Austin v. Secretary of Health and Human Services

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 05-579V
(To be published)
*****************************
* Special Master Corcoran
HOLLY AUSTIN, parent of K.A., a minor, *
* Filed: May 15, 2018
*
Petitioner, * Decision without Hearing;
* Dismissal; Diphtheria Tetanus
v. * acellular-Pertussis (“DTaP”)
* Vaccine; Encephalopathy;
SECRETARY OF HEALTH AND * Developmental Regression; Autism.
HUMAN SERVICES, *
*
Respondent. *
*
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Robert Krakow, Law Office of Robert J. Krakow, P.C., New York, NY, for Petitioner.
Ann D. Martin, U.S. Dep’t of Justice, Washington, DC, for Respondent.
DECISION GRANTING MOTION TO DISMISS CASE1
On May 27, 2005, Holly Austin, on behalf of her son, K.A., filed a petition seeking
compensation under the National Vaccine Injury Compensation Program (“Vaccine Program”).2
In it, Mrs. Austin alleged that a number of childhood vaccines (the Diphtheria Tetanus acellular-
Pertussis (“DTaP”), Hepatitis B (“Hep. B”), and Pneumococcal vaccines that K.A. received on
1
This Decision will be posted on the United States Court of Federal Claims’s website, in accordance with the E-
Government Act of 2002, 44 U.S.C. § 3501 (2012). As provided by 42 U.S.C. § 300aa-12(d)(4)(B), however, the
parties may object to the published Decision’s inclusion of certain kinds of confidential information. Specifically,
under Vaccine Rule 18(b), each party has fourteen days within which to request redaction “of any information
furnished by that party: (1) that is a trade secret or commercial or financial in substance and is privileged or
confidential; or (2) that includes medical files or similar files, the disclosure of which would constitute a clearly
unwarranted invasion of privacy.” Vaccine Rule 18(b). Otherwise, the whole Decision will be available to the
public. Id.
2
The Vaccine Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660,
100 Stat. 3758, codified as amended, 42 U.S.C. §§ 300aa-10 through 34 (2012) [hereinafter “Vaccine Act” or “the
Act”]. Individual section references hereafter will be to § 300aa of the Act.
July 28, 2003; the Influenza (“flu”) vaccine he received on December 15, 2003; the Hib vaccine
he received on June 1, 2004; and the DT vaccine he received on June 8, 2004) caused K.A. to
experience an encephalopathic reaction (accompanied by increased seizure activity), later
manifesting as developmental regression, and ultimately evolving into an autism spectrum
disorder (“ASD”). Petition at 1-2. Years later, Mrs. Austin filed an Amended Petition in August
2017, altering her allegations in an effort to exclude autism as the complained-of injury, and
arguing instead that K.A. had merely experienced seizure activity following each of the
vaccinations listed above, along with developmental regression following the June 8, 2014 DT
vaccination. Am. Pet. (ECF No. 123) at 1-2.
After the parties filed expert reports, and based upon my initial review of the case record
in light of the disposition of similar cases previously adjudicated in the Vaccine Program, I
proposed that the matter be decided without holding an evidentiary hearing, and I invited the
parties to brief the substantive merits of Petitioner’s claim. To that end, Respondent filed a
motion to dismiss, dated October 12, 2017 (ECF No. 127) (“Mot.”), to which Petitioner
responded on November 14, 2017 (ECF No. 129) (“Opp.”).
Having completed my review of the evidentiary record and the parties’ filings, I hereby
GRANT Respondent’s Motion for a Ruling on the Record Dismissing the Case, and DENY
Petitioner’s request for compensation. As discussed in greater detail below, the record does not
support Petitioner’s contention that K.A. suffered an encephalopathy, that he experienced any
non-transient reaction at all to the relevant vaccines, or that the vaccines caused his seizure
activity. In addition, the claim recycles causal theories involving autism as a vaccine injury that
have been universally rejected in the Vaccine Program.
I. FACTUAL BACKGROUND
Birth and Early Medical History
K.A. was born via spontaneous vaginal delivery on January 24, 2003, following a normal
pregnancy. Ex. 3 at 1.3 No concerns or complaints were raised during the pregnancy, labor, or
delivery. Id. Birth weight, head circumference, and length were all within the normal limits. Ex.
2 at 1, 65. K.A.’s hearing and neonatal screens were also normal, and he was discharged one day
later. Id. at 6, 13, 31.
As the contemporaneous medical records reveal, K.A.’s health in his first year of life was
characterized by the kind of illnesses that many otherwise-healthy infants experience. For
example, K.A. was seen on several occasions for a variety of infections (including ear infection,
3
Petitioner’s exhibits in this case are referenced numerically, while Respondent’s exhibits are referenced
alphabetically.
2
URI, and perioral cyanosis). See, e.g., Ex. 3 at 9 (1/25/2003, possible jaundice and observed as
“jittery” in office); Ex. 8 at 47 (4/23/2003, diagnosed with conjunctivitis in left eye and
constipation), 47 (5/2/2003, diagnosed with an ear infection and an upper respiratory infection),
and 51 (5/11/2003, possible sinusitis). In addition, K.A. was treated for oral thrush on June 25,
2003, and pharyngitis on July 8, 2003. Ex. 14 at 20-22. Apart from these minor health problems,
the records from K.A.’s well-child appointments generally indicated that he was progressing
normally from a developmental standpoint.
Receipt of Vaccinations and Subsequent Medical History
K.A. received his first Hep. B vaccination on February 5, 2003, according to his
vaccination record. Ex. 14 at 2. On March 27, 2003, at his two-month well-child visit, he
received his initial round of childhood vaccinations, including the DTaP, Hep B (second dose),
Hib, Pneumovax, and IPV vaccines. Ex. 8 at 26-28; Ex. 14 at 2-3. K.A. received a second round
of vaccinations (including DTaP, IPV, Hib, and Pneumococcal) at his four-month well-child visit
on June 13, 2003, and a third round on July 28, 2003 (including DTaP, Hep B, and Pneumovax).
Ex. 8 at 26, 29; Ex. 14 at 2, 6. The medical records reference no adverse reactions following
receipt of any of these vaccinations.
On July 12, 2003 (about two weeks after K.A.’s last June pediatric visit), Mrs. Austin
went to the emergency room at Franklin Memorial Hospital in Bangor, Maine, complaining that
K.A. had experienced an apparent “acute life-threatening event,” including an episode of starring
and limpness. Ex. 11 at 2. According to the treater’s notes, Petitioner went to pick him up around
6:00 p.m. that evening, and he immediately turned blue and went limp for a period lasting “a few
seconds to minutes.” Id. at 4. She then placed him down on the floor, and he eventually opened
his eyes and became responsive. Id. at 4.
K.A was subsequently transferred to Eastern Maine Medical Center (also in Bangor), and
was placed on cardiorespiratory monitoring throughout his admittance. Ex 11 at 2, 45-47.
Testing noted no abnormalities in his chest cavity or lungs. Id. at 5-6. Treaters also conducted an
upper GI series, which was normal, and noted no further limpness episodes during his hospital
stay. Id. at 2-3, 19-20. As there was some evidence of a cough associated with the episode,
treaters questioned whether Petitioner had observed any reflux, and also did not rule out an ear
infection. After monitoring K.A., and determining that his vitals remained stable, treaters
discharged him with a final diagnosis of an unspecified “acute life-threatening event,”
presumptive gastrointestinal reflux, and left otitis media. Id. at 2. He was proscribed Zantac for
any future problems. Id. K.A.’s treatment plan also included a Good Start formula diet, Tylenol
for temperature increases, and Amoxicillin for his on-going ear infection. Id. at 6. Summary
notes indicated that K.A.’s symptoms did not include muscle twitching or spasm activity. Id. at
4.
3
Two weeks later, on July 28, 2003, K.A. had his six-month well-child visit at Penobscot
Pediatrics, and received his third round of vaccinations (including DTaP, Hep B, and
Pnuemovax). Ex. 8 at 2; Ex. 14 at 2. Once again, no developmental problems were noted. More
specifically, K.A.’s pediatrician, Dr. Elizabeth Trefts, noted that K.A. was alert and happy. Ex. 8
at 30; Ex. 14 at 5. Dr. Trefts’s notes indicated K.A.’s parents had reported that K.A. had been
taken to the emergency room on July 12th for an “episode” which included limpness and a
change in color. Id. The record from this appointment stated that K.A. was diagnosed with reflux
and treated with Zantac. Id. No further episodes of limpness or change in color were noted in the
intervening period. Id.
Acute Onset Seizures
On that same day, a few hours later, K.A. experienced acute onset seizures. Ex. 11 at 55;
Ex. 4 at 11-14. K.A. was taken back to Eastern Main Medical Center and admitted to the
pediatric intensive care unit for cardiopulmonary monitoring. Ex. 11 at 53. During the
admittance process, K.A. experienced an additional four to eight seizures that were observed by
various medical staff members. Id. He was treated with Fosphenytoin4 and Phenobarbital during
the course of his hospitalization. Id. An EEG and MRI completed during the visit were both
normal. Id. Treater notes also indicated that K.A.’s parents voiced some concern that
Moxifloxacin (antibiotic taken by K.A.’s mother while breast-feeding) had caused him to
develop seizures. Id. However, medical staff explained to her that they “could not link the two
together.” Id.
During his hospitalization, K.A. was evaluated by Dr. James Sears, a neurologist. Ex. 11
at 63. Dr. Sears noted that K.A.’s earlier acute life-threatening event from July 12th, when
viewed in conjunction with his current episode, supported a diagnosis of partial seizures. Id. at
64. According to Dr. Sears, the later episode was similar to the earlier one two weeks before –
seizures lasting 30-60 seconds, accompanied by eye deviation, blank stares, brief twitching, and
irregular breathing. Id. Dr. Sears noted that K.A.’s EEG showed prominent artifacts and
indicated some focal slowing, but no abnormal activity. Id. He also opined that K.A.’s MRI
showed normal intracranial activity. Id. Dr. Sears treated K.A. with Fosphenytoin and
maintenance Phenobarbital, with a transition into Dilantin. Id. at 65. Dr. Sears also was aware
that K.A. had received vaccinations earlier that day, but maintained that the vaccines did “not
appear to be [a] substantial element” relating to the seizure episode. Id. at 64. K.A. was
discharged three days later with after a normal physical exam (which included no seizure activity
for three days). Id. at 54.
4
Fosphenytoin is an anticonvulsant drug used to treat epilepsy. Dorland’s Illustrated Medical Dictionary 736 (32nd
ed. 2012) (hereinafter “Dorland’s”). It can be administered intravenously or intramuscularly. Id.
4
Over the next several months, K.A. seemed to be doing well once again. He returned to
Penobscot Pediatrics on August 4, 2003, seven days following his hospitalization. Ex. 8 at 57;
Ex. 14 at 25. The attending pediatrician reported that K.A.’s seizure medications were working,
although he had displayed some minimal staring-type episodes, and there remained some
lingering reflux concerns. Ex. 8 at 57. Following this appointment, K.A. saw Dr. John Hickey of
Pine Tree Pediatrics for a nine-month well child visit on October 3, 2003. Ex. 8 at 14. Dr. Hickey
assessed K.A. as a healthy nine-month old with no developmental problems. Id. K.A. received
his third round of the IPV vaccine on October 31, 2003, and no adverse reaction was noted, with
no additional seizures occurring in the days and weeks immediately thereafter. Ex. 14 at 2; Ex. 8
at 14.
On December 15, 2003, K.A. received an influenza vaccine during a visit to Pine Tree
Pediatrics. Ex. 14 at 2; Ex. 8 at 10. Eight days later, Mrs. Austin called the clinic on December
23, 2003, reporting that K.A. had again experienced seizure activity on the prior night
(December 22nd). Ex. 8 at 11. Mrs. Austin described the episode as lasting five seconds, and
stated that K.A. did not lose consciousness, although he did convulse. Id. Dr. Hickey
recommended that K.A.’s mother continue administering his doses of Phenobarbital. Id. Later
treater records expand this seizure event into a four-part episode, including a December 21st
staring spell (lasting approximately ten seconds), a December 22nd generalized seizure
(including arm/leg stiffness, clenched jaw, and shaking), a December 26th seizure, and a
December 27th seizure. Ex. 5 at 7 (January 6, 2004, appointment with Dr. Stephen Rioux).
2004 Seizure Treatment and Medical Visits
K.A. presented to Dr. Stephen Rioux, a pediatric neurologist at Maine Medical Partners,
on January 6, 2004. Ex. 5 at 7. The Austins provided Dr. Rioux a history of K.A.’s seizure
disorder, and reported that he had done well on medication since his seizures first began in July
2003. Id. Upon examination, Dr. Rioux opined that K.A. likely had a generalized seizure
disorder, adding that it was “possible that quinolones5 transmitted to the child through breast
milk, as well as subsequent immunizations lowered the seizure threshold and may have been
responsible for the timing of the child’s seizures.” Id. However, Dr. Rioux also noted that it was
“unlikely that either of these interventions or agents are responsible for his ongoing seizure
difficulties.” Id (emphasis added). Dr. Rioux recommended that K.A. remain on Phenobarbital
for the time being and schedule a follow-up appointment in six months. Id. During a follow-up
visit on May 6, 2004, he also (at Petitioner’s request) proposed that the schedule for future
vaccines be spread out temporally to reduce the possibility that any single vaccine might trigger
a seizure (although, as indicated above, the record does not suggest that Dr. Rioux believed that
any vaccine was causal of K.A.’s larger seizure activity). Ex. 5 at 7; Ex. 8 at 20-21.
5
Quinolone is a term used to define a group of synthetic antibacterial agents (or antibiotics). Dorland’s at 1567.
Examples include nalidixic acid, cinoxacin, rosoxacin, and fluoroquinolones. Id.
5
Over the next two months, K.A. was brought back to his pediatricians for various
ailments (although not to treat seizures). On February 12, 2004, for example, K.A. was seen by
Dr. Hickey at Pine Tree Pediatrics for an ear check due to restlessness and crying during the
night. Ex. 8 at 13. He was assessed with ear pain and teething. Id. Roughly a month later, on
March 4, 2004, K.A. presented again to Dr. Hickey for his one year well-child visit. Id. at 14.
Upon evaluation, Dr. Hickey noted that K.A. displayed no developmental problems. Id. On
March 10, 2004, K.A. presented again to Penobscot Pediatrics for a five-day history of fever of
up to 104.4 degrees, a cough, and cold symptoms. Id. at 12. K.A.’s treating pediatrician
diagnosed him with a URI and possible respiratory syncytial virus. Id. Two weeks later, on
March, 29, 2004, K.A. was diagnosed with otitis media and viral pharyngitis. Ex. 14 at 30.
