1

In the United States Court of Federal Claims 

OFFICE OF SPECIAL MASTERS

No. 13-483V 

(To be published) 

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

 *

TANISIA CUNNINGHAM, *

legal guardian of G.C.F., * Filed: August 1, 2016 

 *

 Petitioner, * 

 * Vaccine Act Entitlement; Autism 

 v. * Spectrum Disorder; Autoimmunity 

 * 

SECRETARY OF HEALTH AND * 

HUMAN SERVICES * 

 * 

 Respondent. * 

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

Clifford Shoemaker, Vienna, VA, for Petitioner.

Voris Johnson, U.S. Department of Justice, Washington, DC, for Respondent.

DECISION

HASTINGS, Special Master.

This is an action in which the Petitioner, Tanisia Cunningham, seeks an award under the 

National Vaccine Injury Compensation Program (“Program”),1on account of her son G.C.F.’s 

developmental disorder, an autism spectrum disorder, which she asserts has been caused or 

aggravated by an MMR (measles, mumps, rubella) vaccination administered on July 2, 2012. 

For the reasons set forth below, I conclude that Petitioner is not entitled to an award.2

 

1 The applicable statutory provisions defining the Program are found at 42 U.S.C. § 300aa10 et seq. (2012 ed.). Hereinafter, for ease of citation, all "§" references will be to 42 U.S.C. 

(2012 ed.). The statutory provisions defining the Program are also sometimes referred to as the 

“Vaccine Act.” 

2 Although I have considered the entire record, including the voluminous medical records 

and medical literature, in arriving at my decision, I will only discuss evidence specifically 

relevant to resolution of this matter. See Paterek v. Sec’y of Health & Human Servs., 527 Fed. 

App’x 875, 884 (Fed. Cir. 2013). This includes medical literature submitted by both sides. 
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I 

THE APPLICABLE STATUTORY SCHEME 

 Under the National Vaccine Injury Compensation Program, compensation awards are 

made to individuals who have suffered injuries after receiving vaccines. In general, to gain an 

award, a petitioner must make a number of factual demonstrations, including showing that an 

individual received a vaccination covered by the statute; received it in the United States; suffered 

a serious, long-standing injury; and has received no previous award or settlement on account of 

the injury. Finally – and the key question in most cases under the Program – the petitioner must 

also establish a causal link between the vaccination and the injury. In some cases, the petitioner 

may simply demonstrate the occurrence of what has been called a “Table Injury.” That is, it may 

be shown that the vaccine recipient suffered an injury of the type enumerated in the “Vaccine 

Injury Table,” corresponding to the vaccination in question, within an applicable time period 

following the vaccination also specified in the Table. If so, the Table Injury is presumed to have 

been caused by the vaccination, and the petitioner is automatically entitled to compensation, 

unless it is affirmatively shown that the injury was caused by some factor other than the 

vaccination. § 300aa-13(a)(1)(A); § 300aa-11(c)(1)(C)(i); § 300aa-14(a); § 300aa-13(a)(1)(B). 

 In other cases, however, the vaccine recipient may have suffered an injury not of the type 

covered in the Vaccine Injury Table. In such instances, an alternative means exists to 

demonstrate entitlement to a Program award. That is, the petitioner may gain an award by 

showing that the recipient’s injury was “caused-in-fact” by the vaccination in question. § 300aa13(a)(1)(B); § 300aa-11(c)(1)(C)(ii). (“Causation-in-fact” is also known as “actual causation.”) 

In such a situation, the presumptions available under the Vaccine Injury Table are inoperative. 

The burden is on the petitioner to introduce evidence demonstrating that the vaccination initially 

caused, or significantly aggravated, the injury in question. Althen v. HHS, 418 F.3d 1274, 1278 

(Fed. Cir. 2005); Hines v. HHS, 940 F.2d 1518, 1525 (Fed. Cir. 1991). The showing of 

“causation-in-fact” must satisfy the “preponderance of the evidence” standard, the same standard 

ordinarily used in tort litigation. § 300aa-13(a)(1)(A); see also Althen, 418 F.3d at 1279; Hines, 

940 F.2d at 1525. Under that standard, the petitioner must show that it is “more probable than 

not” that the vaccination initially caused or aggravated the injury. Althen, 418 F.3d at 1279. The 

petitioner need not show that the vaccination was the sole cause or even the predominant cause 

of the injury or aggravation, but must demonstrate that the vaccination was at least a “substantial 

factor” in causing or aggravating the condition, and was a “but for” cause. Shyface v. HHS, 165 

F.3d 1344, 1352 (Fed. Cir. 1999). Thus, the petitioner must supply “proof of a logical sequence 

of cause and effect showing that the vaccination was the reason for the injury;” and the logical 

sequence must be supported by “reputable medical or scientific explanation, i.e., evidence in the 

form of scientific studies or expert medical testimony.” Althen, 418 F.3d at 1278; Grant v. HHS, 

956 F.2d 1144, 1148 (Fed. Cir. 1992). 

 The Althen court also provided additional discussion of the “causation-in-fact” standard, 

as follows: 

Concisely stated, Althen’s burden is to show by preponderant evidence that the 

vaccination brought about her injury by providing: (1) a medical theory causally 

connecting the vaccination and the injury; (2) a logical sequence of cause and 

effect showing that the vaccination was the reason for the injury; and (3) a 
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showing of proximate temporal relationship between vaccination and injury. If 

Althen satisfies this burden, she is “entitled to recover unless the [government] 

shows, also by a preponderance of the evidence, that the injury was in fact caused 

by factors unrelated to the vaccine.”

Althen, 418 F.3d at 1278 (citations omitted). The Althen court noted that a petitioner need not 

necessarily supply evidence from medical literature supporting petitioner’s causation contention, 

so long as the petitioner supplies the medical opinion of an expert. (Id. at 1279-80.) The court 

also indicated that, in finding causation, a Program fact-finder may rely upon “circumstantial 

evidence,” which the court found to be consistent with the “system created by Congress, in 

which close calls regarding causation are resolved in favor of injured claimants.” (Id. at 1280.) 

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

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

instruction for resolving causation-in-fact issues. In Capizzano v. HHS, 440 F.3d 1317, 1326 

(Fed. Cir. 2006), the court cautioned Program fact-finders against narrowly construing the 

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

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

in a particular case be sufficient to satisfy that second element of the Althen test. Both Pafford v. 

HHS, 451 F.3d 1352, 1355 (Fed. Cir. 2006), and Walther v. HHS, 485 F.3d 1146, 1150 (Fed. Cir. 

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

causes. DeBazan v. HHS, 539 F.3d 1347 (Fed. Cir. 2008), concerned an issue of what evidence 

the special master may consider in deciding the initial question of whether the petitioner has met 

her causation burden. The issue of the temporal relationship between vaccination and the onset 

of an alleged injury was further discussed in Locane v. HHS, 685 F.3d 1375 (Fed. Cir. 2012), and 

W.C. v. HHS, 704 F.3d 1352 (Fed. Cir. 2013). Moberly v. HHS, 592 F.3d 1315 (Fed. Cir. 2010), 

concluded that the “preponderance of the evidence” standard that applies to Vaccine Act cases is 

the same as the standard used in traditional tort cases, so that conclusive proof involving medical 

literature or epidemiology is not needed, but demonstration of causation must be more than 

“plausible” or “possible.” Both Andreu v. HHS, 569 F.3d 1367 (Fed. Cir. 2009), and Porter v. 

HHS, 663 F.3d 1242 (Fed. Cir. 2011), considered when a determination concerning an expert’s 

credibility may reasonably affect the outcome of a causation inquiry. Broekelschen v. HHS, 618 

F.3d 1339 (Fed. Cir. 2010), found that it was appropriate for a special master to determine the 

reliability of a diagnosis before analyzing the likelihood of vaccine causation. Lombardi v. HHS, 

656 F.3d 1343 (Fed. Cir. 2011), and Hibbard v. HHS, 698 F.3d 1355 (Fed. Cir. 2012), both again 

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

theory of causation. Doe 11 v. HHS, 601 F.3d 1349 (Fed. Cir. 2010) and Deribeaux v. HHS, 717 

F.3d 1363 (Fed. Cir. 2013), both discuss the burden of proof necessary to establish that a “factor 

unrelated” to a vaccine may have caused the alleged injury. 

 Another important aspect of the causation-in-fact case law under the Program concerns 

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

and other scientific evidence relating to causation issues. In Daubert v. Merrell Dow 

Pharmaceuticals, Inc., 509 U.S. 579 (1993), the Supreme Court listed certain factors that federal 

trial courts should utilize in evaluating proposed expert testimony concerning scientific issues. 

In Terran v. HHS, 195 F.3d 1302, 1316 (Fed. Cir. 1999), the Federal Circuit ruled that it is 
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appropriate for special masters to utilize Daubert’s factors as a framework for evaluating the 

reliability of causation-in-fact theories presented in Program cases. 

I also note that while the Petitioner’s primary contention throughout this case has been 

that the MMR vaccination of July 2012 initially caused the autism spectrum disorder of G.C.F., 

late in the case Petitioner’s expert very briefly raised the alternative contention that G.C.F.’s 

vaccination significantly aggravated a preexisting ASD, causing it to worsen. 

The elements of an off-Table significant aggravation case are set forth in Loving v. HHS, 

86 Fed. Cl. 135, 144 (2009). There, the court combined the test from Althen, above, which 

defines off-Table causation cases, with the test from Whitecotton v. HHS, 81 F.3d 1099, 1107 

(Fed. Cir. 1996), which concerns on-Table significant aggravation cases. The resultant test has 

six components, which are: 

(1) the person's condition prior to administration of the vaccine, (2) the person's 

current condition (or the condition following the vaccination if that is also 

pertinent), (3) whether the person's current condition constitutes a 'significant 

aggravation' of the person's condition prior to vaccination, (4) a medical theory 

causally connecting such a significantly worsened condition to the vaccination, 

(5) a logical sequence of cause and effect showing that the vaccination was the 

reason for the significant aggravation, and (6) a showing of a proximate temporal 

relationship between the vaccination and the significant aggravation. 

Loving, 86 Fed. Cl. at 144; see also W.C. v. HHS, 704 F.3d 1352, 1357 (Fed. Cir. 2013) (holding 

that “the Loving case provides the correct framework for evaluating off-table significant 

aggravation claims”).

II

BACKGROUND: THE OMNIBUS AUTISM PROCEEDING (“OAP”)

This case is one of more than 5,400 cases filed under the Program in which petitioners 

alleged that conditions known as “autism” or “autism spectrum disorders” (“ASD”)3 were caused 

 

3

“Autism Spectrum Disorder” is a general classification which as of 2010 included five 

different specific disorders: Autistic Disorder, Childhood Disintegrative Disorder, Asperger’s 

Syndrome, Rett Syndrome, and Pervasive Developmental Disorder Not Otherwise Specified 

(PDD-NOS). King v. HHS, No. 03-584V, 2009 WL 892296 at *5 (Fed. Cl. Spec. Mstr. Feb. 12, 

2010). The term “autism” is often utilized to encompass all of the types of disorders falling 

within the autism spectrum. (Id.) I recognize that since the OAP test cases, the consensus 

description of ASDs, contained now in the “DSM-V” as opposed to the prior “DSM-IV,” revises 

the prior subcategories of ASD set forth in the first sentence of this footnote. However, the 

DSM-V retains the same general description of ASDs. An ASD is a serious form of 

neurodevelopmental disorder defined by a collection of symptoms and behaviors, including 

significant impairment of social interaction and language skills, and the presence of repetitive, 
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by one or more vaccinations. A special proceeding known as the Omnibus Autism Proceeding 

(“OAP”) was developed to manage these cases within the Office of Special Masters (“OSM”). A 

detailed history of the controversy regarding vaccines and autism, along with a history of the 

development of the OAP, was set forth in the six entitlement decisions issued as “test cases” for 

two theories of causation litigated in the OAP (see cases cited below), and will only be 

summarized here. 

A group called the Petitioners’ Steering Committee (“PSC”) was formed in 2002 by the 

many attorneys who represented Vaccine Act petitioners who raised autism-related claims. 

About 180 attorneys participated in the PSC. Their responsibility was to develop any available 

evidence indicating that vaccines could contribute to causing autism, and eventually present that 

evidence in a series of “test cases,” exploring the issue of whether vaccines could cause autism, 

and, if so, in what circumstances. Ultimately, the PSC selected groups of attorneys to present 

evidence in two different sets of “test cases” during many weeks of trial in 2007 and 2008. In 

the six test cases, the PSC presented two separate theories concerning the causation of ASDs. 

The first theory alleged that the measles portion of the measles, mumps, rubella (“MMR”) 

vaccine could cause ASDs. That theory was presented in three separate Program test cases 

during several weeks of trial in 2007. The second theory alleged that the mercury contained in 

thimerosal-containing vaccines could directly affect an infant’s brain, thereby substantially 

contributing to the causation of ASD. That theory was presented in three additional test cases 

during several weeks of trial in 2008. 

Decisions in each of the three test cases pertaining to the PSC’s first theory rejected the 

petitioners’ causation theories. Cedillo v. 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. 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. HHS, No. 01-162V, 

2009 WL 332044 (Fed. Cl. Spec. Mstr. Feb. 12, 2009), aff’d, 88 Fed. Cl. 706 (2009).4 Decisions 

in each of the three “test cases” pertaining to the PSC’s second theory also rejected the 

petitioners’ causation theories, and the petitioners in each of those three cases chose not to 

appeal. Dwyer v. HHS, No. 03-1202V, 2010 WL 892250 (Fed. Cl. Spec. Mstr. Mar. 12, 2010); 

King v. HHS, No. 03-584V, 2010 WL 892296 (Fed. Cl. Spec. Mstr. Mar 12, 2010); Mead v. 

HHS, No. 03-215V, 2010 WL 892248 (Fed. Cl. Spec. Mstr. Mar. 12, 2010). 

The “test case” decisions were comprehensive, analyzing in detail all of the evidence 

presented on both sides. The three test case decisions concerning the PSC’s first theory 

(concerning the MMR vaccine) totaled more than 600 pages of detailed analysis, and were 

solidly affirmed in many more pages of analysis in three different rulings by three different 

judges of the United States Court of Federal Claims, and in two rulings by two separate panels of 

the United States Court of Appeals for the Federal Circuit. The three special master decisions 

 

stereotyped interests. E.g., Snyder v. HHS, No. 01-162V, 2009 WL 332044, at *31 (Fed. Cl. 

Spec. Mstr. Feb. 12, 2009). 

4

 The petitioners in Snyder did not appeal the decision of the U.S. Court of Federal Claims. 
6

concerning the PSC’s second theory (concerning vaccinations containing the preservative 

“thimerosal”) were similarly comprehensive.

 All told, the 11 lengthy written rulings by the special masters, the judges of the U.S. 

Court of Federal Claims, and the panels of the U.S. Court of Appeals for the Federal Circuit 

unanimously rejected the petitioners’ claims, finding no persuasive evidence that either the 

MMR vaccine or thimerosal-containing vaccines could contribute in any way to the causation of 

autism. 

