Allen v. Hhs

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 02-1237V

Filed: September 26, 2015

For Publication

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

COLLEEN BOSTON MADARIAGA and *

JAMES ALLEN, parents and guardians of *

A.A., a minor, * Measles, Mumps, and

* Rubella [“MMR”] Vaccine;

Petitioners, * Autism; Mitochondrial

* Disorder; Diagnosis;

v. * Metabolic Stress;

* Regression; Treating

SECRETARY OF THE DEPARTMENT * Physicians; Expert

OF HEALTH AND HUMAN SERVICES, * Qualifications

*

Respondent. *

*

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

Sylvia Chin-Caplan, Conway, Homer & Chin-Caplan, Boston, MA, for petitioners.

Heather Pearlman, U.S. Dept. of Justice, Washington, D.C., for respondent.

DECISION 1

Vowell, Special Master:

On September 23, 2002, Colleen Allen [“petitioner”] filed a short-form “Petition for

Vaccine Compensation” for compensation under the National Vaccine Injury

Compensation Program, 42 U.S.C. §300aa-10, et seq. 2 [“Vaccine Act” or “Program”] on

behalf of her daughter, A.A. An amended petition, which now constitutes the operative

petition for this claim, was filed on March 1, 2012. 3 On May 9, 2012, petitioner moved

1

The E-Government Act of 2002, Pub. L. No. 107-347, 116 Stat. 2899, 2913 (Dec. 17, 2002) requires

that this decision be publically available. In accordance with Vaccine Rule 18(b), petitioner has 14 days

to identify and move to redact medical or other information, the disclosure of which would constitute an

unwarranted invasion of privacy. If, upon review, I agree that the identified material fits within this

definition, I will redact such material from public access.

2

The National Vaccine Injury Compensation Program [“Vaccine Program”] is set forth in Part 2 of the

National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755, codified as amended,

42 U.S.C. § 300aa-10 et seq. (2012). All citations in this decision to individual sections of the Vaccine Act

are to 42 U.S.C. § 300aa.

3

Hereinafter, unless the context clearly indicates otherwise, any reference to “petition” is to this Amended

Petition.

to amend the case caption to reflect her name change following remarriage, and to add

James Allen, A.A.’s father, as a petitioner.

In summary, petitioners claim that the measles, mumps, and rubella [“MMR”]

vaccine A.A. received on October 23, 2000, caused her to suffer from “mitochondrial

pervasive developmental disorder” 4—a “particular form of autistic spectrum disorder

caused by an inborn error of mitochondrial metabolism.” Petition ¶¶ Introduction, 15.

According to their experts, A.A. had an underlying mitochondrial disorder—present

since birth—that made her vulnerable to the inflammatory effects of the MMR vaccine.

The vaccine, which constituted an immunological stressor, overwhelmed A.A.’s already

impaired mitochondrial function and caused extensive cell death in her brain. As a

result of this damage, she experienced an acute regression and ultimately developed

mitochondrial autism. See Petitioners’ Post-Hearing Brief, filed Nov. 27, 2013, at 30-60.

For the reasons set forth below, I find that the record does not contain

preponderant evidence establishing entitlement to compensation.

I. Procedural History.

A. The Omnibus Autism Program [“OAP”].

Beginning in 1997, but peaking numerically in 2002-03, thousands of petitions

were filed alleging either that the measles, mumps, and rubella [“MMR”] vaccine or

thimerosal, an ethyl mercury preservative used in multi-dose vials of vaccine, caused

ASD. The sheer volume of petitions filed—more than 1,300 new petitions in 2002

alone—led to the creation of the OAP. 5 Omnibus programs had been used previously

to make causation determinations in groups of cases alleging that a particular vaccine

caused a specific injury, but the OAP was, by far, the largest such grouping of similar

cases. 6 By filing their original short-form petition, an abbreviated petition authorized by

Autism General Order #1, petitioners opted into the OAP.

Following a series of meetings with an informal advisory committee comprised of

petitioners’ counsel representing many of the Program claimants plus legal and medical

representatives of the Secretary of Health and Human Services, the Office of Special

Masters adopted a plan that would allow a period of discovery, followed by the selection

and litigation of test cases on the theories of causation presented. Autism General

4

Synonymous with “mitochondrial pervasive development disorder” are the terms “autism secondary to

mitochondrial disease” and “mitochondrial autism.” Tr. at 236-37.

5

See Autism General Order #1, issued July 3, 2002 (found at 2002 WL 31696785, 2002 U.S. Claims

LEXIS 365, or http://www.uscfc.uscourts.gov/sites/default/files/autism/Autism+General+Order1.pdf) (last

visited on Sept. 8, 2015).

6

See Hennessey v. Sec’y, HHS, No. 01-190V, 2009 WL 1709053 (Fed. Cl. Spec. Mstr. May 29, 2009),

aff’d, 91 Fed. Cl. 126 (2010) (discussing the different types of omnibus proceedings conducted in the

Vaccine Program).

2

Order #1 at 2-3. The conclusions reached on general causation in the test cases would

be used to resolve the remaining individual claims. Id. at 3. Petitioners were allowed to

“opt in” or “opt out” of the proceedings and future claimants could automatically “opt in”

by filing the short form petition included as Attachment B to Autism General Order #1.

Autism General Order #1 at 6-8.

Attorneys representing petitioners created the Petitioners’ Steering Committee

[“PSC”] to coordinate the OAP litigative effort. The PSC acknowledged that there was

insufficient evidence at the time the OAP was created to prove vaccine causation, but

averred that such evidence could be found through discovery and ongoing scientific

investigations. Petitioners sought and received an extended period of time to conduct

discovery and prepare to litigate test cases.

Nearly five years after the OAP was created, litigation in the test cases began.

The PSC presented two different theories on the causation of ASD in two sets of test

cases. The first alleged that thimerosal-containing vaccines and the MMR vaccine, in

combination, could cause ASD (Theory 1). The second alleged that thimerosal-

containing vaccines could cause ASD (Theory 2). 7

Decisions in each of the three Theory 1 test cases, which were tried in 2007,

rejected petitioners’ causation theories. Cedillo v. Sec’y, HHS, No. 98-916V, 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); Hazlehurst v. Sec’y, HHS, No. 03-654V, 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); Snyder v. Sec’y, HHS, No. 01-162V, 2009 WL 332044 (Fed. Cl. Spec.

Mstr. Feb. 12, 2009), aff’d, 88 Fed. Cl. 706 (2009). 8

Decisions in the three Theory 2 test cases, which were tried in 2008, also

rejected the causation theory presented. Petitioners did not seek review of the special

masters’ decisions. Dwyer, 2010 WL 892250; King v. Sec’y, HHS, No. 03-584V, 2010

WL 892296 (Fed. Cl. Spec. Mstr. Mar. 12, 2010); Mead, 2010 WL 892248.

An impressive body of medical and scientific evidence was adduced in the OAP

test cases, with the three special masters who heard this evidence finding that the issue

of vaccine causation was “not a close case.” See, e.g., King, 2010 WL 892296, at *90

(emphasis in original); Snyder, 2009 WL 332044, at *198. Each of the three special

7

A detailed discussion of the OAP can be found at Dwyer v. Sec’y, HHS, No. 03-1202V, 2010 WL

892250, at *2 (Fed. Cl. Spec. Mstr. Mar. 12, 2010). In keeping with the intent that the OAP test case

evidence be available to aid in resolving the remaining OAP cases, the evidence (including expert

reports, transcripts of testimony, trial presentation materials (trial exhibits), and lists of the medical

journals and other documents filed by the parties) is posted on the Court of Federal Claims website

(http://www.uscfc.uscourts.gov/docket-omnibus-autism-proceeding) (last visited on May 11, 2015). The

parties in the test case hearings all filed explicit written consent to make these materials publicly

available. See, e.g., Mead v. Sec’y, HHS, No. 03-215V, 2010 WL 892248 (Fed. Cl. Spec. Mstr. Mar. 12,

2010), at *1 n.1 (referencing petitioners’ and respondent’s written consent in that case).

8

Petitioners did not appeal the Court of Federal Claims decision in Snyder to the Federal Circuit.

3

masters independently determined that the medical theories advanced were not reliable

and that the test case petitioners had failed to produce preponderant evidence of

causation. The OAP test case litigation concluded in 2010, with the last Federal Circuit

decision affirming the dismissal of the final Theory 1 test case. 9

During the period between the test case hearings and the final appellate action

on the test case decisions, petitioners in this case, like others in the OAP, were ordered

to file the medical records necessary to establish that the petition was timely filed. See

Order, issued Mar. 13, 2009, at 5. Petitioners filed the required medical records on

June 11, 2009 and July 22, 2009. See Petitioners’ Exhibits [“Pet. Exs.”] 1-10. On

August 14, 2009, respondent filed a statement indicating that the claim was timely filed

and involved a diagnosis of ASD. Because the claim was determined to have been

timely filed, petitioners were ordered to file all remaining medical records. See Order,

issued Aug. 24, 2009, at 1-2. Petitioners filed the required medical records on

November 19, 2009 and December 23, 2009. See Pet. Exs. 11-14.

With appellate review completed, orders were issued on a rolling basis to the

remaining 4,800 petitioners, requiring them to inform the court whether they intended to

dismiss their case or proceed on a different theory or with different evidence.

Petitioners were ordered to inform the court if they wished to proceed with their claim.

See Order, issued May 12, 2011, at 3. If petitioners wished to continue with their claim,

they were ordered to file an amended petition, setting forth their theory of causation. 10

Id. During the next ten months, petitioners filed additional medical records. See Pet.

Exs. 15-20. On March 1, 2012, they filed their amended petition.

B. Procedural History Post-OAP.

On March 15, 2012, I held a telephonic status conference to discuss petitioners’

amended petition and next steps in this case. I ordered petitioners to file any

outstanding medical records and a supplemental statement of completion by March 30,

2012, and expert reports by May 14, 2012. See Scheduling Order, issued Mar. 15,

2012.

On March 30, 2012, petitioners filed a supplemental statement of completion

indicating that they had filed all of the medical records to substantiate the amended

petition.

After requesting and receiving additional time to file their expert reports (see

Motions, filed May 14, 2012; July 16, 2012), petitioners filed an expert report, curriculum

vitae [“CV”], and two supporting documents from Dr. Richard Kelley; and an expert

report, CV, and one article from Dr. Andrew Zimmerman on July 19, 2012. See Pet.

9

Cedillo v. Sec’y, HHS, 617 F.3d 1328 (Fed. Cir. 2010).

10

Petitioners were cautioned that the special masters did not intend to re-litigate the test case theories,

and that a reasonable basis to proceed would require either new evidence on the old theories or new

theories of causation. See Order, issued May 12, 2011, at 2.

4

Exs. 23-26. 11 Although both experts treated A.A., they did so long after onset of her

ASD symptoms.

On November 16, 2012, respondent filed her supplemental Rule 4(c) report; an

expert report, CV, and eight articles from Dr. Stephen Cederbaum; and an expert report,

CV, and seven articles from Dr. Max Wiznitzer, after seeking one extension of time.

See Respondent’s Rule 4(c) report; Respondent’s Exhibits [“Res. Exs.”] A-S.

On January 9, 2013, I held a telephonic status conference pursuant to Vaccine

Rule 5 12 to discuss the expert reports and positions of the parties. During the status

conference, the parties agreed that the case was ready for a hearing to address the

experts’ disagreement with regard to causation. I noted that certain factual disputes still

existed and that I would need the experts to testify on these issues as well. I ordered

the parties to file a joint status report by January 24, 2013, providing possible hearing

dates. See Scheduling Order, issued Jan. 9, 2013.

After the parties filed their joint status report, I scheduled a four-day entitlement

hearing in Washington, D.C. from July 9-12, 2013. See Pre-Hearing Order, issued Jan.

28, 2013. On April 5, 2013, I ordered the parties to file any outstanding evidence on

which they intended to rely by May 24, 2013. See Pre-Hearing Order, issued Apr. 5,

2013, at 1. I also ordered the parties to file (1) a joint submission identifying any

disputed and non-disputed issues; (2) a memorandum containing their basic factual

contentions and applicable legal authority; (3) an affidavit from each fact witness, if not

previously filed; and (4) witness lists. Id. at 2.

Over the next several months, petitioners timely filed additional medical

literature, 13 updated school and medical records, and relevant video evidence.

Respondent also filed additional medical literature. 14 On June 10, 2013, the parties filed

their pre-hearing submissions. Petitioners indicated that they would be calling four

witnesses, including two expert witnesses, to testify at the hearing. See Pet. Pre-

Hearing Submission, filed June 10, 2013, at 34. Respondent indicated that she would

be calling both of her expert witnesses to testify. See Res. Pre-Hearing Submission,

filed June 10, 2013 (ECF No. 80), at 16. Petitioners also filed the affidavits of James

Allen (A.A.’s father) and Susan Edick (A.A.’s aunt), A.A.’s vaccination record, and

additional video and photographic evidence.

11

The supporting documents from Dr. Kelley included A.A.’s amino acid profile (Pet. Ex. 23A) and an

unpublished protocol titled “Evaluation and Treatment of Patients with Autism and Mitochondrial Disease

(Pet. Ex. 23B). Doctor Zimmerman submitted J. Poling, et al., Developmental Regression and

Mitochondrial Dysfunction In a Child with Autism, J. CHILD NEUROL., 21 (2): 170-72 (2006), filed as Pet.

Ex. 25, Tab A [hereinafter “Poling, Pet. Ex. 25A”].

12

RCFC, Appendix B.

13

See Pet. Exs. 27-59, 65-74.

14

See Res. Exs. T-CC.

5

Finally, the parties filed a joint submission identifying the disputed and non-

disputed issues. See Joint Pre-Hearing Submission, filed June 10, 2013 (ECF No. 79).

Specifically, the parties disputed (1) “the state of A.A.’s health and development prior to

October 23, 2000”; (2) whether “A.A. suffer[ed] a developmental regression after her

receipt of the October 23, 2000, MMR vaccination[,]” and, if so, when the regression

occurred; (3) whether the “October 23, 2000, MMR vaccinations cause[d]-in-fact any of

A.A.’s subsequently diagnosed developmental, neurological, or mitochondrial issues”;

and (4) whether “A.A. has a mitochondrial disease[.]” Id. at 1-2.

On June 20, 2013, petitioners filed additional video evidence. See Pet. Ex. 80.

On June 28, 2013, I held a telephonic status conference with the parties to discuss the

pending hearing. I also discussed the video evidence filed by petitioners. Petitioners’

counsel confirmed that the video was a compilation of clips taken from a more complete

recording. I explained that although the edited clips could be used during testimony, the

entire recording should be filed into the record for review. I also requested that any

additional videos of A.A. from the first two years of her life be filed, if available. See

Scheduling Order, issued July 1, 2013.

In compliance with my order, petitioners filed an unedited version of the video.

See Pet. Ex. 81. Petitioners also filed a status report stating that “after a diligent

search, . . . they were unable to locate any additional videos of A.A. from one to two

years of age.” See Status Report, filed July 2, 2013, at 2.

The entitlement hearing was held as scheduled, from July 9-12, 2013. Four

physicians testified at the four day hearing. Mr. Allen and Ms. Edick also testified in

person. A.A. also attended part of the hearing, and I had the opportunity to meet and

speak with her. Following the hearing, I set a schedule for the identification and

correction of transcript errors and the submission of post-hearing briefs. See Post-

Hearing Order, issued on July 30, 2013.

On August 1, 2013, petitioners filed several exhibits used during the hearing.

See Trial Exhibits [“Trial Exs.”] 1-5. On September 3, 2013, I filed Court Exhibit I, a

medical journal article, and provided the parties and their experts an opportunity to

comment on the exhibit. See Res. Resp. to Court’s Sept. 3, 2013 Order and Ex., filed

Sept. 30, 2013; Res. Ex. DD; Pet. Resp. to Court’s Sept. 3, 2013 Order and Ex., filed

Oct. 3, 2013; Pet. Ex. 82.

On September 6, 2013, the parties submitted their joint corrections to the

transcript. A corrected version of the transcript was filed on September 19, 2013. 15

Simultaneous post-hearing briefs were filed on November 27, 2013. On

December 12, 2013, the parties submitted responses to the post-hearing briefs,

completing the record.

15

All references to the transcript are to the corrected version.

6

II. Legal Standards Applying to Off-Table Causation Claims.

When petitioners allege an off-Table injury, eligibility for compensation is

established when, by a preponderance of the evidence, petitioners demonstrate that the

vaccinee received, in the United States, a vaccine appearing on the Table and

sustained an illness, disability, injury, or condition caused by the vaccine or experienced

a significant aggravation of a preexisting condition. They must also demonstrate that

the condition has persisted for more than six months. 16 Vaccine Act litigation rarely

concerns whether the vaccine appears on the Table, the geographical location of

administration, or whether the symptoms have persisted for the requisite time. Rather,

in the very small minority of Vaccine Act cases that proceed to a hearing, the most

common issue to be resolved by the special master is whether the injury alleged was

caused by the vaccine.

To establish legal causation in an off-Table case, Vaccine Act petitioners must

establish by preponderant evidence: (1) a reliable medical theory causally connecting

the vaccination and the injury; (2) a logical sequence of cause and effect showing that

the vaccination was the reason for the injury; and (3) a proximate temporal relationship

between vaccination and injury. Althen v. Sec’y, HHS, 418 F.3d 1274, 1278 (Fed. Cir.

2005); see de Bazan v. Sec’y, HHS, 539 F.3d 1347, 1351-52 (Fed. Cir. 2008); Caves v.

Sec’y, HHS, 100 Fed. Cl. 119, 132 (2011), aff’d per curiam, 463 Fed. Appx. 932 (Fed.