On April 26, 2004, K.A. was seen for his fifteen-month well-child visit at Penobscot
Pediatrics. Ex. 14 at 8. K.A. was due to receive additional vaccines during this visit, but his
parents requested that they not be given pending Dr. Rioux’s evaluation. Id. Office notes
recorded at this time regarding K.A.’s history were somewhat contradictory of the actual medical
history as set forth above. Thus, the record from the April 26th visit states that K.A.’s first seizure
occurred two weeks prior to his six-month vaccinations, and that the cause of his second was
“s/p vaccines”. Id. These notes also indicated (correctly) that K.A. had “4-5 seizures following
[the] flu vaccine” and “seizure #3 . . . temporarily related to [the] flu vaccine,” although the
record does not set forth the actual time interval between (other than recording the first post-flu
vaccine seizure to have begun on December 21st). Id. at 2, 8; see also Ex. 5 at 7; Ex. 8 at 10-11.
No developmental problems were otherwise noted during this visit.
K.A.’s next set of records from Penobscot Pediatrics, dated May 24-28, 2004, include
telephone messages between Mrs. Austin and the doctor’s office concerning her requests to
change K.A.’s immunization schedule. Ex. 14 at 42. According to the notes, Petitioner wanted
K.A. to receive one vaccination at a time per Dr. Rioux’s recommendation, and wholly eliminate
the DTaP vaccination from his schedule. Id. Following these requests, K.A.’s vaccine record
indicated that he received the IPV vaccine on May 25, 2004, a third dose of Hib on June 1, 2004,
and the DT vaccine on June 8, 2004. Id. a 2, 31. Notes from the DT vaccine administration
indicated that K.A. did not experience any post-vaccination seizure activity in the office. Id. at
31. Following the DT vaccination, K.A. presented to his pediatrician on June 11, 2004, with a
two-day history of congestion and fussiness. Id. at 32. He was diagnosed with a URI. Id. Office
notes also indicated that K.A. presented with a small, two centimeter lump on his thigh at the DT
vaccination injection site. Ex. 14 at 32.
6
Return of Seizure Activity and Reported Developmental Problems
On July 5, 2004 (about one month following receipt of the DT vaccine), Petitioner called
Penobscot Pediatricians and reported that K.A. had experienced additional seizures. Ex. 14 at 43.
The attending pediatrician instructed her to consult K.A.’s neurologist, as well as have him
evaluated for developmental delays. Id. at 44. K.A. thereafter presented to a pediatrician,
Michael Ross, four days later, on July 9, 2004. Ex. 14 at 35-36. Dr. Ross’s notes indicated that
K.A. had increased seizure activity during the previous weekend while on a therapeutic level of
Phenobarbital. Id. at 35.
The records from this post-seizure July 2004 treatment visit now set forth – for the first
time in K.A.’s medical history – issues with K.A.’s development. The Austins reported that K.A.
had developed a vocabulary of six to seven words, but had not spoken any words over the
previous three weeks (or since the middle of June), and had displayed a “steady decrease back to
wordless mumbling.” Ex. 14 at 35. Several concerning behaviors were also reported at this time,
including decreased attention span, failure to regard faces, constant looking away, lingering
blank looks, frequent head and ear rubbing, aimless wandering, and unsteady gait. Id. In
addition, the Austins reported that K.A. had experienced three distinct seizure episodes and
several episodes of blank staring the weekend prior. Id. Upon examination, Dr. Ross assessed
K.A. with “seizure disorder and significant developmental delay.” Id. at 36. Dr. Ross
recommended that K.A.’s parents schedule a repeat EEG, orthopedic consultation, and a hearing
assessment, as well as evaluation for developmental problems. Id.
K.A. subsequently returned to Dr. Rioux (his neurologist) for a follow-up visit on July
22, 2004. Ex. 5 at 5-6; Ex. 8 at 20. Dr. Rioux confirmed the reports from the visit earlier that
month with Dr. Ross that K.A.’s developmental status had begun to regress, and noted possible
concerns for autism. Ex. 5 at 6. Dr. Rioux was unsure if the latest episodes were attributable to
K.A.’s seizures, but he conducted a repeat EEG (which was normal) and ordered additional
testing. Id. According to Dr. Rioux’s notes, Mrs. Austin specifically stated her view that K.A.’s
developmental setbacks were associated with the vaccinations he had received, although Dr.
Rioux assured her that no scientific basis existed for a vaccine-induced autism injury. Id.
K.A. was next evaluated at Penobscot County Child Development Services (“CDS”) in
Bangor, Maine, on July 28, 2004. Ex. 11 at 238-47. His reported symptoms at this time included
loss of language, lack of eye contact, poor responsiveness, and unsteady gait. Id. K.A. was
thereafter referred to the Maine General Medical Center’s Developmental Evaluation Clinic
(“DEC”) in Waterville, Maine, and evaluated on September 9, 2004. Ex. 25 at 1-25. Anne
Uecker, Ph.D., a licensed psychologist, determined that K.A. exhibited all six critical indicators
for autism on the Modified Checklist for Autism in Toddlers. Id. at 11-12. She also found that
K.A. was at the eleven-month level on the Bayley Scales of Infant Development. Id. DEC’s
7
assessment for K.A. also included a seizure disorder, severe receptive and expressive language
delays, severe articulation delay, mild gross motor delay, internal tibial torsion and femoral
anteversion, but ruled out Landau-Kleffner syndrome, and Fragile X syndrome. Id. at 2-3. DEC
evaluators recommended speech, occupational and physical therapy, an orthopedic follow-up, a
hearing evaluation, and continued monitoring and treatment for autism. Id. at 3-4.
In August, at his neurologist’s recommendation K.A. was taken to an orthopedic surgeon,
Dr. James Greene, for an evaluation of unsteady gait, plus tripping and falling when walking. Ex.
12 at 1-2. Upon examination, Dr. Greene found that K.A. had excellent circulation in extremities
and normal muscle strength throughout. Id. at 3. Dr. Greene assessed K.A. with femoral
anteversion, internal tibial torsion, physiologic genu varum (bow-leggedness), and a seizure
disorder (all of which Dr. Greene stated were not unusual for a child of K.A.’s age and would
generally resolve in a couple of years). Id. Overall, Dr. Greene recommended additional physical
therapy, with a follow-up visit in six months for another evaluation. Id.
The Austins took K.A. thereafter to a new pediatrician, on September 14, 2004, at
Norumbega Medical Pediatrics in Bangor, Maine, for his eighteen-month visit. Ex. 6 at 2. K.A.’s
health history at this time now officially included autistic regression, and noted that he continued
to take medication for his seizure disorder. Id. Upon evaluation, the treating pediatrician
observed that K.A. had some receptive language, but no words. Id. No physical problems were
otherwise noted, and his overall assessment was consistent with K.A.’s past treaters: autism and
a seizure disorder. Id.
Treatment in 2005 and Beyond
In the twelve-plus years thereafter, K.A. has received many therapeutic interventions and
treatments for his autism - including speech, physical therapy, occupational therapy, dietary
restrictions, hyperbaric oxygen, chelation, methylcobalamin injections, and supplements. See
generally Ex. 10 (dietary restrictions and supplements), 17 (speech therapy), 20 (occupational
therapy), 22 (chelation), and 24 (occupational and physical therapy); see also Ex. 21 at 66
(speech therapy); Ex. 4 at 1, 6-7 (methylcobalamin injections); Ex. 26 (pediatric visit and lab
testing); Ex 32 (occupational and educational therapy). While the Austins have received a variety
of proposals for the etiology of K.A.’s condition, none of the records suggest a plausible
connection between the vaccinations at issue and his subsequent medical and/or developmental
problems.
On March 3, 2005, for example, K.A. was evaluated by Dr. Cheryl Garganta in the
genetics department at the metabolic clinic at Tufts Medical Center in Boston, Massachusetts, to
determine if his autism had a metabolic etiology. Ex. 4 at 10. As the history from this evaluation
indicates, the Austins themselves attributed his neurologic condition and autism symptoms to his
8
vaccinations. Id. Dr. Garganta, however, noted that K.A. had received his vaccinations at an age
where children who were later diagnosed with autism tended to first experience regression. Id. at
12. Dr. Garganta ordered that K.A be tested for Fragile X syndrome, amino acid disorders,
organic acidemias, mitochondrial dysfunction, disorders of creatinine synthesis and transport,
disorders of pyruvate and pyrimidine metabolism, congenital disorders of glycosylation, and
Angelman syndrome (all of which returned normal results apart from an deficiency in
carbohydrate transferring). Id. at 12-13.
Dr. Garganta ultimately could not identify, based on K.A.’s normal lab test results, any
particular adverse genetic condition from which K.A. suffered that could be deemed to have a
metabolic component. Ex. 4 at 3. Certainly, it appeared to her from K.A.’s history that he was
not suffering from any progressive condition that had developmental regression as a side effect;
as she noted, K.A. continued to gain motor milestones, and his regression in language and social
interaction could not therefore be deemed a sign of a neurodegenerative disorder. Id. Overall, Dr.
Garganta opined that K.A.’s health problems were unrelated to his immunizations, although she
recommended that K.A.’s parents schedule a follow-up appointment in a few years, as advances
in testing would likely occur within that time period. Id. at 13.
K.A. returned to Dr. Garganta for follow-up visits on August 10, 2006, and again on
March 3, 2010. Ex. 4 at 2-8. Dr. Garganta again ordered multiple lab tests (including plasma
lactate, serum uric acid, RBC folate, hermatocrit, prolactin, urine organic acids, and lactyl-
lactate) Id. at 1, 3-4, 6-8. Overall, as the notes from this visit indicated, Dr. Garganta once again
concluded that K.A. did not display any medical symptoms associated with a mitochondrial
disease other than autism (indicating a low likelihood of a primary mitochondrial disease, which
would be far more debilitating and progressive in character). Id. at 3. Although she could not rule
out the possibility that K.A. suffered from some kind of mitochondrial dysfunction or cerebral
folate deficiency, K.A.’s symptoms did not in her opinion warrant any invasive procedure. Id. at
4. Dr. Garganta specifically declined to conduct a lumbar puncture or muscle biopsy due to the
lack of clinical marker evidence. Id. She recommended that K.A. reschedule follow-up
appointments every few years. Id. at 5.
On July 10, 2008, K.A. presented to Dr. Wendy Smith, a geneticist at Maine Pediatric
Specialty Group. Ex. 18 at 1. Upon evaluation, Dr. Smith found minimal small joint hyper
extensibility, but no dysmorphic features. Dr. Smith assessed K.A. with autism, and no clear
syndromic diagnosis. Id. at 4. Dr. Smith recommended that K.A. be tested via comparative
genomic hybridization (or microarray), which is used to detect small variants that may offer
some clinical, genetic significance in patients with mental retardation, developmental delays, and
autism. Id. at 5. Dr. Smith also recommended that K.A. continue his current course of therapy
treatment. Id. No follow-up appointment was recommended.
9
On November 3, 2010, K.A. presented to another pediatric neurologist, Dr. Peter
Morrison at Maine Medical Partners, for an autism evaluation. Ex. 15 at 1. As the record from
this visit reveals, Dr. Morrison had agreed to evaluate K.A. due to his history of seizures (even
though autism was outside his scope of practice). Id. After obtaining a brief history of K.A.’s
seizure symptoms, Dr. Morrison noted the Austins’s concern that K.A. had developed a
mitochondrial disorder (leading to autism) due to his exposure to antibiotics in breast milk and
thimerosal in his immunizations. Id. at 2. Upon evaluation, however, Dr. Morrison generally
opined that autism cannot be linked to a specific cause. Id. at 1. He further noted that Petitioner
expressed a concern that K.A. had a cerebral folate deficiency, but stated his view that this type
of deficiency was typically not related to regressive autism. Id. Dr. Morrison did not completely
exclude the possibility that K.A. had some underlying mitochondrial dysfunction, but he noted
that he could not find any systematic signs during his exam. Id.
Updated records filed between December 2014 and February 2015 include various
additional pediatric visits and specialty visits. See generally Ex. 28 (pediatric visit for lab
testing); Ex. 30 (same), Ex. 32 (occupational and educational therapy). None are any more
supportive of the conclusion that K.A.’s autism was vaccine-related. For example, in February
2015, K.A. was seen by another geneticist and mitochondrial specialist, Dr. Fran Kendall6 of
Virtual Medical Practices, LLC, in Atlanta, Georgia. Ex. 29. at 1. Dr. Kendall reviewed various
tests and labs during the visit (including CBC, CMP, CPK, T4, TSH, coenzyme, Q10, carnitine,
vitamin D, and urine amino acid) in order to determine if K.A. displayed clinical symptoms of a
mitochondrial disease. Id. at 4. Upon evaluation, Dr. Kendall opined that K.A.’s autism (along
with general fatigue and constipation), did not suggest that he was experiencing an underlying
mitochondrial disorder. Id. In response to Petitioner’s concerns that K.A.’s condition was
vaccine-caused, Dr. Kendall stated that “no clear proof of causation” existed between the two. Id.
II. EXPERT REPORTS
A. Dr. Yuval Shafrir
Dr. Shafrir prepared two expert reports for Petitioner, both of which attempt to establish a
link between K.A.’s regression/autism and his vaccinations. See Report, dated Nov. 23, 2015,
field as Ex. 34 (ECF No. 94-1) (“Shafrir First Rep.”); Report, dated May 3, 2016, filed as Ex. 35
(ECF No. 105-1) (“Shafrir Second Rep.”). According to Dr. Shafrir, K.A. suffered from an
autoimmune encephalopathy (manifesting as acute onset seizures) that evolved into an autistic
syndrome as a result of receiving the combination of vaccinations outlined above.
6
Dr. Kendall has testified on behalf of other petitioners claiming autism as a vaccine injury. See, e.g., Murphy v.
Sec’y of Health & Human Servs., No. 05-1063V, 2016 WL 3034047 (Fed. Cl. Spec. Mstr. Apr. 25, 2016), mot. for
rev. den’d, 128 Fed. Cl. 348 (2016); Holt v. Sec’y of Health & Human Servs., No. 05-0136V, 2015 WL 4381588(Fed. Cl. Spec. Mstr. June 24, 2015), mot. for rev. den’d, 132 Fed. Cl. 194 (2017).
10
As his CV indicates, Dr. Shafrir is a pediatric neurologist at Sinai Hospital in Baltimore
Maryland. See Shafrir CV, filed as Ex. 36 (ECF No. 122). Dr. Shafrir received his medical
degree from the Tel Aviv University Sackler School of Medicine in Israel, where he also
completed a pediatric residency. Id. at 1. Upon his arrival in the United States, he completed an
additional pediatric residency at Cornell University Medical College and two fellowships, one in
pediatric neurology from Washington University Medical Center in St. Louis, Missouri, and one
in pediatric neurophysiology from Miami Children’s Hospital. Id. at 1-2. Dr. Shafrir is board
certified in pediatric neurology, clinical neurophysiology, and epilepsy. Id. at 2. He has
published over ten peer-reviewed articles and has served on faculty at various medical
institutions around the United States, including Georgetown University School of Medicine, the
University of Oklahoma School of Medicine, and the United Services University of Health
Sciences, in addition to his most recent position the University of Maryland School of Medicine.
