woke
frequently during the night, 15 times a night and could wake up for an hour at a time. She did
not have difficulty walking. All other systems reviewed were negative. Her strength was intact
and equal in all four extremities. Sensation was intact throughout. Id. Dr. El Hage diagnosed
petitioner with chronic fatigue syndrome and chronic migraine without aura. Id. at 17.

On December 12, 2014, petitioner and her mother again saw Dr. Lindstrom. Id. at 13.
Petitioner had general malaise in terms of decreased sleep, daytime fatigue, stressful dreams,
inability to focus, and feeling restless. Id. She had some difficulty with her first semester at
college and took an incomplete in one course. Petitioner had been crying more. She was
interested in going back to see Dr. Nichter whom she had not seen in two years. Id. On physical
examination, petitioner was at times almost tearful. Id. Dr. Lindstrom diagnosed petitioner with
multiple symptoms of mood disorder, not otherwise specified, with some feelings of reliving
stressful dreams, some crying, decreased sleep, and some symptoms of inattention. Dr.
Lindstrom believed petitioner needed a neuropsychiatric evaluation to assess her for inattentive
disorders, post-traumatic stress disorder, and stress reactions. Dr. Lindstrom thought petitioner

37
Ethyl alcohol is ethanol. Dorland’s at 45. Ethanol is “a primary alcohol existing as a transparent,
colorless, volatile, flammable liquid, miscible with water, methanol, ether, chloroform and acetone; it is
formed by microbial fermentation of carbohydrates or by synthesis from ethylene. Excessive ingestion
results in acute intoxication, with psychological, gastrointestinal, neurological, and motor abnormalities. .
. .” Id. at 650.
43
would benefit from counseling. As for orthostatic hypertension, petitioner’s blood pressure was
stable that day. Petitioner had been using table salt. She had chronic migraines headaches for
which she would see Dr. Nichter. Id. at 14.

On December 31, 2014, petitioner and her parents saw Dr. Nichter. Id. at 9. Stress was
an issue for petitioner. Over the last several weeks, she had such difficulty with stress that she
would hyperventilate sometimes and have a 15- and 20-minute period where she was not in
control of herself. This exacerbated over the last few weeks. She had a significant sleep
dysfunction. Before trying to sleep, she would take Tylenol PM, which contains Benadryl, and
then perhaps a glass of wine a few times a week. Id. She had daily headaches. She did not take
any medication for POTS but used various salts. Id. On physical examination, she had normal
gait. Id. at 10. There was nothing to suggest seizures or a neurodegenerative process. She did
not have an upper or lower motor neuron disease. Dr. Nichter found her to be “a bright young
lady who may have put a number of stressors and possibly too many on her plate.” Id. She was
“alert, fluent. She had a wonderful fund of knowledge.” Id. As for petitioner’s sleeping
difficulties, Dr. Nichter stated it “would be helpful to decrease and stop the alcohol. It would be
helpful to stop the Benadryl and Tylenol PM.” Id. Dr. Nichter’s plan was for the family to
consider counseling vs. psychiatry. The family was fine with the plan. Id.

On March 2, 2015, petitioner saw Dr. El Hage for her annual exam. Id. at 6. Her mother
accompanied her. She had chronic daily migraine. Petitioner was using a lot of Aleve (three to
six pills per day at 220 mg. each). She did not have any abnormal neurologic symptoms during
her headaches. As for her POTS, she had frequent pre-syncopal events, but no true syncopal
episodes. She could exercise without difficulty. She denied chest pain or palpitations during
exercise. Id. She drank 16 ounces of coffee with two shots of espresso daily. Id. at 7. She lifted
weights and used the elliptical machine. Her major was theater and political science. She
wanted to do theater professionally. She woke 15 times per night and could wake for an hour at
a time. She felt tired in the morning. All other systems were negative. Id. Overall, petitioner
was doing well except for her chronic migraines. Id. at 8. Dr. El Hage discussed medication
overuse with petitioner and her mother. She recommended that petitioner avoid NSAIDs
(Motrin, Advil, Aleve) and take Tylenol as needed for headache. She should avoid Advil
because it can cause gastrointestinal side effects and renal issues long term. If petitioner
improved, Dr. El Hage would discuss with her that Tylenol can also cause overuse headache and
petitioner should be conscientious with its use long term as well. Id.

On March 16, 2015, petitioner saw Dr. Nichter on an urgent basis in light of increased
seizure. Id. at 4. Petitioner came with her parents. Approximately two to three weeks earlier,
petitioner had increasing headaches. At one point, she came home from college and assumed a
fetal position, crying constantly. She tried oxycodone and slept a while. The headache tended to
be diffuse and pounding with photophobia and phonophobia. Petitioner switched from Aleve to
Tylenol. Yet, on some days, even four days, she took nothing, but on other days, she took five to
seven in a day. Probably, every week, she took at least four pills a week. Medications she tried
but which failed included Topamax, Benzodiazepine, Reglan, and Maxalt. Two precipitating
44
factors contributed to her headaches: (1) academic stressors, and (2) sleep dysfunction. Id.
Petitioner would pull an all-nighter and then have significant headaches. Yet she had a double
major and a minor and was a high achieving student. She did not have any major deficit in terms
of gait, vision, or hearing. She did not have swallowing difficulties. She did not have weakness
or ataxia. She did not have bowel or bladder problems. She used salts and fluids to help her
POTS and they worked reasonably well. Review of systems was benign. Id. On neurological
examination, she was normal. Id. at 5. Dr. Nichter wrote: “She is a bright young lady,
introspective and has a wonderful fund of knowledge.” Id. Dr. Nichter diagnosed her with a
history of migraines and a multifactorial stressful life. She had tried acupuncture without
success. The drug Restoril did not improve her sleep. Dr. Nichter prescribed Elavil. 38 He
advised her to work on her sleep hygiene. Although Dr. Argoff recommended Botox, petitioner
said she did not want it. Dr. Nichter also recommended she increase her dosage of melatonin.
Id.

On May 7, 2015, petitioner saw PA Sujata Kane, complaining of low back pain and a
rash. Id. at 1. Petitioner said she had low back pain for the prior four to five days. She had been
lifting a free weight of approximately 50 pounds, which was heavier than what she usually lifted
in the gym. She knew her posture was not the best when she did this. She also had a rash on her
right lower extremity for two days. Petitioner said she has pre-lupus and a connective tissue
disorder with a history of significantly elevated ANA. She told PA Kane she had never been to a
rheumatologist. She said she was allergic to Ambien, Reglan, Toradol, Compazine, and
Depakote. Id. She said she stopped taking Elavil because she thought it did not work. PA Kane
diagnosed petitioner with a back muscle spasm. Id. at 2.

Expert Reports

On June 24, 2013, petitioner filed the expert report of Dr. Yehuda Shoenfeld, an
immunologist, as Exhibit 24. He worded his report as answers to seven questions the
undersigned raised in the undersigned’s Order to Show Cause, dated November 13, 2012.

In answer to question 1, that petitioner had the same symptoms prior to receiving
Gardasil as she had after Gardasil, Dr. Shoenfeld responded that she had recovered from these
symptoms in 2007 and they did not cause long-term disability. Ex. 24, at 1. 39 Moreover, she
had new symptoms after Gardasil, including recurrent syncope, fatigue, neck pain, joint pains,
numb legs, cognitive disturbances, blurred vision, unrefreshing sleep, tachycardia, dyspnea,
impaired thermoregulation, cold extremities (subsequently diagnosed as Raynaud’s disease), toe
discoloration, excessive hair loss, gastrointestinal disturbances, lessened appetite, altered sense
of taste, and significant weight loss. Id. She also had positive findings for ANA, anti-
phospholipid antibodies, and lupus anticoagulant. Id. Dr. Shoenfeld stated none of these

38
Elavil is an antidepressant also used for chronic pain. Dorland’s at 598, 63
39
Dr. Shoenfeld’s expert report is not paginated. The undersigned is using the page numbers on the top
right of the page that are part of the CM-ECF system.
45
manifestations was present prior to her February 2009 illness. Id. To Dr. Shoenfeld, that meant
Gardasil triggered them. Id. He did not mention, much less discuss, petitioner’s prior viral
illness on February 15, 2009.

In answer to question 2, that the 2007 symptoms dissipated and then returned after the
February 15, 2009 viral illness, Dr. Shoenfeld responded that petitioner’s 2009 viral illness was
only presumed because she had flu-like symptoms such as sore throat and enlarged nodes, but
not actually verified by laboratory testing. Id. Tests for bacterial infection were negative. Id.
Dr. Shoenfeld doubted that petitioner’s flu-like symptoms in 2009 were viral-based because they
are well-recognized symptoms for chronic fatigue syndrome (“CFS”), otherwise known as
myalgic encephalomyelitis. Id. Dr. Shoenfeld believed petitioner satisfied the criteria for CFS
because she had persistent fatigue for over six months, headaches, unrefreshing sleep, and
cognitive disturbances. Id. He then related that flu-like symptoms and CFS are associated with
certain vaccines, particularly vaccines containing aluminum and other adjuvants. Id. He stated
that because vaccines induce an immune response similar to infections, they may also trigger
autoimmune and immune-mediated inflammatory diseases, just as infections do. Id. Unlike
infections, however, vaccines frequently contain adjuvants, and Dr. Shoenfeld stated these
adjuvants enhance immune stimulation above the levels of natural infections. Id. To Dr.
Shoenfeld, this enhancement suggested “vaccines may provoke more exaggerated, anarchic
immune responses than infections.” Id. at 2. He found his observation particularly relevant
because vaccines, including Gardasil, typically are administered repeatedly over relatively short
periods of time, i.e., weeks or months. Id. Dr. Shoenfeld continued that vaccines have been
reported to precede CFS after exposure to multiple vaccinations and/or as an adverse response to
a vaccine adjuvant. Id. He stated that, since petitioner’s symptoms began after her second
Gardasil, “it is probable that her illness was triggered by an exaggerated pathological vaccine-
related autoimmune response.” Id. Dr. Shoenfeld mentioned numerous VAERS reports of
similar adverse manifestations, i.e., headaches, myalgia, fatigue, weakness, dizziness, flu-like
symptoms, autoimmune disorders, with comparable symptom onset, i.e., two to four months,
following receipt of Gardasil booster shots. Id.

In answer to question 3, that all of petitioner’s treating doctors noted the significance of
petitioner’s February 15, 2009 viral illness, Dr. Shoenfeld responded that these doctors only
presumed a virus was the cause based on her symptom presentation and not on any concrete
laboratory findings. Id. But, because flu-like symptoms are recognized as within the CFS
diagnosis, and CFS is “solidly linked” to vaccines, especially those containing aluminum
adjuvant, including Gardasil, he believed petitioner’s flu-like symptoms were due to her CFS and
not to a viral illness. Id. Dr. Shoenfeld also noted that VAERS reports describe flu-like illnesses
and thus are “possible adverse reactions to vaccines.” Id.

In answer to question 4, that there was a two-month interval between petitioner’s second
Gardasil and the onset of her renewed symptoms, Dr. Shoenfeld responded that a two-month
onset is not unusual for vaccine-related cases and has been previously reported after Gardasil.
Id. He noted that this is shown in supplementary Table 1, but did not provide this table with his
46
report. Id. Dr. Shoenfeld then cited to a medical case report of a teenage girl who died
unexpectedly six months after her third Gardasil booster. Id. In the autopsy blood and splenic
tissues HPV-16 L1 gene DNA fragments corresponding to 16 separate Gardasil vials from
different vaccine lots, suspected of being contaminants, were found, suggesting Gardasil caused
her death. Id. at 2-3. These particles were protected from degradation because they were bound
to particulate aluminum adjuvant used in the vaccine formulation. Id. at 3. In another case
report, Dr. Shoenfeld said there were three cases of systemic lupus erythematosus, including
exacerbation of pre-existing lupus, after Gardasil vaccination. Id. Symptom onset was between
two to four months post-vaccination. Id. Dr. Shoenfeld’s search of VAERS reports of those
complaining of flu-like symptoms, chronic fatigue, myalgia, headaches, weakness, dizziness,
joint pains, weight loss, photophobia, and lupus occurred mostly two to four months after
Gardasil. Id. He attributed flu-like symptoms and chronic fatigue to autoimmune illness
following Gardasil acting as the trigger. Id. Dr. Shoenfeld thought that treating doctors do not
attribute these events to the vaccine and frequently misdiagnose them as due to viral or microbial
illness despite lack of corroborative serological evidence. Id.

In answer to question 5, asking how Gardasil significantly aggravated petitioner’s pre-
existing symptoms, Dr. Shoenfeld responded that individual susceptibility factors play an
important role in determining the severity of adverse reactions. Id. Those risk factors include a
previous history of relevant symptoms and a family history of Raynaud’s disease. Id. These
may have made petitioner more susceptible to having a serious adverse reaction after Gardasil.
Id. Referencing a case study, Dr. Shoenfeld said that two out of three lupus cases fitting the
criteria for ASIA following Gardasil were exacerbations of pre-existing conditions. Id. He
noted that 21 percent of hepatitis B vaccine ASIA cases had either a personal or family history of
autoimmune diseases, referencing another article. Id. Since the estimated occurrence of
autoimmunity in the general population is from 5-8 percent, Dr. Shoenfeld suggested that those
with susceptibility are more likely to suffer disease exacerbation after vaccination. Id.

In answer to question 6, asking how the February 15, 2009 viral syndrome is not itself the
trigger of petitioner’s post-viral fatigue syndrome, Dr. Shoenfeld responded that his answers to
questions 2-4 respond to that. Id. at 4. He also stated that based on petitioner’s clinical
presentation, her flu-like symptoms were most likely an adverse reaction to Gardasil. Id.

In answer to question 7, asking why the advice of one of petitioner’s treating doctors, Dr.
Rowe, to increase her salt, exercise, and raise her pillow, was effective and caused her to
improve, Dr. Shoenfeld responded that those suggestions are standard for the management of
POTS and not surprisingly recommended to petitioner. Id. All POTS patients require a high salt
diet, copious fluids, and specific postural exercise training. Id. The high salt and fluid intake
increase the patient’s blood pressure and decrease her orthostatic dizziness. Id. Sleeping in a
position that tilts the head up decreases orthostatic hypotension. Id. Exercise improves
symptoms markedly in POTS patients, especially those with chronic fatigue. Id.

47
 On July 19, 2013, respondent filed the expert report of Dr. J. Lindsay Whitton, an
immunologist, discussing Dr. Shoenfeld’s ASIA hypothesis, and disputing its scientific
credibility. Ex. A.

On July 19, 2013, respondent filed the expert report of Dr. Edward W. Cetaruk, a
toxicologist, discussing Dr. Shoenfeld’s ASIA syndrome, and disputing its reliability. Ex. W.

On December 6, 2013, respondent filed three expert reports: (1) Dr. Carlos Rosé, a
pediatric rheumatologist; (2) Dr. Max Wiznitzer, a pediatric neurologist; and (3) Dr. Stephen
McGeady, a pediatrician and immunologist. Dr. Rosé, the pediatric rheumatologist, states that
petitioner has undifferentiated connective tissue disease (“UCTD”). He states that UCTD is “a
very useful concept to typify individuals who present with clinical and serologic features
suggestive of a connective tissue disease (CTD) but who do not meet criteria for a definable
CTD like Systemic Lupus, Sjögren’s or scleroderma but yet may be at risk for developing a
significant disease over time. Dr. [Michelle] Petri made the diagnosis based on Raynaud’s
symptoms, positive ANA and elevated values for Lupus anticoagulant (hexagonal phospholipid
test). None of [petitioner’s] ongoing additional symptoms (migraine headaches, dizziness, gait
abnormality) was part of her rationale for the clinical diagnosis.” Ex. RRR, at 6.

Dr. Rosé notes that petitioner’s gait abnormality had no physical basis. He notes that
three of petitioner’s treating neurologists diagnosed her with astasia-abasia, i.e., a non-
physiologic phenomenon, “a bizarre gait that does not correspond to any specific area of
neurologic deficit.” Id. at 8. Dr. Rosé also notes that almost two years before her Gardasil
vaccinations, petitioner had migraine and, in 2008 (also pre-vaccination), a mild form of regional
pain syndrome. Id. Dr. Rosé was “of the opinion that her progression to intractable migraine
complicated by astasia-abasia is nothing more than the natural course of chronic pain, a concept
known as pain amplification syndrome.” Id. He also states that the association of conversion
disorder and migraine is “not new or rare.” Id. Dr. Rosé has treated children with chronic pain,
frequently combined with fatigue, migraine, and POTS, and in his 30 years of experience, he has
not found immune or inflammatory mechanisms to be important in those conditions. Id. at 11.
As for Dr. Shoenfeld’s ASIA syndrome, Dr. Rosé doubts it exists. Id. at 12.

