Reed v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

Filed: December 4, 2018

* * * * * * * * * * * * * * *

ERIC REED and JEANNA REED, as * PUBLISHED

Parents and Natural Guardians of *

I.R., a minor, * No. 08-650V

*

Petitioners, * Chief Special Master Dorsey

*

v. * ProQuad Measles, Mumps, Rubella,

* and Varicella (“MMRV”) Vaccine;

SECRETARY OF HEALTH * Autism Spectrum Disorder (“ASD”);

AND HUMAN SERVICES, * Encephalopathy; Mitochondrial

* Dysfunction; Mitochondrial

Respondent. * Disorder.

*

* * * * * * * * * * * * * * *

Anne Carrion Toale, Maglio Christopher and Toale, Sarasota, Florida, for petitioners.

Ryan Daniel Pyles, U.S. Department of Justice, Washington, D.C., for respondent.

ENTITLEMENT DECISION1

On September 15, 2008, Eric Reed and Jeanna Reed (“petitioners”), parents and

guardians of I.R., a minor, filed a Short-Form Autism Petition for Compensation under the

National Vaccine Injury Compensation Program (“the Program”).2 The case was included

1

The undersigned intends to post this Decision on the United States Court of Federal Claims’

website. This means the Decision will be available to anyone with access to the Internet. In

accordance with Vaccine Rule 18(b), petitioners have 14 days to identify and move to redact

medical or other information, the disclosure of which would constitute an unwarranted invasion

of privacy. If, upon review, the undersigned agrees that the identified material fits within this

definition, the undersigned will redact such material from public access. Because this Decision

contains a reasoned explanation for the action in this case, the undersigned is required to post it

on the United States Court of Federal Claims’ website in accordance with the E-Government Act

of 2002. 44 U.S.C. § 3501 note (2012) (Federal Management and Promotion of Electronic

Government Services).

2

The Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, 42

U.S.C. §§ 300aa-10 et seq. (“Vaccine Act” or “the Act”). Hereafter, individual section

references will be to 42 U.S.C. § 300aa of the Act.

1

among the pending claims in the Court’s Omnibus Autism Proceeding (“OAP”).3 At the

conclusion of the OAP test cases, petitioners filed an amended petition alleging that the

combined measles, mumps, rubella, and varicella (“MMRV” or “ProQuad”4) vaccine that I.R.

received at 12 months on December 30, 2005, caused I.R. to “suffer from immunodeficiency

disorder, bowel disease, pathological neuroinflammation, seizure disorder, mitochondrial

disease, and the resulting features of autism spectrum disorder (‘ASD’).” Amended (“Am.”)

Petition dated Feb. 6, 2012, at ¶ 34 (ECF No. 16). Petitioners also alleged at the time that I.R.

suffered a table injury, “post-MMR encephalitis.” Id. at ¶ 35.5 However, petitioners

subsequently filed a second amended petition alleging that I.R. “suffered a significant

aggravation of a preexisting condition, a mitochondrial disorder, causally related to the ProQuad

vaccine administered on December 30, 2005,” which in turn caused I.R. to “suffer from

immunodeficiency disorder, bowel disease, pathological neuroinflammation, seizure disorder,

mitochondrial dysfunction and the resulting features of autism spectrum disorder.” Second Am.

Petition dated Mar. 16, 2015, at ¶¶ 43-44 (ECF No. 85); see also Joint Pre-hearing (“Prehr’g”)

Submission dated Apr. 3, 2015, at 7 (ECF. No. 98).

An entitlement hearing was held on April 28-29, 2015, and June 22-24, 2016, followed

by post-hearing briefing. After a review of the entire record, including medical records,

affidavits, videotape evidence, expert reports, medical literature, hearing testimony, and other

submissions, the undersigned finds that the evidence does not support a finding that petitioners

are entitled to compensation. Accordingly, for the reasons discussed herein, compensation is

denied.

I. Factual Background

The undersigned has considered all the evidence in this case and the record as a whole.

The following summaries are by no means a complete recitation of the relevant facts and

evidence reviewed. See § 300aa–13(a) (stating that the special master should consider the

“record as a whole”).

3

The Omnibus Autism Proceeding consisted of a large group of petitions alleging that certain

childhood vaccinations cause or contribute to the development of a serious neurodevelopmental

disorder known as “autism spectrum disorder” or “autism.” For complete information

concerning the autism proceedings, please see www.uscfc.uscourts.gov/omnibus-autism-

proceeding.

4

ProQuad, a vaccine for the prevention of measles, mumps, rubella, and varicella, is

recommended for children 12 months through 12 years of age. ProQuad, Merck Vaccines,

https://www.merckvaccines.com/Products/ProQuad (last visited Nov. 7, 2018).

5

While petitioners alleged a table encephalopathy in their amended petition, this allegation was

abandoned in their second amended petition. See Second Am. Petition dated Mar. 16, 2015

(ECF No. 85).

2

A. Stipulated Facts

The parties agreed to 29 paragraphs of stipulated facts, set forth in the joint pre-hearing

submission filed on April 3, 2015. Joint Prehr’g Submission at 1-6. Although not repeated here,

the stipulated facts are incorporated in the Decision as if fully set forth. See id. The summary of

additional facts below includes some of the facts set forth in the stipulated submissions, as well

as additional relevant facts that pertain to I.R.’s medical history and the experts’ opinions.

B. Summary of Additional Relevant Facts from the Medical Records

I.R. was born on December 29, 2004. Petitioners’ Exhibit (Pet. Ex.) 4 at 6. He was

conceived through in vitro fertilization (“IVF”) and his mother was induced into labor at 38

weeks. Id. Prior to delivery, I.R.’s mother was placed on bed rest due to preeclampsia and high

blood pressure. Pet. Ex. 2 at 9. At birth, I.R. experienced respiratory depression. Pet. Ex. 4 at 7.

APGAR scores at one and five minutes were four and nine, respectively. Id. at 6. Although I.R.

experienced breathing problems within the first five minutes of birth, his condition improved and

he met all the benchmarks of a healthy newborn. Id. at 7.

i. I.R.’s Medical History Prior to 12-Month Vaccinations

As an infant, I.R. had trouble feeding, was colicky, and had a number of illnesses. See,

e.g., Pet. Ex. 9 at 42. On January 19, 2005, he was noted to have excessive gas, and several days

later, he had vomiting and diarrhea. Pet. Ex. 15 at 3-4. On January 26, 2005, he was reported to

have episodes of crying and screaming. Id. at 5. Zantac was prescribed. Id. In February 2005,

I.R.’s stomach problems persisted and he had another episode of diarrhea that lasted for two

days. Id. at 6-7. In March 2005, he had periods of low grade fever, fussiness, and screaming.

Id. at 8. Later that month, he had another low-grade fever and diarrhea. Id. at 9.

I.R.’s records do not reveal episodes of illness during the summer of 2005. By mid-

October of that year, however, he was ill again, with colds “back to back” and a cough for one

month. Pet. Ex. 15 at 11-12; see also Pet. Ex. 9 at 37. During his 9-month visit on October 13,

2005, I.R. was noted to suffer from a “nasty cough.” Pet. Ex. 9 at 37. I.R.’s mother contacted

his pediatrician’s office with further complaints about his colds on October 27 and 31, 2005.

Pet. Ex. 15 at 11-12. She expressed concern specifically about his “productive cough” and

“constant drainage from nose.” Id. at 11.

I.R.’s illnesses continued through November. Pet. Ex. 9 at 35-36; Pet. Ex. 15 at 13-14.

During a sick visit with his pediatrician on November 1, 2005, I.R. exhibited coughing, fever,

and decreased appetite. Pet. Ex. 9 at 36. On November 16, 2005, I.R. again suffered from a

productive cough and loss of appetite, accompanied by fever and diarrhea. Pet. Ex. 15 at 14. On

November 18, 2005, the intermittent fever, cough, and diarrhea persisted. Id. at 13. At this time,

I.R. was described by his parents as being more fatigued and “sick off and on for weeks.” Id.

3

Records from a November 19, 2005 sick visit also note a recent history of fever, diarrhea, and a

“bad cough.” Pet. Ex. 9 at 35.

ii. I.R.’s Medical History Following 12-Month Vaccinations

At I.R.’s one-year well-child exam on December 30, 2005, his pediatrician, Dr. Brooke

Scherer, noted that I.R. was healthy. Pet. Ex. 9 at 34. I.R.’s 12-month vaccinations for mumps,

measles, rubella, and varicella (“ProQuad”) and for Haemophilus influenza type B and Hepatitis

B (“COMVAX”6) were also administered. Id. Nine days later, on January 8, 2006, I.R. had a

high fever, above 103°, for several days. Pet. Ex. 15 at 17. I.R.’s pediatrician indicated that the

fever could have been a reaction to the ProQuad vaccine.7 Id. at 16.

On February 3, 2006, approximately one month after these vaccinations, I.R.’s mother

called the pediatrician’s office to report that I.R. had a fever and a rash on his face and trunk.

Pet. Ex. 15 at 15. The registered nurse who spoke with I.R.’s mother suggested that the rash was

likely roseola8 based on the mother’s description. Id. On February 24, 2006, I.R. was diagnosed

with pityriasis rosea.9 Pet. Ex. 9 at 33. The rash persisted and led to a return visit on March 23,

2006. Id.

On March 26, 2006, I.R. was seen at the emergency room for fever and vomiting that

began the previous day. Pet. Ex. 4 at 2-3. I.R. had some blueness around his lips and hands and

his fever was 101°. Id. He was diagnosed with viral gastroenteritis and fever. Id. Four days

later, on March 30, 2006, I.R. had his 15-month well-child visit. Pet. Ex. 9 at 32. No

developmental abnormalities were noted and I.R. was assessed as a healthy 15 month old. Id.

6

COMVAX, which has since been discontinued, is a vaccine for the prevention of Haemophilus

influenza type B and Hepatitis B. Licensed Biological Products with Supporting Documents,

U.S. Food & Drug Admin., https://www.fda.gov/BiologicsBloodVaccines/ucm133705.htm (last

visited Nov. 7, 2018).

7

I.R.’s mother reported the fever by telephone. I.R. was not seen by his pediatrician.

8

Roseola is “a type of rose-colored rash seen most often in an infectious disease such as measles

or other exanthematous diseases.” Dorland’s Illustrated Medical Dictionary 1654 (32d ed. 2012)

(“Dorland’s”).

9

Pityriasis rosea is “a common, acute or subacute, self-limited, exanthematous disease of

unknown etiology, whose onset is marked by a solitary pink, reddish, or tan plaque called a

herald patch, usually on the trunk . . . ; subsequent lesions are similar to this but smaller, with

vesicular borders, tending to peel and produce a scaly collarette.” Dorland’s at 1451.

4

At the visit, I.R. received the diphtheria-tetanus-acellular pertussis (“DTaP”) and 7-valent

pneumococcal conjugate vaccine (“PCV7” or “Prevnar 7”10) vaccines. Id.

In April and May of 2006, I.R. visited his pediatrician’s office numerous times. See

generally Pet. Ex. 5; Pet. Ex. 9. On April 11, 2006, the medical record indicates he had been sick

for about a week and a half, with symptoms of fever, cough, and sleeplessness. Pet. Ex. 9 at 31.

On April 24, 2006, he had a rash “all over trunk,” which had been present “x 3 days.” Pet. Ex. 9

at 30. He also had swelling of the face, red ears, and ear drainage. Id. His diagnoses included

right-sided otitis media. Id. On April 27, 2006, I.R. returned and was diagnosed with bilateral

otitis media, conjunctivitis, and petechiae on his earlobes. Pet. Ex. 9 at 29. At a series of three

visits between May 2 and 4, 2006, I.R. was again diagnosed with otitis media and given an

injection of Ceftriaxone, an antibiotic. Pet. Ex. 9 at 26-28. On May 5, 2006, I.R. saw an ear,

nose, and throat (“ENT”) specialist at the Ear Institute of Chicago, who diagnosed bilateral ear

infections and perforated ear drums. Pet. Ex. 6 at 11. I.R.’s past history of fevers ranging from

103° to 105° were attributed to ear infections. Id. Because of I.R.’s repeated illnesses, the ENT

specialist recommended immunoglobulin testing for possible immunodeficiency. Id. I.R.’s

immunoglobulins A and G were both documented as below normal.11 Pet. Ex. 4 at 65-66. At a

follow-up visit on May 12, 2006, I.R. was improved, had no fever, and was described as playful

and active. Pet. Ex. 6 at 10.

Due to his recurrent acute otitis media with high fevers, I.R. had tympanostomy tubes

inserted on May 23, 2006. Pet. Ex. 6 at 3-4. I.R.’s preoperative diagnosis was recurrent acute

otitis media and bilateral middle ear effusion. Id. at 3. The surgeon’s operative report

documents that I.R. had a history of “recurrent acute otitis media over the past several months

developing recurrent high fevers.” Id.

Following his operation, I.R. travelled with his family to Florida for vacation. On May

26, 2006, while in Florida, I.R.’s father called the pediatrician to report that I.R. had a fever of

103.5°. Pet. Ex. 6 at 9. The pediatrician instructed I.R.’s family to take him to an emergency

department. Pet. Ex. 12 at 3-6. The treating physician in Florida ordered a complete blood count

(“CBC”), which was normal, and diagnosed I.R. with a viral infection. Id.

On June 2, 2006, I.R.’s mother called his pediatrician to report that he had petechiae on

his ear lobe. Pet. Ex. 15 at 44. She called again on June 10, 2006, reporting that I.R. had “3

good days last week with no [symptoms]” but that he had developed a low-grade fever a few

days before and was “acting tired.” Id. at 43. On June 14, 2006, I.R.’s mother reported that I.R.

10

Prevnar 7 is a pneumococcal conjugate vaccine for the prevention of pneumococcal disease

and is recommended for all babies and children younger than two years of age. Pneumococcal

Vaccination: What Everyone Should Know, Ctrs. for Disease Control & Prevention,

https://www.cdc.gov/vaccines/vpd/pneumo/public/index.html (last visited Nov. 7, 2018).

Prevnar 13 is the latest iteration of this vaccine. Id.

11

But see infra Section VI.B.ii.e.

5

had a floppy appearance and was stumbling a lot. Id. at 41. He was also irritable, vomiting, and

had a low-grade fever. Id. The following day, I.R. presented to his pediatrician for a sick visit

and was noted to be irritable, imbalanced, and fatigued. Pet. Ex. 9 at 24. The pediatrician

recommended I.R. be seen by an immunologist; he also ordered a head and sinus CT scan, the

results of which were normal. Id.

At his 18-month well-child exam on June 27, 2006, I.R. was noted to stumble less often,

and his petechiae had cleared. Pet. Ex. 9 at 23. At that visit, his parents reported that I.R. had a

10-word vocabulary. Id. No developmental concerns were noted, and I.R. was described as

“healthy.” Id. Between that visit and July 18, 2006, I.R. experienced ear drainage, which was

treated with medication and ear wicks. Id. at 20.

In August 2006, I.R. underwent an immunology evaluation at Loyola Clinic for Asthma,

Allergy, and Clinical Immunology. Pet. Ex. 11 at 2. Although his IgG2 was below normal, it

was attributed to “a frequent delay in immunity seen in young boys.” Id. at 6-7. Based on the

tests and evaluations, the immunologist concluded that I.R.’s immune system responded

normally to environmental challenges relative to his age. Id. at 7.

I.R.’s two-year well-child exam was December 28, 2006. Pet. Ex. 9 at 17. He presented

with no health problems. Id. He could say at least 20 words. Id. Again, no developmental

concerns were noted. Id. In January 2007, I.R. had bilateral otitis media, ear drainage, and

cough, and was treated with ear drops and antibiotics. Id. at 16. I.R. had no other significant

health problems in January or February 2007.

iii. Evaluation and Diagnosis of Autism

I.R.’s mother first expressed concern about his speech development on March 30, 2007,

more than a year after the vaccinations in question, when I.R. was seen for a follow-up

appointment after an ear infection. Pet. Ex. 9 at 15. I.R. was 27 months of age. Id. He was

saying 20 words, but many were difficult to understand. Id. I.R. also seemed frustrated with his

inability to communicate. Id. The pediatrician diagnosed a speech delay and recommended that

he be evaluated through the Early Intervention Program. Id.

On April 18, 2007, I.R. (28 months old) was evaluated by Jump Start Development

(“Jump Start”). Pet. Ex. 9 at 61-66. The evaluation included a parental interview, clinical

observation, and testing with the Battelle Developmental Inventory.12 Id. The examiners

concluded that I.R. had a delay in personal and social skills and referred him for occupational

therapy. Id. at 66.

12

Battelle Developmental Inventory is a comprehensive development test focused on cognitive,

adaptive, motor, communication, and personal-social behavior. It is most often used to

determine if a child is eligible for therapy services. See generally Abbey T. Berls & Irene R.

McEwen, Battelle Developmental Inventory, Physical Therapy, Aug. 1999, at 776-783.

6

On May 1, 2007, occupational therapists documented that I.R. had a delay with grasping

and visual motor integration. Pet. Ex. 9 at 75. They recommended occupational therapy in a

clinical setting and a “sensory diet.” Id. at 76. To rule out hearing problems as a cause for his

language difficulties, I.R. was referred to the Sertoma Speech and Hearing Center for testing and

evaluation. Pet. Ex. 7 at 2. He passed all screening tests and was deemed not hearing impaired.

Id. at 2-3.

On July 24, 2007, I.R. (31 months old) was referred for an evaluation at Advocate Illinois

Masonic Medical Center. Pet. Ex. 9 at 47. The records note that I.R.’s parents were concerned

about his speech delay that began “after four months of illness,” as well as his “difficult

behaviors that may be due to autism.” Id. at 47. I.R.’s language development history was

reported as follows:

[I.R.’s] first words were at 1 year of age, then he had 15 words at 15 months, but

while sick he had no new words and for a long time had the same 15-20 words. He

has had slow progression since he was ill, and now has about 40 words with a few

2-word utterances.