Cir. 2012) (specifying that each Althen factor must be established by preponderant

evidence). The applicable level of proof is the “traditional tort standard of ‘preponderant

evidence.’” Moberly v. Sec’y, HHS, 592 F.3d 1315, 1322 (Fed. Cir. 2010) (citing de

Bazan, 539 F.3d at 1351); Pafford v. Sec’y, HHS, 451 F.3d 1352, 1355 (Fed. Cir. 2006);

Capizzano v. Sec’y, HHS, 440 F.3d 1317, 1320 (Fed. Cir. 2006); Althen, 418 F.3d at

1278). Although special masters are not bound by the formal rules of evidence

generally applicable in federal courts, they are required to find evidence reliable before

they may consider it. Knudsen v. Sec’y, HHS, 35 F.3d 543, 548-49 (Fed. Cir. 1994)

(Petitioner has the burden to present a reliable and reputable medical theory, which

must be “legally probable, not medically or scientifically certain.”); Daubert v. Merrell

Dow Pharmaceuticals, 509 U.S. 579, 590 (1993) (holding that scientific evidence and

expert opinions must be reliable to be admissible). The preponderance standard

“requires the trier of fact to believe that the existence of a fact is more probable than its

nonexistence.” In re Winship, 397 U.S. 358, 371 (1970) (Harlan, J., concurring)

(internal quotation and citation omitted).

Another formulation of the causation requirement in off-Table cases is the “Can it

cause?” and “Did it cause?” inquiries used in toxic tort litigation. These queries are also

referred to as issues of general and specific causation. Prong 1 of Althen has been

characterized as an alternative formulation of the “Can it cause?” or general causation

query. Prong 2 of Althen, the requirement for a logical sequence of cause and effect

16

Section 13(a)(1)(A). This section provides that petitioner must demonstrate “by a preponderance of the

evidence the matters required in the petition by section 300aa–11(c)(1) . . . .” Section 11(c)(1) contains

the factors listed above, along with others not relevant to this case.

7

between the vaccine and the injury, has been characterized as addressing the “Did it

cause?” or specific causation query. See Pafford v. Sec’y, HHS, No. 01-165V, 2004 WL

1717359, at *4 (Fed. Cl. Spec. Mstr. July 16, 2004), aff’d, 64 Fed. Cl. 19 (2005), aff’d,

451 F.3d 1352 (2006). Prong 3 of Althen, the requirement that the injury sustained

occur within a medically appropriate interval after vaccination, is subsumed into the

other inquiries. Even if a particular vaccine has been causally associated with an injury,

petitioner must still establish facts and circumstances that make it more likely than not

that this vaccine caused the particular injury. Timing may be one of those

circumstances.

Whether a case is analyzed under Althen or the “Can it cause?” formulation,

petitioners are not required to establish identification and proof of specific biological

mechanisms, as “the purpose of the Vaccine Act’s preponderance standard is to allow

the finding of causation in a field bereft of complete and direct proof of how vaccines

affect the human body.” Althen, 418 F.3d at 1280. Petitioners need not show that the

vaccination was the sole cause, or even the predominant cause, of the injury or

condition; showing that the vaccination was a “substantial factor” 17 in causing the

condition, and was a “but for” cause, are sufficient for recovery. Shyface v. Sec’y, HHS,

165 F.3d 1344, 1352 (Fed. Cir. 1999); see also Pafford, 451 F.3d at 1355 (petitioners

must establish that a vaccination was a substantial factor and that harm would not have

occurred in the absence of vaccination). Petitioners cannot be required to show

“epidemiologic studies, rechallenge, the presence of pathological markers or genetic

disposition, or general acceptance in the scientific or medical communities to establish a

logical sequence of cause and effect,” Capizzano, 440 F.3d at 1325, but the special

master may certainly consider such evidence when filed. Andreu v. Sec’y, HHS, 569

F.3d 1367, 1379 (Fed. Cir. 2009) (Special masters may consider medical literature and

epidemiological evidence, when it is submitted, in “reaching an informed judgment as to

whether a particular vaccine likely caused a particular injury.”). 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 (Fed. Cir. 1994). Close calls regarding causation must be

resolved in favor of petitioners. Althen, 418 F.3d at 1280; but see Knudsen, 35 F.3d at

550 (when evidence is in equipoise, the party with the burden of proof fails to meet that

burden).

In Vaccine Act cases, special masters are frequently confronted by expert

witnesses with diametrically opposing positions on causation. When experts disagree,

many factors influence a factfinder to accept some testimony and reject other contrary

testimony. 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.

17

The Restatement (Third) of Torts has eliminated “substantial factor” in the factual cause analysis. § 26

cmt. j (2010). Because the Federal Circuit has held that the causation analysis in the Restatement

(Second) of Torts applies to off-Table Vaccine Act cases (see Walther v. Sec’y, HHS, 485 F.3d 1146,

1151 (Fed. Cir. 2007); Shyface, 165 F.3d at 1352), this change does not affect the determination of legal

cause in Vaccine Act cases: whether the vaccination is a “substantial factor” is still a consideration in

determining whether it is the legal cause of an injury.

8

Objective factors, including the qualifications, training, and experience of the expert

witnesses; the extent to which their proffered opinions are supported by reliable medical

research and other testimony; and the factual basis for their opinions are all significant

factors in determining what testimony to credit and what to reject. Lalonde v. Sec’y,

HHS, 746 F.3d 1334, 1340 (Fed. Cir. 2014) (noting that “as the finder of fact, the special

master was responsible for assessing the reliability of [the expert’s] testimony by looking

for reliable medical or scientific support” (citing Moberly, 592 F.3d at 1324-25)).

Congress contemplated that special masters would weigh and evaluate opposing

expert opinions in determining whether petitioners have met their burden of proof.

Congress clearly specified petitioners’ burden of proof in off-Table cases as the

preponderance of the evidence standard. It directed special masters to consider the

evidence as a whole, but stated that special masters are not bound by any particular

piece of evidence contained in the record. 18 In weighing and evaluating expert opinions

in Vaccine Act cases, the same factors the Supreme Court has considered important in

determining their admissibility provide the weights and counterweights. See Kumho

Tire Co. v. Carmichael, 526 U.S. 137, 149-50 (1999); Terran v. Sec’y, HHS, 195 F.3d

1302, 1316 (Fed. Cir. 1999). As the Supreme Court has noted, a trial court is not

required to accept the ipse dixit of any expert’s medical or scientific opinion because the

“court may conclude that there is simply too great an analytical gap between the data

and the opinion proffered.” Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997).

Although the Federal Rules of Evidence and cases interpreting them are not

binding on special masters, they can guide their decisions. Daubert, which interpreted

Rule 702 of the Federal Rules of Evidence, provides a useful framework for evaluating

scientific evidence in Program cases. Terran, 195 F.3d at 1316 (concluding that it was

reasonable for the special master to use Daubert to evaluate the reliability of an expert’s

testimony); Cedillo, 617 F.3d at 1339 (noting that special masters are to consider all

relevant and reliable evidence filed in a case and may use Daubert factors in their

evaluation of expert testimony); Davis v. Sec’y, HHS, 94 Fed. Cl. 53, 67 (2010)

(describing the Daubert factors as an “acceptable evidentiary-gauging tool with respect

to persuasiveness of expert testimony already admitted . . . by special masters in

vaccine cases”); see also Snyder, 88 Fed. Cl. 706, 718 (2009) (quoting Ryman v. Sec’y,

HHS, 65 Fed. Cl. 35, 40-41 (2005) (special masters perform gatekeeping function when

determining “whether a particular petitioner’s expert medical testimony supporting

biological probability may be admitted or credited or otherwise relied upon” and as a

“trier-of-fact [a special master] may properly consider the credibility and applicability of

medical theories”)). The special master’s use of the Daubert factors to evaluate the

reliability of expert opinions in Vaccine Act cases has been cited with approval by the

Federal Circuit more recently in Andreu, 569 F.3d at 1379 and Moberly, 592 F.3d at

1324. See also Vaughan v. Sec’y, HHS, 107 Fed. Cl. 212, 222 (2012) (“The Federal

18

See § 13(a)(1)(A) (preponderance standard); § 13(a)(1) (“Compensation shall be awarded . . . if the

special master or court finds on the record as a whole . . . .” ); § 13(b)(1) (indicating that the court or

special master shall consider the entire record in determining if petitioner is entitled to compensation and

special master is not bound by any “diagnosis, conclusion, judgment, test result, report, or summary”

contained in the record).

9

Circuit has repeatedly stated that the Special Master may refer to Daubert to assess

reliability of expert testimony in vaccine cases.”). Special masters decide questions of

credibility, plausibility, probability, and reliability, and ultimately determine to which side

the balance of the evidence is tipped. See Pafford, 451 F.3d at 1359.

Bearing all these legal standards in mind, I now turn to the evidence presented in

this case.

III. Summary of Relevant Medical Records.

A. Early Medical and Developmental History.

A.A., petitioners’ first child, was born in mid-July, 1999. She was a healthy

newborn, with Apgar scores of 8 and 9. 19 Pet. Ex. 1, p. 19. Her newborn exam was

normal. 20 Pet. Ex. 3, pp. 5, 16.

During her first year of life, A.A. received routine childhood immunizations 21 and

was generally healthy with no major illnesses. Her medical records from Countryside

Pediatrics [“Countryside”], her primary care provider, 22 reflect scheduled well child

examinations, as well as periodic unscheduled visits due to minor illnesses.

A.A. was seen for her two-month well child visit on September 17, 1999, and was

noted to be “doing very well.” Pet. Ex. 9, p. 13. The medical report indicated a normal

physical examination, and normal development as measured by six defined skills,

including whether she regarded a face directly and responded to sound. 23

19

The Apgar score is a numerical assessment of a newborn’s condition (with lower numbers indicating

problems), usually taken at one minute and five minutes after birth. The score is derived from the infant’s

heart rate, respiration, muscle tone, reflex irritability, and color, with from zero to two points awarded in

each of the five categories. See DORLAND’S ILLUSTRATED MEDICAL DICTIONARY (32d ed. 2012)

[“DORLAND’S”] at 1682; NELSON TEXTBOOK OF PEDIATRICS (19th ed. 2011) [“NELSON’S ”] at 536-37.

20

She initially failed the audiological evaluation; however, upon re-testing, her hearing was found to be

within normal limits. Pet. Ex. 3, pp. 13-15.

21

On September 17, 1999, A.A received her first vaccinations, which included the combined diphtheria,

tetanus, and acellular pertussis [“DTaP”]; Haemophilus influenzae Type b [“Hib”]; and the inactivated polio

[“IPV”] vaccines. Pet. Ex. 9, p.1. She received the second round of the same vaccines at her two month

well child visit on November 19, 1999. Id. She received her third DTaP and Hib vaccines at her six

month well child visit on January 21, 2000. Id. She received the varicella and her first hepatitis B

vaccines at her one year well child visit on July 26, 2000. Id.

22

A.A. was evaluated by a variety of health care professionals at Countryside Pediatrics, including

medical doctors, certified pediatric nurse practitioners, and registered nurses. These professionals will all

be referred to as her “pediatrician,” regardless of their credentials.

23

A.A.’s pediatrician made use of developmental checklists with very specific developmental milestones

for specific ages. Those for the two month visit incuded: (1) Regards face directly; (2) Lifts head when

upright; (3) Coos; (4) Smiles; (5) Grasps object when placed in hands; (6) Responds to sound. Pet. Ex.

9, p. 13.

10

On November 11, 1999, at about four months of age, she was seen for an upper

respiratory infection [“URI”]. Pet. Ex. 9, p. 62. She had awakened screaming, with

fever, irritability, and loss of appetite. Id. Her pediatrician gave instructions to call if her

fever exceeded 100 degrees or if she did not improve within three days. Id. On

November 16, 1999, she was seen due to congestion, irritability, and difficulty sleeping,

and was diagnosed with bronchiolitis. Id., p. 61. She returned again on November 19,

1999, with URI symptoms and continued congestion. Id., p. 60.

At her six-month well child visit on January 21, 2000, A.A.’s growth and

development were normal. Pet. Ex. 9, p. 12. The medical report indicated a normal

physical examination, and normal development as measured by eight defined skills,

including whether she laughed and babbled or could sit with little support. 24 Id. On

January 26, 2000, she returned due to a persistent cough and runny nose, which was

diagnosed as a URI. Id., p. 59. She had been pulling at her ears, as well. Id.

A.A. was seen for her nine-month well child visit on April 21, 2000. Pet. Ex. 9, p.

11. The medical report contained no written comments, but indicated a normal physical

examination, and normal development as measured by seven defined skills, including

the ability to imitate “mama, dada.” 25 Id. On April 26, 2000, A.A. returned due to

congestion and a raspy voice. Id., p. 58. After examination, she was diagnosed with

right otitis media [“OM”], bilateral conjunctivitis, and a URI. Id.

On July 24, 2000, A.A. attended her one-year well child examination,

accompanied by her nanny. She was assessed as normal with regard to illness and

accidents, and her temperament, as reported by the nanny, was “no problem.” The

corresponding medical report indicated a normal physical examination, and normal

development as measured by eight defined skills, including whether she could walk two

to three steps or say one to three words. 26 Pet. Ex. 9, p. 10.

B. Administration of Allegedly Causal Vaccination.

As reflected by the medical evidence of record, A.A. did not visit any healthcare

provider between her one-year well child visit and her 15-month checkup. At that

examination, on October 23, 2000, she was tugging at her ears and was reported to

often have a cold. Pet. Ex. 9, p. 9. Her physical examination was normal, although her

tympanic membranes had fluid. Id. She also had normal development as measured by

24

The eight assessed developmental skills were: (1) Reaches for toys; (2) No head lag; (3) Laughs,

babbles; (4) Peak-a-boo, pat-a-cake; (5) Sits with little support; (6) Fearful of strangers; (7) Rolls over; (8)

Bears own weight. Pet. Ex. 9, p. 12.

25

The seven assessed developmental skills were: (1) Pincer grasp; (2) Holds bottle; (3) Imitates mama,

dada; (4) Peak-a-boo, pat-a-cake: (5) Sits well alone; (6) Crawls; (7) Pulls up to stand. Pet. Ex. 9, p. 11.

26

The eight assessed developmental skills were: (1) Precise pincer grasp; (2) Stands alone; (3) Walks 2-

3 steps; (4) Says 1-3 words; (5) Imitates sounds; (6) Eats and drinks sitting up; (7) Points; (8) Waves

“bye-bye.” Pet. Ex. 9, p. 10.

11

five defined skills, including whether she could walk well alone and point at one to two

body parts. 27 Id. At this examination she received her first MMR, second hepatitis B,

and fourth Hib vaccines. Id., p.1. Petitioners claim this MMR vaccine was causal of

A.A.’s current condition.

C. Growth and Development Following the October 23, 2000 Vaccination.

The first reported illness following her 15-month check-up and MMR vaccination

was nearly two months later, on December 18, 2000, when she was treated for a viral

infection and early OM. Pet. Ex. 9, p.57. The examination report from that encounter

reflected that A.A. had vomited the previous night, and awakened with a fever; however,

there is no mention of any behavioral or developmental concerns. Id. On January 25,

2001, she was treated at the Loudon Healthcare Emergency Room for second degree

burns to her hands after she touched a hot fireplace screen at home. Pet. Ex. 22, pp.

18-20.

A.A. was seen for her 18-month 28 well child visit on March 1, 2001. Additionally,

she had a runny nose and was teething. The examination report noted that the burns to

her hands were healing well. Some issues with the previous nanny were reported, but

A.A. was “opening up more” now with a new nanny. Her physical examination was

completely normal, except for a left ear infection. She was prescribed an antibiotic, with

orders to follow up in 10 to 14 days. She was behind on two vaccinations (DTaP and

IPV), which could be administered at the follow-up visit. Her development was again

measured against a defined set of skills; for the first time, A.A. did not display some of

the expected skills. The report indicated that she was fully able to drink from a cup,

walk up steps, point to body parts, and scribble. However, she had not mastered using

a spoon and only took off some clothes. Her ability to build three to four block towers

was not checked as achieved. And, the response to whether she could speak 4-10

words was “? consistency.” Despite diagnosed acute left OM, she was evaluated as a

“well 19 month old.” Pet. Ex. 9, p. 8.

A note dated March 1, 2001 continued the report from A.A.’s 18 month well child

visit. It stated:

Mom reports [decreased] language skills. Baby seems to understand [but]

sometimes refuses to talk/play games. Mom attributes above to change in

nanny – mom wasn’t pleased with nanny. Also child burned hand in

[January 2001]. New nanny seems knowledgeable [about] child

dev[elopment]. Takes [baby] to play groups, library, reads & sings, etc.

Mom to continue to talk to baby, play games, read & sing – but to back off

27

The five evaluated developmental skills were: (1) Drinks from cup; (2) Walks well alone; (3) Crawls up

steps; (4) Rolls and tosses ball; (5) Points at 1-2 body parts. Pet. Ex. 9, p. 9. Language or vocabulary

was not assessed on the examination record, but the Denver II developmental screening form reflected

that she had at least three words at 15 months of age. Id., p. 7

28

A.A. was more than 19 months old at the time of the visit.

12

if this becomes a power struggle [with baby]. [Follow up] if concerned or if

not seeing progress in language dev[elopment] over [the] next 2 months.

Pet. Ex. 9, p. 18.

The examiner also completed the medical portion of the Virginia School Entrance

Health Form, which was required prior to A.A.’s admission to school. The report

generally mirrored the findings noted in the Countryside Pediatrics record described

above and estimated her developmental level to be within normal limits. Pet. Ex. 7, p.

13.