Dr. Wiznitzer, the pediatric neurologist, notes that petitioner had a history of headache
with light and noise intolerance and dizziness in 2007 (pre-vaccination) that persisted and then
resolved. Ex. BBBB, at 9. In February 2009, petitioner had an acute illness with fever, sore
throat, and swollen lymph nodes associated with headache. Id. Her headache quickly evolved
into a chronic daily headache pattern, which stress provoked or exacerbated. Id. Petitioner had
documented give-away weakness and gait disturbance diagnosed as astasia-abasia, which was
not physiologic but a well-known feature of conversion disorder. Id. Dr. Wiznitzer questioned
the diagnosis of petitioner with POTS because there were key clinical features of POTS absent at
the beginning. Id. Petitioner showed changes affecting heart rate, and occasionally blood
pressure, later. Id. Dr. Wiznitzer explains these symptoms by citing the conclusions of Dr. Peter
Rowe of Johns Hopkins Hospital, who, on August 11, 2010, “suspected that [petitioner’s]
48
connective tissue phenotype was allowing excessive vascular compliance in the dependent
circulation and was a factor contributing to her orthostatic intolerance along with deconditioning
which in turn caused a loss of plasma volume.” Id. Dr. Wiznitzer notes that petitioner’s
connective tissue phenotype predates her receipt of Gardasil vaccines in 2008. Id. He also notes
that POTS frequently appears after an identifiable trigger, such as a viral illness or a period of
prolonged disability, which occurs in individuals with chronic daily headache. Id. To Dr.
Wiznitzer, that identifiable trigger, if petitioner’s POTS started in February 2009, was her acute
illness, or if it started months later, her chronic daily headache. Id. Dr. Wiznitzer also notes that
petitioner’s episodes of syncope were associated with her taking Propanolol and they
significantly improved when she stopped taking it. Id. Dr. Wiznitzer concludes that petitioner’s
acute viral illness in February 2009 and the psychological problems associated with her
conversion disorder are sufficient to explain her symptoms. Id. at 10. He states there is no
evidence or biologically plausible model to associate petitioner’s December 2008 Gardasil
vaccinations with her 2009 clinical complaints. Id.

Dr. McGeady, the pediatrician and immunologist, states that ASIA is an unproven
hypothesis. Ex. MMMM, at 4. He opines that there is scant evidence of autoimmunity in
petitioner’s illness. Id. at 5. He notes that Dr. Shoenfeld acknowledges that autoantibodies are
often present for more than a year before any clinical manifestation of disease. Id. None of the
petitioner’s tests for acute inflammation was abnormal: white blood cell numbers, platelet
counts, erythrocyte sedimentation rates (ESR), C-reactive protein determinations, and
complement component determination. Id. Dr. McGeady does not agree that petitioner’s
elevated ANA and hexagonal phospholipids reflected she had an ongoing autoimmune process.
Id. at 6. Although Dr. Shoenfeld described petitioner as having an anamnestic response 40 to
Gardasil vaccine, Dr. McGeady notes that petitioner did not have an abnormal response to her
first vaccination and, after her second vaccination, two months elapsed until the onset of her
symptoms, thus belying an anamnestic response. Id. He notes that petitioner’s symptoms did
closely follow a sore throat, low-grade fever, and possible sinusitis. Id. Dr. McGeady also notes
that the medical records do not contain evidence of an acute inflammatory process following
either petitioner’s first or second Gardasil vaccination. Id. at 6-7. Dr. McGeady comments that
in Dr. Shoenfeld’s paper The Mosaic of Autoimmunity: Hormonal and Environmental Factors in
Autoimmune Disease (2008) which is Ex. 134, Dr. Shoenfeld identifies stress as a trigger for
autoimmune disease. Ex. MMM, at 7. Dr. McGeady notes that when petitioner became
symptomatic, her grandmother had died and her father had surgery. Id. He comments that Dr.
Shoenfeld does not consider stress as a trigger in his opinion, but blames Gardasil instead. Id.

40
An anamnestic response is also called a “secondary immune response,” which occurs “on the second
and subsequent exposures to an antigen; compared to a primary immune response, the lag period is
shorter, the peak antibody titer is higher and lasts longer, IgG production predominates, the antibodies
produced have a higher affinity for the antigen, and a much smaller dose of the antigen is required to
initiate the response.” Dorland’s at 1629.
49
 Dr. McGeady was not impressed with the literature petitioner submitted in defense of the
ASIA syndrome, most of which literature Dr. Shoenfeld wrote. Id. at 8. He states ASIA is not a
generally accepted diagnosis. Id. Dr. McGeady concludes that petitioner was susceptible to
developing an autoimmune disease but, so far, had not done so. Id. at 10. Her susceptibility is
based on a family history of maternal Raynaud syndrome and petitioner’s having an
autoantibody. Id. Dr. McGeady states that whatever condition “beset” petitioner in February
2009 “has defied diagnosis.” Id. POTS alone would not have caused all her symptoms. Id.
Three of her treating doctors opined that her condition had a non-organic cause. Id.

Dr. McGeady attached to his expert report an article entitled Postural tachycardia
syndrome following human papillomavirus vaccination, by S. Blitshteyn, Eur J Neurol
doi:10.1111/ene.12272: 1-5 (Epub Sept. 16, 2013) (see also, 21 Eur J Neurol 1:135-39 (2014)
(references will be to the page numbers of the electronic version filed as exhibit OOOO). 41 In
this article, Dr. Blitshteyn describes six patients who developed POTS six days to two months
after receiving Gardasil. Ex. OOOO, at 1, 2, and 4. Dr. Blitshteyn states that POTS is a
heterogeneous disorder, which may arise from various mechanisms and etiologies, but recently
there is evidence that POTS may be an autoimmune disorder. Id. at 4. Based on the finding of
several types of antibodies in patients with POTS, Dr. Blitshteyn writes she considers POTS “an
attenuated form of autoimmune autonomic neuropathy in a subset of patients.” Id. The
antibodies she describes are to ganglionic N-type acetylcholine receptors, various cardiac
proteins, and ß1/2 adrenergic and M2/3 muscarine receptors. Id. Based on these findings of
several autoantibodies in a subset of patients, Dr. Blitshteyn writes that POTS is considered to be
an autoimmune autonomic neuropathy in that subset of patients. Id. She writes that a virus,
surgery, pregnancy, or trauma are common triggers of POTS in a subset of patients. Id. She
writes possible pathogenesis of the subset of POTS that is autoimmune after Gardasil may
include molecular mimicry in which human papillomavirus vaccine epitopes may induce
formation of cross-reacting antibodies against potential targets of the autonomic ganglia,
neurons, cardiac proteins or ß1/2 adrenergic and M2/3 muscarine receptors. Id. She also states
that bystander lymphocyte activation and a broad spectrum of cytokine responses that human
papillomavirus vaccine elicits may also be involved. Id. Dr. Blitshteyn relates the onset of
POTS in the six subjects of six days to two months post-Gardasil to the onset timeframes of GBS
and acute disseminated encephalomyelitis (“ADEM”) after vaccination, and says they are
consistent with these well-known post-vaccination syndromes. Id.

(Of interest in the instant action is the fact that doctors tested petitioner for reactivity to
ganglionic neurons, and the result of the testing was negative, indicating petitioner’s POTS was
not autoimmune in nature and she was not in the subset of patients who had autoimmune POTS.

41
Petitioner also filed this article as Exhibit 426. Petitioner also filed a Letter to the Editor by Dr.
Blitshteyn entitled Postural tachycardia syndrome after vaccination with Gardasil, 17 Eur J Neurol 7:e52
(2010); doi:10.1111/j.1468-1331.2010.0321.x. Ex. 425. Dr. Blitshteyn writes that an autoimmune
etiology for POTS has been implicated in about 14 percent of patients with POTS after detection of
ganglionic acetylcholine receptor antibody. Id. at 1.
50
Med. recs. at Ex. 8, at 22. Therefore, petitioner’s POTS does not fit within the subset of POTS
Dr. Blitshteyn described in her article as being an autoimmune autonomic neuropathy.)

Dr. Blitshteyn also mentions that two of the patients experienced significant symptomatic
exacerbation following a re-challenge with a subsequent Gardasil vaccination, a phenomenon
suggesting a more robust autoimmune response yielding more severe symptoms with subsequent
receipt of Gardasil vaccine. Id. (Of interest in the instant action is the fact that petitioner had no
adverse reaction to her first Gardasil vaccination, unlike the two patients Dr. Blitshteyn
describes.)

None of the six patients in Dr. Blitshteyn’s study had a family history of autoimmune
disorders. Id. (In the instant action, petitioner has a family history of Raynaud’s syndrome and a
pre-vaccination onset of antinuclear antibodies.) Dr. Blitshteyn concludes her article with the
statement that Gardasil is possibly associated with POTS, but further studies are necessary to
determine if there is a causal relationship. Id. at 5.

On March 13, 2014, Dr. Shoenfeld responded to respondent’s Dr. Rosé’s expert report.
Ex. 472. He dismisses Dr. Rosé’s focus on petitioner’s pre-vaccination history of headaches,
dizziness, photophobia, and phonophobia in 2007 because these symptoms resolved. Id. at 2.
Dr. Shoenfeld states that “the vaccine could have been a possible triggering factor, or at the
very least, the exacerbating factor [emphasis added].” Id. at 3. He adds, “[A[n immune-based
etiology of POTS would support the idea that the vaccine may have been involved . . . .
[emphasis added]” Id. Dr. Shoenfeld admits that not all cases of POTS are autoimmune, and
states a fraction of POTS cases are autoimmune. Id. at 4. Dr. Shoenfeld cites a paper by Dr.
Phillip A. Low and colleagues on POTS, in which they found that ganglionic acetylcholine
receptor antibody was detected in 14.6 percent of the POTS cases. Id. Besides antibody to
ganglionic acetylcholine receptors in POTS patients, Dr. Shoenfeld states other researchers have
identified other autoantibodies, including antibodies to various cardiac proteins, to β1/2-
adrenergic and M2/3 muscarinic receptors, and to calcium channels. Id. at 4-5. He concludes
that some orthostatic syndromes are autoimmune. Id. at 5. In addition, he confirms that
orthostatic hypotension syndromes including POTS are a form of autoimmune autonomic
neuropathy in a subset of patients. Id. at 5-6. He estimates that 40 percent of patients with
chronic fatigue syndrome (“CFS”) also have POTS. Id. at 6.

In discussing petitioner’s case, Dr. Shoenfeld summarizes the letter to the editor and
article of Dr. Blitshteyn (discussed in Dr. McGeady’s expert report). Id. at 7-8. Dr. Shoenfeld
finds it “rather unfortunate” that three of petitioner’s neurologists labeled her symptoms as
psychogenic. Id. at 8.

Dr. Shoenfeld also opines that autoimmune neuropathies associated with Gardasil
vaccination can occur up to four to ten months post-vaccination. Id. at 14.

51
 On September 16, 2014, respondent filed Dr. Cetaruk’s response to Dr. Shoenfeld’s July
3, 2013 report regarding ASIA. Ex. PPPP. Dr. Cetaruk calls Dr. Shoenfeld’s ASIA theory
untested and unestablished. Id. at 3.

On June 22, 2015, respondent filed the supplemental expert report from Dr. Whitton,
again criticizing Dr. Shoenfeld’s ASIA hypothesis. Ex. BBBBBB.

Treating Doctors who Opined Petitioner had no physical abnormality or Gardasil was
unrelated to her symptoms

On May 4, 2009, petitioner and her parents saw Dr. Magdi Sobeih, a behavioral
neurologist, at Children’s Hospital in Boston. Med. recs. Ex. 2, at 1. Dr. Sobeih saw petitioner
to evaluate her headache and walking difficulties. “After a thorough evaluation I have concluded
that there are no neurobiological abnormalities or neuropathological concerns to [L.A.M.]’s
complaints.” Id. He stated, “I do not feel there is any association between the Gardasil HPV
vaccine and the onset of these symptoms.” Id. He continued:

I discussed this at length with the parents. I discussed that this is
presenting as a mood disorder that needs appropriate care. . . . It
would be very important to[o] that [petitioner] continue under the
care of appropriate psychological or psychiatric services and
someone to monitor her response to any medications such as
amitriptyline. However I do not feel there is any need for any
further neurological workup or followup. I discussed this with the
parents and with [petitioner] and I counseled further mental health
care should be provided.

Id. at 3-4.

On May 14, 2009, petitioner and her parents saw Dr. Nichter, a neurologist. Med. recs.
Ex. 553, at 108. Since her last visit, petitioner saw a pediatric neurologist in Boston who felt she
had a major psychological or psychiatric component to her ill-defined headache syndrome, and
was not convinced that petitioner had migraines. Id. Petitioner’s mother stated that petitioner’s
headaches were better but quite variable. Id. What was most pronounced was petitioner’s
abasia-atasia type gait. Id. Petitioner was unable to walk. There was no new weakness. Id. On
physical examination, she had giveaway weakness but, when this problem was mentioned to her,
she had 5/5 strength. Id. at 109. She would bear weight, but had lurching, swaying movements
when trying to walk. She would say “sharp” when a dull object was placed on her leg, but her
responses were inconsistent. Id. Dr. Nichter prescribed a mood elevator (Elavil). Id.

On November 8, 2009, petitioner and her parents saw Dr. Charles Rheeman, a neuro-
ophthalmologist, to evaluate petitioner for difficulty in reading. Med. recs. Ex. 15, at 2. He
wrote in a letter to Dr. Charles Argoff, a neurologist specializing in pain management:
52
 I do not have a good explanation for why she is having trouble
reading. At this point, I could not entirely rule out a non-organic
cause. For example, as far as her difficulty ambulating is
concerned, you told me you did not find any weakness or
numbness on exam. She could barely walk without her mother’s
assistance today. However, the patient’s mom told me [petitioner]
was able to walk about two miles trick or treating on Halloween
night.

Id.

On November 10, 2009, petitioner and her parents went to Johns Hopkins University to
see Dr. David Reid Cornblath, a neurologist, about petitioner’s headaches because he consulted
with Merck regarding Gardasil. Med. recs. Ex. 3, at 7. On physical examination, Dr. Cornblath
found petitioner’s gait striking. Id. at 9. When she walked with her mother, petitioner held on
quite tightly and appeared as though she were going to fall. Id. But, when petitioner walked
with Dr. Cornblath, she hardly required any real assistance. Id. She could rise from a chair
without the use of her hands. Id. Dr. Cornblath’s assessment was that, after a viral infection in
mid-February, petitioner developed what became incapacitating daily headaches. Id. Dr.
Cornblath stated that he discussed Gardasil with petitioner and her parents:

I have explained to the family why I do not believe her current
symptoms can be related to the Gardasil vaccine. We have gone
over the concepts of biological possibility and the kinds of events
of a neuroimmune nature that are known to occur following
vaccines at a low incidence. Her symptoms began two months
after vaccination and were closely in time follow[ing] some sort of
viral infection. Thus, I do not believe there is any relationship
between her current symptoms and her receipt of the Gardasil
vaccine.

Id. Dr. Cornblath also wrote:

There is no clear neurological explanation for her gait dysfunction.
This has been noted multiple times in her past records where her
gait has been called “astasia-abasia.”

At the end of the interview, [petitioner’s mother] asked me if I
thought she was crazy. I told her that she had a serious set of
symptoms for which the doctors had been unable to find the cause.
However, in most people of her age who have a normal neurologic
examination and extensive normal neurological testing, she has an
53
 excellent prognosis for her recovery. I explained . . . however that
a recovery of her medical condition requires close cooperation
with her [doctors] and a positive attitude on her part.

Id.

On November 17, 2009, petitioner and her parents saw Dr. Nichter again. Med. recs. Ex.
553, at 87. He wrote that petitioner had a profound migraine at the end of February, two months
after her Gardasil vaccination. Id. Nerve conduction, EMG, MRI, MRA and lumbar puncture
results were unremarkable. Id. at 87-88. In a personal phone call Dr. Nichter had with Dr.
Cornblath, a neurologist in Baltimore, after petitioner and her parents had seen Dr. Cornblath,
Dr. Cornblath told Dr. Nichter that he thought most of petitioner’s findings were not physiologic
(i.e., had no physical basis). Id. at 88. Petitioner had also seen a neuro-ophthalmologist who
looked at her retina and found her entire eye examination benign. Id. This doctor asked about
the stressors in petitioner’s life. Id. Petitioner’s headaches waxed and waned. Id. Petitioner
walked for probably five miles during a Halloween event the prior evening. Id. On physical
examination, petitioner was quite variable as for weakness. Id. at 89. At times, she was weaker
on the left than on the right, but it was inconsistent. Id. She could barely walk during the
examination, but when petitioner was coming in, she walked from the parking lot to Dr.
Nichter’s waiting room without any assistance. Id. Dr. Nichter’s plan was to discuss with Dr.
Karen Kennette, petitioner’s pediatrician, a psychiatric evaluation for petitioner and whether
petitioner should be on a mild mood elevator. Id. at 90.

On December 4, 2009, petitioner and her parents went to Dr. Michelle A. Petri and Dr.
Saru Sachdeva, rheumatologists, at Johns Hopkins University for a second opinion regarding her
headaches and positive ANA. Med. recs. Ex. 5, at 1. Her mother had possible rheumatoid
arthritis, although the family was not certain about it. Id. at 2. On neurological exam, petitioner
did not have any objective evidence of sensory or motor deficits. Id. at 3. Her Romberg’s test
was negative. Dr. Petri diagnosed petitioner with undifferentiated connective tissue disease
(“UCTD”) based on petitioner’s positive ANA, Raynaud’s disease, livedo, and lupus
anticoagulant. Id. She recommended petitioner take Plaquenil. In answer to petitioner’s
parents’ concern that Gardasil caused petitioner’s headaches, Dr. Petri wrote that symptom onset
was six weeks post-vaccination. (Actually, it was 10 weeks post-vaccination.) Id. Dr. Petri
engaged in a detailed discussion with the family. She said there is a mean of three to four years
between positive serologies and clinical onset of symptoms in systemic lupus erythematosus
(“SLE”). Plaquenil would delay the progression of UCTD to SLE. Ten percent of UCTD
progresses to SLE. Id. Dr. Petri noted that she could not connect petitioner’s UCTD to Gardasil.
Id.