Thus, the proceedings in the six “test cases” concluded in 2010. Thereafter, the Petitioners 

in this case, and the petitioners in other cases within the OAP, were instructed to decide how to 

proceed with their own claims. The vast majority of those autism petitioners elected either to 

withdraw their claims or, more commonly, to request that the special master file a decision denying 

their claim on the written record, resulting in a decision rejecting the petitioner’s claim for lack of 

support. However, a small minority of the autism petitioners have elected to continue to pursue 

their cases, seeking other causation theories and/or other expert witnesses. A few such cases have 

gone to trial before a special master, and in the cases of this type decided thus far, all have resulted 

in rejection of petitioners’ claims that vaccines played a role in causing their child’s autism. See, 

e.g., Henderson v. HHS, No. 09-616V, 2012 WL 5194060 (Fed. Cl. Spec. Mstr. Vowell Sept. 28, 

2012) (autism not caused by pneumococcal vaccination); Franklin v. HHS, No. 99-855V, 2013 

WL 3755954 (Fed. Cl. Spec. Mstr. Hastings May 16, 2013) (MMR and other vaccines found not 

to contribute to autism); Coombs v. HHS, No. 08-818V, 2014 WL 1677584 (Fed. Cl. Spec. Mstr. 

Hastings Apr. 8, 2014) (autism not caused by MMR or Varivax vaccines); Blake v. HHS, No. 03-

31V, 2014 WL 2769979 (Fed. Cl. Spec. Mstr. Vowell May 21, 2014) (autism not caused by MMR 

vaccination); Long v. HHS, No. 08-792V, 2015 WL 1011740 (Fed. Cl. Spec. Mstr. Hastings Feb. 

19, 2015) (autism not caused by influenza vaccine); Brook v. HHS, No. 04-405V, 2015 WL 

3799646 (Fed. Cl. Spec. Mstr. Hastings May 14, 2015) (autism not caused by MMR or Varivax 

vaccines); Holt v. HHS, No. 05-136V, 2015 WL 4381588 (Fed. Cl. Spec. Mstr. Vowell June 24, 

2015) (autism not caused by hepatitis B vaccine); Lehner v. HHS, No. 08-554V, 2015 WL 5443461 

(Fed. Cl. Spec. Mstr. Vowell July 22, 2015) (autism not caused by influenza vaccine); Miller v. 

HHS, No. 02-235V, 2015 WL 5456093 (Fed. Cl. Spec. Mstr. Vowell August 18, 2015) (ASD not 

caused by combination of vaccines); Allen v HHS, No. 02-1237V, 2015 WL 6160215 (Fed. Cl. 

Spec. Mstr. Vowell Sept. 26, 2015) (autism not caused by MMR vaccination); R.K. v. HHS, No. 

03-632V, 2015 WL 10936124 (Fed. Cl. Spec. Mstr. Vowell Sept. 28, 2015) (autism not caused by 

influenza vaccine), aff’d, 125 Fed. Cl. 57 (2016); Hardy v. HHS, No. 08-108V, 2015 WL 7732603 

(Fed. Cl. Spec. Mstr. Hastings Nov. 3, 2015) (autism not caused by several vaccines); Sturdivant 

v. HHS, No. 07-788V, 2016 WL 552529 (Fed. Cl. Spec. Mstr. Hastings Jan. 21, 2016) (autism not 

caused by Hib and Prevnar vaccines); R.V. v. HHS, No. 08-504V (Fed. Cl. Spec. Mstr. Corcoran 

Feb. 19, 2016) (autism not caused by influenza vaccine) (on Court website), aff’d, 2016 WL 

3647786 (Fed. Cl. June 2, 2016); Murphy v. HHS, No. 05-1063V, 2016 WL 3034047 (Fed. Cl. 

Spec. Mstr. Corcoran Apr. 25, 2016) (autism not caused by DTaP or MMR vaccines) (on review). 

In addition, some autism causation claims have been rejected without trial, at times over 

the petitioner’s objection, in light of the failure of the petitioner to file plausible proof of 

vaccine-causation. See, e.g., Waddell v. HHS, No. 10-316V, 2012 WL 4829291 (Fed. Cl. Spec. 

Mstr. Campbell-Smith Sept. 19, 2012) (autism not caused by MMR vaccination); Fester v. HHS, 
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No. 10-243V, 2016 WL 1745436 (Fed. Cl. Spec. Mstr. Dorsey April 7, 2016) (autism not caused 

by measles, mumps, rubella, and varicella (MMRV) vaccine); Fresco v. HHS, No. 06-469V, 

2013 WL 364723 (Fed. Cl. Spec. Mstr. Vowell Jan. 7, 2013) (autism not caused by multiple 

vaccines); Fesanco v. HHS, No. 02-1770, 2010 WL 4955721 (Fed. Cl. Spec. Mstr. Hastings 

Nov. 9, 2010) (autism not caused by multiple vaccines); Miller v. HHS, No. 06-753V, 2012 WL 

12507077 (Fed. Cl. Spec. Mstr. Hastings Sept. 25, 2012) (autism not caused by DTaP or MMR 

vaccines); Pietrucha v. HHS, No. 00-269V, 2014 WL 4538058 (Fed. Cl. Spec. Mstr. Hastings 

Aug. 22, 2014) (autism not caused by multiple vaccines); Bushnell v. HHS, No. 02-1648, 2015 

WL 4099824 (Fed. Cl. Spec. Mstr. Hastings June 12, 2015) (autism not caused by multiple 

vaccines); Bokmuller v. HHS, No. 08-573, 2015 WL 4467162 (Fed. Cl. Spec. Mstr. Hastings 

June 26, 2015) (autism not caused by multiple vaccines); Canuto v. HHS, No. 04-1128, 2015 WL 

9854939 (Fed. Cl. Spec. Mstr. Hastings Dec. 18, 2015) (autism not caused by DTP and DTaP 

vaccines); Valle v. HHS, No. 02-220V, 2016 WL 2604782 (Fed. Cl. Spec. Mstr. Hastings April 

13, 2016) (autism not caused by DTaP vaccine). Judges of this court have affirmed the practice 

of dismissal without trial in such cases. E.g., Fesanco v. HHS, 99 Fed. Cl. 28 (2011) (Judge 

Braden affirming); Canuto v. HHS, No. 04-1128V, 2016 WL 2586510 (Judge Yock affirming). 

 In none of the rulings since the test cases has a special master or judge found any merit in 

an allegation that any vaccine can contribute to causing autism.5

 

5

I am well aware, of course, that during the years since the “test cases” were decided, in 

two cases involving vaccinees suffering from ASDs, Vaccine Act compensation was granted. 

But in neither of those cases did the Respondent concede, nor did a special master find, that there 

was any “causation-in-fact” connection between a vaccination and the vaccinee’s ASD. Instead, 

in both cases it was conceded or found that the vaccinee displayed the symptoms of a Table 

Injury within the Table time frame after vaccination. (See Section I above). 

In Poling v. HHS, the presiding special master clarified that the family was compensated 

because the Respondent conceded that the Poling child had suffered a Table Injury--not because 

the Respondent or the special master had concluded that any vaccination had contributed to 

causing or aggravating the child’s ASD. See Poling v. HHS, No. 02-1466V, 2011 WL 678559, 

at *1 (Fed. Cir Spec. Mstr. Jan. 28, 2011) (a fees decision, but noting specifically that the case 

was compensated as a Table Injury). 

Second, in Wright v. HHS, No. 12-423, 2015 WL 6665600 (Fed. Cl. Spec. Mstr. Sept. 21, 

2015), Special Master Vowell concluded that a child, later diagnosed with ASD, suffered a 

“Table Injury” after a vaccination. However, she stressed that she was not finding that the 

vaccinee’s ASD in that case was “caused-in-fact” by the vaccination--to the contrary, she 

specifically found that the evidence in that case did not support a “causation-in-fact” claim, 

going so far as to remark that the petitioners’ “causation-in-fact” theory in that case was 

“absurd.” Wright v. HHS, No. 12-423, 2015 WL 6665600, at *2 (Fed. Cl. Spec. Mstr. Sept. 21, 

2015). 

The compensation of these two cases, thus does not afford any support to the notion that 

vaccinations can contribute to the causation of autism. In setting up the Vaccine Act 

compensation system, Congress forthrightly acknowledged that the Table Injury presumptions 
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III

PROCEDURAL HISTORY 

Petitioner filed a Petition for Vaccine Compensation on behalf of her son G.C.F. on July 

17, 2013, alleging that G.C.F. suffered a “brain injury” resulting from adverse reactions to one or 

more of many vaccinations administered between March 28, 2011, and July 2, 2012. (Petition 

(“Pet.”), ECF No. 1.) The case was initially assigned to Special Master Millman. (ECF No. 2.) 

On September 24, 2013, Petitioner filed G.C.F.’s medical records marked as Exhibits 1-

13. (ECF Nos. 7-8.) Following an initial status conference, the case was reassigned to me on 

September 25, 2013. (ECF No. 9.) Respondent filed her “Rule 4 report” on December 6, 2013. 

(ECF No. 13). Respondent argued that Petitioner failed to identify an injury or establish a 

sufficient causal medical theory. (ECF No. 13, p. 10.) Respondent further stressed the view that 

G.C.F.’s condition is explained by his autism diagnosis, with onset occurring within the first year 

of life and with no evidence in the record suggesting causation or aggravation by G.C.F’s 

vaccinations. (Id.) 

On July 15, 2014, Petitioner filed an expert medical report by Yuval Shafrir, M.D., 

accompanied by Dr. Shafrir’s curriculum vitae, marked as Exhibits 14 and 15 respectively. 

(ECF Nos. 21-2, 21-3.) In that report, Dr. Shafrir specified that MMR and Varivax (varicella) 

vaccinations administered to G.C.F. on July 2, 2012, caused his developmental disorder. (Ex. 

14, pp. 5-6 and 25 of 27.) Between July 15 and July 24, 2015, Petitioner additionally filed 

Exhibits 16-42, comprising medical literature referenced by Dr. Shafrir. (ECF Nos. 22, 24-26.) 

On December 10, 2014, Respondent filed an amended “Rule 4 report.” (ECF No. 32.) 

Respondent also filed an expert report by Max Wiznitzer, M.D., marked as Exhibit A, and a 

curriculum vitae marked as Exhibit B. (ECF No. 31.) 

On February 4, 2015, Petitioner filed additional medical literature marked as Exhibits 43-

46. (ECF No. 35.) 

Petitioner filed a supplemental expert report by Dr. Shafrir on August 19, 2015, marked 

as Exhibit 48.6(ECF No. 40.) Accompanying literature marked as Exhibits 49-68 was filed 

 

would result in compensation for some injuries that were not, in fact, truly vaccine-caused. H.R. 

Rept. No. 99-908, 18, 1986 U.S.C.C.A.N. 6344, 6359. (“The Committee recognizes that there is 

public debate over the incidence of illnesses that coincidentally occur within a short time of 

vaccination. The Committee further recognizes that the deeming of a vaccine-relatedness 

adopted here may provide compensation to some children whose illness is not, in fact, vaccinerelated.”)

6

 Initially, Petitioner filed Dr. Shafrir’s supplemental report on August 18, 2015, as Exhibit 

47. (ECF No. 39.) However, during the subsequent hearing in this case, Dr. Shafrir explained 

that the report marked as Exhibit 47 omitted a reference and that Exhibit 48 is a corrected 

version of that report. (Tr. 26.) Thus, this Decision will only address Dr. Shafrir’s second 

supplemental report marked as Exhibit 48, and the report marked as Exhibit 47 will not be 

further discussed. 
9

between August 27 and August 31, 2015. (ECF Nos. 43-46.) Updated medical records were 

also filed in August and September of 2015. (ECF Nos. 46, 50-51.) 

On September 4, 2015, Respondent filed as Exhibit C a supplemental expert report by Dr. 

Wiznitzer responsive to Dr. Shafrir’s second report, along with literature marked Exhibits D-F. 

(ECF No. 47.) 

On September 4, 2015, the parties also simultaneously filed Pre-Hearing Submissions. 

(ECF Nos. 48-49.) 

An evidentiary hearing was held at the National Courts Building in Washington, D.C., on 

September 18, 2015. (Transcript of Proceedings (“Tr.”), ECF No. 54.) Testimony by Ms. 

Cunningham, as well as by Drs. Shafrir and Wiznitzer, was heard. (Id.) 

Petitioner filed a Post-Hearing Brief on December 17, 2015, and Respondent filed a 

responsive Post-Hearing Brief on February 4, 2016. (ECF Nos. 57-58.) Petitioner filed a reply 

brief on March 7, 2016. (ECF No. 59.) 

IV

FACTS 

G.C.F. was born on March 26, 2011. (Ex. 10-1, p. 150.) He had a heart murmur. (Ex. 9, 

p. 14.) No medical intervention was planned, and a three-month follow-up echocardiogram was 

scheduled. (Ex. 9, p. 32.) He received his first hepatitis B vaccination on March 28, 2011. (Ex. 

3, p. 5.) 

No concerns were reported at G.C.F.’s well visits on April 11, and May 9, 2011. (Ex. 11, 

pp. 102-04 of 104.) He was seen for another well-child exam on June 17, 2011, at which he 

received several vaccinations. (Id., pp. 100-01.) Again, no significant concerns were reported. 

(Id.) 

There is no record that he was seen again by his pediatrician until January 6, 2012, at 

nine months of age. (Ex. 11, pp. 99-100.) At that time, his development was assessed, and no 

problems were reported. (Id.) During the appointment, G.C.F. again received several 

vaccinations. (Id.)

G.C.F. returned to his pediatrician on March 28, 2012, at twelve months of age. (Ex. 11, 

pp. 97-99 of 104.) His parents reported that he “rocks self to sleep on knees and elbows” and 

“bangs his head on side of crib.” (Id., p. 98.) Developmental notes for that visit note nothing else 

unusual. (Id.) Additional vaccinations were administered. (Id., pp. 98-99.) 

On April 3, 2012, G.C.F. was seen again, and his father reported concern regarding some 

of his child’s behavior, and that he was “concerned about autism.” (Ex. 11, p. 97.) Specifically, 

he reported that when G.C.F. was in his crib, he repeatedly bounced his head off the wall, and 

that when the parents stopped the behavior the child screamed, cried, and threw a tantrum. (Id.) 

G.C.F.’s father showed the physician a video of G.C.F. rocking and banging his head. (Id.) The 

parents also reported that the child did not seem to hurt himself when banging his head, that his 
10

sleep patterns were irregular, and that he did not sleep through the night. (Id.) The doctor’s 

notes indicate that G.C.F.’s general behavior was “developmentally appropriate.” (Id.) The notes 

also state that other than “[r]ecurrent head banging,” there were “[n]o other autistic symptoms.” 

(Id., emphasis added.) A developmental pediatric evaluation and a pediatric neurology 

consultation were recommended. (Id.) 

On Monday, July 2, 2012, G.C.F. returned to his physician for a fifteen-month well-child 

evaluation. (Ex. 11, pp. 96-97.) He was “still banging his head” on hard surfaces, and “holds his 

head in the middle of activities and starts crying.” (Id.) G.C.F.’s developmental progress was 

also noted. (Id.) G.C.F. was given his first MMR (measles, mumps, and rubella) and varicella 

vaccinations. (Id.) 

G.C.F. returned to the pediatrician four days later, on Friday, July 6, with a history of 

fever and continuous crying for two days. (Ex. 11, p. 95.) The next day, on July 7, 2012, G.C.F. 

was admitted to St. Barnabas Medical Center with a runny nose, cough, congestion, and fever. 

(Ex. 2, p. 1 of 19.) G.C.F. arrived in “severe respiratory distress,” with a temperature of 99.9 

degrees. (Ex. 2, p. 2.) His mother reported that he had developed a fever three days prior 

(“Wednesday”) that had subsided with ibuprofen. (Ex. 2, p. 4.) Upon examination, G.C.F. was 

alert. (Ex. 2, p. 5.) He was administered corticosteroids and epinephrine, and was discharged 

the next day on July 8, 2012, with a final diagnosis of “croup,” a type of viral infection. (Ex. 2, 

p. 1; Tr. 137-38.) 