A.A. next visited Countryside on March 23, 2001, due to coughing and

congestion. Also of concern was a reported increase in hearing loss after the “past 3

[bilateral] OM” and her ear tugging. She was diagnosed with a URI and bilateral OM. A

note indicated that A.A.’s “language skills [were] improving” and that she could say “uh-

oh” and “bye, bye.” Pet. Ex. 9, p. 56.

Several weeks later, on April 2, 2001, A.A. was treated for OM. She had

continued tugging at her ears, was “generally feeling miserable,” and had been

“sleeping a lot.” Pet. Ex. 9, p. 55. She also received her third hepatitis B and IPV and

her fourth DTaP vaccines at this examination. Id., p. 1.

On May 7, 2001, A.A. returned to follow up on her three ear infections,

accompanied by her nanny. The examination report noted concerns regarding A.A.’s

hearing, speech/language delay, and vocabulary of about six words. She was

diagnosed again with OM. For the first time, her pediatrician assessed her as

developmentally delayed in speech. Pet. Ex. 9, pp. 19, 54; see also id., p. 7 (Denver

II). 29

A.A. was next seen on June 13, 2001, for a possible urinary tract infection

[“URI”]. Her mother thought she was having problems urinating. She was noted as

crying, but consolable at the appointment. Mrs. Allen was to call if the concerns

persisted. Pet. Ex. 9, p. 53.

D. Diagnosis of and Evaluations for Speech Delay.

A.A.’s two-year well child visit took place on August 6, 2001. Her physical

examination was normal. However, she was again diagnosed as having a

developmental speech delay. The examination was “very difficult,” because A.A. was

29

The Denver Developmental Screening Test [“Denver II”] was a widely used assessment for examining

the developmental progress of young children; however, in recent years the test has fallen out of favor

with some early childhood organizations. See, e.g., Minnesota Department of Health,

http://www.health.state.mn.us/divs/fh/mch/webcourse/ devscrn/instrument.cfm (last visited Sept. 8, 2015)

(not recommended as a developmental screening instrument). The test’s publisher closed in 2015; the

testing materials are no longer available for sale. See Denver Developmental Materials, Inc.,

http://denverii.com/ (last visited Sept. 8, 2015).

13

apprehensive and screamed throughout the encounter. As a result, the examination

report, including the nine-item developmental skills checklist, was not thoroughly

completed. The two skills that were evaluated (“2-3 word sentences” and “repeats

words”) were marked as abnormal. 30 She was referred for speech evaluation. Pet. Ex.

9, p. 4.

A hearing test on August 27, 2001, was inconclusive, and she was re-evaluated

on August 31, 2001. Although testing was again incomplete because A.A. “was very

active and crying,” the obtained results suggested “normal hearing in at least one ear.”

The audiologist recommended A.A. undergo a speech and language evaluation. Pet.

Ex. 5, p. 1.

That speech and language evaluation was conducted on September 5, 2001.

A.A.’s nanny accompanied her to the appointment and served as the informant

regarding her daily communication skills and behaviors. Her parents supplied a written

history. The report noted that A.A.’s medical history was significant for ear infections.

Her developmental milestones were reportedly age-appropriate. Although she was

clumsy with walking, she was able to run and climb with coordination. Her fine motor

skills were still developing. Pet. Ex. 5, p. 4. Her speech and language landmarks were

reported “as age appropriate to a point.” Id., p. 5. She reportedly spoke “her first word

‘Quack’ at 1 year and [spoke] a little more/using animal sounds at 15 months.” Id.

However,

[s]he stopped speaking after having 3 ear infections in a row..[31] She has

just begun to put 2 words together. She has an estimated expressive

vocabulary of 30 words. In the past 6 months she has begun to babble a

lot again. She cries, points, and tugs, as her primary means of

communicating with her parents and nanny. She does not communicate

with peers. [She] reportedly will learn new words, but when she does, . . .

previous learning is lost.

Id.

After testing and examination, the speech-language pathologist provided the

following assessment:

[A.A.] is an attractive young child who would not engage with this

examiner. Based on clinical observations and caregiver’s report, she

presents with delayed receptive language skills and gaps in her

expressive language development. Of greater significance are her poor

pragmatic skills (eye contact, joint attention, etc.) and atypical behaviors:

30

The nine assessed developmental skills were: (1) Uses spoon well; (2) Eats using spoon; (3) Walks up

steps; (4) Knows name; (5) Runs without falling; (6) Builds 5-6 blocks; (7) 2-3 word sentences; (8)

Repeats words; (9) Can do simple tasks. Pet. Ex. 9, p. 4.

31

A.A. was seen for these ear infections on March 1 and 23, and April 2, 2001. Pet. Ex. 9, pp. 8, 54-56.

14

preference of objects over people, sustained odd play, tantrums,

resistance to changes in routine, showing distress for reasons not

apparent to others, lack of response to verbal cues (although hearing tests

in normal range), aloof manner, fascination with venetian blinds/lights,

desire to hold objects daily, and walking on tip toes. These combined

behaviors may suggest that she is experiencing more than just a

developmental delay.

Pet. Ex. 5, p. 11. The speech pathologist “suspect[ed] autism” and recommended that

A.A. “receive evaluation from a pediatric neurologist and/or developmental psychologist

to assess communication and behavioral patterns to determine/rule-out underlying

problems.” Id.

E. Autism Evaluations.

On September 16, 2001, A.A. was seen for a neurologic consultation with Dr.

Bennett L. Lavenstein at Children’s National Medical Center [“Children’s Hospital”], in

Washington, D.C. In the resultant report, Dr. Lavenstein noted that A.A. had been

referred by a speech pathologist who perceived “features of autism” in some of her

behaviors. Pet. Ex. 9, p. 96. He recounted that A.A., by history, had

[d]emonstrated normal behavior in the neonatal course. Subsequently

sat, walked and was appropriate in her milestones . . . . In October of

2000 she had some oral sounds but then subsequently regressed. There

has been some evidence of echolalia. Occasional stereotype movements

have been noted, especially when excited with some hand motions, and

she is noted to walk on her tip toes. At this time, she has been evaluated

in a hearing evaluation with an audiogram that was noted to be normal.

She has no history of seizures. There has been no evidence of

regression.

...

Additional behavioral features reveal that [A.A.] frequently will stare at

lights, stares in the mirror and continues to twirl her hair. She does have

some interaction with those in the environment.

Id.

Her neurologic examination was generally within normal limits, but A.A. was non-

communicative. 32 Pet. Ex. 9, p. 96. According to Dr. Lavenstein, A.A. was “a patient in

whom there may have been development of primitive speech then a regression of

speech, . . . a child who has autistic symptomatology.” Id. He recommended an

additional MRI scan and electroencephalogram [“EEG”] testing to determine whether

32

Reflexes were normal, and she was not hypertonic.

15

“there are features that would be suggestive of the Landau-Kleffner syndrome.” Id., pp.

96-97. 33

Following the neurologic consultation, A.A. underwent further diagnostic testing,

including a cerebral MRI and an EEG, as well as blood plasma analysis to obtain amino

acid levels. A radiological report dated October 3, 2001, indicated A.A.’s cerebral MRI

results were unremarkable. Pet. Ex. 4, p. 76. Similarly, an October 15, 2001, report

indicated that her EEG results were within normal limits. Pet. Ex. 9, p.93. With regard

to her amino acid levels, an October 22, 2001, laboratory report showed “mildly

elevated” tyrosine and lysine, and “borderline high” branched-chain amino acids. The

report stated, however, that clinical correlation was required, and Dr. Lavenstein

indicated they were reported as “non specific” by Dr. Mendel Tuchman, who interpreted

them. Pet. Exs. 10, p. 6; 9, p. 85.

On October 27, 2001, A.A. presented to Loudon Ear, Nose & Throat Specialists

for an evaluation of her recurrent episodes of otitis media. During the consultation,

A.A.’s mother reported that “[o]ver the last 10 months, [A.A.] ha[d] had 4-5 acute [otitis

media] episodes, . . . and, more importantly, ha[d] been diagnosed with speech delay.”

Pet. Ex. 9, p. 92. According to her mother, A.A.’s “regression began when the ear

infections started, and at least some of the developmental delay experts have indicated

that the fluid in her ear and/or recurrent acute infections could be at least part of the

problem.” Id. The physician examined A.A. and confirmed that she suffered from a

speech delay, “since at this age she still has very minimal vocabulary.” Id. She opined

that “her history of recurrent acute otitis media could be contributory since even

transient conductive hearing losses would affect her speech development at this age.”

Id. The physician recommended bilateral myringotomy and ventilation tube placement.

Id. The procedure was performed around October 2001. 34

A.A. was seen repeatedly over an approximately six week period, beginning in

November 2001, for minor illnesses, which included pharyngitis and otitis media. See

Pet. Ex. 9, pp. 43, 45, 47, 49, 51. Reports of behavioral issues were mentioned during

these visits. Id.

On the morning of December 17, 2001, A.A. was taken to the Inova Fairfax

Hospital Emergency Department because of severe pain in her abdomen and groin

area with recurrent bouts of uncontrollable crying and screaming, all of which had begun

approximately one week earlier. Pet. Ex. 4, p. 10. After an initial examination, the

emergency department physician rendered a tentative diagnosis of intermittent

abdominal pain, rule out intussusception and UTI. Id. A barium enema and a kidney,

ureter, and bladder [“KUB”] workup were negative for intussusception, but notable for

33

This evaluation also appears at Pet. Ex. 10, pp. 17-18. Duplicates of other exhibits also appear in

A.A.’s primary care records. I will not identify duplicate citations.

34

Medical records of the procedure were not filed; however, the surgery appears to have occurred around

October 2001. See Pet. Ex. 9, p. 92 (Oct. 27, 2001 audiology consult recommending procedure “in the

near future”); Pet. Ex. 4, p. 28 (Dec. 17, 2001 medical history noting “PE tubes placed ~ 3 mo ago.”).

16

increased stool in the colon, which “[t]he patient was not able to evacuate.” Id., pp. 40-

41. The emergency department recommended that A.A. be admitted to the hospital for

further testing and evaluation. Id., p. 34. A.A.’s pediatrician was informed of her status

and of the available test results, including evidence of thrombocytosis and increased C-

reactive proteins [“CRP”]. Pet. Ex. 9, p. 41. All other tests were negative, but an upper

gastrointestinal [“UGI”] was still needed. Id.

At admission, A.A.’s mother completed a comprehensive pediatric history form

regarding her health and development. Pet. Ex. 4, pp. 56-58. She reported that A.A.

was generally healthy, but noted that she had recently been sick, had allergies to eggs

and dairy, and was “slightly behind” in meeting developmental milestones. Id. She

specifically denied that A.A. had any history of gastrointestinal or genitourinary issues,

or had any ear problems. Id. A.A.’s current medications were listed as Tylenol, smart

oil, good bacteria, and unidentified supplements. Id., p. 56.

Additional history was provided to the attending physician during the admitting

examination: A.A. was reportedly in her usual state of health following a flu-like illness

when she developed increased fatigue, fussiness, and episodes of abdominal and

perineal pain. Her symptoms were accompanied by extreme tantrums, during which

she placed her hands near her perineal/paravaginal area and screamed uncontrollably.

The episodes, which started about one week earlier, occurred several times per day

and lasted for 20-30 minutes. Pet. Ex. 4, p. 28; see also id., p. 18 (pediatric history

taken by resident).

As for her earlier medical history, the attending physician recounted her burn

injury in January 2001 and a history of multiple ear infections requiring a myringotomy in

October 2001. Pet. Ex. 4, p. 28; see also id., p. 18. The physician also noted that A.A.

had undergone an EEG and MRI in October 2001 with normal results “per Dr.

Lavenstein.” Id., p. 28. Concerning her development, the physician reported that A. A.

had a language delay and toe walked, but noted that she “runs [up and down] stairs,

self feeds, [and] can speak in sentences, but talks little.” Id. Her speech reportedly had

increased after her myringotomy. Id. No history of behavioral problems was reported.

Id., p. 18. With regard to her diet, the physician noted that A.A.’s food allergies were

discovered by way of a home ELISA [enzyme-linked immunosorbent assay] test

administered by her parents. Id., p. 28. A.A. was currently “followed by a nutritionist”

and had a diet free of dairy and eggs and supplemented with vitamins. Id.

A.A. remained in the hospital overnight and was discharged on December 18,

2001. Pet. Ex. 4, p. 7. A hospital pediatric consultation report dated that day

summarized the results of various tests undertaken during A.A.’s hospitalization. The

consulting physician stated:

[A.A.’s] work up so far has included a [KUB x-ray] which is notable for

increased stool in the colon as well as a normal barium enema and normal

pelvic ultrasound with Doppler. Of note, she does have thrombocytosis

with platelets of 947 and mildly elevated CRP of 1.32. Mild anemia with

17

hemoglobin of 11.2[,] but with normal electrolytes, liver function tests and

urinalysis. An electroencephalogram being done today . . . is pending. 35

Pet. Ex. 4, p. 21.

The consultant noted that A.A.’s physical examination was normal and stated

that “[a]t this point, it is unclear if her colicky pain is clearly gastrointestinal related or

not. It is possible that she may be having some post infection enteropathy which is

worsened with her constipation.” Pet. Ex. 4, p. 21. He recommended an upper GI

examination to “rule out malrotation with intermittent volvulus and ischemia,” additional

blood work, and continued Milk of Magnesia “to clean her out.” Id. The upper GI study

performed the following day, December 19, 2001, was negative for any abnormalities,

including malrotation or duodenal obstruction. Id., p. 5.

On December 20, 2001, A.A was seen at Countryside for repeat blood testing.

The medical report noted that A.A. was feeling better. Pet. Ex. 9, p. 39. However, on

December 31, 2001, A.A.’s mother telephoned Countryside seeking an appointment.

She reported that A.A. was “hysterical, upset since [2:30 a.m.], throwing things.” She

stated that A.A. had been “evaluated at Fairfax Hospital [two] weeks [earlier] for these

same symptoms, EEG done, upper and lower GI, barium enema done, no cause was

found.” Id., p. 37. An appointment was scheduled for later that day. The corresponding

medical report noted that A.A.’s mother requested a toxicology workup for metals and

expressed concern about her decreased language ability. The possibility of autism was

raised. Id., p. 36.

On January 3, 2002, A.A. was evaluated by a gastroenterologist for constipation.

The consultation report recounted that A.A. had recently been hospitalized “for extreme

episodes of rage/irritability.” Pet. Ex. 9, p. 90. It noted that neurological evaluation was

in progress “for possible developmental disorders.” Id. Abdominal x-rays taken during

hospitalization “revealed large amount of retained stool” and the upper GI study was

normal. Id. The physician conducted a physical examination with normal findings. Id.

A diagnosis of constipation was made. Id.

On January 14, 2002, A.A.’s parents telephoned Countryside to discuss her

status. During the call, A.A.’s father stated “that he [was] 100% sure that [A.A.’s]

problems [we]re from her MMR immunization. 36 Her behavior started 30 days post

35

The EEG results were normal. Pet. Ex. 4, p. 39.

36

On January 28, 2002, Mrs. Allen was interviewed by a Loudon Public Schools social worker who was

preparing a sociocultural assessment as part of A.A.’s application for special education services. During

the interview she reported that A.A.’s “development was fine until 10-23-00 when she had her MMR

vaccination.” Pet. Ex. 8, p. 47. However, a few days later, on February 1, 2002, Mrs. Allen reported to a

school psychologist that A.A. “was very outgoing and her language skills were developing within normal

limits” until “[a]bout a year ago,” when her “speech skills began to regress and she began to struggle in

social situations.” Pet. Ex. 8, p. 27. This time frame coincides with her three ear infections, which

occurred in March and April 2001. See Pet. Ex. 9, pp. 8, 54-56.

18

MMR.” Pet. Ex. 9, p. 35. He had been doing his own research on the Internet and had

ordered several dietary supplements, including pills to improve brain function and help

the body eliminate harmful metals. 37 Id. He also stated that they had seen a nutritionist

named Kelly Dorfman who gave them “smart oil” to improve A.A.’s intelligence by 15

percent. Id.

On January 14-15, 2002, Dr. Lavenstein administered a 24-hour DigiTrace EEG

to record A.A.’s brain activity. The corresponding report noted that A.A. had “a history

of seizures. First episode was December 2001 and last episode was [January 13,

2002]. They seem to occur every day. Patient has a history of speech delay. These

[seizures] appear to be temper tantrum-like events.” Pet. Ex. 10, p. 1. Doctor

Lavenstein stated that the EEG recorded several of these tantrum events, but “[a]t no

time was there any evidence of a[n] electrographic seizure correlate.” Id. The EEG

revealed “no premonitory electrographic discharge” or “evidence of any focal

epileptiform disturbance.” Id. His impression was: “This 24 hour EEG correlating with

any temper tantrums does not reveal any evidence of paroxysmal abnormality and is

within normal limits.” Id.

In a letter dated February 2, 2002, Dr. Lavenstein provided his conclusions and

recommendations in light of the various tests performed to date. With regard to her

sleep problems, he advised that A.A. undergo a polysomnogram for further sleep

analysis, as she had a sleep disorder. Pet. Ex. 9, p. 85. Concerning her developmental

delays and behavioral problems, Dr. Lavenstein raised concern “about the possibility of

autism,” as there was “past development of primitive speech, then regression of speech

in the setting of a positive family history of epilepsy in a child who does have autistic

symptomatology.” Id. Neurologic testing showed no evidence of Landau-Kleffner

syndrome, and an MRI scan was within normal limits. Id. Laboratory studies to date

were basically normal, including an amino acid screen. Id. Although there “were some

borderline levels of tyrosine and lysine[, t]hese were felt to be nonspecific[.]” Id. Dr.