On May 20, 2010, petitioner and her parents saw Dr. Nichter, who noted that petitioner
had headache with major visual complaints and abnormal autonomic function, although other
aspects of autonomic dysfunction, such as sweating, bowel, bladder, and gastric emptying, had

54
been totally normal. Med. recs. Ex. 18.3, at 2-3. Dr. Nichter stated, “One cannot cogently bring
all components to her history into a single story.” Id.

On August 11, 2010, petitioner saw Dr. Peter C. Rowe at Johns Hopkins University for
further evaluation of her orthostatic intolerance, fatigue, and other problems. Med. recs. Ex. 6, at
4. Dr. Rowe assessed petitioner as having “a post viral fatigue illness that now meets criteria for
chronic fatigue syndrome given her fatigue for more than 6 months, post exertional worsening of
the malaise, new-onset headaches, myalgias, cognitive problems, and unrefreshing sleep.” Id. at
7. He said, “I suspect the connective tissue phenotype is allowing excessive vascular compliance
in the dependent circulation, and is a factor contributing to her orthostatic intolerance, along with
the deconditioning, which in turn causes a loss of plasma volume.” Id. Petitioner was still
deconditioned. He suggested petitioner increase her exercise and improve her conditioning
status with physical therapy. Id. For the orthostatic intolerance, Dr. Rowe suggested she raise
the head of her bed and wear compression garments. She could use postural counter-maneuvers
such as clenching her fists when she began to stand or when she felt lightheaded. He also
suggested petitioner receive two-liter infusions of normal saline over one to two hours to
modulate autonomic tone. Id.

On November 21, 2012, petitioner and her mother saw Dr. Jennifer Lindstrom, a
pediatrician and internal medicine specialist. Med. recs. Ex. 552, at 23. Petitioner’s mother
believed that Gardasil caused all her medical problems, including gait instability, severe
headaches, an elevated ANA, and orthostatic hypotension. Id. Petitioner had been on multiple
headache medications without success. Hypnosis failed to help her and she refused to follow up
with neurology again. Petitioner saw a rheumatologist about her elevated ANA and was
diagnosed with undifferentiated connective tissue disease. She had not followed up on this. Dr.
O’Brien, recommended petitioner take midodrine and Florinef for her orthostatic hypotension,
but she was no longer taking them. She instead tried to follow a high sodium diet. Id. Petitioner
was drinking four to eight alcoholic drinks on the weekend, which qualified as binge drinking.
Id. at 24.

On December 12, 2014, petitioner and her mother again saw Dr. Lindstrom. Id. at 13.
Petitioner had general malaise in terms of decreased sleep, daytime fatigue, stressful dreams,
inability to focus, and feeling restless. Id. Dr. Lindstrom recommended petitioner get a
neuropsychiatric evaluation and counseling. Id. at 14.

On December 31, 2014, petitioner and her parents saw Dr. Nichter, the neurologist. Id. at
9. Stress was an issue for petitioner. Over the last several weeks, she had such difficulty with
stress that she would hyperventilate sometimes and have a 15- and 20-minute period where she
was not in control of herself. This exacerbated over the last few weeks. She had a significant
sleep dysfunction. Before trying to sleep, she would take a Tylenol PM, which contains
Benadryl, and then perhaps a glass of wine a few times a week. Id. She had daily headaches.
She did not take any medication for POTS but used various salts. Id. On physical examination,

55
she had normal gait. Id. at 10. Dr. Nichter’s plan was for the family to consider counseling vs.
psychiatry. The family was fine with the plan. Id.

Besides Dr. Nichter, Drs. Rheeman and Lindstrom attributed petitioner’s problems to
stress.

TESTIMONY

Petitioner testified first. Tr. at 14. At the time of the hearing, petitioner was participating
in an acting apprenticeship, which was in addition to her college curriculum. Id. at 15. She
stated she would love to be an actor and was passionate about the theater. Id. Petitioner said her
disability made every day a struggle. Id. She felt as if she were going to pass out three times a
day and she watched everything she ate and drank. Id. Petitioner said the headaches were
debilitating, but she pushed through every day because acting is what she wants to do and makes
her happy, even though she is in pain and struggling. Id. at 15-16. She said it was worth fighting
for. Id. at 16. She said there were days when her right knee hurts a lot because of all she has
been through relearning how to walk. Id. But, “for the most part we learn as actors that your
body is your instrument and you have to take care of it in certain ways, and sometimes it’s very
difficult to do with all of my medical list of injuries and everything.” Id.

Petitioner testified that she feels normal on some days and then, on other days, she has to
drag herself out of bed, stop crying, and continue with the day. Id. It changes from day to day.
Id. Every day, she wakes with a headache and goes to sleep with a headache. Id. at 17. She
constantly watches her blood pressure, her heart, and her head. Id. She has a migraine every day
that never goes away. Id. at 19. She has some limb stiffness and pain depending on the weather
patterns. Id. at 20. She was wheelchair-bound for seven months because she lost feeling in her
legs before she relearned how to walk. Id. She never used crutches before or after the
wheelchair. Id. at 21. She would fall down all the time. Id. She still faints, but she fights it. Id.
at 24. She has learned certain tricks like clenching her fists or sitting down and then getting back
up. Id. She watches her salt and sugar intake. Id. She estimates she has seen about 16 doctors,
if not more. Id. at 27. She has a top ten list of people she dislikes the most, and they are the
doctors that called her crazy. Id. at 28. She said, “I am not some case. I am a human being.
Please listen to me.” Id. One of those doctors worked at Boston Children’s Hospital and two
doctors worked at Johns Hopkins. Id. at 29. She said that the first doctor “with the great idea of
me being chronically insanely ill” was Dr. Sobeih, but Dr. Nichter has been her friend
throughout this entire process. Id. at 29-30. She said Dr. Nichter has no idea how to help her
and no answers, but he is the person she goes to if she has a problem. Id. at 30-31.

Petitioner had strep a few times when she was in elementary school. Id. at 32. She gets
rashes occasionally. Id. at 33. She has sworn off all medications except for birth control and
occasional ibuprofen. Id. at 34. She told her doctors she wanted to go “all natural” and live
without constantly having to take medicine. Id. at 35. She feels medication is not a necessity for
her anymore because it was just not doing anything. Id. Her doctors never really had an answer.
56
Id. at 36. They would all prescribe drugs in their specific field but no miracle drug to help. Id. at
37. She is off all the drugs. They were nothing and did not do very much; they did not help. Id.
at 38. The pain in her head was directing vivid dreams when she tried to sleep. Id. She does not
sleep very well. Id. She normally wakes more tired than when she went to sleep, and coffee is
her “friend.” Id. at 38-39. She wakes probably every twenty minutes to an hour and one-half, or
at least five times a night. Id. at 39. Most of the time, it is pain that wakes her. Id. Last year,
her grades were between 3.7 and 3.8. Id. She said she does pretty well in school and always has.
Id. at 39-40.

She just finished playing Maria in Shakespeare’s “Twelfth Night” as part of her acting
apprenticeship. Id. at 45. She was in rehearsal from 2:00 p.m. to 10:00 p.m. and was very tired,
“but it’s what I like to do.” Id. at 46. Acting is “a different place” and “you fuel yourself with
everything . . . to get yourself ready to be in this place.” Id. She lifts weights and goes to the
gym. Id. at 47. She wants to be the healthiest she can be. Id. She does squats, dead lifts, and
other forms of lunges with a bar that has weights on the sides. Id. The bar she uses weighs 35 to
45 pounds, and normally she puts 10 to 15 pounds on each side of the bar. Id. at 48. The 60- to
70-pound weighted bar is on her shoulders while she is doing squats and lunges, and she does
three sets of eight to ten repetitions. Id. She alternates between squats and lunges. Id. at 49. At
school, she goes to the gym two or three times a week. Id. She will exercise legs one day and
arms another day, and leave abdominals, cardiovascular and other things for a third day. Id. at
50. For cardiovascular, she normally uses a stationary bike or possibly the elliptical. Id. When
she goes to the gym, she drinks extra water and has some sugar or salt, and she feels good. Id. at
51. When she was in elementary school, she did plays, but she was mostly obsessed with
playing soccer. Id. She got into the theater program in high school and did a lot of backstage
work. Id. at 52. She has earned ten weeks of a 50-week requirement to earn an Actors’ Equity
card. Id. at 66-67. Petitioner drinks two to three cups of caffeinated coffee daily. Id. at 84-85.

Petitioner’s father testified next. Id. at 107. He is a cardiac surgeon at Albany Medical
Center. Id. at 108. Before receiving Gardasil, petitioner was very involved in soccer and had a
multitude of fractures with repeated visits to an orthopedic surgeon. Id. at 110. Eight weeks
after petitioner’s Gardasil vaccination, petitioner had a headache. Id. He thinks petitioner saw a
total of 20-25 doctors. Id. at 114. The closest they came to a diagnosis was at Johns Hopkins
where Dr. Peter Rowe diagnosed petitioner with chronic fatigue and POTS. Id. at 114. Dr.
Nichter, a pediatric neurologist at Albany Medical Center, has been providing continual support
to petitioner and her parents. Id. at 117-18. Dr. Nichter could never explain what petitioner’s
movement disorder was. Id. at 118. He was a cheerleader for petitioner to go to physical
therapy and go back to being functional. Id. None of the many medications Dr. Nichter
prescribed for petitioner worked. Id. at 119. When petitioner would curl up in a ball and sob
from headache pain, she would use oxycodone or hydrocodone. Id. at 119-20.

57
 Petitioner’s father focused on Gardasil as the cause of petitioner’s complaints when he
and his wife heard about a girl, Natalie Rowan, 42 who lives less than two blocks away from them
who had almost the identical symptoms petitioner had and had received Gardasil with the same
lot number as petitioner received. Id. at 121-20. Petitioner’s father never thought petitioner’s
illness was psychosomatic. Id. at 130.

Petitioner’s father prepared a summary of all of petitioner’s visits to doctors, but he did
not give this summary to Dr. Sandler, the psychiatrist, because petitioner and her parents saw Dr.
Sandler before petitioner’s father created the summary. Id. at 134. At the time petitioner saw
her personal care physician on February 26, 2009 with symptoms consistent with a viral or
bacterial infection, petitioner’s father wrote a prescription for Cipro for petitioner for presumed
sinusitis. Id. at 151-52. Petitioner’s father stated petitioner started fainting in the spring of 2009,
although his summary of petitioner’s medical records states she started fainting in October 2009.
Id. at 157-58.

Dr. Yehuda Shoenfeld, an immunologist, testified next for petitioner. Id. at 174. Dr.
Shoenfeld has edited and written almost 60 books on different aspects of autoimmune disorders.
Id. at 191. His opinion in the instant action is that Gardasil caused petitioner’s condition. Id. at
193. Dr. Shoenfeld said at least 12 different doctors saw petitioner before and after the
vaccination, and they were perplexed regarding her diagnosis. Id. at 193-94. He stated nobody
knew the right diagnosis. Id. at 194. Dr. Shoenfeld said three diagnoses were correct: chronic
fatigue syndrome, postural orthostatic tachycardia syndrome or POTS, and undefined connective
tissue disease or UCTD. Id. Doctors did not diagnose her with these three diseases before her
Gardasil vaccination. Id. Dr. Shoenfeld did not include migraine headaches as part of the three
diagnoses because “[m]igraine is a disease by itself.” Id. He stated migraine is a neurovascular
condition, which does not have an autoimmune etiology. Id. at 194-95.

He said petitioner has lupus anticoagulant, but she does not have antiphospholipid
syndrome. Id. at 195. He stated she is at great risk for developing autoimmune diseases, one of
which might be antiphospholipid syndrome. Id. Antiphospholipid syndrome or APS appears in
40 percent of cases of systemic lupus erythematosus or SLE. Id. at 196. Petitioner has

42
Natalie Rowan’s father Michael Rowan filed a petition on behalf of his minor daughter on May 3,
2010. When Natalie reached her majority, she became petitioner. Petitioner’s counsel in Rowan, Patricia
Ann Finn, is the same counsel for petitioner in the instant action (although petitioner at the time of filing
the instant action, i.e., who is the current petitioner’s father, was pro se until Ms. Finn filed a motion to
substitute in order to represent petitioner seven months after the filing of the petition). Petitioner’s expert
in Rowan, Dr. Yehuda Shoenfeld, is the same expert for petitioner in the instant action. Now-Chief
Special Master Nora Beth Dorsey dismissed Rowan. Rowan v. Sec’y of HHS, No. 10-272V, 2014 WL
7465661 (Fed. Cl. Spec. Mstr. Dec. 8, 2014). Petitioner appealed the dismissal. Judge Francis Allegra
affirmed the dismissal. 2015 WL 3562409 (Fed. Cl. May 18, 2015 (under seal); reissued June 9, 2015).
Petitioner appealed Judge Allegra’s affirmance of the dismissal to the Federal Circuit Court of Appeals.
The Federal Circuit dismissed the appeal because petitioner failed to file her appellate brief within the
time allotted and thus failed to prosecute. No. 15-5119 (Fed. Cir. 2015).
58
antinuclear antibody or ANA, lupus anticoagulant, and a positive rheumatoid factor. Id. at 197.
Doctors did not test for these autoantibodies before petitioner’s Gardasil vaccination. Id. at 199.
Dr. Shoenfeld believes that if doctors had tested petitioner before her Gardasil vaccination, they
would have detected these autoantibodies. Id.

Dr. Shoenfeld testified that antinuclear antibodies frequently occur in chronic fatigue
syndrome. Id. He said POTS and chronic fatigue syndrome are overlapping diagnoses and go
together quite often. Id. He mentioned that two papers say they are actually the same disease.
Id. Dr. Shoenfeld stated petitioner did not have joint pains before her Gardasil vaccination, but
she has them now, i.e., swollen knees, ankles, wrists. Id. at 199-200. She also had a rash. Id. at
200. Dr. Michelle Petri, petitioner’s rheumatologist, diagnosed petitioner with undefined
connective tissue disease because she could not say which one petitioner has. Id. at 201. Dr.
Shoenfeld said petitioner could develop rheumatoid arthritis, systemic lupus erythematosus, or
scleroderma. Id.

Before Gardasil vaccination, Dr. Shoenfeld said petitioner had headaches, phonophobia,
photophobia, some dizziness, and some fatigue. Id. After Gardasil vaccination, she had bad
headache, squeezing pain, vertigo, protracted headache, fainting while standing, sleeping
disturbances, memory problems, and abdominal complaints, the last three characteristic of
chronic fatigue syndrome. Id. at 201-02. Dr. Shoenfeld testified that petitioner’s enlarged lymph
nodes, fever, fatigue, and dizziness were clinical manifestations compatible with chronic fatigue
syndrome. Id. at 204.

Dr. Shoenfeld said that a two-month interval between Gardasil and onset was reasonable.
Id. at 206. Autoimmune disease is progressive. Autoantibodies also develop progressively. Id.
These autoantibodies may have developed sequentially to each other and not on the same date.
Id. at 206-07. Dr. Shoenfeld explained that the adjuvant in the vaccine causes the disease and
stimulates the immune system. Id. at 207. The adjuvant remains for weeks in the muscle where
the vaccine where the person received the injection. Id. This muscle was biopsied and scientists
found aluminum (the adjuvant) there. Id. The purpose of adjuvant is to enhance the immune
system. Id. In a vaccinee with a hyperactive immune system, usually a woman because women
have a better immune system than men, the vaccinee is more prone to develop autoimmune
disease. Id. at 207-08. Adjuvant is an environmental factor causing autoimmune disease. Id. at
208. People involved in sports also are more likely to respond to immunizations. Id. at 209.

Dr. Shoenfeld testified that petitioner’s doctors were not aware of the signs and
symptoms of very early autoimmune disease that Gardasil induced, and diagnosed petitioner
with a psychiatric problem. Id. at 212. Dr. Shoenfeld asked if petitioner’s joint pains, rash, and
livedo were psychiatric. Id. He also asked if petitioner could induce three different
autoantibodies due to a psychiatric problem. Id. at 213. He believed that eventually all
petitioner’s 12 doctors would have recognized she developed a classic autoimmune reaction after
Gardasil. Id. In conclusion, Dr. Shoenfeld said petitioner has classic undefined connective
tissue disease, which will most probably evolve into a well-defined autoimmune disease, chronic
59
fatigue syndrome, POTS, and three different autoantibodies. Id. at 214. Chronic fatigue can be
associated with headache. Id.