Id. at 3, 4-5.7
Dr. Shafrir opined that the DTaP vaccine K.A. received on July 28, 2003, triggered
seizures and “started an encephalopathic process, which was exacerbated by his . . . influenza
vaccination [on December 15, 2003] and greatly exacerbated by his . . . DT vaccination [on June
8, 2004].” Shafrir First Rep. at 45, 38.
Dr. Shafrir’s First Expert Report
Dr. Shafrir’s report began with an overview of K.A.’s health course and regression
following his vaccinations. He pointed specifically to K.A.’s immediate onset of seizure activity
following the July 28, 2003 DTaP vaccination as direct evidence of an encephalopathy. Shafrir
First Rep. at 36. Dr. Shafrir did not deem his conclusion undermined, however, by the fact that
K.A.’s EEG and MRI findings (conducted during his hospitalization) were both normal, or that
K.A. had presented to the hospital without fever (or any other symptoms consistent with an
encephalopathic reaction). Id. He also identified an instance in the record where K.A.’s treating
pediatrician recommended that K.A.’s future vaccinations be spread out over time as this “may
reduce the risk of seizures.” Id. at 37 (Ex. 8 at 21). Apart from these factual references, Dr.
Shafrir offered no additional discussion of any purported evidence of encephalopathy in K.A.’s
health record. The remainder of his discussion of K.A.’s records center on the temporal
association between K.A.’s DT vaccination the following year (on June 8, 2004), and his onset
7
Dr. Shafrir has testified on behalf of petitioners asserting autism as a vaccine injury on numerous occasions. See,
e.g., Cunningham v. Sec’y of Health & Human Servs., No. 13-482, 2016 WL 4529530 (Fed. Cl. Spec. Mstr. Aug. 1,
2016), mot. for rev. den’d, 2017 WL 1174448 (Fed. Cl. Jan. 25, 2017); R.V. v. Sec’y of Health & Human Servs., No.
08-504V, 2016 WL 3882519 (Fed. Cl. Spec. Mstr. Feb. 19, 2016), mot. for rev. den’d, 127 Fed. Cl. 136 (2016);
Lehner v. Sec’y of Health & Human Servs., No. 08-554V, 2015 WL 5443461 (Fed. Cl. Spec. Mstr. July 22, 2015).
His credibility on the topic has been sharply questioned by other special masters. See, e.g, Cunningham, 2016 WL
4529530, at *15-16.
11
of regression around two weeks later (which he also labeled as encephalopathic in origin). Id. at
37; Shafrir Second Rep. at 5.
Dr. Shafrir analogized K.A.’s alleged vaccine injury, autism, to epilepsy, arguing that
their neurologic origins and course are congruent. Shafrir First Rep. at 38. Dr. Shafrir asserted
that an association between seizures, epilepsy, and autism has in fact been observed in several
medical articles. Id.; see, e.g., E. Saemundsen, et al., Autism Spectrum Disorders in Children
with Seizures in the First Year of Life—A Population-based Study, 48 Epilepsia 1724 (2007),
filed as Ex. 34 (ECF No. 94-5) (cohort study concluding that prevalence of ASD is higher in
children with history of seizures in first year of life); J. Lugo, et al., Early-Life Seizures Result in
Deficits in Social Behavior and Learning, 256 Exp. Neuro. 74, 78 (2014), filed as Ex. 34 (ECF
No. 94-9) (animal laboratory study concluding that early-life seizures result in significant
reduction in social behavior in mice); P. Bernard, et al., Behavioral Changes Following a Single
Episode of Early-Life Seizures Support the Latent Development of an Autistic Phenotype, 44
Epilepsy & Behavior 78, 78 (2015), filed as Ex. 34 (ECF No. 94-10) (animal laboratory study
concluding that early-life seizures resulted in permanent physiological and behavioral changes in
rat models, consistent with clinical and experimental ASD).8 While Dr. Shafrir acknowledged
that K.A.’s medical history does not support a diagnosis of epilepsy, he nevertheless maintained
that K.A.’s seizure condition is connected to his autism diagnosis. Shafrir First Rep. at 38. 9
Dr. Shafrir next considered a genetic component associated with both epilepsy and
autism, and the degree to which it may establish an autoimmune basis for autism. As Dr. Shafrir
explained, abnormalities in the Caspr2 gene10 have been suggested to have a causal relationship
with both autism and epilepsy in infants. Shafrir First Rep. at 38-39; see K. Strauss, et al.,
8
Dr. Shafrir also relied on two papers drawing an association between autism and seizure disorders. See M. Matsuo,
et al., Characterization of Childhood-onset Complex Partial Seizures Associated with Autism-Spectrum Disorder, 20
Epilepsy & Behavior 527 (2011), filed as Ex. 34 (ECF No. 94-6) (cohort study concluding that ASD is “very
common” in patients with childhood development of complex seizures); P. Bernard, et al., Early Life Seizures:
Evidence for Chronic Deficits Linked to Autism and Intellectual Disability Across Species and Models, 263 Exp.
Neurol. 72, 76 (2015), filed as Ex. 34 (ECF No. 94-8) (reviewing recent developments concerning the association
between ELS and autism, and concluding the causal relationship is still in its infancy).
9
Dr. Shafrir’s report also discusses literature evidencing signs of epileptic discharge following DTaP and DT
vaccinations. Shafrir First Rep. at 41; S. Nouna, et al., Adverse Effects on EEG and Clinical Condition After, 32
Acta Paediatrica Japonica 357 (1990), filed as Ex. 34 (ECF 96-8) (Nouna). Dr. Shafrir asserted that Nouna described
the appearance of epileptic discharges in the EEG of children with a history of seizure disorder after DTaP
vaccination (who had a normal EEG prior to vaccination). Shafrir First Rep. at 41. As noted above, however, K.A.’s
EEG is not consistent with an epilepsy diagnosis, and he has never received such a diagnosis either.
10
Caspr2, also known as contactin associated protein like 2 (CNTNAP2), is a gene responsible for coding proteins
which function in the vertebrate nervous system as cell adhesion molecules and receptors. Caspr 2 proteins also
mediate interactions between neurons and glia during nervous system development and are involved in localization
of potassium channels. See CNTNAP2: Contactin Associated Protein Like 2, NCBI,
https://www.ncbi.nlm.nih.gov/gene/26047 (last accessed on May 3, 2018).
12
Recessive Symptomatic Focal Epilepsy and Mutant Contactin-Associated Protein-Like 2, 354
New Eng. J. Med. 1370 (2006), filed as Ex. 34-11 (ECF No. 95-2); D. Obregon, et al., Potential
Autoepitope within the Extracellular Region of Contactin-Associated Protein-Like 2 in Mice, 4
Bit. J. Med. & Med. Research 416 (2014), filed as Ex. 34-13 (ECF No. 95-4) (“Obregon”).11 In
Obregon, researchers identified the Caspr2 protein as a target for autoantibodies found in the
serum of autistic children. Shafrir First. Rep. at 39. Obregon’s authors used protein sequence
databases to show homology between several amino acid sequences in infectious agents and the
Caspr2 protein (including three segments of five to six amino acids in the filamentous
hemagglutinin in the Bordetella pertussis vaccine) – thereby suggesting an autoimmune
component to these conditions. See, e.g, G. Lilleker, et al., VGKC Complex Antibodies in
Epilepsy Diagnostic Yield and Therapeutic Implications, 22 Seizures 776 (2013), filed as Ex. 34-
14 (ECF No. 95-5). However, it does not appear that Dr. Shafrir has opined that a gene mutation
theory is applicable in the present matter, or even that K.A. had the Caspr2 mutation (let alone
any genetic disorder at all relevant to his vaccine injury claim).
As additional support for the autoimmune character of the injury in question, Dr. Shafrir
relied on a variety of case reports and studies that he maintained associate DTaP or other
vaccines with various antibody-mediated autoimmune encephalopathies12 – and in particular
anti-NMDA-receptor encephalitis.13 First Shafrir Rep. at 40; S. Irani, et al, N-methyl-D-aspartate
Antibody Encephalitis: Temporal Progression of Clinical and Paraclinical Observations in a
Predominantly Non-paraneoplastic Disorder of Both Sexes, 133 Brain 1655, 1655-67 (2010),
11
In his supplemental report, Dr. Shafrir noted that Obregon included a “significant error.” Shafrir Second Rep. at 7.
Specially, the filamentous hemagglutinin protein does not contain certain amino acid sequences (CSSR2 and
CSSR3) as Obregon purports to show. Id. However, Dr. Shafrir indicated in his supplemental report that he did not
rely exclusively on these two sequences in opining on molecular mimicry in the present context. Id. Thus, in his
view Obregon’s other statements relating to homology between the components in the DTaP vaccine and human
proteins (other than CSSR2 and CSSR3) remain reliable. Id.12
Dr. Shafrir also cited literature discussing the causal relationship between autoimmune encephalitis in the context
of anti-VGKC (voltage-gated potassium channel proteins) autoantibodies, and the capacity for such an encephalitis
to in turn produce developmental regression. First Shafrir Rep. at 42, 43-44. R. Dhamija, et al., Neuronal Voltage-
gated Potassium Channel Complex Autoimmunity in Children, 44 Pediatric Neurol. 275, 275 (2011), filed as Ex. 43
(ECF No. 97-4) (“Dhamija”). Dhamija was conducted by the Mayo Clinic and involved twelve patients, all with
positive anti-VGKC antibodies; one patient was a twenty-nine month old who suffered autistic regression following
receipt of the pertussis vaccine. According to Dr. Shafrir, the Dhamija authors concluded that the regression was the
direct result of the cross-reaction. Shafrir Rep. at 43. However, Dhamija specifically attempts to document
autoimmunity targeting VGKC complexes in the sera of children. More specifically, the authors conclude that larger
case studies are needed to investigation the association between autism/developmental regression and the presence
of VGKC antibodies. The paper does not otherwise suggest the vaccine was itself causal. Dhamija at 1, 6.
13
Anti-NMDA-receptor encephalitis is an autoimmune, neurologic disease where the body creates antibodies
against the NMDA receptors in the brain, disrupting signaling patterns in the brain and causing brain inflammation.
Symptoms can include a paranoia, aggression, speech problems, movement disorders, and autonomic dysfunction.
See Anti-NMDAR Encephalitis: What is Anti-NMDA Receptor Encephalitis, Cent. for Autoimmune Neurology,
Perleman Sch. Med. U. Penn., https://www med.upenn.edu/autoimmuneneurology/nmdar-encephalitis.html (last
accessed on May 3, 2018).
13
filed as Ex. 34 (ECF No. 96-9) (thirteen-year-old female received DTaP vaccine one day prior to
seizure onset); J. Dalmau, et al., Clincal Experience and Laboratory Investigations in Patients
with Anti-NMDAR Encephalitis, 10 Lancet Neuro. 63, 66 (2011), filed as Ex. 34 (ECF No. 96-
10) (two patients out of four hundred developed anti-NMDAR encephalitis after the flu vaccine
and one patient developed symptoms after a receipt of a DTaP booster vaccination). Indeed – Dr.
Shafrir maintained that reliable literature actually establishes a causal connection between
NMDA-receptor encephalitis and autistic regression. See O. Scott, et al., Anti-N-Methyl-D-
Aspartate (NMDA) Receptor Encephalitis: An Unusual Cause of Autistic Regression in a
Toddler, J. Child Neuro. (2013), filed as Ex. 34 (ECF No. 97-5) (“Scott”) (case report finding
that 33-month-old patient with NMDAR encephalitis developed autistic syndrome, but
concluding only that NMDAR encephalitis was a possible cause, and noting that further studies
will be needed). Although Dr. Shafrir acknowledged that autoimmune encephalitis in children is
“exceedingly rare . . . as there are only a small number of cases in which autoimmune
encephalitis led to autistic syndrome[,]” he maintained that the phenomenon is still significant
and supportive of his theory. Shafrir First Rep. at 44. There is, however, no evidence herein that
K.A. possessed the autoantibodies associated with NMDA encephalitis (or any other known
autoantibody-driven encephalitis), and he certainly was never so diagnosed.
Dr. Shafrir next attempted to propose a specific mechanism by which the DTaP vaccine
could have produced an initial encephalopathic reaction in K.A. – molecular mimicry. As the
literature filed in support of this concept explains, molecular mimicry is a process occurring
when the body is exposed to a foreign antigen (whether via infection or the components of a
vaccine) that resembles, or “mimics,” a self-structure, resulting in a cross-reaction when
antibodies produced by the immune system to attack the foreign antigen also mistakenly attack
the self. See N. Agmon-Levin, et al., Vaccines and Autoimmunity, 5 Perspectives 648 (2009),
filed as Ex. 24 (ECF No. 96-5) (“Agmon-Levin”); Shafrir First Rep. at 40. Dr. Shafrir proposed
that the immune attacks occurring in K.A.’s brain were “probably related to an increase in the
level of antibodies against brain proteins,” in combination with K.A.’s weakened state as a result
of earlier vaccinations. Id.In support of the above, Dr. Shafrir relied on literature exploring the possibility that
molecular mimicry was the applicable mechanism by which a specific formulation of the flu
vaccine caused a narcolepsy outbreak in Europe. M. Partinen, et al., Increased Incidence and
Clinical Picture of Childhood Narcolepsy Following the 2009 H1N1 Pandemic Vaccination
Campaign in Finland, 7 PlosOne E33723 (2012), filed as Ex. 34 (ECF No. 96-4) (“Partinen”).
Partinen discussed protein sequence fragments common to both the flu virus and the H1N1 flu
vaccine, hypothesizing that these fragments could generate a cross-reactive immune response to
a self receptor in the brain linked to narcolepsy based on similarities between the two. Partinen
did not, however, involve the DTaP vaccine—the vaccine implicated in Dr. Shafrir’s theory –
14
and the article by its own terms involves a distinguishable condition that only shares with autism
its neurologic character.14
Dr. Shafrir also attempted to establish protein sequential homology between components
of the DTaP vaccine and human protein structures in the body. First Shafrir Rep. at 39-40; D.
Kanduc, et al., Peptide Cross-Reactivity: The Original Sin of Vaccines, Frontiers Bioscience,
filed as Ex. 34-15 (ECF No. 95-6) (“Kanduc”). Kanduc examined the tetanus toxins in the DTaP
vaccine and determined sufficient identity existed between sequential fragments of those vaccine
components and multiple genes and channel receptors in the body (including sodium channels,
and the KCMA1, CAC1C, GBRB2, and NLGN3 genes). Shafrir First Rep. at 39. Researchers
have also analyzed the pertussis bacterium and found a large amount of homology between the
pertussis hemagglutinin protein component and several synaptic proteins (for example SCN8A).
Id. at 39-40. Dr. Sharfri acknowledged that Kanduc did not analyze actual sequences in human
patients or animal models, but he maintained the study lends support for a theory based on
molecular mimicry reactivity and vaccine injuries at large. Id. at 40.