Lavenstein recommended that A.A. begin taking Klonopin to help her sleep. Id. He

noted that A.A. was to see Dr. Zimmerman in the near future. Id.

F. Evaluations and Treatment at the Kennedy Krieger Children’s Hospital.

On February 13, 2002, A.A. was evaluated by Dr. Gerald Raymond at the

Neurobehavioral Unit of the Kennedy Krieger Institute in Baltimore, Maryland. Pet. Ex.

6, p. 25. The initial evaluation report noted that A.A.’s parents were concerned about

her “loss of language and social skills, and frequent temper tantrums.” 38 Id. According

to her parents, A.A. “sat up independently at 6-months and walked by 12-months.” Id.

At the time of the evaluation, she was able to use a sippy cup, spoon, and a fork, “but

37

Mr. Allen specifically identified the following websites: www.life-enhancement.com;

www.extremehealth.com.

38

Contemporaneous with the initial visit, A.A.’s parents completed a developmental and medical history

form to provide background information for Dr. Raymond’s evaluation. Pet. Ex. 6, pp. 39-44.

19

sometimes [ate] with her hands.” Id. She also assisted with dressing and undressing,

but was not toilet-trained. Id. The report continued:

Loss of language skills was noted at approximately 16-months. Prior to

that, she was reportedly able to make ‘animal sounds’ such as ‘roar!’ when

asked, and was able to state her age. Parents feel that loss of skills was

concomitant [sic] with her 15 month MMR vaccination. She has made

some improvements since that time and is now able to count some

objects. She occasionally uses words or phrases spontaneously, such as

“daddy go look.” She may say “French fries” when the family goes to

McDonald’s. She has made better eye contact recently, since starting

dietary supplements.

Id.

With regard to her previous medical history, Dr. Raymond noted the placement of

tympanostomy tubes due to frequent otitis media, and recounted her normal

neurological evaluation in September 2001, and hospitalization for severe temper

tantrums in December 2001. Pet. Ex. 6, pp. 25-26. He also noted that A.A. had been

taking a dietary supplement, “which include[d] chelation with EDTA,” for approximately

three weeks. 39 Id., p. 26. The supplement had reportedly improved her behaviors. Id.

She was also prescribed Klonopin. Id.

Following physical examination with normal results, Dr. Raymond assessed A.A.

as “a 2-year, 6-month-old child who has had regression of language and social skills by

parental report.” Pet. Ex. 6, p. 27. He noted that her “[l]oss of language could be

suggestive of Landau-Kleffner’s syndrome; however, multiple EEG studies done in the

past have been normal.” Id. Of specific concern were A.A.’s “poor pragmatic skills,

limited eye contact, and stereotypies. These features, with a history of regression, are

suggestive of autistic disorder. In her case, based on findings, Rett Syndrome should

also be considered.” Id. He recommended continued use of Klonopin to manage her

behaviors, but cautioned use of the dietary supplement. Id. He also recommended

karyotype, fragile X DNA, and Rett studies. 40 Id.

That same day, A.A. was seen by Dr. Andrew Zimmerman, a pediatric

neurologist at the Kennedy Krieger Institute, for further evaluation of autistic symptoms.

Pet. Ex. 6, p. 23. Dr. Zimmerman’s report included the following history:

The parents report normal development until 11/00, when she underwent

regression 1-2 weeks following MMR immunization, with loss of language

and eye contact as well as social interaction. She is currently undergoing

39

Testing of A.A.’s hair reportedly had revealed “high metal content and arsenic.” Pet. Ex. 8, p. 47.

40

Fragile X genetic testing was normal. Pet. Exs. 6, p. 71; 15, p. 120. Rett syndrome genetic testing was

normal. Pet. Exs. 6, pp. 72-73; 15, pp.121-22. Both tests were performed on February 14, 2002.

20

vitamin therapy and ‘GI support’, and has had trace metal testing of the

hair. She has been followed by Dr. Bennett Lavenstein and had normal

EEGs, including an overnight study, and cranial MRI scan. She has

shown increasing toe walking in recent months. Father feels her eye

contact is improving since starting ‘oral chelation’, which is obtained

through the mail. She uses up to 100 words inconsistently and tends to

lose single words that she has once used. She is now sleeping through

the night, though she has had episodes of awakenings every 2 hours, and

will have rage episodes with hitting her head and pulling her hair.

Id.

A.A. reportedly had exhibited “repetitive behaviors, hair-twirling and echolalia.”

Pet. Ex. 6, p. 23. Doctor Zimmerman assessed “her rating on the Childhood Autism

Ratings scale [as] 35-37, in the moderately autistic range.” Id. He noted that there was

no family history of autism, and A.A. was an only child. Id. He conducted a physical

examination:

On exam, [A.A. was] fussy and reactive, does not engage or sustain eye

contact. Occasional word sounds [were] heard, as she responds to her

parents and seeks their attention briefly, and they are responsive to her. . .

. The cranium appears relatively small compared to the face, with large

features, and head circumference [in the] 50th percentile . . . . Tone is

moderate and symmetrical. She does not engage in a ball game, but

reaches into the can to obtain one. She climbs up and down a set of

steps repeatedly, has mild truncal instability but no tremor or movement

disorder. . . . Toe walking is persistent and increases with an instability of

her gait. The feet are plethoric in appearance (and are reported to change

color from pink to blue at times without apparent cause). Brief

hyperventilation episodes were reported on the exam earlier today.

Id.

Dr. Zimmerman concluded that A.A. “present[ed] an atypical history and

appearance consistent with an encephalopathy and a pervasive development disorder

(autism spectrum).” Pet. Ex. 6, p. 24. Because of her “history of regressive

encephalopathy,” he recommended genetic testing, as well as testing of quantitative

plasma amino acids and urine organic acids. Id. He also recommended that she

continue her treatment with Klonopin. Id.

On July 15, 2002, A.A. returned to Dr. Zimmerman for a follow-up appointment.

During the visit, A.A.’s mother reported that she had experienced “an increase in

language functions” due to her involvement in an infants and toddlers program, but had

“lost some ground” after the program ended for the summer. Pet. Ex. 6, p. 21. Doctor

Zimmerman noted that A.A. “ha[d] functional language, [but her] pragmatics [we]re still

21

poor and she [did] not readily engage or relate.” Id. He planned to begin to taper her

Klonopin dosage over the next few weeks. Id.; see also id., p. 88.

The report indicated that urinary organic acids had not been obtained, but that

“[g]enetic testing was normal, including chromosomes and DNA for fragile X. Rett

syndrome genetic testing was normal. There is no family history of hearing loss or

muscle weakness (mitochondrial disorder).” Pet. Ex. 6, p. 21. With regard to behavior,

Dr. Zimmerman reported that “[s]he marche[d] around the room and [was] continuously

active. She jump[ed] and ha[d] some hand flapping with excitement.” Id. He stated

that they again “reviewed the history of her loss of functions following MMR vaccine.

She has regressive encephalopathy with development of PDD (autism spectrum

disorder).” Id. He recommended that she have Applied Behavior Analysis [“ABA”]

therapy. 41 Id.

In addition to ABA therapy, Dr. Zimmerman recommended additional testing,

including “quantitative urinary organic acids, fasting serum lactic acid, serum

chemistries with liver function tests (especially AST), as well as CK (CPK),” 42 in view of

the possibility of mitochondrial disorder. Pet. Ex. 6, p. 21. He stated “[m]itochondrial

disorders are difficult to diagnose, and some of them are responsive to specific vitamin

therapies.” Id. He noted at the conclusion of his report that A.A. “had normal

quantitative amino acids, including the alanine/lysine ratio.” Id.

On November 4, 2002, A.A. returned to Dr. Zimmerman for a follow-up visit. A

nursing report noted that A.A. was non-compliant and crying during intake procedures.

Pet. Ex. 6, p. 86. It also noted that she was being treated with vitamin therapy. Id.

During the examination, A.A.’s mother reported increased sensory sensitivities and

agitation since she stopped taking Klonopin. Pet. Exs. 6, p.19. But she noted that A.A.

was “showing more responsiveness in her therapies and [was] using a few words.” Id.

With regard to test results, Dr. Zimmerman noted that

[l]aboratory testing again showed a normal amino acid profile. Her plasma

lactate was 2.2 mM/L (0.7-2.1) and CPK was 196 IU/L (0-165) . . . and

calcium 10.6 (8.5-10.4). She was struggling when the test was done and,

by report, the tourniquet was not removed. These findings are further

suggestive of a mitochondrial disorder but not clearly diagnostic.

...

We were able to obtain a urine specimen for quantitative organic acids

that will be sent to Dr. Kelly’s lab, and we also obtained a carnitine profile

41

ABA therapy consists of the “application of learning theory based on operant conditioning” and “is the

only intervention recommended by the Surgeon General” for ASD. Dwyer, 2010 WL 892250, at 272,

n.650 (internal citations omitted).

42

Blood chemistry results (Aug. 7, 2002). Pet. Ex. 6, pp. 69-70. Plasma amino acid results (Aug. 29,

2002). Id., pp. 66-67.

22

and will request repeat AST and CK determinations.[43] We will then begin

a trial of carnitine (Carnitor) increasing as tolerated up to 500 mg or 5 cc

t.i.d. . . . She will also take folic acid 0.5 mg daily. We will later consider

addition of other vitamins to the regimen depending on results. We will

also consider further evaluation for mitochondrial disorder with spinal fluid

lactic acid and/or muscle biopsy. We also obtained a carnitine profile

today.

Pet. Ex. 6, p.19.

Doctor Zimmerman prescribed carnitine and folic acid and ordered a follow-up in

three months. The discharge diagnosis was “encephalopathy.” Pet. Ex. 6, p. 85.

On November 15, 2002, A.A. was seen at Countryside due to a reported seizure

that morning. Pet. Ex. 9, p. 2. The medical record reflects that A.A. had a “grand mal”

seizure, which lasted approximately three minutes. Id. She was taken to Countryside

on the advice of Dr. Zimmerman. Id. Physical examination was normal. Id. A.A.’s new

“vitamin therapy” was mentioned. Id., p. 24. On November 23, 2002, A.A. was treated

for pharyngitis and viral infection. Id., p. 23. She reportedly “missed school all week.”

Id.

On January 13, 2003, A.A. had another EEG, the results of which indicated “a

focal cerebral disturbance of the right temporal region, but possibly involving the right

cerebral hemisphere diffusely.” Pet. Ex. 6, p. 54. The reporting physician noted “no

clear epileptiform discharges,” but could “not rule out an epileptic disorder.” Id. He

recommended an imaging study be performed “to evaluate for structural abnormalities.”

Id.

A.A. was seen at Countryside on January 21, 2003, due to another reported

grand mal seizure that morning, which lasted about two minutes. Pet. Ex. 9, p. 22. The

medical report noted that she was scheduled to see Dr. Zimmerman the following day,

but that he wanted her to be seen at Countryside “because she ha[d] had 4 seizures

since [the] new year.” Id. Physical examination was normal, with the exception of an

inflamed right tympanic membrane, diagnosed as acute OM. Id.

On January 22, 2003, A.A. returned to Dr. Zimmerman for a follow-up visit. Dr.

Zimmerman discussed A.A.’s most recent EEG results and noted that she had had four

“generalized tonic-clonic seizures, apparently nonfocal, over the past several weeks

after starting a trial of Carnitor (L-carnitine), [which] was discontinued about 3 weeks

ago.” Pet. Ex. 6, p. 15. Although her last seizure occurred the previous day and she

was presently alert, her mother observed “intermittent episodes of convergence spasm

43

The report from the repeat testing noted these results as “CK = 201 IU/L (24-170); Calcium 10.7 [8.5-

10.4]; AST 44 U/L (0-31); CO2=19; carnitine profile normal; organic acids – normal.” Pet. Ex. 6, p. 19;

see also Pet. Exs. 6, p. 56 (Johns Hopkins lab report dated Nov. 4, 2002); 6, p. 57 (KKI genetics lab

report dated Nov. 7, 2002); 6, p. 58 (KKI mass spectrometry lab report dated Nov. 8, 2002).

23

of the eyes” during the “past week or so.” Id. A.A.’s speech, however, had reportedly

improved while taking Carnitor. Id.

Doctor Zimmerman noted a limited familial history of seizures, but stated that

A.A.’s MRI films from October 2001 appeared normal, “showing no focal abnormalities

on the right side.” Pet. Ex. 6, p. 15. He recounted that she had “a history of normal

development until about 2 weeks after her MMR immunization at 18 [sic] months of age.

Up to that time, she knew her colors and was using words and was pointing. She

began repetitive behaviors and declined in her speech production with her regression.”

Id. The seizures, however, were “a new onset.” Id. This history is significantly different

from the medical records showing A.A.’s skill level at the time of vaccination and from

the histories provided before her parents asserted that the MMR vaccine was causal.

See, e.g., Pet. Ex. 9, p. 10 (pediatrician assessment at one-year checkup indicating

A.A. knew one to three words); Pet. Ex. 5, p. 4 (parental report to speech-language

pathologist on September 5, 2001, stating that A.A. spoke “her first word ‘Quack’ at 1

year and [spoke] a little more/using animal sounds at 15 months”), p. 5 (she “stopped

speaking after having 3 ear infections in a row”); Pet. Ex. 9, p. 96 (parental report to Dr.

Lavenstein on September 6, 2001, that at 15 months A.A. “had some oral sounds”; Dr.

Lavenstein’s characterization of her speech at that time as “primitive”).

Doctor Zimmerman planned a repeat EEG in six weeks, after starting A.A. on

Depakote. “Depending on the results of her repeat EEG . . . we may wish to repeat her

MRI scan, if right sided or other focal abnormalities persist.” Pet. Ex. 6, p.15. He also

recommended updated bloodwork for “CBC, AST and a valproic acid level.” Id. Any

decision “to reinstitute treatment with carnitine and other ‘mitochondrial vitamins’” would

be determined at a later date. Id. Dr. Zimmerman prescribed Depakote and ordered a

follow-up in six weeks. Id. The discharge diagnosis was, again, encephalopathy. Id.,

p. 82.

Another EEG was performed on March 3, 2003, pursuant to Dr. Zimmerman’s

order. Pet. Ex. 6, p. 50. The record reflected “no seizure discharges or localizing signs”

and was improved as compared to the one obtained on January 13, 2003. Id. The

examiner also noted that “[t]he focal attenuation of activity noticed over the right side on

the previous recording was not present in the current record; however, it must be kept in

mind that there were fewer recording channels in the current record.” Id.

That same day, A.A. was also seen by Dr. Zimmerman. He noted that A.A. was

currently taking Depakote and had only “a single seizure [the previous] week after sleep

deprivation and none ha[d] recurred.” Pet. Ex. 6, p. 13. He also reported that “[s]everal

studies suggest[ed] that [A.A.] has signs of a mitochondrial disorder.” Id. As a result,

he contacted Dr. Richard Kelley and asked him to review A.A.’s chart. Id. He intended

to ask Dr. Kelley to see A.A. clinically “to review studies[,] comment on any further

testing[,] . . . [and] recommend treatment.” Id. In the meantime, Dr. Zimmerman started

A.A. on coenzyme Q, folic acid, and thiamine; however, restarting Carnitor would be

postponed “pending Dr. Kelley’s recommendation.” Id.

24

On April 8, 2003, A.A. was seen by Dr. Richard Kelley, a metabolic specialist at

the Kennedy Krieger Institute, for further evaluation and recommendations for

treatment. Pet. Ex. 6, p. 3. In his report, Dr. Kelley recounted A.A.’s relevant history, as

provided by her parents and medical records. Id. Consistent with previous accounts,

A.A. reportedly “did well in the neonatal period and appeared to be a healthy, thriving

girl for the remainder of the first year.” Id. “[L]anguage acquisition continued to develop

normally up until the age of 15 months when, approximately one to two weeks after her

MMR immunization, [A.A.] progressively lost most of her language, visual contact, and

normal social interaction over several weeks.” Id. Extensive testing and evaluation “to

determine the cause of the losses [provided] no explanation for her autistic regression.”

Id. Then, in February 2002, A.A. was seen by Dr. Zimmerman. Although she had

regained some of her language, “and to some degree, her socialization” by the time of

the evaluation, “she continued to have major behavioral problems, including self-injury.”

Id. At that examination, she demonstrated “persistent toe-walking as well as some gait

instability, suggesting . . . a primary neurological disorder and not idiopathic autistic

spectrum disorder.” Id.

In view of the “early regressive nature of [A.A.’s] pervasive developmental

disorder and the abnormalities in [her] neurological examination, Dr. Zimmerman was

concerned that [she] might have a metabolic disease or other genetic disorder causing

her progressive developmental and neurological losses.” Pet. Ex. 6, p. 3. He “obtained

a number of basic laboratory studies for diagnosis of inborn errors of metabolism.” 44 Id.

These showed several abnormalities, including an increased plasma

alanine level, increased ratio of AST to ALT, mildly increased creatine

kinase level, mildly increased blood lactate level, and electrolyte evidence

of a mild metabolic acidosis. Negative diagnostic testing for identifiable

causes of autistic spectrum disorder included Fragile X testing, Rett

syndrome mutation analysis, plasma carnitine profile, and urinary organic

acid analysis. Taken together, the laboratory abnormalities suggested an

inborn error of mitochondrial energy metabolism. Interesting with regard

to [A.A.’s] having a possible mitochondrial disorder is that, although frank

hypoglycemia has never been documented, [A.A.] seems to [be] very

sensitive to fasting and, according her parents, ‘melts’ if she misses a

between-meal snack. She also sometimes becomes ‘stuporous’ within 15

to 20 minutes of a meal and often wants to eat in the middle of the night.

Id.