Dr. Shoenfeld testified that petitioner always had a tendency for autoimmune diseases
genetically because her mother has Raynaud’s phenomenon. Id. at 215. Even though petitioner
did not develop a full-blown autoimmune disease, Raynaud’s quite often characterizes patients
with different connective tissue disease or precedes connective tissue disease in the future. Id. at
215-16. As for headaches, they are a very common complaint. Id. at 216. Dr. Shoenfeld does
not believe petitioner had migraine headaches before Gardasil vaccination. Id. Migraine has
nothing to do with chronic fatigue syndrome because migraine is not an autoimmune disease. Id.
It is very common in young females, particularly when they start to menstruate and particularly
after menstruation. Id.

When petitioner was complaining pre-Gardasil that she had the feeling she was swaying
as if on a boat, Dr. Shoenfeld testified that this was not POTS. Id. at 217. He said POTS occurs
when someone rises from a recumbent position to the erect position and then experiences a fall in
blood pressure and an increase in heart rate (tachycardia), associated with fainting. Id. Dr.
Shoenfeld said that petitioner did not have POTS before receiving Gardasil. Id.

In describing two plausible mechanisms of causation in this case, Dr. Shoenfeld said the
first is classic molecular mimicry. Id. In Gardasil, in the structure of the viral particles, called
the L1, is a portion denoted as numbers 16 and 18, which have molecular mimicry found in
many constituents of the human body. 43 Id. at 218. Channels of calcium and potassium, active
in our autonomic nervous system, are some of those bodily constituents. Id. The autonomic
nervous system adjusts our blood vessels from the supine position, where they are dilated, to the
erect position, where they must be squeezed to enable the blood to flow to the brain. Id.
Gardasil generates autoantibodies against these constituents into the nervous system, causing
malfunction of the system and POTS. Id. at 218-19. Because the adjuvant is in the vaccine, the
molecular mimicry is also there. 44 Id. at 219.

43
Petitioner filed articles discussing HPV L1: Potential cross-reactivity between HPV16 L1 protein and
sudden death-associated antigens by D. Kanduc, 9 J Exp Ther Oncol 159-65 (2011) (P. Ex. 502, also filed
as P. Ex. 546) (matches between HPV16 L1 and human proteins which, when altered, are associated with
cardiovascular diseases and arrhythmogenic disorders); Quantifying the possible cross-reactivity risk of
an HPV 16 vaccine by D. Kanduc, 8 J Exp Ther Oncol 65-76 (2009) (P. Ex. 503, also filed as P. Ex. 547)
(host tissues expressed antigens sharing sequences with possible physical consequences such as spinal
muscular atrophy, cardiovascular and musculoskeletal abnormalities, and increased risk of coronary
artery disease).
44
Petitioner filed articles relating HPVL1 gene DNA to aluminum adjuvant: Detection of human
papillomavirus L1 gene DNA fragments in postmortem blood and spleen after Gardasil vaccination—A
case report by S.H. Lee, 3 Advances in Bioscience & Biotechnology 1214-24 (2012) (P. Ex. 30, also filed
as P. Ex. 147 and P. Ex. 339) (presence of HPV16 L1 gene DNA in blood and spleen of teenage girl who
suddenly died six months after receiving Gardasil; interprets gene fragments not degrading over six
months after vaccination to binding to particulate aluminum adjuvant in HPV vaccine); Detection of
60
 Dr. Shoenfeld said the second plausible mechanism is small fiber neuropathy, 45 which is
also probably an autoimmune condition, and results from a viral constituent that most probably
causes an autoantibody that destroys the ending of fibers in the skin. Id. The regular nerve
fibers are not affected and an EMG would be normal. Id. A neurologist will use a biopsy to
diagnose small fiber neuropathy. Id. Doctors found that half of patients with chronic fatigue
syndrome, fibromyalgia, and POTS had biopsies, which indicated small fiber neuropathy. Id.
Petitioner never had a biopsy. Id. at 220. Dr. Shoenfeld concluded there are at least two
mechanisms by which Gardasil can cause a malfunctioning of the autonomic nervous system. Id.
at 219.

To Dr. Shoenfeld, the fact that petitioner had clinical manifestations and abnormal
laboratory findings (lupus anticoagulant, rheumatoid factor, ANA) after Gardasil within two
months means Gardasil caused them. Id. at 220. Dr. Shoenfeld means all the adjuvants in
Gardasil, not just aluminum, caused the autoimmunity. Id. at 221, 227. He said that his
testimony is descriptive of the ASIA syndrome because adjuvants induce autoimmune diseases,
i.e., undefined connective tissue disease, SLE, antiphospholipid syndrome, chronic fatigue
syndrome, and POTS. Id. at 234. His opinion is that a combination of the effects of the surface
antigen of the human papillomavirus, plus adjuvants in general, is the cause of petitioner’s
illnesses. Id. at 237. He believes petitioner suffers from an autoimmune condition that adjuvants
and the virus particles induced. Id. at 238-39. The adjuvant alone could have caused her
injuries, but we do not know. Id. at 239. Dr. Shoenfeld said that, in this case, the adjuvant
contributed to the condition because, without the adjuvant, there would not have been an
enhanced immune response to the viral particles in Gardasil. Id. at 248. In general, he thinks
adjuvant alone can cause autoimmunity, but, in this case, a combination of the adjuvant with the
vaccine caused petitioner’s autoimmune condition. Id. at 249, 256. Petitioner did not have
macrophagic myofasciitis syndrome. Id. at 257.

Respondent’s counsel realized that Dr. Shoenfeld was not basing his theory of causation
on aluminum adjuvant alone causing petitioner’s conditions, i.e., he was veering away from his
ASIA theory which posits causation from aluminum as a vaccine adjuvant without adding in any
other components of the vaccine. Id. at 239-88. Through an extensive series of questions and
answers, Dr. Shoenfeld stated he was no longer relying on certain articles dealing with ASIA that
petitioner had filed as evidence, but on the other hand, he was relying on other articles. For
example, he relied on an article on aluminum injections in mice causing motor deficits and motor

human papillomavirus (HPV) L1 gene DNA possibly bound to particulate aluminum adjuvant in the HPV
vaccine Gardasil® by S.H. Lee, 117 J Inorganic Biochemistry 85-92 (2012) (P. Ex. 31, also filed as P. Ex.
148 and P. Ex. 338) (analysis of 16 Gardasil samples results in residual HPV DNA fragments bound to
adjuvant, presumably aluminum, but clinical significance requires further investigation).
45
“Small fiber neuropathies lead to pain and temperature sensory loss, painless ulceration, injury, and
neuropathic joint degeneration . . . .” Peripheral Neuropathy, Vol. 1, at 1146 (eds. P.J. Dyck, et al. 4th ed.
2005). Petitioner was never diagnosed with small fiber neuropathy.
61
neuron degeneration because that would show aluminum adjuvant can cause small fiber
neuropathy even though there is no proof that petitioner has small fiber neuropathy. Id. at 263.
At this point, the undersigned stated it was not helpful to prove a mechanism for an illness
petitioner did not have. Id. at 264. The undersigned offered to give petitioner time to obtain a
biopsy to prove that she has small fiber neuropathy. Id. Dr. Shoenfeld stated the theory of
aluminum causing small fiber neuropathy was helpful because it was a “possible theory” in
petitioner’s case. Id. The undersigned then stated the standard of proof is probability, not
possibility. Id. At which point, Dr. Shoenfeld testified that it is probable that petitioner has
small fiber neuropathy because half the patients in the paper he was discussing had small fiber
neuropathy. Id. at 265-66. The undersigned rejected that petitioner has small fiber neuropathy
based on half of the subjects in the paper having small fiber neuropathy. Id. at 266. Petitioner’s
attorney said she would consider having petitioner undergo a biopsy to determine if she has
small fiber neuropathy and would let the undersigned know the next day. Id. at 267-68. Dr.
Shoenfeld then said in answer to respondent’s counsel’s question that he did not know if
aluminum adjuvant alone could cause small fiber neuropathy. Id. at 268.

Because Dr. Shoenfeld was no longer advancing an adjuvant only theory as the
explanation for how Gardasil can cause various illnesses, respondent opted to no longer rely on
the expert testimony of Drs. Cetaruk and Whitton. Id. at 301. The undersigned asked Dr.
Shoenfeld if he agreed that there was no physical reason for petitioner to have been in a
wheelchair. Id. at 304. Dr. Shoenfeld responded yes. Id. Then he said that chronic fatigue or
extreme fatigue might have been the reason petitioner did not walk. Id. He said these are
subjective symptoms and we cannot understand how much she was fatigued. Id. He said there
are two kinds of fatigue: (1) muscle fatigue, and (2) fatigue from the brain. Id. at 304-05. Many
patients with POTS and chronic fatigue syndrome also have depression. Id. at 305. Petitioner
had difficulties with smell and taste. He said difficulty with smell is quite often associated with
depression. Id. Autoantibodies can be associated with depression. Id. at 307. He and his co-
authors injected into mice an antibody from the blood of patients who were depressed and had
lupus. Id. Mice in a bucket of water will swim. Id. But the mice who were injected with the
antibody from depressed lupus patients did not swim; they floated. Id. Dr. Shoenfeld said they
floated because they were depressed. Id. When Dr. Shoenfeld gave the depressed mice smells,
such as orange, citron, grapefruit, or lavender, i.e., aromatherapy, they woke up and began to
swim. Id. at 308. Dr. Shoenfeld concluded that depression can have an autoimmune origin and
is involved with the lack of smell because the antibody binds to the limbic area of the brain,
responsible for both emotions and smell. Id. He said women who are depressed do not smell,
and they splash too much perfume on themselves. Id. When they stop being depressed, they feel
awful for splashing too much perfume on themselves and stop doing so. Id. Relating this to
petitioner, Dr. Shoenfeld said that petitioner was depressed and lost her sense of smell. Id.
These symptoms joined with her feeling she could not walk and she took to a wheelchair. Id.
He said this is a repeated complaint of many patients with POTS. Id. at 309.

In light of Dr. Nichter’s note that petitioner walked unaided from the parking lot to his
office, but then could only walk with assistance inside his office, the undersigned queried Dr.
62
Shoenfeld’s analysis that petitioner’s depression, difficulty smelling, and needing a wheelchair
were linked. Id. at 310-11. Dr. Shoenfeld replied that in POTS, as in many autoimmune
diseases, the manifestations are not continuous and persistent. Id. at 311. He also said that
POTS is not continuous but may be intermittent. Id. The undersigned also queried petitioner’s
walking probably five miles during a Halloween event, but when Dr. Nichter tested her for
weakness, petitioner’s response varied. Id. at 312. Because of petitioner’s variability in physical
testing of strength, Dr. Nichter noted he was going to discuss the results of her examination with
petitioner’s personal care physician, i.e., Dr. Kennette, and recommend a psychiatric evaluation
and a mild mood elevator. Id. Dr. Shoenfeld responded that, eventually, petitioner developed
autoimmune phenomena, and he assumes petitioner was at the incubation stage when she had
these inconsistent behaviors. Id. at 315. He admitted that mood has a physiological basis. Id. at
316. But, he also said that psychiatric manifestations have an organic source in the brain. Id. at
317. He said different chemicals in someone’s brain can affect his or her mood, and one of the
examples is smell, which can affect mood. Id. If smell is affected, so is taste. Id. at 318.

Dr. Shoenfeld stated that petitioner does not fulfill the criteria for systemic lupus
erythematosus because she does not have four out of eleven criteria; she has three out of eleven.
Id. at 318-19. He does not think petitioner has SLE, but she has a good chance of developing
SLE in the future. Id. at 319. She could develop antiphospholipid syndrome. Id.

On cross-examination, Dr. Shoenfeld stated petitioner does not have acute cerebellar
ataxia. Id. at 347. He has between 50 and 100 chronic fatigue patients and treats almost none of
them with immune suppressants. Id. at 370, 372. He has between 10 to 20 POTS patients, most
of whom overlap with chronic fatigue. Id. at 372-73. He does not treat any of them with
immunosuppressants because they have severe side effects. Id. Dr. Shoenfeld recommended
vitamin D in large doses, i.e., 2,000 units per day, to prevent or slow down the process of
autoimmune disease. Id. at 389. For molecular mimicry to occur, at least three weeks and
sometimes more weeks are necessary to generate autoantibodies. Id. at 375. Then the
autoantibodies need to increase in titer to reach and penetrate the target organ. Id. This takes
weeks. Id. An article by Arbuckle 46 about military personnel who developed lupus showed that
their blood, taken 10 years earlier before they became symptomatic and which was still
preserved, contained autoantibodies of anti-CCP and rheumatoid factor. Id. at 387, 392. To
explain why it could take 10 years for someone with autoantibodies to manifest autoimmune
disease, Dr. Shoenfeld stated sometimes the process is prolonged and sometimes a person needs
another hit. Id. at 388. The slow process is called incubation time. Id. This is why petitioner is
at great risk of eventually developing autoimmune disease – she has three autoantibodies. Id. at
389.

Dr. Shoenfeld set the interval between petitioner’s second Gardasil vaccination and the
onset of her POTS at two months. Id. at 392. Dr. Shoenfeld stated we can never know if

46
Arbuckle, M.R., et al., Development of Autoantibodies before the Clinical Onset of Systemic Lupus
Erythematosus, 349 NEJM 1526-33 (2003). P. Ex. 334.
63
petitioner had a positive rheumatoid factor, lupus anticoagulant, and elevated ANA before her
Gardasil vaccinations because she was not tested for them, but she was genetically prone to
develop them. Id. at 393. He said petitioner is part of a family with autoimmune disease. Id. at
395. For example, petitioner’s mother has Raynaud’s phenomenon. Id. In addition, petitioner’s
maternal grandmother has thyroid disease. Id. Most thyroid disease is autoimmune. Id. at 396.
To Dr. Shoenfeld, the first “hit” (i.e., cause) is genetics. Id. at 395. The second “hit” for
autoimmune disease could be a vaccine, silicon implant, infections, etc. Id. at 395-96.

Dr. Max Wiznitzer testified for respondent. Id. at 410. He is a pediatric neurologist with
patient care and teaching responsibilities. Id. at 411-12. He has had patients with POTS, chronic
fatigue syndrome, autoimmune disease, and headache disorders. Id. at 415, 416, 418, 419. He
sits on the editorial boards for Lancet Neurology and the Journal of Child Neurology. Id. at 423.

Dr. Wiznitzer’s opinion is that Gardasil did not cause petitioner a neurological injury. Id.
at 425. In June 2007, petitioner had a headache lasting for at least a week, associated with
dizziness, and light and noise intolerance, but no vomiting or fever. Id. On February 21, 2009,
petitioner had a bad headache that tended to persist, with noise intolerance, similar to her
complaint in 2007. Id. Cold symptoms, nausea, and dizziness occurred a week before it,
consistent with an acute viral infection. Id. at 425-26. Petitioner continued to have headaches
from that time forward and went to an emergency room in early March for an evaluation,
involving a neurologist. Id. at 426. She had her first brain MRI in 2007 and her second brain
MRI in 2009 because of her headache. Id. She continued to have headache, vertigo, and
photophobia that caused daily dysfunction. Id.

Dr. Wiznitzer testified that petitioner’s neurologic examination did not show any
abnormalities of strength or tone. Id. She reported some walking issues and reduced her
activities because of the constant headache complaints. Id. By September, she was having
fainting spells, seeing black dots in front of her eyes. Id. Dr. Peter Rowe diagnosed petitioner
with POTS in August 2010, after a cardiology evaluation in December 2009. Id. at 427.
Petitioner testified that she continues to have headache complaints and some lightheadedness and
dizziness intermittently. Id. Her blood tests showed a positive ANA and rheumatoid factor, and
the equivalent of a lupus anticoagulant. Id. At Dr. Rowe’s request, petitioner had an extensive
battery of tests against antibodies, including against the P/Q calcium channel, acetylcholine
receptor, and various other things, all of which were negative. Id. Petitioner’s current diagnosis
is POTS and chronic daily headache syndrome. Id. at 428.

Petitioner had a viral illness on February 26, 2009. Id. This was about 11 weeks after
her second Gardasil vaccination. Id. at 429. Her cold was not due to the vaccination. Id.
Petitioner had had a prior headache event in 2007, which was unrelated to any vaccination. Id.
Acute viral illnesses can trigger chronic daily headaches and transform an individual who had
episodic headaches into having chronic daily headaches. Id. On March 6, 2009, petitioner went
to the emergency room at Albany Medical Center. Id. at 430. The record said that petitioner’s
Romberg was negative, but she appeared to overcorrect with loss of balance. Id. Her gait was
64
narrow-based but ataxic with her requiring assistance in order to walk without falling. Id. The
diagnosis was headache and ataxia. Id. Dr. Wiznitzer disagreed that petitioner had ataxia. Id. at
431. Dr. Nichter, a pediatric neurologist, saw petitioner in the ER on the same date, and noted
that petitioner had a normal gait. Id. Dr. Nichter wrote that she had a tandem gait with an ever
so slight wobble. Id. She hopped on one foot and two feet, and squatted without difficulty. Id.
His diagnosis was that petitioner did not have concerning ataxia or vertigo. Id.

