Pearson v. Secretary of Health and Human Services ( 2019 )

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
Filed: July 31, 2019
* * * * * * * * * * * * * * *
STEVEN PEARSON, * PUBLISHED
*
Petitioner, * No. 16-9V
*
v. * Chief Special Master Dorsey
*
SECRETARY OF HEALTH * Dismissal Decision; Influenza (Flu)
AND HUMAN SERVICES, * Vaccine; Transverse Myelitis; Onset.
*
Respondent. *
*
* * * * * * * * * * * * * * *
Randall G. Knutson, Knutson & Casey Law Firm, Mankato, MN, for petitioner.
Lisa A. Watts, U.S. Department of Justice, Washington, DC, for respondent.
DECISION1
I. INTRODUCTION
On January 4, 2016, Steven E. Pearson (“petitioner”) filed a petition under the National
Vaccine Injury Compensation Program (“Vaccine Act” or “the Program”),2 42 U.S.C. § 300aa-
10 et seq. (2012) alleging that as a result of receiving an influenza (“flu”) vaccine on October 18,
2012, he suffered from transverse myelitis (“TM”). Petition at 1-2. Respondent argued against
compensation, stating that “the record fails to establish a more likely than not causal connection
between petitioner’s flu vaccination and his subsequent condition.” Respondent’s Report
1
Because this Decision contains a reasoned explanation for the action in this case, the
undersigned is required to post it on the United States Court of Federal Claims’ website in
accordance with the E-Government Act of 2002. 44 U.S.C. § 3501 note (2012) (Federal
Management and Promotion of Electronic Government Services). This means the Decision will
be available to anyone with access to the Internet. In accordance with Vaccine Rule 18(b),
petitioner has 14 days to identify and move to redact medical or other information, the disclosure
of which would constitute an unwarranted invasion of privacy. If, upon review, the undersigned
agrees that the identified material fits within this definition, the undersigned will redact such
material from public access.
2
The National Vaccine Injury Compensation Program is set forth in Part 2 of the National
Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755, codified as amended,
42 U.S.C. §§ 300aa-10 to -34 (2012). All citations in this decision to individual sections of the
Vaccine Act are to 42 U.S.C. § 300aa.
1
(“Resp. Rept.”) at 10 (ECF No. 17). Respondent also contended that “as an initial matter, the
diagnosis . . . is unclear,” and that petitioner “has failed to establish that the onset of his
symptoms, approximately eleven weeks after vaccination, occurred within a medically
acceptable time frame for a causal association.” Id.
After carefully analyzing and weighing the evidence presented in this case in accordance
with the applicable legal standards, the undersigned finds that petitioner has failed to provide
preponderant evidence that the flu vaccine he received on October 18, 2012, caused his TM.
Therefore, this case must be dismissed.
II. PROCEDURAL HISTORY
The petition was filed in this matter on January 4, 2016,3 along with petitioner’s medical
records and affidavit. Petitioner’s Exhibits (“Pet. Exs.”) 1-7 (ECF No. 1). Petitioner filed
additional medical records on April 22, 2016, and a Statement of Completion on May 18, 2016.
Pet. Exs. 8-13 (ECF No. 11); Pet. Statement dated May 18, 2016 (ECF No. 12). On September
12, 2016, respondent filed his Rule 4(c) Report, recommending against compensation. Resp.
Rpt. at 2.
On October 27, 2016, the undersigned advised the parties during a Rule 5 status
conference that litigative risk assessment was appropriate and encouraged them to pursue
informal resolution. Order dated Oct. 27, 2016 (ECF No. 19). On December 5, 2016,
respondent indicated that the parties had reached a tentative settlement. 15-Week Stipulation
Order dated Dec. 6, 2016 (ECF No. 22). However, on February 24, 2017, respondent informed
the undersigned that the authorized representative of the Attorney General had declined to grant
settlement authority for the proposed settlement. Resp. Status Rept. dated Feb. 24, 2017 (ECF
No. 23).
A status conference was held in March 2017 to determine next steps in the case, and the
parties agreed that petitioner should file an expert report. Order dated Mar. 9, 2017 (ECF No.
24). On May 9, 2017, petitioner filed additional medical records and an expert report by Dr.
James Dahlgren, MD. Pet. Exs. 14-16 (ECF No. 25). On August 3, 2017, respondent filed a
responsive expert report by Dr. Timothy Vartanian, M.D., Ph.D. Resp. Exs. A-B (ECF No. 31).
On September 25, 2017, the undersigned ordered petitioner to file an affidavit regarding
the onset of his transverse myelitis, a supplemental expert report, and a motion for a ruling on the
record or status report. Order dated Sept. 25, 2017 (ECF No. 32). Petitioner filed his affidavit
on October 11, 2017, a supplemental expert report by Dr. Dahlgren on November 13, 2017, and
a motion for a ruling on the record on November 14, 2017. Pet. Affidavit (“Aff.”) dated Oct. 11,
2017 (ECF No. 33); Pet. Ex. 17 (ECF No. 34); Pet. Motion (“Mot.”) dated Nov. 14, 2017 (ECF
3
Based on the onset date alleged in the petition, petitioner would have been required to file his
claim by December 31, 2015, in order to comply with the statute of limitations. See § 16(a)(2).
However, as respondent noted, the U.S. Court of Federal Claims was closed on December 31,
2015; this petition was filed on January 4, 2016, the date the Court reopened. Resp. Rept. at 2
n.2; see also Vaccine Rule 19(a)(1)(c).
2
No. 35). On November 27, 2017, respondent filed a motion requesting the opportunity to have
Dr. Vartanian respond to the four points raised in the undersigned’s September 25, 2017 Order,
in light of Dr. Dahlgren’s submission. Resp. Mot. dated Nov. 27, 2017 (ECF No. 36). The
motion was granted, and respondent filed a responsive report by Dr. Vartanian on January 19,
2018. Order dated Nov. 27, 2017 (ECF No. 37); Resp. Ex. C (ECF No. 39).
Petitioner subsequently filed updated neurology records on May 17, 2018, and an expert
report from his treating neurologist, Dr. Scott Lipson, M.D., on May 25, 2018. Pet. Ex. 18 (ECF
No. 46); Pet. Exs. 19-20 (ECF No. 47). On August 9, 2018, respondent filed a second
supplemental report by Dr. Vartanian, and on September 6, 2018, petitioner submitted a final
supplemental report from Dr. Lipson. Resp. Ex. D (ECF No. 51); Pet. Ex. 21 (ECF No. 52).
On November 1, 2018, the undersigned held a status conference and explained to the
parties that after reviewing the supplemental expert reports from Dr. Lipson and Dr. Vartanian,
she had preliminarily determined that petitioner was not entitled to compensation. Order dated
Nov. 2, 2018 (ECF No. 54). The undersigned suggested that petitioner file a renewed motion for
a ruling on the record, which petitioner filed later that day. Id.; Pet. Mot. dated Nov. 1, 2018
(ECF No. 53). Respondent filed his response to petitioner’s motion for a ruling on the record on
November 30, 2018. Resp. Response dated Nov. 30, 2018 (ECF No. 55).
This matter is now ripe for adjudication.
III. FACTUAL SUMMARY
A. Medical History Prior to Vaccination
Mr. Pearson was born on December 31, 1953. Pet. Ex. 1. His medical history is
significant for hearing loss, vertigo, right hip pain, depression, and anxiety. Pet. Ex. 8 at 5. In
the three years preceding the vaccination at issue, he received medical care from his primary care
physician, Dr. David E. Dennis. Petitioner saw Dr. Dennis several times in 2009 for upper
respiratory infection with bronchitis, infected nasal septum, tinnitus due to cerumen impaction,
dizziness, elevated blood pressure, and depression. Pet. Ex. 8 at 3-6.
In 2010 through 2012, petitioner saw Dr. Dennis for various complaints. In 2010,
petitioner experienced dizzy spells thought to be due to anxiety, excessive alcohol use, or
Meniere’s Disease. Pet. Ex. 8 at 8-9, 21. Petitioner also complained of right lower back pain
and was diagnosed with lumbar sprain and right sacroiliitis. Id. at 22-28; Pet. Ex. 9 at 134.
Lumbar spine X-rays showed degenerative changes, especially at L4-5. Pet. Ex. 8 at 23. In 2011
and 2012, petitioner had left knee pain that resolved with medication and time. Id. at 32-35, 38.