In view of the “biochemical evidence for a mitochondrial disorder . . ., and

because of success in treating similar children with pharmacological amounts of

mitochondrial cofactors,” Dr. Zimmerman had started A.A. on “stepwise

supplementation with carnitine, thiamine, and folic acid[.]” Pet. Ex. 6, p. 4. A.A.

became “very excitable and agitated on carnitine,” however, and also experienced

44

The report summarized the results of the diagnostic testing undertaken to date. Pet. Ex. 6, pp. 4-5.

25

several grand mal seizures. Id. Treatment with carnitine was discontinued and an

anticonvulsant was prescribed. Id. With regard to the effectiveness of carnitine, Dr.

Kelley noted:

Although there was suspicion that the seizures had been brought on by

treatment with carnitine, [A.A.’s] last seizure prior to initiation of

anticonvulsive therapy occurred three weeks after stopping carnitine.

After starting treatment with Depakote, [A.A.] . . . had no further seizures.

However, [she] remains significantly more excitable and agitated than

prior to initiation of any of these medications and supplements. As a

result, [A.A.’s] parents suspect that some of [her] worsening behavior has

been caused by Depakote. Also important is that [A.A] was noted to be

much more alert and focused in school after starting treatment with

carnitine, an observation that was made by teachers who at the time were

unaware of [her] new medication.

Id.

Doctor Kelley noted that A.A. did not have a history of any significant illness or

hospitalizations. Pet. Ex. 6, p. 4. It is not clear whether Dr. Kelley was unaware of her

previous hospitalization for tantrums and constipation in December 2001, or whether he

did not consider this event significant. He stated that “[a]part from the above history,

[A.A. showed] no signs or symptoms of a metabolic disease such as food intolerance,

chronic vomiting or diarrhea, recurrent infections, abnormal rashes, unusual odors, or

decompensation with otherwise simple childhood infections (apart from the MMR

immunization).” Id. He noted, however, that she “may have had more than the usual

number of ear infections and has required frequent treatment with antibiotics as well as

bilateral tympanostomy.” Id. A complete physical examination was not undertaken, as

the “visit was primarily for consultation regarding pharmacological treatment.” Id., p. 5.

In his assessment, Dr. Kelley explained:

Although autism in most children remains a diagnosis without known

cause, [A.A.] . . . has many of the historical and laboratory characteristics

that we now associate with a particular form of autistic spectrum disorder

caused by an inborn error of mitochondrial metabolism. Children with this

disorder (possibly a group of disorders), typically appear to be normal for

their first 12 months or more before a viral illness or other stress[,] such as

an immunization[,] provides the critical metabolic stress that sufficiently

taxes or compromises energy metabolism in the brain to precipitate acute

or subacute cognitive and motor deterioration. For reasons that most

likely are explained by changes in neurotransmitter receptor densities in

the brain, the period between 12 and 36 months is the time when children

with these mitochondrial disturbances appear to be most susceptible to

brain injury. Such injury may occur once or several times with additional

stresses, or, more rarely, a child may regress for many months, even in

26

the absence of specific stresses like infections or immunizations. Most

likely because the greatest susceptibility for brain [sic] occurs during a

peak period of language and social development, children who sustain this

type of mitochondrial injury often develop signs of autistic spectrum

disorder.

Id.

He then stated:

In addition to historical information consistent with an inborn error of

energy metabolism, [A.A.’s] laboratory studies are similar to those of other

children with autistic spectrum disorders and mitochondrial disease, which

for shorthand we call ‘mitochondrial PDD.’ These include a distinctly

increased level of plasma alanine relative to essential amino acids, a high

ratio of AST to ALT, mildly increased creatine kinase level, and mild

metabolic acidosis. Although [A.A.’s] plasma lactate level was only

borderline increased at 2.2 mM, the lack of a distinct lactic acidosis in

children with mitochondrial PDD together with an increased alanine level

is quite characteristic. This is also consistent with muscle biopsy studies

in mitochondrial PDD children, which typically show a significant block at

the level of complex I, the primary site of oxidation of pyruvate. Alanine,

being the amino acid form of pyruvate, is secondarily increased, but more

useful as a diagnostic marker because its degree of elevation can be

expressed relative to other amino acids, and it is not subject to artifacts

commonly encountered in doing pyruvate and lactate measurements. The

mildly increased levels of AST and creatine kinase are presumed to reflect

the involvement of muscle tissue, which, second only to the brain, has the

highest demand for mitochondrial energy metabolism.

Id., pp. 5-6.

Doctor Kelley also discussed A.A.’s “hyperactivity reaction” to carnitine, which he

explained was “not uncommon in mitochondrial PDD.” Pet. Ex. 6, p. 6. With regard to

her first seizure, he found it unlikely, “based on extensive international experience with

carnitine treatment of metabolic disorders, that carnitine could be the primary cause of a

seizure disorder, only the particular factor that demonstrates a child’s predisposition to

having seizures. Indeed, seizures are relatively common in mitochondrial PDD before

any pharmacological treatments are begun.” Id. Despite A.A.’s reaction, Dr. Kelley

believed carnitine was beneficial and recommended A.A. restart the treatment. Id. In

addition, he recommended “starting the combination of vitamins now commonly used in

the treatment of mitochondrial diseases.” 45 Id. The vitamin therapy was planned to

continue “until at least age five years. Id. In the meantime, Dr. Kelley encouraged A.A.

to “continue to be followed by Dr. Zimmerman and her developmental specialists to

monitor her progress.” Id. Although he found it unnecessary that she return for

45

The vitamin mixture was coenzyme Q10, vitamins C and E, thiamine, and lipoic acid. Pet. Ex. 6, p. 7.

27

“continued formal evaluation” at his clinic, he offered to provide advice or consultation

as necessary regarding adjustments to her medications. Id., p. 7.

Finally, Dr. Kelley noted that although “the specific genetic lesion or lesions

causing mitochondrial PDD” are not known, mitochondrial enzymatic analysis of muscle

biopsies from “several similar children” have “almost always [shown] exactly the same

biochemical profile.” Pet. Ex. 6, p. 7. As a result, “undertaking an invasive and

expensive muscle biopsy at this time would not seem to have any practical value.” Id.

On July 14, 2003, A.A. returned to Dr. Zimmerman for a follow-up visit. He noted

that she had been doing “remarkably well on the mitochondrial regimen” and provided a

favorable evaluation. Pet. Ex. 6, p. 1. He reported:

Today her eye contact is notably improved and she sustains it for several

seconds and is briefly interactive. She plays with imagination with a toy

stove and stays busy with it. She is heard to sing words clearly and is

using single words and word combinations. Her sleep has improved,

although she is up about once per week during the night and is ‘wired’ for

a few hours. This is gradually improving. She has remained seizure free

on Tegretol . . . . She still is having difficulty with transitions and sensory

sensitivities. Her growth has improved with increase in weight . . . from

60th to 95th percentile, and height . . . represents increase from 50th to

75th percentile in the last four months.

Id.

Doctor Zimmerman noted that A.A.’s positive response to the mitochondrial

regimen indicated a possible “underlying mitochondrial dysfunction which may be from a

nuclear gene that affects the mitochondria.” Pet. Ex. 6, p. 1. He ordered bloodwork and

a follow-up in three months. Id.; id, p. 76; see also Pet. Ex. 15, pp. 98-99 (laboratory

results).

On July 14, 2003, Dr. Kelly provided a letter excusing A.A. from further

vaccination due to her condition. The letter stated that A.A. “has autistic spectrum

disorder and biochemical evidence of a mitochondrial disease.” It explained that “the

physiological stress of a vaccine” can trigger the “onset of brain injury in children with

mitochondrial disease . . . as was the case for [A.A.] at the time of her MMR

immunization.” For this reason, it was recommended that A.A. not receive any further

MMR or cellular pertussis vaccines until she passed “the window of greatest

vulnerability for brain injury,” which in children with A.A.’s “type of metabolic disorder” is

six years of age. Pet. Ex. 11, p. 162.

On October 27, 2003, A.A. returned to Dr. Zimmerman for a follow-up visit. The

medical report reflected that A.A. “seem[ed] to be doing quite well on the mitochondrial

vitamin supplements.” Pet. Ex. 11, p. 160. She had been seizure free since January

2003, and the plan was to taper her off the anticonvulsant once she reached the two-

28

year point. Id. Laboratory results were generally within normal limits, including a

comprehensive metabolic panel. Id.; see also Pet. Ex. 12, pp. 52-53.

On March 15, 2004, A.A. presented for a routine neurology follow-up with Dr.

Zimmerman. According to her parents, A.A. had recently experienced a “regression” in

her behaviors and skills. Pet. Ex. 11, pp. 155-56. She was having increased sensory

integration problems, including frequent temper tantrums, and appeared less happy

than usual. Id. Additionally, certain behaviors had returned or increased, including

teeth grinding, stereotypic behaviors, humming, and toe walking. Id., p. 155. It had also

become harder for her to transition to new situations and she was observed by her

parents and teachers to be “more lethargic” and “less focused in the afternoon.” Id., pp.

155-56. Of particular concern was a teacher report that A.A. had recently had a brief

staring spell and “did not respond for a short time.” Id., p. 155. Her father also reported

observing a possible seizure-like episode, but was not certain. Id. Although A.A.

“continue[d] to speak occasionally” and “respond to specific choices given to her, [she

did] not make spontaneous speech.” Id. She was “learning things,” but her parents

were considering her placement in “a special education kindergarten program where

she w[ould] be pulled into regular programs in school.” Id., p. 156. It was noted that

A.A. “ha[d] been on the mitochondrial vitamins for one year . . . with no change in the

dosage.” Id., p. 155.

The impression was that A.A. had undergone a regression in her behaviors and

skills. Pet. Ex. 11, p. 156. The plan was to slowly increase her mitochondrial vitamins

to their target dosage. Id. The possible staring spells were “concerning,” so the plan

was to increase her anticonvulsant medication. Id., p. 157. A follow-up was scheduled

in three months. Id. Subsequent laboratory results were generally within normal limits,

with the exception of creatine, AST, and her platelet count. Pet. Ex. 12, pp. 48-49. Her

plasma carnitine was within normal limits. Pet. Ex. 12, p. 50.

On June 14, 2004, A.A. returned for a neurology follow-up with Dr. Zimmerman.

The medical report reflected that A.A. had improved since the previous visit and

“continued to do quite well on the mitochondrial vitamins.” Pet. Ex. 11, p. 148. She was

kept at her current levels, with no intention of ending the treatment “anytime soon, since

they seem to be working very effectively.” Id. Because she had been seizure-free for a

year and a half, they planned to begin tapering her anticonvulsant medications. Id.

By December 2005, A.A. was off her anticonvulsant medication and doing well.

Pet. Ex. 11, p. 135-36. In December 2008, Dr. Zimmerman planned to taper A.A. off of

the vitamin cocktail to determine whether there was “still indication of mitochondrial

dysfunction.” Pet. Ex. 12, p. 1. Although it is not clear from the record whether this

occurred, Dr. Zimmerman later wrote, in a June 21, 2010 evaluation, that A.A. continued

to have “clinical suggestion of mitochondrial dysfunction.”46 Pet. Ex. 15, p. 1. As of the

46

In his evaluation, Dr. Zimmerman noted: “When she was off all mitochondrial vitamins she seemed to

regress and Father has noted that she improves after each morning dose of Carnitor[.] . . . Mother is not

sure whether there is benefit from it, but agrees to continue with the treatment.” Pet. Ex. 15, p. 1.

29

most current record, A.A. continued to take Carnitor and the mitochondrial cocktail. Pet.

Ex. 64, pp. 1-2.

Petitioners submitted medical records dated through April 2012, at which time

A.A. was 12 years old. The records reflected regular treatment with her pediatrician 47

and ongoing care with Dr. Zimmerman and others at KKI. Pet. Exs. 61, pp. 16, 18-20,

23-28, 30-31, 33-34 (Countryside Pediatrics); 15, pp. 1, 49-52 (KKI); 64, pp. 1-2 ( KKI).

IV. Summary of Fact Testimony and Supporting Evidence.

At the July 10, 2013 hearing, A.A.’s father, James Allen, and her maternal aunt,

Susan Edick, testified with regard to A.A.’s health and development prior to her October

23, 2000 MMR vaccination, and the changes they observed over the ensuing months.

Mr. Allen and Ms. Edick provided additional evidence in the form of written affidavits.

See Pet. Exs. 78, 79. Video and photographic evidence was also submitted. See Pet.

Exs. 60, 75, 80, 81 (video); 76 (photos); Trial Exs. 1-3 (photos).

A. Mr. James Allen.

Mr. Allen testified that A.A. had a “healthy” birth and was regularly evaluated by

her pediatrician, who expressed no concerns during her first year of development.

Neither of A.A.’s parents had any concerns about her development either. Tr. at 6-7;

Pet. Ex. 78 at 2.

A.A. reached a notable milestone just prior to her first birthday, when she took

her first steps during a family vacation to the Outer Banks over the 4th of July holiday.

Tr. at 7-8; Pet. Ex. 78 at 2. A photograph taken during the trip showed A.A. standing on

the beach, smiling and playfully tugging on a rope attached to a boogie board. 48 Mr.

Allen recalled that A.A. was happy on the trip, laughing and giggling. Tr. at 8; Pet. Ex.

78 at 2. He noted that “[o]nce she started walking, it wasn’t long before she was

running, too.” Tr. at 8.

Early on, she also developed “a strong liking [for] the water” and enjoyed going to

the swimming pool. Tr. at 9. Mr. Allen stated that they frequently took A.A. to a local

swimming pool where she “would go in the wading pool and splash with other children.”

Pet. Ex. 78 at 3. One of her favorite places, though, was a large waterpark near their

home. Tr. at 9; Pet. Ex. 78 at 3. He recalled that whenever A.A. visited the park, she

was actively engaged with her surroundings—running, splashing, and playing with other

children. Tr. at 9; Pet. Ex. 78 at 3. Her affinity for water was reportedly illustrated by a

photo of A.A. with her mother in a pool. 49 The photo, which showed A.A. “kind of doing

47

A.A. continued to suffer from recurrent OM.

48

A photograph of the trip to the Outer Banks was used as Pet. Trial Ex. 1.

49

A photograph of her swimming with her mother was used as Pet. Trial Ex. 3. Mr. Allen noted that A.A.

was looking directly at the camera in the photograph. Tr. at 17.

30

the doggie paddle thing,” was taken during “the summer of 2000, around her birthday.”

Tr. at 17.

With regard to her personality, A.A. was becoming “kind of a jokester.” Tr. at 9.

For example, when asked “how big” she was, A.A. would “smile, extend her arms and

say ‘Soooo big’ and wait for everyone to laugh.” Pet. Ex. 78 at 4; see also Tr. at 9-10.

She could tell “knock-knock” jokes, too, although she “hadn’t quite learned to hold back

her laughter until the punch line[.]”50 Pet. Ex. 78 at 3-4; see also Tr. at 10. She also

loved animals and often played with the family’s dogs. Tr. at 10; Pet. Ex. 78 at 5.

Mr. Allen testified that members of both sides of the family observed A.A. during

her first year, and none expressed concern or reported any strange behaviors. Tr. at

11-12. Indeed, she “was actually accelerating, growing.” Tr. at 12. According to Mr.

Allen, she played well with other children, had no difficulty with eye contact, and

responded when called to by name. Tr. at 10-12. She was “very social.” Tr. at 11. In

fact, by her first birthday, A.A. reportedly had learned to use “well over 100 words.” Tr.

at 70-72. In view of the other evidence regarding A.A.’s language at one year of age,

this testimony cannot be accurate.

On her first birthday (July 21, 2000), A.A.’s parents threw a small party attended

by family and friends. Tr. at 12-13. A photograph taken that day shows A.A. next to her

birthday cake. 51

In the fall of that year, over the Labor Day holiday, petitioners visited A.A.’s

maternal aunt and family [“the Edicks”] at their home in Syracuse, New York. Pet. Ex.

78 at 3. Mr. Allen described A.A. as active during their stay and specifically recalled her

playing croquet with him and several of her cousins in the backyard. Id. at 4. Although

“she could only hit the ball about three feet, . . . she tried. She knew how to play. She

understood the colors.” Tr. at 33; see also Pet. Ex. 78 at 4. One of his memories was

of her “saying she was ‘a big girl’ while holding the croquet mallet and trying to hit the

ball.” Pet. Ex. 78 at 4. A photograph taken that weekend 52 showed A.A. outside during

a game of croquet, standing independently with a ball in her hands.

On October 14, 2000, the family visited a local pumpkin patch to purchase a few

pumpkins. Mr. Allen recalled that A.A. was full of energy that day and enjoyed the

experience. He specifically remembered her playing on playground equipment and

50

This statement is simply not credible. At one year of age, A.A.’s pediatrician assessed her with having

one to three words, which was considered to be normal development. Pet. Ex. 9, p. 10. Two to three

word sentences were not expected until age two years. See Pet. Ex. 9, p. 4. Indeed, petitioners

themselves reported that A.A. spoke her first word “quack” at one year and spoke “a little more/using

animal sounds” at 15 months. See Pet. Ex. 5, p. 5.

51

A photograph on her first birthday was used as Pet. Trial Ex. 2.

52

Pet. Ex. 76; see Tr. at 115 (Ms. Susan Edick testified that she took the photograph on September 3,

2000).

31

helping to choose the pumpkins. Tr. at 19-20. “She was like a kid in a candy store,

basically.” Tr. at 21. Video from that day showed A.A. walking and touching the

pumpkins. 53 In one segment, she was seen “pushing” a wheelbarrow while holding her

mother’s hand. Tr. at 20. Mr. Allen also thought she might have danced to some music

playing in the background. Tr. at 21. His recollection from that activity was of A.A.

“engaging with people, . . . with her mom and her dad, too.” Tr. at 22.