Id. at 48. Dr. Michael Cupoli, M.D., and other examiners13 assessed I.R.’s developmental and

behavioral skills to determine whether he was delayed as compared to his peers14 and to measure

his age equivalency.15 Id. at 49. I.R. exhibited a significant delay in both cognitive and social-

emotional skills. Id. Based on the testing, he was diagnosed with a sensory processing disorder,

disruptive behavior disorder, and mixed language disorder, and was recommended for

occupational therapy. Id. at 52. I.R. was also evaluated for autism through informal observation,

which yielded unclear results. Id. The examiners recommended that I.R. undergo further testing

to discern whether he had a definitive diagnosis of autism. Id. They also encouraged metabolic

and genetic testing for I.R. Id.

On October 12, 2007, I.R. (33 months) was evaluated for “diagnostic clarification” at the

Children’s Research Triangle. Pet. Ex. 10 at 5. I.R. had difficulty maintaining eye contact and

engaging with the examiners. Id. at 7-8. The examiners concluded that I.R.’s developmental

delays were characteristic of autistic disorder. Id. at 8. Based upon his Childhood Autism

13

Dr. Michael Cupoli is a developmental and behavioral pediatrician. The other examiners

included occupational therapists Lori N. Osborne, Ph.D., and Deborah Margulis, M.S.; physical

therapist Lara Miller; and developmental therapist Melba Carter. See Pet. Ex. 9 at 47.

14

I.R. was 45% delayed in cognitive skills, according to the Mullen Scale of Learning. Pet. Ex.

9 at 49. He was 42-52% delayed in social-emotional development measured by an informal

observation through the Childhood Autism Rating Score (“CARS”) and the Hawaii Early

Learning Profile. Id. I.R.’s gross motor skills showed no delay. Id.

15

I.R.’s level of cognitive skills was assessed as equivalent to a 17-month old and his social-

emotional skills were between 15 and 18 months. Pet. Ex. 9 at 49.

7

Rating Score (“CARS”)16 of 39, I.R. was placed in the severe autistic range. Id. Upon

completion of the evaluation, I.R. was diagnosed with “Autistic Disorder.” Id. at 9. Early

Intervention through the Early Childhood Program was recommended. Id.

Shortly before I.R.’s third birthday, on November 8, 2007, he was seen at the Pfeiffer

Treatment Center, where he underwent biochemical testing.17 Pet. Ex. 8 at 24. After discussing

I.R.’s medical and nutritional history, the physician recommended that I.R. start a gluten and

casein18 free diet and take methyl-B-12 injections. Id. at 32. On December 12, 2007, the Pfeiffer

Treatment Center notified I.R.’s parents that his lab results showed a zinc deficiency and

elevated copper levels. Id. at 48.

At his three-year well-child exam on December 28, 2007, I.R.’s pediatrician noted that

his speech was improving. Pet. Ex. 9 at 11. I.R. was assessed as a well child with autism. Id.

At his four-year visit on January 15, 2009, I.R.’s pediatrician documented that his autism was

less severe. Pet. Ex. 29 at 14.

iv. Genetic Testing and Evaluations for Mitochondrial and

Immunological Disorders

After I.R. received his diagnosis of autism, he underwent testing to identify a causal or

contributing underlying genetic or mitochondrial disorder. On June 26, 2009, I.R. saw Dr.

Marvin R. Natowicz during a stay in the pediatric epilepsy unit at the Cleveland Clinic. Pet. Ex.

29 at 63. Dr. Natowicz was asked to evaluate I.R. to determine a “possible genetic and/or

metabolic basis” for his ASD. Id. Prior diagnostic testing was reviewed and reported as follows:

cranial CT scan (June 2006) normal; blood lymphocyte karyotype (2007) normal; Fragile X

syndrome testing (2007) negative; CBC (2006, 2007, 2009) negative; comprehensive serum

chemistry panel (2007, 2009) negative; serum CK (2007) normal; serum TSH and free T4 (2007)

normal; blood ammonia (2009) normal; IgG (2006) low at 563; IgM (2006) normal; IgA (2006)

low at less than 47; IgG, IgM, and IgA (2006) normal. Id. at 66-67.

16

CARS is a scale used by clinicians to measure the indicators of autism. Ctr. for Autism

Research, http://www.carautismroadmap.org/childhood-autism-rating-scale/ (last visited Nov. 7,

2018).

17

The Pfeiffer Treatment Center (now the Pfeiffer Medical Center) focuses on treating

biochemical imbalances in children through vitamin, minerals, and other nutrient supplements.

Pfeiffer Medical Ctr., http://www.hriptc.org/index.php (last visited Nov. 7, 2018).

18

Casein is a protein present in all mammals’ milk. The most common foods that contain casein

are milks, ice cream, sour cream, yogurt, butter, lunchmeats, and cheese. A casein-free diet

eliminates all foods that contain ingredients that have mammals’ milk. What is Casein?, Talk

About Curing Autism, http://www.tacanow.org/family-resources/what-is-casein/ (last visited

Oct. 9, 2018).

8

I.R.’s physical examination was normal except for findings of a “large body size w/o

disproportionate macrocephaly” and mild hyper-extensibility of hips and fingers. Pet. Ex. 29 at

67-68. Neurological examination was notable for his “neurodevelopmental phenotype, . . . mild

diffuse hypotonia and a question of mild gross motor clumsiness.” Id. at 68. Dr. Natowicz noted

that I.R.’s clinical history, physical exam, and prior diagnostic evaluation did not suggest any

basis for his ASD. Id. I.R.’s motor clumsiness and “possible intolerance of fasting raise[d] a

question of an underlying metabolic basis for his condition,” but Dr. Natowicz stated that a

metabolic condition was not a certainty since no other history or lab data strongly supported a

metabolic cause. Id. In addition to considering a metabolic cause, Dr. Natowicz also wondered

whether I.R. might have a “monogenic non-syndromic process,” given his history of staring

episodes and his EEG pattern. Id. Lastly, Dr. Natowicz proposed the possibility of an

“underlying chromosomal” disorder, noting that the prior chromosomal studies lacked the

“substantial power to detect subtle cytogenic lesions.” Id.

Dr. Natowicz ordered diagnostic tests to screen for metabolic causes or risk factors for

I.R.’s ASD, but no such causes or risk factors were found. Pet. Ex. 29 at 68-69. Blood lactate

levels, pyruvate levels, the plasma acylcarnitine profile, urinalysis, the urinary acylglycine

profile, urinary organic acid analysis, urinary guanidinoacetate analysis, and creatine analysis

were all normal. Id. Plasma amino acid analysis revealed mildly increased plasma glycine19 and

a relative increase in plasma alanine, but the “absolute level of alanine was normal.” Id. DNA

sequencing of the SCN1A gene was normal, although Dr. Natowicz did not rule out other genetic

mutations. Id. The oligonucleotide-based chromosomal microarray analysis and cranial MR

were also normal. Id. The EEG showed “benign focal epileptiform discharges of childhood.”

Id. Testing also did not reveal chromosomal abnormalities. Id. While acknowledging the limits

of diagnostic testing, Dr. Natowicz concluded that it was unlikely that I.R. had a metabolic

disorder because the tests did not reflect evidence of “organic acidemias and mitochondrial

cytopathies, disorders of mitochondrial fatty acid beta-oxidation, [or] disturbances of creatine

synthesis and transport.” Id. He encouraged I.R.’s parents to revisit the issue of genetic

etiologies in the future, given ongoing research and development in the area of ion channel

defects caused by genetic mutations. Id.

On September 24, 2009, I.R. was seen by Dr. Richard E. Frye at University of Texas

Physicians in Houston. Pet. Ex. 25 at 132-34. Dr. Frye noted I.R.’s abnormal EEG and history

of immunoglobulin abnormalities, and recommended testing for cerebral folate deficiency and

medication to treat the abnormal discharges seen on the EEG. Id. at 134. Numerous diagnostic

tests were ordered, including a lumbar puncture. Id. at 88-98.

After the above testing revealed low levels of IgG, I.R. underwent a second

immunological evaluation, this one by Dr. Sudhir Gupta, Chief of Immunology at the University

of California, Irvine. Pet. Ex. 29 at 103. In a letter dated December 18, 2009, Dr. Gupta noted

19

The increase in plasma glycine was not thought significant because I.R. had been receiving

dimethylglycine. Pet. Ex. 29 at 69.

9

I.R.’s “impressive history of recurrent acute and chronic otitis media treated with several courses

of antibiotic.” Id. Given I.R.’s history of ear infections, decreased levels of IgG, and the fact

that he lacked antibodies to polio even though he received the polio vaccine, Dr. Gupta

diagnosed I.R. with “hypogammaglobulinemia with specific antibody deficiency” and

recommended IVIG treatments. Id. Dr. Gupta did not express an opinion about whether I.R. had

a mitochondrial disorder.

On February 25, 2010, Dr. Frye held a conference call with I.R.’s mother and physicians

regarding analysis of I.R.’s cerebrospinal fluid (“CSF”).20 Pet. Ex. 25 at 85. Dr. Gupta

confirmed “elevations in cytokines” consistent with an inflammatory process; Dr. Krigsman (a

GI physician) noted “inflammation in the GI tract”; and Dr. Frye noted “decreased BH4

[consistent with] inflammation.” Id. Dr. Frye also thought I.R. might possibly have a

“secondary mito deficiency due to inflammation,” but added that it was “probably mild

considering the few mito markers found.” Id. Thus, as of February 25, 2010, Dr. Frye

considered the possibility of a mitochondrial deficiency, but had not diagnosed I.R. with a

mitochondrial disorder due to the paucity of diagnostic markers.

To complete his evaluation for a metabolic or mitochondrial disorder, I.R. underwent a

right quadriceps muscle biopsy in February 2011. Pet. Ex. 25 at 18. The biopsy showed “very

good differentiation of [muscle] fiber types,” but no necrosis, regeneration, or phagocytosis. Id.

The biopsy did not show “‘ragged-red’ or ‘ragged-blue’ fibers.” Id. Electron microscopy

revealed “several accumulations of intermyofibrillar enlarged mitochondria,” but “no crystalloid

inclusions.” Pet. Ex. 21 at 2. Mitochondrial respiratory chain enzyme analysis (“ETC”)

performed on the muscle revealed increased citrate synthase activity, suggesting “mitochondrial

proliferation,” a possible “adaptive response to mitochondrial dysfunction.” Pet. Ex. 22 at 3.

Genetic testing for the PTEN mutation21 detected a benign sequence variant. Pet. Ex. 27

at 4. A screening panel for common mutations and deletions in mitochondrial DNA, performed

in May 2011, found no abnormal mutations. Id. at 12. In October 2011, Dr. Frye ordered a

Transgenomic NuclearMitome Test, a “comprehensive gene panel for variants in 448 nuclear

genes important for mitochondrial function.” Pet. Ex. 30 at 4. The test revealed that I.R. had “a

variant of unknown significance in KIAA0196, a gene with autosomal dominant disease

20

Of note, serology studies also performed on I.R.’s CSF in February 2010 revealed that no

antibodies were detectable for Rubeola (measles) or Rubella. Pet. Ex. 25 at 86.

21

“The PTEN gene provides instructions for making an enzyme that is found in almost all tissues

in the body. The enzyme acts as a tumor suppressor, which means that it helps regulate cell

division by keeping cells from growing and dividing too rapidly or in an uncontrolled way.”

PTEN gene, Genetics Home Reference, U.S. Nat’l Library of Med., https://ghr.nlm.nih.gov/

gene/PTEN# (last visited Nov. 7, 2018).

10

inheritance,” and that [t]his genotype could be consistent with spastic paraplegia type 8.”22 Id. at

1. The test also showed that I.R. is a “carrier for a predicted deleterious variant in the POLG, a

gene with autosomal recessive and autosomal dominant disease inheritance.” 23 Id.

On August 31, 2011, using the Morava criteria,24 Dr. Frye concluded that I.R. had “a

probable mitochondrial disorder.” Pet. Ex. 25 at 7. Dr. Frye gave I.R. a score of 7 points,

including 3 points for his history of regression and seizures, 2 points for elevated alanine, and 2

points for the abnormal electron microscopy skeletal muscle biopsy findings. Id.

C. Summary of Affidavits, Fact Testimony, and Additional Evidence

Both of I.R.’s parents provided detailed affidavits about I.R.’s health and development

prior to the December 30, 2005 vaccinations and the changes they observed over the ensuing

months and years. See Pet. Exs. 16-17. Additionally, Mrs. Reed provided oral testimony during

the first day of hearing on April 28, 2015. See Transcript (“Tr.”) at 10-102. Home videos were

also submitted into the record. See Pet. Exs. 138-44.

i. Jeanna Reed Affidavit

Mrs. Reed recounted that prior to receiving the ProQuad and COMVAX vaccines on

December 30, 2005, when he was one year old, I.R. was meeting or exceeding “[a]ll of his

developmental milestones.” Pet. Ex. 16 at 1. She recalled that “[h]e understood commands, he

waved, he said ‘mama, dada, banana’ to name a few words.” Id. He was an “absolutely healthy

one year old.” Id.

22

“Spastic paraplegia type 8 is part of a group of genetic disorders known as hereditary spastic

paraplegias. These disorders are characterized by progressive muscle stiffness (spasticity) and

the development of paralysis of the lower limbs (paraplegia).” Spastic paraplegia type 8,

Genetics Home Reference, U.S. Nat’l Library of Med., https://ghr.nlm.nih.gov/condition/spastic-

paraplegia-type-8 (last visited Nov. 7, 2018).

23

“The POLG gene provides instructions for making the active piece, called the alpha subunit, of

a protein called polymerase gamma (pol γ). . . . Pol γ is a DNA polymerase, which is a type of

enzyme that ‘reads’ sequences of DNA and uses them as templates to produce new DNA.”

POLG gene, Genetics Home Reference, U.S. Nat’l Library of Med., https://ghr.nlm.nih.gov/

gene/POLG (last visited Nov. 7, 2018). DNA polymerases play important roles in the replication

of cells’ genetic material and the repair of DNA and have an important function in mitochondria.

Id. “Mitochondria each contain a small amount of DNA, known as mitochondrial DNA

(mtDNA), which is essential for the normal function of these structures. Pol γ is the only DNA

polymerase that is active in mitochondria and that can replicate mtDNA.” Id.

24

The Morava criteria are discussed further below. See infra Section VI.C.i. They are part of a

“consensus mitochondrial disease scoring system . . . established to facilitate the diagnosis in

patients with a suspected mitochondrial disorder.” Pet. Ex. 71 at 1.

11

A week later, on January 7, 2006, I.R. “came down with a 103+ fever,” which “went up

to 104+” the following day. Pet. Ex. 16 at 1. Because Mrs. Reed was concerned about his

temperature, as well as his unsteadiness when walking, she contacted the pediatrician’s office.

Id. She called the pediatrician’s office again on January 9, when a rash that “looked like the

chicken pox” appeared on his body. Id. She was “reassured this was normal.” Id.

In early February 2006, I.R. developed another high fever, which resolved after three

days, and then a rash on his face and trunk. Pet. Ex. 16 at 2. On February 3, 2006, Mrs. Reed

called the pediatrician’s office to report his condition and inquire about the rash. Id. She

recalled being “reassured by the nurse that it was most likely Roseola and that it would resolve.”

Id. A few weeks later, I.R. developed a rash on his back “that seemed to be spreading in

patches[,] and his cheeks . . . were also very red.” Id. Additionally, he seemed fatigued and

lacked coordination. Id. At an office visit on February 24, 2006, I.R. was diagnosed with

pityriasis rosea. Id. The rash persisted over the next month and spread to his shoulders. Id. At

an office visit on March 23, 2006, I.R.’s pediatrician continued the diagnosis of pityriasis rosea

and reassured that “it would resolve within eight to ten weeks.” Id.

On March 26, 2006, I.R. was taken to an emergency room for fever, vomiting, and blue-

appearing lips and hands, and was diagnosed with viral gastroenteritis and fever. Pet. Ex. 16 at

2. I.R. attended his 15-month checkup a few days later, on March 30, 2006, and was noted to be

“developmentally fine” and “overall a healthy 15[-]month old.” Id. At that visit, he received

DTaP and Prevnar vaccines. Id.

Beginning in April and extending through May, I.R. had a series of illnesses, with

numerous calls and visits to his pediatrician’s office. Pet. Ex. 16 at 2-3. The day after his March

30 visit, Mrs. Reed recalled I.R. having “dark red circles under his eyes” and a “puffy and

swollen” face. Id. at 2. Over the next few weeks he continued to have facial swelling and

developed cough, fever, and rash, as well as otitis media and conjunctivitis. Id. None of the

prescribed treatments, including eye drops, Amoxicillin, and Benadryl, had much effect. Id. On

April 26, 2006, I.R. had “dark purple dots that looked like blood and . . . ‘splotches’ on the

bottom of his earlobes.” Id. Mrs. Reed sent pictures to I.R.’s pediatrician and took I.R. for an

office visit the following day. Id. I.R. was diagnosed with petechiae and a complete blood count

was ordered. Id. The next morning, the I.R. “woke up with petechiae on his forearm down to his

hand.” Id. Despite this development, I.R.’s blood results returned normal, providing “a moment

of relief.” Id.

I.R.’s fever returned a few days later with more severe symptoms. Pet. Ex. 16 at 3. On

May 2, 2006, I.R. was seen by his pediatrician, who determined the best treatment was to

administer a series of antibiotic injections over three consecutive days. Id. The antibiotic

appeared to help. Id. On May 5, 2006, I.R. was seen by an ENT for evaluation of his recurrent

ear infections. Id. at 4. The ENT “ordered an immunoglobulin analysis to evaluate for possible

immunodeficiency.” Id. The results showed below normal levels of immunoglobulin A and G.