In 2012, petitioner had an upper respiratory tract infection, situational anxiety, depression, a
fungal infection in his feet, and cerumen impaction of his ears. Id. at 37, 39-40. He also
reported a history of blurred vision in his right eye.4 Id. at 41.
4
Another physician was treating petitioner for this ailment, but Dr. Dennis commented that
petitioner was “simply going to have to live with this blurriness.” Pet. Ex. 8 at 41.
3
B. Date of Vaccination
Petitioner received the flu vaccination at issue on October 18, 2012. Pet. Ex. 8 at 1. Of
note, he also received seasonal flu vaccinations on October 19, 2011; September 26, 2013; and
November 6, 2014. Id. Aside from petitioner’s allegations related to the flu vaccine
administered on October 18, 2012, no documentation in the medical records indicates that
petitioner had any adverse reaction to his other flu vaccinations.
C. Subsequent Clinical Course
On November 8, 2012, petitioner saw Dr. Dennis for a “health maintenance
examination.” Pet. Ex. 8 at 41. Petitioner reported that he consumed four beers every day and
experienced stress due to family issues. Id. There was no indication at this visit that petitioner
had any adverse reaction to his flu vaccine the previous month.
Petitioner next saw Dr. Dennis on January 4, 2013. He complained of “pain of the left
chest going down the left arm” with painful skin, sensitive to touch. Pet. Ex. 8 at 47. Dr. Dennis
did not document how long these symptoms had been present. Physical examination revealed
scratching of the skin on the left side, with “exquisitely painful pressure points on [his] back and
down [his] left arm.” Id. Dr. Dennis diagnosed petitioner with herpes zoster (shingles) “prior to
the eruption of vesicles.” Id.
Petitioner returned to Dr. Dennis on January 28, 2013, still complaining of pain in his left
arm. Pet. Ex. 8 at 50. Dr. Dennis noted that petitioner “never did develop vesicles, so we are not
entirely sure that he ever had shingles, though we treated him for the same due to the radicular
nature of this pain.” Id. In addition to symptoms in the left arm, petitioner also complained of
“tingling and itching of the left leg and left abdomen.” Id. Petitioner had a “little follicular rash
of the left shoulder,” but no other rash. Id. Dr. Dennis diagnosed petitioner with pruritis with no
“particular etiology” and “[v]ague chest pain and pressure with left arm discomfort.” Id.
Cardiac studies were ordered, which showed normal heart function with no evidence of cardiac
ischemia. Id. at 54-56.
On March 21, 2013, petitioner saw Dr. Keith Hansen for lower back pain after slipping
on ice. Pet. Ex. 8 at 57. He was diagnosed with left sacroiliac strain and treated with a Medrol
Dosepak. Id. On May 30, 2013, petitioner again presented to Dr. Dennis’s office with “herpetic
neuralgia pain left chest and arm,” which had worsened over the last few days. Id. at 60. Dr.
Dennis noted that petitioner’s “herpetic infection was quite some time ago.” Id. Dr. Dennis
diagnosed petitioner with post-herpetic neuropathy and prescribed gabapentin. Id. Petitioner
returned for follow-up on June 13, 2013, and reported that although the gabapentin helped, he
continued to have “zingers that come through.” Id. at 61. Dr. Dennis increased the dose of
gabapentin. Id. At his return visit on July 3, 2013, petitioner reported that the medication was
controlling his symptoms. Id. at 62. No documentation from the visits of January 2013 through
March 2013 suggests that petitioner had leg weakness, gait problems, or urinary retention.
Petitioner did not return to Dr. Dennis for herpetic neuropathy symptoms until September
26, 2013, when he again complained of “left arm pain going down the inside of the left arm,”
4
which he attributed to shingles. Pet. Ex. 8 at 65. Dr. Dennis noted that petitioner previously
only exhibited “one tiny lesion on the back” that may have been a zoster lesion. Id. At this
point, Dr. Dennis decided to “totally reassess” the problem since petitioner never had the “classic
blistery shingles rash.” Id. Dr. Dennis ordered an MRI of the cervical spine. Id. Incidentally,
petitioner also received a seasonal flu vaccine at this visit. Id. No documentation suggests that
petitioner had any adverse reaction to this vaccination.
An MRI of the cervical spine was performed September 27, 2013. It showed a “T2
hyperintense focus in the lower cervical and upper thoracic [spinal] cord at the C7-T1 level.”
Pet. Ex. 8 at 76. No appreciable enhancement was noted. Id. Differential diagnoses included
demyelinating conditions like multiple sclerosis (“MS”) or “other forms of myelitis, including
infection or idiopathic transverse myelitis.” Id. After receiving the results of the MRI, Dr.
Dennis ordered additional diagnostic tests including sedimentation rate, C-reactive protein,
ANA, and Lyme titer, which were all normal. Id. at 68, 71, 80-81. A brain MRI showed no
“evidence of acute intracranial abnormality.” Pet. Ex. 9 at 87. Dr. Dennis referred petitioner to a
neurologist, Dr. Alireza Yarahmadi, for consultation. Id. at 87-89.
Dr. Yarahmadi first saw petitioner on October 3, 2013. Dr. Yarahmadi noted that
“[a]pproximately 10 months ago [petitioner] started noticing paresthesia and pain over his left
chest and left shoulder.” Pet. Ex. 9 at 88. Petitioner compared his pain to an“electric shock or
stabbing feeling.” Id. Physical examination revealed “decreased sensation in distribution of C6
and C7 dermatomes on the left side.” Id. at 89. Impression was “[m]yelitis extending from left
C7 to T1 for up to 5 cm . . . . Etiology is unknown.” Id. Dr. Yarahmadi ordered additional
diagnostic testing to “look for autoimmune/infectious causes.” Id.
Petitioner returned for a follow-up appointment with Dr. Yarahmadi on October 17,
2013. The results of an NMO antibody test5 were normal, as were the other laboratory tests. Pet.
Ex. 13 at 16-17. Cerebrospinal fluid showed “slightly elevated ACE and protein,” but also
revealed normal oligoclonal bands6 and IgG index. Id. Dr. Yarahmadi diagnosed petitioner with
myelitis from left C4 to T1. Id. He concluded that the most likely causes were related to
infection, autoimmunity, or malignancy. Id. He did not document vaccination as a possible
cause.
Dr. Yarahmadi next saw petitioner on September 30, 2014. Petitioner reported residual
paresthesia and pain in his left shoulder and arm. Pet. Ex. 13 at 23. Repeat thoracic MRI
showed persistent abnormal findings at T1. Id. Dr. Yarahmadi documented that petitioner’s
workup was unremarkable for “autoimmune, metabolic, and infectious causes.” Id. at 24.
Petitioner was offered a second opinion but elected to “continue with conservative measures.”
Id.
5
An NMO antibody test screens for the autoantibody NMO-IgG, also known as aquaporin-4,
which assists doctors with early diagnosis of NMO. Neuromyelitis optica, Mayo Clinic,
https://www.mayoclinic.org/diseases-conditions/neuromyelitis-optica/diagnosis-treatment/drc-
20375655 (last visited June 11, 2019).
6
Two oligoclonal bands in the CSF were noted on the lab report. Pet. Ex. 13 at 30.
5
In February 2015, petitioner had numbness, tingling, and weakness of his left leg, and he
was diagnosed with radiculopathy. Pet. Ex. 11 at 316-17. Physical therapy was prescribed. Id.
No reference was made to abnormal gait or urinary retention at that time. On August 27, 2015,
petitioner was once again evaluated by Dr. Yarahmadi. A repeat MRI again showed myelitis
extending from left C7 to T1. Pet. Ex. 13 at 27. A subsequent MRI performed September 5,
2017, also showed stable intramedullary7 hyperintensity present from T1-2 to C7. Pet. Ex. 18 at
11.
On November 28, 2017, petitioner saw a second neurologist, Dr. Maria J. Servioli Verde.
Dr. Verde noted that in December 2012, petitioner “started to experience numbness, tingling, and
pain at the level of the left axillary region and shoulder, and pectoral area.” Pet. Ex. 18 at 4.
Petitioner reported that two months before his symptoms began, he received the flu vaccine. Id.
