In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

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

K.O., parent of * No. 13-472V 

A.F., a minor, * Special Master Christian J. Moran 

 Petitioner, * 

 * Filed: July 7, 2016 

v. * Reissued: January 3, 2017 

 * 

SECRETARY OF HEALTH * Entitlement; Pneumococcal Conjugate 

AND HUMAN SERVICES, * (“PCV”) Vaccine; Opsoclonus 

 * Myoclonus Syndrome (“OMS”). 

 Respondent. * 

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

Ronald C. Homer and Meredith Daniels, Conway, Homer & Chin-Caplan, P.C., 

Boston, MA, for petitioner;

Heather L. Pearlman, United States Dep’t of Justice, Washington, DC, for 

respondent. 

PUBLISHED DECISION DENYING COMPENSATION1

 K.O. filed a petition on behalf of her minor son, A.F., alleging that the 

pneumococcal conjugate (“PCV”) vaccine caused him to develop opsoclonus 

myoclonus syndrome (“OMS”). K.O. is seeking compensation pursuant to the 

National Childhood Vaccine Injury Compensation Program, codified at 42 U.S.C. 

§ 300aa−10 through 34 (2012).

To connect the PCV vaccine and A.F.’s OMS, K.O. relied upon the opinion 

of a pediatric neurologist, Spencer Weig. Dr. Weig opined that A.F. developed 

OMS on August 25, 2010, asserting that the PCV vaccination A.F. received on 

July 14, 2010, provoked the condition under the theory of molecular mimicry. 

The Secretary disagreed with K.O.’s claim. The Secretary presented the 

opinion of neurologist Eric Lancaster. Dr. Lancaster opined that the onset of 

 1 After this decision was issued, the petitioner filed a motion to redact her name to initials 

pursuant to Vaccine Rule 18(b). That motion was granted. Order, filed Nov. 30, 2016. 
2 

A.F.’s OMS was August 28, 2010, and asserted that the medical evidence did not 

support the theory proposed by Dr. Weig. 

K.O.’s case falters for two independent reasons. First, the theory she 

presents, molecular mimicry, is far too general to be persuasive. She has not 

offered sufficient evidentiary justification for a finding that Dr. Weig’s opinion is 

reliable. Second, the onset of A.F.’s OMS occurred outside the time that both Dr. 

Weig and Dr. Lancaster accepted as medically acceptable. Because K.O. did not 

prove, by a preponderance of the evidence, that the PCV vaccine can cause OMS, 

and did not show A.F.’s OMS arose in the acceptable time, K.O. did not meet her 

burden of proof. Thus, she is not entitled to compensation. 

I. Background2

Section A provides a brief overview of OMS. Section B summarizes the 

experts’ qualifications. Section C delineates the relevant events in A.F.’s medical 

history. 

 2

 The undersigned has considered all the evidence. Cf. Moriarty v. Sec’y of Health & 

Human Servs., No. 2015-5072, 2016 WL 1358616 (Fed. Cir. Apr. 6, 2016) (stating special 

master erred in not considering the entire record). Although the undersigned does not discuss all 

the evidence, the undersigned discusses the evidence (documentary and testimonial) that the 

undersigned finds most relevant. The process of determining the relevancy of any piece of 

evidence is informed by the undersigned’s experience as a special master generally. The 

undersigned has reviewed the expert reports several times, beginning when they were initially 

filed. In preparing the order requesting briefs before the hearing, the undersigned reviewed the 

expert reports and the articles cited in those reports. The parties provided their views of the 

relevance of the articles in their pre-hearing briefs. The parties’ briefs, in turn, provided a 

foundation for asking questions at the hearing. The witnesses’ testimony further refined and 

highlighted the most important articles that the parties discussed in their briefs after the hearing. 