G.C.F. next saw his pediatrician on July 24, 2012. (Ex. 11, p. 94.) G.C.F. had broken out 

in a rash “all over [his] body” that had appeared the day before. (Id.) His parents reported that 

he had “not been doing too well since administration of MMR and varicella about 3 weeks ago.” 

(Id.) G.C.F.’s repeated head-banging was again reported, as was an upcoming evaluation at 

Children’s Specialized Hospital (“CSH”). (Id.) The pediatrician felt that the rash was “probably 

related to a varicella vaccine adverse event.” (Id., p. 95.) 

On October 3, 2012, at eighteen months of age, G.C.F. was seen at CSH by Mary Van 

Horn, a nurse practitioner, for an initial neurodevelopmental evaluation. (Ex. 5, pp. 40-44 of 48.) 

The notes indicate that G.C.F.’s parents expressed concern about “developmental delays and the 

possibility of an autism diagnosis,” and that “they began having concerns [when G.C.F. was] 11 

months old.” (Id., p. 40.) G.C.F.’s parents reported a number of specific concerns, including 

head-banging, severe tantrums, that their son inconsistently responded to his name, lack of 

pointing, lack of gestures, using “Mama” and “Dada” only non-specifically, poor eye contact, 

lack of single words up to 16 months, and repetitive use of toys.7(Id., pp. 40-41.) G.C.F.’s 

parents were also noted as having reported a “regression” in language and social skills (id., p. 

41), while nurse Van Horn assessed that he was “speech-delayed” (id., p. 43). Ms. Van Horn 

concluded that G.C.F. was “a child who should be considered at risk for autism.” (Id., p. 43.) A 

follow-up was recommended with Dr. Malia Beckwith, a developmental pediatrician. (Id.) 

 

7 Petitioner’s expert contended that nurse Van Horn’s report contained “a lot of errors.” 

(Ex. 14, p. 10.) Significantly, however, the only error Dr. Shafrir specifically noted was that 

nurse Van Horn incorrectly recorded that G.C.F.’s mother had taken Aldactone for hypertension 

during pregnancy instead of Aldomet. (Id.) 
11

On October 20, 2012, G.C.F. received an initial evaluation by the New Jersey Early 

Intervention System. (Ex. 1, p. 35.) G.C.F. scored significantly below the mean in the 

“Personal/Social,” “Adaptive,” “Communication,” and “Cognitive” testing categories. (Ex. 1, p. 

38.) 

On October 23, 2012, G.C.F. was evaluated for speech therapy at Children's Specialized 

Hospital, by speech/language pathologists Kristen Martinez and Laura Watson. (Ex. 1, pp. 2-10

of 85.) He was seen for concerns related to expressive and receptive language delays. (Id., p. 2.) 

The “age of onset” is listed as “7-12 months.” (Id.) It was noted that G.C.F. had no history of 

developmental regression. (Id., p. 3.) Testing of G.C.F.’s expressive and receptive language 

skills showed that he was below the limits expected for his age in both categories, thereby 

confirming a diagnosis of expressive/receptive language disorder. (Id., pp. 5-6, 8.) 

On January 22, 2013, at twenty-one months of age, G.C.F. was seen by Dr. Beckwith, a 

developmental pediatrician. (Ex. 5, pp. 18-24 of 48.) Dr. Beckwith reviewed G.C.F.’s earlier 

visit with nurse Van Horn. (Id., p. 18.) G.C.F.’s mother reported to Dr. Beckwith that her son’s 

behaviors “continued to be very challenging,” that he had inconsistent eye contact, did “not often 

respond to his name,” had “limited” communication abilities, and engaged in “repetitive 

behavior.” (Id.) Based on G.C.F.’s history and his clinical evaluation, Dr. Beckwith noted that 

G.C.F. met the criteria for an “autistic disorder.” (Id., p. 22.) 

G.C.F. had another appointment with Dr. Beckwith on April 16, 2013. (Ex. 5, pp. 10-14 

of 48.) G.C.F.’s mother described G.C.F.’s behaviors since the previous visit to Dr. Beckwith. 

(Id., p. 10.) A neurologic review stated that "no regression or loss of skills has been noted." (Id., 

p. 11.) Dr. Beckwith’s diagnostic impression continued to be “autistic disorder,” along with 

mixed expressive receptive language disorder, sensory integration concerns, and significant 

feeding rigidity. (Id., pp. 12-13.) 

Since then, G.C.F., tragically, has continued to suffer from a severe neurodevelopmental 

disorder, characterized as an autism spectrum disorder. (E.g., Ex. 5, pp. 4-7; Tr. 17-22.) 

V 

SUMMARY OF THE EXPERT WITNESSES’ QUALIFICATIONS AND OPINIONS 

 In this case, Petitioner and Respondent each presented an expert report and testimony 

from a medical expert. At this point, I will briefly summarize both the qualifications and the 

opinions of these expert witnesses. 

A. Petitioner’s expert, Dr. Yuval Shafrir

1. Qualifications 

 Yuval Shafrir, M.D., attended the Sackler School of Medicine in Tel Aviv, Israel, 

graduating magna cum laude in 1982. (Ex. 15, p. 1.) After graduation, he spent more than two 

years in pediatric residencies before moving to the United States, where he continued as a 

pediatric resident at the North Shore University Hospital in New York from February 1986 to 
12

June 1988. (Id.) Dr. Shafrir then completed a pediatric neurology fellowship at Washington 

University in St. Louis from 1988 to 1991. (Id.) He continued the following year to complete a 

fellowship in pediatric neurophysiology and epileptology at Miami Children's Hospital. (Id.)

Dr. Shafrir was certified by the American Board of Pediatrics. (Ex. 15, p. 2.) He also 

received certification from the American Board of Psychiatry and Neurology, with a special 

qualification in Child Neurology. (Id.) In 1998, he was certified by The American Board of 

Clinical Neurophysiology. (Id.) He maintains a license to practice medicine in Maryland. (Id.) 

Currently, Dr. Shafrir works in private practice as a pediatric neurologist in Baltimore, 

MD. (Ex. 15, p. 3.) He has held several teaching positions since 1988, including assistant 

professor in neurology and pediatrics at the United Services University of the Health Sciences, F. 

Edward Herbert School of Medicine, a position which he has held for over 20 years. (Ex. 15, p. 

3.) Since 2004 he has also been an assistant professor in the Department of Pediatrics at the 

University of Maryland School of Medicine, in Baltimore, Maryland. (Id.) 

Dr. Shafrir has published twelve medical journal articles and ten abstracts. (Ex. 15, pp. 

3-6.) He has also presented numerous lectures in pediatric neurology, primarily on the subject of 

seizures. (Ex. 15, pp. 6-8.) Dr. Shafrir is not a member of any professional associations. (Tr. 

75.) 

2. Summary of Dr. Shafrir’s opinion

According to Dr. Shafrir, G.C.F. had not displayed any symptoms of autism prior to July 

2, 2012. (Ex. 14, p. 18 of 27; Tr. 33-34, 38.) Then, he contends, G.C.F. experienced a dramatic 

developmental regression between July 2 and his evaluation on October 3, 2012. (Tr. 76-77.) 

Significantly, this opinion is based, in part, on Dr. Shafrir’s rejection of G.C.F.’s head-banging 

behavior in early 2012 as a symptom of autism. (Ex. 14, p. 18.) 

Based on his understanding of G.C.F.’s medical history, Dr. Shafrir theorized that G.C.F. 

suffered an “encephalopathy” (brain injury), which caused his autistic symptoms. (Ex. 14, p. 

25.) Dr. Shafrir argued that this encephalopathy was likely caused by an autoimmune reaction to 

the MMR vaccination that G.C.F. received on July 2, 2012.8 (Id.) (An autoimmune reaction 

means that the MMR caused G.C.F.’s immune system to attack his own brain; the immune 

system components (“antibodies”) that carry out an autoimmune reaction are described as 

“autoantibodies.”) 

In support of his theory that G.C.F.’s condition is autoimmune, Dr. Shafrir pointed to an 

extensive rash that G.C.F. experienced about three weeks following his MMR and varicella 

immunizations on July 2.9 (Tr. 78-79.) Although Dr. Shafrir conceded that the rash itself is not 

 

8

In his expert report, Dr. Shafrir opined that the autoimmune reaction was to the 

“combined MMR and varicella” vaccinations. (Ex. 14, p. 25.) During the hearing, however, Dr. 

Shafrir stated instead that his theory is actually specific to the MMR vaccination. (Tr. 80.) He 

admitted that his earlier inclusion of the varicella vaccine as causal was an “error.” (Id.) 

9 Though Dr. Shafrir is clearly of the opinion that G.C.F.’s rash was vaccine-caused, he 

was inconsistent in his opinion regarding the precise cause of the rash. In his initial report, he 
13

evidence of autoimmunity, he opined that the severity of the rash provided evidence that G.C.F. 

had an abnormal immune system and was susceptible to autoimmunity. (Id.) 

While Dr. Shafrir admitted that the “exact mechanism [of causation] is very frequently 

impossible to prove,” his expert report cited theories such as, “molecular mimicry,” “bystander 

activation,” “epitope spreading,” and “polyclonal activation,” as possible mechanisms of how a 

vaccination might trigger an autoimmune disease. (Ex. 14, p. 21.) During the hearing, however, 

Dr. Shafrir discounted the possibility of “polyclonal activation” (Tr. 40), and never explained the 

“epitope spreading” and “bystander activation” mechanisms. He stated that the “probable”

mechanism was molecular mimicry. (Tr. 40.) 

Dr. Shafrir cited a number of medical articles which, he said, offered support to his 

theory that autoimmunity could play a role in autism, and/or that the MMR vaccine can cause an 

autoimmune reaction. (Ex. 14, pp. 22-24.) Dr. Shafrir further contended that his theory of 

causation of autism is supported by his idea that autism is an “epidemic,” and therefore its 

prevalence cannot be explained solely by genetics. (Tr. 29-33.) 

In his supplemental report, Dr. Shafrir sought to further bolster his opinion by 

analogizing to research indicating that a disorder known as “narcolepsy” can be caused by a type 

of influenza vaccine. (Ex. 48.) 

B. Respondent’s expert, Dr. Max Wiznitzer 

1. Qualifications 

Max Wiznitzer, M.D., received his B.S. degree in medical education in 1975, and a 

medical degree in 1977, both from Northwestern University. (Ex. B, p. 1.) He completed a 

residency in pediatrics in 1980, at the Children’s Hospital Medical Center in Cincinnati, Ohio. 

(Ex. B, p. 1.) He then completed a one-year fellowship at the Cincinnati Center for 

Developmental Disorders, a three-year fellowship in pediatric neurology at the Children’s 

Hospital of Philadelphia, and a two-year fellowship at the Albert Einstein College of Medicine in 

New York, studying higher cortical functions. (Ex. B, pp. 1-2.) 

Dr. Wiznitzer has received appointments to practice at several hospitals, including: the 

Department of Neurology of Montefiore Medical Center in New York; the Department of 

 

did not specify which of G.C.F.’s vaccinations he felt caused the rash, but indicated that the 

pediatrician felt it was the varicella. (Ex. 14, p. 19.) In his supplemental report, he clearly 

attributed the rash to the MMR vaccination, stating that “[t]he MMR immunization produced 

fever and rash indicating more significant system infection by the vaccine viruses, most likely 

the measles.” (Ex. 48, p. 1.) During the hearing, he confirmed that his opinion was that the rash 

was caused by the MMR vaccine, but then immediately, and inexplicably, seemed to endorse the 

pediatrician’s diagnosis of a varicella-caused rash. (Tr. 79.) 

For his part, Dr. Wiznitzer opined that the rash was unlikely to be caused by the MMR 

vaccine, because it was pruritic (itchy), which is more consistent with a varicella rash. (Tr. 98-

100.) 
14

Neurology at Bronx Municipal Hospital Center; and the Rainbow Babies and Children’s Hospital 

in Cleveland. (Ex. B, p. 2.) He has served as a consultant in pediatrics and neurology at several 

other hospitals as well. Dr. Wiznitzer has also maintained a continuous practice as an associate 

pediatrician and associate neurologist at University Hospitals of Cleveland since 1986. (Ex. B, 

p. 2.) 

At Rainbow Babies and Children’s Hospital in Cleveland, Dr. Wiznitzer served as CoDirector of the Rainbow Autism Center in 1991; as Chief of the Division of Pediatric Neurology 

from 1992 to 1995; and as the Director of the Rainbow Autism Center from 1992 through 2010. 

(Ex. B, p. 3.) He has taught pediatrics and neurology since 1986 at the Case Western Reserve 

University School of Medicine, and in 2013 he became Professor of Pediatrics at the school. 

(Ex. B, p. 2.) Although he no longer directs the autism center, he estimates that in his current 

practice at least 25% of his patients have been diagnosed with autism. (Tr. 85.) 

Dr. Wiznitzer is certified by the American Board of Pediatrics. (Ex. B, p. 5.) He also 

received certification from the American Board of Psychiatry and Neurology, with a special 

qualification in Child Neurology. (Id.) In 2004, the American Board of Psychiatry and 

Neurology certified his competence in Neurodevelopmental Disabilities. (Id.) He maintains 

licenses to practice medicine in Ohio, Pennsylvania, and New York. (Id.) 

Dr. Wiznitzer has been a reviewer of articles for many medical journals, most notably for 

Pediatric Neurology, Lancet Neurology, and the Journal of Child Neurology, and has also served 

on the editorial boards of those three journals. (Ex. B, p. 6.) He currently serves on a multitude 

of medical advisory groups at the local, state, and national levels. (Id., pp. 6-9.) Dr. Wiznitzer 

has published sixty-seven medical articles, eleven book chapters, and fifty-five abstracts. (Id., 

pp. 13-23.) He has also presented numerous lectures at the invitation of community 

organizations concerning childhood developmental disorders, primarily on the subject of autism. 

(Id., pp. 24-54.) He has been extensively engaged in autism-related research since 1986. (Tr. 

83-86.) He has participated in developing diagnostic tests for autism. (Tr. 86.) He currently is 

part of a committee of the American Academy of Neurology developing guidelines for autism 

management. (Id.) 

2. Summary of Dr. Wiznitzer’s opinion

Dr. Wiznitzer strongly disagreed with Dr. Shafrir’s causation theory. In Dr. Wiznitzer’s 

view, G.C.F. is properly diagnosed as a young boy with an autism spectrum disorder (Ex. A, p. 

7), who showed significant signs of that ASD prior to his vaccinations of July 2, 2012. (Id.) Dr. 

Wiznitzer also stated that the “[e]volution of [G.C.F.’s] ASD fits *** identified development 

trajectories” of autism. (Id.) Furthermore, he disagreed with Dr. Shafrir that G.C.F.’s medical 

record is either “suggestive of or consistent with [G.C.F. having] an underlying immune 

disorder.” (Id.) 

 Dr. Wiznitzer’s expert report and hearing testimony noted a number of specific citations 

from Dr. Shafrir’s references which he believes are contrary to Dr. Shafrir’s hypothesis. (Ex. A, 

pp. 7-9; Tr. 103-24.) Contrary to Dr. Shafrir, Dr. Wiznitzer does not believe that the role of 

immune dysfunction and autoimmunity in autism is well supported, nor does he believe that such 

a theory is supported by Dr. Shafrir’s references. (Ex. A, p. 8.) Furthermore, Dr. Wiznitzer 

noted that the studies which Dr. Shafrir referenced for the proposition that autoimmune 
15

encephalitis has been described as a cause of autism, included participants whose “clinical 

presentation” is “not applicable in the case of [G.C.F.],” and that G.C.F.’s clinical history is not 

consistent with an autoimmune encephalitis. (Id., pp. 8-9.) 

VI

SUMMARY OF MY OPINION 

 After careful consideration of the entire record of this case, I find that Petitioner and Dr. 