Petitioner also indicated that eight years earlier, he had temporary loss of vision in his right eye,
and over the last year, he had noticed progressive weakness of the left leg extremity such that he
occasionally dragged the leg. Id. He stated that he had experienced leg weakness since his
symptoms began, with waxing and waning of his leg symptoms. Id. Dr. Verde also noted that
petitioner did not report pain in general, but that he did have residual paresthesias and pain in the
left shoulder, along with occasional urinary incontinence.8 Id. Physical examination revealed
“[d]ecreased vibration and pinprick in the dorsal aspect of left foot” and erythrocyanosis of the
left foot. Id. at 6. Petitioner was noted to “slightly drag the left leg.” Id. Dr. Verde’s diagnosis
was TM and abnormal evoked potential9 of the right eye. Id. at 7. Although Dr. Verde noted
that petitioner reported receiving a flu shot two months before his symptoms began, Dr. Verde
did not document this vaccination as a possible cause of petitioner’s TM. Id.
D. Affidavits
In his initial affidavit, Mr. Pearson averred that he received a flu vaccine on October 18,
2012. Pet. Ex. 2 at ¶ 3. After receiving the vaccination, he states that he began experiencing
pain in the upper left side of his chest and arm. Id. at ¶ 4. He was diagnosed with TM
approximately one year later, on October 3, 2013. Id. at ¶ 5.
Petitioner executed a subsequent affidavit on October 9, 2017, in which he asserted that
he “believe[s] the symptoms initially began in November 2012.” Aff. dated Oct. 11, 2017 (ECF
No. 33) at ¶ 2. He also recalled a “very specific episode” of pain in mid-December 2012. Id. at
7
“Intramedullary” means “within the spinal cord.” Dorland’s Illustrated Medical Dictionary 954
(32d ed. 2012).
8
Petitioner saw urologist Dr. Orville Jacobs on December 11, 2014, for an unrelated problem
and denied any bladder or bowel concerns. Pet. Ex. 9 at 22.
9
Evoked potential, in the visual context, means “changes in the evoked cortical potential when
the eye is stimulated by light; variations are diagnostic for abnormalities of the visual system and
for other disorders, particularly neurological disorders such as multiple sclerosis, that have visual
symptoms.” Dorland’s at 1505.
6
¶ 3. Petitioner stated, however, that he “[did] not know the exact date of the onset of the
symptoms.” Id. at ¶ 2.
IV. Transverse Myelitis
Transverse myelitis is a rare disease “in which inflammation of the spinal cord results in
neurological deficits, manifesting as weakness, sensory loss and autonomic dysfunction.” Resp.
Ex. C, Tab 3 (Borchers 2012) at 1. The etiology is thought to be multi-factorial and due to a
combination of “genetic, immunological, hormonal and environmental factors.” Pet. Ex. 23,
Ref. 1 (Agmon-Levin 2009) at 2. “[U]p to 40% of TM cases are associated with a preceding
infectious illness, mostly within a month of TM onset.” Id. The cause of acute TM is generally
not identified, and thus, the cause is referred to as idiopathic. Resp. Ex. C, Tab 3 (Borchers
2012) at 2.
When TM is coupled with demyelination of the optic nerve, it is referred to as
neuromyelitis optica (“NMO”). Pet. Ex. 23, Ref. 1 (Agmon-Levin 2009) at 2. TM and NMO are
“part of a spectrum of inflammatory demyelinating disorders, which also includes acute
disseminated encephalomyelitis [“ADEM”] and MS.” Resp. Ex. C, Tab 3 (Borchers 2012) at 2.
TM is usually monophasic but can be recurrent in up to 25% of cases. Id. NMO events can
occur “months, years or even decades apart and . . . the disease takes a recurrent or
relapsing/remitting course in > 80% of patients.” Id.
TM is suspected when a patient has “acute or subacute motor, sensory, bladder, and/or
bowel dysfunction with a presence of a sensory level.” Resp. Ex. A at 5. Early symptoms
generally include “sensory dysfunction, paresthesias or pain in the back, abdomen or the
extremities, and an often ascending pattern of numbness or weakness of the legs, whereas the
upper extremities are less frequently and generally less severely affected.” Resp. Ex. C, Tab 3
(Borchers 2012) at 8. Symptoms progress over hours or days, “with a majority of patients
reaching their maximum deficient within 7 days, although full evolution may take up to 21
days.” Id. Two-thirds of patients lose their ability to walk, and almost all have urinary retention.
Id. Outcome ranges from full recovery to death from respiratory failure. Id. Diagnostic testing
may include cerebrospinal fluid (“CSF”) analysis, which may reveal CSF pleocytosis,
characteristic of spinal cord inflammation. Pet. Ex. 23, Ref. 1 (Agmon-Levin 2009) at 1. IgG
index may be abnormally elevated. Id. Most importantly, MRI may reveal the presence of
spinal cord lesions. Id.
V. EXPERT OPINIONS
A. Petitioner – Dr. James Dahlgren, M.D.
i. Qualifications
Dr. Dahlgren earned his B.A. from the University of California at Los Angeles, and his
M.D. from the University of California at San Francisco. Pet. Ex. 22 at 1. After completing
residencies at both Boston Veteran’s Hospital in Boston and Cedars-Sinai Medical Center in Los
Angeles, he served as a fellow in infectious diseases at UCLA Medical Center. Id. Dr. Dahlgren
7
has held several academic appointments, including Assistant Professor of Medicine at the UCLA
School of Medicine from 1975-1977, and Assistant Clinical Professor of Medicine at the
University of California at Los Angeles School of Medicine from 1977-2011. Id. at 2. His CV
lists 39 publications that he has authored or co-authored, along with a number of abstracts and
presentations. Id. at 3-9. Dr. Dahlgren is board certified in internal medicine. Id. at 1.
ii. Opinion
1. Althen Prong One
Dr. Dahlgren opined that the flu vaccine caused an autoimmune phenomenon that
contributed to the development of petitioner’s TM. Pet. Ex. 16 at 11. He suggested several
potential mechanisms whereby vaccines can cause “altered immune function,” including
molecular mimicry; epitope spreading; polyclonal activation of B lymphocytes, causing
enhanced production of cytokines; T cell mediated immune response to oligodendrocytes; and
autoimmune/inflammatory syndrome induced by adjuvants (“ASIA”). Id. at 4-11. Dr. Dahlgren
also opined that petitioner had a genetic susceptibility to autoimmune conditions because his
father suffered from Guillain-Barre Syndrome (“GBS”). Id. at 11. Other than listing them in his
expert report, Dr. Dahlgreen did not describe or develop the theories of epitope spreading,
polyclonal activation of B lymphocytes, or T cell mediated immune response to
oligodendrocytes. He focused principally on two theories: molecular mimicry and adjuvant-
induced autoimmunity.
Dr. Dahlgren claimed that the adjuvants in vaccines cause an increase in cytokines and
autoantibodies, which cause autoimmune diseases. Pet. Ex. 16 at 4-9. He stated that the flu
vaccine contains the adjuvants squalene and aluminum, which lead to autoimmune diseases,
adding that “[i]t is likely that [petitioner’s] trivalent influenza vaccine contained squalene as an
adjuvant.” Id. at 5. Dr. Dahlgren asserted that animal models show that squalene “is a powerful
inducer of cytokines” that cause autoimmunity. Id. at 5. He suggested that in a susceptible
person, an adjuvant can trigger the immune system. Id. at 8.
Dr. Dahlgren maintained that in addition to inducing cytokines, adjuvants themselves can
cause autoimmune or inflammatory conditions. Pet. Ex. 16 at 8. He cited a study by Khan, et
al., for the proposition that aluminum adjuvant in the HPV vaccine can cause damage to neurons
in the brain. Id. at 9; see generally Pet. Ex. 25, Ref. 30 (Khan 2013). In addition to squalene and
aluminum, Dr. Dahlgren opined that other adjuvants, including silicon, mineral oil, guaiacol, and
iodine gadital, can cause autoimmune disease. Pet. Ex. 16 at 9. Dr. Dahlgren cited Korn-
Lubetzki, et al., in support of his theory that the adjuvants in the flu vaccine may play a role in
the development of autoimmune disease. Id. at 4; see generally Pet. Ex. 23, Ref. 2 (Korn-
Lubetzki 2011).10 The Korn-Lubetzki study raised the question of whether adjuvants “might”
play a role in development of TM, but did not study the issue or reach any conclusions. Pet. Ex.
23, Ref. 2 (Korn-Lubetzki 2011) at 2. Likewise, the Agmon-Levin study discussed interest in
10
Petitioner did not proffer any evidence to show that the flu vaccine at issue contained any of
these adjuvants.
8
the adjuvant mechanism of causation, but only suggested that adjuvants “might be responsible.”
Pet. Ex 23, Ref. 1 (Agmon-Levin 2009) at 5.