Mr. Allen also videotaped A.A. at home on that same day in various situations—

from running around the house to eating dinner. 54 In one clip, A.A. was standing in her

crib looking at the camera. Mr. Allen described her as “a little grumpy” after having just

awakened from a nap. Tr. at 15. In another, she was in the bathtub splashing and

playing with some toys. Mr. Allen noted that she made eye contact and was “very

interactive.” Id. During her bath, A.A. was playing with a rubber ducky and splashed

herself with water, “which she liked to do.” Id. He recalled her saying “quack, quack”

when asked what sound a duck makes, although the sound does not appear on the

videos. Tr. at 15-17. She “loved to make animal sounds,” but her “first words were da-

da.” Tr. at 15. 55

After her bath, A.A. was videotaped playfully running around her parents’

bedroom. See Pet. Ex. 60. When asked if she was vocalizing during the clip, Mr. Allen

responded: “Yes. A little bit. Really she was kind of doing the quack-quack still after

the bath, yeah.” Tr. at 18. In a subsequent segment, she was engaged in a “game”

with her father that involved her being chased “down the main hallway on the second

floor.” Tr. at 25. “That was a tickler bug thing . . . you know ‘I’m going to get you[.]’”

Tr. at 25. In the clip she also kissed her favorite stuffed toy—a teddy bear. Tr. at 26. In

another scene, A.A. danced to a song playing on Sesame Street. Tr. at 28- 29. A later

clip showed her seated in a high chair eating dinner. At the end of that clip she

appeared to imitate her father. He explained: “I was doing the ‘rah’ and she was doing it

back.” Tr. at 29.

On October 23, 2000, A.A. received a MMR vaccination. Although Mr. Allen was

present at the appointment, he could not recall any details. Tr. at 102-04. He did,

however, remember noticing changes in her behavior following the appointment, but not

necessarily on that day. Tr. at 73. He specifically recollected a developing awareness

that something was wrong during a neighborhood Halloween party the family attended

on October 29, 2000. Tr. at 77. The daytime, outdoor event included treats, games,

and a participatory parade for the children to show off their costumes. Tr. at 30-31; Pet.

53

Video of A.A. on October 14, 2000. Pet. Ex. 60.

54

Video of A.A. on October 14, 2000. Pet. Ex. 60. Despite confessing his love for recording his

daughter’s life (Tr. at 14.), Mr. Allen was able to find video from only three events of her entire childhood.

In view of his comments, I find the lack of other videos from holidays or birthdays in this period

inexplicable and concerning for spoliation of evidence.

55

This statement is contrary to earlier reports. See, e.g., Pet. Ex. 5, p. 5 (reporting that her first word was

“quack”).

32

Ex. 78 at 4-5. She did not want to walk in the parade and displayed little interest in

interacting with other children or participating in the activities. Tr. at 31; Pet. Ex. 78 at 4-

5. She really “seemed inattentive and passive.” Pet. Ex. 78 at 5. She “just stood in one

place like a mannequin”—she “looked stoned.” Tr. at 31. While there were “brief

moments” when she “would take one step, two steps here, one or two steps [t]here,”

she did not really walk, and definitely did not run. Tr. at 36-37.

Mr. Allen contrasted this behavior with her actions over the Labor Day weekend,

when she eagerly played croquet in her aunt’s backyard. Tr. at 32-33. On that

occasion, she was “interacting and playing games”—she wanted “to be like a big girl,” to

understand the rules and learn how to play. Tr. at 32-33. At the Halloween party,

however, she did not play games, or want to walk, stand, or interact with the other kids.

He recalled thinking that “maybe she’s really shy or something.”

In video taken during the neighborhood Halloween party, A.A. was seen standing

with other children waiting for family and friends to take photographs of the group. 56 Tr.

at 35. Mr. Allen recalled that afterwards A.A. just stood in place until every other child

had left. Id. He thought she would want to follow them for the parade, but she did not.

Id. Rather than walk, she allowed her mother to carry her for a while and then push her

in a cart. Id. Mr. Allen observed the absence of eye contact or any sounds during the

segment and noted that when they spoke to her, she showed no response. Tr. at 35-

36. “You can hear the birds, but you don’t hear her.” Tr. at 36.

Her disinterest “was kind of startling” to him—“[i]t was a big change.” Tr. at 37.

In the past, she would have had “her hands in everything.” Tr. at 38. But on that day

she was not engaged. Id. As an example, he remembered that they tried without

success to get her to play a beanbag toss game. Id. They “had to walk it up . . . and

she’d put it through the hole and that was it.” Id. The other children “sort of ran by her.”

Id. He remembered thinking “maybe she’s got a bug or something or maybe she’s just

having a bad day.” Id.

According to Mr. Allen, that day (October 29, 2000) marked the beginning of

noticeable changes in A.A.’s behavior. Tr. at 38. From there she gradually stopped

speaking and interacting, and her personality changed. Id.

That night, when she developed a fever and refused to eat, petitioners became

concerned. Tr. at 78. Because her fever was over 100 degrees, they contacted A.A.’s

doctor, who told them to administer Tylenol and to call back or come in if the fever did

not subside. Tr. at 78-79. There is no record of this telephone call. The fever lasted

four days, during which it “kind of spiked and . . . went down and spiked again.” Tr. at

39-40. As a result of her illness, A.A. was unable to trick-or-treat on Halloween night.

Id.; see also Tr. at 79-80 (testified that they contacted doctor twice); Pet. Ex. 78 at 5.

They did not take her to the doctor. Tr. at 80-81.

56

Video of A.A. on October 29, 2000. See Pet. Ex. 80, 81.

33

Mr. Allen stated that he and A.A.’s mother speculated as to the cause of the

illness, but remained uncertain. Initially, they wondered if it was something she had

eaten—perhaps too much candy or she had developed an allergy. Tr. at 40-41. They

also considered that it was a “’bug,’ like the flu[,]” or that she was maybe teething. As a

new parent, the situation “was disconcerting.” Tr. at 41; see also Pet. Ex. 78 at 5.

However, this was not A.A.’s first illness.

According to Mr. Allen, A.A.’s behavior changed significantly after the fever. He

stated that she was sleepy, cried at night, and wanted to go to bed early. Tr. at 81. She

no longer was “talkative” and would not respond or make eye contact. Tr. at 41. She

also stopped “watching Sesame Street and dancing.” Id. Instead, she would sit on the

carpet and pull pieces of thread. Id. She “wasn’t mobile like other kids.” Id. He could

not recall, though, whether he or his wife contacted A.A.’s physician about her

worsening symptoms. Tr. at 81-82; see also Tr. at 45.

Over the Veterans Day weekend in November 2000, the Edicks visited

petitioners at their home in Virginia. Tr. at 42. During their visit, the two families made

a trip to the National Zoo in Washington, D.C. Id. The zoo was A.A.’s “favorite place”

because she liked animals—especially monkeys, which she previously had watched

with fascination. Tr. at 42; Pet. Ex. 78 at 5. On this occasion, however, she was

disinterested, and cried and fussed. Tr. at 43. Mr. Allen recalled thinking that “her

behavior and lack of activity was because she was recovering from a bug.” Pet. Ex. 78

at 5; see also Tr. at 43, 83. Because of her tantrums and crying, the trip was cut short.

Tr. at 43; Pet. Ex. 78 at 6. “During this weekend,” he also “noticed that [A.A.] seemed

unsteady on her feet” and often “crawl[ed] to her destination.” Pet. Ex. 78 at 5. She

talked less, too. Tr. at 84. Petitioners did not take A.A. to the doctor, however. Tr. at

83-84.

Later that month, on Thanksgiving, the family gathered at Mr. Allen’s

grandfather’s farm. Tr. at 43. At some point that day, Mr. Allen recalled talking to his

mother about his concerns. Tr. at 44. He stated that she expressed concern, too,

because A.A. was crawling more than walking. Id. She also seemed content to sit

alone by herself. Tr. at 45; see also Pet. Ex. 78 at 6. This was noticeably different from

her behavior on October 14th, when she was “running around, . . . interactive with other

kids.” Tr. at 45. In retrospect, Mr. Allen wished that he had called the doctor, but stated

that other than reporting that he could not “get a great Kodak moment,” he was not sure

what he would have said. Tr. at 45.

Throughout the month of December 2000 “all [A.A.] wanted to do was sleep.”

Pet. Ex. 78 at 7. She also had frequent tantrums. Tr. at 86. “Her temperament

changed from a child with a big personality to one who would only smile occasionally.

Mostly, however, she stared off into space[.]” Pet. Ex. 78 at 7. On December 18, 2000,

A.A. was seen by her pediatrician; however, Mr. Allen could not recall whether he

attended or what was discussed. 57 Tr. at 84. Her behavioral problems continued to

57

The medical record on December 18, 2000, reflects a diagnosis of early OM. Pet. Ex. 9, p. 57.

34

Christmas, which made the holiday a “disappointment.” Tr. at 46. Petitioners stayed

home for Christmas and were joined by A.A.’s maternal grandparents. Id. Although

there were a lot of gifts, A.A. showed no interest in opening any of them on Christmas

morning. Tr. at 46; Pet. Ex. 78 at 7. She even “cried when a gift was placed in front of

her and left the room.” Pet. Ex. 78 at 7. Mr. Allen remembered that she “still seemed

sickly,” having had an earache the prior week. Tr. at 46. Mr. Allen shot video on

Christmas Day, 58 but noted that most of the clips showed “the good moments”—

because “she was crying a lot,” they had to reshoot numerous times. Tr. at 47-48. He

remembered that she was miserable “[t]hrough the entire day all the way up to dinner”

and was put to bed early. Tr. at 49. “For a kid on Christmas,” her behavior was “kind of

surprising.” Tr. at 48. He contrasted her unhappiness with how she behaved on her

birthday: “opening every little gift . . . and . . . going through the cake.” Tr. at 50.

The day after Christmas, A.A. appeared to feel better, so petitioners tried again

to get some “Kodak moments.” Tr. at 50. However, despite being more cooperative,

her behavior was still unusual. Though she showed increased interest in her toys, she

did not play with them “appropriately.” Tr. at 50. For example, one of the gifts was a set

of toy kitchenware, which she banged against a nearby clock and stacked in piles

instead of pretending to fix food. Tr. at 50-51. Mr. Allen stated that this was unusual—

“before[,] she wasn’t like that.” Tr. at 51. “She was in a world of her own.” Pet. Ex. 78

at 7.

After Christmas, A.A. “never really went back to where she was,” and it was

“years” before she started talking again. Tr. at 51. Petitioners eventually decided to

seek the help of specialists, because they had received no “clear answers” from her

treating physicians. Tr. at 52. He recalled the frustration he felt:

I’m going to the pediatrician and they’re treating her ear, they’re treating

her nose, they’re treating her finger, they’re treating her bellyache, they’re

treating her fever. They’re treating symptoms; they’re not treating the

whole problem. . . . And you walk out and you feel better for about a half a

day until you’re home again.

Tr. at 52. However, the medical records reflect that A.A.’s pediatrician was actively

engaged in her care and responsive to her parents’ concerns.

On March 1, 2001, petitioners took A.A. to her 18-month well child visit. Tr. at

86. Although he could not remember anything specific about the visit, Mr. Allen knew

he was concerned about her loss of speech and eye contact. Tr. at 86-87. According

to the pediatrician’s notes of that visit, A.A. did not display some of the expected skills

for a child her age, including the ability to speak 4-10 words. See Pet. Ex. 9, p. 8. It

was noted that there had been “problems” with the previous nanny, but that A.A. was

“opening up more” with the replacement. Id. The record indicated that Mrs. Allen 59

58

Video of A.A. on December 25, 2000. Pet. Exs. 74, 81.

59

The medical records of this visit do not indicate whether Mr. Allen was present.

35

expressed concern over A.A.’s language skills, noting that she “seems to understand

[but] sometimes refuses to talk/play games.” Pet. Ex. 9, p. 18. Mrs. Allen attributed this

to the previous nanny, with whom she was not pleased. Id. The pediatrician advised

Mrs. Allen to follow up if concerned or not seeing progress in language development

over the next two months. Id.

On Easter, April 15, 2001, the family visited Mr. Allen’s sister at her home, also in

Virginia. Pet. Ex. 78 at 7. Mr. Allen remembered family members noting a “dramatic

change” in A.A.’s behavior from when they saw her on her birthday and at

Thanksgiving. Id. His sister, for instance, noticed that A.A. would not respond when

called to by name. Id. at 8. Eventually his sister became “so concerned” about the

changes she saw, that she and A.A.’s mother jointly called A.A.’s pediatrician “to see if

[she] had lost her hearing.” Id. About this time, A.A. also “began tip toe walking and

hand flapping,” as well as humming and pacing back and forth. Id.; but see Tr. at 87

(toe walking began “later in the year of 2001”; and the hand-flapping did not become

“prevalent” until “around the Children’s Hospital time frame” in September). To those

who knew her, it was “becoming increasingly apparent that something was wrong.” Pet.

Ex. 78 at 8.

On April 24, 2001, Mr. Allen completed an application for A.A.’s admission to the

Village Green Day School. Tr. at 87-88. On the application, he reported that his

daughter did not have temper tantrums and noted no physiological, behavioral, or

developmental problems or difficulties, including in the areas of speech, hearing, and

mobility. See Pet. Ex. 7, pp. 7-8. He did mention, however, that she had a tantrum on a

seven-hour family trip to New York. Id. When asked to explain his responses, he

stated: “I was a first-time parent. I didn’t see my daughter as having problems. I didn’t

see her as abnormal. I didn’t know if any of these behaviors were normal or abnormal.

So that’s probably why I wrote that.” Tr. at 90. He also noted: “At that point in time, no

doctor had told me that there was anything wrong with her.” 60 Tr. at 91.

In late August and early September 2001, A.A. was examined at Blue Ridge

Speech and Hearing for a suspected hearing problem related to her recurrent OM. The

resultant examination report noted that A.A. had reportedly “said her first word ‘quack’ at

one year and [spoke] a little more/using animal sounds at 15 months, [but] stopped

speaking after having three ear infections in a row.” Tr. at 92 (quoting Pet. Ex. 5, p. 5).

When asked if this was accurate, Mr. Allen clarified that A.A. “began to stop speaking in

between each ear infection – that sentence reads as if after the three ear infections, she

stopped speaking.” Tr. at 93. Instead, “she had three ear infections as her language

skills were deteriorating.” Tr. at 93. The report concluded with a tentative diagnosis of

autism. Tr. at 53; see also Pet. Ex. 78 at 8-9.

60

This report may be technically correct in that a diagnosis of speech/language delay was not made until

May 2001, but it was clear from the March 1, 2001 well child visit that A.A.’s mother had concerns about

her development, and said that she refused to talk and play games. Pet. Ex. 9, p. 18

36

According to Mr. Allen, he and his wife were surprised by the diagnosis—in fact,

it was the “first time” that he had heard the word “autism.” Tr. at 53. He recalled staying

up every night, reading “about autism until 3 or 4 in the morning. During those hours,

[A.A] would wake up screaming and the only thing that would calm her down was

watching cartoons with music in our bedroom.” Pet. Ex. 78 at 9; see also Tr. at 96, 98-

100.

On September 6, 2001, petitioners consulted with Dr. Lavenstein, a neurologist

at Children’s Hospital in Washington, D.C. Tr. at 55. He ordered additional testing, the

results of which supported the ASD diagnosis. Pet. Ex. 78 at 10. Mr. Allen then

“applied to get [A.A.] into Kennedy Krieger through a referral” and was successful. Tr.

at 57; Pet. Ex. 78 at 10.

Additionally, during this period A.A. underwent a bilateral tympanostomy to treat

her recurrent OM. 61 The procedure reportedly did nothing to improve her behavior—

“she was still not responding.” Tr. at 53. She was also taken to the Fairfax Hospital

Emergency Department during the Christmas season in 2001 because of “one of [her]

screaming episodes.” Pet. Ex. 78 at 9. Testing revealed that she was “suffering from

intestinal blockages. She was not digesting the food and it was acting like a poison in

her body.” Pet. Ex. 78 at 9. Petitioners eventually learned that A.A. had allergies to

dairy and eggs—a condition commonly found in children with autism. Pet. Ex. 78 at 9.

When asked to identify the time frame in which he first connected the MMR

vaccine to A.A.’s problems, Mr. Allen reported that it “was a slow gradual process of

kind of putting one and one together and coming up with two.” Tr. at 96. Although he

could not say for sure, he thought it was “probably . . . late 2001.” Tr. at 97. To assist

his memory during testimony, Mr. Allen was shown a January 2002 medical record,

which reflected his statement that he was “100 percent sure that [A.A.]’s problems are

from her MMR immunization. Her behavior started 30 days post-MMR.” Tr. at 97

(quoting Pet. Ex. 9, p. 35). In view of the record, Mr. Allen testified: “At that time, if I

said I was 100 percent certain, I meant it.” Tr. at 97.

In January 2002, petitioners were notified that A.A. would no longer be allowed to

attend Village Green Day School due to behavioral difficulties. Tr. at 106. Mr. Allen

recalled that “during that time frame . . . she was having the screaming fits.” Tr. at 106.

In February 2002, petitioners met with Dr. Zimmerman for the first time. Tr. at

57. After an extensive workup, Dr. Zimmerman validated the ASD diagnosis. Tr. at 58.

He then recommended that A.A. be tested for mitochondrial disorder to help guide her

treatment. Id. Mr. Allen remembered that the testing, which involved obtaining a blood

specimen, was very difficult because A.A. struggled against the procedure. Tr. at 58-

59. After obtaining the results, Dr. Zimmerman informed petitioners that A.A. “tested

positive for mitochondrial disorder” and referred them to Dr. Kelley for further testing

and evaluation. Tr. at 59.