Shafrir have failed to demonstrate that it is “more probable than not” 10 that G.C.F.’s MMR 

vaccination of July 2, 2012, had any role in initially causing, or in aggravating, G.C.F.’s autism 

spectrum disorder, or his autistic symptoms. First, Dr. Shafrir based his opinion on an incorrect 

assumption concerning the onset of G.C.F.’s autistic symptoms. (See Section VII of this 

Decision, below.) Second, Respondent’s expert Dr. Wiznitzer is far more qualified to opine 

concerning the causation of autism, and was a much more persuasive witness in this case. 

(Section VIII.) Third, after a review of all the evidence, including medical articles, I find that 

Dr. Shafrir failed to demonstrate in general that the MMR vaccination can result in 

autoimmunity causing autism or autistic symptoms. (Section IX.) Fourth, even if it were 

assumed that the MMR vaccine is capable of causing autism or autistic symptoms via 

autoimmunity, there is no evidence of autoimmunity or abnormal immune system activity in 

G.C.F.’s own case. (Section X.) Next, Petitioner and Dr. Shafrir did not demonstrate any 

validity to their alternative “significant aggravation” argument in this case. (Section XI.) 

 And finally, in Section XII below, I will summarize why the Petitioner’s case fails the 

Althen criteria for showing that a vaccine “initially caused” an injury, as well as the 

Althen/Loving criteria for showing that a vaccine “significantly aggravated” an injury. 

VII

DR. SHAFRIR’S OPINION IS BASED ON THE INCORRECT ASSUMPTION THAT 

THE ONSET OF G.C.F.’S ASD SYMPTOMS OCCURRED AFTER THE 

VACCINATION IN QUESTION 

One basic deficiency in Dr. Shafrir’s causation opinion in this case is that he based his 

opinion on a false assumption regarding the onset of G.C.F.’s autism. Specifically, Dr. Shafrir 

opined that G.C.F. experienced the first symptoms of his ASD between July and October of 

2012, following his MMR vaccination on July 2, 2012. (Tr. 36; Ex. 14, p. 18.) Dr. Wiznitzer, 

however, contended that a careful review of the record indicates that G.C.F. had exhibited 

symptoms of his ASD well prior to July of 2012, including his head-banging in March of 2012. 

 

10 Petitioner has the burden of demonstrating the facts necessary for entitlement to an award 

by a “preponderance of the evidence.” § 300aa-12(a)(1)(A). Under that standard, the existence 

of a fact must be shown to be “more probable than its nonexistence.” In re Winship, 397 U.S. 

358, 371 (1970) (Harlan, J., concurring). 
16

(Tr. 87, 93-96; Ex. A, p. 7.) Dr. Wiznitzer opined that G.C.F. followed one of the typical 

patterns of ASD onset. (Ex. A, p. 7; Tr. 100-02.) For the reasons described below, I find Dr. 

Wiznitzer’s interpretation of the record concerning this issue to be more persuasive. 

A. Contrary to Dr. Shafrir’s contention, G.C.F.’s head-banging was a symptom of his ASD.

Dr. Shafrir did not dispute the fact, well documented in the medical records, that in 

March of 2012 G.C.F. began intentionally and repeatedly banging his head on hard surfaces. Dr. 

Shafrir, however, contended that G.C.F.’s head-banging was not a sign of autism. (Ex. 14, p. 18; 

Tr. 36-37, 76.) In that regard, Dr. Shafrir suggested that G.C.F.’s pediatrician did not view the 

head-banging as diagnostic of ASD. (Tr. 36-37.) Dr. Shafrir further cited a study which 

concluded that children who display head-banging at about age 1 typically have “no serious 

behavioral sequelae.”11 (Tr. 36-37; Ex. 16, p. 647.) Dr. Shafrir further stated, based on his own 

clinical practice, that the head-banging behavior in some children is likely in reaction to a 

headache or infantile migraine. (Ex. 14, p. 6.) 

Dr. Shafrir’s opinion regarding the head-banging is flawed. First, his insistence that 

G.C.F.’s pediatrician rejected the idea of his head-banging as a symptom of ASD is incorrect. It 

is true that the pediatrician, Dr. Dosunmu, noted at G.C.F.’s visit on April 3, 2012, that G.C.F. 

was “developmentally appropriate” and demonstrated “social skills appropriate for age.” (Ex. 

11, p. 97 of 104.) However, at the same time, she also referred G.C.F. for evaluation by a 

pediatric neurologist and a developmental pediatrician, specifically for the recurrent headbanging, noting that G.C.F. had “no other autistic symptoms” (emphasis added). (Id.) Thus, in 

sending G.C.F. to a specialist, and saying that he had no “other” symptoms of autism, G.C.F.’s 

pediatrician was clearly indicating a concern that the head-banging might be a symptom of 

autism. 

To be sure, Dr. Wiznitzer did not claim that based on the head-banging symptom alone, 

G.C.F. could have been diagnosed for certain with autism in March or April of 2012. Dr. 

Wiznitzer did not dispute the article submitted by Dr. Shafrir (Ex. 16) indicating that many 

children go through a head-banging stage with no permanent consequences. But he explained 

that in retrospect, knowing as we do that G.C.F. in fact began exhibiting other clear-cut 

symptoms of autism later in 2012, he can state that the head-banging was an early symptom of 

autism in G.C.F. (Tr. 96; see also Tr. 87, 94, 102.) In this regard, Dr. Wiznitzer pointed out that 

another scientific article, published in 2007, states that head-banging can be one of the 

stereotyped, repetitive behaviors that form a key part of autism. (See Ex. D, Johnson, et al., 

Identification and Evaluation of Children with Autism Spectrum Disorders, 120 Pediatrics 1183, 

at 1193-94.) Indeed, Dr. Shafrir himself characterized head-banging as “not infrequent” among 

the ASD population.12 (Ex. 14, p. 18.) In addition, as Dr. Wiznitzer pointed out (Tr. 96), when 

 

11 See Ex. 16, K. Abe, et al., Natural History and Predictive Significance of Head-Banging, 

Head-Rolling and Breath-Holding Spells, 26 Dev. Med. & Child Neurology 644 (1984). 

12 The Abe study cited by Dr. Shafrir was attempting to assess the “predictive value” of 

head-banging. (Ex. 16, p. 1183.) Thus, even accepting that study at face value, the study would 

not support the contention that head-banging is not a symptom associated with ASD, only that it 

is not predictive of ASD. Moreover, even if the Abe and Johnson studies were in conflict, I 

would still give greater weight to the Johnson study. I note that whereas the Johnson study was 
17

the developmental pediatrician Dr. Beckwith definitely diagnosed G.C.F. with an autism disorder 

on January 22, 2013, she specifically noted “repetitive motor mannerisms of head-banging” as 

one of his symptoms of autism. (Ex. 5, p. 23 of 48.) Similarly, nurse Van Horn on Oct. 3, 2012, 

listed head-banging as one of the symptoms supporting her conclusion that G.C.F. was “at risk” 

for autism. (Ex. 5, p. 43 of 48.) 

Dr. Wiznitzer also pointed out (Tr. 96) that G.C.F.’s head-banging in March of 2012 was 

“more than simple head-banging,” because when his parents tried to stop the behavior, he would 

scream, cry, and throw a tantrum (Ex. 11, p. 97 of 104), thus further indicating that G.C.F.’s 

head-banging in early 2012 was an early symptom of his autism. 

B. Other evidence of symptoms of autism in G.C.F. predating the July 2012 vaccinations 

 Dr. Wiznitzer also pointed out (Tr. 95) that in April of 2012 his pediatrician noted that

G.C.F. suffered from a sleep disturbance, including a failure to sleep through the night (Ex. 11, 

p. 97 of 104). Dr. Wiznitzer explained that 20 to 25 percent of autistic children under age 4 will 

have a similar sleep disturbance. (Tr. 95.) Thus, I credit Dr. Wiznitzer’s view that, again with 

the benefit of hindsight, the sleep disturbance in early 2012 was likely another early symptom of 

autism. 

Further, on October 3, 2012, when G.C.F.’s parents expressed concerns about his 

“developmental delays and the possibility of an autism diagnosis,” they specifically stated that 

“they began having concerns [when G.C.F. was] 11 months old.” (Ex. 5, p. 40 of 48.) Similarly, 

on October 23, 2012, G.C.F’s parents reported that the “age of onset” of his language delays was 

“7-12 months.” (Ex. 1, p. 2 of 85.) G.C.F. was 11 months old several months before the MMR 

vaccination that Dr. Shafrir implicates, which was administered on July 2, 2012, at around age 

15 months. Thus, these two reports are further significant indications that G.C.F. was exhibiting 

early symptoms of his ASD in the spring of 2012, well before the vaccination in question. And 

similarly, Dr. Wiznitzer opined that, based on his review of G.C.F.’s medical records, he 

perceived a “stagnation” or “difference” in G.C.F.’s language development, in the period when 

G.C.F. was between “seven and 12 months of age.” (Tr. 93.) 

C. Dr. Shafrir was mistaken in asserting that G.C.F.’s pediatrician in April 2012 wrote that 

G.C.F. did not have autism at that time. 

 Dr. Shafrir asserted on several occasions that G.C.F.’s pediatrician wrote in the child’s 

records in the spring of 2012 that G.C.F. specifically did not have symptoms of autism at that 

time. (E.g., Tr. 33-34, 36, 160; Ex. 14, p. 18 of 27.) Dr. Shafrir, however, was, deliberately or 

not, misconstruing the pediatric records. To be sure, as noted above, on April 3, 2012, the 

 

published in 2007, the Abe study was published in 1984 and was based on questionnaires 

completed between 1975 and 1982. (Ex. 16, p. 1184.) As Dr. Wiznitzer explained, diagnostic 

criteria for ASD have changed over the years and were much more rigid 30 years ago. (Tr. 139-

40.) Moreover, he noted that the public was less aware of the condition. (Id.) In that regard, I 

note that the Abe study offers no indication that children were specifically screened for ASD. 

(Ex. 16.) In contrast, the much more recent Johnson article was specifically intended to address 

the identification of children with ASD. (Ex. D.) 
18

pediatrician found G.C.F. to be “developmentally appropriate,” with “social skills appropriate.” 

(Ex. 11, p. 97 of 104.) However, at the same time, based specifically upon the head-banging 

symptom, she referred G.C.F. for evaluations by a pediatric neurologist and a developmental 

pediatrician, and noted only that G.C.F. at the time had “no other autistic symptoms” in addition 

to the head-banging. (Id.) The pediatrician’s full notation, therefore, clearly indicates that she 

was concerned that the head-banging might be a symptom of autism, and wanted that possibility 

evaluated by a specialist. Dr. Shafrir, therefore, was clearly wrong in asserting that the 

pediatrician’s notations concerning “appropriate” development on April 3, 2012, was a flat 

statement that G.C.F. was definitely not displaying any symptoms of autism at that time. 

D. Dr. Shafrir’s incorrect assumption regarding the onset of G.C.F.’s ASD is fatal to his 

causation opinion. 

 I find as a matter of fact, based on the evidence cited in Sections VII(A), (B), and (C) 

immediately above, that the first symptoms of G.C.F.’s autism occurred several months prior to 

his MMR vaccination of July 2, 2012. But throughout his expert reports and his hearing 

testimony, Dr. Shafrir consistently based his causation opinion in this case on the assumption 

that the onset of G.C.F’s autistic symptoms took place after his MMR vaccination on July 2, 

2012, between July 2 and his visit to the nurse practitioner on October 3, 2012.13 

Thus, Dr. Shafrir’s causation opinion is simply at odds with the record of this case, which 

shows that G.C.F.’s autism pre-dated the July 2012 vaccination implicated by Dr. Shafrir’s 

theory. Therefore, as a threshold matter, even before considering the details of Dr. Shafrir’s 

theory, I find his opinion utterly unpersuasive, because it is based upon a key misassumption of 

fact. Dobrydnev v. HHS, 566 Fed. Appx. 976, 982-83 (Fed. Cir. 2014) (holding that the special 

master was correct in noting that “when an expert assumes facts that are not supported by 

preponderance of the evidence, a finder of fact may properly reject the expert’s opinion”)(citing 

Brooke Group Ltd. v. Brown & Williamson Tobacco Corp., 509 U.S. 209, 242 (1993)). 

VIII 

DR. WIZNITZER WAS A MUCH MORE QUALIFIED AND PERSUASIVE WITNESS 

THAN DR. SHAFRIR IN THIS CASE 

Given that Dr. Shafrir’s causation theory in this case was based upon an incorrect 

assumption concerning the onset of G.C.F.’s symptoms of autism, I could end my discussion of 

this case with Section VII. However, in the interest of completeness, I will also point out, in 

Sections VIII, IX, X, and XI of this Decision, the other ways in which Dr. Shafrir’s theory was 

flawed, and in which Dr. Wiznitzer’s testimony was more persuasive. 

 

13 In one answer to a leading question by Petitioner’s counsel during the evidentiary 

hearing, Dr. Shafrir suggested that if the July 2 vaccination did not initially cause G.C.F.’s ASD, 

it could have “significantly aggravated” that ASD. (Tr. 38.) I will deal with that “significant 

aggravation” claim later in this Decision, in Section XI. 
19

A. Dr. Wiznitzer is much better qualified to opine concerning autism. 

 Both Dr. Shafrir and Dr. Wiznitzer are board-certified pediatric neurologists, which gives 

both at least a basic qualification to opine here, since autism is a neurological diagnosis. 

However, Dr. Wiznitzer is far better qualified to opine concerning autism, since he has devoted 

much of his career to specializing in autism. 

At Rainbow Babies and Children’s Hospital in Cleveland, Dr. Wiznitzer served as CoDirector of the Rainbow Autism Center in 1991, and as the Director of the Rainbow Autism 

Center from 1992 through 2010. (Ex. B, p. 3.) Although he no longer directs the autism center, 

he estimates in his current practice at least 25% of his patients have been diagnosed with autism. 

(Tr. 85.) Of Dr. Wiznitzer’s published medical articles, medical text chapters, and medical 

abstracts, many concern autism. (Ex. B, pp. 13-23.) He has presented numerous lectures at the 

invitation of community organizations concerning childhood developmental disorders, primarily 

on the subject of autism. (Ex. B, pp. 24-54.) He has been extensively engaged in autism-related 

research since 1986. (Tr. 83-86.) He has participated in developing diagnostic tests for autism. 

(Tr. 86.) He currently is part of a committee of the American Academy of Neurology that 

develops guidelines for autism management. (Id.) 

Dr. Shafrir’s curriculum vitae and testimony show no similar specialization in or 

extensive experience in the specific field of autism. Therefore, Dr. Wiznitzer’s qualifications to 

opine concerning the causation of autism are much superior.14

 

B. Dr. Wiznitzer was a much more persuasive witness in this case.

 In addition to being much better qualified, I found that Dr. Wiznitzer was a far more 

persuasive witness in this case as well. As for Dr. Shafrir, I simply did not find him to be a 

solid, thoughtful, or persuasive witness. As noted in multiple instances above and below, Dr. 

Shafrir often overstated the significance of the materials upon which he was relying. This was 

true of both his analysis of the medical literature he cited, as well as his analysis of G.C.F.’s own 

medical records. He sometimes contradicted himself or changed his testimony. In contrast, Dr. 

Wiznitzer was far more measured and credible as a witness. 

 As one glaring example, noted above, Dr. Shafrir repeatedly insisted that G.C.F.’s 

pediatrician in April 2012 found explicitly that G.C.F. did not have autistic symptoms at that 

time -- when in fact the actual record of the visit of April 3, 2012, tells a much different story, 

that the pediatrician found generally normal development but was concerned with the headbanging as a potential symptom of autism. (See discussion at Section VII(C) above.) 