Id. At a follow-up visit, the ENT recommended ear tubes be inserted to relieve I.R.’s ear

12

problems. Id. The procedure was performed on May 23, 2006. Id. Another immunoglobulin

test was performed, but this one returned with normal results. Id.

While vacationing in May 2006, I.R.’s fever and petechiae returned, and he suffered

diarrhea. Pet. Ex. 16 at 4. He was examined at a nearby emergency room and diagnosed with

another “viral syndrome.” Id. Throughout the month of June 2006, I.R. continued to experience

a variety of symptoms, including fever, petechiae, diarrhea, vomiting, poor appetite, irritability,

and lethargy. Pet. Ex. 16 at 4. By his 18-month checkup on June 27, 2006, he “seemed to be

getting better” physically, although his behavior was “becoming a bit more challenging.” Id.

The month of July 2006 saw fewer illnesses, and I.R. was “very active.” Pet. Ex. 16 at 5. The

results of an immunology consult and testing at Loyola Medical Hospital on July 24, 2006,

returned as “normal for his age.” Id.

By I.R.’s second birthday in late December 2006, changes in his behavior were starting to

cause concern. Pet. Ex. 16 at 5. Mrs. Reed recalled that he had difficulty sitting still and “was

very frustrated with his speech.” Id. She also remembered that “[t]ime outs were not [an]

effective” form of discipline and that he “seemed to like the physical side of punishment.” Id.

For instance, when they “would put him on the step he would throw himself on it.” Id.

Mrs. Reed’s affidavit also described at length her family’s subsequent efforts to diagnose

I.R.’s condition and care for him. Pet. Ex. 16 at 5-10. She testified similarly during the hearing,

though with some additional detail. Tr. 10-101.

ii. Eric Reed Affidavit

Mr. Reed explained that due to his work schedule, his interactions with I.R. were mostly

limited to evenings and weekends. Pet. Ex. 17 at 1. He indicated that Mrs. Reed watched I.R.’s

development and progress every moment on a daily basis. Id. Nonetheless, Mr. Reed indicated

that he did notice that I.R. tended to get really sick a couple days after regular doctor’s visits and

vaccinations, noting in particular that I.R. had episodes of 104° to 105° fevers for several days in

a row. Id. After noticing this trend, Mr. Reed indicated that he also noticed I.R.’s development

begin to taper off. Id. at 2. Mr. Reed recalled that his speech declined and that he stopped using

words he had been using on a regular basis. Id. He placed this changed at between about one

year of age and eighteen months of age. Id. Mr. Reed also indicated that he observed a change

in temperament as well, noting that after his vaccinations he became hard to manage and very

erratic. Id. Additionally, Mr. Reed described the efforts that his family made to address I.R.’s

condition. Id. at 2-3. Mr. Reed did not testify during the hearing.

iii. Home Videos

In addition to oral and written testimony, petitioners provided extensive video footage

showing I.R. at home and engaged in daily family activity from about six months of age to

shortly after his second birthday. Specifically, the videos were filed on seven discs marked as

13

petitioners’ Exhibits 138 through 144 and include footage from July 10, 2005, to January 23,

2007.

II. Procedural Background

Petitioners filed their claim on September 15, 2008. The case was included in the OAP.25

Supporting evidence was also filed in the form of medical records, labeled as Exhibits 1-15 (ECF

No. 6), and affidavits, labeled as Exhibits 16-17 (ECF No. 7).

On December 12, 2008, respondent filed his Rule 4(c) Report, stating that the case was

not appropriate for compensation. Respondent’s Report (“Resp. Rept.”) dated Dec. 12, 2008

(ECF No. 8). Over the next three years, petitioners filed additional medical records, labeled as

Exhibits 18-19 (ECF No. 9), Exhibit 20 (ECF No. 12), Exhibit 21 (ECF No. 13), and Exhibits

22-29 (ECF No. 14). Petitioners filed an amended petition on February 6, 2012. Amended

(“Am.”) Petition dated Feb. 6, 2012 (ECF No. 16).

Thereafter, another special master received the case and set a deadline for petitioners to

file an expert report. See Order dated Feb. 7, 2012 (ECF No. 18). Petitioners subsequently filed

more records, labeled as Exhibits 30-31 (ECF Nos. 19, 22), and eventually the expert report of

Andrew W. Zimmerman, M.D., designated as Exhibit 32 (ECF No. 27). The special master

25

The OAP was created to manage more than 5,400 petitions alleging that autism or autism

spectrum disorder was caused by either the measles, mumps, and rubella (“MMR”) vaccine or

thimerosal, an ethylmercury preservative used in multi-dose vials of vaccines. See Autism

General Order #1, 2002 WL 31696785 (Fed. Cl. Spec. Mstr. Jul. 3, 2002). Three special masters

conducted separate proceedings in test cases involving these two theories of autism causation.

All found that the petitioners had not provided preponderant evidence of causation, indicating

that the cases were “not a close case.” King v. Sec’y of Health & Human Servs., No. 03-584,

2010 WL 892296, at *90 (Fed. Cl. Spec. Mstr. March 12, 2010) (emphasis removed).

Motions for review were denied in all three cases. Two of the three decisions in the Theory 1

test cases were appealed to the Federal Circuit. Cedillo v. Sec’y of Health & Human Servs., No.

98-916, 2009 WL 331968 (Fed. Cl. Spec. Mstr. Feb. 12, 2009), aff’d, 89 Fed. Cl. 158 (2009),

aff’d, 617 F.3d 1328 (Fed. Cir. 2010); Hazelhurst v. Sec’y of Health & Human Servs., No. 03-

654, 2009 WL 332306 (Fed. Cl. Spec. Mstr. Feb. 12, 2009), aff’d, 88 Fed. Cl. 473 (2009), aff’d,

604 F.3d 1343 (Fed. Cir. 2010). Petitioners in the third test case did not appeal the Court of

Federal Claims’ decision. Snyder v. Sec’y of Health & Human Servs., No. 01-162, 2009 WL

332044 (Fed. Cl. Spec. Mstr. Feb. 12, 2009), aff’d, 88 Fed. Cl. 706 (2009). Petitioners did not

seek review of the special masters’ decisions in the Theory 2 test cases. Dwyer v. Sec’y of

Health & Human Servs., No. 02-1202, 2010 WL 892250 (Fed. Cl. Spec. Mstr. March 12, 2010);

King v. Sec’y of Health & Human Servs., No. 03-584, 2010 WL 892296 (Fed. Cl. Spec. Mstr.

Mar. 12, 2010); Mead v. Sec’y of Health & Human Servs., No. 03-215, 2010 WL 892248 (Fed.

Cl. Spec. Mstr. Mar. 12, 2010). For a comprehensive discussion of the OAP and proceedings

after the conclusion of the test case litigation, see Sturdivant v. Sec’y of Health & Human Servs.,

No. 07-788, 2016 WL 552529 (Fed. Cl. Spec. Mstr. Jan. 21, 2016).

14

ordered petitioners to file a supplemental expert report from Dr. Zimmerman because the one

submitted appeared to “not attribute the alleged vaccine-related injury to a vaccine.” Order dated

Aug. 15, 2012 (ECF No. 28).

The following month, petitioners filed the results of amino acid testing performed by

Richard I. Kelley, M.D., Ph.D., and his interpretation of those results. Pet. Ex. 33 (ECF No.

30).26 On October 15, 2012, petitioners filed Dr. Zimmerman’s supplemental expert report. Pet.

Ex. 34 (ECF No. 31).

On February 1, 2013, respondent filed the expert reports of Bruce H. Cohen, M.D., and

Max Wiznitzer, M.D., along their curriculum vitae (“CV”) and other supporting materials. Resp.

Exs. A-E (ECF No. 34). On February 8, 2013, respondent filed a supplemental Rule 4(c) Report,

maintaining his position that this case was not appropriate for compensation and should be

dismissed. See Resp. Suppl. Rept. dated Feb. 8, 2013 (ECF No. 37).

On February 28, 2013, the special master convened a telephonic status conference to

discuss petitioners’ claim. During the discussion, petitioners’ counsel asked that a hearing in this

case be delayed until she had an opportunity to further consult with experts. The special master

granted petitioners’ request and ordered the filing of regular status reports until petitioners

deemed the case ready for hearing. See Order dated Feb. 28, 2013 (ECF No. 38). For nearly a

year and a half, petitioners filed status reports documenting their efforts to obtain additional

expert evidence. They also filed more medical records during this period, identified as Exhibits

35-38 (ECF Nos. 40-41, 43).

On August 14, 2014, petitioners filed the expert report of Dmitriy Niyazov, M.D. Pet.

Ex. 39 (ECF No. 52). Petitioners subsequently filed Dr. Niyazov’s CV as Exhibit 40 (ECF No.

54) and supporting medical literature as Exhibits 41-65 (ECF No. 56). On October 29, 2014,

respondent filed the expert report of Shawn E. McCandless, M.D., along with his CV and

supporting medical literature. Resp. Exs. F-G (ECF No. 59). On December 1, 2014, petitioners

filed the transcript of a proceeding of the Committee to Review Adverse Effects of Vaccines.

Pet. Ex. 66 (ECF No. 61). The proceeding, which featured respondent’s expert Dr. Cohen,

occurred on August 26, 2009.

On December 5, 2014, petitioners filed a status report stating that the case was now ready

for an evidentiary hearing. Petitioners planned to present the testimony of Drs. Zimmerman and

Niyazov. See Status Report dated Dec. 5, 2014 (ECF No. 62). The special master ordered

respondent to file a status report indicating which experts she intended to present at hearing.27

Order dated Dec 9, 2014 (ECF No. 63). In the interim, the undersigned received the case. See

Order Reassigning Case dated Dec. 11, 2014 (ECF No. 64).

26

The Exhibit was previously filed incompletely (ECF No. 29).

27

The status report was not filed.

15

On January 7, 2015, respondent filed a supplemental expert report from Dr. Cohen.

Resp. Ex. H (ECF No. 66). The following day, the undersigned convened a status conference to

discuss possible hearing dates and to confirm which experts would testify. Additionally, the

undersigned afforded petitioners time to file a supplemental expert report in response to Dr.

Cohen’s supplemental report, provided it did not delay the hearing. See Order dated Jan. 8, 2015

(ECF No. 67). On January 26, 2015, in response to the parties’ feedback, the undersigned

ordered the entitlement hearing for April 28-29, 2015, and set pre-hearing deadlines. Prehr’g

Order dated Jan. 26, 2015 (ECF Nos. 69, 70 (revised)).

From January through April 2015, petitioners filed additional evidence, including

medical and other records, demonstrative materials, and supporting literature.28 Likewise,

respondent filed additional supporting literature.29 On March 16, 2015, petitioners filed a second

amended petition. Second Am. Petition dated filed Mar. 16, 2015 (ECF No. 85). That same day,

petitioners moved for leave to file the report of an expert specializing in the retrospective review

of home videos in cases of early autism. Motion (“Mot.”) dated Mar. 16, 2015 (ECF No. 84).

On March 25, 2015, petitioners and respondent filed their pre-hearing memoranda. (ECF

Nos. 90-91). The following day, the undersigned convened a pre-hearing status conference to

discuss the upcoming hearing, as well as petitioners’ pending motion to file the additional expert

report. At the conclusion of the conference, the parties requested an opportunity to confer and to

file a status report proposing next steps, including whether the hearing should be postponed. The

undersigned granted the parties’ request but ordered petitioners to file the videos they planned to

have their expert analyze. See Order dated Mar. 26, 2015 (ECF No. 95).

On March 31, 2015, petitioners filed a joint status report informing the undersigned that

the parties wished to proceed as scheduled. Joint Status Report dated Mar. 31, 2015 (ECF No.

96). Petitioners also noted that they and respondent had agreed to “table” the issue of video

analysis. Id. Petitioners, however, reserved the right to present a video expert at a later date, and

respondent reserved the right to challenge the merits of any motion by petitioners to add such an

expert. Id.

On April 3, 2015, petitioners filed a Joint Pre-hearing Submission setting forth stipulated

facts, disputed facts, issues not in dispute, and issues remaining to be resolved. Joint Submission

dated Apr. 3, 2015 (ECF No. 98). The parties also reiterated their agreement to table the video

28

Pet. Ex. 67 (ECF No. 68); Pet. Exs. 68-84 (ECF No. 71); Pet. Exs. 85-93 (ECF No. 77); Pet.

Exs. 94-97 (ECF No. 78); Pet. Ex. 98 (ECF No. 79); Pet. Ex. 99 (ECF No. 80); Pet Exs. 100-106

(ECF No. 81); Pet. Exs. 107-109 (ECF No. 86); Pet. Exs. 110-119 (ECF No. 87); Pet. Ex. 120

(ECF No. 88); Pet. Ex. 121 (ECF No. 99); Pet. Ex. 122 (ECF No. 102); Pet. Ex. 123 (refiling of

Exhibit 73) (ECF No. 105).

29

Resp. Ex. H, Tabs 1-9 (ECF No. 72); Resp. Ex. H, Tabs 10-18 (ECF No. 73); Resp. Ex. J

(ECF No. 101); see also Resp. Ex. C, Tabs 1-4 (refiled) (ECF No. 92); Resp. Ex. H, Tabs 2, 4-9

(refiled) (ECF No. 93); Resp. Ex. H, Tabs 10-13, 15, 16, 18 (refiled) (ECF No. 94).

16

analysis issue, adding that neither would offer any testimony about the home videos at hearing.

Id. at 1. In light of this agreement, the parties further agreed that petitioners need not file the

home videos. Id.

On April 22 and 24, 2015, a few days before the hearing, respondent filed the testimony

of Diane Griffin, M.D., Ph.D., an immunologist.30 Respondent stated that the testimony, which

was taken during the OAP, was responsive to petitioners’ argument “that the MMR vaccine has

an immunosuppressive effect.” Notice of Filing dated Apr. 22, 2015, at 1 (ECF No. 101).

Respondent argued that the testimony, which was precisely on point, was appropriately filed in

the current case, as it had been “part of the OAP.” Id. Respondent also noted that petitioners

had not “designated an immunologist or virologist to address their assertions,” and that none of

their current experts had addressed their argument regarding the immunosuppressive effect of the

MMR vaccine. Id. Petitioners did, however, specifically rely on one of Dr. Griffin’s articles.

Id.

The following day, petitioners filed a motion to strike Dr. Griffin’s testimony. Mot.

dated Apr. 25, 2015 (ECF No. 104). Petitioners argued that the testimony was irrelevant and

would “confuse the task of fact-finding” in this case. Id. at 2. They additionally asserted that the

admission of the testimony “would be a failure of due process” because they would be unable “to

confront and cross-examine the witness.” Id.

At the commencement of the entitlement hearing on April 28, 2015, the undersigned

heard oral arguments from the parties concerning petitioners’ motion to strike. The undersigned

granted petitioners’ motion on the basis that respondent had filed the Exhibit outside the time

frame set forth in the pre-hearing order. See Order dated May 1, 2015 (ECF No. 106). The

undersigned, however, granted respondent permission to resubmit the testimony if, at the

conclusion of the hearing, he determined it was still needed. Id.

The hearing proceeded for two full days, recessing on April 29 with testimony remaining.

During the proceeding, petitioners offered the testimony of Mrs. Reed and Dr. Niyazov, and

respondent offered that of Drs. McCandless and Cohen. The parties also produced evidence

during the hearing that had not been entered into the record.31 The undersigned ordered these

documents to be filed within 30 days. See Order dated May 1, 2015 (ECF No. 107).

On May 7, 2015, the undersigned convened a status conference to inquire about the

availability of the parties’ counsel and experts to reconvene and conclude the hearing. See Order

dated May 8, 2015 (ECF No. 109). The parties provided several possible dates and discussed

30

Resp. Ex. I (ECF Nos. 101, 103) (subsequently stricken pursuant to order dated May 1, 2015

(ECF No. 106)). An unrelated medical article, filed as Exhibit J, was not stricken.

31

Pet. Ex. 124 (ECF No. 108); Pet. Exs. 125-34 (ECF No. 116); Pet. Exs. 135-37 (ECF No.

117); Resp. Exs. K-N (ECF No. 118).

17

which experts would offer testimony. Id. at 1. Respondent had not decided whether he would

move for the admission of Dr. Griffin’s transcript testimony and requested more time to make a

determination. Id. Petitioners renewed their objection and advised that they would likely obtain

an opposing expert if the testimony was admitted. Id. Finally, petitioners stated that they did not

intend to obtain a video analysis expert to opine concerning I.R.’s development or to submit any

video evidence. Id. at 2.

On May 27, 2015, the parties requested hearing dates of September 9-10, 2015. See

Order dated May 27, 2015 (ECF No. 115). Petitioners now stated that it was their intention to

call an unidentified video expert, as well as Drs. Zimmerman and Niyazov. Id. Respondent

stated that Drs. Cohen and Wiznitzer would testify, as well as an expert responsive to petitioners’

video expert. Id. In view of the number of experts testifying, and the parties’ difficulty

managing their time during the previous hearing, the undersigned informed the parties that an

additional day of hearing was necessary to ensure receipt of all anticipated testimony. Id.

On June 9, 2015, the parties confirmed their availability to reconvene the hearing on

September 9-11, 2015, in Washington, D.C. See Order dated June 10, 2015 (ECF No. 119).

Petitioners also identified Ashley Freuler, Ph.D., as their video analysis expert. Id. The

undersigned set deadlines for the submission of Dr. Freuler’s expert report, and a responsive

report from a yet-to-be-identified expert for respondent. Id. On July 10, 2015, petitioners filed

Dr. Freuler’s expert report and CV as Exhibits 145-46 (ECF No. 124) and supporting medical

literature as Exhibits 147-70 (ECF No. 125). Petitioners also filed select home video footage as

Exhibits 138-44 (ECF No. 123).

On June 22, 2015, respondent submitted a status report stating her desire to resubmit Dr.

Griffin’s transcript testimony. Status Report dated June 22, 2015 (ECF No. 120). Petitioners

again moved to “exclude inadmissible evidence.” Mot. dated June 22, 2015 (ECF No. 121).