The undersigned is reasonably confident that this process has brought to his attention any piece 

of evidence that would significantly contribute to analyzing K.O.’s claim. See Vaccine Rule 

8(b)(1).
3 

A. Opsoclonus Myoclonus Syndrome 

OMS is a rare neurological condition defined by acute onset of rapid and 

chaotic eye movements (opsoclonus) and jerking of the limbs and trunks 

(myoclonus) in conjunction with other conditions, including ataxia and behavioral 

irritability. Exhibit 18, tab C (Katherine K. Matthay, Opsoclonus myoclonus 

syndrome in neuroblastoma: a report from a workshop on the dancing eyes 

syndrome at the advances in neuroblastoma meeting in Genoa, Italy, 2004, 228 

Cancer Lett. 275 (2005)) at 276; exhibit D (Barbara Hero, Update on Pediatric 

Opsoclonus Myoclonus Syndrome, 44 Neuropediatrics 324 (2013)) at 324; exhibit 

18, tab D (K. Ki Pang, A prospective study of the presentation and management of 

dancing eye syndrome/opsoclonus–myoclonus syndrome in the United Kingdom, 

14 European J. of Pediatr. Neurol., 156 (2010)) at 156. Most, but not all, pediatric 

patients with OMS also have a diagnosis of a neuroblastoma.

3

 The etiology of 

OMS is believed to be autoimmune in nature. Exhibit 18, tab B (M. Kinsbourne, 

Myoclonic encephalopathy of infants, 25 J. Neurol. Neurosurg. Psychiatr. 271 

(1962)) at 276; exhibit 18, tab C at 276-77; exhibit D at 324; Tr. 52-53, 61, 154. 

OMS is diagnosed upon the presentation of a patient with various 

prodromal4 symptoms with irritability being the most common. Neurologic 

symptoms of ataxia, falling, and myoclonus are most often experienced with 

behavioral problems becoming more prevalent. OMS is commonly misdiagnosed 

as acute cerebellitis. Exhibit J (Elizabeth D. Tate, Neuroepidemiologic Trends in 

105 US Cases of Pediatric Opsoclonus-Myoclonus Syndrome, 22 J. of Pediatr. 

Oncol. Nurs., 8 (2005)) at 10.

B. Expert Qualifications

K.O. relies upon the expert opinion of Spencer Weig. Dr. Weig is a boardcertified pediatrician and neurologist with a special qualification in child 

neurology. Exhibit 18 at 1; exhibit 19 at 2. He graduated from Mt. Sinai School of 

 3

 A neuroblastoma is a sarcoma consisting of malignant neuroblasts, usually arising in the 

autonomic nervous system or in the adrenal medulla. It is considered a type of neuroepithelial 

tumor and affects mostly infants and children up to 10 years of age. Dorland’s Illus. Med. 

Dictionary at 1263 (32d ed. 2012). 

4

 A prodrome is a premonitory symptom or precursor; a symptom indicating the onset of 

a disease. Dorland’s at 1522. 
4 

Medicine in 1973 and, after practicing for several years, completed residencies and 

a fellowship in child neurology. He practiced child and adult neurology 

continuously for 24 years. Exhibit 18 at 1. Dr. Weig has treated 10 to 12 patients 

with opsoclonus myoclonus syndrome over the course of his career. Exhibit 18 at 

1; Tr. 10. He remains active in the Departments of Neurology and Pediatrics at the 

University of North Carolina at Chapel Hill School of Medicine. Exhibit 18 at 1. 

The Secretary relies upon the expert opinion of Eric Lancaster. Dr. 

Lancaster completed his PhD focused on neuroscience and MD degrees at the 

University of Maryland in 2002 and 2003, respectively. He completed a residency 

in neurology and multiple fellowships in neuromuscular study. He is the author of 

22 peer-reviewed publications with many concerning autoimmune neurological 

disorders. Exhibit A at 1; exhibit B at 3-4. Dr. Lancaster’s current practice 

primarily focuses on research of autoimmune brain and nerve diseases. Tr. 101. 

Dr. Lancaster has treated one patient with opsoclonus myoclonus syndrome. 

Exhibit A at 1. He currently serves as an assistant professor of neurology at the 

University of Pennsylvania. Exhibit B at 1.

C. A.F.’s Medical History

A.F. was born on July 15, 2009, and developed normally for the first year. 