Dr. Wiznitzer finds it significant that petitioner did not have ataxia on March 6, 2009. Id.
at 432. Dr. Wiznitzer said that the ER doctor did not know as much about ataxia as Dr. Nichter,
a pediatric neurologist. Id. Dr. Wiznitzer testified it is not plausible that a person with
significant ataxia will have a narrow base to her gait. Id. Dr. Wiznitzer then stood up in the
courtroom and demonstrated what he was saying. Id. at 433. Normally, people typically stand
with a narrow base, meaning with their feet maybe six inches to a foot apart. Id. A person with
ataxia, i.e., unsteadiness, looks like he is drunk. Id. A drunk person cannot stand with his feet
together. Id. That is why the police test a driver by having him walk a line, which is a narrow
base. Id. A drunk driver will stand with his feet about two feet apart as he walks, and is
unsteady and will typically fall over. Id. at 433-34. If, however, someone walks with a narrow
base and yet is unsteady, that is not ataxia. Id. at 434.

Moreover, Dr. Wiznitzer testified, ataxia does not come and go. Id. If petitioner truly
had ataxia on March 6, 2009, it would not be there for the emergency room doctor and gone
when Dr. Nichter examined her. Id. Dr. Shoenfeld postulated that petitioner’s ataxia was
immune-mediated, but if it were, the ataxia would not have gone away. Id. Dr. Wiznitzer’s
opinion is that petitioner never had ataxia. Id. at 435. Dr. Wiznitzer called what petitioner had a
gait disturbance. Id. In 2007, petitioner also had a gait disturbance, where she needed support
when she was not feeling well. Id. at 435. Petitioner’s episode on June 6, 2007 could be due to
ataxia or vertigo when doctors diagnosed her with a migraine headache since either ataxia or
vertigo is a known accompaniment of migraine. Id. at 436. Dr. Wiznitzer testified that this
March 6, 2009 emergency room record was the only place in petitioner’s medical records where
a doctor (a non-neurologist) mentioned ataxia, and none of her neurologists stated she had ataxia.
Id. at 437.

Dr. Wiznitzer turned to an August 2009 physical therapy record, which stated petitioner’s
physical presentation with immobility continued to be incongruent with objective measurements.
Id. He said that note was consistent with the doctors’ diagnosis of petitioner with astasia-abasia.
Id. The way petitioner moved was not consistent with the features of her actual exam. Id. at
438. People with astasia-abasia maintain a narrow base when they walk and appear to fall or
bump into things, but never suffer any serious injuries. Id. They may have giveaway weakness
of the extremities so that, as they walk, suddenly, their knees seem to give out from under them.
Id. Astasia-abasia is not a gait that is physiologic in nature. Id. Astasia-abasia does not look
like ataxia. Id. It also does not look like dystonia, rigidity, chorea, or any of the other movement
disorders that neurologists typically see. Id. Dr. Wiznitzer testified that there is no doubt that
petitioner had astasia-abasia. Id. at 439. Dr. Sobeih in Boston diagnosed petitioner with astasia-
65
abasia on May 4, 2009. Id. Dr. David Cornblath from Johns Hopkins diagnosed petitioner with
astasia-abasia. Id. Petitioner’s treating pediatric neurologist Dr. Nichter diagnosed petitioner
with astasia-abasia on May 28, 2009 and July 6, 2009. Id. Dr. Argoff was also concerned about
petitioner’s gait because he could not categorize it. Id. at 441.

Dr. Wiznitzer and other neurologists get patients all the time for evaluation of their gait to
determine if their gait has an organic origin or is symptomatic of a conversion disorder. Id. at
439-40. The latter is a disorder of the mind. Id. at 440. Astasia-abasia does not indicate a
neurologic injury, but is a psychological disorder, part of the somatoform disorders in the
Diagnostic and Statistical Manual of Mental Disorders (“DSM”). Id. It is a problem with
standing and/or walking that no organic problem can explain, which means the individual has no
identifiable problem with strength, tone, coordination, or sensation. Id. The article to which Dr.
Shoenfeld referred during his testimony (Ex. 504, a case report of acute cerebellar ataxia 12 days
after HPV vaccination) is irrelevant to this case because petitioner did not have a chronic or
acute ataxia syndrome, and, in any event, a case report does not prove causation. Id. at 442, 443.

Dr. Wiznitzer disagreed with Dr. Shoenfeld that petitioner lost her sense of smell. Id. at
443. The medical records state that petitioner complained certain smells bothered her. Id.
Another record says altered taste and smell, not lost taste and smell. Id. 444. Petitioner
complained that food tasted weird, and was either too salty or too bitter. Id. at 446. Petitioner
said smells annoyed her. Id. Another record states petitioner had a heightened sense of smell
and taste. Id. at 447. She found many tastes noxious. Id. Dr. Shoenfeld used loss of smell as
the reason to refer to a mouse model to hypothesize an antibody mechanism, but Dr. Wiznitzer
said this has no relation here because petitioner did not lose her sense of smell. Id.

In November 2009, petitioner saw Dr. Nichter, who performed a neurological
examination. Id. at 447-48. Petitioner was quite variable as to weakness. Id. at 449. At times,
she was weaker on the left than on the right side, but the weakness was inconsistent. Id.
Petitioner could barely walk during the examination, but when she came from the parking lot,
she walked to the waiting room without assistance. Id. Petitioner could not jump on two feet
without some assistance, but at other times, she was able to jump perfectly fine. Id. Dr.
Wiznitzer called this a waxing/waning examination. Id. He stated this was clearly not ataxia.
Id. Moreover, when someone manifests waxing/waning strength and she does not have
myasthenia gravis (and even with myasthenia, someone would need a nap or medication to
regain strength), then the only explanation is conversion disorder. Id.

Dr. Wiznitzer defined POTS as consisting of complaints of dizziness, and
lightheadedness, with perhaps seeing spots before one’s eyes. Id. at 450. It occurs when
someone goes from the lying position to the standing position. Id. If the patient lies down, he or
she feels much better. Id. POTS is associated with an increase in heart rate. Id. The person
feels lightheaded, dizzy, faint, a little nauseated, maybe has spots before his or her eyes, due to
inadequate blood flow to the brain. Id. at 452. Generally, people do not pass out, but can have
near syncope. Id. Petitioner herein never had a tilt table test. Id. at 453. The undersigned then
66
asked petitioner’s father if petitioner had ever had a tilt table test and he said no. Id. He said that
Dr. Peter Rowe said he was confident just from his examination of petitioner that she had POTS.
Id. Dr. Wiznitzer accepts that petitioner has POTS. Id. at 454. POTS is a problem with
neurological control of circulation. Id. Some cases of POTS are immune-mediated. Id. A small
number of POTS patients have ganglionic isotope choline receptor antibodies. Id. However,
petitioner was tested for those ganglionic antibodies and the result was negative. Id. Petitioner
had no measurable level of ganglionic isotope choline receptor antibodies. Id. Neurologists can
diagnose POTS. Id.

Dr. Wiznitzer sees POTS patients in his practice. Id. at 455. Deconditioning can cause
POTS. Id. POTS can also happen after an acute illness, after surgery, and if someone is lying or
sitting around and becomes deconditioned. Id. If someone develops POTS from an illness, it
can be concomitant with the illness or within a week or two after it. Id. at 455-56. Dr. Rowe
noted in his record that petitioner did not walk much until August 2009. Id. at 457. Dr.
Wiznitzer’s opinion is that petitioner’s onset of POTS was when she reported fainting spells in
September or October 2009. Id. at 458. Petitioner did complain in March and April 2009 about
headaches and gait problems, but her gait was actually astasia-abasia, which does not reflect poor
coordination. Id. Petitioner’s complaint in March and April 2009 was not due to weakness. Id.
However, if we consider petitioner’s complaint of lightheadedness as due to POTS, her onset of
POTS might have been in March or April 2009. Id. at 459. She did not have POTS in June 2007
when she had an episode of dizziness. Id. at 459-60.

Dr. Wiznitzer stated that his POTS patients do not normally present with headaches. Id.
They normally present with complaints of dizziness, lightheadedness, and weakness. Id. Later,
they may start complaining of headaches. Id. He thinks petitioner’s headaches were related to
her viral illness. Id. One can have headaches with chronic fatigue syndrome. Id. at 461. Dr.
Wiznitzer has no opinion about the onset of petitioner’s chronic fatigue syndrome. Id.

In discussing Dr. Shoenfeld’s hypothesis that there are amino acid sequences on the L1
protein of HPV, specifically HPV16, which set off molecular mimicry in the vaccinee, Dr.
Wiznitzer said he disagreed. Id. at 461-62. Dr. Shoenfeld’s theory assumes that a five-amino
acid sequence is sufficient to cause an antibody to form. Id. at 462. But the sequence is too
small to cause antibody formation. Id. Rather, one would need at least 10-15 amino acids to
have a chance to form an antibody. Id. at 463. Even a five-amino acid sequence forming an
antibody does not equal a functional antibody that harms someone. Id. We have numerous
antibodies in our blood which are detectible, but do not cause problems. Id. Dr. Shoenfeld also
assumes that this hypothetical antibody can get to the target of interest and, if it does, that it can
actually bind to the target of interest. Id. The assumption also is that if the antibody binds to the
target, it will disrupt the function of the molecule and that this molecule has anything to do with
petitioner’s problems. Id. Dr. Wiznitzer testified that Dr. Shoenfeld’s hypothesis is conjecture
built upon speculation. Id. at 463-64.

67
 Dr. Wiznitzer testified that Dr. Shoenfeld testified about a CACNA1C gene product,
quoting from Kanduc’s paper. Id. at 464. This gene product helps make a calcium channel
known as an L voltage-gated calcium channel, which is calcium channel 1.2. Id. This calcium
channel is not present in the peripheral autonomic nervous system. Id. There are different
channels in the peripheral autonomic nervous system. Id. Since the L voltage-gated calcium
channel, i.e., calcium channel 1.2, is not present in the peripheral autonomic nervous system, the
antibody cannot attack it. Id. That channel is located in the brain. Id. at 465. There is no
peripheral nerve involvement or peripheral autonomic nerve involvement. Id. at 466, 467.

Dr. Wiznitzer testified that Dr. Shoenfeld’s other hypothesis was that this hypothetical
antibody would target a calcium channel in the heart and cause POTS. Id. at 480. Dr. Wiznitzer
does not know any good biological model to support that hypothesis. Id. When that calcium
channel becomes dysfunctional, the person develops true arrhythmias and heart disturbances. Id.
at 481. Brugada syndrome 47 is tachyarrhythmia 48 with the risk of sudden death, not a little bit of
increase in heart rate when someone stands. Id. If a targeted calcium channel in the heart caused
cardiac dysfunction, the blood pressure would be low and the person would not have POTS. Id.
Because of the low blood pressure, it would not matter whether the person was standing or lying
down. Id. at 482.

Dr. Wiznitzer explained petitioner’s reeling back and forth as the result of a combination
of lightheadedness from the discomfort of her headache and the headache. Id. at 471. Later on,
she had the POTS-type of complaint, which made her feel a bit unsteady. Id. We know she had
astasia-abasia, which is conversion disorder. Id. Depression does not cause the kind of gait
petitioner had. Id. at 472. Dr. Wiznitzer agreed with Dr. Shoenfeld that petitioner had a change
in her mood, i.e., depression, which sent her to a wheelchair for seven months. Id. Dr. Wiznitzer
has patients who are depressed and stop their activities. Id. They sit in their room all the time.
Id. Their mood heightens whatever somatic complaints they have. Id. at 463. However,
petitioner’s depression was not immune-mediated in this case. Id. Someone with a conversion
disorder does not have frank anxiety or depression. Id. at 474. A conversion disorder exists
because of some psychological process that is so bothersome to someone that she manifests it in
a different way, e.g., through gait disturbance. Id. at 474-75. This decreases the psychic pain
associated with confronting the issue she does not want to confront. Id. at 475. That is the
primary gain for conversion disorder. Id. at 476. The secondary gain for conversion disorder is
to get a lot of attention. Id. Dr. Wiznitzer believes that petitioner’s chronic daily headache is
due to stress because when she returned to school, her headaches increased. Id. at 477. There
has to be a psychological component to petitioner’s headaches. Id. at 478.

47
Brugada syndrome is “a type of ion channelopathy characterized by sudden, idiopathic ventricular
fibrillation in an apparently healthy person, often resulting in death (sudden adult or sudden arrhythmia
death syndrome). It is autosomal dominant and occurs most often in males of Southeast Asian origin.”
Dorland’s at 1823.
48
Tachyarrhythmia is “any disturbance of the heart rhythm in which the heart rate is abnormally
increased, usually to greater than 100 beats per minute in an adult.” Dorland’s at 1867.
68
 Since Dr. Shoenfeld testified that petitioner might have small fiber neuropathy, Dr.
Wiznitzer defined it. Id. at 484. Small fiber neurons are unmyelinated, and deal with touch,
temperature, and autonomic functions such as sweating. Id. Petitioner’s physical examination
did not have small fiber neuropathy features present. Id. at 486. In POTS, a subset of patients
can also have small fiber neuropathy. Id. at 487. If someone had an antibody that attacked the
heart, the person would have heart damage. Id. at 489. Medical literature has not reported that
POTS is associated with primary cardiac dysfunction. Id. Dr. Wiznitzer has had patients with
cardiomyopathy and doctors have not diagnosed them with POTS. Id.

Referring to petitioner’s exhibit 425, a letter to the editor concerning someone who had
POTS two weeks after a Gardasil vaccination, 49 Dr. Wiznitzer stated that a temporal association
after a vaccination does not imply causal association. Id. at 491. Articles that compare computer
models of proteins in vaccines to human proteins are not taking into account the configuration of
the protein in the human being. Id. at 494. Homology on a two-dimensional plain means
nothing. Id. at 495-96. We do not know if the components of human papillomavirus vaccine,
e.g., L1 protein, generate an antibody and, if they do, whether the antibody does anything. Id. at
496.

Dr. Wiznitzer commented on the case report Dr. Shoenfeld and coauthors published
about petitioner’s case, filed as Exhibit 470.50 Id. at 502-03. Dr. Wiznitzer said the case report
was not an accurate factual synopsis of petitioner’s history because it omitted her conversion

49
Postural tachycardia syndrome after vaccination with Gardasil by S. Blitshteyn, 17 Eur J Neurol 7:e52
(2010); doi:10.1111/j.1468-1331.2010.0321.x. Dr. Blitshteyn writes that an autoimmune etiology for
POTS has been implicated in about 14 percent of patients with POTS after detection of ganglionic
acetylcholine receptor (“AChR”) antibody. Id. at 1.
50
Petitioner filed a draft of a case report as Ex. 470, Appendix B. Manuscript file (Dr. Shoenfeld referred
to this manuscript in his response to respondent’s expert Dr. Rosé’s expert report). Dkt entry no. 53. The
manuscript is a draft of a case report entitled Postural Orthostatic Tachycardia With Chronic Fatigue
After HPV Vaccination as Part of the “Autoimmune/Auto-inflammatory Syndrome Induced by
Adjuvants”: Case Report and Literature Review by L. Tomljenovic, S. Colafrancesco, C. Perricone, and
Y. Shoenfeld [petitioner’s expert herein]. The authors sent the draft to the Journal of Investigative
Medicine High Impact Case Reports. P. Ex. 471 is an e-mail from the editorial office of the Journal of
Investigative Medicine High Impact Case Reports, dated January 16, 2014, saying the journal had
accepted the draft for publication. Dkt entry no. 54. The Journal of Investigative Medicine High Impact
Case Reports is an open-access journal from the American Federation for Medical Research published by
SAGE. afmr.org/JIMHICR.cgi (last visited: Jan. 25, 2017). The published version of Ex. 470 is available
at doi:10.1177/2324709614527812. The “Declaration of Conflicting Interests” section at the end of the
case report states “the following potential conflicts of interest with respect to the research, authorship,
and/or publication of this article: Y. Shoenfeld is currently providing expert testimony in cases involving
adverse reactions to the HPV and other vaccines in the US National Vaccine Injury Compensation
Program (including this case).” Id. at 6. The “Authors’ Note” above the “Declaration of Conflicting
Interests” states that petitioner gave her informed consent to present her case in the case report. Id.
69
disorder and astasia-abasia. Id. at 503. The case report says “gait disturbance,” which is too
vague since petitioner did not have true leg weakness according to a neurologic examination. Id.
at 506. There was nothing wrong with her motor system, her sensory system, or her balance
system. Id. Dr. Wiznitzer disagrees with Dr. Sandler’s opinion that petitioner did not have
psychosomatic symptoms. Id. at 508-09. Dr. Sandler’s conclusion flies in the face of all the
other information in the medical records, including that she had depression. Id. at 509. It does
not mention mood disturbance either. Id. at 503. Dr. Wiznitzer said Dr. Shoenfeld did not put
all the facts in his case note. Id. He quoted Dr. Sandler, the psychiatrist, saying petitioner did
not have psychosomatic symptoms, but ignored the conclusions of those who did not agree with
him. Id. When someone writes a case note, he should put all the facts in, not just the facts with
which he agrees. Id.

Dr. Wiznitzer’s opinion is that HPV vaccine had nothing to do with petitioner’s ailments.
Id. at 504. She developed a chronic daily headache after an acute febrile illness in February
2009. Id. Later, she developed POTS. Id. She had a conversion disorder manifested as astasia-
abasia. Id. Then doctors tested her blood and found rheumatologic abnormalities. Id. Doctors
later diagnosed her with chronic fatigue syndrome. Id.