Respondent filed a timely response. Resp. Resp. to Mot. dated July 9, 2015 (ECF No. 122).

On July 16, 2015, the undersigned convened a telephonic status conference to discuss the

pending hearing. See Order dated July 20, 2015 (ECF No. 126). The parties confirmed that their

experts remained available to testify; however, Dr. Freuler, petitioners’ video analysis expert,

would have to testify via videoconferencing. Id. at 1. After an extended discussion about this

development, the undersigned advised that Dr. Freuler’s testimony would not be conducive to

long-distance videoconferencing and that petitioners would have to devise an alternate plan.32

Id. As for the identity of respondent’s video analysis expert, respondent reported that Dr.

Wiznitzer had been selected and that his report was forthcoming. Id. Finally, the undersigned

addressed petitioners’ renewed motion to exclude Dr. Griffin’s testimony. Id. at 2. The parties

agreed that a decision on the motion should be stayed pending further proceedings, but that the

transcript testimony would remain excluded at the hearing. Id.

32

The parties agreed to consider a change of venue to enable Dr. Freuler to testify in person.

Order dated July 20, 2015, at 1 (ECF No. 126).

18

On July 29, 2015, the parties informed the undersigned that the hearing would need to be

rescheduled. See Order dated July 31, 2015 (ECF No. 127). The undersigned ordered a joint

status report in 30 days proposing new dates. Id. On August 28, 2015, respondent filed Dr.

Wiznitzer’s responsive video analysis report and supporting articles as Exhibit O, Tabs 1-5 (ECF

No. 130).33 That same day, the parties chose February 4-5, 2016, as the new dates, and

confirmed Washington, D.C., as the location.34 See Order dated Aug. 31, 2015 (ECF No. 131).

They advised, however, that because of certain scheduling conflicts with two experts, an

additional proceeding would be needed.35 Id.

On December 16, 2015, petitioners informed the undersigned that their video expert, Dr.

Freuler, had unexpectedly resigned from the case due to a personal crisis. See Order dated Dec.

18, 2015 (ECF No. 138). Petitioners had retained another expert to review the videos and

prepare a report. Id. As a consequence of this development, the parties were no longer prepared

for the hearing in February and proposed that the hearing now be held on June 22-24, 2016. Id.

The undersigned approved these dates and rescheduled the hearing. See Prehr’g Order dated Jan.

12, 2016 (ECF No. 140).

Over the next several months, the parties filed additional evidence and various pre-

hearing submissions.36 On February 22, 2016, petitioners filed the report of their new video

expert, Kaitlyn Wilson, Ph.D., along with her CV, as Exhibits 176-77 (ECF No. 142).

Supporting literature was subsequently filed as Exhibits 178-84 (ECF No. 143). On March 24,

2016, respondent filed a second supplemental expert report from Dr. Wiznitzer, along with

supporting literature, as Exhibit P, Tabs 1-3 (ECF No. 144). Petitioners filed a pre-hearing brief

on May 6, 2016 (ECF No. 145), and respondent filed one on May 31, 2016 (ECF No. 149).

On June 8, 2016, the undersigned convened a pre-hearing status conference. See Order

dated June 10, 2016 (ECF No. 153). The parties confirmed that they were prepared to resume

the entitlement hearing. Id. at1. During the conference, the undersigned learned that petitioners’

counsel had not provided respondent’s counsel with certain hearing-related materials, including a

detailed list of the video segments to be discussed by petitioners’ video expert. Id. at 2. The

33

Petitioners elected to not file a reply supplemental expert report from Dr. Freuler. Status

Report dated Sept. 4, 2015 (ECF No. 132).

34

Subsequently, the parties requested that the hearing be rescheduled for February 3-4, 2016.

See Order dated Sept. 8, 2015 (ECF No. 133).

35

The parties selected June 22-23, 2016, for a third proceeding with the two experts. See Order

dated Nov. 9, 2015 (ECF No. 137).

36

Pet. Exs. 171-73 (literature) (ECF No. 139); Pet. Exs. 174-75 (medical records) (ECF No.

141); Pet. Exs. 185-91 (literature) (ECF No. 148); Pet. Exs. 192-93 (updated CV for Dr.

Niyazov; literature) (ECF No 152); Pet. Ex. 194 (medical records) (ECF No. 154); Pet. Exs. 195-

97 (literature and demonstrative exhibit) (ECF No. 155).

19

undersigned reminded the parties that “‘ambush’ tactics have no place in the Vaccine Program,”

and she instructed them to share such information prior to the hearing.37 Id. Respondent’s

counsel stated that he did not have an illustrative presentation prepared for the hearing but would

share it with opposing counsel if one was created. Id. In any case, respondent’s counsel agreed

to file a list of the video clips to be discussed by his expert.38 Id. The undersigned also briefly

discussed respondent’s request to refile the testimony of Dr. Griffin and petitioners’ renewed

motion to exclude. Id. The undersigned informed the parties that a decision on this issue would

not be made until the hearing concluded, and as such, the testimony would remain excluded from

the hearing. Id. The undersigned also acknowledged respondent’s objection to petitioners’

submission of additional articles unrelated to the video testimony and unreferenced by any of

their experts. Id. Respondent requested and was granted relief to supplement the record, if

necessary, after the hearing. Id.

On the morning of the first day of the continued hearing, petitioners filed a motion in

limine to exclude, postpone, or limit the planned video testimony. Mot. in Limine dated June 22,

2016 (ECF No 157). Petitioners argued that they had been unfairly prejudiced when, in

compliance with the undersigned’s order, they filed a streamlined list “of actual presentation

footage” to be shown at the hearing, while respondent subsequently designated all of the video

footage for possible use. Id. at 1-2. Petitioners asserted that this allowed respondent to better

prepare for the cross-examination of petitioners’ video expert and the direct examination of his

own expert, while precluding petitioners from doing the same. Id. at 2-3. Petitioners proposed

several remedies, involving various combinations of excluding, postponing, or limiting the

anticipated testimony. Id. at 3. The undersigned addressed petitioners’ pending motion at the

start of the hearing. Tr. 563-73. Following a lengthy discussion, the parties reached a

compromise agreement that allowed both parties to present their video testimony as anticipated.

Id.

The hearing thereafter proceeded as planned from June 22 to 24, 2016, in Washington,

D.C., with Drs. Niyazov, Zimmerman, and Wilson testifying for petitioners, and Drs. Cohen and

Wiznitzer testifying for respondent. Following the hearing, the undersigned ordered petitioners

to report whether they intended to offer rebuttal testimony, and whether they wished to file a

post-hearing brief. The parties were also ordered to submit any evidence produced during the

hearing but not yet filed into the record.39 See Order dated June 27, 2016 (ECF No. 158).

37

That same day, petitioners’ counsel filed a list of the video clips Dr. Wilson intended to

display and discuss during the hearing. Status Report dated June 8, 2016 (ECF No. 151).

38

Respondent filed the list of video clips Dr. Wiznitzer intended to reference during his

testimony. Status Report dated June 20, 2016 (ECF No. 156).

39

Pet. Exs. 198-202 (responsive report of Dr. Wilson; literature) (ECF No. 166); Pet. Ex. 203

(Dr. Wilson’s PowerPoint presentation) (ECF No. 167); Pet. Ex. 204 (compilation of

mitochondrial exhibits) (ECF No. 173); Pet. Ex. 205 (mutation database) (ECF No. 177); Resp.

Exs. Q-R (ECF No. 168); Resp. Ex. S (demonstrative video clips) (ECF No. 169).

20

On August 16, 2016, petitioners filed a status report stating they did not intend to provide

rebuttal testimony from Drs. Zimmerman or Wilson. Status Report dated Aug. 16, 2016 (ECF

No. 175). However, they were undecided about refuting respondent’s recently filed Exhibit R (a

printout of a database of mutations in DNA polymerase gamma (POLG) discussed at hearing)

and they requested additional time to make that decision. On September 15, 2016, petitioners

filed a rebuttal to Exhibit R from Dr. Niyazov, along with supporting materials.40

On September 30, 2016, respondent requested and was granted an opportunity to file a

supplemental report from Dr. Cohen responsive to Dr. Niyazov’s rebuttal report addressing

Exhibit R. See Order dated Sept. 30, 2016 (ECF No. 185). The supplemental report and

supporting literature were filed on October 28, 2016.41 On October 31, 2016, petitioners filed a

motion to strike Dr. Cohen’s supplemental report and supporting literature. Mot. dated Oct. 31,

2016 (ECF No. 187). A response and reply were filed in due course. Resp. Resp. to Mot. dated

Nov. 22, 2016 (ECF No. 189); Pet. Reply to Resp. Resp. to Mot. dated Dec. 2, 2016 (ECF No.

190).

On January 9, 2017, petitioners filed their post-hearing brief. Pet. Posthr’g Br. dated Jan.

9, 2017 (ECF No. 193). On April 5, 2017, respondent file his post-hearing brief. Resp. Posthr’g

Br. dated Apr. 5, 2017 (ECF No. 196). Petitioners filed a reply post-hearing brief on April 28,

2017. Pet. Reply Posthr’g Br. dated Apr. 28, 2017 (ECF No. 198). The evidentiary record is

now closed and the case is ripe for adjudication.

III. Rulings on Pending Motions

Two evidentiary motions remain pending in this case. They are (1) petitioners’ motion to

exclude Dr. Griffin’s testimony, and (2) petitioners’ motion to strike Dr. Cohen’s supplemental

report, Exhibit T, including accompanying tabs 1 through 4. These motions are resolved within

the analysis below. The motion to exclude Dr. Griffin’s testimony is addressed in Section

VI.B.i, below. For the reasons discussed there, petitioners’ motion to exclude Dr. Griffin’s

testimony is DENIED as MOOT. The motion to strike Dr. Cohen’s supplemental report is

addressed in Section VI.C.ii, below. For the reasons discussed there, petitioners’ motion is

DENIED.

IV. Standards for Adjudication

A. Petitioners’ Burden in Vaccine Program Cases

The Vaccine Act established the Program to compensate vaccine-related injuries and

deaths. § 300aa-10(a). “Congress designed the Vaccine Program to supplement the state law

40

Pet. Exs. 206-09 (ECF No. 181).

41

Resp. Ex. T, Tabs 1-4 (ECF No. 186).

21

civil tort system as a simple, fair and expeditious means for compensating vaccine-related

injured persons. The Program was established to award ‘vaccine-injured persons quickly, easily,

and with certainty and generosity.’” Rooks v. Sec’y of Health & Human Servs., 35 Fed. Cl. 1, 7

(1996) (quoting H.R. Rep. No. 908 at 3 (1986), as reprinted in 1986 U.S.C.C.A.N. at 6287,

6344).

To establish causation-in-fact, a petitioner must show by a preponderance of the evidence

that but for the vaccination, the petitioner would not have been injured, and that the vaccination

was a substantial factor in bringing about the injury. Cedillo v. Sec’y of Health & Human

Servs., 617 F.3d 1328, 1338 (Fed. Cir. 2010); Shyface v. Sec’y of Health & Human Servs., 165

F.3d 1344, 1352 (Fed. Cir. 1999). Proof of actual causation must be supported by a sound and

reliable “medical or scientific explanation that pertains specifically to the petitioner’s case,

although the explanation need only be ‘legally probable, not medically or scientifically certain.’”

Moberly v. Sec’y of Health & Human Servs., 592 F.3d 1315, 1322 (Fed. Cir. 2010) (quoting

Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 548-49 (Fed. Cir. 1994)); see also

Grant v. Sec’y of Health & Human Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992) (“[P]etitioners

must show a medical theory causally connecting the vaccination and the injury.”). “[A]

petitioner must demonstrate the reliability of any scientific or other expert evidence put forth to

carry their burden. Expert testimony, in particular, must have some objective scientific basis in

order to be credited by the Special Master.” Jarvis v. Sec’y of Health & Human Servs., 99 Fed.

Cl. 47, 54-55 (2011) (citing Moberly, 592 F.3d at 1322; Cedillo, 617 F.3d at 1339; Terran v.

Sec’y of Health & Human Servs., 195 F.3d 1302, 1316 (Fed. Cir. 1999)).

Causation is determined on a case-by-case basis, with “no hard and fast per se scientific

or medical rules.” Knudsen, 35 F.3d at 548. A petitioner may use circumstantial evidence to

prove the case, and “close calls” regarding causation must be resolved in favor of the petitioner.

Althen v. Sec’y of Health & Human Servs., 418 F.3d 1274, 1280 (Fed. Cir. 2005).

To receive compensation under the Program, petitioners must prove either (1) that I.R.

suffered a “Table Injury” – i.e., an injury listed on the Vaccine Injury Table – corresponding to a

vaccine that he received, or (2) that I.R. suffered an injury that was actually caused by the

vaccine (or vaccines) he received. See §§ 13(a)(1)(A) and 11(c)(1); Capizzano v. Sec’y of

Health & Human Servs., 440 F.3d 1317, 1319-20 (Fed. Cir. 2006). Petitioners must show that a

vaccine was “not only a but-for cause of the injury but also a substantial factor in bringing about

the injury.” Moberly, 592 F.3d at 1321 (quoting Shyface, 165 F.3d at 1352-53).

Although the Vaccine Table includes an injury of encephalopathy (or encephalitis)

suffered five to 15 days after administration of the MMRV vaccine or one of its components,

petitioners did not pursue the Table Injury. Moreover, to qualify as a Table Injury, the

encephalopathy petitioners claims I.R. suffered would have to satisfy the more narrow definition

of encephalopathy contained in the Qualifications and Aids to Interpretation (“QAI”) section of

22

the Vaccine Injury Table.42 See 42 C.F.R. § 100.3(c)(2). Here, the medical records and expert

reports do not support an allegation of a Table encephalopathy, even if petitioners had decided to

pursue that allegation.

Because petitioners cannot show that I.R. suffered a Table injury, they must prove that a

vaccine or vaccines I.R. received caused his injury. To do so, they must show by preponderant

evidence (1) a medical theory causally connecting a vaccine and I.R.’s injury (“Althen Prong

One”); (2) a logical sequence of cause and effect showing that a vaccine was the reason for his

injury (“Althen Prong Two”); and (3) a showing of a proximate temporal relationship between a

vaccine and his injury (“Althen Prong Three”). Althen, 418 F.3d at 1278; § 13(a)(1) (requiring

proof by a preponderance of the evidence).

Since Althen, the Federal Circuit has addressed the causation-in-fact standard in several

additional rulings, which have affirmed the applicability of the Althen test and afforded further

instruction for determining causation-in-fact. In Capizzano v. Sec’y of Health & Human Servs.,

440 F.3d 1317, 1326 (Fed. Cir. 2006), the court cautioned Program fact-finders against narrowly

construing the second element of the Althen test, confirming that circumstantial evidence and

medical opinion, sometimes in the form of notations of treating physicians in the vaccinee’s

medical records, may in a particular case be sufficient to satisfy that second element of the

Althen test. Both Pafford v. Sec’y of Health & Human Servs., 451 F.3d 1352, 1355 (Fed. Cir.

2006), and Walther v. Sec’y of Health & Human Servs., 485 F.3d 1146, 1149-50 (Fed. Cir.

2007), discussed the issue of which party bears the burden of ruling out potential non-vaccine

causes. DeBazen v. Sec’y of Health & Human Servs., 539 F.3d 1347, 1350-52 (Fed. Cir. 2008),

explored what evidence the special master may consider in deciding the initial question of

whether the petitioner has met her causation burden. The issue of the temporal relationship

between vaccination and the onset of an alleged injury was further discussed in Locane v. Sec’y

of Health & Human Servs., 685 F.3d 1375, 1380-81 (Fed. Cir. 2012), and W.C. v. Sec’y of

Health & Human Servs., 704 F.3d 1352, 1358 (Fed. Cir. 2013). Moberly v. Sec’y of Health &

Human Servs., 592 F.3d 1315, 1322-23 (Fed. Cir. 2010), concluded that the “preponderance of

the evidence” standard that applies to Vaccine Act cases is the same as the standard used in

traditional tort cases, so that conclusive proof involving medical literature or epidemiology is not

needed, but demonstration of causation must be more than “plausible” or “possible.” Both

Andreu v. Sec’y of Health & Human Servs., 569 F.3d 1367, 1379 (Fed. Cir. 2009), and Porter v.

Sec’y of Health & Human Servs., 663 F.3d 1242, 1253-54 (Fed. Cir. 2011), considered when a

determination concerning an expert’s credibility may reasonably affect the outcome of a

causation inquiry. Broekelschen v. Sec’y of Health & Human Servs., 618 F.3d 1339, 1345-46

(Fed. Cir. 2010), found that it was appropriate for a special master to determine the reliability of

42

As explained in Waddell, “[t]he scope of the medical term ‘encephalopathy’ is more expansive

than the narrower, statutory definition set forth in the Table.” Waddell v. Sec’y of Health &

Human Servs., No. 10-316, 2012 WL 4829291, at *12 (Fed. Cl. Spec. Mstr. Sept. 19, 2012).

Encephalopathy as generally used means “any degenerative disease of the brain.” Dorland’s at

614. “The QAI definition of acute encephalopathy simply does not encompass every type of

brain dysfunction to which the broader meaning of ‘encephalopathy’ applies.” Blake v. Sec’y of

Health & Human Servs., No. 03-31, 2014 WL 2769979, at *6 (Fed. Cl. Spec. Mstr. May 21,

2014).

23

a diagnosis before analyzing the the likelihood of vaccine causation. Lombardi v. Sec’y of

Health & Human Servs., 656 F.3d 1343, 1351-52 (Fed. Cir. 2011), and Hibbard v. Sec’y of

Health & Human Servs., 698 F.3d 1355, 1364-65 (Fed. Cir. 2012), both again explored the

importance of assessing the accuracy of the diagnosis that supports a claimant’s theory of

causation. Doe 11 v. Sec’y of Health & Human Servs., 601 F.3d 1349, 1356-58 (Fed. Cir. 2010),

and Deribeaux v. Sec’y of Health & Human Servs., 717 F.3d 1363, 1369 (Fed. Cir. 2013), both

discuss the burden of proof necessary to establish that a “factor unrelated” to a vaccine may have

caused the alleged injury.