An additional causal theory proposed by Dr. Dahlgren is molecular mimicry, which he
described as an “accidental failure to recognize” one’s own “cell, tissue or protein,” resulting in
an attack on “normal and healthy tissue.” Pet. Ex. 16 at 4. He asserted that the “antibodies that
attack the myelin” are “known to occur from vaccinations.” Id. at 11. Here, Dr. Dahlgren
pointed to Agmon-Levin, a study which asserted that antigens and self-antigens are the most
common mechanism by which infections trigger TM and hypothesized that “it is reasonable to
assume” that vaccines induce autoimmunity in the same manner as “infectious antigens.” Pet.
Ex. 23, Ref. 1 (Agmon-Levin 2009) at 4; see also Pet. Ex. 16 at 2-3. The authors of this study
did not explain the basis for this assumption. Dr. Dahlgren also cited a study by Sato, et al.,
which did not ultimately support the mechanism of molecular mimicry. See generally Pet. Ex.
23, Ref. 3 (Sato 2011). At the conclusion of the study, the authors stated, “we could not find any
data directly suggesting molecular mimicry between the nervous tissue and influenza vaccines.”
Id. at 4.
Underlying both causal theories is Dr. Dahlgren’s opinion that certain persons are
susceptible to autoimmune illnesses due to their genetics. See Pet. Ex. 16 at 8. Dr. Dahlgren
observed that petitioner’s father had “an autoimmune illness of Guillain-Barre syndrome, which
is compatible with a genetic susceptibility in this family.” Id. at 11.
Dr. Dahlgren pointed to a number of case reports describing patients who developed TM
following vaccination. Pet. Ex. 16 at 4-9. One of these, Agmon-Levin, summarizes 37 cases of
TM associated with a host of different vaccines. See generally Pet. Ex. 23, Ref. 1 (Agmon-Levin
2009). However, of the 37 cases, only two were reported following the flu vaccine; these cases
involved adults ages 42 and 70, with onset nine and seven days following vaccination,
respectively. Id. at 3. The authors conclude that the “rarity of post-influenza-vaccination
neurological complications reported in recent years makes it impossible to establish a definite
causal relation.” Id. at 4. Of note, the authors pointed out that adverse neurological events have
declined since the introduction of the HA form of the vaccine,11 prepared from human stock of
the virus. Id. Moreover, some of the cases were associated with live virus vaccines, unlike the
influenza vaccine, which is an “inactivated or killed viral vaccine.” Id.
2. Althen Prong Two
Regarding Prong Two, Dr. Dahlgren made the following conclusory statement: “The
logical sequence is [petitioner] developed a well-known but rare complication from a influenza
vaccine. There is no other risk factor for his illness.” Pet. Ex. 16 at 11. In his second report, Dr.
Dahlgren provided some context. He opined that the symptoms that began in petitioner’s left
axillary region and shoulder, reported to his doctor on January 4, 2013, were the first
manifestations of his TM. Pet. Ex. 17 at 2. Dr. Dahlgren did not reference any facts or evidence
11
Hemagglutinin, also known as HA, is “an agglutinin, e.g., an antibody or lectin, that
agglutinates erythrocytes.” Dorland’s at 830.
9
from petitioner’s clinical course or medical records that support his causal theories of vaccine
causation based on either molecular mimicry or adjuvant-induced TM.
3. Althen Prong Three
Dr. Dahlgren opined that a temporal association of three months from vaccine to onset is
appropriate. Pet. Ex. 16 at 11. He cited the table of cases from the Agmon-Levin study for the
proposition that onset of TM can range from two days, to three months, to nine years in cases of
oral polio vaccine. Id. at 3. However, he did not address the fact that the two cases of TM
following flu vaccine occurred within nine days of vaccination, not three months. Dr. Dahlgren
did not provide any literature or other foundational support for his opinion that three months is
an appropriate temporal association for his proposed causal theories.
B. Dr. Scott Lipson, M.D.
i. Qualifications
Dr. Lipson received a B.A. from Harvard University and an M.D. from New York
University School of Medicine. Pet. Ex. 20 at 1. He completed his residency at Harvard
University’s Beth Israel Deaconess Medical Center, followed by a fellowship in Clinical
Neurophysiology at the University of Illinois Medical Center at Chicago. Id. Dr. Lipson is
board certified in general neurology and clinical neurophysiology, and he currently practices at
Neurology Consultants/EMG Centers of Chicagoland. Id. He has also co-authored three
publications. Id. at 2.
ii. Opinion
Petitioner submitted two reports by Dr. Lipson. See Pet. Exs. 19, 21. In both reports, Dr.
Lipson framed his opinions relative to those of Dr. Vartanian, respondent’s expert neurologist,
whose opinions are discussed below. Dr. Lipson did not offer a causal theory or mechanism
whereby the flu vaccine can cause TM. He did not offer a logical sequence of cause and effect
or otherwise opine that petitioner’s flu vaccine caused TM. He did, however, opine regarding
onset.
Dr. Lipson provided the following narrative of petitioner’s clinical history:
Mr. Pearson received an influenza vaccination of October 18, 2012 (as well as on
three other occasions: October 18, 2011; September 26, 2013; and November 6,
2014). He reported symptoms of left axillary/shoulder/chest pain to Dr. David
Dennis on January 4, 2013 (History provided to neurologist, Dr. Maria J. Servioli
Verde, on August 29, 2016 related a symptom onset in [December] 2012, not
further specified). Initial diagnosis from Dr. Dennis is herpes zoster, either with or
without a rash and he received treatment with acyclovir and oral
methylprednisolone. MRI C-spine with and without contrast from September 27,
2013 showed abnormal T2 signal hyperintensity in the central/left cervical cord
from C7-T1. Serum blood test workup included elevated ACE levels but was
10
otherwise unremarkable. MRI of the brain and lumbar spine did not show any other
significant findings. NMO/aquaporin-4 antibody testing was negative. CSF studies
showed mild protein elevation but were otherwise unremarkable as well. Mr.
Pearson’s clinical presentation is consistent with transverse myelitis.
Pet. Ex. 19 at 1. Although Dr. Lipson opined that petitioner’s clinical course was consistent with
TM, as stated above, he did not opine that the flu vaccine caused petitioner’s TM.
Dr. Lipson offered two opinions as to onset – one based on petitioner’s initial symptoms,
and the other based upon the MRI performed in September 2013. In his initial report, he opined
that the onset of petitioner’s TM occurred 10-11 weeks after his flu vaccine. Pet. Ex. 19 at 2.
Dr. Lipson stated:
The first manifestation of [petitioner’s TM] consist of his left shoulder/axilla and
chest pain, corresponding to the C7-T1 spinal level affected. The first date for
which he sought medical attention for those symptoms is January 4, 2013 with Dr.
Dennis, nearly 11 weeks after the influenza vaccination of October 18, 2012. The
only other reference in the medical record as to symptom onset occurs several years
after the fact during his visit with Dr. Maria J. Servioli Verde on August 29, 2016
(“. . . 2 months before his symptoms started in 10/2012, he received the flu
vaccine”).
Dr. Dennis does not specify in his evaluation of January 4, 2013 how long
[petitioner] had experienced his shoulder/axillary pain. . . . To a reasonable degree
of medical certainty, therefore, the date of onset occurred in the first days of January
2013. One can therefore place the onset of [TM] 10-11 weeks after the influenza
vaccination.”
Id. Dr. Lipson also provided a second opinion as to onset, in agreement with Dr. Vartanian’s
interpretation of petitioner’s September 26, 2013 MRI. Dr. Lipson reviewed the interpretation of
petitioner’s MRI, as well as screenshots of the images themselves, and expressly agreed with Dr.
Vartanian’s position that onset occurred within 1-2 months of the MRI. Pet. Ex. 21 at 2. This
interpretation places onset of petitioner’s TM in July or August 2013, nine or more months after
his flu vaccination.
While Dr. Lipson opined in his first report that petitioner’s clinical presentation was
consistent with TM, it was not clear whether Dr. Lipson’s opinion referred to petitioner’s initial
presentation in January 2013, or his ultimate diagnosis of TM in October 2013. See Pet. Ex. 19
at 1. In his supplemental report, Dr. Lipson resolved this uncertainty when he opined that
petitioner’s initial presentation in January 2013 was “most consistent” with shingles “based on
the dermatomal restriction, character of the pain and presence of pruritis.” Pet. Ex. 21 at 1.