 Another example is that Dr. Shafrir first pointed to a combination of the MMR and 

varicella vaccinations administered on July 2, 2012, as causing G.C.F.’s disorder (Ex. 14, p. 25), 

then at the hearing implicated only the MMR vaccination (Tr. 80). A further example was Dr. 

Shafrir’s inconsistent and confusing testimony as to whether it was the MMR or the varicella 

 

14 Similarly, in R.K. v. HHS, No. 03-632V, 2015 WL 10936124, at *57, 59 (Fed. Cl. Spec. 

Mstr. Sept. 28, 2015), Special Master Vowell concluded that Dr. Shafrir’s experience concerning 

autism was heavily outweighed by that of the Respondent’s expert. 
20

vaccination that caused G.C.F.’s rash some three weeks later. (See discussion at p. 12, fn. 9, 

above.) 

 Yet another example of this contrast between the experts was Dr. Shafrir’s criticism of 

Dr. Wiznitzer’s testimony regarding the limitations of CDC data of the prevalence of autism. 

Looking at the actual CDC reports cited by Dr. Shafrir, however, the very points raised by Dr. 

Wiznitzer were identified as significant limitations by the CDC itself. Thus, Dr. Shafrir seems to 

have been less than adequately familiar with his own source material. See discussion at Section 

IX(A) below.

 This is not the first time that Dr. Shafrir has been criticized for this very type of 

inconsistent and unsupported testimony. In particular, in recent cases in which he has testified 

for petitioners in cases involving vaccinees suffering from autism, Dr. Shafrir’s testimony has 

been repeatedly rejected and criticized. For example, in a case where Dr. Shafrir presented a 

theory similar to his presentation in this case, the special master concluded that “Dr. Shafrir’s 

opinions are wishful thinking premised on unverified and unsupported assumptions.” Lehner v. 

HHS, 08-554V, 2015 WL 5443461, at *45 (Fed. Cl. Spec. Mstr. Vowell July 22, 2015.) The 

special master added that Dr. Shafrir “was unable to explain coherently his theory of causation,” 

that his testimony was “vague” in nature, and that he simply “parroted key phrases, such as 

molecular mimicry,” without being able to explain them well. (Id.) 

 Similarly, in R.K. v. HHS, supra, the same special master observed that Dr. Shafrir’s 

testimony, again involving a similar causation theory in an autism case, involved “harangues” 

(id. at *68) and “attacks *** leveled without apparent support” (id. at *97). She noted that Dr. 

Shafrir was “fervent but without any support.” (Id. at *106.) She summarized that the “theories 

espoused by Dr. Shafrir are unreliable.” (Id. at *110.) Based on my impression of Dr. Shafrir’s 

performance in this case, I am compelled to concur with Special Master Vowell’s comments. 

See also R.V. v. HHS, 08-504V (Fed. Cl. Spec. Mstr. Corcoran Feb. 19, 2016) (rejecting Dr. 

Shafrir’s theory that the vaccinee’s autism resulted from an encephalopathy caused by an 

autoimmune reaction to a vaccination); Wright v. HHS, No. 12-423V, 2015 WL 6665600, at *2 

(Fed. Cl. Spec. Mstr. Sept. 21, 2015) (special master found Dr. Shafrir’s theory of causation in 

an autism case to be “absurd”). 

It is also noteworthy that despite advancing a theory steeped in immunology, Dr. Shafrir 

is not himself an immunologist. To the extent he claimed expertise in neuroimmunology, that 

assertion is not supported by his curriculum vitae. (Tr. 25-26; Ex. 15.) This fact makes Dr. 

Shafrir’s overstatements all the more unpersuasive, because he does not have any established 

clinical or research background to support statements that are not fully confined to the medical 

literature he cited. Although Dr. Wiznitzer likewise lacks any background in immunology, the 

initial burden of proof rests with Petitioner, and the unsupported assertions were Dr. Shafrir’s. 

Dr. Wiznitzer’s testimony more closely adhered to the conclusions of the medical literature cited. 

For all of these reasons, I conclude that Dr. Wiznitzer was a more credible and more 

persuasive witness in this case. See, e.g., Hennessey v. HHS, No. 01-190V, 2009 WL 1709053, 

*42 (Fed. Cl. Spec. Mstr. May 29, 2009) (“When experts disagree, many factors influence a factfinder to accept some testimony and reject other contrary testimony. Objective factors, including 

the qualifications, training, and experience of the expert witnesses and the extent to which their 

proffered opinions are supported by reliable medical research, other testimony, and the factual 
21

basis for their opinions, are all significant in determining what testimony to credit and what to 

reject.”).) 

IX 

DR. SHAFRIR FAILED TO DEMONSTRATE IN GENERAL THAT THE MMR 

VACCINATION CAN RESULT IN AUTOIMMUNITY CAUSING AUTISM OR 

AUTISTIC SYMPTOMS 

 Dr. Shafrir attempted to demonstrate in general that the MMR vaccination can cause a 

chronic autoimmune attack on the brain, resulting in autistic symptoms. This general 

proposition, however, turned out to be poorly supported, quite speculative, and not persuasive. 

A. Dr. Shafrir’s theory derives in part from an unsupported assumption that autism is an 

“epidemic.”

 

Dr. Shafrir’s theory is predicated in part upon his unsupported insistence that autism is 

best understood as an “epidemic.” Both experts in this case agreed that autism is a disorder or 

syndrome rather than a specific disease with a specific cause, and that the causation of autism is 

not fully understood. (Tr. 28, 134.) Both experts also agreed that at least some ASD cases are 

explained by known genetic defects. (Tr. 29-30, 131.) Where the two experts disagreed, 

however, is in the relative prevalence of genetically-based autism. Whereas Dr. Wiznitzer 

opined that the vast majority of ASD cases will ultimately be explained genetically (Tr. 131), Dr. 

Shafrir suggested that most cases of ASD are part of a large autism “epidemic,” ruling out 

genetics as a sole cause (Tr. 30-33). That difference of opinion is foundational to Dr. Shafrir’s 

theory; he stressed that, although his purported explanation is just one minor cause of ASD 

among many (Tr. 56), his theory is supported by the fact that, as an epidemic, autism must 

necessarily have an environmental trigger in many cases (Tr. 30-33, 46, 56, 158). 

As far as the record of this case goes, Dr. Shafrir’s contention that autism represents an 

epidemic is based on two sources of information, CDC (Centers for Disease Control) statistics 

and his own personal observations. (Tr. 30-33, 153-57.) Petitioner has submitted into evidence 

in this case CDC statistics on the increasing prevalence of autism diagnoses from 2000-2010. 

(See Exs. 60, 63-68.) Dr. Shafir indicated that the CDC data “succinctly describes the autism 

epidemic,” and that he submitted that material “to counteract any possible claim that what 

[G.C.F.] suffered [was] ‘genetic.’” (Ex. 48, p. 3.) He also stressed that his own professional 

experience is consistent with a steady rise in autism diagnoses. (Tr. 157.) 

Dr. Wiznitzer, however, argued that the rise in ASD diagnoses reported by the CDC is 

not necessarily explained as an actual rise in the incidence of autism. (Tr. 138-42.) He noted 

that there are a number of factors that may contribute to the increasing number of diagnosed 

cases. Specifically, he noted that there is still disagreement over when to use the ASD label. 

(Tr. 141-42.) He also suggested that both diagnostic criteria and public awareness have changed 

over the years, leading to identification and inclusion of less obvious or less severe cases. (Tr. 

138-40.) In this regard, Dr. Wiznitzer stressed that the CDC statistics show an increasing IQ 

level, suggesting that the population being identified has not remained consistent. (Id.) Finally, 
22

he also noted that risk factors for autism, such as the age of the parents, has changed over time. 

(Tr. 140-41.) 

I find Dr. Wiznitzer’s explanation to be sound. More significantly, however, Dr. 

Shafrir’s position is fatally undercut by his own citations. The CDC reports that petitioner filed 

in this case explicitly caution against drawing exactly the conclusion that Dr. Shafrir has 

suggested. For example, the Community Report From the Autism and Developmental 

Disabilities Monitoring (ADDM) Network, filed by Petitioner as Exhibit 61, states that “for such 

complex conditions like ASDs, no single factor can explain why more children are being 

identified with ASDs. Some of the increase likely has been due to changes in the diagnosis and 

treatment of ASDs, some to greater awareness, and some to better record keeping, although 

exactly how much is due to these factors is unknown.” (Ex. 61, p. 43.) Likewise, the yearly data 

reports themselves stress the same limitation for the interpretation of the data. For example, the 

surveillance summary for 2008 states that “[t]hese data confirm that the estimated prevalence of 

ASDs identified in the ADDM network surveillance populations continues to increase. The 

extent to which these increases reflect better case ascertainment as a result of increases in 

awareness and access to services or true increases in prevalence of ASD symptoms is not 

known.” (Ex. 68, pp. 3-4.) Thus, Dr. Wiznitzer’s testimony better reflects the actual content of 

the CDC materials than does Dr. Shafrir’s.15

Nor, for that matter, even if an epidemic increase in autism was established, would that 

necessarily point to the type of trigger Dr. Shafrir posited in this case. Dr. Wiznitzer opined that 

to the extent that ASD is not explained by genetics alone, it would involve pre-natal factors. (Tr. 

130-31, 142-44.) For his part, Dr. Shafrir testified that the environmental factor he cites as 

necessary to the epidemic would be something “affecting either the mother or the child,” 

suggesting that Dr. Shafrir at least contemplates the possibility that the cause of the epidemic he 

posits could be prenatal factors, and not necessarily tied to post-natal environmental factors. (Tr. 

46-47.) Thus, despite Dr. Shafrir’s repeated emphasis, the concept of an autism “epidemic,”

even if credited, would still be of minimal value in resolving this case. 

In short, although serious questions obviously remain, there is simply not preponderant 

evidence in this case that the undisputed rise in identified cases of autism is equivalent to a true 

increase in the prevalence of autism. And even if there has been some increase, the extent and 

cause of that increase remain unclear. Dr. Shafrir’s eagerness to call it an “epidemic,” and to 

 

15 For a further discussion of the issue of the increases in diagnoses of autism in recent 

years, see Snyder v. HHS, No. 01-162V, 2009 WL 332044 (Fed. Cl. Spec. Mstr. Feb. 12, 2009), 

at *34-35. There, Special Master Vowell discussed the very extensive evidence concerning that 

issue brought forth in the autism “test cases” cited at Section II of this Decision above. She 

found that at least part of the increase in diagnoses is explained (as Dr. Wiznitzer testified in this 

case) by changes in autism definitions, and in better awareness and better ascertainment of 

autism. (Id.) She concluded that it is unclear whether other factors are also in part causative of 

the increase in diagnoses, but found that overall, the evidence concerning the increase in autism 

diagnoses did not support the idea that vaccines are causing any part of the increase. (Id. at *35.) 
23

draw causal inferences from that label, is speculative and premature at best.16

 Moreover, even if 

I were to accept Dr. Shafrir’s testimony regarding epidemic autism at face value, it still would 

not have the significance to the specific theory that he claims. 

B. Dr. Shafrir has not persuasively linked autism to autoimmunity. 

Regardless of whether there is an autism epidemic, Dr. Shafrir’s theory of autoimmune 

encephalopathy leading to autism would still be quite speculative. Dr. Shafrir relied upon studies 

which, when closely examined, do not offer strong support to his general theory. Dr. Shafrir’s 

interpretation of the studies that he referenced is questionable at best. 

Dr. Wiznitzer, on the other hand, disputed that any of these studies supported Dr. 

Shafrir’s causation theory, and opined that there is not sufficient reason to conclude that autistic 

symptoms can be caused by chronic autoimmunity. (Tr. 103-124.) For the reasons discussed 

below, I agree. 

1. Dr. Shafrir’s own statements admit, in essence, that his autoimmunity theory 

amounts to mere speculation. 

At multiple times, Dr. Shafrir candidly acknowledged the limitations of the state of 

scientific knowledge regarding autoimmunity and its alleged potential role in autism. He stated 

that “autoimmune is a very important new concept in neurology” (Ex. 48, p. 3), but conceded 

that the articles he cited do not prove that autism is an autoimmune disease (Tr. 67-68), and that 

“we don’t talk about proof” when it comes to autoimmune disease (Tr. 61). Indeed, he 

characterized important aspects of his own theory as unprovable “assumptions.” (Tr. 39.) He 

testified that “unfortunately, the field of autoimmune encephalopathy is in its very beginning, 

and we don’t know to what extent those patients may have autoimmune encephalitis or 

autoimmune – or autoantibodies against the brain. I think it’s something that we’ll wait for a lot 

of research***.” (Tr. 46-47.) He acknowledged that Dr. Wiznitzer was correct in saying that one 

of Dr. Shafrir’s cited articles “doesn’t prove anything.” (Tr. 67.) 

After viewing his entire presentation, I conclude that, as Dr. Shafrir himself seemed to 

acknowledge, his entire general theory concerning a role for autoimmunity in autism amounts to 

mere speculation. 

 

16 To the extent Dr. Shafrir has urged such speculation as an underlying rationale for 

accepting his theory, his opinion is diminished in my view. That is, in offering an unqualified 

opinion that an autism “epidemic” exists, particularly in light of the limitations expressed in his 

own source material, Dr. Shafrir has again shown his propensity for overstatement. Thus, his 

general credibility is also diminished. 
24

2. The articles upon which Dr. Shafrir relied do not provide strong support for his 

theory. 

a. Studies which, Dr. Shafrir asserted, show that autoimmunity and immune 

dysfunction are “established” as causing autism

Dr. Shafrir first cited a number of studies for the proposition that autoimmunity and 

immune dysfunction play a role in causing autism, contending that such a role is “wellestablished.” (Ex. 14, p. 22.) Dr. Wiznitzer, however, disputed that Dr. Shafrir’s references 

supported his claim that autoimmunity in autism is well-established, or even likely. (Ex. A, p. 8; 

Tr. 104-24.) Dr. Wiznitzer explained that most of Dr. Shafrir’s cited articles involve various 

autoimmune conditions that are quite distinct from autism. (Ex. A, pp. 8-9; Tr. 105-12.) Based 

upon my own review of these studies, I agree with Dr. Wiznitzer. 

For example, the Gesundheit paper is a review article cited among Dr. Shafrir’s sources,

evaluating prior studies “associating ASD with the immune system.” (Ex. 26, p. 1.) Contrary to 

Dr. Shafrir’s assertion, the authors ultimately concluded that “none of these studies sufficiently 

explain whether the immune system underlies the pathology of ASD in a causative way, whether 

immune interferences create vulnerability to other pathogens responsible for ASD, or whether a 

third, yet unknown factor is responsible for both the pathology of ASD and for the aberrant 

immune response in ASD.” (Ex. 26, p. 6.) 

Similarly, with regard to Dr. Shafrir’s particular contention that autistic children show 

higher levels of autoantibodies against neuronal cells, the Mazur-Kolecka article concluded that 

although “[r]ecent developments indicate a possible pathogenic role of autoantibodies in CNS 

[central nervous system] disorders,” “[i]n autism, the potential role of autoantibodies *** is 

unknown.” (Ex. 30, p. 7, emphasis added.) Dr. Wiznitzer further stressed that although the 

Mazur-Kolecka study found autoantibodies among a higher percentage of children with ASD 

than without, the study nonetheless found autoantibodies in both populations, leaving the 

significance of the autoantibodies unclear. (Ex. A, p. 8.) 