Where, as here, petitioners in a cause-in-fact or “off Table” case seek to prove that their

vaccination aggravated a pre-existing injury, the court must apply three additional factors

originating from the standard for assessing aggravation claims in “Table” injury cases. See

Loving v. Sec’y of Health & Human Servs., 86 Fed. Cl. 135, 144 (Fed. Cl. 2009). The additional

Loving factors require petitioners to demonstrate aggravation by addressing (1) the vaccinee’s

condition prior to the administration of the vaccine, (2) the vaccinee’s current condition, and (3)

whether the vaccinee’s current condition constitutes a “significant aggravation” of the condition

prior to the vaccination. Id.

Another important aspect of the causation-in-fact case law under the Vaccine Act

concerns the factors that a special master should consider in evaluating the reliability of expert

testimony and other scientific evidence. In Daubert v. Merrell Dow Pharm., Inc., 509 U.S. 579

(1993), the Supreme Court listed certain factors that federal trial courts should utilize in

evaluating proposed expert testimony concerning scientific issues. In Terran, 195 F.3d at 1316,

the Federal Circuit ruled that it is appropriate for special masters to utilize the Daubert factors as

a framework for evaluating the reliability of causation-in-fact theories presented in Program

cases.

B. Law Governing Factual Determinations

The process for making factual determinations in Vaccine Program cases begins with

consideration of the medical records. See § 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.” § 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)

(emphasizing that it is within the special master’s discretion to afford greater weight to

contemporaneous medical records than to other evidence, such as oral testimony given at a later

date).

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

24

health problems). Curcuras v. Sec’y of Health & Human Servs., 993 F.2d 1525, 1528 (Fed. Cir.

1993); Doe/70 v. Sec’y of Health & Human Servs., 95 Fed. Cl. 598, 608 (2010) (“Given the

inconsistencies between petitioner’s testimony and his contemporaneous medical records, the

special master’s decision to rely on petitioner’s medical 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). This presumption is based on the linked propositions that (1) sick people visit medical

professionals; (2) sick people honestly report their health problems to those professionals; and

(3) 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. 11-685, 2013

WL 1880825, at *2 (Fed. Cl. Spec. Mstr. Apr. 10, 2013); Curcuras, 26 Cl. Ct. 537, 543 (1992),

aff’d, 993 F.2d 1525 (Fed. Cir. 1993) (“It 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, they should be

afforded substantial weight. See Lowrie v. Sec’y of Health & Human Servs., No. 03-1585, 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. Curcuras, 993 F.2d at 1528;

see also Murphy v. Sec’y of Health & Human Servs., 23 Cl. Ct. 726, 733 (1991) (favorably

citing the special master’s determination that “oral testimony which is in conflict with

contemporaneous documents is entitled to little evidentiary weight”), aff’d, 968 F.2d 1226 (Fed.

Cir. 1992).

However, compelling oral testimony may be more persuasive than written records in

some situations, 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) (“[L]ike 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 (“Written 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 special master must evaluate the witness’ credibility before determining the weight

to afford such testimony. See Andreu v. Sec’y of Health & Human Servs., 569 F.3d 1367, 1379

(Fed. Cir. 2009); 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. 90-2808, 1998 WL 408611, at *5 (Fed. Cl. Spec. Mstr. June 30, 1998)). In

25

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 of Health & Human Servs., 110 Fed. Cl. 184, 203-04 (2013), aff’d, 746

F.3d 1334 (Fed. Cir. 2014). In determining whether to afford greater weight to contemporaneous

medical records than to contrary testimony, there must be evidence that this decision was the

result of a rational determination. Burns, 3 F.3d at 416-17.

V. Expert Testimony

Petitioners allege that I.R. “suffered a significant aggravation of a preexisting condition, a

mitochondrial disorder, causally related to the ProQuad vaccine administered on December 30,

2005,” which in turn caused I.R. “to suffer from immunodeficiency disorder, bowel disease,

pathological neuroinflammation, seizure disorder, mitochondrial dysfunction and the resulting

features of autism spectrum disorder.” Second Am. Petition at ¶¶ 43-44. Regarding this

proposition, the following expert evidence was heard.

A. Petitioners’ Experts

i. Dmitriy Niyazov, M.D.

Dmitriy Niyazov, M.D., was proffered by petitioners without objection as an expert in the

areas of genetics and mitochondrial medicine. Tr. 114.

a. Education and Background

Dr. Niyazov earned his undergraduate degree in biology from the University of

California at Los Angeles in 1996 and his M.D. from the University of Rochester School of

Medicine in 2001. Pet. Ex. 192 at 1; Tr. 105-06. He completed residencies in otolaryngology

and medical genetics at Emory University School of Medicine. Id. Dr. Niyazov is licensed to

practice medicine in the state of Louisiana and is a diplomate of the American Board of Medical

Genetics. Id.

Currently, Dr. Niyazov is section head of medical genetics in the department of pediatrics

at the Ochsner Clinic Foundation in New Orleans, Louisiana. Pet. Ex. 192 at 1; Tr. 105. He is

also an instructor in the combined medical student and residency program at Ochsner Clinic and

Tulane University School of Medicine and a senior lecturer for the joint medical student program

between Ochsner Clinic and the University of Queensland School of Medicine. Pet. Ex. 192 at

2; Tr. 106. Dr. Niyazov specializes in mitochondrial medicine as a branch of genetics. Tr. 106.

Previously, he was a research associate in the departments of human genetics and biomedical

engineering at Emory University School of Medicine. Pet. Ex. 192 at 2.

26

Dr. Niyazov is a fellow of the American College of Medical Genetics and is also

affiliated with the American Society of Human Genetics and the Mitochondrial Medicine

Society. Pet. Ex. 192 at 1. He is a member of the editorial board of both Clinical Syndromology

and the Journal of Molecular Genetics and Metabolism. Id. Dr. Niyazov lists 30 publications on

his CV, as well as numerous presentations. Pet. Ex. 192 at 2-13; Tr. 106-07.

b. Opinion

Applying two different sets of diagnostic criteria, as well as noting the presence of a

heterozygous POLG mutation (explained below), Dr. Niyazov opined that I.R. “experienced

developmental regression and autism, caused by a vaccine reaction, which exacerbated his

deficient cellular energy metabolism due to his POLG mutation.” Pet. Ex. 39 at 4. Dr. Niyazov

also asserted that “it’s more likely than not that [I.R.]’s infection rate increased with more

vaccinations because his immune system was weakened by the vaccinations and his

[mitochondrial disorder]. Even if infections played a role in [I.R.]’s regression and autism, the

vaccinations were a substantial factor in causing the injury without which it wouldn’t have

occurred.” Id. at 5. Dr. Niyazov further opined:

When a stress event such as infection or vaccine (both of which carry antigens)

enters the body it produces inflammatory response and catabolism which requires

a significant amount of ATP. Immune response to vaccines has been shown to last

for weeks and months and vaccination was unequivocally demonstrated to cause

oxidative stress in humans. Developmental regression is a hallmark of

[mitochondrial disorders] but a certain magnitude of threshold need to be exceeded

to trigger decompensation and ATP depletion. Each individual affected person

has his or her own threshold based on a variety of cumulative factors over a period

of time such as degree and duration of an impact in relationship to this person’s

percentage of mitochondrial heteroplasmy in different organs and tissues.

Moreover, owing to its waxing and waning nature, [mitochondrial disorders] can

cause mitochondrial dysfunction that can reach this threshold more than once[,]

often triggered by a catabolic stressor as in the case of [I.R.]’s vaccinations which

served as catabolic events that expedited the threshold of his regression after both

12- and 15-month shots.43

Pet. Ex. 39 at 5-6 (internal citations omitted).

43

Although Dr. Niyazov’s report references vaccines other than the ProQuad vaccine that I.R.

received on December 30, 2005, petitioners allege that only the ProQuad vaccine caused any

injury. See Second Am. Petition at ¶¶ 43-44. Furthermore, consideration of I.R.’s other

vaccinations would not change the undersigned’s analysis.

27

ii. Kaitlyn Wilson, Ph.D.

Kaitlyn Wilson, Ph.D., was proffered by petitioners without objection as an expert in

speech-language pathology and as an expert in Retrospective Video Analysis (“RVA”) in autism.

Tr. 621.

a. Education and Background

Dr. Wilson earned her undergraduate degree in communication sciences and disorders

from Florida State University in Tallahassee, Florida, in 2004 and a master’s degree and

doctorate in speech and hearing sciences from the University of North Carolina at Chapel Hill in

2006 and 2012, respectively. Pet. Ex. 177 at 1. In 2014, she completed a post-doctoral

fellowship at the Kennedy Krieger Institute, where she worked in the Center for Autism and

Related Disorders. Id. at 2. She is licensed by the Maryland State Board of Audiologists,

Hearing Aid Dispensers, and Speech-Language Pathologists. Id. She is also certified as a

speech-language pathologist by ASHA, the American Speech-Language-Hearing Association.

Id.

Currently, Dr. Wilson is an assistant professor and clinical supervisor in the department

of audiology, speech-language pathology, and deaf studies at Towson University. Pet Ex. 177 at

1. Previously, she worked for six years, dating back to her time as a graduate research assistant

with Dr. Grace Baranek from 2004 to 2006, with the Program in early Autism Research,

Leadership, and Service (“PEARLS”) based at the University of North Carolina Chapel Hill. Id.

at 3; Tr. 585, 594, 597.

Dr. Wilson is a peer reviewer for several publications, including the Journal of Early

Intervention, the Journal of Autism and Developmental Disorders, and the Journal of Speech,

Language, and Hearing Research. Pet Ex. 177 at 8. She is a member of both the International

Society for Autism Research and the American Speech-Language Hearing Association. Id. She

lists seven journal articles and two book chapters on her CV, as well as numerous presentations.

Id. at 4-6.

b. Opinion

Upon review of the video footage filed in this case, Dr. Wilson opined that “I did not find

clear markers of autism in the earliest home videos provided for [I.R.]. Many children who will

later be diagnosed with autism exhibit characteristics, or red flags, prior to their first birthday. I

begin to see clear (vs. ambiguous or possible) markers that raise red flags for autism starting

around 15 months of age and after. . . . Later videos primarily focused on the baby brother and

the context became increasingly non-continuous.” Pet. Ex. 176 at 4.

28

iii. Andrew Zimmerman, M.D.

Andrew Zimmerman, M.D., was proffered by petitioners without objection as an expert

in pediatric neurology with specialty in autism. Tr. 681.

a. Education and Background

Dr. Zimmerman earned his undergraduate degree in Germanic languages and literatures

from Princeton University in 1966 and this M.D. from Columbia University in 1970. Pet. Ex.

125 at 1; Tr. 678-80. He completed a residency in pediatrics at C.S. Mott Children’s Hospital,

University of Michigan Hospitals, in 1972 and a residency in neurology at Johns Hopkins

Hospital in 1977. Pet. Ex. 125 at 1. He is licensed to practice medicine in Maryland and

Massachusetts and is board certified in pediatrics as well as psychiatry and neurology, with

special competence in child neurology. Id. at 13.

Currently, Dr. Zimmerman is an associate professor in epidemiology at Johns Hopkins

Bloomberg School of Public Health as well as an associate professor of pediatrics and neurology

at Harvard Medical School. Pet. Ex. 125 at 2. He is also a clinical professor of pediatrics at the

University of Massachusetts Medical School. Id. Dr. Zimmerman is a staff physician at both

Johns Hopkins Hospital (pediatric neurology) and Kennedy Krieger Institute (neurology and

developmental medicine). Id. He is also the Director of Medical Research for the Center for

Autism and Related Disorders at Kennedy Krieger Institute. Id. He has had numerous prior

academic and hospital appointments. Id. at 1-2.

Dr. Zimmerman has been a conference organizer for Autism Speaks, past President of

Medical Staff at Kennedy Krieger Institute, and a panel member for the National Institutes of

Health Development Conference on Neurofibromatosis. Pet Ex. 125 at 3. He is a member of,

inter alia, the American Academy of Neurology as well as the American Academy of Pediatrics,

for which he was a member of the Executive Committee for the Section on Neurology from 1998

to 2001. Id. He is a peer reviewer for many publications, including the New England Journal of

Medicine, Pediatrics, the Journal of Autism and Developmental Disorders, Autism Research, and

the Journal of Child Neurology. Id. at 4-5. He lists 78 peer-reviewed publications on his CV, as

well as numerous presentations. Id. at 16-22; Tr. 680-81.

b. Opinion

Dr. Zimmerman opined that “[i]t is my opinion, based on a reasonable degree of medical

certainty, that [I.R.]’s autistic regression following immunizations can be explained by the

underlying genetic, metabolic and immune abnormalities that have been carefully documented in

his medical record.” Pet. Ex. 32 at 1. Dr. Zimmerman explained the basis for his opinion as

follows:

29

From my previous experience and subsequent studies by others, it is apparent that

certain abnormalities of cellular mitochondrial energy metabolism are associated

with a susceptibility to developmental regression leading to autism. The

relationship of immune dysfunction to mitochondrial abnormalities in such children

is not known, but may also be related to the underlying genetic abnormality and

compounds their susceptibility to metabolic stress during infections or with certain

immunizations.

Id.

With regard to the facts of this case, Dr. Zimmerman opined:

[I.R.]’s initial reaction to vaccination on January 18, 2006 at 12 months of age, with

a rash and temperature of 104° (diagnosed as roseola), was followed by recurrent

infections for 5 months. Neurological symptoms became clinically evident at 17

months in postural unsteadiness and ataxia of gait, then regression in both language

and social skills around 24 months of age. The evolution of immunological stress

following immunization, combined with the underlying mitochondrial disorder, led

to the diagnosis of autism.

Pet. Ex. 32 at 1.

B. Respondent’s Experts

i. Shawn McCandless, M.D.

Shawn McCandless, M.D., was proffered by respondent as an expert in clinical genetics,

as well as mitochondrial and metabolic disorders and general pediatrics. Tr. 334. The

undersigned accepted him as an expert in mitochondrial disorders, including respiratory chain

disorders. Tr. 343.

a. Education and Background

Dr. McCandless earned his undergraduate degree in chemistry from Westminster College

in 1984 and his M.D. from Temple University School of Medicine in 1988. Resp. Ex. L at 1. He

initially completed a residency in pediatrics at the University of Wisconsin Hospital and Clinics

from 1988 to 1991, before later completing a residency in medical genetics and a fellowship in

biochemical genetics at University Hospitals of Cleveland through Case Western Reserve

University. Id. He is licensed to practice medicine in the state of Ohio and is certified in clinical

biochemical genetics by the American Board of Genetics and in clinical genetics by the

American Board of Medical Genetics. Id. at 1-2; Tr. 329. He is also board certified in pediatrics.

Tr. 329.

Currently, Dr. McCandless is an associate professor of genetics, pediatrics, and pathology

at Case Western Reserve University and University Hospitals Case Medical Center, where is he

30

also the director of the Center for Human Genetics, residency director of the department of

genetics, medical director of the Prader-Willi Syndrome Clinic, and associate director of the

Center for Inherited Disorders of Energy Metabolism. Resp. Ex. L at 1-2. Prior to joining Case

Western Reserve University, he was an assistant professor of pediatrics in the division of

genetics and metabolism at the University of North Carolina School of Medicine. Id. at 1.

Dr. McCandless has served numerous professional committees and organizations. He is a

section editor for the Medical Genetics Inservice Exam on behalf of the Association of

Professors of Human and Medical Genetics. Resp. Ex. L at 3. He is chair of both the Genetics

Education Committee at the University Hospitals Case Medical Center and the Newborn

Screening Committee at University Hospitals of Cleveland, as well as a member of the

Laboratory Subcommittee of the Ohio Newborn Screening Advisory Council. Id. He is also a

peer reviewer for several journals, including the Journal of Inherited Metabolic Diseases,

Genetics in Medicine, Pediatrics, and the American Journal of Medical Genetics. Id. at 2. His

CV lists 36 peer-reviewed articles, along with various other publications and one patent. Id. at 4-

12.

b. Opinion

Dr. McCandless agreed with Dr. Niyazov’s assessment that I.R. had a likely deleterious

POLG mutation but disputed that a heterozygous POLG mutation could cause disease. Resp. Ex.

F at 4-5. With regard to the potential for a mitochondrial disorder diagnosis based on I.R.’s

medical history, Dr. McCandless observed:

I find no records supporting myopathy, nor is there clear documentation by an

objective observer of loss of neurodevelopmental milestones, with the possible

exception of the balance problem . . . . Development of ataxia is not really

regression, as defined by a loss of previously attained milestones, as ataxia does not

represent an earlier developmental stage. Rather, ataxia should be considered a

new neurological finding. I find no convincing documentation of many [of] the

cardinal signs of MRI changes in the brain, mitochondrial diseases, myopathy,

cardiomyopathy, hearing loss, diabetes, autonomic dysfunction, significant

hypotonia, hematological problems or kidney disease.

Id. at 4.

Dr. McCandless disputed Dr. Niyazov’s application of the mitochondrial disorder

diagnostic criteria and criticized Dr. Niyazov for conflating mitochondrial dysfunction with

mitochondrial disease (or disorder). Resp. Ex. F at 5-6. Dr. McCandless opined that “[i]n this

case, the sum of testing that reflects mitochondrial function is normal, and the likelihood that this

child has a primary mitochondrial disease is extremely low.” Id. at 5.

Additionally, Dr. McCandless disputed Dr. Niyazov’s suggestion that there is a causative

link between mitochondrial dysfunction, immunological dysfunction, and oxidative stress that

31

could explain how a vaccine induces autistic regression. Resp. Ex. F at 6. He also disputed Dr.