In addition to offering molecular mimicry as a possible mechanism, Dr. Shafrir
maintained that the pertussis vaccine is generally a strong inducer of brain inflammation. Shafrir
First Rep. at 41; S. Lassman, et al., Induction of Type 1 Immune Pathology in the Brain
Following Immunization Without Central Nervous System Autoantigen in Transgenic Mice with
Astrocyte-Targeted Expression of IL-12, 167 J. Immunol. 5485 (2001), filed as Ex. 34-25 (ECF
No. 96-7). Lassman analyzed the peripheral immune system stimulation in mice (using the
pertussis toxin) and found that mice immunized with the toxin developed neurological
symptoms. Lassman at 5-7. Although Dr. Shafrir acknowledged that the mice used in the
experiment had an “engineered” immune system, he maintained that the study should not be
discounted as unpersuasive in support of a vaccine-induced pertussis encephalopathy. Shafrir
First Rep. at 41.
Dr. Shafrir concluded his first report by discussing the extent to which genetically-
determined immune dysfunction could provide a fertile environment for the development of
autism. Shafrir First Rep. at 44; R. Sacco, et al., Genome-Wide Expression Studies in Autism
Spectrum Disorders: moving from Neurodevelopment to Neuroimmunology Genomics,
Proteomics, and the Nervous System, 2 Adv. Neurobio. 469 (2011), filed as Ex. 38 (ECF No. 97-
10); P. Goines, et al., Cytokine Dysregulation in Autism-Spectrum Disorders (ASD): Possible
14
Dr. Shafrir’s supplemental report additionally included some discussion of the role inflammatory cytokine
production can play with regard to vaccine-induced encephalopathies in the DTaP/epilepsy context. Shafrir Second
Rep. at 3-4. He appears to have offered it, however, mainly in support of Petitioner’s argument that K.A.’s onset was
medically acceptable, rather than to establish some other mechanistic basis by which the DTaP vaccine could cause
encephalopathy – and I do not find that the limited evidence he offers relating to the above was sufficient from a
preponderant basis in any event.
15
Role of the Environment, 36 Neurotoxicol. Teratol. 67-81 (2013), filed as Ex. 37 (ECF No. 97-9).
Because, he opined, “the only documented effective therapy for autism is immunosuppressive
therapy,” an exaggerated immune response must in turn have some relationship with autism.
Shafrir First Rep. at 44; M. Chez, et al., Immune Therapy in Autism: Historical Experience and
Future Directions with Immunomodulatory Therapy, 7 Neurotherapeutics 293 (2010), filed as
Ex. 34 (ECF No. 98-5) (“Chez”); F. Duffy, et al., Corticosteroid Therapy in Regressive Autism:
A Retrospective Study of Effects on the Frequency Modulated Auditory Evokes Response
(FMAER), Language, and Behavior, 14 BMC Neuro. 1 (2014), filed as Ex. 34 (ECF No. 98-6)
(“Duffy”). These studies, however, simply discuss the effectiveness of steroid treatment as it
relates to autism, and do not conclude or explore the thesis on behalf of which they have been
invoked. Moreover, K.A. has not been shown to have a dysfunctional immune system – let alone
one caused by genetic mutation or similar factors.
Dr. Shafrir’s Supplemental Expert Report
Dr. Shafrir’s supplemental report mainly sought to address the report of Respondent’s
expert, Dr. Gregory Holmes. In response to Dr. Holmes’s critiques of the proffered causation
theory in this case, Dr. Shafrir argued that it was not his intent to opine that a vaccine could
cause autism directly, but instead to demonstrate that (based upon literature cited in his earlier
report) vaccinations could cause autoimmune phenomena, presumably with developmental
injuries as a secondary effect. Second Shafrir Rep. at 5. While acknowledging the literature he
offered involved patients with clinical pictures different from K.A.’s herein, Dr. Shafrir
nevertheless maintained that “newly emerging” concepts in the field of pediatric neurology
connected together into a plausible theory of causation. Id.Dr. Shafrir also attempted to clarify statements in his first report relating to the nature of
immune dysfunction in autism. Shafrir Second Rep. at 6. In his view, autoimmunity is a major
factor underlying the pathophysiology and risk factors involved in autistic syndrome. Id. For
support, Dr. Shafrir relied on the papers cited in his original report, but also submitted for
consideration additional literature published after he wrote his initial report in this case, all of
which, he argued, establish a reliable association between autism and an increased susceptibility
for autoimmune disorders, although all conclude that additional research is necessary to
determine the causal nature.15
15
See, e.g., M. Careaga, et al., Immune Endophenotypes in Children with Autism Spectrum Disorder, 15 Biol.
Psychiatry 738, 738-60 (2015), filed as Ex. 35 (ECF No. 106-7) (study examining immune responses in male
children, fifty with autism and sixteen without, and determining that autistic patients experienced greater cytokine
production/greater behavioral impairment after lipopolysaccharide stimulation); C. McDougle, et al, Toward an
Immune-Mediated Subtype of Autism Spectrum Disorder, 18 Brain Research 72, 72-92 (2015), filed as Ex. 35 (ECF
No. 106-8) (paper discussing the relationship between familial autoimmune disorders and autism, post-mortem
neuroimaging studies, present animal model work in ASD, and immunotherapy drug treatment for ASD, and
suggesting that future research could help define the role of immune factors and inflammation in ASD); O. Zerbo, et
al., Immune-Mediated Conditions in Autism Spectrum Disorders, 46 Brain Behav. Immun. 232, 232-36 (2015), filed
16
Dr. Shafrir further maintained that K.A.’s medical record supported his contention that
K.A. had experienced an “immune attack” on the brain (a point Dr. Holmes endeavored to
refute) resulting in encephalopathy. Shafrir Second Rep. at 4. In so doing, Dr. Shafrir admitted
that he could identify no evidence in K.A.’s medical records supporting his contention that K.A.
suffered from immune dysfunction, or that his purported encephalopathy had been caused by an
autoimmune process in the first place. Id. at 5, 7. But he maintained that the lack of evidence of
an autoimmune response could be attributable to the fact that none of K.A.’s treaters ever looked
for it. Id. More broadly, Dr. Shafrir argued that K.A.’s medical record demonstrated a repeated
series of neurological reactions to separate vaccinations at different times, even though he could
not pinpoint the abnormality that caused each. Id. at 6. K.A., in his view, had experienced several
encephalopathic episodes following his immunizations, which he deemed “compatible with [an
autoimmune reaction] possibility.” Id. at 7.
Dr. Shafrir particularly took issue with Dr. Holmes’s assertion that K.A.’s seizure
disorder began before the July 28, 2003 vaccinations. Shafrir Second Rep. at 1. In so arguing, Dr.
Shafrir maintained that one of K.A.’s treaters, Dr. Rioux, had erred in his characterization of
K.A.’s seizure disorder (when conducting an EEG during a July 22, 2004 office visit) as
“ongoing,” when in fact K.A. had experienced no ongoing seizures until after K.A.’s receipt of
the flu vaccine in December 2003. Id. at 1. Further, Dr. Shafrir contended that Dr. Rioux
incorrectly labeled K.A.’s July 22, 2004 sleeping-state EEG report as normal. Id. According to
Dr. Shafrir, the report was conducted during wakefulness only, and thus could not be read as Dr.
Holmes proposed. Id.Finally, Dr. Shafrir attempted to bulwark the concept that the timeframe of K.A.’s
injuries was medically acceptable, addressing Dr. Holmes’s brief criticism of Petitioner’s
assertion that an autoimmune reaction is possible within hours of a vaccination.16 Shafrir Second
Rep. at 3. In his view, a period of several hours is a sufficient period of time for an immune
reaction to occur. Id. For support, Dr. Sharfir listed a host of articles discussing an acceptable
timeframe for an immune response. Id., citing D. Skowronski, et al., Injection-site Reactions to
Booster Doses of Acellular Pertussis Vaccine: Rate, Severity, and Anticipated Impact, 112
Pediatrics E453, E456 (2003), filed as Ex. 35 (ECF No. 105-10) (“Skowronski”) (DTaP
injection-site reaction can occur in two to three hours following vaccination); N. Matin, et al.,
as Ex. 35 (ECF No. 106-9) (case-control study suggesting that children with autism have elevated presence of
specific immune-related comorbidities, but concluding that more research is needed to determine the type of
association that exists between the two); L. Matelski, et al., Thinking Outside the Brain, 67 J. Autoimmun. 1, 1-7
(2016), filed as Ex. 35 (ECF No. 106-10) (paper discussing, among other things, the evidence of the immune
system’s role in ASD, including maternal infection during pregnancy, familial autoimmunity, immune cell
anomalies found in children with ASD).
16
It does not appear that Dr. Shafrir addressed symptom onset in his first report, apart from a passing conclusory
reference that onset occurred within an “expected” timeframe. Shafrir First Rep. at 45.
17
Epilepsy and Innate Immune System: A Possible Immunogenic Predisposition and Related
Therapeutic Implications, 11 Human Vaccines & Immunotherapeutics, 2021, 2023 (2003), filed
as Ex. 35 (ECF No. 106-1) (innate immune system reaction, such as increased glial and
microglial cells can produce pro-inflammatory cytokines within minutes of onset of seizures); Y.
Kashiwagi, et al., Production of Inflammatory Cytokines in Response to Diphtheria-Pertussis-
Tetanus (DPT), Haemophilus Influensae Type B (Hib), and 7-Valent Pneumococcal (PCV7)
Vaccines, 10 Human Vaccines Immunotherapeutics 677, 677-85 (2014), filed as Ex. 35 (ECF
No. 106-5) (cytokine production began six hours after stimulation with vaccinations, including
DPT, Hib, and PVC7). He did not, however, provide any basis derived from his own experience
to explain why the facts of this case were consistent with such literature, nor did he go into detail
as to his specific views on this causation factor (apart from opining that the literature cited above
is sufficient to support his contention that an autoimmune reaction can occur within hours of a
vaccination).
B. Dr. Gregory Holmes
Dr. Holmes provided one expert report for Respondent. Dr. Holmes is board certified by
the American board of Psychiatry and Neurology with a special qualification in child neurology.
Report, dated Feb. 2, 2016 (ECF No. 102-1) (Ex. A) (“Holmes Rep.”) at 1; ECF No. 102-2 (Ex.
B) (“Holmes CV”). He received his bachelor’s degree from Washington and Lee University and
his medical degree from the University of Virginia. Holmes CV at 2. Following medical school,
Dr. Holmes completed two residencies, one in pediatrics from Yale University School of
Medicine and another in neurology from the University of Virginia. Id. Currently, Dr. Holmes is
a professor of neurological sciences and pediatrics, and chair of the neurological sciences
department at the University of Vermont College of Medicine in Burlington, Vermont. Holmes
Rep. at 1. His expertise is focused on pediatric neurology with an emphasis in pediatric epilepsy.
Id. Previously, Dr. Holmes held positions at both Dartmouth-Hitchcock Medical Center and
Children’s Hospital in Boston. Holmes CV at 3.
Dr. Holmes has demonstrated expertise in the fields of child neurology and epilepsy. He
has served on the editorial board of multiple peer-reviewed journals, including the Journal of
Epilepsy and the Journal of Child Neurology. Holmes CV at 8. He has also served as a primary
investigator during multiple clinical evaluations involving antiepileptic drugs. Id. at 4-5. Today,
Dr. Holmes routinely serves as a lecturer for the American Academy of Clinical
Neurophysiology and the American Academy of Neurology, and he has also published
extensively in the field of pediatric neurology. See generally Holmes CV.
Dr. Holmes asserted that Dr. Shafrir had provided no compelling causation theory that
vaccines can cause autism. Holmes Rep. at 22.17 In particular, he dismissed the scientific and
17
Indeed, Dr. Holmes stated that he found Dr. Shafrir’s overall opinion somewhat confusing, noting that it was not
18
medical literature offered in support of the argument that vaccines, through the mechanism of
molecular mimicry, can cause autoimmune phenomena as speculative at best, or inapplicable to
the present case (for example, Partinen, which involved flu vaccine-caused narcolepsy and not
autism). Id. at 22. Dr. Holmes also emphasized that molecular mimicry is a pathological
mechanism that can more easily be triggered by an infectious agent than a vaccine. Id.; M. De
Martino, et al., Vaccines and Autoimmunity, 26 Int’l J. Immunopathol. & Pharmacol. 433, 433
(2013), filed as Ex. A-31 (ECF No. 118-1) (concluding that vaccines are not a source of
autoimmune diseases, but rather that infectious agents are the primary trigger of autoimmune
mechanisms).
Dr. Holmes next attacked the basis for Dr. Shafrir’s opinion that autoimmune encephalitis
caused K.A.’s autism. Holmes Rep. at 23. One article Dr. Shafrir heavily relied upon for this
argument (R. Dhamija, et al., Neuronal Voltage-gated Potassium Channel Complex
Autoimmunity in Children, 44 Pediatric Neurol. 275, 275 (2011), filed as Ex. 43 (ECF No. 97-4)
(“Dhamija”)), for example, did not implicate any vaccine as the cause of the patient’s
encephalopathy, but rather asserted that the condition could be caused by a familial history or
viral illness. Id.; Dhamija at 6-7. Dr. Holmes also dismissed literature discussing the
developmental regression of a 33-month-old patient who was found to have anti-NMDA receptor
antibodies in his cerebrospinal fluid, noting that the autoimmune response therein was not
considered to have been vaccine-mediated. Holmes Rep. at 23-24; see Scott at 691-94. While Dr.
Holmes agreed that autoimmune encephalitis can in rare circumstances lead to autistic behavior
in a small number of cases, K.A.’s medical history did not establish he had experienced an
autoimmune encephalitis at any time. Id.18
Dr. Holmes also discussed the relationship between seizures, epilepsy, and autism
emphasized by Dr. Shafrir. Even though autism does not have a clear etiology, the prevalence of
autism in individuals with epilepsy is 22.2 percent higher than in the general population, and Dr.
Holmes acknowledged that children who experience seizures early in life also develop ASDs at a
higher rate. Holmes Rep. at 20; see A. Selassie, et al., Epilepsy Beyond Seizure: A Population-
Based Study of Comorbidities, 108 Epilepsy Research 305, 305 (2014), filed as Ex. A-4 (ECF
No. 115-4). However, he denied that this created a causal relationship between the two,
suggesting instead that pathophysiological properties shared between the two “far more likely”
explained the symptoms K.A. experienced. Holmes Rep. at 21.
clear from Dr. Shafrir’s report if he was arguing that K.A. had developed autism due to a toxin in one of his
vaccines, a poor immune response, or via molecular mimicry. Holmes Rep. at 21-22.
18
Dr. Holmes similarly contested Dr. Shafrir’s basis for his argument that the pertussis vaccine is a strong inducer
of brain inflammation, and could therefore encourage encephalopathy. Holmes Rep. at 23. Although Dr. Holmes
agreed with Dr. Shafrir’s assertion that a pertussis vaccine-induced encephalopathy was possible (albeit rare), he
maintained his view that no record evidence indicated that K.A. had ever experienced any kind of immune
19
In response to Dr. Shafrir’s discussion of immune dysfunction and autoimmunity in
autism, Dr. Holmes countered that the medical literature in fact did not support the conclusion
that autism is an autoimmune disorder. First Holmes Rep. at 24. Thus, Dr. Holmes dismissed Dr.