11
C. Dr. Timothy Vartanian, M.D., Ph.D.
i. Qualifications
Dr. Vartanian earned his B.A. from Oakland University, and both his Ph.D. and M.D.
from the University of Chicago. Resp. Ex. B. at 2. After completing a neurology residency at
Massachusetts General Hospital, he completed fellowships in Boston at Beth Israel Hospital and
Harvard Medical School. Id. at 3. Dr. Vartanian has taught courses at Harvard Medical School
on topics such as CNS myelination. Id. at 3, 5. He has co-authored 56 studies, and he serves as
an ad hoc reviewer for a number of publications, including the New England Journal of
Medicine, the Journal of Neuroscience Research, and the Journal of Comparative Neurology. Id.
at 13-20.
Currently, Dr. Vartanian serves as a professor of Neurology and Neuroscience at Weill
Cornell Medical College, and he practices at the Judith Jaffe Multiple Sclerosis Center. Resp.
Ex. A at 1; Resp. Ex. B at 4. He is board certified in adult neurology. Resp. Ex. B. at 4.
ii. Opinion
1. Althen Prong One
Dr. Vartanian disagreed with Dr. Dahlgren that any evidence supported a causal
association between the flu vaccine and TM. Resp. Ex. A at 5. He explained that it is
“generally agreed in the scientific community that we cannot determine causality through
individual case reports,” citing a study by Rasmussen, et al., for this general proposition. Id. at
7; see generally Resp. Ex. A, Tab 1 (Rasmussen 2012). Dr. Vartanian noted that approximately
1,400 new cases of TM are diagnosed each year. Resp. Ex. A at 6 (citing Transverse Myelitis
Fact Sheet, Nat’l Inst. of Neurological Disorders & Stroke, http://www.ninds.nih.gov/disorders/
transversemyelitis/detail_transversemyelitis.htm (last visited June 18, 2019)). He further
observed that the Agmon-Levin study cited by petitioner summarized cases reported in the
literature over a period of 39 years. Id. Assuming 1,400 cases of TM were diagnosed per year,
one would expect approximately 54,600 new cases of TM over the time period covered by
Agmon-Levin. Id. Yet, out of thousands of newly diagnoses cases, Agmon-Levin only
associated two TM cases with flu vaccines. See id. Additionally, Dr. Vartanian noted, the
authors did not provide any statistical analysis to “discern the probability of chance occurrence
versus causal occurrence.” Id. at 7.
Dr. Vartanian also disagreed that adjuvants in vaccines can cause TM. He explained that
the articles cited by Dr. Dahlgren in support of this theory are not relevant because they have “no
temporal, physiologic, or pathologic similarities to [petitioner’s] case.” Resp. Ex. A at 7. For
example, in the Lujan study, sheep were given vaccines against ovine pathogens that contained
the adjuvants aluminum and thimerosal. See Pet. Ex. 25, Ref. 29 (Lujan 2013). However, as Dr.
Vartanian emphasized, “the lambs received a total of 14 inoculations” over 9 months, and thus
“[t]he adjuvant exposure in these lambs was significantly higher than that of [petitioner].” Resp.
Ex. A at 8. Moreover, in the sheep study, subsequent pathology slides revealed histopathological
lesions not relevant to this case. Id.
12
With regard to petitioner’s theory that the flu vaccine can cause TM through the
mechanism of molecular mimicry, Dr. Vartanian responded that the autoantibodies that cause
TM “are not known.” Resp. Ex. A at 6. In support of his conclusion, he cited a study by
Borchers, et al. Id.; see also Resp. Ex. C, Tab 3 (Borchers 2012). This study discussed possible
mechanisms whereby activation of an autoimmune response may cause TM, stating that
molecular mimicry has “long been thought to play a primary role in triggering a variety of
autoimmune diseases. However, evidence has remained elusive in most cases, with the possible
exception of [GBS].” Resp. Ex. C, Tab 3 (Borchers 2012) at 12. The authors reviewed current
findings and noted growing evidence that antibodies targeting the aquaporin-4 water channel of
the central nervous system may play a pathogenic role in NMO and TM. Id. at 1.
Dr. Vartanian also contested Dr. Dahlgren’s claim that petitioner was genetically
predisposed to TM. Dr. Vartanian rebutted this assertion by stating that there is “no
epidemiologic evidence that individuals with a family history of GBS are more likely to develop
[TM].” Resp. Ex. A at 6.
2. Althen Prong Two
Dr. Vartanian opined that there was no logical sequence of cause and effect because
petitioner’s clinical presentation in January 2013 was “most consistent” with shingles and not
TM, “based on the dermatome restriction, character of the pain and presence of pruritis.” Resp.
Ex. C at 1. Noting that petitioner subsequently developed symptoms of numbness and leg
weakness, Dr. Vartanian attributed petitioner’s initial symptoms to varicella zoster.12 Id. at 3.
The evolution of petitioner’s course was prolonged, and thus, atypical of acute TM, which
usually progresses from onset of symptoms to maximum deficit within 72 hours. Id. at 5. Thus,
Dr. Vartanian concluded, petitioner’s symptoms were more consistent with varicella zoster
myelitis. Id. at 5.
3. Althen Prong Three
Dr. Vartanian observed that the symptoms that led to petitioner’s TM diagnosis were first
reported on January 4, 2013, approximately 11 weeks after vaccination. Resp. Ex. A at 10. He
maintained that “11 weeks falls well outside generally accepted time frames for post-
immunization induced pathology.” Id. However, Dr. Vartanian also acknowledged that the
difficulty in placing the onset of TM in January 2013 is that petitioner’s clinical course was
prolonged and atypical for TM. Resp. Ex. C at 3. He emphasized that while “[t]he clinical
course of transverse myelitis from onset of symptoms to maximal deficit is 12-72 hours
typically,” petitioner did not reach maximal deficit until 12 months after onset. Id. at 5. Thus,
Dr. Vartanian asserted in the alternative that petitioner’s January 2013 symptoms were likely
caused not by TM, but by varicella zoster. Id. at 1. Petitioner’s varicella zoster reactivation, Dr.
Vartanian explained, subsequently caused him to develop TM. Id. at 5. Based on petitioner’s
September 2013 MRI, which showed an increased T2 signal in the spinal cord from C7 to T1,
12
Varicella zoster virus, or human herpesvirus 3, is the virus that causes chickenpox and shingles
(herpes zoster). Dorland’s at 853, 1703, 2017, 2024.
13
Dr. Vartanian opined that the onset of petitioner’s TM was “within 1-2 months of the MRI.” Id.
at 12.
VI. DISCUSSION
A. Standards for Adjudication
The Vaccine Act was established to compensate vaccine-related injuries and deaths.
§ 10(a). “Congress designed the Vaccine Program to supplement the state law civil tort system
as a simple, fair and expeditious means for compensating vaccine-related injured persons. The
Program was established to award ‘vaccine-injured persons quickly, easily, and with certainty
and generosity.’” Rooks v. Sec’y of Health & Human Servs., 35 Fed. Cl. 1, 7 (1996) (quoting
H.R. Rep. No. 908 at 3, reprinted in 1986 U.S.C.C.A.N. at 6287, 6344).
Petitioner’s burden of proof is by a preponderance of the evidence. § 13(a)(1). The
preponderance standard requires a petitioner to demonstrate that it is more likely than not that the
vaccine at issue caused the injury. Moberly v. Sec’y of Health & Human Servs., 592 F.3d 1315,
1322 n.2 (Fed. Cir. 2010). In particular, petitioner must prove that that the vaccine was “not only
[the] but-for cause of the injury but also a substantial factor in bringing about the injury.” Id. at
1321 (quoting Shyface v. Sec’y of Health & Human Servs., 165 F.3d 1344, 1352-53 (Fed. Cir.
1999)); Pafford v. Sec’y of Health & Human Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006). A
petitioner who satisfies this burden is entitled to compensation unless respondent can prove, by a
preponderance of the evidence, that the vaccinee’s injury is “due to factors unrelated to the
administration of the vaccine.” § 13(a)(1)(B).
B. Legal Framework
i. Statute of Limitations
The statute of limitations, or the time frame within which a vaccinee or their legal
representative must file a claim, is outlined in § 16(a)(2) of the Vaccine Act:
[I]f a vaccine-related injury occurred as a result of the administration of such
vaccine, no petition may be filed for compensation under the Program for such
injury after the expiration of 36 months after the date of the occurrence of the first
symptom or manifestation of onset or of the significant aggravation of such injury.
§ 16(a)(2) (emphasis added). This time period runs from the manifestation of the first
objectively cognizable symptom, whether or not that symptom is sufficient for diagnosis.