Dr. Stephen J. McGeady, a retired immunologist who now practices pediatrics one and
one-half days a week, testified second for respondent. Id. at 543-44. He also lectures medical
students in allergy and immunology. Id. at 546. He is board-certified in pediatrics, allergy and
immunology, and diagnostic laboratory immunology. Id. at 548. His research interest centers
around the field of immune deficiency. Id. at 549. His opinion is that petitioner’s HPV
vaccinations on August 26, 2008 and December 3, 2008 did not injure her. Id. at 555. He
disagrees with Dr. Shoenfeld’s analysis because, if petitioner had reacted abnormally to HPV
vaccination, he would expect inflammatory mechanisms to be present that would cause tissue
damage. Id. at 558. For instance, her erythrocyte sedimentation rate (“sed” rate), C-reactive
protein (“CRP”), and platelet count should have risen. Id. Sometimes the complement
components and white cell count could also be elevated. Id.

Dr. McGeady defined chronic fatigue syndrome as resulting in various aches and pains,
including headache, and a general malaise. Id. at 559. Doctors do not treat chronic fatigue
patients with immune system suppressants. Id. at 559-60. Chronic fatigue syndrome is not an
autoimmune disease. Id. at 560. Doctors also do not treat POTS patients with immune system
suppressants. Id. at 560. Migraine headaches are not an immune disease. Id. at 561. Doctors do
not treat migraine headache patients with immune system suppressants. Id.

Dr. McGeady said petitioner’s first symptoms, a sore throat, headache, and low-grade
fever, suggested she had a virus. Id. at 562. Petitioner’s first test on March 3, 2009 was a
complete blood count (“CBC”), consisting of measurements of hemoglobin, hematocrit, the
white blood cell count, and a differential. Id. at 563. The results did not show any markers of
inflammation or heightened immune response. Id. Petitioner’s three tests for Lyme disease were
negative. Id. at 566.
70
 Dr. McGeady thinks that petitioner was positive for antinuclear antibodies (“ANA”) as
early as 2004 (years before her HPV vaccinations in 2008) because an elevated ANA would
affect the results of her Epstein-Barr virus (“EBV”) nuclear antigen test administered April 5,
2004, the results of which were “weakly positive at 1 to 10.” This result was identical to the
result of the EBV nuclear antigen test done March 3, 2009 (after petitioner received two HPV
vaccinations in 2008). Id. at 571-72. Petitioner’s weakly positive EBV nuclear antigen result
conflicted with the negative results for current or past infection with EBV in the negative IgM
and IgG tests. Id. at 566-67. Those negative tests would indicate that she had never been
exposed to EBV. Id. at 567, 568. Dr. McGeady said his analysis of these test results is
consistent with Dr. Shoenfeld’s citation of the Arbuckle article that ANA can be positive for very
long periods of time before the onset of clinical symptoms. Id. at 572. Arbuckle discussed the
testing of blood of former servicemen before they had clinical onset of rheumatoid arthritis. 51 Id.
Dr. McGeady continued his explanation of the significance of the weakly positive EBV nuclear
antigen test four years before petitioner received HPV vaccine. Id. at 573. ANA, being
antinuclear antibody, and EBV nuclear antigen share some nuclear components; therefore, a
positive ANA could have confounded the test results of the EBV nuclear antigen. Id. Dr.
McGeady cannot think of any other reason for the confounding of the EBV test results, with IgM
and IgG testing negative for EBV exposure, but EBV nuclear antigen testing weakly positive.
Id.

Dr. McGeady continued with an analysis of the April 6, 2009 blood tests, which showed
a normal CBC and C-reactive protein, meaning that petitioner did not have inflammation. Id. at
575, 576. The liver produces C-reactive protein and the production increases when there is
inflammation. Id. at 576. On April 6, 2009, petitioner’s ANA test result was elevated at 1 to 640
with a speckled pattern. Id. at 577. Petitioner had a negative result of testing for DNA anti-
double stranded antibodies, which is a test for lupus. Id. at 577, 578. Under the direction of the
immunologist Dr. Meuwissen, petitioner was tested for IgG, IgM, IgA, and IgE on June 30, 2009
and the test results were normal. Id. at 578, 579. On June 30, 2009, petitioner’s ANA test result
was the same as April 6, 2009. Id. at 580. Further testing showed that petitioner is not immune-
deficient. Id. at 583. Petitioner had a normal result to testing of complement, which showed she
did not have antibody-mediated inflammation. Id. at 584, 585. On September 16, 2009,
petitioner’s cerebrospinal (“CSF”) fluid was tested and the result did not reveal an inflammatory
process in the central nervous system. Id. at 587.

51
Arbuckle and his co-authors examined serum samples from 130 patients who were or had been in the
military and who had systemic lupus erythematosus. P. Ex. 334, at 3. They found that the time from
detection of a positive antinuclear antibody to clinical symptoms in 78% of the patients was 9.2 years,
although the amount of time ANA was present was limited by the earliest date of the blood sample. Id.
They conclude that some autoantibodies, such as ANA, usually precede the onset of SLE by many years.
Id. at 6. They also note that ANA are relatively common in normal persons who have never had clinical
symptoms of rheumatic disease. Id.
71
 Dr. Kremer, petitioner’s second neurologist, ordered testing on October 27, 2009. Id. at
588. Petitioner’s CBC and sedimentation rate were normal. Id. at 589, 592. Petitioner did not
have significant inflammation. Id. at 593. On September 12, 2011, petitioner’s rheumatoid
factor was slightly elevated at 22, when the laboratory’s range of normal was less than 20. Id. at
595, 596. Since petitioner previously had a positive ANA and lupus anticoagulant, the finding of
a slightly elevated rheumatoid factor is not surprising since it is another autoantibody. Id. at 596.
The finding indicates that petitioner was making autoantibodies and is at least a candidate for
some sort of autoimmune condition. Id. at 597. The result of petitioner’s test for antibody to
ganglion neurons was zero, which does not suggest that her POTS was autoimmune. Id. at 600.

Dr. McGeady proceeded to discuss one of the two Kanduc articles (P. Ex. 502) submitted
into evidence. Id. at 602. Kanduc and her co-authors looked at a sequence of five amino acids
and found that the L1 protein had 34 pentamers in the viral capsid protein, which matched
similar sequences in the human proteome. Id. at 602-03. But this was just a computer match.
Id. at 603. Of the 34 matches, five amino acids were identical. Id. Dr. McGeady agrees with
Dr. Wiznitzer’s criticism of the Kanduc paper because it was a two-dimensional, rather than a
three-dimensional, homology. Id. Dr. McGeady explained that where an antibody binds is
called an epitope. Id. There are two types of epitope, one linear and the other conformational.
Id. Amino acids are not present in nature in a linear configuration, like a string with lights on it.
Id. at 603-04. In nature, amino acids are arrayed in loops and twisted around one another in
unusual shapes. Id. at 604. An antibody can be directed against a linear epitope or a
conformational epitope (which consist of the tips of two or three of these loops). Id. The fact
that five amino acids in the L1 protein match five amino acids in the human proteome says
absolutely nothing about the type of configuration where they are found in either the L1 protein
or the human proteome. Id. A scientist has to do x-ray crystallography studies to determine
these appropriate configurations and the Kanduc study does not report that the authors did this.
Id. The Kanduc authors discuss the astronomical odds of arriving at a match. Id. at 605. Dr.
McGeady testified that a five-amino acid sequence would not be sufficient to induce homology.
Id. at 606.

Dr. McGeady said that the beginning of developing antibody response against a cell
protein is three days. Id. at 609. The primary response occurs in five or six days with IgM,
which will fade, and then one gets IgG, and after 14 days, that fades. Id. at 610. A person would
manifest a response depending on whether this is the first time the person is exposed to this cell
protein or this is a recall response, i.e., a secondary response. Id. A primary response would
occur in two weeks because it takes that long to get a significant titer of antibodies. Id. Dr.
McGeady would expect the furthest response to be three to four weeks for an antibody-mediated
response to a neoantigen. Id. at 611. He does not think an 11-week onset of symptoms is likely.
Id. at 612. He would be suspicious of anything occurring beyond four weeks. Id. at 613.

Dr. McGeady testified that if a person received a vaccine he had previously received, the
onset of symptoms would be greatly accelerated. Id. The antibody production would be well on
its way in three or four days and you would expect clinical symptoms sooner than four weeks.
72
Id. at 614. His opinion is that HPV vaccine was most unlikely to have played any role in
petitioner’s alleged injuries. Id. at 615. On cross-examination, Dr. McGeady admitted that
petitioner’s positive ANA, positive lupus anticoagulant, and positive rheumatoid factor indicate
an autoimmune disorder. Id. at 617-18.

Responding to the undersigned’s question to Dr. Shoenfeld regarding Dr. McGeady’s
testimony that petitioner’s EBV nuclear antigen pre-vaccination was weakly positive as a
consequence of an elevated ANA, Dr. Shoenfeld stated he disagreed. Id. at 626. Yet, Dr.
Shoenfeld’s stated, “Antinuclear antibodies can cause [a] false positive of EB virus,” which is
exactly what Dr. McGeady said. Id.

Dr. McGeady later stated that since petitioner’s EBV IgG and IgM were negative on
testing on April 5, 2004, she could not have had an Epstein-Barr infection to account for the
positive EBV nuclear antigen result on April 5, 2004. Id. at 734. The positive EBV nuclear
antigen in 2004 in the absence of EBV infection supports Dr. McGeady’s opinion that her
positive EBV nuclear antigen in 2004 reflected her having a positive ANA in 2004. Id. at 735.

On cross-examination, Dr. McGeady said it was quite difficult to say what caused
petitioner’s undifferentiated connective tissue disease because he does not believe anyone knows
that. Id. at 744-45. Petitioner does have a family history to support that disease. Id. at 745. He
agrees with Dr. Wiznitzer that petitioner had elements of a conversion reaction. Id. As for Dr.
Sandler, the psychiatrist who saw petitioner a couple of times, and his professional opinion that
petitioner did not have psychosomatic disorder, Dr. McGeady stated, in comparing Dr. Sandler
to Sigmund Freud, who saw patients for months before he figured out what conflict they had:

[T]o go from that [seeing a patient for months] to a single visit or a
visit or two or three in which the patient was seen and to say, oh,
well, there’s nothing there, I think that’s a little unrealistic in face
of the findings that have been presented in this case.

Id.

There followed a discussion of petitioner’s negative testing for acetycholine receptor
(“AChR”), ganglionic neuronal antibody which resulted in zero. Id. at 750. Subsequent testing
for AChR, ganglionic neuronal antibody resulted in less than or equal to 0.02. Id. at 751. Dr.
McGeady testified that these negative results strongly suggest that petitioner’s POTS was not
autoimmune. Id.

Dr. Shoenfeld then stated that Dr. McGeady was incorrect because there exist other
autoantibodies, for which petitioner was not tested. Id. at 752. Dr. Shoenfeld said the fact that
the antibodies for which petitioner was tested were negative does not exclude autoimmunity. If
they had been positive, her POTS would have been autoimmune. The fact that the tests were

73
negative does not exclude autoimmunity. Id. In POTS, there are at least six or seven different
autoantibodies. Id. at 753. Petitioner was not tested for them. The following colloquy occurred:

THE COURT: All right. So, what we have is that the one test for
antibodies, which was ganglionic neurons, was tested twice and
was negative, and so we have no proof that she has autoimmune
POTS, because the other tests were not done.
DR. SHOENFELD: Yes.
THE COURT: Would you agree with that?
DR. SHOENFELD: Yes. It does not exclude autoimmunity.
…THE COURT: What you do not want to hear is she doesn’t
have autoimmune POTS, because all of the testing that could have
been done wasn’t done, but I’m saying to you I have no proof that
she does have autoimmune POTS. All I have is proof that there is
no antibody to ganglionic neurons because the testing was
negative. Would you agree, Doctor?
DR. SHOENFELD: I agree.

Id. at 753-54.

Dr. Carlos D. Rosé, a pediatric rheumatologist, testified third for respondent. Id. at 645.
He is the chief of pediatric rheumatology of the Division of Pediatric Rheumatology at Thomas
Jefferson University. Id. at 647. He treats patients with undifferentiated connective tissue
disease. Id. at 648. He also trains medical students, residents, and fellows. Id. at 649.

Dr. Rosé’s opinion in this case is that Gardasil vaccine had no relationship with
petitioner’s rheumatic condition. Id. at 659. He stated that on April 2, 2008 (pre-vaccination),
petitioner visited her orthopedist, Dr. Richard Uhl, who had been following her for hand trauma
with persistent pain. Id. at 659-60. He was suspicious of petitioner’s having reflex sympathetic
dystrophy, which is a form of regional limb pain related to amplified pain, and recommended she
take Neurontin for pain. Id. at 660. An MRI of petitioner’s upper extremity was done. In
addition, Dr. Rosé saw a bone scan done which showed petitioner had decreased profusion in
that hand. To Dr. Rosé, this signifies that petitioner had a tendency to develop chronic and
amplified pain in 2008. Id. Petitioner’s tendency to amplify pain occurred before petitioner’s
first Gardasil vaccination on August 26, 2008. Id. at 660-61.

Dr. Rosé stated amplified pain syndrome is an umbrella term used to refer to children and
adults who suffer a disproportionate amount of pain after minor trauma. Id. at 661. It is also
specifically well known as reflex sympathetic dystrophy. Individuals with reflex sympathetic
dystrophy tend to get fibromyalgia at an older age. Id. Reflex sympathetic dystrophy is
characterized by localized swelling, changes in the color of the skin, changes in temperature both
perceptional and by examination, and by allodynia, which is a pain response to stimuli that are
not nociceptive, i.e., not necessarily normally causing pain. Id. at 662. This is also known as
74
hyperaesthesia. “Aesthesia” means sensation, and “allodynia” means pain sensation. Id.
Petitioner’s hand pain exceeded the limits of where the hand fracture was. Id. at 663. Another
term used for this is complex regional pain syndrome, and it is the most accepted term. Id. at
664. Chronic fatigue syndrome is related to regional pain syndrome if someone has
fibromyalgia, but not if someone does not have fibromyalgia. Id. at 665. The incidence of
chronic headache among persons with amplified pain is higher than the general population. Id.
Headache pain is associated with chronic pain. Id. On June 9, 2008, petitioner’s orthopedist, Dr.
Uhl, used the term “complex regional pain syndrome” in reference to petitioner. Id. at 666.

Dr. Rosé agrees that petitioner has undifferentiated connective tissue disease (“UCTD”).
Id. at 668. Undifferentiated connective tissue disease describes patients with symptoms also
seen in inflammatory connective tissue diseases, i.e., lupus, scleroderma, dermatomyositis, and
mixed connective tissue disease. Patients with UCTD have some of the specific symptoms or
laboratory tests of connective tissue diseases but do not meet the criteria for any particular
connective tissue disease. Id. That is why their disease is “undifferentiated.” Id. at 669. Dr.
Rosé, in referring to specific symptoms petitioner has, meant her Raynaud’s syndrome.
Petitioner has antinuclear antibodies, low titer lupus anticoagulant by the hexagonal test, and
livedo (which represents a pathology in the dermal vessels, meaning the blood vessels of the
deeper layers of the skin, which are dilated or inflamed, causing a bluish discoloration of the
skin). Id. at 669-70.

Dr. Rosé said he knows Dr. Petri, petitioner’s second rheumatologist, very well. Id. at
171. Dr. Petri made the diagnosis of UCTD based on petitioner’s having Raynaud’s, antinuclear
antibodies, lupus anticoagulant, and livedo. Id. at 673-74. Dr. Rosé said that patients with
UCTD have three possible outcomes: (1) developing a full-blown connective tissue disease that
meets the criteria for diagnosis that were missing, (2) remaining as UCTD, or (3) having the
UCTD fade away and disappear. Id. at 674-75. The most common time period when an adult
with UCTD might develop a full-blown connective tissue disease is about five years. Id. at 679.
The most common full-blown connective tissue disease is lupus. Id. at 680.

Dr. Rosé put the onset of petitioner’s UCTD as April 2009 when she had the first positive
ANA. Id. But petitioner could have been ANA positive before, in 2004, according to the false
positive EBV test. Nothing in the record says when petitioner’s Raynaud began. Dr. Rosé cited
petitioner’s exhibit 334, the Arbuckle article studying Army recruits’ sera and discovering that
they had ANA positivity way before they had clinical symptoms of lupus. Id. Petitioner has
livedo reticularis, which means mimicking a mesh. Id. at 684. It is known to be associated with
the presence of antiphospholipid syndrome or lupus anticoagulant. Id. at 685. Dr. Rosé’s
opinion is that petitioner has an autoimmune disease called UCTD. Id. at 685-86. UCTD is
probably inflammatory in some of its manifestations. Id. Raynaud is not inflammatory, but
arthritis is inflammatory. Id. at 687.

Dr. Rosé said he was having difficulties establishing the source of petitioner’s joint pain.
Id. at 688. Two rheumatologists examined petitioner and did not report objective evidence of
75
arthritis, i.e., joint swelling or limitation of range of motion. Id. Petitioner complained of joint
pain that was arthralgic. Id. at 688-89. However, petitioner also had pain amplification
syndrome and may have had something similar to fibromyalgia, making it difficult for Dr. Rosé
to say it was arthralgia. Id. at 689. Her joint pain could be attributed to the UCTD or to her
other pain amplification symptoms. Id. Dr. Rosé pointed out one negative predictor of
petitioner’s UCTD evolving into a full-blown connective tissue disease: her negative anti-DNA
antibody. Id. The presence of anti-DNA antibody when someone has UCTD is very specific for
lupus, but petitioner had negative anti-DNA antibody. Id. at 690. In addition, it has been five
years since petitioner was tested and she has not developed a full-blown syndrome. It looks like
she has been lucky not to evolve into a full-blown connective tissue disease, i.e. lupus,
scleroderma, dermatomyositis, or rheumatoid arthritis. Id. Dr. Rosé would put petitioner in the
non-evolving UCTD group. Id. at 691.