Shafrir’s reasoning that autism must be autoimmune because the only documented effective
therapy for autism is immunosuppressive steroid therapy. Id.; M. Chez, et al., Immune Therapy
in Autism: Historical Experience and Future Directions with Immunomodulatory Therapy, 7
Neurotherapeutics 293 (2010), filed as Ex. A-38 (ECF No. 118-8) (stating that neither
immunization nor thimerosal exposure has been conclusively linked to autism); F. Duffy, et al.,
Corticosteroid Therapy in Regressive Autism: A Retrospective Study of Effects on the Frequency
Modulated Auditory Evoked Response (FMAER), Language, and Behavior, 14 BMC Neurol. 70
(2014), filed as Ex. A-39 (ECF No. 118-9). Rather, Dr. Holmes argued that there are many other
effective treatments having nothing to do with immunology, such as behavioral therapies. Id.; see
D. Granpeesheh, et al., Applied Behavior Analytic Interventions for Children with Autism: A
Description and Review of Treatment Research, 21 Ann. Clin. Psychiatry 162 (2009), filed as
Ex. A-40 (ECF No. 118-10). Overall, Dr. Holmes maintained that the usefulness of treating ASD
patients with steroids “does not indicate that autism is a disorder of autoimmunity.” Holmes Rep.
at 24.
In Dr. Holmes’s view, K.A.’s autism disorder could not be associated with any of the
vaccines he received. Holmes Rep. at 24. Rather, Dr. Holmes attributed K.A.’s immediate
symptoms to his seizure disorder (which he opined began approximately two weeks prior to
K.A.’s July 28, 2013 vaccinations), with the autism symptoms that K.A. later displayed in 2004
reflective of a typical ASD clinical course. Id. at 21, 22. In so arguing, Dr. Holmes
acknowledged that K.A. had experienced an additional cluster of seizures following the vaccines
received on July 28, 2013, but maintained that “onset of afebrile seizures within hours of the
vaccination would make an autoimmune cause of the seizures untenable.” Id.The record otherwise, in Dr. Holmes’s view, established that the July 28th seizures were
not reflective of an encephalopathic reaction to vaccination (for example, K.A.’s EEG and MRI
scan conducted that same day produced normal results). First Holmes Rep. at 20. Dr. Holmes
also maintained that the medical record did not support Dr. Shafrir’s assertion that K.A. had
experienced an autoimmune encephalopathy and/or recurring “immune attacks” on the brain as a
result of any of his vaccinations, pointing out that there was no evidence of neurologic injury or
deterioration, and that none of K.A.’s treaters ever proposed that he had suffered an
encephalopathy. Holmes Rep. at 21-22.
dysfunction reflective of such a process. Id.20
III. PROCEDURAL HISTORY
As noted above, this action (originally assigned to former Special Master Hastings) was
initiated in May 2005, nearly thirteen years ago. Petition at 1. Petitioner filed this claim in
conjunction with the Omnibus Autism Proceedings (“OAP”)19, resulting in a long hiatus in the
progress of this matter while the OAP was concluded. See Order, dated Mar. 15, 2010 (ECF No.
11). The case was formally separated from the OAP on January 12, 2011, in light of Petitioner’s
expressed desire to proceed on an alternate theory. See Order, dated Jan. 12, 2011 (ECF No. 15);
Order, dated Sept. 30, 2011 (ECF No. 18). Petitioner filed the majority of the medical records
associated with this case in February 2012 (ECF No. 27).
Petitioner’s original counsel withdrew from the case on August 7, 2012 (ECF No. 38).
After counsel’s withdrawal, Special Master Hastings directed Petitioner to file an expert report
on or before March 4, 2013 (ECF No. 40). Thereafter, Petitioner made numerous requests for
extensions of time to file the expert report. See ECF Nos. 41, 44, 47. In the interim, Respondent
filed his Rule 4(c) Report in September 2013 (ECF No. 49) contesting the propriety of
compensation.
On January 9, 2014, Petitioner obtained new counsel. ECF Nos. 52-53. That same day,
Special Master Hastings again directed Petitioner to file a status report within thirty days,
19
In the OAP, thousands of petitioners’ claims that certain vaccines caused autism were joined for purposes of
efficient resolution. A “Petitioners’ Steering Committee” was formed by many attorneys who represent Vaccine
Program petitioners, with about 180 attorneys participating. This group chose “test” cases to represent the entire
docket in the OAP, with the understanding that the outcomes in these cases would be applied to cases with similar
facts alleging similar theories.
The Petitioners’ Steering Committee ultimately chose six test cases to present two different theories regarding
autism causation. The first theory alleged that the measles portion of the MMR vaccine precipitated autism, or, in
the alternative, that MMR plus thimerosal-containing vaccines caused autism, while the second theory alleged that
the mercury contained in thimerosal-containing vaccines could affect an infant’s brain, leading to autism.
The first theory was rejected in three test case decisions, all of which were subsequently affirmed. See generally
Cedillo v. Sec’y of Health & Human Servs., No. 98-916V, 2009 WL 331968 (Fed. Cl. Spec. Mstr. Feb. 12, 2009),
mot. for review den’d, 89 Fed. Cl. 158 (2009), aff’d, 617 F.3d 1328 (Fed. Cir. 2010); Hazlehurst v. Sec’y of Health
& Human Servs., No. 03-654V, 2009 WL 332306 (Fed. Cl. Spec. Mstr. Feb. 12, 2009), mot. for review den’d, 88
Fed. Cl. 473 (2009), aff’d, 605 F.3d 1343 (Fed. Cir. 2010); Snyder v. Sec’y of Health & Human Servs., No. 01-
162V, 2009 WL 332044 (Fed. Cl. Spec. Mstr. Feb. 12, 2009), aff’d, 88 Fed. Cl. 706 (2009).
The second theory was similarly rejected. Dwyer v. Sec’y of Health & Human Servs., No. 03-1202V, 2010 WL
892250 (Fed. Cl. Spec. Mstr. Mar. 12, 2010); King v. Sec’y of Health & Human Servs., No. 03-584V, 2010 WL
892296 (Fed. Cl. Spec. Mstr. Mar. 12, 2010); Mead v. Sec’y of Health & Human Servs., No. 03-215V, 2010 WL
892248 (Fed. Cl. Spec. Mstr. Mar. 12, 2010).
After the OAP’s conclusion, a total of 11 lengthy decisions by special masters, the judges of the U.S. Court of
Federal Claims, and the panels of the U.S. Court of Appeals for the Federal Circuit had unanimously rejected the
petitioners’ claims. These decisions found no persuasive evidence that the MMR vaccine or thimerosal-containing
vaccines caused autism. The OAP proceedings concluded in 2010.
21
updating the Court on the status of the expert report (originally requested in March 2013). See
ECF No. 52. Petitioner continued to request extensions of time to file an expert report from
January 2014 to November 2015, finally filing Dr. Shafrir’s first report on November 23, 2015.
Thereafter, Respondent filed an expert report from Dr. Holmes on February 18, 2016, with Dr.
Shafrir’s supplemental report filed on May 4, 2016.
The case was reassigned to me on April 19, 2017 (ECF No. 109). On May 5, 2017, I held
a status conference with the parties after reviewing the case record and each side’s expert reports
in greater detail. By this point, it was evident that Petitioner’s causation theory relied on the
determination that K.A. had experienced a vaccine-induced encephalopathic reaction that was
subsequently exacerbated by additional vaccinations, and that resulted in seizures plus eventual
developmental regression (and an autism diagnosis). But it was equally evident that the medical
record (which contained the most probative and reliable evidence as to K.A.’s history) did not
support Petitioner’s contentions. I thus informed Petitioner that I had serious concerns about the
claim’s viability, in light of both the history of Program claims asserting a similar theory, as well
as my own experience deciding similar cases in which vaccinations were alleged to have been
linked to an autism injury.
Given the above, during the May 2017 conference I proposed that, in lieu of a hearing,
the parties brief Petitioner’s claim, and I set a schedule for so doing in a Non-PDF Order, dated
May 5, 2017. Over several months, the parties filed their respective briefs, as referenced at the
outset of this decision, on August 14, 2017, and October 12, 2017, respectively. Along with her
brief, Respondent filed a Motion for Ruling on Record. ECF No. 127. Prior to filing her brief in
support of her claim, Petitioner filed an Amended Petition on August 11, 2017 (ECF No. 123). In
it, Petitioner specifically deleted autism as an alleged injury, and instead asserted only a vaccine-
induced developmental regression (accompanied by increased seizure activity) as the alleged
vaccine-caused injuries.
IV. Parties Respective Arguments
Petitioner’s Brief
In her opening brief, Petitioner maintains that she has established preponderant evidence
in support of her causation-in-fact claim under each of the three prongs set forth by the Federal
Circuit in Althen v. Sec’y of Health & Human Servs., 418 F.3d 1274, 1278 (Fed. Cir. 2005). First,
Petitioner proposes that Dr. Shafrir has offered a reliable theory establishing that vaccines can
cause autoimmune encephalopathies, later capable of producing developmental regression (and
ultimately evolving into an autism diagnosis). Mem. at 50-51. For the second, “did cause” prong,
Petitioner argues that K.A.’s medical records support a causal connection between the July 28,
22
2013 vaccination and onset of his seizures. Mem. at 52. In particular, Petitioner cites to one
instance in the medical record where a treating pediatrician made a reference to spreading out
future vaccinations over a period of time to reduce possible immune system stimulation and risk
of further seizure activity (Ex. 8 at 2), which she argues shows that K.A.’s treaters were
concerned about the relationship between his seizures and additional vaccinations. Id. at 52-53.
Petitioner otherwise relies on the fact that K.A. experienced seizures post-vaccination on two
occasions, followed by developmental regression after a third-vaccination to establish a logical
cause and effect sequence. Id. at 53.
Finally, Petitioner contends that the timeframe in which K.A.’s vaccine reaction and
subsequent developmental problems occurred was medically appropriate. Mem. at 53. She notes
that Dr. Shafrir’s report (showing that the medical concept of anamnesis20 does not prescribe a
timeframe for sensitization reactions, for example) supports the conclusion that four hours is an
acceptable timeframe for an onset of seizures following vaccination, as in K.A.’s case. Id. at 54.
Furthermore, Petitioner argues that this same concept would support an onset of seizures within
six days of K.A.’s flu vaccine, and onset of developmental regression within a month of K.A.’s
DT vaccine. Id.
Petitioner also asserts that a hearing should be held, to permit a closer examination of the
facts and expert opinions set forth herein, especially because (in her view) the causation theory
asserted herein differs from those examined in the OAP. Mem. at 46-47. It also appears from
Petitioner’s brief that she is concerned that K.A.’s autism diagnosis, coupled with the case’s
former inclusion in the OAP, will be overemphasized in rendering a decision. Id. Furthermore,
Petitioner argues that the medical facts of the present case (described as “three episodes of post-
vaccine seizures, coupled with dramatic regression after [a] third”) merit the kind of detailed
evaluation more likely at a hearing. Id. at 48.
Respondent’s Brief
Respondent contests the adequacy of Petitioner’s showing so much that he maintains
reasonable basis for the claim is in question. First, Respondent argues that the medical record
does not support Petitioner’s contention that K.A. suffered any encephalopathy post-vaccination.
Mot. at 6. Rather, K.A. developed a seizure disorder in 2003 prior to vaccination (which he was
subsequently treated for), and later developed autism in 2004. Id.
Second, Respondent proposes that Petitioner’s causation theory is deficient, as it
improperly (and broadly) concludes that vaccines can cause an autoimmune reaction via
20
Anamnesis, or immunologic memory, refers to “the elevated immune response following a secondary or tertiary
administration of immunogen to a recipient previously primed or sensitized to the immunogen (i.e. the secondary
response).” Illustrated Dictionary of Immunology 39 (3rd ed. 2009), filed as Ex. 35 (105-8).
23
molecular mimicry that will eventually result in developmental regression or an autism
diagnosis. Mot. at 6-7. In fact, Dr. Shafrir’s theory (based primarily on literature suggesting only
possible associations between vaccine-induced encephalopathies manifesting as ASD) has been
fully adjudicated and determined to be unreliable in numerous other cases. Mot. at 5, 8-13; see,
e.g., R.V. v. Sec’y of Health & Human Servs., No. 08-504V, 2016 WL 3882519 (Fed. Cl. Spec.
Mstr. Feb. 19, 2016), mot. for review den’d, 127 Fed. Cl. 136 (2016). Respondent argues that
such cases are not factually distinguishable in any meaningful sense, and that Petitioner’s theory
represents “an effort to avoid the unfavorable precedent facing petitioners who attempt to
advance a case alleging that vaccines cause autism . . . .” Mot. at 13.
Finally, Respondent proposes that Dr. Shafrir lacks sufficient expertise on the
immunologic or molecular biologic issues implicated in his theory to even opine reliably as to
the issues in the present matter. Mot. at 8-9.
Petitioner’s Reply
On Reply, Petitioner asserts that Respondent has “distorted the facts” in K.A.’s medical
records as they apply to his initial, purportedly pre-vaccination seizure event. Reply at 10. K.A.’s
treating doctor, Petitioner maintains, actually described this event as merely an “acute life-
threatening event” (with a presumption of gastrointestinal reflux), and not a seizure, and that
only one treater later characterized it as a seizure during subsequent treatment visits. Id. (citing
Ex. A at 20). Otherwise, Petitioner maintains that K.A.’s onset of seizures (following his
vaccinations between June 2003 and December 2003),21 followed by his onset of autistic features
post-vaccination in 2004, “infuses [P]etitioner’s case with credibility.” Id. at 14. Petitioner
repeats her earlier concerns that Respondent overemphasizes K.A.’s autism diagnosis in her
causation analysis (as opposed to the seizure evidence). Id. at 3. Overall, Petitioner continues to
assert that the present case is distinguishable from other autism cases based on the medical facts,
and that Respondent’s reliance on K.A.’s autism diagnosis as relevant to the case herein should
be disregarded. Id. at 3-7.
IV. APPLICABLE LEGAL STANDARDS
A. Petitioner’s Burden in Vaccine Program Cases
To receive compensation in the Vaccine Program, a petitioner must prove either: (1) that
he suffered a “Table Injury” – i.e., an injury falling within the Vaccine Injury Table –
21
Petitioner’s Reply also repeats her earlier arguments that K.A.’s medical record clearly documents evidence of
encephalopathy, including “loss of balance, weakness or numbness in part of [K.A.’s] body, blurred speech or loss
of speech, ataxia, cognitive impairment, agitation, [and] sleeplessness.” Mot. at 14. However, Petitioner cites no
record support for these assertions.
24
corresponding to one of the vaccinations in question within a statutorily prescribed period of
time or, in the alternative, (2) that his illnesses were actually caused by a vaccine (a “Non-Table
Injury”). See Sections 13(a)(1)(A), 11(c)(1), and 14(a), as amended by 42 C.F.R. § 100.3; §
11(c)(1)(C)(ii)(I); see also Moberly v. Sec’y of Health & Human Servs., 592 F.3d 1315, 1321
(Fed. Cir. 2010); Capizzano v. Sec’y of Health & Human Servs., 440 F.3d 1317, 1320 (Fed. Cir.