Carson v. Sec’y of Health & Human Servs., 727 F.3d 1365, 1369 (Fed. Cir. 2013). Whether a
petitioner knows the cause of his injury is not significant for purposes of the statute of
limitations. Cloer v. Sec’y of Health & Human Servs., 654 F.3d 1322, 1330-35 (Fed. Cir. 2011)
(en banc).
14
ii. Causation
To receive compensation under the Program, petitioner must prove either: (1) that he
suffered a “Table Injury”—i.e., an injury listed on the Vaccine Injury Table—corresponding to a
vaccine that he received, or (2) that he suffered an injury that was caused by a vaccination. See
§§ 13(a)(1)(A) and 11(c)(1); Capizzano v. Sec’y of Health & Human Servs., 440 F.3d 1317,
1319-20 (Fed. Cir. 2006). Petitioner must show that the vaccine was “not only a but-for cause of
the injury but also a substantial factor in bringing about the injury.” Moberly, 592 F.3d at 1321(quoting Shyface, 165 F.3d at 1352-53).
Because petitioner does not allege that he suffered a Table injury, he must prove that the
vaccine caused his TM. To do so, he must establish, by preponderant evidence: (1) a medical
theory causally connecting the vaccine and his injury (“Althen Prong One”); (2) a logical
sequence of cause and effect showing that the vaccine was the reason for his injury (“Althen
Prong Two”); and (3) a showing of a proximate temporal relationship between the vaccine and
his injury (“Althen Prong Three”). § 13(a)(1); Althen v. Sec’y of Health & Human Servs., 418
F.3d 1274, 1278 (Fed. Cir. 2005).
The causation theory must relate to the injury alleged. Thus, petitioner must provide a
reputable medical or scientific explanation that pertains specifically to this case, although the
explanation need only be “legally probable, not medically or scientifically certain.” Knudsen v.
Sec’y of Health & Human Servs., 35 F.3d 543, 548-49 (Fed. Cir. 1994). Petitioner cannot
establish entitlement to compensation based solely on assertions. Rather, a vaccine claim must
be supported either by medical records or by the opinion of a medical doctor. § 13(a)(1). In
determining whether petitioner is entitled to compensation, the special master shall consider all
material contained in the record, including “any . . . conclusion, [or] medical judgment . . . which
is contained in the record regarding . . . causation.” § 13(b)(1)(A). The undersigned must weigh
the submitted evidence and the testimony of the parties’ offered experts and rule in petitioner’s
favor when the evidence weighs in his favor. See Moberly, 592 F.3d at 1325-26 (“Finders of
fact are entitled—indeed, expected—to make determinations as to the reliability of the evidence
presented to them and, if appropriate, as to the credibility of the persons presenting that
evidence”); Althen, 418 F.3d at 1280 (noting that “close calls” are resolved in petitioner’s favor).
iii. Evaluation of Expert Testimony
Another important aspect of the causation-in-fact case law under the Vaccine Act
concerns the factors that a special master should consider in evaluating the reliability of expert
testimony and other scientific evidence. In Daubert v. Merrell Dow Pharm., Inc., the Supreme
Court listed certain factors that federal trial courts should utilize in evaluating proposed expert
testimony concerning scientific issues. 509 U.S. 579 (1993). In Terran v. Sec’y of Health &
Human Servs., the Federal Circuit ruled that it is appropriate for special masters to utilize the
Daubert factors as a framework for evaluating the reliability of causation-in-fact theories
presented in Program cases. 195 F.3d 1302, 1316 (Fed. Cir. 1999).
Daubert instructs fact-finders to consider (1) whether a theory or technique can be (and
has been) tested; (2) whether the theory or technique has been subjected to peer review and
15
publication; (3) whether there is a known or potential rate of error and whether there are
standards for controlling the error; and (4) whether the theory or technique enjoys general
acceptance within a relevant scientific community.” Terran, 195 F.3d at 1316 n.2 (citing
Daubert, 509 U.S. at 592-95). In addition, where both sides offer expert testimony, a special
master’s decision may be “based on the credibility of the experts and the relative persuasiveness
of their competing theories.” Broekelschen v. Sec’y of Health & Human Servs., 618 F.3d 1339,
1347 (Fed. Cir. 2010) (citing Lampe v. Sec’y of Health & Human Servs., 219 F.3d 1357, 1362
(Fed. Cir. 2000)). However, nothing requires the acceptance of an expert’s conclusion
“connected to existing data only by the ipse dixit of the expert,” especially if “there is simply too
great an analytical gap between the data and the opinion proffered.” Snyder v. Sec’y of Health
& Human Servs., 88 Fed. Cl. 706, 743 (2009) (quoting Gen. Elec. Co. v. Joiner, 522 U.S. 146(1997)).
A treating physician’s opinions are considered “quite probative,” as treating physicians
are in the “best position” to evaluate the vaccinee’s condition. Capizzano, 440 F.3d at 1326.
However, no treating physician’s views bind the special master, per se; rather, their views should
be carefully considered and evaluated. § 13(b)(1); Snyder, 88 Fed. Cl. at 745 n.67. Each
opinion from a treating physician should be weighed against other, contrary evidence present in
the record – including conflicting opinions from other treating physicians. Hibbard v. Sec’y of
Health & Human Servs., 100 Fed. Cl. 742, 749 (Fed. Cl. 2011), aff’d, 698 F.3d 1355 (Fed. Cir.
2012); Caves v. Sec’y of Health & Human Servs., 100 Fed. Cl. 119, 136 (Fed. Cl. 2011), aff’d,
463 F. App’x 932 (Fed. Cir. 2012); Veryzer v. Sec’y of Health & Human Servs., No. 06-522V,
2011 WL 1935813, at *17 (Fed. Cl. Spec. Mstr. Apr. 29, 2011), aff’d, 100 Fed. Cl. 344 (2011).
iv. Diagnosis
The Federal Circuit has made clear that “identifying [the petitioner’s] injury is a
prerequisite” to the Althen analysis. Broekelschen v. Sec’y of Health & Human Servs., 618 F.3d
1339, 1346 (Fed. Cir. 2010). However, it is not necessary to diagnose an exact condition. The
Federal Circuit has explained: “The function of a special master is not to ‘diagnose’ vaccine-
related injuries, but instead to determine ‘based on the record evidence as a whole and the
totality of the case, whether it has been shown by a preponderance of the evidence that a vaccine
caused the petitioner’s injury.’” Lombardi v. Sec’y of Health & Human Servs., 656 F.3d 1343,
1351 (Fed. Cir. 2011) (citing Andreu v. Sec’y of Health & Human Servs., 569 F.3d 1367, 1382
(Fed. Cir. 2009)).
C. Analysis
i. Althen Prong One: Petitioner’s Medical Theory
Under Althen Prong One, petitioner must set forth a medical theory explaining how his
flu vaccine could have caused his TM. Andreu v. Sec’y of Health & Human Servs., 569 F.3d
1367, 1375 (Fed. Cir. 2009); Pafford, 451 F.3d at 1355-56. Petitioner’s theory of causation must
be informed by a “sound and reliable medical or scientific explanation.” Knudsen, 35 F.3d at
548; see also Veryzer v. Sec’y of Health & Human Servs., 98 Fed. Cl. 214, 223 (2011) (noting
that special masters are bound by both § 13(b)(1) and Vaccine Rule 8(b)(1) to consider only
16
evidence that is both “relevant” and “reliable”). If petitioner relies upon a medical opinion to
support his theory, the basis for the opinion and the reliability of that basis must be considered in
the determination of how much weight to afford the offered opinion. See Broekelschen, 618
F.3d at 1347 (Fed. Cir. 2010) (“The special master’s decision often times is based on the
credibility of the experts and the relative persuasiveness of their competing theories.”); Perreira
v. Sec’y of Health & Human Servs., 33 F.3d 1375, 1377 n.6 (Fed. Cir. 1994) (stating that an
“expert opinion is no better than the soundness of the reasons supporting it”) (citing Fehrs v.
United States, 620 F.2d 255, 265 (Ct. Cl. 1980)).
Petitioner’s theory of causation, as outlined in Dr. Dahlgren’s first expert report, relies on
several faulty premises. Pet. Ex. 16 at 11. The undersigned will consider each in turn.
Molecular Mimicry and Adjuvants
Dr. Dahlgren asserted that “human and animal studies show[] that vaccine and adjuvants
excite a large increase in cytokines and . . . autoantibodies, resulting in autoimmune disease.”