Moreover, an additional study cited by Dr. Shafrir (Ashwood and Van de Water) also 

cautioned that “the pathophysiological significance of these antibodies reported in children with 

autism is uncertain.” (Ex. 29, p. 559.) The authors further cautioned that “the presence of 

autoantibodies in the serum of these patients may be a secondary phenomenon.” (Ex. 29, p. 560.)

In other words, as Dr. Wiznitzer testified, the authors in a number of the articles on which 

Dr. Shafrir relied acknowledged themselves that their results were merely speculative, not 

probative, concerning a causal role for autoimmunity in autism. (Tr. 104.) Others of these 

authors acknowledged that there is “no scientific evidence that vaccinations can be directly 

associated with the development of autoimmune diseases.” (Id.) 

b. Studies regarding immunosuppressive therapy in ASD 

Dr. Shafrir also cited studies purporting to show that immunosuppressive therapy can 

reverse the course of autism. (Ex. 14, p. 22; Tr. 68-69.) During the hearing, however, Dr. 

Shafrir himself noted the limited value of these immunosuppressive therapy studies, 
25

acknowledging that they were not controlled and suggesting other unspecified issues with the 

studies. (Tr. 69.) In any event, these studies are wholly tentative in their conclusions. 

For example, the Golla article explicitly states that the efficacy of treating autism with 

steroids has not been established. (Ex. 35, p. 2.) The Duffy paper states that “[t]he current study 

does not suggest that steroids ‘cure’ regressive autism nor does it claim proof of the value of 

pharmacological treatment of regressive autism.” (Ex. 34, p. 17 (emphasis in original).) The 

Chez article, a review article of prior studies on the subject, concludes by noting significant 

shortcomings among prior studies and stating that further studies are “desperately needed.” (Ex. 

33, p. 7.) 

c. Articles reporting on anti-VGKC antibodies and anti-NMDAR antibodies as 

causes of autoimmune encephalitis. 

Dr. Shafrir also cited several studies (Exs. 36-40) involving anti-VGKC17 antibodies and 

anti-NMDAR18 antibodies, as alleged evidence that autoimmune encephalitis has been described 

as a cause of autism. (Ex. 14, p. 22.) Dr. Wiznitzer did not dispute the diagnosis of autoimmune 

encephalitis among the subjects of those studies, but contended that the clinical picture of those 

subjects is different from the usual clinical picture of autism (Tr. 107-10), and not comparable to 

G.C.F.’s clinical history. (Ex. A, pp. 8-9.) He testified that the autoimmune encephalitis profile 

described in those studies “is not the autistic spectrum disorder that is described in this case.” 

(Tr. 110.) 

Dr. Shafrir sought to counter Dr. Wiznitzer’s observation by contrasting the brief case 

descriptions contained in the encephalitis articles against the many pages of G.C.F.’s medical 

records in evidence. (Tr. 70.) Dr. Shafrir contended that the fact that G.C.F. exhibited 

symptoms of autism in addition to those described in the studies should not be viewed as 

significant. (Id.) Dr. Wiznitzer’s observation, however, is not so easily dismissed. Dr. 

Wiznitzer did not merely observe that G.C.F. had additional ASD symptoms relative to the study 

subjects, he opined that the usual clinical picture of autism, as well as G.C.F.’s own clinical 

history, is clearly distinct from those known to be experiencing encephalitis. (Ex. A, pp. 8-9; Tr. 

110.) 

Significantly, in addition to opining that G.C.F. exhibited significant ASD symptoms 

such as restricted interests and repetitive behaviors not seen among the encephalitis study 

subjects, Dr. Wiznitzer also identified the presence of additional symptoms of encephalitis 

among the study subjects, symptoms which are not found in G.C.F.’s history. (Ex. A, pp. 8-9.) 

Specifically, he noted that these studies found the subject children to have experienced loss of 

established language progressing to mutism, movement disorders, swallowing problems, and 

seizure disorders, none of which G.C.F. exhibited. (Ex. A, p. 8.) 

 

17 “VGKC” stands for voltage-gated potassium channel. (See, e.g., Ex. 36, p. 1.) 

18 “NMDAR” stands for N-methyl-d-aspartate receptor.” (See, e.g., Ex. 37, p. 2.) 
26

Moreover, Dr. Wiznitzer persuasively testified that G.C.F.’s additional ASD symptoms 

are also significantly different from symptoms of NMDAR encephalitis. At the hearing, Dr. 

Wiznitzer stressed that patients with NMDAR encephalitis experience neurobehavioral or 

neuropsychiatric problems such as seizure, catatonia, withdrawn behavior, and mutism. (Tr. 

105-06.) He explained that while some of these behaviors can be mistaken for signs of autism at 

a superficial level in young children, the difference between autistic behaviors and encephalitis is 

distinct among teens and adults. (Id.) In that regard, Dr. Wiznitzer opined that G.C.F.’s 

additional ASD behaviors such as repetitive movements and restricted interests represent an 

additional diagnostic prong under the standard criteria for autism diagnosis that is not present 

among those experiencing encephalitis. (Tr. 106-07.) Contrary to Dr. Shafrir’s suggestion that 

the absence of those symptoms among the encephalitis study subjects is simply an issue of 

brevity, Dr. Wiznitzer opined that those symptoms are highly relevant to distinguishing between 

encephalitis and autism. (Tr. 107.) 

Additionally, Dr. Wiznitzer further noted that the NMDAR encephalitis study subjects 

demonstrated no improvement absent immunotherapy. (Ex. A, p. 8.) Unlike those with 

autoimmune encephalitis, however, G.C.F. did improve over time without immunotherapy, 

which is consistent with the expected prognosis for ASD, which Dr. Wiznitzer described as a 

course of variable improvement. (Ex. A, p. 8; Tr. 149-50.) 

Significantly, Dr. Shafrir did not himself attempt to explain how a typical autism clinical 

picture, or G.C.F.’s own clinical history, could be viewed as conforming to an NMDAR 

encephalitis or VGKC encephalitis diagnosis, leaving Dr. Wiznitzer’s opinion virtually 

unchallenged. The fact that these studies suggest that certain presentations of these types of 

encephalitis may include some symptoms potentially consistent with ASD is of small import,

when the typical autism course and G.C.F.’s own clinical course remain distinct from such 

encephalitis, and there is no evidence to suggest that G.C.F. ever experienced encephalitis. 

For all these reasons, I found that the literature concerning the autoimmune encephalitis 

cases did not provide strong support for Dr. Shafrir’s theory that autism can be the result of 

autoimmunity. 

d. The Kayser/Dalmau and Obregon articles 

In further support of his autoimmunity theory, Dr. Shafrir cited studies by Kayser and 

Dalmau, and by Obregon, et al. (Ex. 14, pp. 23-24; Exs 40-41.) According to Dr. Shafrir, these 

studies show a connection between autoimmune encephalitis and autism, because they show 

antibodies targeting a brain protein known as “Caspr2.” (Ex. 14, pp. 23-24.) The 

Kayser/Dalmau article, however, posits a link between autoimmunity and some forms of 

neuropsychiatric disease, but does not say that autism can be the result of autoimmunity. (Ex. 

40.) And Dr. Dalmau himself testified for the Respondent in another Program case in which Dr. 

Shafrir presented a similar causation theory, and opined that “based on his own experience in 

investigating and researching autoimmune encephalitis, vaccination does not play any role in its 

development.” (Lehner v. HHS, 2015 WL 5443461 at *48.) 

Dr. Shafrir put particular stress on the Obregon article, which he cited for the proposition 

that the MMR vaccine could cause antibodies to attack the Caspr2 protein, thereby causing injury 
27

to the brain. (Tr. 38-40; Ex. 41, p. 24.) Specifically, Dr. Shafrir contended that the Obregon 

study demonstrated “homology”

19 between certain proteins in the measles, mumps, and rubella 

viruses, and amino acid sequences in the Caspr2 protein. (Ex. 14, p. 24.) According to Dr. 

Shafrir, such homology makes the Caspr2 protein a likely candidate for “molecular mimicry,” in 

which, Dr. Shafrir suggested, antibodies created by the immune system to attack the MMR 

viruses instead attack the Caspr2 protein in the brain. (Id.) Dr. Shafrir further stressed that the 

Caspr2 protein has itself been associated with autism. 20 (Tr. 39-40; Ex. 14, p. 24.) (The Caspr2 

protein is also known as the CNTNAP-2 protein.) (Ex. 41, p. 2 of 17.) 

Dr. Wiznitzer, however, raised a number of criticisms of the Obregon study, which Dr. 

Shafrir left completely unrebutted. (Tr. 113-21.) First, Dr. Wiznitzer questioned the purported 

finding of homology. According to Dr. Wiznitzer, the Obregon study looked at a “very small” 

sequence of amino acid and added to that sequence in order to match the sequence in the 

vaccine. (Tr. 114-15.) This means that the vaccine and the Caspr2 protein are not homologic,

and therefore leaves the study resting on an unsupported assumption. (Tr. 115.) Moreover, Dr. 

Wiznitzer contended that homology by itself would still not be sufficient to prove that molecular 

mimicry is occurring.21 (Tr. 123-24.) Next, Dr. Wiznitzer challenged the study’s finding that the 

Caspr2 protein is associated with autism. (Tr. 115-16.) Dr. Wiznitzer noted that the study 

population, with 18 controls and 26 autistic subjects, was very small. (Tr. 116.) He also noted 

that the two groups were mismatched in age and sex ratio. (Id.) Importantly, the study authors 

themselves acknowledge these very limitations and characterized them as “significant.” (Ex. 41, 

p. 13.) Dr. Wiznitzer pointed out additional problems with the Obregon article, and summarized 

that “the Obregon paper is of no value in this hearing at all. *** There are too many flaws in it, 

too many mistakes in it for it to have any practical utility.” (Tr. 121.) 

Although Dr. Shafrir further addressed the Obregon study in his rebuttal testimony, he 

did not address these specific points of Dr. Wiznitzer concerning the reliability of the findings. 

(Tr. 157-58, 159-60.) Moreover, Dr. Shafrir appeared to concede that the Obregon study suffers 

significant weaknesses, characterizing it only as a “pathfinder study” in need of replication. (Tr. 

157-58.) He acknowledged that the article “doesn’t prove anything at this point,” but merely 

 

19

“Homology” means, in the context of our autoimmunity discussion, that the Caspr2 

protein is alleged to be similar enough in molecular structure to proteins in the MMR vaccine 

that the immune system mistakenly attacks the Caspr2 protein. (See Tr. 114.) 

20 In his expert report, Dr. Wiznitzer was critical of Dr. Shafrir’s citation in his own report 

of the Kayser and Dalmau study. (Ex. A, p. 9.) Dr. Shafrir quoted language suggesting that 

autoantibodies against Caspr2 have been found in cases of autoimmune encephalitis with 

autistic-like symptoms. (Ex. 14, p. 23.) Dr. Wiznitzer intimated that Dr. Shafrir had 

misleadingly truncated the quotation, noting that the complete quote described additional 

symptoms that made clear that the condition examined, including the purported Caspr2 genetic 

link to autism, does not match G.C.F.’s clinical presentation. (Ex. A, p. 9.) 

21 Dr. Shafrir agreed with Dr. Wiznitzer that homology is not enough in itself to 

demonstrate autoimmunity. (Tr. 55.) 
28

suggests a “possible” way by which the MMR vaccination might cause the onset of autism. (Tr. 

55.) 

e. The narcolepsy articles 

Dr. Shafrir attempted to further bolster his theory by submitting a supplemental expert 

report (Ex. 48), in which he cited a number of articles regarding cases of a condition known as 

“narcolepsy” reported following administration of a Pandemrix influenza vaccine in Finland. He 

contended that the narcolepsy cases support his theory by providing an example of the same 

mechanism of autoimmunity proposed in this case -- i.e., molecular mimicry resulting in 

autoimmune attacks against brain proteins. (Ex. 48, pp. 1-2.) Dr. Shafrir acknowledged during 

the hearing, however, that these studies do not even establish that narcolepsy actually is an 

autoimmune condition, rendering the comparison meaningless. (Tr. 60.) In any event, I do not 

see how evidence of a different vaccine possibly acting via molecular mimicry upon a different

target to produce a different injury significantly supports Dr. Shafrir’s theory of causation in this

case. The narcolepsy cases tell us nothing about whether autism can be a product of 

autoimmunity and, if so, whether it could be triggered by the MMR vaccine at issue in this case. 

Dr. Wiznitzer additionally noted (Ex. C, p. 1; Tr. 111-13) that the relationship between 

Pandemrix and narcolepsy was supported by positive epidemiological studies showing a 

statistical association between that vaccine and narcolepsy, whereas the epidemiological 

evidence regarding MMR and autism shows no association. (See Ex. F, pp. 145-48, and 

discussion at Section IX(C)(1) of this Decision, below.) 

f. Summary concerning articles on which Dr. Shafrir relied 

In short, I have reviewed all of the articles upon which Dr. Shafrir relied for his theory 

that autoimmunity can cause autism in general, and the discussions of those articles by Drs. 

Shafrir and Wiznitzer. Based on that review, I acknowledge that some of these articles, and the 

articles taken as a whole, suggest the possibility of a role for autoimmunity in autism. However, 

that possibility has certainly not been proven likely to the level of “more probable than not.” I 

am not persuaded that the articles provide more than mere tentative or theoretical support for Dr. 

Shafrir’s suggestion that autism can be the result of autoimmunity. In fact, it is clear that Dr. 

Shafrir overstated the findings of the studies he submitted. The papers cited by Dr. Shafrir for 

the most part are far more tentative than he suggested, and provide only weak evidence of a 

possible association between autoimmunity and autism. Dr. Shafrir admitted as much during the 

hearing, effectively endorsing Dr. Wiznitzer’s critique and conceding that none of the articles he 

cited establish autoimmunity as a cause of autism. (Tr. 67-68.) According to Dr. Shafrir, the 

studies “just demonstrated that those autoantibodies exist,” not that they cause autism. (Tr. 68.) 

Particularly in light of all the other shortcomings of Dr. Shafrir’s presentation, this is simply 

inadequate. 

3. Summary: Dr. Shafrir has not adequately supported his general theory that 

autoimmunity can cause autism. 

In short, for all of the reasons set forth in this Section IX(B) of this Decision, I find that 

Dr. Shafrir has not demonstrated his general theory that it is “more probable than not” that 
29

autism can be caused by autoimmunity. I found Dr. Wiznitzer’s testimony to the contrary to be 

more persuasive. 

To be sure, some of the studies cited by Dr. Shafrir at least raise a credible question

concerning whether autistic symptoms might in some cases be the product of autoimmunity. 

This general question may be the subject of further study. However, based on the evidence in 

the record of this case, I find that it has not been shown to be “more probable than not” that 

autism can be caused by autoimmunity.22 

C. Even assuming that autoimmunity can result in autistic symptoms, there has been no 

showing that the MMR vaccine can cause such autoimmunity. 

 Even if Dr. Shafrir were able to demonstrate that it is probable that autistic symptoms can 

be caused by autoimmunity (which he has not), he would still need to demonstrate that it is 

probable that the MMR vaccination can cause such autoimmunity. This he has also failed to do. 

1. Published studies concerning MMR and autism make Dr. Shafrir’s 

MMR/autoimmunity theory seem unlikely. 

Respondent filed excerpts from an extensive 2012 report of the Institute of Medicine 

(IOM), which specifically evaluated whether there is a causal relationship between the MMR 

vaccine and autism. (Ex. F.) The IOM Committee’s conclusion, considering all the available 

evidence on the issue, was that the “evidence favors rejection of a causal relationship between 

MMR vaccine and autism.” (Id., p. 153, emphasis added.) 

Further, the IOM Committee evaluated multiple epidemiologic studies which examined 

the question of whether any association exists between the MMR vaccination and autism. All of 

the studies that the Committee found most probative, found no association between the MMR 

vaccine and autism. (Ex. F, pp. 145-48.) 