2006).22 In this case, Petitioner does not assert a Table claim.
For both Table and Non-Table claims, Vaccine Program petitioners bear a
“preponderance of the evidence” burden of proof. Section 13(1)(a). That is, a petitioner must
offer evidence that leads the “trier of fact to believe that the existence of a fact is more probable
than its nonexistence before [he] may find in favor of the party who has the burden to persuade
the judge of the fact’s existence.” Moberly, 592 F.3d at 1322 n.2; see also Snowbank Enter. v.
United States, 6 Cl. Ct. 476, 486 (1984) (mere conjecture or speculation is insufficient under a
preponderance standard). Proof of medical certainty is not required. Bunting v. Sec’y of Health &
Human Servs., 931 F.2d 867, 873 (Fed. Cir. 1991). In particular, a petitioner must demonstrate
that the vaccine was “not only [the] but-for cause of the injury but also a substantial factor in
bringing about the injury.” Moberly, 592 F.3d at 1321 (quoting Shyface v. Sec’y of Health &
Human Servs., 165 F.3d 1344, 1352-53 (Fed. Cir. 1999)); Pafford v. Sec’y of Health & Human
Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006). A petitioner may not receive a Vaccine Program
award based solely on his assertions; rather, the petition must be supported by either medical
records or by the opinion of a competent physician. Section 13(a)(1).
In attempting to establish entitlement to a Vaccine Program award of compensation for a
Non-Table claim (which is the kind of claim asserted in this matter), a petitioner must satisfy all
three of the elements established by the Federal Circuit in Althen: “(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, 418 F.3d at 1278.
Each of the Althen prongs requires a different showing. Under Althen prong one,
petitioners must provide a “reputable medical theory,” demonstrating that the vaccine received
can cause the type of injury alleged. Pafford, 451 F.3d at 1355-56 (citations omitted). To satisfy
this prong, the petitioner’s theory must be based on a “sound and reliable medical or scientific
explanation.” Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 548 (Fed. Cir. 1994).
Such a theory must only be “legally probable, not medically or scientifically certain.” Id. at 549.
22
Decisions of special masters (some of which I reference in this ruling) constitute persuasive but not binding
authority. Hanlon v. Sec’y of Health & Human Servs., 40 Fed. Cl. 625, 630 (1998). By contrast, Federal Circuit
rulings concerning legal issues are binding on special masters. Guillory v. Sec’y of Health & Human Servs., 59 Fed.
Cl. 121, 124 (2003), aff’d, 104 F. App’x 712 (Fed. Cir. 2004); see also Spooner v. Sec’y of Health & Human Servs.,
No. 13-159V, 2014 WL 504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014).
25
Petitioners may satisfy the first Althen prong without resort to medical literature,
epidemiological studies, demonstration of a specific mechanism, or a generally accepted medical
theory. Andreu v. Sec’y of Health & Human Servs., 569 F.3d 1367, 1378-79 (Fed. Cir. 2009)
(citing Capizzano, 440 F.3d at 1325-26). Special masters, despite their expertise, are not
empowered by statute to conclusively resolve what are essentially thorny scientific and medical
questions, and thus scientific evidence offered to establish Althen prong one is viewed “not
through the lens of the laboratorian, but instead from the vantage point of the Vaccine Act’s
preponderant evidence standard.” Id. at 1380. Accordingly, special masters must take care not to
increase the burden placed on petitioners in offering a scientific theory linking vaccine to injury.
Contreras v. Sec’y of Health & Human Servs., 121 Fed. Cl. 230, 245 (2015) (“[p]lausibility . . .
in many cases may be enough to satisfy Althen prong one” (emphasis in original)). But this does
not negate or reduce a petitioner’s ultimate burden to establish his overall entitlement to damages
by preponderant evidence. W.C. v. Sec’y of Health & Human Servs., 704 F.3d 1352, 1356 (Fed.
Cir. 2013) (citations omitted).
The second Althen prong requires proof of a logical sequence of cause and effect, usually
supported by facts derived from a petitioner’s medical records. Althen, 418 F.3d at 1278; Andreu,
569 F.3d at 1375-77; Capizzano, 440 F.3d at 1326; Grant v. Sec’y of Health & Human Servs.,
956 F.2d 1144, 1148 (Fed. Cir. 1992). In establishing that a vaccine “did cause” injury, the
opinions and views of the injured party’s treating physicians are entitled to some weight. Andreu,
569 F.3d at 1367; Capizzano, 440 F.3d at 1326 (“medical records and medical opinion testimony
are favored in vaccine cases, as treating physicians are likely to be in the best position to
determine whether a ‘logical sequence of cause and effect show[s] that the vaccination was the
reason for the injury’”) (quoting Althen, 418 F.3d at 1280). Medical records are generally viewed
as particularly trustworthy evidence, since they are created contemporaneously with the
treatment of the patient. Cucuras v. Sec’y of Health & Human Servs., 993 F.2d 1525, 1528 (Fed.
Cir. 1993).
However, medical records and/or statements of a treating physician’s views do not per se
bind the special master to adopt the conclusions of such an individual, even if they must be
considered and carefully evaluated. Section 13(b)(1) (providing that “[a]ny such diagnosis,
conclusion, judgment, test result, report, or summary shall not be binding on the special master
or court”); Snyder v. Sec’y of Health & Human Servs., 88 Fed. Cl. 706, 746 n.67 (2009) (“there
is nothing . . . that mandates that the testimony of a treating physician is sacrosanct—that it must
be accepted in its entirety and cannot be rebutted”). As with expert testimony offered to establish
a theory of causation, the opinions or diagnoses of treating physicians are only as trustworthy as
the reasonableness of their suppositions or bases. The views of treating physicians should also be
weighed against other, contrary evidence also present in the record – including conflicting
opinions among such individuals. Hibbard v. Sec’y of Health & Human Servs., 100 Fed. Cl. 742,
26
749 (2011) (not arbitrary or capricious for special master to weigh competing treating
physicians’ conclusions against each other), aff'd, 698 F.3d 1355 (Fed. Cir. 2012); Caves v. Sec’y
of Health & Human Servs., 100 Fed. Cl. 119, 136 (2011), aff'd, 463 F. App’x 932 (Fed. Cir.
2012); Veryzer v. Sec’y of Health & Human Servs., No. 06-522V, 2011 WL 1935813, at *17
(Fed. Cl. Spec. Mstr. Apr. 29, 2011), mot. for review den’d, 100 Fed. Cl. 344, 356 (2011), aff’d
without opinion, 475 Fed. App’x 765 (Fed. Cir. 2012).
The third Althen prong requires establishing a “proximate temporal relationship” between
the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been equated to
the phrase “medically-acceptable temporal relationship.” Id. A petitioner must offer
“preponderant proof that the onset of symptoms occurred within a timeframe which, given the
medical understanding of the disorder’s etiology, it is medically acceptable to infer causation.”
Bazan v. Sec’y of Health & Human Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The
explanation for what is a medically acceptable timeframe must also coincide with the theory of
how the relevant vaccine can cause an injury (Althen prong one’s requirement). Id. at 1352;
Shapiro v. Sec’y of Health & Human Servs., 101 Fed. Cl. 532, 542 (2011), recons. den’d after
remand, 105 Fed. Cl. 353 (2012), aff’d mem., 2013 WL 1896173 (Fed. Cir. 2013); Koehn v.
Sec’y of Health & Human Servs., No. 11-355V, 2013 WL 3214877 (Fed. Cl. Spec. Mstr. May
30, 2013), mot. for review den’d (Fed. Cl. Dec. 3, 2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).
B. Law Governing Factual Determinations
The process for making determinations in Vaccine Program cases regarding factual issues
begins with consideration of the medical records. Section 11(c)(2). The special master is required
to consider “all [] relevant medical and scientific evidence contained in the record,” including
“any diagnosis, conclusion, medical judgment, or autopsy or coroner’s report which is contained
in the record regarding the nature, causation, and aggravation of the petitioner’s illness,
disability, injury, condition, or death,” as well as “the results of any diagnostic or evaluative test
which are contained in the record and the summaries and conclusions.” Section 13(b)(1)(A). The
special master is then required to weigh the evidence presented, including contemporaneous
medical records and testimony. See Burns v. Sec’y of Health & Human Servs., 3 F.3d 415, 417
(Fed. Cir. 1993) (it is within the special master’s discretion to determine whether to afford
greater weight to contemporaneous medical records than to other evidence, such as oral
testimony surrounding the events in question that was given at a later date, provided that such a
determination is evidenced by a rational determination).
Medical records that are created contemporaneously with the events they describe are
presumed to be accurate and “complete” (i.e., presenting all relevant information on a patient’s
health problems). Cucuras, 993 F.2d at 1528; Doe/70 v. Sec’y of Health & Human Servs., 95
Fed. Cl. 598, 608 (2010) (“[g]iven the inconsistencies between petitioner’s testimony and his
contemporaneous medical records, the special master’s decision to rely on petitioner’s medical
27
records was rational and consistent with applicable law”), aff’d, Rickett v. Sec’y of Health &
Human Servs., 468 F. App’x 952 (Fed. Cir. 2011) (non-precedential opinion). This presumption
is based on the linked propositions that (i) sick people visit medical professionals; (ii) sick
people honestly report their health problems to those professionals; and (iii) medical
professionals record what they are told or observe when examining their patients in as accurate a
manner as possible, so that they are aware of enough relevant facts to make appropriate treatment
decisions. Sanchez v. Sec’y of Health & Human Servs., No. 11-685V, 2013 WL 1880825, at *2
(Fed. Cl. Spec. Mstr. Apr. 10, 2013); Cucuras v. Sec'y of Health & Human Servs., 26 Cl. Ct. 537,
543 (1992), aff’d, 993 F.2d 1525 (Fed. Cir. 1993) (“[i]t strains reason to conclude that petitioners
would fail to accurately report the onset of their daughter’s symptoms. It is equally unlikely that
pediatric neurologists, who are trained in taking medical histories concerning the onset of
neurologically significant symptoms, would consistently but erroneously report the onset of
seizures a week after they in fact occurred”).
Accordingly, if the medical records are clear, consistent, and complete, then they should
be afforded substantial weight. Lowrie v. Sec’y of Health & Human Servs., No. 03-1585V, 2005
WL 6117475, at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed, contemporaneous medical
records are generally found to be deserving of greater evidentiary weight than oral testimony –
especially where such testimony conflicts with the record evidence. Cucuras, 993 F.2d at 1528;
see also Murphy v. Sec’y of Health & Human Servs., 23 Cl. Ct. 726, 733 (1991), aff'd, 968 F.2d
1226 (Fed. Cir.), cert. den’d, Murphy v. Sullivan, 506 U.S. 974 (1992) (citing United States v.
United States Gypsum Co., 333 U.S. 364, 396 (1947) (“[i]t has generally been held that oral
testimony which is in conflict with contemporaneous documents is entitled to little evidentiary
weight.”)).
However, there are situations in which compelling oral testimony may be more
persuasive than written records, such as where records are deemed to be incomplete or
inaccurate. Campbell v. Sec’y of Health & Human Servs., 69 Fed. Cl. 775, 779 (2006) (“like any
norm based upon common sense and experience, this rule should not be treated as an absolute
and must yield where the factual predicates for its application are weak or lacking”); Lowrie,
2005 WL 6117475, at *19 (“[w]ritten records which are, themselves, inconsistent, should be
accorded less deference than those which are internally consistent”) (quoting Murphy, 23 Cl. Ct.
at 733). Ultimately, a determination regarding a witness’s credibility is needed when determining
the weight that such testimony should be afforded. Andreu, 569 F.3d at 1379; Bradley v. Sec’y of
Health & Human Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).
When witness testimony is offered to overcome the presumption of accuracy afforded to
contemporaneous medical records, such testimony must be “consistent, clear, cogent, and
compelling.” Sanchez, 2013 WL 1880825, at *3 (citing Blutstein v. Sec’y of Health & Human
Servs., No. 90-2808V, 1998 WL 408611, at *5 (Fed. Cl. Spec. Mstr. June 30, 1998)). In
28
determining the accuracy and completeness of medical records, the Court of Federal Claims has
listed four possible explanations for inconsistencies between contemporaneously created medical
records and later testimony: (1) a person’s failure to recount to the medical professional
everything that happened during the relevant time period; (2) the medical professional’s failure
to document everything reported to her or him; (3) a person’s faulty recollection of the events
when presenting testimony; or (4) a person’s purposeful recounting of symptoms that did not
exist. La Londe v. Sec’y Health & Human Servs., 110 Fed. Cl. 184, 203-04 (2013), aff’d, 746
F.3d 1334 (Fed. Cir. 2014). In making a determination regarding whether to afford greater
weight to contemporaneous medical records over contrary testimony, there must be evidence that
this decision was the result of a rational determination. Burns, 3 F.3d at 417.
C. Analysis of Expert Testimony
Establishing a sound and reliable medical theory often requires a petitioner to present
expert testimony in support of his claim. Lampe v. Sec’y of Health & Human Servs., 219 F.3d
1357, 1361 (Fed. Cir. 2000). Vaccine Program expert testimony is usually evaluated according to
the factors for analyzing scientific reliability set forth in Daubert v. Merrell Dow Pharm., Inc.,
509 U.S. 579, 594-96 (1993). See Cedillo v. Sec’y of Health & Human Servs., 617 F.3d 1328,
1339 (Fed. Cir. 2010) (citing Terran v. Sec’y of Health & Human Servs., 195 F.3d 1302, 1316
(Fed. Cir. 1999)). “The Daubert factors for analyzing the reliability of testimony are: (1) whether
a theory or technique can be (and has been) tested; (2) whether the theory or technique has been
subjected to peer review and publication; (3) whether there is a known or potential rate of error
and whether there are standards for controlling the error; and (4) whether the theory or technique
enjoys general acceptance within a relevant scientific community.” Terran, 195 F.3d at 1316 n.2
(citing Daubert, 509 U.S. at 592-95).
The Daubert factors play a slightly different role in Vaccine Program cases than they do
when applied in other federal judicial fora (such as the district courts). Daubert factors are
usually employed by judges (in the performance of their evidentiary gatekeeper roles) to exclude
evidence that is unreliable and/or could confuse a jury. In Vaccine Program cases, by contrast,
these factors are used in the weighing of the reliability of scientific evidence proffered. Davis v.
Sec’y of Health & Human Servs., 94 Fed. Cl. 53, 66-67 (2010) (“uniquely in this Circuit, the
Daubert factors have been employed also as an acceptable evidentiary-gauging tool with respect
to persuasiveness of expert testimony already admitted”). The flexible use of the Daubert factors
to evaluate the persuasiveness and reliability of expert testimony has routinely been upheld. See,
e.g., Snyder, 88 Fed. Cl. at 742-45. In this matter (as in numerous other Vaccine Program cases),
Daubert has not been employed at the threshold, to determine what evidence should be admitted,
but instead to determine whether expert testimony offered is reliable and/or persuasive.