Pet. Ex. 16 at 11. Although he proposed several mechanisms that might provoke this result, he
focused on molecular mimicry and ASIA. Neither mechanism satisfies the demands of Althen
Prong One.
Molecular mimicry points to “the ability of viral or bacterial antigens to induce cross-
reactive immune responses against self antigens.” Resp. Ex. C, Tab 3 (Borchers 2012) at 11.
But while this mechanism “has long been thought to play a primary role in triggering a variety of
autoimmune diseases . . . evidence has remained elusive in most cases, with the possible
exception of [GBS].” Id. at 12. Other studies have clarified that “present data tend to exclude a
causal mechanistic role for molecular mimicry in the genesis of autoimmunity.” Resp. Ex. C,
Tab 15 (Trost 2010) at 3. Afterall, “it is difficult to reconcile the enormous number of viral and
bacterial peptides disseminated throughout the human proteins with a fundamental role for
molecular mimicry in the etiology of certain autoimmune conditions.” Id.Likewise, the undersigned finds that petitioner has not established a sufficient link
between ASIA and the flu vaccine. Ever since Dr. Yehuda Shoenfeld and his colleagues coined
the term in 2011, ASIA has intrigued many researchers. See Pet. Ex. 25, Ref. 24 (Shoenfeld
2011). However, that research has not provided a “sound and reliable” mechanism that might
link TM to the flu vaccine. For instance, one study submitted by petitioner examined post-
vaccination adverse events “of potential autoimmune origin” and found “no significant
difference between MF59-adjuvanted and non-adjuvanted influenza vaccines.” Pet. Ex. 25, Ref.
22 (Pellegrini 2009) at 5. On the subject of adjuvants, Dr. Vartanian provided a particularly
effective rebuttal of petitioner’s medical literature. The provided ASIA studies, he notes, “bear
no temporal, physiologic, or pathologic similarities to [petitioner’s] case.” Resp. Ex. A at 7. In
the Lujan study, for instance, lambs received a total of 14 vaccines in less than one year,
exposing them to a significantly higher level of adjuvants than petitioner and producing
strikingly different symptoms. Pet. Ex. 25, Ref. 29 (Lujan 2013); see also Resp. Ex. A at 8. The
Poddighe case report is similarly inapplicable. There, the patient received the HPV vaccine,
rather than the flu vaccine. Pet. Ex. 25, Ref. 28 (Poddighe 2014). Moreover, while that patient
seemed to suffer from a somatoform illness that “could be interpreted as a case of ASIA,” her
17
treating physicians ultimately concluded that “a diagnosis of any definite organic or immune-
mediated disease could not be made.” Id. at 5; see also Resp. Ex. A at 9.
Case Reports
Dr. Dahlgren relied on “multiple cases reported in the literature of patient’s developing
TM and other autoimmune diseases including many different vaccines, including influenza
vaccine.” Pet. Ex. 16 at 11. As a preliminary matter, the undersigned acknowledges that “[c]ase
reports generally carry limited weight on the issue of causation,” in part because they “lack
controls and thus do not provide the level of information or detail found in epidemiologic
studies.” Bast v. Sec’y of Health & Human Servs., No. 01-565V, 2012 WL 6858040, at *38
n.104 (Fed. Cl. Spec. Mstr. Dec. 20, 2012), appeal dismissed sub nom. M.S.B. ex rel. Bast v.
Sec’y of Health & Human Servs., 579 F. App’x 1001 (Fed. Cir. 2014). Respondent, conversely,
has provided literature that answers these reports with much more thorough analysis of the
alleged relationship between vaccines and demyelinating diseases. See, e.g., Resp. Ex. C, Tab 3
(Borchers 2012) at 12 (discussed above); Resp. Ex. C, Tab 3 at 5 (concluding that “[v]accination
does not appear to increase the short-term risk of relapse in multiple sclerosis”); Resp. Ex. C,
Tab 19 (IOM 2012) at 5 (concluding that “the mechanistic evidence regarding an association
between influenza vaccine and onset of MS in adults [is] lacking”).13
Likewise, petitioner’s heavy reliance on the Agmon-Levin paper provides little support
for his theory. This study provided a comprehensive survey of 39 years of TM cases, yet it
uncovered only two cases that could be hypothetically linked to a flu vaccine. Pet. Ex. 23, Ref. 1
(Agmon-Levin 2009); see also Resp. Ex. A at 6 (estimating that “[o]ver the 39-year period that
[Agmon-Levin] covered, the cumulative number of [TM] cases would be an estimated 54,600”).
Moreover, as Dr. Vartanian pointed out, the data set examined by the study includes a number of
complex variables: “incidence of [TM], the frequency of each of the relevant vaccines, time from
vaccination to symptoms, the presence or absence of infection clinically, . . . the presence or
absence of infection documented by acute and convalescent titers . . . for relevant organisms, and
seasonable variation.” Resp. Ex. A at 7. The fact that the authors “provide no statistical analysis
to discern the probability of chance occurrence versus causal occurrence” severely limits the
study’s relevance to our Althen inquiry. See id.13
The undersigned also notes that when post-vaccination demyelinating diseases are discussed in
the literature, they are often associated with vaccines other than the flu vaccine. See, e.g., Pet.
Ex. 23, Ref. 10 (Holt 1976) (diffuse myelitis reported following rubella vaccination); Pet. Ex. 24,
Ref. 11 (Trevisani) (TM following Hepatitis B vaccination); Pet. Ex. 24, Ref. 12 (Joyce 1995)
(TM following measles, mumps, and rubella vaccination); Pet. Ex. 24, Ref. 13 (Matsui 2002)
(TM following Japanese B encephalitis vaccination); Pet. Ex. 24, Ref. 14 (Das 2007) (TM
following typhoid vaccination); Pet. Ex. 24, Ref. 15 (Read 1992) (TM following tetanus toxoid
vaccination). She emphasizes, however, that “without any empirical evidence that the theory
actually applies to the influenza vaccine and TM, the first prong of Althen would be rendered
meaningless.” Caves v. Sec’y of Health & Human Servs., 100 Fed. Cl. 119, 135 (2011), aff’d
without opinion, 463 F. App’x 932 (Fed. Cir. 2012).
18
Genetic Susceptibility
Dr. Dahlgren maintained that “some people have a susceptibility to develop an
autoimmune response to a vaccine,” and that petitioner’s family history indicates such a “genetic
susceptibility.”14 Pet. Ex. 16 at 11. The parties’ medical literature suggests that this could be
true. See Pet. Ex. 25, Ref. 27 (Tomljenovic 2014) at 2 (“[T]he importance of genetic
background in autoimmune diseases is well documented.”); Resp. Ex. C, Tab 3 (Borchers 2012)
at 11 (correlating NMO with a family history of autoimmune disease). However, this alleged
susceptibility only supports petitioner’s causal mechanism if “[t]here is no other risk factor for
his illness,” as Dr. Dahlgren opined. See Pet. Ex. 16 at 11. As the undersigned will explain
below, another risk factor unrelated to the vaccination was very likely at play.
ii. Althen Prong Two: Logical Sequence of Cause and Effect
Under Althen Prong Two, petitioners must prove by a preponderance of the evidence that
there is a “logical sequence of cause and effect showing that the vaccination was the reason for
the injury.” Capizzano, 440 F.3d at 1324 (quoting Althen, 418 F.3d at 1278). “Petitioner must
show that the vaccine was the ‘but for’ cause of the harm . . . or in other words, that the vaccine
was the ‘reason for the injury.’” Pafford, 451 F.3d at 1356 (internal citations omitted).
Even assuming that the flu vaccine could cause TM, the undersigned finds that it did not
do so in this case. As Dr. Vartanian observed, the “prolonged progression of the clinical course”
seen in petitioner’s case “is atypical for [TM].” Resp. Ex. C at 3. Although petitioner claims an
onset of December 31, 2012, his symptoms continued to worsen over an extended period of time,
and he was not diagnosed with TM until October 3, 2013. “This would suggest clinical
progression over months or even a year, which is exceedingly unusual.” Id. In contrast, most
TM sufferers advance from onset of symptoms to maximum deficit within weeks, days, or even
hours. Id.; see also Resp. Ex. C, Tab 2 (Berman 1981) at 3 (observing intervals between earliest
symptoms and maximum deficit of 2 hours to 14 days); Resp. Ex. C, Tab 3 (Borchers 2012) at 8
(observing intervals between earliest symptoms and maximum deficit of 1 to 21 days); Resp. Ex.