Of course, if MMR were causing only a very small percentage of autism cases, these 

epidemiologic studies might not have had sufficient power to identify an association; 

epidemiologic studies, by their very nature, cannot prove for certain that Factor A never causes 

Condition B. However, especially since Dr. Shafrir urges that MMR vaccines are contributors to 

a large “epidemic” of autism, both the findings of the epidemiologic studies described above, and 

the conclusion of the IOM Committee, tend to cast significant doubt on Dr. Shafrir’s theory. 

 

22 In another recent Vaccine Act case, Dr. Shafrir similarly testified that a vaccine (in that 

case an influenza vaccine) could cause an autoimmune reaction, resulting in autism or in an 

encephalopathy manifesting as autistic symptoms. R.K. v. HHS, No. 03-632V, 2015 WL 

10936124, at *103-04 (Fed. Cl. Spec. Mstr. Sept. 28, 2015). In that case, he relied upon some of 

the same articles and arguments that he raised in this case. Id. at *105-06. Special Master 

Vowell rejected Dr. Shafrir’s autoimmunity theory. (Id. at *92, 101-06.) She found one part of 

that theory to be “completely speculative.” (Id. at *105.) She also found that his attempt to 

“demonstrate the capacity of the vaccine to cause such [an autoimmune] reaction were not only 

circular, they utterly failed.” (Id. at *109.) 
30

2. Dr. Shafrir’s attempt to theorize how the MMR vaccine might trigger autoimmunity 

was not persuasive. 

In Section IX(B)(2)(d) above, I have already discussed Dr. Shafrir’s attempt to show that 

the MMR vaccine could prompt an autoimmune attack on the brain as the result of an alleged 

similarity (“homology”) between certain proteins in the measles, mumps, and rubella viruses and 

amino acid sequences in the Caspr2 brain protein. For the reasons set forth in that section, I 

found Dr. Wiznitzer’s criticisms of the Obregon study to be persuasive, and Dr. Shafrir’s 

approach to be less than persuasive. 

Thus, even if it were to be assumed that autoimmunity can play a role in autism, 

nevertheless it has not been shown to be probable that the MMR vaccine could cause an ongoing 

autoimmunity condition resulting in autistic symptoms.23 

X 

THERE IS NO EVIDENCE OF ANY ABNORMAL IMMUNE REACTION OR 

ANY AUTOIMMUNITY IN G.C.F. 

Even if Dr. Shafrir had demonstrated in general that the MMR vaccine can result in 

autoimmunity causing autism or autistic symptoms, he still failed to show that such an 

occurrence caused the specific autism or autistic symptoms of G.C.F. Since Dr. Shafrir 

theorized that G.C.F.’s injury is explained as autoimmune encephalopathy manifesting as ASD 

(Tr. 40-41), his opinion is predicated on the idea that G.C.F. himself had an immune dysfunction 

and/or an abnormal immune reaction to his vaccination in question. However, G.C.F.’s own 

medical history does not establish that any such abnormality or reaction existed in G.C.F.

For example, Dr. Shafrir acknowledged that there was never any test performed in 

G.C.F.’s case that would demonstrate the autoimmune response that he has theorized. (Tr. 39, 

 

23 Petitioner stresses in her post-hearing reply brief, filed March 7, 2016, that a petitioner 

need not show the exact mechanism of injury (p. 6), and that a petitioner need not demonstrate 

that her theory is “generally accepted” in the medical community (p. 7). Petitioner is correct on 

both of these legal points. If a petitioner can show, based upon the overall record, that an injury 

was “more likely than not” caused by a vaccination, then that petitioner becomes entitled to a 

Program award whether or not the mechanism of injury is demonstrated, or the petitioner’s 

medical theory has gained “general acceptance.” In this case, however, I found Dr. Shafrir’s 

overall presentation to be speculative, dubious, and less persuasive than the presentation of Dr. 

Wiznitzer. Based on the entire record, I do not find it to be “more probable than not” either that 

the MMR vaccine can cause or aggravate autism by any mechanism, or that it did cause or 

aggravate G.C.F.’s autism. 

 

 Further, I note that in reaching my resolution of this case I have fully considered both of 

the post-hearing briefs filed by Petitioner. 
31

78.) Similarly, Dr. Wiznitzer stressed that G.C.F. never displayed any symptoms that would 

reasonably have prompted referral to an immunologist. (Tr. 122-23.) Dr. Shafrir also 

acknowledged that there was no EEG, MRI, or other evaluation, that would have tested for 

encephalopathy. (Tr. 45.) Dr. Shafrir failed to point to any indication that any of G.C.F.’s 

treating physicians believed that his autistic symptoms were the result of an autoimmune 

encephalopathy, or that G.C.F. was referred to an immunologist. 

Instead, Dr. Shafrir stated that in the absence of any testing that showed a defective 

immune system or autoimmunity, he based his opinion of an autoimmune encephalopathy “[o]n 

the symptoms and the time course” of G.C.F.’s condition. (Tr. 78.) But Dr. Shafrir failed to 

explain that answer in any persuasive fashion. Of course, he did express the belief (an incorrect 

belief, as shown above in Section VII of this Decision) that G.C.F.’s first symptoms of autistic 

behavior arose in the three-month period soon after his MMR vaccination of July 2012, but even 

if that belief were true, that would not support a conclusion that an autoimmune reaction was 

attacking G.C.F.’s brain. 

Dr. Shafrir did point to one symptom of G.C.F. that he claimed supported his 

autoimmunity theory -- the severe rash which G.C.F.’s pediatrician described on July 24, 2012. 

(Ex. 11, p. 94.) Although Dr. Shafrir conceded that the rash itself was not evidence of 

autoimmunity, he opined that the severity of the rash provided evidence that G.C.F. had an 

abnormal immune system and was susceptible to autoimmunity. (Tr. 78-79.) This assertion, 

however, was entirely unsupported. Although rashes are well-known reactions to both the MMR 

and varicella vaccinations,24 Dr. Shafrir provided no explanation or citation to support his 

contention that such a reaction, if severe enough, could constitute evidence of an abnormal 

immune system. Dr. Shafrir ultimately conceded that “the rash had nothing to do with 

autoimmune.” (Tr. 78.) His only potential explanation was to assert that, since G.C.F. was 

prescribed acyclovir, a varicella treatment, his immune system must have had difficulty handling 

the vaccine strain of the virus. (Ex. 14, p. 19.) However, there is no notation in G.C.F.’s 

medical records suggesting that the pediatrician felt that G.C.F. had an abnormal immune 

system, or should see an immunologist. 

For his part, Dr. Wiznitzer disputed Dr. Shafrir’s contentions concerning G.C.F.’s rash 

and immune system. Dr. Wiznitzer indicated that there is no available literature suggesting that 

the severity of one’s rash is indicative of one’s immune status. (Tr. 122.) Dr. Wiznitzer found in 

G.C.F.’s records no evidence supporting the idea that his ASD was caused by an autoimmune 

reaction. (Tr. 103.) Significantly, neither Dr. Shafrir nor Dr. Wiznitzer is an immunologist.25 

This fact is particularly significant in terms of Dr. Shafrir’s attempt, based on minimal to no 

 

24 For example, Dr. Wiznitzer testified that reports of adverse events following 

immunization show that between 5-20% will develop a rash. (Tr. 121.) 

25 During the hearing, Dr. Shafrir did testify that he has treated a number of patients 

experiencing severe neuroimmunological conditions. (Tr. 25.) However, nothing in his 

testimony establishes that treating neuroimmunological conditions is a significant part of his 

practice. (Tr. 25-26.) Moreover, nothing in Dr. Shafrir’s CV suggests that he has focused on 

neuroimmunology or immunology in any significant way. (Ex. 15.) 
32

evidence, to establish that G.C.F. had an abnormal immune system, especially since the 

Petitioner bears the burden of proof in this case. After considering the testimony of both experts,

I was not persuaded by Dr. Shafrir that G.C.F.’s rash constituted evidence that he had an 

abnormal immune system. 

In sum, there is no significant evidence in the record to suggest that G.C.F. had an 

abnormal immune system, or suffered from autoimmune encephalopathy as Dr. Shafrir suggests. 

Concerning G.C.F.’s rash, Dr. Shafrir has presented no basis, other than his own ipse dixit as a 

non-immunologist, to conclude that such a rash is evidence of any immune system abnormality. 

Thus, even if I were to accept the validity of Dr. Shafrir’s general theory that autoimmunity 

could cause autism, it would be pure speculation to assert that it could explain G.C.F.’s autism.

XI

“SIGNIFICANT AGGRAVATION” CLAIM

A. General 

 As noted above, Dr. Shafrir spent all of his expert reports, and virtually all of his hearing 

testimony, on his theory that the MMR vaccination of July 2, 2012 caused the initial onset of 

G.C.F.’s autism symptoms. However, at one point in his testimony he was asked a leading 

question by his counsel: 

Q: Now, if the head banging -- the earlier head banging from a couple of months 

before, *** if that were a symptom of autism, would you then say that the vaccines given 

on July 2 significantly aggravated that condition? 

 A: Yes. 

(Tr. 38.) Thus, by merely saying “yes,” Dr. Shafrir in effect presented a “significant 

aggravation” argument, as an alternative to his primary argument that the MMR vaccination of 

July 2, 2012, caused the initial onset of G.C.F.’s autism spectrum disorder. 

 However, the above-quoted question and answer constituted the entirety of Dr. Shafrir’s 

discussion of his alternative “significant aggravation” claim. Dr. Shafrir never explained that 

claim. Thus, I must reject it as unexplained. 

Of course, presumably Dr. Shafrir would say, if questioned, that his “significant 

aggravation” claim would be based on the same proposed causal mechanism as his “initial onset” 

theory -- i.e., that the MMR vaccine caused G.C.F.’s immune system to attack his own brain. 

However, for the reasons stated above, I have found that Dr. Shafrir failed to demonstrate that it 

is “more probable than not” that autism can be the result of an autoimmune encephalopathy, or 

that the MMR vaccine can cause such an autoimmune encephalopathy, or that his MMR vaccine 

did initially cause G.C.F.’s own autism symptoms via this mechanism. For the same reasons, I 

also find that there is no good reason to believe that G.C.F.’s MMR vaccination of July 2, 2012 

“significantly aggravated” his already existing autism. 
33

B. Temporal relationship 

 Although Dr. Shafrir never added any explanation to his one-word alternative “significant 

aggravation” claim quoted above, I do note that he made some comments suggesting a temporal 

relationship between G.C.F.’s MMR vaccination of July 2, 2012, and his autism symptoms. I 

note here that I have considered these comments, but find that they offer no significant support to 

a conclusion that the MMR vaccination caused either the initial onset or a significant aggravation 

of G.C.F.’s autism.

 At one point, Dr. Shafir pointed (Tr. 77) to the statement in the pediatric record of July 

24, 2012, that G.C.F. had “not been doing too well” since July 2 (Ex. 11, p. 94). He implied that 

the “not been doing too well” referred to the onset or increase of autistic symptoms. But that 

statement that G.C.F. “has not been doing too well” is much more likely explained, as Dr. 

Wiznitzer testified (Tr. 97-98), by the fact that in the week after July 2, G.C.F. had a severe 

croup infection, which caused him to be hospitalized. (Ex. 11, p. 95; Ex. 2, pp. 1-5 of 19.) 

During his testimony, Dr. Shafrir acknowledged the croup diagnosis, and agreed that it was 

infectious and unrelated to G.C.F.’s vaccinations. (Tr. 42-43.) Thus, the “not been doing too 

well” notation does not imply that G.C.F. had a sudden spike in autistic symptoms in the three 

weeks after his July 2 MMR vaccination. Indeed, the record of July 24, 2012, constitutes 

important evidence to the contrary. If in fact G.C.F. had a sharp increase in autistic symptoms in 

the three-week period prior to July 24, 2012, such increase most likely would have been noted at 

the pediatrician visit of July 24.26 

 Next, Dr. Shafrir noted the fact that over a three-month period after the July 2 

vaccination, G.C.F. undoubtedly did have a significant increase in his autistic symptoms. That 

is, before July 2, G.C.F. had some autistic symptoms -- the head-banging, the sleep disturbance, 

and the incipient language delays that caused his parents to say in October of 2012 that the onset 

of his language delays occurred at “7-12 months” or “11 months.” (See discussion at Section 

VII(B) above.) But by October 3, 2012, G.C.F. undoubtedly had much stronger symptoms of 

 

26 In this regard, I note that in resolving this case, I have not failed to consider the testimony 

of the Petitioner, G.C.F.’s mother, who testified at the evidentiary hearing. I have no reason to 

conclude that Mrs. Cunningham was not presenting her best memory of the events of 2012. 

Indeed, for the most part, Mrs. Cunningham’s testimony did not differ from the description of 

those events contained in the medical records. However, at one point, she testified that a “couple 

days” after his hospitalization of July 7-8, 2012, G.C.F. became “disconnected,” and at some 

unspecified time, apparently soon afterward, he stopped talking, socializing, and making eye 

contact. (Tr. 14.) I do not doubt that G.C.F. exhibited those behaviors at some point in time 

prior to October of 2012, but I cannot accept as accurate that those behaviors took place 

suddenly, within a few days of that hospitalization, as Mrs. Cunningham’s testimony may have 

implied. If such an abrupt behavioral change had occurred at that time, G.C.F.’s mother very 

likely would quickly have taken him to his pediatrician. Moreover, if those symptoms had in 

fact taken place prior to his pediatrician visit on July 24, 2012, those symptoms would certainly 

have been reported during that visit. 
34

autism -- greater language delay, repetitive use of toys, inconsistent response to his name, poor 

eye contact, etc. (Ex. 5, pp. 40-41.) 

However, the fact that G.C.F.’s autistic symptoms worsened in the three-month period 

after July 2, 2012, does not support a finding that his MMR vaccination “significantly 

aggravated” his autism. First, Dr. Shafrir never so testified. Second, Dr. Wiznitzer explained 

that G.C.F.’s overall course of autistic symptoms fit within one of the typical courses of 

symptoms in an autistic individual. (Ex. A, p. 7; Tr. 100-02.) In other words, G.C.F.’s autistic 

symptoms happened to worsen during that time period, as part of the ordinary course of his 

autism. Therefore, I do not find that G.C.F.’s tragic worsening of autistic symptoms between 

July 2 and October 3 of 2012 supports a conclusion that he experienced a “significant 

aggravation” of his pre-existing autism as a result of his MMR vaccination of July 2, 2012. 

 

XII

PETITIONER’S CASE FAILS THE TESTS REQUIRED BY ALTHEN AND 

LOVING

 In this part of my Decision, I will explain how this case fits specifically within the 

interpretive standards set forth in the Althen and Loving decisions. (As noted in Section I above, 

Althen provides the legal framework for attempts to establish “initial causation,” while Loving

provides the framework for evaluating “significant aggravation” claims.) The short answer is 

that I find that Petitioner’s case clearly does not satisfy the standards presented in either Althen

or Loving.

 In this regard, as previously noted, Dr. Shafrir devoted all of his expert reports, and all 

but one word of his hearing testimony, to the claim that the MMR vaccination of July 2, 2012 

initially caused G.C.F.’s autism or autistic symptoms. But as explained in Section XI, Dr. 

Shafrir also briefly suggested that the vaccination significantly aggravated a preexisting autism 

spectrum disorder. It is clear that Petitioner has clearly failed to provide adequate evidence for 

either claim, for the reasons set forth in detail above. But, in this Section of my Decision, I will 

analyze Petitioner’s case first under Althen, summarizing why I have rejected Petitioner’s “initial 

causation” argument. Then I will analyze Petitioner’s case under the six-part Loving/Althen test, 

summarizing my rejection of their alternative “significant aggravation” claim.