Respondent frequently offers one or more experts of his own in order to rebut a
petitioner’s case. Where both sides offer expert testimony, a special master’s decision may be
29
“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, 219 F.3d at 1362). However, nothing requires the acceptance of an expert’s
conclusion “connected to existing data only by the ipse dixit of the expert,” especially if “there is
simply too great an analytical gap between the data and the opinion proffered.” Snyder, 88 Fed.
Cl. at 743 (quoting Gen. Elec. Co. v. Joiner, 522 U.S. 146 (1997)); see also Isaac v. Sec’y of
Health & Human Servs., No. 08-601V, 2012 WL 3609993, at *17 (Fed. Cl. Spec. Mstr. July 30,
2012), mot. for review den’d, 108 Fed. Cl. 743 (2013), aff’d, 540 Fed. App’x 999 (Fed. Cir.
2013) (citing Cedillo, 617 F.3d at 1339).
D. Consideration of Medical Literature
Both parties relied on a few pieces of medical and scientific literature in this case in
support of their respective positions. I have reviewed all of the medical literature submitted in
this case, although my decision does not discuss each filed article in detail. Moriarty v. Sec’y of
Health & Human Servs., No. 2015-5072, 2016 WL 1358616, at *5 (Fed. Cir. Apr. 6, 2016)
(“[w]e generally presume that a special master considered the relevant record evidence even
though he does not explicitly reference such evidence in his decision”) (citation omitted).
E. Determination to Resolve Case without Hearing
I have opted to decide entitlement in this case based on written submissions and
evidentiary filings, including the expert reports filed by each side. The Vaccine Act and Rules
not only contemplate but encourage special masters to decide petitions on the papers rather than
via evidentiary hearing, where (in the exercise of their discretion) they conclude that the former
means of adjudication will properly and fairly resolve the case. Section 12(d)(2)(D); Vaccine
Rule 8(d). The choice to do so has been affirmed on appeal. See Hooker v. Sec’y of Health &
Human Servs., No. 02-472V, 2016 WL 3456435, at *21 n.19 (Fed. Cl. Spec. Mstr. May 19,
2016) (citing numerous cases where special masters decided on the papers in lieu of hearing and
that decision was upheld). I am simply not required to hold a hearing in every matter, no matter
the preferences of the parties. Hovey v. Sec’y of Health & Human Servs., 38 Fed. Cl. 397, 402-03
(1997) (special master acted within his discretion in denying evidentiary hearing); Burns, 3 F.3d
at 417; Murphy v. Sec’y of Health & Human Servs., No. 90-882V, 1991 WL 71500, at *2 (Ct. Cl.
Spec. Mstr. Apr. 19, 1991).
ANALYSIS
After careful review of the expert reports, medical records, and the arguments of both
sides, and taking into account my own experience resolving similar claims (as well as numerous
parallel decisions from other Vaccine Act cases), I conclude that Petitioner has not established
preponderant evidence in favor of her claim.
30
A. K.A. Did Not Experience a Post-Vaccination Encephalopathy.
Petitioner’s claim depends on a fact finding that K.A. suffered from an encephalopathy
prior to his alleged regression and/or seizures and other symptoms – making that a threshold
matter for resolution. See Broekelschen, 618 F.3d at 1346 (when an injury or diagnosis is
disputed, and “the proposed injuries differ significantly in their pathology,” the special master
may “first find which of [the] diagnoses was best supported by the evidence presented in the
record before applying the Althen test so that the special master could subsequently determine
causation relative to the injury”). The facts from the medical records, however, do not support
the conclusion that K.A. experienced any kind of encephalopathy reaction after his July 28,
2013, vaccinations (or subsequent vaccinations in December 2013 and June 2014). See Ex. 11 at
64-65.
As I have discussed in prior decisions, although the term “encephalopathy” is less strictly
defined in the context of a non-Table claim, it nevertheless is not so elastic as to include any
possible type of brain injury no matter the degree. Murphy v. Sec’y of Health & Human Servs.,
No. 05-1063V, 2016 WL 3034047, at *25-26 (Fed. Cl. Spec. Mstr. Apr. 25, 2016), mot. for
review den’d, 128 Fed. Cl. 348 (2016); see also Wright v. Sec’y of Health & Human Servs., No.
12-423V, 2015 WL 6665600, at *6 (Fed. Cl. Spec. Mstr. Sept. 21, 2015). Thus, even though a
petitioner with a non-Table causation-in-fact claim may evade some of the Table’s requirements
for establishing an encephalopathy (such as that it is both “acute” and “chronic” as defined by
the Table’s “Qualifications and Aids to Interpretation” (“QAI”) (42 C.F.R. § 100.3(b)(2)), a non-
Table petitioner will still need to point to reliable evidence from the record establishing that the
injured party’s symptoms were sufficiently evident and severe to constitute an encephalopathy.
Murphy, 2016 WL 3034047, at *32 (record did not support contention that child had experienced
a post-vaccination encephalopathy).
The decisions of other special masters in non-Table cases have identified the specific kinds
of evidentiary factors that would suggest an individual had experienced an encephalopathy.
These include evidence of crying, anorexia, insomnia, fever, moodiness, irritability, and/or
depression. See, e.g., Cook v. Sec’y of Health & Human Servs., No. 00-331V, 2005 WL
2659086, at *14 (Fed. Cl. Spec. Mstr. Sept. 21, 2005); Noel v. Sec’y of Health & Human Servs.,
No. 99-538V, 2004 WL 3049764, at *17 (Fed. Cl. Spec. Mstr. Dec. 14, 2004) (non-Table
encephalopathy at issue characterized by moaning, high-pitched and eerie crying, and
unresponsiveness). While a petitioner might reasonably also seek to include seizures in that
partial list, proof of seizures alone is generally not considered sufficient to establish an
encephalopathy. See, e.g., Borin v. Sec’y of Health & Human Servs., No. 99-491V, 2003 WL
21439673, at *8 (Fed. Cl. Spec. Mstr. May 29, 2003) (“[a] child with no symptoms other than
31
seizures who is alert, well-appearing, non-toxic, behaving normally, playful, interactive, smiling,
and cooing does not have an acute encephalopathy, either Table or non-Table.”).
Because of the above, special masters have been reluctant to make a finding of
encephalopathy solely where an injured party displays symptoms manifesting only as seizures,
without something also indicating greater brain dysfunction or the presence of inflammation.
See, e.g., Oliver v. Sec’y of Heatlh & Human Servs., No. 10-394V, 2017 WL 747846, at *27
(Fed. Cl. Spec. Mstr. Feb. 1, 2017) (denying entitlement where petitioner experienced seizure
within 24 hours post-vaccination, but returned to baseline and experienced no other
encephalopathic symptoms), aff’d, 133 Fed. Cl. 341, 353 (2017), appeal docketed, No. 17-2540
(Fed. Cir. Sept. 13, 2017); Mohamud v. Sec’y of Health & Human Servs., No. 09-812V, 2013
WL 5314611, at * 11 (Fed. Cl. Spec. Mstr. Aug. 30, 2013) (denying entitlement where petitioner
experienced seizure within 24 hours of vaccination, but MRI and EEG were normal and no other
evidence indicated the presence of brain inflammation).
Here, proof that K.A. experienced a non-Table encephalopathy would need to include
medical record evidence detailing severe symptomology (similar to that mentioned above) in
addition to seizure activity. But the record in this case establishes only that K.A. developed acute
onset seizures immediately following his receipt of the July 28, 2003 vaccinations. The record is
subsequently bereft of evidence corroborative of encephalopathy. On the contrary, K.A.
appeared healthy and normal both at the time of his July vaccinations (after his arguable first
seizure (Ex. 8 at 30; Ex. 14 at 5)), as well as immediately thereafter (Ex. 8 at 57), and then was
deemed generally healthy from a neurologic standpoint as well in the months thereafter before
his next significant seizure activity in December 2003. In addition, K.A.’s EEG (a test which
would more likely than not reveal neurological damage) performed on the same day as his July
vaccinations was normal (Ex. 11 at 53), as was his MRI conducted that same day (Ex. 11 at 53).
And none of K.A.’s treaters ever proposed that he suffered from an encephalopathic reaction.
Indeed, Dr. Spears, K.A.’s treating neurologist, was aware that K.A. had received vaccinations
earlier that day, but concluded that they were not likely causative of his condition. Ex. 11 at 64.
Similarly, K.A.’s records surrounding his seizure episode in December 2013 do not allow
for the conclusion that he more likely than not suffered any type of encephalopathy following the
receipt of the flu vaccine roughly one week prior. Ex. 8 at 11. First, the renewed seizure activity
occurred a few days after vaccination rather than immediately (unlike the July 2013 incident),
and in response to a different vaccine. Second, K.A. subsequently saw another neurologist, Dr.
Rioux, who (like Dr. Sears) opined that K.A.’s seizure disorder was unrelated to his
vaccinations. Ex. 5 at 7. Accordingly, this instance, like the July 2013 seizure instances, can only
invoke the temporal relationship between vaccine receipt and seizure to establish evidence of
encephalopathy.
32
I also take note of K.A.’s ensuing medical history, between the time of his July 2003 and
December 2003 seizure events. Those records generally establish that K.A.’s anti-seizure
treatments were effective, and display no larger concerns about his development or status. Ex. 8
at 14, 57; Ex. 14 at 2-5, 25. And the record of later vaccines K.A. received in June 2004 (closer
in time to when his developmental problems manifested) is similarly characterized by an absence
of evidence that could be interpreted as indicia of encephalopathy, while also being temporally
attenuated by almost a month from any additional seizure activity. Ex. 14 at 35-36. The overall
record simply does not support the conclusion that K.A. ever experienced a post-vaccination
encephalopathy at any time.23
B. Petitioner Has Not Established a Reliable or Persuasive Causation Theory.
Dr. Shafrir maintained that a component in the DTaP vaccine could initiate an
autoimmune process and thereby produce an encephalopathy (somehow encouraged by the other
vaccinations K.A. experienced) sufficient to result in developmental regression a year later.
Petitioner did not offer direct evidentiary support establishing the capacity of DTaP vaccines to
function as alleged, in this or other analogous circumstances. Nor did Dr. Shafrir invoke any
persuasive studies involving these vaccines, or others, and their roles in incidents of
developmental regression.
Instead, Dr. Shafrir relied on a loose chain of circumstantial propositions in order to
establish Petitioner’s causation theory. But (and even though circumstantial evidence is wholly
acceptable as a general matter in Vaccine Program cases) those propositions were themselves
insufficiently supported with reliable scientific evidence required to conclude that the overall
theory was plausible. As another special master noted in considering the Althen prong one
analysis, “[t]he weight to be given an expert’s opinion is based in part on the size of the gap
between the science and the opinion proffered.” Isaac v. Sec’y of Health & Human Servs., No.
08-601V, 2012 WL 3609993, at *17 (Fed. Cl. Spec. Mstr. July 30, 3012), aff’d, 108 Fed. Cl. 743(2013) aff’d, 540 F. App’x 999 (Fed. Cir. 2013). That gap is quite wide in this case.24
23
It is instructive to compare the facts of this case with those exceedingly rare cases in which a claimant has
established an encephalopathy resulting in ASD-like symptoms (although both involved Table claims in which
causation was assumed). In one such instance, the vaccinated child developed a very high fever within 48 hours of
vaccination, thereafter displaying crying, sleeplessness, and significant motor problems, all of which were
documented in the medical record. Poling v. Sec’y of Health & Human Servs., No. 02-1466V, 2011 WL 678559, at
*1 (Fed. Cl. Spec. Mstr. Jan. 28, 2011). In another, the vaccinated child received a multi-virus vaccine and then
experienced a seizure on the trip home from the vaccination, followed by a week of noticeably decreased levels of
consciousness and lethargy. Wright v. Sec’y of Health & Human Servs., No. 12-423V, 2015 WL 6665600 (Fed. Cl.
Spec. Mstr. Sept. 21, 2015). In Petitioner’s case, by contrast, there are no records establishing any sort of proximate
temporal reaction to the vaccines that would support a finding that K.A. experienced such an encephalopathy.
24
I also note (as I have in other cases) that Dr. Shafrir lacks the qualifications necessary to offer persuasive expert
testimony regarding the propensity of vaccines to cause neurologic injury sufficient to result in autism. See T.M. v.
Sec’y of Health & Human Servs., No. 08-284V, 2016 WL 11087157, at *28 (Fed. Cl. Spec. Mstr. Aug. 9, 2016),
33
For example, certain literature offered in support of Petitioner’s theory, like Partinen, not
only involved a different vaccine and injury (the flu vaccine and narcolepsy), but also centered
on a pathologic process reasonably understood to be autoimmune – something that cannot
possibly be said for autism or developmental regression. Partinen at 7-8. In addition, the
literature cited with regard to anti-NMDAR or anti-VGKC autoantibody-mediated
encephalitis establishes only weak evidence of a possible association between
autoimmunity and autism. See, e.g., Dhamija at 6-7. Notably, Petitioner offered no record
evidence that relevant testing suggested that K.A. had either of these antibodies in his
body (close-in-time to the vaccine or any time thereafter). Similarly, articles such as
Agmon-Levin were simply too broad in focus to constitute persuasive support for the theory
offered in this case; simply because other vaccines have been linked to other kinds of
autoimmune-associated conditions does not mean the same can be concluded to have occurred in
this case. See R.K. v. Sec’y of Health & Human Servs., No. 03-0632V, 2015 WL 10936124 (Fed.
Cl. Spec. Mstr. May 23, 2016) (categorizing Dr. Shafrir’s theory as a “one size fits all” approach
to autoimmune reactions), mot. for review den’d, 125 Fed. Cl. 57 (2016), aff’d, 671 F. App’x 792
(2016).
Petitioner’s causation theory has an even more fundamental weakness: its striking
similarity to theories universally rejected in the Vaccine Program. To date, every non-Table
claim seeking compensation for autism injuries purportedly related to a vaccine and litigated
since completion of the OAP has failed. See, e.g., Hardy v. Sec’y of Health & Human Servs., No.
08-108V, 2015 WL 7732603, at *4-5 (Fed. Cl. Spec. Mstr. Nov. 3, 2015) (referencing eleven
autism claims unsuccessfully tried, plus six that were rejected (over the petitioners’ objections)
without trial). I myself have tried several such cases, with the same result. See, e.g., Anderson v.
Sec’y of Health & Human Servs., No. 02-1314V, 2016 WL 8256278 (Fed. Cl. Spec. Mstr. Nov.
1, 2016), mot. for rev. den’d, 131 Fed. Cl. 735 (2017), aff’d, 717 F. App’x 1009 (Fed. Cir. 2018);
T.M. v. Sec’y of Health & Human Servs., No. 08-284V, 2016 WL 11087157, at *28 (Fed. Cl.