C, Tab 6 (Christensen 1990) at 6 (observing intervals between earliest symptoms and maximum
deficit of 1 hour to 20 days). Petitioner’s September 2013 MRI results cast further doubt on his
proposed sequence of cause and effect. Based on the radiologist’s interpretation of the images,
Dr. Vartanian opined (and Dr. Lipson agreed) that “the onset of the TM is probably within 1-2
months of the MRI.” Resp. Ex. C at 12.
Petitioner’s ultimate diagnosis of TM has never been disputed, but his initial diagnosis is
a more complex question. Although Dr. Dennis may have eventually abandoned his opinion that
petitioner suffered from varicella zoster (or herpes zoster) in January 2013, Dr. Vartanian argued
persuasively that this diagnosis was correct all along. Varicella zoster reactivation is a relatively
common ailment – approximately 1 million new cases are diagnosed annually in the United
States, and 90% of these patients are immunocompetent. Resp. Ex. D, Tab 1 (Gilden 2014) at 3-
14
The undersigned notes that Dr. Vartanian disagreed. See Resp. Ex. A at 6 (“There is no
epidemiologic evidence that individuals with a family history of GBS are more likely to develop
transverse myelitis.”).
19
4. Indeed, petitioner’s initial left arm and chest pain is characteristic of post-herpetic neuralgia,
“the most common neurologic complication of zoster.” Id. at 6; Resp. Ex. C at 4-5. Moreover,
varicella zoster myelitis is a known complication of varicella zoster reactivation, which
“[i]mportantly . . . may develop without rash.” Resp. Ex. D, Tab 1 (Gilden 2014) at 8; see also
Resp. Ex. C at 2 (noting that “Herpes Zoster sine herpete can cause focal myelitis at the relevant
segmental levels”). And as Dr. Vartanian observed, the fact that petitioner’s January 2013
symptoms were “treated early and appropriately with high dose anti-viral agents” would have
“reduce[d] the likelihood of lesion formation.” Resp. Ex. C at 2. Naturally, the fact that Dr.
Lipson concurred with Dr. Vartanian’s opinion gives it additional weight. See Pet. Ex. 21 at 1.
The undersigned finds that petitioner’s January 2013 symptoms indicated varicella zoster
(shingles), not early signs of TM. This conclusion resolves any disparity between the typical
progression of TM and the clinical course exhibited by petitioner. In reaching this conclusion,
the undersigned does not determine the cause of petitioner’s TM. While Dr. Vartanian opined
that petitioner’s clinical course is typical of varicella zoster myelitis,15 he also allowed that
petitioner’s TM may simply be idiopathic.16 Resp. Ex. C at 2. But the undersigned does
determine that whatever the cause of petitioner’s TM, his October 2012 flu vaccination was not
involved.
iii. Althen Prong Three: Proximate Temporal Relationship
Under Althen Prong Three, petitioner must provide “preponderant proof that the onset of
symptoms occurred within a time frame for which, given the understanding of the disorder’s
etiology, it is medically acceptable to infer causation-in-fact.” De Bazan, 539 F.3d at 1352. The
acceptable temporal association will vary according to the medical theory advanced in the case.
See Pafford, 451 F.3d at 1358. A temporal relationship between a vaccine and an injury,
standing alone, does not constitute preponderant evidence of vaccine causation. See, e.g.,
Veryzer v. Sec’y of Health & Human Servs., 100 Fed. Cl. 344, 356 (2011) (explaining that “a
temporal relationship alone will not demonstrate the requisite causal link and that petitioner must
posit a medical theory causally connecting the vaccine and injury”).
Over the course of these proceedings, petitioner has asserted two different onset dates.
Both dates are problematic. If petitioner’s symptoms began on December 31, 2012, as he claims
in his petition, onset would have occurred too late to be considered medically appropriate. If
petitioner’s symptoms arose in mid-November 2012, as he suggests in his affidavit, petitioner
would run afoul of the statute of limitations.
15
As Dr. Vartanian explains, “The diagnosis of [varicella zoster] mediated transverse myelitis, is
confirmed by identification of the viral genome in CSF by . . . PCR and by the presence of anti-
[varicella zoster] antibodies in the CSF.” Resp. Ex. D at 1. Since petitioner did not undergo
such testing, the diagnosis cannot be conclusively confirmed. See id.16
After all, “a significant fraction of all [TM] is not associated with an antecedent infection or
illness and is thus technically idiopathic.” Resp. Ex. C at 6.
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1. December 31, 2012 Onset
Assuming an onset date of December 31, 2012, 74 days (10.6 weeks) elapsed between
petitioner’s vaccination and the first appearance of his symptoms. The medical literature filed by
both parties weighs heavily against such a protracted onset period. Although many of
petitioner’s studies do not specifically address the flu vaccine or TM, those that do allege the
following onset timeframes:
Study Onset Period Following Flu Vaccination
Pet. Ex. 23, Ref. 1 (Agmon-Levin 2009)17 7 days; 9 days
Pet. Ex. 23, Ref. 2 (Korn-Lubetzki 2011) 1 month
Pet. Ex. 23, Ref. 3 (Sato 2011) 1 month
Pet. Ex. 23, Ref. 4 (Nakamura 2003) 7 days
Pet. Ex. 23, Ref. 5 (Bakshi 1996) 4 weeks
Pet. Ex. 23, Ref. 6 (Wells 1971) 2 days; 29 days
Such shorter onset timeframes are, as other special masters have observed, “wholly consistent
with the recognized acute nature of TM.” Bender v. Sec’y of Health & Human Servs., No. 11-
693V, 2018 U.S. Claims LEXIS 903, at *91 (Fed. Cl. Spec. Mstr. July 2, 2018), mot. for review
denied, 141 Fed. Cl. 262 (2019). Thus, petitioner’s own literature reinforces the undersigned’s
conclusion that a 74-day onset period is medically and scientifically unacceptable. Moreover,
when determining the appropriate onset for a post-vaccination demyelinating disease, the
undersigned’s fellow special masters have reached very similar conclusions. See, e.g., Bender,
2018 U.S. Claims LEXIS 903, at *89-95 (determining that 42 days was not a medically
acceptable timeframe for TM following Hepatitis A or meningococcal vaccines); Taylor v. Sec’y
of Health & Human Servs., No. 13-700V, 2018 U.S. Claims LEXIS 425, at *67 (Fed. Cl. Spec.
Mstr. Mar. 9, 2018) (finding that the proposed onset timeframe of 11 weeks between flu
vaccination and onset of a demyelinating disease was “entirely too long”). Petitioner has
provided no evidence that would lead the undersigned to deviate from this paradigm.
2. Mid-November 2012 Onset
Petitioner filed his petition on January 4, 2016, claiming an onset date of December 31,
2012. Because the Court was closed on New Year’s Eve, and did not reopen until January 4,
petitioner appeared to have just barely complied with the Vaccine Act’s 36-month statute of
limitations. However, in his October 2017 affidavit, petitioner stated that he “believe[s] the
symptoms initially began in November 2012,” and that he “recall[s] a very specific episode in
17
Dr. Dahlgren seemed to cite this study for the proposition that an onset of “even longer than
three months in some cases” may be appropriate. See Pet. Ex. 17 at 3-4; Pet. Ex. 16 at 2-3.
Critically, however, the cases with longer onset timeframes all involved vaccines other than the
flu vaccine at issue here. See Pet. Ex. 17 at 4. The letter from Dr. Yehuda Shoenfeld, filed with
petitioner’s literature, suffers from the same flaw. While Dr. Shoenfeld claims that “the
incubation time for induction of autoimmunity following vaccination can be more than 3 years,”
he does not appear to cite any literature or other support involving the flu vaccine. See Pet. Ex.
25, Ref. 25 (Schoenfeld 2012).
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mid-December 2012.” Aff. at ¶¶ 2-3. An onset date of November 2012, or even mid-December
2012, would make compliance impossible. Moreover, petitioner has not demonstrated the kind
of extraordinary circumstances that would allow him to invoke equitable tolling.
VII. CONCLUSION
TM has caused significant distress in petitioner’s life over the past few years, and the
undersigned empathizes with his dedicated search for medical and scientific answers. However,
for all the reasons discussed above, the undersigned finds that petitioner has not established by
preponderant evidence that he is entitled to compensation and his petition must be dismissed. In
the absence of a timely filed motion for review pursuant to Vaccine Rule 23, the Clerk of the
Court SHALL ENTER JUDGMENT in accordance with this Decision.
IT IS SO ORDERED.
s/Nora Beth Dorsey
Nora Beth Dorsey
Chief Special Master
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