61

See n.34, supra, dating the procedure as likely occurring in October 2001.

37

When petitioners met with Dr. Kelley, he confirmed that A.A. had a mitochondrial

disorder and explained his recommended treatment was a “vitamin cocktail” that

included Coenzyme Q10. Tr. at 61-62. Mr. Allen testified that after A.A. began the Dr.

Kelley’s prescribed treatment, her behavior slowly, but steadily improved. Tr. at 62-63;

Pet. Ex. 78 at 10. Although she continued to toe-walk on occasion and have difficulty in

social situations, other areas were positively changed. Tr. at 63. For example, she

began to make eye contact, “her voice came back,” she was better able “to

conceptualize, particularly . . . in reading,” and her confidence increased. Tr. at 63.

As of the time of the hearing, A.A. was, according to Mr. Allen, progressing in her

development and doing well in school. 62 Tr. at Tr. at 63-68. Although her social skills

were “not quite there,” she was learning to interact with her peers and had made a

friend at school; however, she was generally more comfortable around adults. Tr. at 63-

64. He indicated that she still had stereotyped and repetitive motor mannerisms, but

took medication to reduce these symptoms. Tr. at 65-67. She also continued to take

“part of the cocktail.” Tr. at 65.

B. Ms. Susan Edick.

Ms. Edick testified that she was employed as a special education teacher in New

York State. Tr. at 108. She earned a Bachelor of Science in education and special

education from Syracuse University and a Masters of Science in education from State

University of New York in Cortland. Pet. Ex. 79 at 1-2. She was certified in New York

State in “Special Education for Infants to Adults, Early Childhood Education, Elementary

Education for Grades K-6 and Reading/Literacy Education for Grades K-12.” Pet. Ex.

79 at 2.

According to Ms. Edick, her training included learning the signs and symptoms of

various developmental disorders, including “emotional [and] learning disabilities and

autism.” 63 Tr. at 109. Two classes in particular focused on autism, with exercises on

how to identify autistic behaviors and educate children with the disorder. Tr. at 109-10.

She also studied normal growth and development in children of school age. Tr. at 109.

In the field of education, Ms. Edick worked as a K-4 resource teacher, performed

student teaching in an early education program with special needs children, and taught

special education children in an integrated co-teaching classroom. Tr. at 110. Some of

her responsibilities have included test modification, evaluation and support of student

Individualized Education Plans [“IEPs”], and identification and improvement of areas of

weakness, such as “social behavioral” issues or a “learning disability in reading and

writing.” Tr. at 110-11. Over the course of her career, Ms. Edick has both taught

62

Mr. Allen reported that A.A. was a “straight A” student in her program. Tr. at 64, 68. She was looking

forward to attending high school the following year. Tr. at 68.

63

It is unclear whether Ms. Edick had training and experience in identifying developmental disorders in

pre-school-age children.

38

autistic children and been responsible for identifying those with autism spectrum

disorder symptoms who might require intervention. Tr. at 111. She stated that in her

work she might, for example, identify “learning disabilities or learning patterns in kids or

serve on the committee for the school . . . [to] recommend further testing with a

psychologist or with speech and language therapists or with specialists, ear, nose and

throat, or doctors.” Tr. at 111.

Ms. Edick testified that, as a close relative, she had frequent opportunities to visit

petitioners and observe A.A.’s growth and development. Tr. at 112; see also Pet. Ex.

79 at 2. She also spoke often with A.A.’s mother—her sister—on the telephone. Tr. at

112. “[W]e would discuss different activities, what was going on with them in life or

family.” Tr. at 112.

Though she did not attend A.A.’s first birthday party, she remembered seeing

A.A. when petitioners visited over the Labor Day weekend in September, when she was

almost 14 months old. Tr. at 112; see also Pet. Ex. 79 at 2-3. According to Ms. Edick,

A.A. seemed “very happy, very healthy” during their stay. Tr. at 113. From what she

observed, A.A. “seemed very normal, [with] typical development for a child socially,

cognitively, physically. She was walking. She was talking, typical vocabulary, one-word

vocabulary.” Tr. at 113. A.A. sometimes used gestures to communicate, such as

pointing, bouncing, or taking one by the hand. Tr. at 113, 123. However, Ms. Edick

specifically recalled that she could say “the words that a child would have at that time”

and “numbers and count a little bit.” Tr. at 113. She estimated that A.A. knew

“approximately 12 to 20 words at that time.” 64 Tr. at 123. None of A.A.’s behaviors at

that time concerned her. Tr. at 113, 115. “She enjoyed playing . . . peek-a-boo, playing

so big. If you asked her how old she was, she would hold up her finger, one.” Tr. at

113. She appeared to understand what was being said and “would look to you to

interact and . . . play.” Tr. at 113. Ms. Edick noted A.A.’s eye contact in the photo taken

of her playing croquet in her yard—“she was laughing and smiling for the camera.” Tr.

at 114 (discussing Pet. Ex. 76).

On Halloween, Ms. Edick recalled speaking to her sister on the telephone and

asking if A.A. was dressing up to go trick-or-treating. Tr. at 116. She replied that A.A.

“hadn’t been feeling well, she was running a fever and had been for a few days.” Tr. at

116; see also Tr. at 123; Pet. Ex. 79 at 3. Her sister promised to “dress her up another

day and . . . send pictures when she’s feeling better.” Tr. at 116.

On Veterans Day weekend, the Edicks visited petitioners at their home. Tr. at

116; see also Pet. Ex. 79 at 3. During that visit, she became “very concerned because .

. . it was apparent that [A.A.] was showing signs of development[al] regression, which

included . . . an absence of speech and communication . . . [and] eye contact. Tr. 116-

64

This estimate contrasts with Mr. Allen’s testimony that A.A. knew “well over 100 words” by her first

birthday (Tr. at 70-72) and the earlier report that she spoke “her first word ‘Quack’ at 1 year and [spoke] a

little more/using animal sounds at 15 months” (Pet. Ex. 5, p. 5). A.A.’s pediatrician assessed her as

having one to three words at her one-year well child visit. Pet. Ex. 9, p. 10.

39

17; see also Tr. at 124; see also Pet. Ex. 79 at 3. Her behavior was noticeably

changed.

She tended to just want to [lie] on the floor, or if we tried to pick her up,

she didn’t want us to touch her or pick her up. She would just stare at her

hand, stare at her bear, stare at the carpet and pick the threads in the

carpet. And it was quite alarming to me.

Tr. at 117.

And when the families visited the National Zoo, “[s]he stayed in her stroller all

day” and showed “no interest in anything at the zoo.” Tr. at 117; see also Pet. Ex. 79 at

3. Ms. Edick remembered that A.A. “cried a lot, whimpered” – “it was a very difficult trip

for her.” Tr. at 117-18; see also Tr. at 128; Pet. Ex. 79 at 4. Following the visit, Ms.

Edick “may have said something” about her concerns to A.A.’s parents, but she did

recall talking to her own parents “because [she] was very concerned[,] especially since

[A.A.] had show[n] typical development in September.” Tr. at 119; see also Tr. at 124-

25, 130-31; Pet. Ex. 79 at 4. She stated that what she saw “really affected” her

because A.A.’s “behaviors were autistic-type behaviors on the spectrum, signs of it.” Tr.

at 119; see also Pet. Ex. 79 at 4. She was not certain, though, that A.A. actually had

autism and hoped instead that the behaviors were due to an illness. Tr. at 127, 130.

In December, Ms. Edick asked her parents to observe A.A. during their

Christmas visit and report back on her behaviors and whether she had improved. Tr. at

119; see also Tr. at 124-25, 130. When they returned home, they informed Ms. Edick

that the signs she had observed were “still apparent.” Tr. at 119. They also expressed

that “they were extremely upset because [A.A.] was having constant tantrums . . .

throwing herself back and hitting her head on the floor.” Tr. at 119; see also Pet. Ex. 79

at 4. Because of her behaviors, they left without seeing her open any gifts. Tr. at 119.

Ms. Edick stated that she spoke with her sister after the holidays and “asked her at

different times to talk to their pediatrician, . . . or follow through with a specialist, an ear

nose and throat person to see if there was anything wrong with [A.A.’s] hearing or

behavior.” Tr. at 126.

In April 2001, their families gathered together for Easter. At that time, A.A. “was

walking again, but . . . still did not communicate through speech or many gestures.” Tr.

at 120; see also Tr. at 128. Ms. Edick also recalled that she “did not want to socially

interact with her grandparents or anyone,” or engage in any age-appropriate activities.

Tr. at 120. Also of concern was her unresponsiveness “to her name or commands” in

potentially dangerous situations. Tr. at 120; see also Pet. Ex. 79 at 5. She observed

A.A. to “just run randomly” into the woods or a nearby yard and that she did “not

respond to her name or commands.” Tr. at 120; see also Pet. Ex. 79 at 5. According to

Ms. Edick, this was different from her previous behavior. Previously A.A. “always

responded and stayed around people”—[i]f you called her, she would come to you.” Tr.

at 120.

40

In the summer of 2001, the Edicks visited petitioners. During their stay, she

noted that some of the abnormal behaviors were persisting—“she still did not

communicate, she still was not talking,” and she still did not “have a lot of eye contact.”

Tr. at 121; see also Pet. Ex. 79 at 5. She also remembered that A.A. “was having a lot

of crying and tantrums[,] . . . did not want to keep her clothes on[,]” and appeared to be

“experiencing some . . . sensory issues[.]” Tr. at 121-22.

Ms. Edick indicated that she was not surprised when A.A. was evaluated on the

autism spectrum, as she eventually suspected—and suggested—that autism was a

possibility. Tr. at 122, 133-34. By that point, petitioners also did not seem too

surprised, either. Tr. at 133. Although it was “very devastating” to accept, they had

been seeking answers for some time—“it was such a bad period of time for them.” Tr.

at 133.

V. Expert Qualifications.

Four physicians offered opinions on vaccine causation and other matters in

dispute. All of the experts were well-qualified to offer opinions in this case. Petitioners’

experts opined that A.A. had an underlying mitochondrial disorder that made her

vulnerable to the inflammatory effects of the MMR vaccine she received at her 15-

month well child visit. As a result of her vaccination, she experienced a rapid regression

and ultimately developed “mitochondrial autism.” Respondent’s experts opined that

A.A. did not have a mitochondrial abnormality or suffer a rapid regression. Instead, she

exhibited signs of autism prior to vaccination and followed a typical course thereafter. In

their view, the MMR vaccine did not aggravate an underlying condition or cause her to

develop ASD.

A. Petitioners’ Experts.

Petitioners presented testimony from two experts: Dr. Andrew W. Zimmerman,

an expert in pediatric neurology, and Dr. Richard I. Kelley, an expert in metabolism.

Both physicians were involved in A.A.’s treatment and were familiar with her general

medical history and development; however, neither was a treater at the time of

vaccination or a contemporaneous witness to the onset of her condition. As such, these

particular treating physicians are no more knowledgeable about what actually transpired

after the vaccination than any other physician who testified in this case.

1. Andrew W. Zimmerman, M.D. 65

Doctor Zimmerman earned his medical degree from Columbia University. Tr. at

289. He completed a pediatric internship at the University of Michigan, and a neurology

residency at Johns Hopkins Hospital. Tr. at 289-90. Following his residency, Dr.

65

Doctor Zimmerman’s CV was filed as Pet. Ex. 26, and his expert report was filed as Pet. Ex. 25.

41

Zimmerman worked for eight years 66 as a faculty member at the University of

Connecticut. Tr. at 290. Thereafter, he went into private practice for 11 years and “then

returned to [the] Kennedy Krieger Institute and Johns Hopkins in 1994 for the next 16

years.” Id.

For the past several years, he has worked at Massachusetts General Hospital as

director of clinical trials at the Lurie Center for Autism, where he conducts drug trials on

children with autism. Tr. at 290. He also is an associate professor of neurology at the

Harvard Medical School. Id. His academic responsibilities involve teaching medical

students, residents, and fellows. Tr. at 291. He is board certified in pediatrics and

pediatric neurology. Id. He has published over 70 peer-reviewed articles—many

focused on autism. Id.; see also Pet. Ex. 26 at 16-22. Doctor Zimmerman works with

various hospital committees in his capacity at the Lurie Center and serves as the

scientific advisory chair on the board of directors of the Fetal Physiology Foundation.

Tr. at 291; Pet. Ex. 26 at 3.

2. Richard I. Kelley, M.D., Ph.D. 67

Doctor Kelly earned his medical degree and a Ph.D. in pathology/molecular

biology from the University of Pennsylvania, where he participated in a combined

Ph.D./M.D. program. Tr. at 135; Pet. Ex. 24 at 1. He completed a residency in

pediatrics and a postdoctoral fellowship in medical genetics at The Children’s Hospital

of Philadelphia [“CHOP”], after which he spent approximately five years on the CHOP

faculty in the departments of metabolism and genetics. Tr. at 135-36; Pet. Ex. 24 at 1.

Subsequently, he joined the faculty of the department of pediatrics at Johns Hopkins

University School of Medicine [“JHU”] and also became a staff physician at the Kennedy

Krieger Institute [“KKI”]. Id. Both institutions are located in Baltimore, Maryland.

Doctor Kelley is currently a professor of pediatrics at JHU and director of the

division of metabolism at KKI. Tr. at 136; Pet. Ex. 24 at 1. In addition to an active

clinical practice, he oversees several KKI laboratories that conduct biochemical and

genetic testing. Tr. at 136-37. He is also “the principal advisor for the neurology

division” and a coordinator for the “neurogenetics division.” Tr. at 137. His academic

responsibilities include teaching medical residents, “mostly . . . on an individual basis,”

and performing “consultations . . . when a question falls into [his] areas of expertise.” Id.

He is board certified in pediatrics, clinical genetics, biochemical genetics, and

cytogenetics. Tr. at 138; Pet. Ex. 24 at 13. Doctor Kelley stated that he is regularly

consulted as a mitochondrial expert both domestically and internationally. Tr. at 139-40.

He is “the go-to person” for certain developmental diseases and has been consulted on

66

Doctor Zimmerman testified that he was on the faculty for eight years; however, his resume indicated

that it was between six and seven years (January 1977 to August 1983). Pet. Ex. 26 at 1-2.

67

Doctor Kelley’s CV was filed as Pet. Ex. 24, and his expert report was filed as Pet. Ex. 23.

42

a number of “puzzling case[s]” involving “Smith-Lemli-Opitz syndrome, Barth syndrome,

mitochondrial disease, chondrodysplasia punctata, [and] Zellweger syndrome.” Id.

His publications include more than 100 peer-reviewed scientific articles and 12

book chapters. Pet. Ex. 24 at 2-11. He has written about “a fairly broad spectrum of

metabolic abnormalities that largely come from clinical practice.” Tr. at 138. His work

has “been largely with metabolic and so-called inborn errors of metabolism;” however,

the focus of his research “basically depends on what comes up in the clinic or . . . our

laboratory” at any given time. Id.

Doctor Kelley previously served on numerous committees and boards, including

journal review boards. Pet. Ex. 24 at 13-14. However, he resigned or withdrew from

them beginning around 2006, when demands on his time increased. Tr. at 141.

B. Respondent’s Experts.

Respondent presented testimony from two experts: Dr. Max Wiznitzer, an expert

in pediatric neurology and developmental disabilities, and Dr. Stephen Cederbaum, an

expert in pediatrics, inborn errors of metabolism and mitochondrial disease, and

genetics.

1. Max Wiznitzer, M.D. 68

Doctor Wiznitzer earned his medical degree from Northwestern University, and

completed a pediatrics residency at the Cincinnati Children’s Hospital. Tr. at 476. He

also completed fellowships in development disorders at the Cincinnati Center for

Developmental Disorders and in child neurology at the University of Pennsylvania

System and at the Children’s Hospital in Philadelphia. Id. Additionally, he completed a

National Institutes of Health National Research Service Award Fellowship in disorders

of higher cortical function in children at the Albert Einstein College of Medicine in New

York. Id.

Since 1986, Dr. Wiznitzer has been a full-time staff neurologist at Rainbow

Babies and Children’s Hospital in Cleveland, Ohio. Tr. at 477. In his capacity, Dr.

Wiznitzer has treated “thousands of children and . . . adults” with autism. Tr. at 482. He

has “an extremely busy clinical practice” that provides him the opportunity to “see

patients four to five half-days a week.” Tr. at 480. He routinely reads EEGs, assists the

epilepsy team when a member is out of town, and works “at least eight weeks in the

year on the inpatient medical service,” where he is responsible for “any children

admitted to the neurology service” and provides consults on any neurology questions.

Tr. at 480-81.

Additionally, Dr. Wiznitzer is a professor of pediatrics and neurology and

international health at Case Western Reserve University School of Medicine. Tr. at 477.

68

Doctor Wiznitzer’s CV was filed as Res. Ex. L, and his expert report was filed as Res. Ex. K.

43

He has conducted research in a variety of areas, with a special interest in autism, which

he began studying in 1986. Tr. at 481. As a researcher, he has been involved in “two

seminal studies looking at the differentiation between autism, kids with developmental

language disorder, and children [with] mental retardation.” Id. Most recently, he

participated in a study with high-functioning autistic children that sought “to alter the[ir]

developmental trajectory” through “a pharmacologic intervention.” Tr. at 481-82.

Doctor Wiznitzer is board certified in pediatrics, neurodevelopmental disabilities,

and neurology, with special qualification in child neurology. Tr. at 477. He has

published 60 peer-reviewed articles, 11 book chapters, and numerous abstracts. Res.

Ex. L at 13-23. He also writes questions for the neurodevelopmental disability board

certification exam. Tr. at 483. Doctor Wiznitzer regularly lectures on autism spectrum

disorders and developmental disabilities at national and international meetings. Tr. at

482. He is a member of numerous professional organizations, editorial boards, and

advisory groups. Tr. at 477-80.