Zimmerman’s assertion that vaccines may induce autistic regression in a child with

mitochondrial disease. Id. at 7.

ii. Bruce Cohen, M.D.

Bruce Cohen, M.D., was proffered by respondent and admitted without objection both as

an expert in neurology with special qualification in child neurology and as an expert in

mitochondrial disease. Tr. 449.

a. Education and Background

Dr. Cohen earned his undergraduate degree in Chemistry from Washington University in

St. Louis, Missouri, in 1978 and his M.D. at the Albert Einstein College of Medicine at Yeshiva

University in New York, New York, in 1982. Resp. Ex. K at 1. After medical school, Dr.

Cohen completed both a pediatric residency and a pediatric neuro-oncology fellowship at the

Children’s Hospital of Philadelphia, as well as a pediatric neurology residency at Columbia

Presbyterian Medical Center. Id. Dr. Cohen is licensed to practice medicine in the state of Ohio.

Id. at 2. He is a fellow of the National Board of Medical Examiners and the American Board of

Psychiatry and Neurology with special competence in child neurology. Resp. Ex. K at 2; Tr. at

441.

Currently, Dr. Cohen serves as the director of neurology and the director of the

Neurodevelopmental Science Center at the Children’s Hospital Medical Center of Akron, where

he maintains a clinical practice. Resp. Ex. K at 2; Tr. 443-44. He is also a professor of

pediatrics at Northeast Ohio Medical University, specializing in child neurology, mitochondrial

disease, and neuromuscular disease. Resp. Ex. K at 2; Tr. 443-44. He has had prior academic

and medical appointments with Case Western Reserve University, Hillcrest Hospital, Cleveland

Clinic, and Ohio State University. Resp. Ex. K at 2. He has been involved with mitochondrial

disorder patient care since 1983. Tr. 444.

Dr. Cohen is a member of, inter alia, the American Academy of Neurology, the Child

Neurology Society, the Mitochondrial Research Society, and the Mitochondrial Medicine

Society. Resp. Ex. K at 2; Tr. 443. He is a past president of both the Professors of Child

Neurology and the Mitochondrial Medicine Society. Resp. Ex. K at 2. He has served on a

multitude of committees and advisory groups, both nationally and at the Cleveland Clinic, and is

on the editorial board of four academic journals. Id. at 3-5. Dr. Cohen listed 91 peer-reviewed

articles on his CV, as well as 30 book chapters and an edited journal volume. Id. at 33-40. He

co-authored several of the medical journal articles extensively discussed in this case.

b. Opinion

Dr. Cohen agreed that “[a] subset of children with autism do have mitochondrial

disease,” but countered that “there is insufficient medical evidence to suggest any link between

vaccines and mitochondrial regression.” Resp. Ex. A at 7-8. He noted that I.R.’s clinical

features of autism improved over time and are “most consistent with the diagnosis of pervasive

32

developmental disorder” with “no evidence of a single encephalopathic event.” Id. at 7. Dr.

Cohen opined that “[t]he medical evaluation performed does not indicate this patient has a

mitochondrial illness” and further that “[t]he analyte screening (chemical biomarkers) did not

indicate any ongoing systemic mitochondrial dysfunction.” Id. at 5-6. He further opined:

[T]he child does not display any classic features of a child with mitochondrial

disease: brain lesions on MRI consistent with a metabolic process, movement

disorder, apneas, ptosis, external ophthalmoplegia, retinitis pigmentosa, optic

atrophy, high-frequency hearing loss, cardiomyopathy, cardiac conduction defect,

exocrine pancreatic failure, liver disease, myopathy, or neuropathy. Although

pervasive development disorders and autism can be seen in mitochondrial

disorders, those children have either additional clinical features or diagnostic

biochemical-genetic-histological features that extend beyond the EEG finding,

epilepsy (although epilepsy has not been confirmed in this case), or a single episode

of regression (which is known to occur in autism).

Id. at 6-7. Dr. Cohen additionally disputed that “immunizations cause enough oxidative stress

(metabolic stress or immunological stress) to trigger mitochondrial dysfunction resulting in a

clinical demise.” Id. at 7.

iii. Max Wiznitzer, M.D.

Max Wiznitzer, M.D., was proffered by respondent as an expert in pediatric neurology

with specialty in autism, including autism diagnosis and developmental pediatrics. Tr. 793.

Petitioners did not object to Dr. Wiznitzer’s admission as an expert in pediatric neurology and

autism.44 Tr. 779, 783.

a. Education and Background

Dr. Wiznitzer received his B.S. in medical education in 1975 and a medical degree in

1977, both from Northwestern University. Resp. Ex. Q at 1. He completed a residency in

pediatrics in 1980 at the Children’s Hospital Medical Center in Cincinnati, Ohio. Id. He then

completed a one-year fellowship at the Cincinnati Center for Developmental Disorders, a three-

year fellowship in pediatric neurology at the Children’s Hospital of Philadelphia, and a two-year

fellowship at the Albert Einstein College of Medicine in New York, where he studied higher

cortical functions. Id. at 1-2. Dr. Wiznitzer is certified by the American Board of Pediatrics. Id.

at 5. He also received certification from the American Board of Psychiatry and Neurology, with

a special qualification in Child Neurology. Id. In 2004, the American Board of Psychiatry and

Neurology certified his competence in neurodevelopmental disabilities. Id. He maintains

licenses to practice medicine in Ohio, Pennsylvania, and New York. Id.

44

However, petitioners do challenge Dr. Wiznitzer’s qualifications specific to his opinion

competing against the opinion of their expert, Dr. Wilson, with regard to review of the home

videos filed in this case. Pet. Posthr’g Br. at 18-20. This issue is addressed in Section VI.A.i.C,

below.

33

Currently, Dr. Wiznitzer is a professor of pediatrics and neurology at Case Western

Reserve University. Resp. Ex. Q at 2. He is also an associate pediatrician and neurologist at

University Hospitals of Cleveland. Id. Dr. Wiznitzer has received appointments to practice at

several hospitals for various lengths of time, including the Department of Neurology of

Montefiore Medical Center in New York; the Department of Neurology at Bronx Municipal

Hospital Center; and Rainbow Babies and Children’s Hospital in Cleveland. Id. He has served

as a consultant in pediatrics and neurology at several other hospitals as well. Id. At Rainbow

Babies and Children’s Hospital, Dr. Wiznitzer served as Co-Director of the Rainbow Autism

Center in 1991; Chief of the Division of Pediatric Neurology from 1992 to 1995; and the

Director of the Rainbow Autism Center from 1992 through 2010. Id. at 2-3.

Dr. Wiznitzer has been a reviewer of articles for many medical journals, most notably for

Pediatric Neurology, Lancet Neurology, and the Journal of Child Neurology, where he also

served on the editorial boards. Resp. Ex. Q at 6. He has served on a multitude of medical

advisory groups at the local, state, and national levels. Id. at 6-9. Dr. Wiznitzer has published 73

medical articles and 11 book chapters. Id. at 13-20.

b. Opinion

Dr. Wiznitzer disputed that I.R.’s autism could be explained by his vaccinations. Resp.

Ex. C at 12. He opined that I.R. was properly diagnosed with autism before age three and that he

does not have any history of regression, persistent unsteadiness, or ataxia. Id. at 11-12. He

further opined that there is no correlation between I.R.’s illnesses and the appearance of his

autistic features, and noted that language delay is known to be an initial manifestation of autism

spectrum disorders. Id. Dr. Wiznitzer also opined that I.R.’s subsequent improvement, with a

later diagnosis of pervasive development disorder not otherwise specified (PDD-NOS), is

consistent with “a known developmental trajectory for autistic disorder.” Id. at 11. Upon

subsequent review of the video footage filed in this case, Dr. Wiznitzer opined, in contrast to Dr.

Wilson, that I.R. “clearly showed ASD signs in 2005 and prior to his MMR and varicella

vaccinations on 12/30/05 and showed no obvious functional deterioration in the months after that

time.” Resp. Ex. O at 3.

VI. Findings of Fact

Before reaching the substance of petitioners’ medical theory regarding causation, a

number of disputed factual points must be resolved. In particular, three significant aspects of

I.R.’s health status remain in dispute. These are the onset and course of I.R.’s autism, his

immune status, and his metabolic status. Petitioners assert that I.R. was neuro-typical during his

first year of life and prior to administration of his 12-month vaccines. They further allege that he

experienced a regression after those vaccinations. Petitioners also allege that I.R.’s ProQuad

vaccine, which includes MMR, caused a temporary immunosuppression and, moreover, that I.R.

has experienced longstanding immunodeficiency. Finally, petitioners allege that I.R. has a

mitochondrial disorder or dysfunction. The undersigned will address each of these assertions in

turn.

34

A. The Onset and Course of I.R.’s Autism

Among the factual disagreements in this case, the parties disagree regarding the onset,

course, and nature of I.R.’s autism. In order to fully evaluate petitioners’ claim of vaccine

causation, it is first necessary to determine when I.R.’s autism first manifested and whether I.R.

experienced a developmental regression following his vaccinations.

i. The undersigned finds that I.R.’s autism manifested prior to his first

birthday and prior to the vaccinations at issue.

A significant point of factual dispute in this case relates to the age at which I.R.’s autism

first manifested. Petitioners contend that I.R. was developmentally typical until one year of age,

after which he began showing signs of autism following his allegedly injury-causing

vaccinations, which became clear by 15 months of age. Pet. Posthr’g Br. at 40-41. Respondent

contends that I.R.’s autism actually manifested much earlier, during his first year of life and prior

to the vaccinations at issue in this case. Resp. Posthr’g Br. at 18-20.

Record evidence touching on this issue includes medical records, baby book entries,

parental and expert testimony, and home videos. However, most of the attention paid to the

question of when I.R.’s autism manifested has been devoted to analysis of the home videos,

which show I.R. in his home environment from about six months of age until shortly after his

second birthday. Resolving this factual issue requires weighing the testimony and opinions of

several competing experts.45

Upon the undersigned’s review of the record evidence as a whole, including the video

footage filed in this case, the undersigned finds preponderant evidence that I.R.’s autism began

to manifest by the time he reached 12 months of age, prior to the vaccinations alleged to have

caused his injuries.

a. Early Detection of ASD

As described in the factual history above, concerns about I.R.’s development were first

raised to his pediatrician at about 27 months of age, when Mrs. Reed expressed concern about

I.R.’s speech development. After several evaluations, he was subsequently diagnosed as autistic

at about 33 months of age. However, age of diagnosis is not equivalent to age of onset or

manifestation, and in any event, both parties contend that I.R.’s autism manifested well before 27

months of age. Rather, children are most commonly diagnosed as autistic at about two years of

age due to the fact that parents and pediatricians are not able to pick up on the more subtle early

manifestations of autism. See Tr. 658.

45

Petitioners had filed a motion to exclude, postpone, or limit respondent’s expert testimony

regarding the home videos. Mot. in Limine dated June 22, 2016 (ECF No. 157). Petitioners

argued that respondent was overbroad in designating video clips for presentation at the hearing,

resulting in unfair surprise. Id. The parties resolved the issue by agreeing to a modified order of

witness presentation. Tr. 563-72.

35

Symptoms of autism are age dependent and diagnosis of ASD relies on the ability to

reliably detect more subtle behaviors that emerge during infant development. Pet. Ex. 150 at 1.

For example, the common symptoms of restricted interests and repetitive behaviors are not

expected until two to three years of age. Tr. 857. Earlier studies suggested that an accurate

autism diagnosis was not possible prior to two years of age. Pet. Ex. 150 at 1; Tr. 801-02.

However, more recent studies have established that onset can actually be discerned much earlier.

For example, one 2010 paper explained:

Retrospective studies have demonstrated that children with early-onset ASD differ

from age-matched children with delayed and typical development in orienting to

name, gaze to faces, joint attention, and affect sharing. Differences are most

evident in the second year of life but some studies have detected signs of ASD

before the first birthday. This early onset pattern is thought to occur in the majority

of individuals with ASD.

Resp. Ex. P, Tab 2 at 1. Experts for both parties (Dr. Wilson for petitioner and Dr.

Wiznitzer for respondent) agree that the age at which a reliable diagnosis can be made is

moving, and that more subtle signs of autism can often be observed as early as the first

year of life. Pet. Ex. 176 at 3; Tr. 660-61, 668-69, 795-96. Dr. Wilson in particular

views RVA research as a driving force in lowering the age of first diagnosis. Tr. 593,

668-69.

In describing what autistic behaviors might be visible during the first year of life, Dr.

Wilson summarized: “[D]uring the first year of life, children with autism (when compared to

typically developing children) are distinguished by reduced social interaction, absence of social

smiling, lack of facial expression, failure to orient to name, lack of joint attention, decreased

orienting to faces, and abnormal muscle tone, posture and movement patterns.”46 Pet. Ex. 176 at

3 (internal citations omitted) (quoting Pet. Ex. 145 at 2). During the hearing, Dr. Wilson further

explained these symptoms with reference to a list created by Autism Speaks! regarding “red

flag” behaviors that may indicate a child is at risk for autism. Tr. 637. Specifically, Dr. Wilson

highlighted the following:

• No big smiles or other warm, joyful expressions by six months or thereafter;

• No back-and-forth sharing of sounds, smiles, or other facial expressions by nine months;

• No babbling at all by 12 months;

• No back-and-forth gestures such as pointing, showing, reaching, or waving by 12

months;

• No words by 16 months;

• No meaningful two-word phrases by 24 months;

• Any loss of speech, babbling, or social skills at any age.

46

Additional behaviors were listed in a more qualified manner as “hav[ing] been mentioned as

potentially being diagnostic.” Pet. Ex. 176 at 3. Dr. Wilson also cited repetitive play as a sign of

autism generally but did not cite an age of onset for that behavior. Id. Dr. Wiznitzer opined,

however, that repetitive behaviors and restricted interests do not present in the first year of life

and may not present until age two to three. Tr. 857.

36

Id.

Dr. Witznitzer did not challenge Dr. Wilson’s description of these early signs of autism

but stressed some caveats. Dr. Wiznitzer opined that patterns are more significant than isolated

behaviors. Tr. 797-800. He also indicated that the relevant question regarding these red flag

behaviors is not “you do the act or you don’t do the act,” but rather the quality of the interaction

and social intent. Tr. 801-02. Both experts agree that a child ultimately diagnosed as having

autism will display typical behaviors some of the time. Tr. 654-55, 801-02.

Additionally, experts for both parties agreed that hyporesponsiveness to pain is a possible

“red flag” sign of autism. Resp. Ex. O at 2; Pet. Ex. 176 at 8. Specifically, Dr. Wilson opined

that additional red flags for autism include “lack of response to pain and lack of response to loud

sounds.” Pet Ex. 176 at 8. She indicated that “[t]hese characteristics are not indicative of autism

on their own, but in conjunction with the other atypical traits noted, they become consistent with

autism features.” Id.

b. Retrospective Video Analysis Generally

Since I.R. was not evaluated for autism until later in life, the most significant source of

evidence regarding his first-year behavior is home videos filmed by his parents, reviewed

through the lenses of RVA. Petitioners characterize RVA as “a respected and scientifically valid

research method which has been instrumental in guiding current early identification of autism.”

Pet. Posthr’g Br. at 14 (citing Pet. Ex. 165). Respondent’s expert, Dr. Wiznitzer, likewise opined

that RVA can be useful in determining autism onset, so long as there is sufficient footage to

discern patterns of behavior. Tr. 794. And indeed, RVA has been used in prior cases within this

Program and has been found to be a useful diagnostic tool. See, e.g., R.K. v. Sec’y Health &

Human Servs., No. 03-632, 2015 WL 10936124, at *67-69 (Fed. Cl. Spec. Mstr. Sept. 28, 2015),

mot. for rev. denied, 125 Fed. Cl. 57, aff’d, 671 F. App’x 792 (mem.).

Numerous RVA studies related to autism have been filed in this case. See, e.g., Pet. Ex.

107 (Osterling); Pet. Ex. 109 (Baranek); Pet. Ex. 147 (Adrien); Pet. Ex. 148 (Adrien); Pet. Ex.

150 (Baranek); Pet. Ex. 151 (Baranek); Pet. Ex. 153 (Bernabei); Pet. Ex. 161 (Maestro); Pet. Ex.

169 (Werner); Resp. Ex. O, Tab 1 (Palomo), Tab 3 (Costanzo), Tab 4 (Ozonoff), Tab 5

(Maestro). In addition, both parties have filed and cited a 2009 literature review article that

surveys prior RVA studies and discusses their utility. Pet Ex. 165 (Saint-Georges).

Methodology and objective vary quite a bit among the different studies. Nonetheless, all of these

studies involve trained screeners viewing home video footage to determine whether autistic-like

behaviors are evidenced. A significant advantage of RVA is that it allows for ecological

validity. That is, the reviewer is able to observe a child in his usual environment, where he or

she is more comfortable and behaving in his or her usual manner. Pet. Ex. 109 at 2.

Nonetheless, RVA has significant limitations. The most notable limitations of home

video review are uncertainty regarding whether the videos are representative of a child’s overall

behavior (parents may selectively film pleasant or favorable situations such as reaching

milestones); a risk that the cross-section of observable behaviors may not be adequate to analyze

infrequent or context-dependent situations; and a tendency by parents to use compensatory

37

strategies to coax more social behavior from their children. See, e.g., Pet. Ex. 165 at 7; Pet. Ex.