A. Applying the Althen standard to Petitioner’s “initial causation” claim

First, I will analyze the Petitioner’s “initial causation” claim, utilizing the Althen

standard. 

The U.S. Court of Appeals for the Federal Circuit declared in Althen that it is a 

petitioner’s burden:

to show by preponderant evidence that the vaccination brought about her injury 

by providing: (1) a medical theory causally connecting the vaccination and the 

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

the reason for the injury; and (3) a showing of a proximate temporal relationship 

between vaccination and injury. 
35

Althen, 418 F.3d at 1278 (citations omitted). There can be no doubt whatsoever that the Althen

test ultimately requires that, as an overall matter, a petitioner must demonstrate that it is “more 

probable than not” that the particular vaccine was a substantial contributing factor in causing or 

aggravating the particular injury in question. That is clear from the statute itself, which states 

that the elements of a petitioner’s case must be established by a “preponderance of the evidence.” 

(§ 300aa-13(a)(1)(A).) In the pages above, of course, I have already set forth in detail my 

analysis in rejecting Petitioners’ “actual causation” theory, including their “initial causation” 

portion of that theory, in this case. In this part of my Decision, then, I will briefly explain how 

that analysis fits specifically within the three parts of the Althen test, enumerated in the first 

sentence of the Althen excerpt set forth above. The short answer is that I find that Petitioners 

“initial causation” claim in this case clearly does not satisfy the Althen test. 

1. Relationship between Althen Prongs 1 and 2

One interpretive issue with the Althen test concerns the relationship between the first two 

elements of that test. The first two prongs of the Althen test, as noted above, are that the 

petitioners must provide “(1) a medical theory causally connecting the vaccination and the 

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

reason for the injury.” Initially, it is not absolutely clear how the two prongs differ from each 

other. That is, on their faces, each of the two prongs seems to require a demonstration of a 

“causal” connection between “the vaccination” and “the injury.” However, a number of Program 

opinions have concluded that these first two elements reflect the analytical distinction that has 

been described as the “can cause” vs. “did cause” distinction. That is, in many Program opinions 

issued prior to Althen involving “causation-in-fact” issues, special masters or judges stated that a 

petitioner must demonstrate (1) that the type of vaccination in question can cause the type of 

injury in question, and also (2) that the particular vaccination received by the specific vaccinee 

did cause the vaccinee’s own injury. See, e.g., Kuperus v. HHS, 2003 WL 22912885, at *8 (Fed. 

Cl. Spec. Mstr. Oct. 23, 2003); Helms v. HHS, 2002 WL 31441212, at *18 n. 42 (Fed. Cl. Spec. 

Mstr. Aug. 8, 2002). Thus, a number of judges and special masters of this court have concluded 

that Prong 1 of Althen is the “can cause” requirement, and Prong 2 of Althen is the “did cause” 

requirement. See, e.g., Doe 11 v. HHS, 83 Fed. Cl. 157, 172-73 (2008); Nussman v. HHS, 83 

Fed. Cl. 111, 117 (2008); Banks v. HHS, 2007 WL 2296047, at *24 (Fed. Cl. Spec. Mstr. July 

20, 2007); Zeller v. HHS, 2008 WL 3845155, at *25 (Fed. Cl. Spec. Mstr. July 30, 2008). And, 

most importantly, the Federal Circuit confirmed that interpretation in Pafford, ruling explicitly 

that the “can it?/did it?” test, used by the special master in that case, was equivalent to the first 

two prongs of the Althen test. Pafford v. HHS, 451 F.3d at 1352, 1355-56 (Fed. Cir. 2006). 

Thus, interpreting the first two prongs of Althen as specified in Pafford, under Prong 1 of Althen 

a petitioner must demonstrate that the type of vaccination in question can cause the type of 

condition in question; and under Prong 2 of Althen that petitioner must then demonstrate that the 

particular vaccination did cause the particular condition of the vaccinee in question. 

 Moreover, there can be no doubt whatsoever that the Althen test ultimately requires that, 

as an overall matter, a petitioner must demonstrate that it is “more probable than not” that the 

particular vaccine was a substantial contributing factor in causing the particular injury in 

question. That is clear from the statute itself, which states that the elements of a petitioner’s case 

must be established by a “preponderance of the evidence.” § 300aa-13(a)(1)(A). And, whatever 

is the precise meaning of Prongs 1 and 2 of Althen, the overall evidence in this case falls far 
36

short of demonstrating that it is “more probable than not” that the MMR vaccine that G.C.F. 

received on July 2, 2012, contributed to the causation of his tragic neurodevelopmental disorder. 

2. Petitioner has failed to establish Prong 1 of Althen in this case.

 As explained above, under Prong 1 of Althen a petitioner must provide a medical theory 

demonstrating that the type of vaccine in question can cause the type of condition in question. 

Petitioner’s primary theory in this case is that G.C.F.’s MMR vaccination of July 2, 2012 

initially caused G.C.F.’s autism or autistic symptoms, via an autoimmune process. However, as 

described above in Sections VIII and IX, Dr. Shafrir has not demonstrated that the MMR 

vaccination can cause an autism spectrum disorder or autistic symptoms. Thus Petitioner’s claim 

clearly fails under Althen Prong 1.

3. Petitioner has failed to establish Prong 2 of Althen in this case.

Under Prong 2, the Petitioner needs to show that it is “more probable than not” that 

G.C.F.’s MMR vaccination of July 2, 2012, did initially cause G.C.F.’s own condition. But this 

they have also failed to do, for all of the reasons detailed above in Sections VII, VIII, and X of 

this Decision. 

4. Petitioner has failed to establish Prong 3 of Althen in this case.

 Since I have explained why Petitioner has failed to satisfy the first and second prongs of 

Althen, I need not discuss why Petitioner’s case also fails to satisfy the third prong, in which the 

Petitioner must show that the timing of the onset of symptoms fits the Petitioner’s causation 

theory. However, as discussed above in Section VII, the evidence shows that G.C.F. was 

suffering from an autism spectrum disorder prior to the vaccination in question, so that clearly 

Petitioner has failed to establish Prong 3 in this case, as well. 

B. Applying the Loving/Althen standard to Petitioner’s “significant aggravation” claim

As explained at Section XI above, Petitioner’s unexplained alternative “significant 

aggravation” claim must also be rejected, for the reasons set forth therein. However, in the 

interest of completeness, I will now address why Petitioner’s “significant aggravation” claim 

clearly fails the Loving/Althen standard. 

1. Analysis of a “significant aggravation” issue is guided by the ruling in Loving.

 The Vaccine Act states that “[t]he term ‘significant aggravation’ means any change for 

the worse in a preexisting condition which results in markedly greater disability, pain or illness 

accompanied by substantial deterioration of health.” §300aa-33(4). 

 The elements of an off-Table significant aggravation case were set forth in Loving v. 

HHS, 86 Fed. Cl. 135, 144 (2009). The United States Court of Appeals for the Federal Circuit 

acknowledged that “the Loving case provides the correct framework for evaluating off-table 

significant aggravation claims,” in W.C. v. HHS, 704 F.3d 1352, 1357 (Fed. Cir. 2013). Thus, 

the Federal Circuit Court of Appeals, which sets binding precedent for decisions by the Office of 

Special Masters, endorsed the use of a six-part test for significant aggravation, which was first 
37

elaborated in Loving. A petitioner must prove by preponderant evidence that a vaccination 

caused significant aggravation by showing: 

(1) the person’s condition prior to administration of the vaccine, (2) the person’s 

current condition (or the condition following the vaccination if that is also 

pertinent), (3) whether the person’s current condition constitutes a ‘significant 

aggravation’ of the person’s condition prior to vaccination, (4) a medical theory 

causally connecting such a significant worsened condition to the vaccination, (5) a 

logical sequence of cause and effect showing that the vaccination was the reason 

for the significant aggravation, and (6) ... a proximate temporal relationship 

between the vaccination and the significant aggravation. 

W.C. v. HHS, 704 F.3d at 1357 (Fed. Cir. 2013). 

 The standard elaborated in Loving, and endorsed in W.C. v. HHS, combines 

elements from previous Federal Circuit decisions. W.C. v. HHS, 704 F.3d at 1357 (“The 

Loving test combines the first three Whitecotton factors, which establish significant 

aggravation, with the Althen factors, which establish causation.”) Since the last three 

elements of the Loving test include the entirety of the Althen test, with insignificant 

wording modifications, the analysis of those three elements would be the same using 

either standard. 

2. Analysis of this case, under the six-part Loving/Althen test 

 In this Section, I will discuss why Petitioner has failed to satisfy the six-part Loving test 

to establish the existence of vaccine-related significant aggravation of a preexisting condition. 

a. What was G.C.F.’s condition prior to the administration of the vaccinations 

in question? 

As explained in Section VII above, on July 2, 2012, much of G.C.F.’s development 

seemed normal. However, with the benefit of hindsight, the evidence indicates that G.C.F. had 

already displayed several symptoms of an autistic spectrum disorder prior to that date. (See 

discussion at Section VII, above.) 

b. What was G.C.F.’s condition “following” the vaccination in question, and 

what is his current condition? 

 As explained above (Section XI(B)), the evidence in this case indicates that G.C.F. did 

not suffer any sharp increase in autistic symptoms in the first three weeks after his MMR 

vaccination of July 2, 2012. However, as also explained in Section XI(B), he clearly did suffer a 

substantial increase during the three months after that vaccination. Therefore, I find that 

G.C.F.’s condition three weeks after the vaccination was substantially unchanged from his prevaccination condition with respect to autistic symptoms, but significantly worse by three months

after vaccination. 
38

Further, by January of 2013, six months after the vaccination in question, G.C.F. was 

formally diagnosed with autism. (Ex. 5, p. 22.) Tragically, since then G.C.F. has proved to have 

a very significant neurodevelopmental disorder, which has been classified as an Autism 

Spectrum Disorder -- that is his “current condition.” 

c. G.C.F.’s disorder legally constitutes a “significant aggravation” of his

autism spectrum disorder.

 

As explained in the prior paragraph, I would have to reject any allegation that G.C.F.’s 

disorder significantly worsened within three weeks after the vaccination in question. However, 

his disorder had significantly worsened by three months after that vaccination. Further, in the 

Loving/Althen formulation set forth in W.C. and quoted above, another question posed is whether 

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

condition prior to vaccination. W.C., 704 F.3d at 1357. And as to that question, my conclusion 

is that G.C.F.’s “current condition” is significantly worse than his condition appeared 

immediately prior to the vaccination in question. Therefore, following the standard set forth in 

Loving and W.C., G.C.F.’s condition three months post-vaccination and his “current condition” 

both do amount to a “significantly aggravation” of his pre-existing autism spectrum disorder --

though the worsening has definitely not been shown to have been related to his vaccination. 

d. Petitioner has failed to establish Prong 4 of Loving/Prong 1 of Althen. 

 As discussed above, Prongs 4, 5, and 6 of the Loving test are, in effect, the same as 

Prongs 1, 2, and 3 of the Althen standard. Under Prong 4 of Loving and Prong 1 of Althen, a 

petitioner must provide a medical theory demonstrating that the type of vaccine in question can 

cause a significant worsening of the type of preexisting condition of the vaccinee. In this case, 

however, for the reasons stated above, in Sections VIII, IX, and XI, the Petitioner has failed to 

show that the vaccination in question can aggravate an autism spectrum disorder. As explained 

in Section XI above, Dr. Shafrir did not provide any explanation at all as to why or how he 

believes that an MMR vaccination could worsen an autism spectrum disorder. 

 Accordingly, Petitioner has wholly failed to establish Prong 4 of Loving/Prong 1 of 

Althen in this case. 

e. Petitioner has failed to establish Prong 5 of Loving/Prong 2 of Althen 

in this case. 

Under Prong 5 of Loving/Prong 2 of Althen, the Petitioner needs to show that it is “more 

probable than not” that G.C.F.’s MMR vaccination of July 2, 2012, did aggravate the autism 

spectrum disorder of G.C.F. himself. But she has failed to do so. As explained at Section XI 

above, Dr. Shafrir did not give any explanation at all of why or how the MMR vaccination in 

question might have aggravated G.C.F.’s own disorder. 

Accordingly, Petitioner has failed to establish Prong 5 of Loving/Prong 2 of Althen in this 

case.

f. Petitioner has failed to establish Prong 6 of Loving/Prong 3 of Althen 

in this case. 
39

Since I have explained why Petitioners have failed to satisfy the first and second prongs 

of Althen (4th and 5th prongs of Loving), I need not discuss why Petitioner’s case also fails to 

satisfy the Prong 3 of Althen/Prong 6 of Loving. However, again in the interest of completeness, 

I will analyze whether there was “a showing of a proximate temporal relationship” between the 

MMR vaccination and the worsening of G.C.F.’s autism spectrum disorder. 

As explained above, the medical records, specifically the notes of G.C.F.’s visit of July 

24, 2012, indicate that G.C.F.’s autism symptoms did not suddenly worsen within three weeks of 

his MMR vaccination of July 2, 2012. On the other hand, the record of October 3, 2012, shows 

that his symptoms did substantially worsen within three months of that vaccination. However, 

since Dr. Shafrir never explained his one-word “significant aggravation” claim, he never stated 

whether he believes that a worsening within three months would constitute a sufficient 

“proximate temporal relationship” to indicate that the vaccination was responsible for that 

worsening. Therefore, Petitioner has also failed to establish Prong 6 of Loving/Prong 3 of Althen 

as to Petitioner’s significant aggravation claim. 

g. Summary concerning Althen/Loving test. 

Having failed to establish Prongs 4, 5, and 6 of the Loving test, Petitioner has failed to 

prove her “significant aggravation” claim in this case. 

C. This not a close case.

As noted above, in Althen, the Federal Circuit indicated that the Vaccine Act involves a 

“system created by Congress, in which close calls regarding causation are resolved in favor of 

injured claimants.” Althen, 418 F.3d at 1280. Accordingly, I note here that this case is 

ultimately not a close call. For all the reasons set forth above, I find that Dr. Shafrir’s causation 

theory was quite speculative, while Respondent’s expert was far more persuasive.27

XII

CONCLUSION 

The record of this case demonstrates plainly that G.C.F. has suffered a tragic medical 

disorder. Thus, I feel deep sympathy for G.C.F. and his mother. Further, I find it unfortunate 

that my ruling in this case means the Program will not be able to provide funds to assist this 

family, in caring for a child who suffers from a serious disorder. However, I must decide this 

case not on sentiment, but by analyzing the evidence. Congress designed the Program to 

compensate only the families of individuals whose injuries or deaths can be linked causally, 

 

27 It should be noted that in this case the Petitioner never came close to carrying her burden 

of making a “prima facie” case showing that G.C.F. suffered a vaccine-caused or vaccineaggravated injury. Therefore, the burden never shifted to Respondent to demonstrate that 

G.C.F.’s disorder was “due to factors unrelated to the administration of the vaccine.” §300aa13(a)(1)(B). 
40

either by Table Injury or presumption or by preponderance of “causation-in-fact” evidence, to a 

listed vaccine. In this case, the evidence advanced by Petitioner has fallen far short of 

demonstrating such a link. Accordingly, I conclude that the Petitioner in this case is not entitled 

to a Program award on G.C.F.’s behalf.28

IT IS SO ORDERED. 

 

 /s/ George L. Hastings, Jr. 

 George L. Hastings, Jr. 

 Special Master 

 

28 In the absence of a timely-filed motion for review of this Decision, the Clerk of the Court 

shall enter judgment accordingly.