2. Stephen D. Cederbaum, M.D. 69

Doctor Cederbaum earned his medical degree from New York University School

of Medicine, and completed an internship and residency at Washington University

School of Medicine in St. Louis. Tr. at 376. Subsequently he worked for the National

Institutes of Health, fulfilling his military service obligation, where he conducted

biochemical research. Id. He then returned to Washington University for training in

medical genetics, after which he accepted a position at the University of California at

Los Angeles [“UCLA”]. Id. At UCLA, Dr. Cederbaum taught medical students, cared for

patients with genetic disorders (particularly those with inborn errors of metabolism), and

conducted basic scientific research, with a focus on urea cycle disorders and inborn

errors. Tr. at 377-78.

Doctor Cederbaum is board certified in clinical genetics and biochemical

genetics. Tr. at 378. He has published 150 peer-reviewed articles and 80 to 90

chapters and other contributions. Tr. at 379. Although he has not published extensively

in the field of mitochondrial disease, he considered himself a “pioneer” on the subject

due to his publication of “one of the first cases of mitochondrial disorders” in the 1970s.

Id. He also “was a pioneer in the area of pyruvate hydrogenase deficiency, developing

the first dietary therapy for it.” Id. He has also lectured on mitochondrial disease

nationally and internationally. Tr. at 381.

He is currently a professor emeritus at UCLA, which has allowed him to continue

many of his previous pursuits, but at a reduced level of responsibility. Tr. at 377. He

remains current with developments, research, and literature in the field of inborn errors

of metabolism, and is a reviewer for a variety of journals. Tr. at 377, 379-80. Doctor

Cederbaum has received notable honors and awards and remains a member of several

69

Doctor Cederbaum’s CV was filed as Res. Ex. B, and his expert report was filed as Res. Ex. A.

44

professional societies, including the American College of Medical Genetics, of which he

was a founding member. Tr. at 380.

Doctor Cederbaum also works as a medical monitor for the mitochondrial

research program at Columbia University. Tr. at 380. He previously worked in that

capacity for the University of Florida. Id. Doctor Cederbaum explained that a medical

monitor acts as an unbiased evaluator when questions arise about the safety of

participants involved in research studies. Id.

VI. Causation Evidence.

A. Medical Literature.

The volume of medical literature submitted into the record renders a separate

summary of each article impractical. Although I read and considered every piece of

medical literature in the record, only the articles addressed by the experts or that I relied

upon in coming to my conclusion will be specifically referenced below.

B. Expert Opinion and Testimony.

1. Doctor Zimmerman.

In his expert report, submitted prior to hearing, Dr. Zimmerman recounted that

A.A. “had normal development until 16 months when she regressed in language and

social skills within 1 – 2 weeks following immunization with MMR vaccine.” Pet. Ex. 25

at 1. Based on her history, his evaluation and testing, and her response to treatment,

Dr. Zimmerman concluded that A.A. “had a disorder of mitochondrial metabolism

associated with autistic regression.” Id. at 2. The report, however, contained no

statement addressing the role of the MMR vaccine in the development of this condition.

Doctor Zimmerman began his direct testimony at hearing with a review of A.A.’s

medical history and his involvement in her treatment. He first saw A.A. at an initial

evaluation on February 13, 2002, when she was 30 months of age. He recalled that

she presented with “a history of autism following regression.” Tr. at 292. Based on

parental report, she regressed “one to two weeks following her MMR immunization” with

a “los[s of] language and eye contact and social interaction.” Id. He stated that her

early development “appeared to be normal” from “all standpoints”—she “had met all her

milestones.” Tr. at 292-93. Because of her history and presentation, Dr. Zimmerman

“initiated a workup of genetic and metabolic studies.” Id. 70

70

In his evaluation, Dr. Zimmerman wrote that A.A. “presents an atypical history and appearance

consistent with an encephalopathy and a pervasive developmental disorder (autism spectrum). A history

of regressive encephalopathy suggests the need for genetic testing, chromosomes and DNA for fragile X

and quantitative plasma amino acids and urine organic acids.” Pet. Ex. 6, p. 24. He also “requested

genetic testing to rule out Rett syndrome.” Id.

45

In response to questioning on cross examination, Dr. Zimmerman stated that the

history he gave of A.A.’s regression in language and social skills shortly after her MMR

immunization was based entirely on statements from her parents. Tr. at 347-48. He

also indicated that prior to her initial evaluation he had not reviewed any of her medical

records, although he has since done so. 71 Id. When asked whether he found any

indication in the medical records of developmental abnormalities or changed behavior

within one to two weeks of her immunization, he stated “I don’t believe so, no.” Tr. at

348.

During his testimony, Dr. Zimmerman viewed and commented on several

segments of home video taken on October 14, 2000, about nine days before A.A.’s

immunization. Petitioners argued that the video provides a demonstrative baseline for

her pre-vaccination behavior and developmental achievement. In the video, which was

taken at petitioners’ home, A.A. seemed “quite lively.” Tr. at 294. She appeared to

respond to her name and play appropriately with toys, and said “quack” when asked

what noise a duck makes. Tr. at 294-95. When questioned about her age, she

indicated with a raised finger that she was one year old. Doctor Zimmerman assessed

this behavior as appropriate for A.A.’s age. Tr. at 295. He also observed that in an

earlier frame she was “pointing with [her] index finger”—an “important prelinguistic

gesture that children develop around one year of age[.]” Tr. at 295-96.

He further noted that A.A. was appropriately interactive with her parents. Tr. at

296. “She’s smiling and responsive and looking at the camera. I think she’s actually

making eye contact with the person who’s taking the film.” Tr. at 297. As for her

language development, she was “not forming words,” but “making word sounds.” Tr. at

297. This was not a point of concern, but instead, evidence that “she’s developing

language.” Tr. at 297. For example, when she said “moo” in response to the question

“What does a cow say?”, she was not simply repeating a sound someone made to her,

but responding to a question. Tr. at 298. “She’s practicing to be two.” Tr. at 298.

On cross examination, Dr. Zimmerman stated that a 15-month-old child would

typically have three words with meaning. Tr. at 343. When asked whether he heard

A.A. say any words in the above-described video clip, he stated: “I guess the ‘quack,’

and at one point she said ‘moo.’” Tr. at 344. He also recalled her “babbling some word

sounds,” but no other specific words. Id. When pressed whether he believed “moo”

and “quack” were words rather than sounds, he stated that “moo” was a word in this

context because A.A.’s response “was prompted only by the question, not by the

sound.” 72 Tr. at 344.

71

I directed Dr. Zimmerman to consider the initial audiological evaluation of A.A. from Blue Ridge Speech

& Hearing, which states: “Speech and language landmarks were reported as age-appropriate to a point,

said first word at one year, spoke a little more at 15 months, stopped speaking after having three ear

infections in a row.” Tr. at 368 (quoting Pet. Ex. 5, p. 5). I asked him whether he still would have

attributed A.A.’s regression to her MMR vaccination had he seen that record or been provided that history

by her parents. Tr. at 368. He responded: “I would have taken this into consideration, yes.” Id.

72

On redirect, Dr. Zimmerman confirmed that “moo” is a legitimate word. He stated that the 1983 edition

of Webster’s Dictionary “clearly says it’s a verb, to make the characteristic sound of a cow. So, she had a

46

He was also questioned about his comment that A.A. appeared to be making eye

contact with the person taking the video. Tr. at 344-45. When asked whether he could

differentiate between her “interacting or making eye contact with the person,” and her

simply “looking at the camera,” he conceded that he could not know what she was

looking at. Tr. at 345.

In response to my questioning, Dr. Zimmerman confirmed that he saw A.A.

pointing on the video, but that he did not see any evidence of her using words, “except

[for] what we have said, the – saying ‘moo’ and ‘quack’.” Tr. at 358. As for her raising a

finger to show her age, he agreed that the action was not an indication that she knew

her numbers, but that she had been “keyed or trained or talked to about putting that

finger up.” Tr. at 358; see also Tr. at 683-84. He also indicated that her reported ability

to name colors was probably overstated based on the level of development he saw on

the video. Tr. at 358-59 (citing Pet. Ex. 6, p. 15 (reporting that prior to her regression

“she knew her colors and was using words and was pointing”)). 73 “It would be a little

advanced, actually.” Tr. at 359.

In a later segment of the video, A.A. demonstrated normal gross motor skills by

running around the house. Tr. at 295. Doctor Zimmerman commented that “[s]he has

quite a good running gait for a child of that age.” Tr. at 298. He also noted that she

stood “without difficulty” and was “quite independent.” Tr. at 298. In another clip, she

was seen actively exploring her surroundings, responding to the word “no”, and feeding

herself—behaviors he judged as age-appropriate. Tr. at 299. When the video

concluded, Dr. Zimmerman stated that A.A. “appear[ed] normal in . . . all respects.” Tr.

at 299.

On redirect, Dr. Zimmerman was asked to elaborate on the development that he

saw during the October 14 video which he considered to be normal. Tr. at 674. He

stated that overall he “thought the language, the social interaction and her movements

were normal. Her activities . . . were appropriate for age.” Tr. at 674-75. It is unclear

why he considered her language to be normal and age appropriate. He previously

testified that a 15-month old child would have three words with meaning, but

characterized A.A.’s speech, as seen in the video, as “babbling” and stated that she

was not forming words. See Tr. at 297, 344.

word.” Tr. at 677; see also Tr. at 680 (recross). He emphasized that it is a “meaningful” word “which is

recognized.” Tr. at 677. I conclude that “moo” was not a word that A.A. used to communicate; rather, it

was a response to “what does the cow say,” just as holding up her index finger was a trained response to

a question about her age.

73

See also Tr. at 33 (Mr. Allen stating that A.A. “understood the colors” of the croquet balls when she

played the game over the Labor Day holiday in September 2000). I have no difficulty accepting that she

understood that the balls were of different colors, and that one particular colored ball was “hers,” but that

is a far cry from knowing colors and labeling items with their color when asked to do so—a more common

meaning for “knowing her colors.”

47

Doctor Zimmerman also was asked to specifically comment on what he

considered to be developmentally normal in A.A.’s behavior at the pumpkin patch that

same day. Tr. at 675. In response, he identified her interest in the pumpkins and her

ability to stoop and recover when playing with them. Id. She had a good running gait

and was stable when walking. Id. He noted “a lot of facial expression” and “some

reciprocal interaction with her parents.” Id. He further noted that he did not perceive

any difference in her behavior at the pumpkin patch from the earlier scenes when she

was alone with her parents at home. Id.

Doctor Zimmerman was asked to review the medical record of A.A.’s 15-month

well child visit, which occurred on October 23, 2000. 74 Tr. at 300. He stated that the

record reflected “normal” development on all measured criteria. Tr. at 301. It also

indicated that she received three vaccinations on that occasion: “MMR number one, Hib

booster, and Hep-B.” Tr. at 301.

Petitioners played several segments of home video taken on October 29, 2000,

six days after A.A.’s immunization. Petitioners argued that the video shows marked

changes in A.A.’s behavior. The video captured various moments during the pre-

Halloween party that took place outdoors in petitioners’ neighborhood.

After viewing the video, Dr. Zimmerman observed that A.A. seemed “less lively,”

had “virtually no facial expression,” and looked as though she did not “feel well.” Tr. at

301; see also Tr. at 678 (redirect). He also noted that she did not look at the camera or

interact with her parents. Id. And although she walked at times, it seemed “stilted.” Tr.

at. 301; see also Tr. at 682 (recross). During one clip, A.A. is seen walking with her

parents but was “not showing much expression on her own and [didn’t] seem to be [as]

interested in things, as she was before.” Tr. at 302; see also Tr. at 677-78 (redirect);

682 (recross). In response to my questioning, Dr. Zimmerman reiterated that he

thought A.A.’s “motor activity was diminished” and that she had less facial emotion as

compared to her behavior on October 14. Tr. at 684-85.

Doctor Zimmerman indicated that the behavioral changes seen in the video

correlated with the parental report that A.A. changed “within one to two weeks of the

MMR immunization.” Tr. at 302-03.

I asked Dr. Zimmerman whether the October 23 well child record reflected

symptoms of an illness or a cold. Tr. at 353-54. He responded that it noted ear tugging,

nasal congestion for one week, and treatment with the antibiotic amoxicillin. Tr. at 354.

He confirmed that treatment with amoxicillin was indicative of an ear infection. Id. I

then recalled his statement that A.A. appeared ill in the October 29th video and asked

whether her behavior could have been the result of the illness reflected in the medical

record. Id. He stated that he “would expect if the amoxicillin were treating an ear

infection, that she would have felt better by . . . six days later.” Id. He agreed, however,

that if the infection was viral rather than bacterial, she might have still felt ill. Id.

74

Pet. Ex. 9, p. 9.

48

I also asked Dr. Zimmerman about differences between the videos with regard to

environment. Tr. at 355. He noted that the first video was taken at home, while the

second was shot “outside in a party atmosphere.” Id. He acknowledged that “they

[we]ren’t directly comparable” and discussed the impact that environment can have on a

child’s behavior. Tr. at 355-56. For example, if she were really shy, she might not feel

comfortable participating in the activities. He stated, though, that he “would have

expected her to be more reactive to her parents . . . and have more expression.” Tr. at

356. Overall, however, he did not think the environment was a factor. Tr. at 679

(redirect).

Petitioners showed home video taken on Christmas Day 2000. Doctor

Zimmerman observed that “[t]his [was] two months later, the opening [of] presents, and

she doesn’t show, again, interaction with the parents or . . . the toys. Tr. at 303. She

also was “not vocalizing like she was initially” and “show[ed] very little facial expression,

if any[.]” Tr. at 303.

Doctor Zimmerman was then asked to opine on the significance of the behavioral

changes seen in the videos. Specifically, were they due to a transitory illness or

possibly the result of her vaccination? He stated that, in his view, the post-vaccination

videos indicated that her changes were not due to a temporary sickness, because she

would have improved by Christmas. Tr. at 303. Instead, “her condition five days after

the doctor’s visit appeared to persist . . . two months later.” Tr. at 303-04.

On cross examination, Dr. Zimmerman was asked whether he had seen any

video of A.A. taken during the two-month period between October 29th and December

25th, or reviewed any medical records from that same period. Tr. at 346. He stated

that apart from petitioners’ affidavits, he had not seen any contemporaneous evidence.

Tr. at 346.

Doctor Zimmerman next discussed his initial evaluation of A.A. on February 13,

2002. See Pet. Ex. 6, p. 23. In his report he noted that “[s]he was fussy and showed

many features of autism; she didn’t engage or sustain eye contact; she had word

sounds . . . and would seek her parents’ attention at times[.]” Tr. at 304. She was

reluctant to engage in “ball-play” and demonstrated “mild instability in her truncal gait.”

Tr. at 305. He stated that her history and physical presentation—specifically, her “lack

of language [and] eye contact, and repetitive behaviors,” as well as her lack of

reciprocation—led him to conclude that she “had an autism spectrum disorder.” Tr. at

305.

Following his diagnosis, he ordered genetic and metabolic testing in an effort to

discover the cause of her condition. Tr. at 305. The genetic test results were normal;

however, several lab studies “showed . . . differences in her amino acids and liver

enzymes, such as AST [aspartate transaminase] and ALT [alanine transaminase] and

CK [creatine kinase].” Tr. at 306.

49

On cross examination, Dr. Zimmerman was asked to elaborate on his statement

in his initial evaluation that A.A. “presents an atypical history and appearance consistent

with an encephalopathy and a pervasive developmental disorder, autism spectrum.” Tr.

at 348 (citing Pet. Ex. 6, p. 24). In response to questioning, he clarified that what he

was “really saying” was that she had “atypical development.” Tr. at 348. He stated that

he was trying to express that “[r]egression is not typical development.” Tr. at 348. He

also found the “rapidity of her regression to be striking.” Tr. at 349. It was “somewhat

unusual" and not characteristic of those seen in the general autism spectrum disorder

population. Tr. at 349.

I questioned Dr. Zimmerman regarding the asserted rapidity of A.A.’s regression.

Specifically, I asked him to consider the time period between the October 14 (pre-

vaccination) video and the December 25 (post-vaccination) video, without regard to the

October 29 video, and state whether he would still consider the behavioral changes to

be rapid. Tr. at 353. He responded: “Three months would not be rapid, no.” Tr. at 353.

A.A. was next seen by Dr. Zimmerman on July 15, 2002. Doctor Zimmerman

reviewed the follow-up note he wrote after that visit. 75 He stated that he “wanted to get

further testing and recommended the organic acids” and other tests because he

suspected “that she might have mitochondrial problems.” Tr. at 306-07. The basis for

this belief was A.A.’s “apparently rapid deterioration following her MMR vaccine”—a

pattern he had seen in other children with mitochondrial problems. Tr. at 307. He

stated that he has “seen about 20 [children] over the years who have had this pattern

and . . . then show up with elevated CK, AST, and alanine.” Tr. at 307. He noted that

“most” of the cases “were in conjunction with Dr. Kelley,” but that he had “seen them

separately from consultation with him.” Tr. at 307. Doctor Zimmerman confirmed that

he ordered additional testing, including “lactic acid, serum chemistries, liver functions,

[and] CK – CPK [creatine phosphokinase].” Tr. at 308.

A neurology clinic follow-up note from A.A.’s next visit, on November 4, 2002,

reflected the results of her laboratory testing. 76 Doctor Zimmerman recounted that “her

lactate was slightly elevated, but CK was elevated, as was her AST.” Tr. at 309. With

regard to her elevated lactate, he explained that any struggling during the procedure

would likely have affected the results

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