Dr. Rosé agrees that petitioner has a low positive and a moderately positive lupus
anticoagulant. Id. at 711-12. But petitioner was positive for only one of the tests for the lupus
anticoagulant, the most sensitive of all of them. Id. at 713. Whenever you increase sensitivity,
however, you lose specificity. Id. Doctors did two tests for petitioner’s lupus anticoagulant, the
hexagonal and the mixing test. Id. at 715. The hexagonal was positive but the mixing test was
negative. Id. Dr. Rosé does not think petitioner has gastrointestinal manifestations of UCTD. Id.
at 717. None of the two rheumatologists who saw petitioner reported that petitioner had a malar
rash. Id. at 718. Dr. Nichter wrote a letter dated March 1, 2010 stating that petitioner’s
occasional vesicular rash did not meet the criteria for a butterfly rash of SLE. Id. at 719-20. Dr.
Petri prescribed Plaquenil, a mild immune suppressor, for petitioner. Id. at 721. Petitioner tried
Plaquenil for several days but did not see any improvement. Id. at 724. Dr. Rosé said it would
have taken at least three to four months for petitioner to see any improvement in her Raynaud’s
disease. Id.

Dr. Rosé said that petitioner’s incongruent test results in 2004 for viral capsid antibodies
and the Epstein-Barr nuclear antigen are possibly due to immunofluorescent interference from
the presence of antinuclear antibodies. Id. at 767. The presence of antinuclear antibodies
preceding clinical disease is very common. Id. at 768. His opinion is that petitioner’s two
Gardasil vaccinations played no role in the development of her positive antinuclear antibodies
and undifferentiated connective tissue disease. Id. He does not know of any scientifically
reliable evidence that Gardasil vaccine causes undifferentiated connective tissue disease. Id. at
771.

Dr. Rosé agreed that petitioner’s gait could be described as astasia-abasia and that she
had conversion disorder. Id. at 786. Conversion disorder is not the same as malingering. Id. at
788. Dr. Rosé attempted to explain why both Dr. Shoenfeld and the psychiatrist Dr. Sandler
missed the diagnosis of conversion disorder. Id. Dr. Rosé repeated Dr. Shoenfeld’s comment in
one of his responses that “he has no business looking at the gait.” Dr. Rosé said Dr. Shoenfeld
was probably right. Doctors should do physical examinations, but they have so many other
things to do that they do not do physical examinations. Id. Dr. Rosé thought Dr. Sandler, the
76
psychiatrist who saw petitioner in September 2009, wanted to help her with hypnosis and other
treatments. Dr. Rosé continued, “[i]t’s not that he completely dismissed that she had some
psychological problem of whatever cause. . . .” Id.

Dr. Rosé testified that petitioner’s gait problem had nothing to do with her UCTD. Id. at
789. He could not explain her gait disorder as being caused by any inflammatory or organic
disease. Id. Petitioner’s variable strength and weakness during physical examinations also
suggests a nonorganic cause. Id. at 790. He would call this variability somatization. Id. at 791.
Conversion disorder is classified under somatoform disorders, meaning psychosomatic. Id. As
for POTS, the majority of POTS cases have not yet been proven to be autoimmune. Id. at 792.
POTS is not associated with undifferentiated connective tissue disease. Id. at 793. Dr. Peter
Rowe, a Johns Hopkins specialist, whom Dr. Rosé knows, tested petitioner on August 11, 2010,
and he discussed in his notes her loose-jointedness in the context of his using the phrase
“connective tissue”. Id. at 794-95. This is not the same as undifferentiated connective tissue
disease. Id. at 795. The reason Dr. Rowe was discussing petitioner’s loose-jointedness is that
individuals with loose joints can have more loose blood vessels which allow more blood pooling
when they stand up, leading to POTS. Id.

Dr. Rosé discussed R. Ex. BBBBBBB (7B), which is the Wang article 52 for which
petitioner filed an abstract marked as P. Ex. 88. Id. at 801. Wang does not say that POTS is an
autoimmune disease. Id. at 803. Wang and his co-authors were looking for things intrinsic to
the heart to which autoantibodies could be made. Id. at 804. In Wang’s experiment, proteins
were the targets of the autoantibodies. Id. at 807. Dr. Rosé said none of what Wang did has
anything to do with POTS, which is a neurocardiopathy, not a cardiopathy. Id. POTS is not an
intrinsic cardiac disease. Id. at 811. Dr. Rosé is in the mainstream of the medical community
that views POTS as an autonomic nervous system disease, not a cardiac autoimmune disease. Id.

The undersigned asked Dr. Wiznitzer, respondent’s expert neurologist, to comment. Id.
at 812. He said the total study population for Wang was seven controls and ten subjects. Wang
and his co-authors found 18 unique spots in the POTS patients, but there were 16 spots that the
controls shared with the POTS patients, which means that the controls had autoantibodies that
were of no functional consequence vis a vis POTS. Id. They were of no functional consequence
because the controls did not have clinical symptoms of POTS. Everyone has some antibodies
52
Wang, X.L. et al., Autoimmunoreactive IgGs from patients with postural orthostatic tachycardia
syndrome, 6 Proteomics Clin Appl 615-25 (2012). Wang notes that anti-ganglionic acetylcholine
receptor (AChR) antibodies are present in 10-15% of POTS patients. Id. at 621. AChR was not one of
the cardiac membrane proteins Wang’s study detected because the AChR in hearts are of the muscarinic,
not the neuronal nicotinic, subtype. Id. Wang, in a section titled “Limitations of the study,” identifies a
list of 40 unique cardiac membrane proteins that were potential targets of autoantibodies in POTS
patients, but states that further confirmation is necessary with a much larger number of patients and
controls to make any conclusion. Id. at 624. Another limitation Wang mentions is he did not know the
functional consequence of IgG binding to specific target cardiac membrane proteins, the same point he
makes in the conclusion of his study as well. Id. He suggests further studies be done. Id.
77
circulating that have an autoantibody nature. Id. Where the antibodies bind in terms of the
proteins involved in Wang, they were not part of the regulation of the autonomic nervous system.
Id. at 813. If Dr. Wiznitzer had designed this study, he would have needed a much larger
population, not seven controls, and he would have chosen another one or two organs in the body,
not the heart, to see if there were similar cross-reactivity or these were just nonspecific
antibodies in the bloodstream. Id. All Wang did was find something and say he does not know
what it means. Id. at 814. Just because an autoantibody binds does not mean it causes problems.
All seven controls in Wang’s study had evidence of autoantibodies but did not have POTS. Id.
Dr. Wiznitzer said that all of us carry antinuclear antibodies and about 10 percent of the
population carries them without disease. Id. at 815.

Dr. Shoenfeld contributed to the discussion and said that all of us have autoantibodies,
called natural autoantibodies, in very low titers. Id. at 817. Our body uses them to clean out our
system. They clean DNA by binding to them and taking them out. It is not surprising to find a
normal person binding to different proteins in his body. Id. Dr. Shoenfeld stated it was possible
that 100 percent of POTS was autoimmune, but he does not know yet. Id. at 819. However, he
admitted that POTS can be non-autoimmune: “I don’t say that POTS cannot be non-
autoimmune.” Id.

Dr. Rosé stated that the Wang paper concluding the autoantibodies they found in the ten
subjects and seven controls were pathogenic is still too premature. Id. at 821. Wang himself
said his study was preliminary or a pilot. Id. Dr. Rosé stated that testing of petitioner for
antibodies showing her POTS was autoimmune were negative. Id. at 822. Some doctors
consider chronic fatigue syndrome to be autoimmune. Id. at 826. The most common cause of
chronic fatigue is sleep deprivation. Id. Dr. Rosé mostly deals with chronic fatigue syndrome as
a sleep abnormality. Id. at 827. Doctors do not use immunosuppressive therapies to treat
chronic fatigue syndrome. Id. Chronic fatigue syndrome and POTS overlap in symptoms. Id. at
830. He does not consider chronic fatigue syndrome to be autoimmune. Id. at 831. He has a lot
of patients with chronic fatigue syndrome. Id. Dr. Rosé’s opinion is that HPV vaccine had
nothing to do with petitioner’s symptoms. Id. at 833.

On cross-examination, petitioner’s counsel asked Dr. Rosé if his opinion that petitioner’s
HPV vaccination did not cause her chronic fatigue syndrome would change if there were
evidence that petitioner’s neighbor Natalie Rowen had the same symptoms after Gardasil
vaccination. Id. at 841. Dr. Rosé said no.

On redirect examination, Dr. Wiznitzer discussed the psychiatrist Dr. Sandler’s failure to
find that petitioner had evidence of a psychosomatic condition and, therefore, could not have had
a conversion disorder. Id. at 848. The Diagnostic and Statistical Manual, 5th ed. (“DSM-V”),
from the American Psychiatric Association, modified the definition of “conversion disorder” to
stress the primacy of the neurologic examination and stated definitively that a psychological
problem may not be identifiable at the time of diagnosis. Id. at 848-49. Neurologists believe
that they do not need psychiatric input to diagnose conversion disorder. Id. at 849. A conversion
78
disorder is particularly appropriate if the patient has astasia-abasia. Id. Petitioner’s father then
asked if Dr. Nichter, petitioner’s neurologist, ever used the term “conversion disorder” in his
notes, and the undersigned said no. Id. at 850. Dr. Wiznitzer said “no” in agreement but added
that Dr. Nichter described all the features of conversion disorder in his notes. Id. Petitioner’s
father then said he would not deny petitioner had a strange gait, which could not be explained
physiologically, 53 but, he said, at no point did petitioner’s treating physicians label her as having
a conversion disorder. 54 Id. at 850-51. Petitioner’s father added that he was involved with all of
petitioner’s treating physicians, and Dr. Wiznitzer was not. Id. at 851. Dr. Wiznitzer replied that
multiple treaters for petitioner used “astasia-abasia” to describe her gait. He added that astasia-
abasia is a recognized movement disorder that is part of conversion disorder. Id.

In repeated criticism of the Wang article (P. Ex. 88 for the abstract; R. Ex. BBBBBBB
for the full article), Dr. Wiznitzer noted that not all the subjects in Wang’s analysis had identified
immunoreactive spots. Id. at 853. He said that no subject had the same spot. In other words, it
was not as if all seven subjects had the same spot. Id. The authors did not describe whether the
individuals they studied had high or low titers. Id. at 853-54. Dr. Wiznitzer called Wang’s
article “a preliminary hypothesis-generating study.” Id. at 854.

Petitioner’s father then asked Dr. Wiznitzer questions, beginning with the statement that
he is a cardiac surgeon, not a neurologist. Id. at 856. He asked how often Dr. Wiznitzer sees
POTS patients, and Dr. Wiznitzer replied about once a month. Id. Petitioner’s father said that
his medical center’s pediatric neurology clinic consisting of four or five pediatric neurologists
sees POTS only once a year. Id. at 857. His attention then turned to Dr. Wiznitzer’s prior
testimony about blood pressure, and Dr. Wiznitzer clarified that when voltage-gated calcium
channel 1.2 is dysfunctional, it is associated either with a rhythm disturbance, i.e., an arrhythmia,
or with an abnormality such as congestive heart failure or cardiac hypertrophy. Id. at 857-58.

Dr. Shoenfeld gave rebuttal testimony. Id. at 862. He said that before she received
Gardasil vaccine, petitioner did not have POTS, chronic fatigue syndrome, UCTD, or livedo. Id.

53
“Physiologic” means “normal; not pathologic, characteristic of or conforming to the normal functioning
or state of the body. . . .” Dorland’s at 1444. What petitioner’s father meant when he said he would not
deny petitioner had a strange gait that could not be explained physiologically, he meant there was no
normal explanation for her strange gait.
54
Petitioner’s father is incorrect. Petitioner’s pediatrician, Dr. Kennette, twice mentioned conversion
syndrome in her notes, and one of petitioner’s physical therapists mentioned conversion syndrome in her
notes. On April 24, 2009, petitioner’s father phoned Dr. Kennette’s office, concerned that petitioner had
muscle pains. Dr. Kennette’s note questioned whether petitioner’s symptoms represented a myositis
syndrome or conversion syndrome because of petitioner’s astasia-abasia. Med. recs. Ex. 12, at 40. On
May 5, 2009, Dr. Kennette filled out a child and adolescent psychiatric telephone consultation request to
Four Winds Foundation, asking if a psychiatrist would see petitioner for the working diagnosis of
conversion syndrome. Id. at 48. On July 14, 2009, physical therapist Adrienne Fil noted that petitioner’s
physical presentation with mobility continued to be incongruent with objective measurements, raising the
possibility of conversion disorder. Med. recs. Ex. 11, at 8.
79
at 863. Petitioner had three autoantibodies: ANA, lupus anticoagulant, and rheumatoid factor.
Id. at 864. Petitioner had hair loss, which is an additional criterion for lupus. She had rash,
which some said was butterfly but others said it was not butterfly. She had constipation. She
had joint pains and swollen joints. Arthralgia is also a criterion for lupus. Id. Petitioner had
smell and taste issues, sleeping disturbances, and cognitive impairment. Id. at 864-65. She
never had any of these manifestations before receiving Gardasil vaccine, and all these
manifestations occurred within two months or ten weeks of the Gardasil vaccination. Id. at 865.

Dr. Shoenfeld continued that, before Gardasil vaccination, petitioner was active, and
played soccer. After vaccination, she was limited in her physical activity. His hypothesis, which
he called plausible, is that petitioner had an autoimmune response to Gardasil. He stated that
vaccines can cause autoimmune responses by many mechanisms. Dr. Shoenfeld believes, in this
case, that the vaccine antigen crossreacted with different constituents in petitioner’s body,
existing in her heart and calcium channels, producing autoantibodies. Id. These autoantibodies
caused dysfunction of her autonomic nervous system, the sympathetic, and parasympathetic
affecting her heart, and the peripheral nervous system. Id. at 866. He said the peripheral
nervous system and the autonomic nervous system innervate the heart, which belongs to the
autonomic nervous system. Id.

Dr. Shoenfeld denied there is evidence that petitioner had antinuclear antibodies before
she received Gardasil vaccine. Id. at 868. Dr. Shoenfeld accused respondent’s experts of stating
that conversion reaction caused all of petitioner’s symptoms, including UCTD, livedo, lupus
anticoagulant, ANA, and rheumatoid factor. Id. at 868-69. Dr. Shoenfeld denied that petitioner
had a pre-existing infection before her symptoms began because she did not have an increase in
white blood cells on testing of her blood. Id. at 869. Petitioner’s C-reactive protein (“CRP”)
was normal in all her studies. Id. at 870. Dr. Shoenfeld said that CRP is normal in lupus, but
increased when there is infection. Id.

Dr. Shoenfeld said that antiphospholipid syndrome is not an inflammatory disease. Id. at
871. Dr. Shoenfeld denied petitioner ever had an infection in the third week of February 2009.
Id. The only pre-symptom event that Dr. Shoenfeld would accept was Gardasil vaccine. Id. at
872. He said that Gardasil can cause POTS, and that POTS and UCTD are autoimmune
diseases. Id. at 872-73. The failure of doctors and scientists to find an autoantibody does not
exclude autoimmune etiology. Id. at 874. In only 40 percent of many classic autoimmune
diseases do doctors find autoantibodies. Id. This just means the doctors did not do all the work
to find them. Id. at 874-75. Dr. Shoenfeld mentioned that he has never had a private practice.
Id. at 875. Dr. Shoenfeld said that livedo is associated with antiphospholipid syndrome. Id.

Dr. Shoenfeld was working on a paper studying 100 UCTD patients with no definite
autoimmune disease compared to 100 controls. Id. at 880-81. The authors discovered a
significantly higher number of patients with UCTD who had a prior vaccination in comparison to
the 100-person control group. Id. at 881.

80
 Dr. Shoenfeld stated that petitioner’s pre-vaccination testing showing a weakly positive
Epstein-Barr virus nuclear antigen did not mean that she had antinuclear antibody. Id. at 882.
She was not tested for antinuclear antibody before the vaccination. It appeared after the
vaccination. Id. Petitioner did not have anti-double stranded DNA, but she did have
anticardiolipin and antiphospholipid. Id. at 884. Therefore, petitioner is at great risk of
developing autoimmune disease and belongs in the evolving group. Id.

DISCUSSION

To satisfy her burden of proving causation in fact, petitioner must prove by preponderant
evidence: “(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.” Althen v. Sec’y
of HHS, 418 F.3d 1274, 1278 (Fed. Cir. 2005). In Althen, the Federal Circuit quoted its opinion
in Grant v. Secretary of Health and Human Services, 956 F.2d 1144, 1148 (Fed. Cir. 1992):

A persuasive medical theory is demonstrated by “proof of a logical
sequence of cause and effect showing that the vaccination was the
reason for the injury[,]” the logical sequence being supported by
“reputable medical or scientific explanation[,]” i.e., “evidence in
the form of scientific studies or expert medical testimony[.]”