150 at 10-11. An additional concern related to study methodology, discussed more fully below,

is the difficulty of overcoming subjective interpretive differences among video reviewers when

analyzing the footage.

c. Retrospective Video Analysis in This Case

Petitioners’ testifying expert on RVA was Kaitlyn Wilson, Ph.D. Dr. Wilson holds a

Ph.D. in speech and hearing sciences and has participated in multiple studies regarding RVA

intended to identify early manifestations of autism. During the hearing, Dr. Wilson was admitted

without objection as an expert in speech and language pathology and in use of RVA with regard

to autism. Tr. 621. Upon review of the video footage available in this case, Dr. Wilson opined

that the first atypical behavior I.R. exhibited occurred when he hit his head and had a minimal

reaction on January 5, 2006, when he was between 12 and 13 months of age. Pet. Ex. 176 at 6,

8; Tr. 629-30. She further opined that it was not until approximately 15 months of age that I.R.’s

autism became clear and apparent.47 Pet. Ex. 176 at 8.

Respondent presented competing expert testimony from Dr. Max Wiznitzer, a pediatric

neurologist with special interest in autism. Dr. Wiznitzer’s testimony was admitted without

objection as being expert in pediatric neurology with a specialty in autism and developmental

pediatrics, including diagnosis.48 Tr. 779, 783. Dr. Wiznitzer’s review of the video footage, as

well as the medical records and other evidence, led him to conclude that, although I.R.’s

condition became more apparent in his second year of life, he showed early signs of autism prior

to 12 months of age and that what he experienced was a slow evolution of atypical behaviors

increasing over time. Resp. Ex. O at 2-3; Tr. 831-32, 840-42.

Upon review of the videos filed in this case, as well as the competing expert opinions, a

number of considerations lead the undersigned to conclude that Dr. Wiznitzer’s opinion is more

persuasive on the whole. First, the undersigned finds that Dr. Wiznitzer has presented persuasive

testimony regarding potential red flag findings within the first year of life that Dr. Wilson has not

persuasively addressed in her own review of the videos at issue. Second, the undersigned finds

that Dr. Wilson failed to identify I.R.’s first instance of hyporesponsiveness. Third, the

47

The record also contains a report filed by petitioners from an additional RVA expert, Dr.

Freuler. Pet. Ex. 145. However, Dr. Freuler did not ultimately testify in this case, providing no

opportunity for respondent to cross-examine. Moreover, her report is largely cumulative of Dr.

Wilson’s opinion. Thus, the undersigned does not give Dr. Freuler’s report significant weight

and will not discuss Dr. Freuler’s report at length. Nonetheless, it has been considered as part of

the following analysis. Like Dr. Wilson, Dr. Freuler did not report any “red flag” findings prior

to 12 months of age. Pet. Ex. 145 at 5-7. Both Dr. Wilson and Dr. Freuler identified minimal

reactions to a head bump January 5, 2006, and a balloon pop on January 25, 2006, as the first

two atypical behaviors observed. Pet. Ex. 145 at 5-7; Pet. Ex. 176 at 6. Some of their

observations regarding subsequently dated videos differ.

48

However, petitioners do challenge Dr. Wiznitzer’s credentials regarding RVA. Pet. Posthr’g

Br. at 18-20. This point is further addressed below.

38

undersigned finds it significant that while Dr. Wiznitzer’s opinion accords with what is known of

autism onset, Dr. Wilson struggled to reconcile her findings with these facts. The undersigned

will address each of these points in turn and will then address additional arguments raised by

petitioners in their post-hearing brief.

1. Dr. Wiznitzer provided persuasive observations

regarding the video footage.

During the course of the hearing, each expert showed several video clips and provided

their analysis. In total, there are video clips from 12 different dates during I.R.’s first year of life

for which there is competing expert testimony in the record.49 In addition, there were video clips

highlighted by each expert for which there is no directly competing expert testimony from the

other party.50 Interpreting these videos is very challenging. In many instances these two experts

drew different conclusions based on very subtle distinctions. However, the undersigned is

persuaded that Dr. Wiznitzer has raised instances of potential signs of autism visible during the

first year of life.

For example, in a video dated August 25, 2005, according to Dr. Wiznitzer, I.R. shows a

lack of good eye contact and babble, fails to respond to his name being called several times, and

doesn’t look at another person who takes an object from him. Resp. Ex. O at 4; Tr. 813-14. In

contrast, Dr. Wilson opined during the hearing regarding the same video that I.R. laughed, pulled

to stand, and responded to his name with eye contact. Tr. 641. In her report, she identified

typical behaviors of mouthing objects and making vowel sounds. Pet. Ex. 176 at 5. Upon the

undersigned’s review, both experts are accurately discussing different aspects of the same video.

For instance, although Dr. Wilson is correct that at one point I.R. responded to his name, Dr.

Wiznitzer is also correct that a different point in the video shows I.R. repeatedly failing to do so.

Dr. Wiznitzer also testified that a series of video clips from July 2005, when I.R. was

about six to seven months old, demonstrated instances of limited eye contact, a lack of facial

49

These clips are dated: July 12, 2005; July 15, 2005; July 18, 2005; August 21, 2005; August

25, 2005; October 6, 2005; October 30, 2005; November 15, 2005; November 20, 2005;

November 26, 2005; December 20, 2005; and December 29, 2005. Although the undersigned

has reviewed all of the videos filed in this case, this decision will explicitly address only a few

examples.

50

Dr. Wilson testified regarding videos dated July 10, 2005; July 22, 2005; September 16, 2005;

October 31, 2005; November 6, 2005; and November 24, 2005. Dr. Wiznitzer testified regarding

videos dated July 23, 2005; August 9, 2005; September 4, 2005; November 25, 2005; and

December 10, 2005. Additionally, Dr. Wiznitzer extended his review of the videos far beyond

the first year of life. While Dr. Wilson testified only regarding video clips up to I.R.’s first

birthday (and her report additionally includes observations through August 2006), Dr. Wiznitzer

also testified regarding later clips dated January 5, 2006; January 7, 2006; January 10, 2006;

January 25, 2006; February 17, 2006; February 26, 2006; March 26, 2006; March 31, 2006;

April 3, 2006; August 2, 2006; August 16, 2006; August 18, 2006; August 27, 2006; October 5,

2006; and December 29, 2006.

39

expression, and a lack of alerting (e.g., no reaction to sneeze).51 Tr. 807-10. That is, he opined

to a lack of the dynamic, sustained interaction that would typically be expected. Id. He also

testified that a video clip from December 10, 2005, just weeks prior to I.R.’s first birthday,

additionally demonstrated minimal vocalizations, and vocalizations limited in their range, that

suggest a developing language issue. Tr. 821-22. Although Dr. Wilson identified competing

typical behaviors from the same time periods in her report (Pet. Ex. 176 at 4), she did not directly

address the behaviors identified by Dr. Wiznitzer.52

In another instance, the undersigned found that Dr. Wilson’s opinion was not persuasive

in itself. For example, in one instance Dr. Wiznitzer cast doubt on Dr. Wilson’s observation of

typical behavior without necessarily offering a strong competing opinion. In a video dated

December 20, 2005, Dr. Wilson opined that I.R. engaged in a waving gesture directed at his

mother. Tr. 645. Dr. Wiznitzer, however, opined that typical versus atypical behavior is

difficult to discern from the video. Tr. 822-23. Dr. Wiznitzer characterized the video as

showing an unprompted up and down of I.R.’s arm and suggested that he could not see an intent

for attention. Resp. Ex. O at 6; Tr. 822-23.

The undersigned is not persuaded by Dr. Wilson’s opinion on this point, in part because it

was inconsistently offered. When Dr. Wilson first discussed this December 20 clip at the

hearing, she described it as a “social gesture of waving directed towards mom” without

qualification. Tr. 645. Later, in testimony rebutting Dr. Wiznitzer’s opinion, she conceded that

due to I.R.’s early age the wave was “not perfectly executed,” but maintained her view that it

represented a social gesture. Tr. 651-52. In her earlier report, however, Dr. Wilson described

the clip only as “possible” waving and smiling, seeming to acknowledge that the action was

ambiguous.53 Pet. Ex. 176 at 6.

Upon the undersigned’s review of the entirety of video footage, neither expert has a

monopoly on correct interpretation.54 However, on the whole, the undersigned is not persuaded

51

This refers to the following video clips presented during the hearing: July 23, 2005, at 6:48:15

to 6:48.38; July 27, 2005, at 10:12:00 to 10:12:20; and July 27, 2005, at 10:13:50 to 10:14:55.

52

Dr. Wilson’s report identifies a range of expressions, including smiles and concern, on July 27,

2005, but does not address the video footage discussed by Dr. Wiznitzer from July 15 or July 23.

Pet. Ex. 176 at 4. Her only observation regarding the December 10, 2005 video is that his first

steps were age appropriate. Id. at 6.

53

Nonetheless, she did code it as a typical rather than ambiguous behavior.

54

The undersigned stresses that it would not be practical to describe the competing opinions

regarding every video in evidence in this case. There is simply too much footage. However, the

undersigned’s opinion is based on review of the video footage as a whole. The above-described

opinions are only a few examples of instances where the undersigned finds Dr. Wiznitzer more

persuasive. There are more. Additionally, there are other instances not cited where Dr. Wilson

has credibly challenged Dr. Wiznitzer’s observations. For example, as stressed in petitioners’

post-hearing brief, the undersigned agrees that Dr. Wiznitzer’s observation that I.R. did not smile

40

that Dr. Wilson has fully accounted for all of the possible red flag behaviors present in the video

clips as presented by Dr. Wiznitzer (also including the hyporesponsiveness discussed separately

below). Rather, the undersigned finds that Dr. Wiznitzer’s competing testimony is credible and

that, coupled with the video evidence, it provides preponderant evidence that I.R.’s autism

predated his first birthday. See, e.g., R.K., 2015 WL 10936124, at *65 (similarly noting that

“[o]n the whole, however, I attach less weight to Dr. Megson’s report than I do to Dr. Miller’s

testimony because Dr. Megson’s characterizations of the videos run counter to what I observed

while viewing them”).

2. Dr. Wilson failed to identify the first appearance of

hyporesponsiveness.

Another significant issue weighing against Dr. Wilson’s interpretation of the video

evidence is her misplacement of the onset of I.R.’s hyporesponsive behavior. Dr. Wilson opined

that, having reviewed all of the video footage in this case, the first “red flag” incident was a

“minimal response” to pain when I.R. fell and hit his head on January 6, 2006. Pet. Ex. 176 at 6;

Tr. 627-29. And indeed, as previously noted, experts for both parties agree that

hyporesponsiveness to pain is a possible “red flag” sign of autism. Resp. Ex. O at 2; Pet. Ex. 176

at 8. Yet Dr. Wilson failed to record, or “code,” two substantially similar incidents occurring

prior to I.R.’s first birthday.55 Thus, the undersigned finds that Dr. Wilson has misplaced the

onset of this behavior. The onset of hyporesponsiveness within the first year of life further

supports Dr. Wiznitzer’s opinion in this case, while also casting doubt on the accuracy of Dr.

Wilson’s opinion.

In the video identified as a red flag by Dr. Wilson, I.R. is toddling around in a hallway

near a staircase on January 5, 2006. He is between 12 and 13 months old. As he moves around,

he loses his balance and falls sideways, striking his head against the wall. A thudding noise is

audible, but I.R. has no apparent reaction.

at his mother in the video on October 31, 2005, should not be credited as an atypical behavior

since I.R. was distressed by his Halloween costume. Pet. Posthr’g Br. at 22. However, other

examples listed in petitioners’ post-hearing brief are less persuasive. For example, petitioners

assert that Dr. Wiznitzer opined that I.R. demonstrated an “inadequate wave.” Id. As described

above, the question was not whether I.R.’s wave was adequately executed, but whether the

behavior was intended to be a wave. The undersigned agrees that the video is ambiguous in that

regard.

55

In fact, I.R.’s baby book suggests a third instance. In an entry for September 15, 2005 (when

I.R. was about eight to nine months old), Mrs. Reed wrote: “Swimming/learned to paddle/you

love to splash/fell on your chin/bleeder in the pool – but you never cry.” Pet. Ex. 73 at 12. Dr.

Wiznitzer classified this as evidence of hyporesponsiveness. Tr. 863-64. Dr. Wilson declined to

opine on the entry, because she had not reviewed the baby book. Tr. 655-56.

41

A very similar incident occurred on August 25, 2005, when I.R. was approximately eight

to nine months old. In the video of that date, I.R. can be heard striking his head.56 As in the later

January 6, 2006 video, there is an audible thud as his head strikes a hard surface. I.R. shows no

reaction to the strike. Mrs. Reed can be heard gasping audibly. Moreover, she expresses

surprise that I.R. is not reacting, saying “it’s so painful, it has to be . . .” Pet. Ex. 139.

As compared to the January 5, 2006 incident, the August 25, 2005 video reflects an

incident just as likely to be painful, and I.R.’s reaction is every bit as muted in the earlier video

as it is in the later January 5, 2006 video. However, in her expert report, Dr. Wilson’s only

observation about the August 25, 2005 video is that I.R. can be heard making vowel sounds. Pet.

Ex. 176 at 5. Her only testimony regarding this video concerned observations – challenged by

Dr. Wiznitzer – that he laughs, responds to his name, and pulls to stand. Tr. 641.

Additionally, the videos in evidence show that on November 15, 2005, when I.R. was

about 10 to 11 months old, I.R. again fell and hit his head while playing with a window curtain.

As with the videos of August 25, 2005, and January 6, 2006, there is an audible thud when his

head strikes the hard surface, despite the camera in this instance being some distance away. As

with the August 25, 2005 video, Mrs. Reed again makes a comment on film that suggests

surprise at I.R.’s lack of reaction. Like the August 25, 2005 incident, the undersigned finds that

the video shows an incident as likely to have caused I.R. pain as the January 5, 2006 incident.

Again, I.R.’s reaction is equally muted. Yet Dr. Wilson’s observations regarding this video

make no mention of the head bump or of I.R.’s muted reaction. In her report, comment on the

November 15, 2005 video is limited to observations regarding his playing of peekaboo and his

response to his name. Pet. Ex. 176 at 5. Her testimony regarding this video addresses only I.R.’s

affect while playing peekaboo. Tr. 650.

During the hearing, the undersigned questioned Dr. Wilson about these prior first-year

falls. Dr. Wilson explained that she felt the falls occurring during the first 12 months of life were

not painful falls. Tr. 672. She further suggested that she has observed in her clinical practice

and in parenting that a crying response to such a fall is often conditioned by the parents and

onlookers reacting in such a way as to elicit that response. Id. She speculated that I.R.’s parents

may not be the type of parents that encourage a crying response. Id. With regard to the specifics

of her review of the videos, Dr. Wilson indicated that “[w]hen I did note that it looked like a

painful fall, you know, you hear a bang or something like that.” Tr. 672-73. Dr. Wilson did

seem to acknowledge that Mrs. Reed appeared concerned by the falls on the video, but ultimately

suggested that in contrast to the fall on January 5, 2006, the prior falls were “just a stumble, no

reason for a cry really.” Tr. 673.

This testimony does not align with the undersigned’s review of the videos. The various

impacts described above were not significantly distinguishable in their severity. Moreover, as

noted above, contrary to Dr. Wilson’s suggestion that I.R.’s parents may not be the types to elicit

a crying response, Mrs. Reed did appear to express concern about the falls and did, in particular,

56

Although the camera pulls away a moment before I.R.’s head strikes the hard surface, the

video clearly shows that I.R. is about to fall.

42

audibly respond each time I.R. hit his head, though she did not react to the extent of intervening

in I.R.’s activities.

Most significantly, and again contrary to Dr. Wilson’s suggestion, the undersigned noted

that each of the prior falls resulted in an audible noise similar to the noise heard upon the January

5, 2006 fall; yet this was Dr. Wilson’s stated basis for distinguishing one fall from another.

Accordingly, the undersigned does not find any basis in the record for Dr. Wilson’s decision to

categorize or code the August 25, 2006 and November 15, 2006 falls differently than the January

5, 2006 fall. Thus, the undersigned finds that Dr. Wilson has misidentified the onset of I.R.’s

hyporesponsiveness, which actually occurred prior to I.R.’s first birthday.57

The undersigned finds Dr. Wilson’s misidentification of the August 25 and November 15

falls significant for two reasons. First, although Dr. Wilson opined that hyporesponsiveness

alone is not indicative of autism, her opinion was predicated on the complete absence of any “red

flag” type behaviors during I.R.’s first year of life. Specifically, Dr. Wilson opined in pertinent

part:

Other red flags noted after [I.R.]’s first birthday included his lack of response to

pain and his lack of response to loud sounds (e.g., balloon popping in video 4).

These characteristics are not indicative of autism on their own, but in conjunction

with the other atypical traits noted, they become consistent with autism features.

The pattern of behaviors noted in this qualitative analysis shows a clear emergence

of autism characteristics following [I.R.]’s first birthday, with no clear cause for

concern prior to 12 months of age.

Pet. Ex. 176 at 8 (emphasis original). Second, at no point did Dr. Wilson offer any additional

explanation of how her opinion would change – or more to the point, not change – if she

accepted any of Dr. Wiznitzer’s competing observations or if the undersigned otherwise found

that certain of I.R.’s autistic behaviors emerged prior to 12 months of age.

Thus, having concluded that I.R. demonstrated the same hyporesponsive behavior

identified by Dr. Wilson, but as early as eight to nine months of age, the undersigned is left with

an expert opinion that is premised on an incorrect factual assumption. It is, therefore, far less

persuasive as a whole. See, e.g., Hennessey v. Sec’y of Health & Human Servs., 2009 WL

1709053, at *42 (Fed. Cl. Spec. Mstr. May 29, 2009) (“When experts disagree, . . . [o]bjective

factors, including the qualifications, training, and experience of the expert witnesses and the

extent to which their proffered opinions are supported by reliable medical research, other

testimony, and the factual basis for their opinions, are all significant in determining what

testimony to credit and what to reject.”). As the Supreme Court has noted, a trial court is not

required to accept medical or scientific opinion “that is connected to existing data only by the

ipse dixit of the expert,” because the “court may conclude that there is simply too great an

57

Of note, Dr. Wiznitzer cited the November 15, 2005 head bump in his supplemental expert

report as an example of hyporesponsiveness similar to the January 5, 2006 incident. Resp. Ex. O

at 2. He did not, however, offer an opinion regarding the August 25, 2005 fall.