Spec. Mstr. Aug. 9, 2016), mot. for rev. den’d, 133 Fed. Cl. 78 (2017); Murphy, 2016 WL
3034047, at *25-26; R.V., 2016 WL 3882519.
mot. for rev. den’d, 133 Fed. Cl. 78 (2017). Although Dr. Shafrir is competent to testify on a wide array of
neurological disorders (including autism itself), he is not an immunologist, and has no relevant background
experience treating or studying the effects of vaccines on individuals. I have considered his testimony carefully, but
it is reasonable to afford it significantly less weight since it comes from a person who lacks the qualifications
necessary to advance it. Daubert v. Merrell Dow Pharm., Inc., 43 F.3d 1311, 1317 (9th Cir. 1995) (“[o]ne very
significant fact to consider is whether the experts are proposing to testify about matters growing naturally and
directly out of research they have conducted independent of the litigation, or whether they have developed their
opinions expressly for purposes of testifying”). Dr. Shafrir’s qualifications and expertise have similarly been called
into question by other special masters, and his testimony described as vague and poorly supported – a criticism
leveled against him herein as well by Dr. Holmes. See, e.g., Lehner v. Sec’y of Health & Human Servs., No. 08-
554V, 2015 WL 5443461 (Fed. Cl. Spec. Mstr. July 22, 2015).
34
Petitioner argues that the theory offered in this case is qualitatively different. But other
petitioners have similarly attempted to recast their claim that a vaccine caused an autism injury
as a claim that the vaccine precipitated some form of encephalopathy (more often than not
autoimmune in nature) that later produced developmental problems (whether or not they are
defined as an ASD) due to the resulting neurologic injury. See, e.g., Cunningham v. Sec’y of
Health & Human Servs., No. 13-483V, 2016 WL 4529530 (Fed. Cl. Spec. Mstr. Aug. 1, 2016),
mot. for review den’d, 2017 WL 1174448 (Fed. Cl. Jan. 25, 2017). Such efforts have been
correctly understood as seeking to evade the weight of negative precedent involving autism
claims – as here. Cunningham, 2017 WL 1174448, at *7-8 (“[r]egardless of petitioner’s attempt
to differentiate this case from other autism cases by creating this second step, the Special Master
rightfully classified this case as an autism case”).
All in all, the theory proposed herein is too similar to previously-rejected theories to find
it reliable and persuasive – and has significant lapses in its chain of propositions in any event.
C. Petitioner Has Not Established that K.A.’s Vaccines Did Cause
Encephalopathy or Seizures Resulting in Autism.
Petitioner’s obligation under the second Althen prong was to demonstrate a logical
sequence of cause and effect connecting the particular facts of her case to her medical theory.
See, e.g., Sturdivant v. Sec’y of Health & Human Servs., No. 07-788V, 2016 WL 552529, at *18
(Fed. Cl. Spec. Mstr. Jan. 21, 2016) (discussing that prong two requires a fact-based inquiry into
whether the vaccine in question did cause the particular injury). But her theory depended on
acceptance of her allegation that K.A. suffered from an encephalopathy – a conclusion the record
does not support, and thereby rendering it impossible for her to establish that the vaccines K.A.
received caused injury.
Even if, however, I had found that K.A. had experienced one or more encephalopathies –
or that his seizure disorder was reflective of an encephalopathy – I would still be unable to find
based upon the present record that any of the vaccines he received caused that injury. There is no
evidence in the record that K.A. was undergoing an autoimmune process of the kind Petitioner’s
causation theory suggests he should have been experiencing in connection with his alleged
encephalopathy. Indeed, Dr. Shafrir acknowledged that (a) K.A.’s clinical picture was different
from articles cited pertaining to autoimmune encephalopathies, (b) K.A.’s records do not indicate
a history of autoimmune disease, and (c) no medical evidence otherwise exists to establish the
autoimmune character of K.A.’s injuries. Ex. 35 at 5, 7.
Moreover, there is credible evidence in the record that K.A. experienced a seizure-like
episode prior to the series of vaccinations received on July 28, 2003, and which are alleged to
have triggered his first encephalopathy. See Ex. 11 at 2-12. Although attending physicians
labeled this initial episode as an “acute life-threatening event,” later-in-time treaters reasonably
35
took it into account in understanding K.A.’s overall condition, deeming it a seizure episode
related to K.A.’s subsequent activity. See Ex. 11 at 64; Ex. 14 at 8. The medical record in any
Program case must be looked at from an overall standpoint, as evidence that treaters understand
at one point may later be viewed otherwise after the passage of time, and after more facts are
adduced in the course of treatment. See, e.g., Bell v. Sec’y of Health & Human Servs., No. 13-
709V, 2016 WL 8136297, at *24-25 (Fed. Cl. Spec. Mstr. Dec. 1, 2016); Blackburn v. Sec’y of
Health & Human Servs., No. 10-410V, 2015 WL 425935, at *25 (Fed. Cl. Spec. Mstr. Jan. 9,
2015). Petitioner did not successfully rebut the reasonable inference that the pre-July incident
was related to the subsequent seizure series, and that inference casts further doubt on Petitioner’s
contention that K.A.’s vaccines caused an encephalopathy or seizure disorder (if not completely
eliminating the possibility that the July 2003 vaccine initiated a process later resulting in
developmental problems and/or autism).
In addition, K.A.’s treaters largely did not opine that he had suffered a vaccine-induced
injury (encephalopathic or any other). Admittedly, as Petitioner points out, at least one of K.A.’s
treaters (Dr. Rioux) allowed for the vaccination schedule to be adjusted based on parental
concerns about possible negative effects (Ex. 14 at 8, 42; Ex. 8 at 20-21; Ex. 5 at 7-8).
Thereafter, K.A.’s mother relayed her concerns (along with Dr. Rioux’s “recommendation”) to
K.A.’s pediatrician during subsequent office visits (Ex. 14 at 8, 42). This alone is not sufficiently
strong and probative evidence of a treater view that the vaccine was causal. Although a treating
physician’s recommendation to withhold a particular vaccination can be probative evidence of a
causal link between the vaccination and an injury sustained, special masters are less likely to find
a causal link where the treater does not seem to have a sound scientific rationale – or, as here,
offers no explanation at all. See e.g., Mosely v. Sec’y of Health & Human Servs., No. 08-724V,
2015 WL 2354316, at *18 (Fed. Cl. Spec. Mstr. Apr. 27, 2015) (physician’s recommendation to
withhold vaccination unpersuasive causation evidence where the same treater offered no
explanation for his statements); Arango v. Sec’y of Health & Human Servs., No. 09-318V, 2012
WL 4018028, at *21 (Fed. Cl. Spec. Mstr. Aug. 23, 2012) (physician’s recommendation to
withhold vaccination unpersuasive where the same treater testified that the vaccine was not the
cause of the injury), aff’d, 109 Fed. Cl. 335 (2013). Here, the statements made by K.A.’s mother
to his pediatrician are uncorroborated by evidence of affirmatively-voiced treater opinion that
any of the vaccines K.A. received had any connection at all to his injuries,25 and thus could
reasonably be interpreted as a physician acquiescing to a caregiver concern rather than an
informed decision bearing strongly on causation.
25
Although Dr. Rioux’s office notes indicate that he could find no precise etiology for K.A.’s seizure disorder, he
allowed for the possibility that a combination of antibiotics and vaccinations could have “lowered [K.A.’s] seizure
threshold.” Ex. 5 at 8. As noted earlier, however, Dr. Rioux ultimately opined that K.A.’s immunizations were not
responsible for his on-going seizure difficulties. Id.36
D. Petitioner Has Not Shown the Timeframe for Development of his Injuries
was Medically Acceptable.
The component of Dr. Shafrir’s theory addressing the timeframe in which the various
vaccines that allegedly injured K.A. would do so is deficient both in specific and general ways.
Looking only at the specific support offered for the theory reveals numerous unreliable
inconsistencies. Thus, and as Respondent argued, although Dr. Shafrir attempted to bulwark the
exceedingly short timeframe between the July 2003 vaccinations and K.A.’s subsequent acute
onset seizures (which would, according to Petitioner, provide some initial evidence of the
supposed encephalopathy), the scientific evidence provided in support was inconsistent with the
aspects of his theory relating to the biologic mechanism that he proposed had caused K.A.’s
reaction, molecular mimicry, which his own literature (and/or counter evidence offered by Dr.
Holmes) suggested would take somewhat longer. See Holmes Rep. at 21; Mot. at 15 n.10. His
timing arguments also conflated evidence pertaining to the timeframe in which adaptive immune
responses (like an autoimmune process mediated through molecular mimicry) would occur with
evidence bearing on the comparatively shorter timeframes involved in innate responses (such as
an injection site or hypersensitivity reaction). See, e.g., Skowronski at E456. These
inconsistencies are not adequately resolved in Dr. Shafrir’s reports.
More generally, however, and relying on incontrovertible facts from K.A.’s medical
history, it is impossible to discern an explanation in this case that can credibly and persuasively
harmonize the varying response times at issue. Ignoring the initial, potentially-related seizure
incident that predated the late-July 2003 vaccinations, K.A. experienced seizures (a) the same
day as the July 2003 vaccinations, (b) none after vaccines received in the fall of 2003, (c)
approximately a week after the December 2003 flu vaccine was administered, and (d) about a
month after two more vaccines were administered in June 2004 on two different occasions. The
temporal irregularity of these reactions is not consistent with what would be seen in the context
of “challenge-rechallenge,” where reactions to a series of vaccines should occur in increasingly
shorter intervals. See e.g., Gramza v. Sec’y of Health & Human Servs., No. 15-247, 2018 WL
1581674, at *10, 24 (Fed. Cl. Spec. Mstr. Feb. 5, 2018), appeal docketed, No. 15-247 (Fed. Cl.
Mar. 7, 2018). Petitioner’s Althen prong three showing also cannot explain why no evidence of
developmental regression is seen before July 2004 – a year from the first alleged reaction, and
with no evidence in that period that developmental problems had begun. Petitioner’s expert and
the various pieces of literature filed in connection cannot provide a reasonable, reliable
framework that makes scientific sense of this ambiguous and inconsistent fact pattern.
E. This Case was Properly Resolved without a Hearing.
In ruling on the record, I am declining Petitioner’s request for a hearing. The choice of
how best to resolve this case is a matter that lies generally within my discretion, but given
Petitioner’s protestations I shall explain my reasoning.
37
A hearing provides a petitioner with the opportunity to put on live testimony, which aids
the special master most in cases where witness (or expert) credibility is at issue, or where there is
a need to pose questions to a witness in order to obtain information not contained in, or not self-
evident from, the existing filings. See, e.g., Hooker v. Sec’y of Health & Human Servs., No. 02-
472V, 2016 WL 3456435, at *21 (Fed. Cl. Spec. Mstr. May 19, 2016) (discussing a special
master’s discretion in holding a hearing and the factors that weighed against holding a hearing in
the matter); Murphy v. Sec’y of Health & Human Servs., No 90-882V, 1991 WL 71500, at *2
(Fed. Cl. Spec. Mstr. Apr. 19, 1991) (no justification for a hearing where the claim is fully
developed in the written records and the special master does not need to observe the fact
witnesses for the purpose of assessing credibility), aff’d, 1991 WL 74931 (Fed. Cl. Apr. 25,
1991) aff’d, 968 F.2d 1226 (Fed. Cir. 1992). It may also permit a claimant to expand upon or
illuminate points already set forth in paper filings, or respond to unanticipated questions raised in
the matter – but again, only where necessary to reach a decision.
Prior decisions have recognized that a special master’s discretion in deciding whether to
conduct an evidentiary hearing “is tempered by Vaccine Rule 3(b),” or the duty to “afford[] each
party a full and fair opportunity to present its case.” Hovey v. Sec’y of Health & Human Servs.,
38 Fed. Cl. 397, 400-01 (1997) (citing Rule 3(b)), appeal dismissed, 135 F.3d 773 (Fed. Cir.
1997). But that rule also includes the obligation of creation of a record “sufficient to allow
review of the special master’s decision.” Id. Thus, the fact that a claim is legitimately disputed,
such that the special master must exercise his intellectual faculties in order to decide a matter, is
not itself grounds for a trial (for if it were, trials would be required in every disputed case).
Special masters are expressly empowered to resolve fact disputes without a hearing, and may do
so if the record at issue has been sufficiently developed to determine that each side’s “full and
fair” opportunity has not been abridged.
In this case, live witness testimony was not required in order for me to reach a reasoned
decision. The record itself was expansive and contained sufficient evidence upon which to base
this decision. As the lengthy procedural history indicates, Petitioner was given ample extensions
of time in which to obtain an expert report, and to marshal the arguments she made in opposing
Respondent’s motion on the record. The flaws in Petitioner’s theory and factual arguments were
self-evident from review of the medical records and the expert reports submitted, which relied
heavily on speculative assertions and statements unsupported by the contemporaneous medical
record and not bulwarked by sufficient reliable scientific evidence. And, as noted above,
Petitioner’s expert offered opinions regarding autism or developmental regressions as a vaccine
injury - consistent with theories that have previously been deemed scientifically unreliable and
unpersuasive. I have heard Dr. Shafrir testify in a similar context before, and relying on similar
scientific evidence, and need not hear him again to understand the logic of his position from the
filed written reports. See, e.g., T.M., 2016 WL 11087157, at *10-15; R.V., 2016 WL 3882519, at
38
*15-20. I simply did not require oral testimony to decide the case. On the contrary: the
congruence of the theory espoused herein with numerous, previously-rejected variations on the
same theme, plus based upon my own prior experiences with the theory, counseled against
expending the time and effort a hearing entails.26
At bottom, the most significant issue in deciding whether to hold a hearing is whether the
refusal to do so will deprive the claimant of the fair opportunity to prosecute her case. Petitioner
here has received such an opportunity. Her counsel has litigated to trial many similar claims
involving the same kind of injuries, and is well aware of how such claims have fared; the likely
outcome would have been no different had a trial been held, regardless of Petitioner’s hopes. A
hearing would also have unnecessarily postponed the date by which the matter could be fully
resolved. Such circumstances ultimately counseled in favor of resolving the matter on the papers.
CONCLUSION
The record does not support Petitioner’s contention that the vaccines K.A. received
could, or did, cause his developmental regression, seizure disorder, or autism, nor has she
established it more likely than not that he ever suffered from a post-vaccine encephalopathy
injury. Petitioner has not established entitlement to a damages award, and therefore I must
DISMISS her claim.
In the absence of a timely-filed motion for review (see Appendix B to the Rules of the
Court), the Clerk shall enter judgment in accordance with this decision.27
IT IS SO ORDERED.
/s/ Brian H. Corcoran
Brian H. Corcoran
Special Master
26
The decision not to hold a hearing because the claim reflected a frequently-litigated theory is not something that
would only ever negatively impact a petitioner. The opposite circumstances – where a petitioner asserted a claim
that has repeatedly succeeded in the past – would motivate me to act in the same manner, and propose to Respondent
that either the case be settled or that it too be resolved on the papers.
27
Pursuant to Vaccine Rule 11(a), the parties may expedite entry of judgment by filing a joint notice renouncing
their right to seek review.
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