Althen, 418 F.3d at 1278.

Without more, “evidence showing an absence of other causes does not meet petitioners’
affirmative duty to show actual or legal causation.” Grant, 956 F.2d at 1149. Mere temporal
association is not sufficient to prove causation in fact. Id. at 1148.

Petitioner must show not only that but for Gardasil, she would not have had all the
illnesses about which she complains, but also that the vaccine was a substantial factor in causing
her illnesses. Shyface v. Sec’y of HHS, 165 F.3d 1344, 1352 (Fed. Cir. 1999).

The question arose whether the onset of petitioner’s undifferentiated connective tissue
disease (“UCTD”) arose before or after Gardasil vaccination, raising the question of whether
Gardasil significantly aggravated her UCTD. Section 300aa-33(4) defines “significant
aggravation” as follows:

The term “significant aggravation” means any change for the
worse in a preexisting condition which results in markedly greater
disability, pain, or illness accompanied by substantial deterioration
of health.

42 U.S.C. § 300aa-33(4).
81
 Because of the multiple illnesses petitioner alleged through her father when he was the
initial petitioner plus the additional illnesses that petitioner’s expert Dr. Shoenfeld raised at the
hearing, the undersigned will discuss each illness individually.

Migraine headaches

The original petitioner (petitioner’s father) alleged in the petition that Gardasil
administered December 3, 2008 caused his daughter (the current petitioner) severe headaches,
photophobia, phonophobia, dizziness, and gait disturbances. These all fall under the rubric of
migraine headache. Petitioner had these symptoms in the beginning of June 2007, more than one
year before she received her first Gardasil vaccination on August 26, 2008. On June 6, 2007, she
complained to her pediatrician Dr. Karen Kennette that when she stood up, she felt very dizzy.
She felt as if she were on a boat. Her gait was slightly slow secondary to her headaches. Dr.
Kennette examined petitioner in a dark room where petitioner was wearing dark sunglasses.
Because the headache persisted, petitioner underwent on June 7, 2007 a brain MRI, which was
normal. On June 8, 2007, petitioner’s mother called Dr. Kennette to say petitioner was still
complaining of a headache and was absolutely no better. She had to lie in a dark room. On June
8, 2007, petitioner went to Albany Medical Center Emergency Department, where petitioner
gave a history that three weeks earlier, she was refereeing a soccer game and felt as if her head
were spinning. She also had a headache and had to sit down. The episode resolved. But a week
before she came to the hospital, she had another headache similar to the first one. It was bilateral
and frontal. Her dizziness was mild. But she also had photophobia, phonophobia, and
associated nausea. The neurologist on call diagnosed migraine.

On August 14, 2007, petitioner complained to Dr. Kennette of fatigue.

Between petitioner’s first Gardasil on August 26, 2008, and her second Gardasil on
December 3, 2008, she had no complaints other than injury to her left ankle and a fractured left
fibula.

Two and three-quarter months after the second Gardasil, petitioner saw Dr. Kennette on
Thursday, February 26, 2009, complaining of a bad headache she had on February 21, 2009,
weak pain, nausea, fever, dizziness, and photophobia. Her father prescribed on February 19,
2009 Cipro for presumed sinusitis. Some of the possible side effects of Cipro include headache,
dizziness, pain, nausea. See n.8 supra. Petitioner started taking Cipro two days before the onset
of her headache. Dr. Kennette diagnosed petitioner with photophobia, bitemporal squeezing
pain, and migraine. Petitioner walked out of Dr. Kennette’s office holding onto her mother’s
arm. Dr. Kennette presumed petitioner had sinusitis.

Petitioner’s headache continued until she went to Albany Medical Center Emergency
Department on March 6, 2009 where she saw a number of doctors including the neurologist Dr.
Nichter. She improved briefly the next day, but her headaches continued. On March 31, 2009,
82
Dr. Kennette’s office received a telephone call from petitioner’s mother. She wanted the lot
number of Gardasil that petitioner had received. She said that petitioner’s headaches had been
ongoing since petitioner received Gardasil. In addition, a friend had received the same lot
number of Gardasil and she had the same problem as petitioner.

Also on March 31, 2009, Dr. Kennette filled out a VAERS (Vaccine Adverse Event
Reporting System) form, writing that petitioner received Gardasil on December 3, 2008 and the
onset of her vaccine reaction on February 21, 2009 or eleven weeks and three days later. Med.
recs. Ex. 12, at 34. The only adverse event Dr. Kennette described was protracted headache. Id.
Dr. Kennette states petitioner recovered. Id.

Dr. Shoenfeld, petitioner’s expert, testified at the hearing that migraine headache is not an
autoimmune disease, but a neurovascular one. He did not testify that Gardasil caused
petitioner’s migraine headache.

Althen analysis

Petitioner failed to prove that Gardasil can cause migraine headache (prong one of
Althen). Petitioner failed to prove that Gardasil did cause her migraine headache (prong two of
Althen). Petitioner failed to prove that two and three-quarter months after Gardasil until the
onset of migraine headache is an appropriate interval to prove causation of migraine headache
(prong three of Althen).

POTS

Dr. Shoenfeld testified that petitioner’s POTS began two months to 10 weeks after her
second Gardasil. However, petitioner did not have the symptoms of POTS until either
September or October 2009 according to petitioner’s medical records, petitioner’s father’s
summary of the medical records, petitioner’s affidavit, and petitioner’s father’s affidavit. The
hallmark of POTS is feeling faint when rising from a supine position, when blood pressure
becomes low and the heart rate rises. Petitioner did not have these symptoms until she had been
sitting in a wheelchair for seven months. The first notice of petitioner’s swaying, saying her legs
felt like jello, was on April 6, 2009, which was four months after her second Gardasil. She had
no problem getting up. Her problem was leaning when she walked. Dr. Nichter diagnosed her
with a wobbly gait, but no vertigo or ataxia. By April 22, 2009, petitioner felt her legs were not
part of her body. She was under a lot of stress at home because her maternal grandmother died
and her father had surgery.

According to petitioner’s father’s summary of the medical records, petitioner had been
seeing black spots and then falling to the floor with tachycardia on October 6, 2009. R. Ex.
AAAAAAA, at 3. Petitioner’s affidavit recounts the same history. P. Ex. 554, at 4. Petitioner’s
father’s affidavit also recounts the same history. P. Ex. 551, at ¶ 35.

83
 Dr. Wiznitzer testified that petitioner’s POTS began late September or early October
2009 due to deconditioning. His testimony is in accordance with medical literature 55 that both
parties filed in this case. Dr. Shoenfeld, on the other hand, insisted that petitioner’s POTS began
two months to 10 weeks after petitioner’s second Gardasil. This makes no sense in light of the
failure of petitioner to manifest symptoms of POTS until late September or early October.

The complicating picture in Dr. Shoenfeld’s analysis of petitioner’s medical history is
that she was manifesting symptoms in April 2009 that had no biologic explanation, what
petitioner’s father called a strange gait that had no biophysiologic explanation. Her conversion
disorder or psychosomatic symptoms seem to have been in imitation of Natalie Rowan’s taking
to a wheelchair after receiving the same lot of Gardasil as petitioner. Natalie lived less than two
blocks away from petitioner. Petitioner’s father testified, and the medical history from
petitioner’s mother’s statements confirms, that petitioner’s father was influenced to file suit
because of Natalie Rowan’s suit in the Vaccine Program.

Dr. Shoenfeld based his rejection of petitioner’s having conversion disorder on the
psychiatrist Dr. Sandler’s meeting with petitioner on September 1, 2009, one week after
petitioner’s parents asked him to determine if petitioner had psychological symptomatology. Dr.
Sandler did not read petitioner’s medical records. He did not examine petitioner. Because
petitioner looked him in the eyes when she spoke and she was alert, oriented, and very
cooperative, he concluded she did not have psychosomatic symptoms. This was not a valid basis
for determining if petitioner were manifesting psychosomatic symptoms six months earlier. An
opinion without a reasonable basis is worthless. Davis v. Sec’y of HHS, 20 Cl. Ct. 168, 173
(1990) (“conclusions . . . are only as good as the reasons and evidence that support them”). Yet
Dr. Shoenfeld relied on Dr. Sandler’s opinion, not only in his testimony, but also in the case
report he and three co-authors published in 2014 on petitioner’s case (Ex. 470, see n.53 supra). 56

Seven of petitioner’s treating doctors opined that her inability to walk, her variable and
inconsistent weakness, and her inability to see were not manifestations of a physical illness: Dr.
Sobeih, Dr. Nichter, Dr. Rheeman, Dr. Cornblath, Dr. Petri, Dr. Rowe, and Dr. Lindstrom.
Three of them, Drs. Nichter, Rheeman, and Lindstrom, attributed petitioner’s complaints to her
inability to deal with stress. The Federal Circuit in Capizzano emphasized that the special
masters are to evaluate seriously the opinions of petitioner’s treating doctors since “treating

55
For example: P. Ex. 485: Postural Tachycardia Syndrome (POTS) by P.A. Low, et al., 20 J Cardiovasc
Electrophysiol 352-58, 356 (2009) (some POTS patients “may have a strong deconditioning
component”); P. Ex. 532: The Postural Orthostatic Tachycardia Syndrome: Definitions, Diagnosis, and
Management by Y. Kanjwal, et al., 26 PACE 1747-57, 1754 (2003) (prolonged immobilization is a
potentially reversible cause of POTS); R. Ex. AAAA, Postural Tachycardia Syndrome: A Heterogeneous
and Multifactorial Disorder by E.E. Benarroch, 87 Mayo Clinic Proc 12:1214-25, 2015 (2012) (physical
deconditioning has an important role in POTS patients).
56
Petitioner’s father testified that petitioner did not have psychosomatic symptoms, but did admit that her
strange gait had no physiological explanation. Dr. Shoenfeld did not rely on petitioner’s father’s opinion.
84
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.” 440 F.3d at 1326. See
also Broekelschen v. Sec’y of HHS, 618 F.3d 1339, 1347 (Fed. Cir. 2010); Andreu v. Sec’y of
HHS, 569 F.3d 1367, 1375 (Fed. Cir. 2009).

The undersigned finds that the onset of petitioner’s POTS was in late September or early
October 2009, 10 or 11 months after her second Gardasil.

The nature of petitioner’s POTS also was controversial. Dr. Shoenfeld testified that
petitioner’s POTS was autoimmune. However, doctors tested her on two separate occasions to
see if she had anti-ganglionic antibodies, and the results were both times negative. Dr. Shoenfeld
said if they had tested her for other antibodies, they would have been positive. But that is pure
speculation. The medical literature from Dr. Blitshteyn shows that the majority of POTS is not
autoimmune. P. Ex. 426; R. Ex. OOOO. Dr. Shoenfeld said he would not deny that non-
autoimmune POTS exists. The only evidence in this case is that petitioner’s POTS is not
autoimmune. Therefore, Dr. Shoenfeld has failed to prove that Gardasil caused petitioner’s
POTS because, in addition to giving an incorrect onset, his opinion was based on his assumption
that petitioner’s POTS was autoimmune.

Althen analysis

Petitioner has failed to prove that Gardasil can cause non-autoimmune POTS (prong one
of Althen). Petitioner has failed to prove that Gardasil did cause her non-autoimmune POTS
(prong two of Althen). Petitioner has failed to prove that 10 or 11 months after Gardasil is an
appropriate interval to prove causation of non-autoimmune POTS (prong three of Althen).

Chronic Fatigue Syndrome

Dr. Shoenfeld testified that petitioner’s sore throat the third week of February 2009 was
the onset of her chronic fatigue syndrome. However, petitioner’s father diagnosed her with
sinusitis and gave her Cipro, an antibiotic. The undersigned sees no reason to doubt petitioner’s
father’s diagnosis. Moreover, one would expect that someone with chronic fatigue syndrome
would complain of fatigue. Only after she stopped sleeping due to her migraine headaches did
she complain of fatigue. The undersigned accepts Dr. Wiznitzer’s testimony that her chronic
fatigue syndrome occurred after she had been sitting in a wheelchair for seven months because
petitioner was deconditioned. Dr. Peter C. Rowe of Johns Hopkins made an interesting
observation on August 11, 2010 that petitioner had a connective tissue phenotype which allowed
excessive compliance in her dependent circulation and was a factor contributing to her
orthostatic intolerance, along with her deconditioning, which in turn caused a loss of plasma
volume.
Althen analysis

85
 Petitioner has failed to prove that Gardasil can cause chronic fatigue syndrome (prong
one of Althen). Petitioner has failed to prove that Gardasil did cause her chronic fatigue
syndrome (prong two of Althen). Petitioner has failed to prove that 10 or 11 months after
Gardasil is an appropriate interval to prove causation of chronic fatigue syndrome (prong three of
Althen).

UCTD

Dr. Petri of Johns Hopkins diagnosed petitioner with undifferentiated connective tissue
disorder (“UCTD”) on December 4, 2009 in light of her positive ANA, Raynaud’s disease,
livedo, and lupus anticoagulant. The reason Dr. Petri diagnosed petitioner with UCTD was that
petitioner did not have a discrete rheumatological disease. The onset of petitioner’s UCTD was
disputed at the hearing. Dr. Shoenfeld at first said the onset was after Gardasil because that was
when doctors tested petitioner for ANA. Then he thought better of that statement in light of the
fact that doctors had not tested petitioner for ANA before vaccination. Moreover, the Arbuckle
article (P. Ex. 334) which showed that autoantibodies can be present in non-symptomatic lupus
patients for up to 9.4 years earlier meant that petitioner likely had autoantibodies before she
became symptomatic as well.

The undersigned finds the Arbuckle article persuasive in finding that petitioner probably
had autoantibodies pre-Gardasil vaccination for which doctors did not test until after vaccination.
Petitioner has a family propensity for rheumatologic disease as petitioner’s mother has
Raynaud’s disease as well. As for Dr. Shoenfeld’s opinion that Gardasil is the cause of
petitioner’s manifesting livedo around both knees and forearms sometime during 2009, which
together with the positive antibody, lupus anticoagulant, and rheumatoid factor led to the
diagnosis of UCTD, the Federal Circuit has held that timing is not enough. Grant, 956 F.2d at
1148. Even the fact that UCTD is an autoimmune disease is not sufficient to pin causation on
Gardasil because UCTD manifests over time. See, e.g., Arbuckle, P. Ex. 334, at 1532: “Our
results show that clinical SLE [lupus] is preceded by complicated autoimmune changes that are
usually under way for many years before diagnosis.”

The undersigned finds particularly interesting that in the case report Dr. Shoenfeld
published in 2014, Dr. Shoenfeld did not emphasize petitioner’s UCTD, but listed it as a minor
criterion for his suggested criteria of ASIA. P. Ex. 470 at 3, 6. Most of Dr. Shoenfeld’s
discussion of petitioner’s history in that case report revolves around POTS and CFS as major
criteria supporting his ASIA theory. At some time between the publication of that case report
and the hearing in this case, Dr. Shoenfeld elevated the importance of UCTD as one of the
illnesses that Gardasil caused.

Of special note is that petitioner’s treating rheumatologist Dr. Petri stated in her medical
records that she could not connect petitioner’s UCTD to Gardasil.

Althen analysis
86
 Petitioner has failed to prove that Gardasil can cause or significantly aggravate UCTD
(prong one of Althen). Petitioner has failed to prove that Gardasil did cause or significantly
aggravate her UCTD (prong two of Althen). Petitioner has failed to prove that clinical and
laboratory substantiation of UCTD occurring months after Gardasil is an appropriate interval to
prove causation or significant aggravation of UCTD (prong three of Althen).

Small Fiber Polyneuropathy

Dr. Shoenfeld mentioned another illness, small fiber polyneuropathy, which he thought
petitioner might have although there is no proof that she has it since she has never manifested
symptoms of it, and no treating doctor diagnosed her with it. Petitioner had the option of having
tests done to prove that she has small fiber polyneuropathy but either she did not undergo the
tests or, if she did, they proved negative. In either event, petitioner failed to prove she has small
fiber polyneuropathy.

Althen analysis

Petitioner has failed to prove that Gardasil can cause small fiber polyneuropathy (prong
one of Althen). Petitioner has failed to prove that Gardasil did cause small fiber polyneuropathy
(prong two of Althen). Petitioner has failed to prove that an unknown interval between a
presumed small fiber polyneuropathy after Gardasil is an appropriate interval to prove causation
(prong three of Althen).

Petitioner has failed to make a prima facie case of causation in fact that Gardasil caused
any of the illnesses alleged in the petition or the illnesses Dr. Shoenfeld added at the hearing.

The undersigned DISMISSES this case for failure to make a prima facie case.

CONCLUSION

This petition is DISMISSED. In the absence of a motion for review filed pursuant to
RCFC, Appendix B, the clerk of the court is directed to enter judgment herewith. 57

IT IS SO ORDERED.

January 31, 2017 s/Laura D. Millman
DATE Laura D. Millman
Special Master

57
Pursuant to Vaccine Rule 11(a), entry of judgment can be expedited by each party, either separately or
jointly, filing a notice renouncing the right to seek review.
87