43

analytical gap between the data and the opinion proffered.” Gen. Elec. Co. v. Joiner, 522 U.S.

136, 146 (1997).

Additionally, separate and apart from her ultimate conclusion regarding the trajectory of

I.R.’s autism, this issue calls into question the reliability and credibility of Dr. Wilson’s review

of the videos and each of her resulting observations. Specifically, the undersigned’s review of

the record evidence described above suggests that Dr. Wilson did not in all instances

acknowledge or characterize similar events similarly across the multiple videos in this case. This

is particularly problematic, because Dr. Wilson’s opinion is premised on her claimed expert

demonstration that there is a complete absence of atypical behaviors prior to 12 months of age,

whereas Dr. Wiznitzer has opined that such behaviors were present during that earlier period,

only more subtle. Yet, the undersigned’s own review reveals that Dr. Wilson’s underlying

assertion is not necessarily credible, because her observations are not consistent between the two

periods even with regard to incidents that are readily comparable and not at all subtle.58 As the

Federal Circuit noted, “[a]ssessments as to the reliability of expert testimony often turn on

credibility determinations, particularly in cases . . . where there is little supporting evidence for

the expert’s opinion.” Moberly, 592 F.3d at 1325-26; see also Snyder, 88 Fed. Cl. at 718

(quoting Ryman v. Sec’y of Health & Human Servs., 65 Fed. Cl. 35, 40-41 (2005)) (noting that

special masters perform a gatekeeping function when determining “whether a particular

petitioner’s expert medical testimony supporting biological probability may be admitted or

credited or otherwise relied upon”).

3. Dr. Wiznitzer’s opinion accords with known patterns of

ASD onset.

The undersigned further stresses that the persuasiveness of Dr. Wiznitzer’s observations

is bolstered by the fact that his opinion is fully consistent with known patterns of ASD onset. Dr.

Wilson, in contrast, struggled to articulate how her findings in this case square with what is

known about autism.

As noted above, Dr. Wiznitzer stressed that patterns of behavior are more significant to

determining ASD onset than isolated behaviors. Resp. Ex. P at 2. He also persuasively testified

that the pattern of ASD onset he observed in I.R.’s case is consistent with one of the known,

major patterns of ASD onset, namely subtle or insidious onset of atypical behaviors during the

first year of life followed by divergence of social behaviors, becoming more evident around 18-

24 months of age. Tr. 859-60. In particular, Dr. Wiznitzer identified a pattern of behavior

during I.R.’s first year of life including quiet or somber behavior, decreased eye contact, less

58

The undersigned also notes that although Dr. Freuler discussed hyporesponsiveness in her

report, Dr. Freuler coded the January 5, 2006 video as atypical not due to hyporesponsiveness,

but because of unsteady gait and motor dyspraxia. Pet. Ex. 145 at 6. This may explain why Dr.

Freuler similarly did not code the prior falls as atypical. It is clear from Dr. Wilson’s report,

however, that it is the hyporesponsiveness to pain, rather than the unsteadiness that led to the

fall, which caused Dr.Wilson to code the January 5, 2006 fall as atypical. Pet. Ex. 176 at 6, 8.

Thus, even if Dr. Freuler was consistent in opining that none of the falls were concerning for

hyporesponsiveness, Dr. Wilson’s observations remain inconsistent.

44

interaction, and a paucity of expected language and vocalization for a child of his age. Tr. 840-

42. These observations are fully consistent with the “red flag” items presented by Dr. Wilson

and with the literature filed in this case, and are consistent with what is typically known as early

onset autism.59 Tr. 637; see generally Pet. Ex. 165 (describing early onset autism as including

social and communicative impairments at a lower rate in the first year, with increasing socio-

interactive difficulties and loss of previously seen behaviors as poorer social interest evolves in

the second year). Moreover, by highlighting later videos as well, Dr. Wiznitzer persuasively

demonstrated how these patterns of behavior became more evident over time.

In contrast, Dr. Wilson has presented findings in this specific case that are potentially at

odds with her characterization of her prior RVA study experience, which forms the basis for her

expertise. That is, Dr. Wilson explained that RVA researchers should be able to discern the

signs of autism earlier than parents or clinicians. Tr. 661. She also noted that prior studies have

predicted autism with 94% accuracy at nine to 12 months of age. Tr. 665-67 (citing Pet. Ex. 150

(Baranek)). Yet Dr. Wilson identified no signs of ASD prior to twelve months of age, despite

the fact that I.R. is known to have been subsequently diagnosed as autistic.

Asked by the undersigned during the hearing whether it is typical that children later

diagnosed as having autism would not show many significant red flag-type behaviors between

nine to 12 months of age (i.e., I.R.’s presentation as posited by Dr. Wilson’s testimony), Dr.

Wilson replied that “I would say it’s unusual.” Tr. 663. Dr. Wilson did not provide any

explanation during the hearing of what significance should be attached to the fact that her

findings are unusual or why, in light of that characterization, her conclusion should be credited

over Dr. Wiznitzer’s competing expert opinion.60 Indeed, when asked if she would include

trajectories of autism as part of her expertise, Dr. Wilson effectively demurred, stating only that

she has read about it in the literature but has not included it in her research. Tr. 670.

Following the hearing, Dr. Wilson provided a supplemental report. Pet Ex. 198. In that

report, she expressed that “[t]here is currently no simple answer to the question of how common

early onset autism is in relation to late onset autism.” Id. Citing one review article by Ozonoff,

et al., and one Medwire News report, Dr. Wilson further expressed that patterns of ASD onset

59

In their post-hearing brief, petitioners were critical of the fact that Dr. Wiznitzer did not

independently provide any objective or published criteria by which to compare I.R.’s behavior.

Pet. Posthr’g Br. at 14 n.25. This is not entirely true. Although not stressed in his opinion, Dr.

Wiznitzer cited medical literature regarding this point in his second supplemental report. Resp.

Ex. P at 2. In any event, the undersigned notes that she had no difficulty matching Dr.

Wiznitzer’s observations to the first-year signs of autism described by Dr. Wilson.

60

In her report, Dr. Freuler went a step further, suggesting not just that I.R. represents an unusual

case at the margins of RVA reliability, but actually positing that the unusual lack of red flag

behaviors is suggestive of an atypical pattern of autism. Pet. Ex. 145 at 5. Dr. Freuler wrote that

I.R. demonstrated a pattern of development that “support[s] an atypical trajectory of autistic

features. In my experience of reviewing hundreds of hours of early home movies of infants and

toddlers who went on to have a diagnosis of autism, I have very rarely (if ever) seen a lack of

ANY red flags in the first year of life prior to an onset of clinical symptoms.” Id.

45

are more complex and varied than simple groups of onset patterns. Id. (citing Pet. Ex. 199

(Ozonoff 2008) and Pet. Ex. 200 (Mahendra 2012)).61

The Ozonoff article notes that “[t]here is evidence that the traditionally defined categories

of early onset and regressive autism are overly narrow prototypes” and that “[t]here is ample

evidence of other ways in which symptoms emerge that are not captured by these prototypes.”

Pet. Ex. 199 at 7. Nonetheless, when discussing a hypothesized additional onset pattern wherein

intact early social development gives way to a later failure to progress, the authors stated that

“[n]o empirical research has been conducted on this pattern and very little is known about

whether it differs from other onset patterns in phenotypic features unrelated to symptom

emergence.” Id. at 6. The authors propose:

[S]ymptom emergence may better be characterized as a continuum. The two

extremes of this continuum are anchored by traditional defined prototypical early

onset and regressive cases, but many intermediate phenotypes containing mixed

features and varying degrees of early deficits, subtle diminishments, failures to

progress, and frank losses are also possible. We propose that variable combinations

and timings of these processes across children lead to symptoms exceeding the

threshold for diagnosis at different points in the first 24 months for different

children . . . .

Id. at 7.

Dr. Wilson concluded her supplement report by noting that “autism is a highly complex

developmental disorder with multiple genetic factors and patterns of progression. The [RVA]

methodology I used to examine I.R.’s early home videos cannot rule out late onset autism, but

does offer valuable information about the likelihood (or not) of early onset autism.” Pet. Ex.

198. Given her findings in this case – in which, given I.R.’s subsequent history, she effectively

concludes there is late onset autism – this is an equivocal conclusion. Moreover, Dr. Wilson

conceded during the hearing that RVA is still an evolving methodology. She acknowledged that

in terms of screening for earlier diagnosis, “we’re not there yet in every way.” Tr. 660-61. She

further explained that notwithstanding the success of RVA studies, “we still need more

information.” Tr. 667-68. Ultimately, she also acknowledged, perhaps consistent with her

findings in this case, that it is easier to pick up on autism at later ages “across the board,”

regardless of methodology.62 Tr. 668.

ii. Petitioners’ Additional Arguments

Petitioners raise several additional arguments in their post-hearing brief as to why Dr.

Wilson’s opinion should be accorded greater weight than Dr. Wiznitzer’s. The undersigned does

not find these arguments persuasive. Moreover, even if fully credited, none of these arguments

61

The Mahendra report is not a study and to the extent it does discuss prior studies, it does not

discuss them by name or even confirm whether the studies discussed were published.

62

Dr. Wiznitzer likewise stressed that diagnosis at one year of age is very difficult. Tr. 795-96.

46

is sufficient to overcome the undersigned’s findings with regard to the substance of Dr. Wilson’s

opinion. Nonetheless, the undersigned addresses each in turn.

a. First Year Medical Records

In their post-hearing brief, petitioners note that I.R.’s medical records report completely

normal development during the first year of life. Pet. Posthr’g Br. at 13. Specifically, petitioners

cite I.R.’s four-month, six-month, nine-month, and 12-month well-child visits. Pet. Ex. 9 at 34-

39. Petitioners also stress that Dr. Niyazov and Dr. Cohen both opined based on the medical

records that I.R. had normal development in his first year.63 Pet. Posthr’g Br. at 6 (citing Tr.

118, 228, 511-12).

The undersigned does take notice of the fact that I.R.’s pediatric medical records reflect

normal development through at least 12 months of age. Indeed, this fact was stipulated by the

parties prior to the hearing. Joint Prehr’g Submission at 1. However, this fact does not carry a

great deal of significance. Dr. Wilson testified that parents and clinicians commonly do not

become concerned about potential signs of autism until about 18 months to two years of age. Tr.

658-59. Dr. Wiznitzer similarly testified that children are typically referred for autism

evaluation after 18 to 24 months of age and that earlier referrals are less common. Tr. 881.

Moreover, Dr. Wiznitzer testified that the 12-month developmental screening in this case did not

account for the types of social behaviors he observed upon his review of the videos filed in this

case. Tr. 904-05. And indeed, petitioners note in their post-hearing brief that due to her

concerns regarding I.R.’s health status and her uncertainty as a first-time parent, Mrs. Reed

recognized some of I.R.’s developmental issues only in hindsight. Pet. Posthr’g Br. at 36-37.

Thus, the fact that I.R.’s medical records do not reflect the signs of autism discussed by

Dr. Wiznitzer is not surprising. Moreover, in light of the extensive expert evidence presented in

this case, the videos filed from I.R.’s first year of life remain the most illuminating evidence

regarding whether he demonstrated atypical behaviors prior to his first birthday. In that regard,

petitioners’ own expert confirmed that there was more than the usual amount of video footage

available in this case and that the amount was sufficient to detect atypical behaviors. Tr. 621-22.

Although the medical records provide some corroboration for Dr. Wilson’s opinion, that

corroboration is not very meaningful in light of her own testimony that parents and clinicians do

not typically recognize the early signs of autism.

b. Experts’ Credentials

Petitioners also allege a qualifications gap between Drs. Wilson and Wiznitzer, favoring

petitioners’ own expert. Petitioners argue, in effect, that Dr. Wilson’s history of participating in

RVA studies makes her more qualified to judge the videos filed in this case and determine the

age of onset for I.R.’s autism. Petitioners do not go so far as to argue that Dr. Wiznitzer’s

63

In the testimony cited by petitioners, Dr. Niyazov did not specifically address the basis for his

opinion regarding I.R.’s first year development. Although I.R. did have office visits with Dr.

Niyazov, these visits occurred later in life. Therefore, Dr. Niyazov’s opinion is necessarily based

on record review or later parental report.

47

testimony should be precluded, but implicitly argue that Dr. Wilson’s opinion should be afforded

greater weight. Pet. Posthr’g Br. at 18 n.33. The undersigned disagrees.

Dr. Wilson’s bona fides in the specific area of RVA are well established. She worked for

six years with the Program in early Autism Research, Leadership, and Service (“PEARLS”)

based at the University of North Carolina Chapel Hill, which is recognized as one of five main

research groups driving study in this field. Tr. 585, 594, 597; Pet. Ex. 165 (Saint Georges) at 5.

Dr. Wilson described the extensive training necessary to participate as a coder in the PEARLS

research and estimates that she has observed video footage of over 100 children. Tr. 576-77,

595-602. Dr. Wilson is published in this area as well. Tr. 602-10; Pet. Ex. 181 (Watson).

In contrast, Dr. Wiznitzer has not published in this area and has not suggested that he has

participated in any RVA studies. He described himself as “familiar” with the literature. Tr. 792.

Rather, Dr. Wiznitzer’s experience with RVA stems from his use of video review as part of his

clinical practice. Resp. Ex. 0 at 2; Tr. 792-93. Dr. Wiznitzer himself characterized his use of

video review as “occasional” and estimated that he reviews patient video about once a month.

Tr. 893. However, Dr. Wiznitzer noted that he has been doing so for many years, characterizing

the timeframe as dating back to when videos were available only on VCR cassette tapes. Tr.

792. In addition to his academic appointments, Dr. Wiznitzer has been a continuously practicing

clinician since 1984. Resp. Ex. Q at 2-3.

Regarding that clinical experience, petitioners stress that Dr. Wiznitzer testified that he

does not currently have any patient under 18 months of age and that patients are usually 18

months old by the time they are referred to him. Pet. Posthr’g Br. at 18-19 (citing Tr. 881, 883).

Dr. Wiznitzer testified, however, that he has evaluated less than ten patients under the age of one

for autism, but several dozen children 12-15 months old. Tr. 881. Dr. Wiznitzer also

specifically confirmed in his testimony that his experience with video review, which he has been

doing for decades to assist in diagnosis, involves videos recorded when his patients were

younger, including during the first year of live. Tr. 792, 896-97. Dr. Wiznitzer estimates that

up to 30% of his practice is devoted to children with autism. Tr. 880.

Petitioners further stress that Dr. Wiznitzer does not see well babies, suggesting that he

has “almost no experience evaluating 0-12 month olds who are ‘typical.’” Pet. Posthr’g Br. at 26

(citing Tr. 886). Dr. Wiznitzer testified, however, that as a pediatric neurologist he regularly

consults on cases involving infants for a variety of issues. Tr. 885. Dr. Wiznitzer clarified that

he sees infants with suspected neurological concerns, but that many of these conditions do not

affect their development. Tr. 886. Additionally, he noted that he is trained not only in

pediatrics, but in developmental pediatrics. Tr. 885. In any event, Dr. Wiznitzer also

persuasively explained that knowing normal social behavior, and variations on social behavior,

are an inherent part of making an autism diagnosis in the clinical context. Tr. 789-90.

Importantly, to the extent that the above points raised by petitioners arguably reveal

significant nuances regarding the relevancy of Dr. Wiznitzer’s clinical experience, these points

also highlight Dr. Wilson’s comparative lack of clinical experience. Dr. Wilson’s CV lists only

two years of clinical experience in speech-language pathology at Kennedy Krieger from 2006 to

2008. Pet. Ex. 177 at 1. She testified that her duties in her current teaching position, which she

48

has held since 2014, also involve supervision of graduate students engaged in clinical speech-

pathology work. Tr. 575. And in any event, although Dr. Wilson has identified a clear research

interest in early identification of autism, she has not demonstrated that any of her clinical, as

opposed to research, experience involves patients in the 0-12 month age range.64

Moreover, Dr. Wilson seemed to acknowledge that her observations may be limited by

her particular field. With specific regard to this case, she acknowledged that petitioners’ other

RVA expert, Dr. Freuler, may have picked up on additional atypical behaviors by virtue of her

training in occupational therapy. Tr. 632-33. Dr. Wilson also admitted that she has not

personally researched trajectories of autism. Tr. 670. This is significant, because diagnosis of

autism is a clinical exercise that extends far beyond speech pathology. See, e.g., King, 2010 WL

892296, at *79 (noting that “autism is considered both a neurologic and a psychiatric disorder”

and that “psychologists are also often the specialists who diagnose autism”); see also Snyder,

2009 WL 332044, at *32 (“With the exception of Rett’s disorder, all ASDs are diagnosed by

comparing behavioral symptoms exhibited by a child against an established set of broad

diagnostic criteria. The diagnosis is made by direct observation, videos of the child, and from

parental reports, as there is no biochemical test for ASD.”).

These points go to the core of the difference between these two experts. While Dr.

Wilson clearly has research experience and training specific to RVA that Dr. Wiznitzer lacks,

Dr. Wiznitzer has a depth and breadth of clinical experience in pediatric neurodevelopment and

autism that Dr. Wilson cannot match. Dr. Wiznitzer persuasively asserted that, notwithstanding

the research methodologies involved in RVA studies, video review itself can be an extension of

clinical care and diagnosis. Tr. 903. Petitioners, on the other hand, have not established that the

video format itself in any way prevents Dr. Wiznitzer from utilizing the full breadth of his

clinical skills. Thus, the undersigned disagrees that Dr. Wilson’s testimony is entitled to greater

weight based on her credentials. While these two experts have different strengths, the

undersigned stresses that both are qualified to opine in this case regarding the manifestation of

I.R.’s autism.

This text is long and has been trimmed here. Open the source document for the complete record.