See generally exhibit 5 at 1-24. At his one-year child health check on July 14, 

2010, A.F. received the PCV vaccine. Id. at 23. 

A few weeks later, on August 11, 2010, A.F. was seen by pediatrician 

Meredith Saillant presenting with a carbuncle5 that she eventually diagnosed as 

“furuncle of face.”6

 Id. at 25. In Dr. Lancaster’s opinion, the presence of the 

furuncle within a month before onset of OMS was a better temporal fit for an 

“autoimmune encephalitis after immune stimuli” as the mechanism of A.F.’s OMS 

than the PCV vaccination. Tr. 147. Dr. Weig disagreed, stating that between the 

furuncle and vaccine, the vaccine more likely than not triggered the OMS. Tr. 156. 

 5

 A carbuncle is a necrotizing infection of skin and subcutaneous tissue composed of a 

cluster of boils (furuncles), usually due to Staphylococcus aureus, with multiple formed or 

incipient drainage sinuses. Dorland’s, at 289; Tr. 146, 169. 

6

 A furuncle is a painful nodule formed in the skin by circumscribed inflammation of the 

dermis and subcutaneous tissue after staphylococci enter through the hair follicles. Dorland’s, at 

751; Tr. 146, 169. 
5 

K.O. recalled A.F. experiencing constipation on August 25, 2010. She gave 

him prune juice and noted some improvement. Exhibit 13 at ¶ 4. A.F. had an eye 

exam on August 27, 2010, with unremarkable results and Dr. Rebecca Maida

concluding that “[A.F.’s] eyes are healthy.” Exhibit 8 at 7. The normal eye exam, 

Dr. Weig opined, indicated that A.F. was not experiencing opsoclonus at the time. 

Tr. 37. Dr. Lancaster asserted that a normal eye exam rules out opsoclonus and he 

further asserted that a doctor would not miss opsoclonus during an eye exam. Tr. 

151. 

The day after his eye examination, A.F. was taken to the emergency room 

due to increased fussiness, crying, drooling, unsteadiness, and lack of bowel 

movement. Exhibit 4 at 8. An abdominal x-ray revealed a “large amount of 

stool.” A.F. was discharged in good condition with instructions for the family to 

use glycerin suppositories and prune juice. Id. at 9-10. 

The following day, on August 29, 2010, A.F. was taken to the emergency 

room again for being “inconsolable of late” and complaints that he “[c]ried 

inconsolably for 4 [hours]” when being put down for a nap. Exhibit 6 at 282, 287; 

Tr. 19. The family reported that A.F. was more uncoordinated than usual, 

wobbling and flopping, and that he had been constipated for several days. Exhibit 

6 at 287. The family also reported that A.F. was no longer constipated or fussy as 

he had been the previous night. Id. at 282. The doctor’s neurologic exam was 

normal, noting that A.F. was “[f]ussy with exam but consolable.” Id. at 283. A 

consultation with a neurologist was arranged. Id. at 284-86.

Dr. Weig opined that the irritability and inconsolable crying were prodromal 

symptoms of OMS. Dr. Weig also asserted that A.F.’s irritability and inconsolable 

crying started no later than August 25, 2010, based on the affidavit of K.O. and the 

medical records of Dr. David Coulter. Tr. 39-41. Dr. Lancaster disagreed, 

asserting that the medical records and histories provided by K.O. indicate that A.F. 

was constipated on August 25, 2010, and did not experience any OMS-like 

symptoms until later on August 28. Tr. 107-08.

During a consultation on August 29, 2010, neurologist David Coulter 

documented the concerns of lethargy, inconsolability, and coordination issues. 

Exhibit 6 at 290. Dr. Coulter noted some weakness attributing it to “the setting of 

constipation or mild illness (though he has had no evidence of recent illness).” Id. 

at 289. Dr. Coulter concluded that the neurologic exam was normal with follow up 

suggested in two weeks. Id. 
6 

A.F. saw a physician with Dr. Saillant’s practice, Marshall Reiner, on 

August 30, 2010, for a follow-up after the emergency room visit. While the 

parents complained that A.F. had regressed and been “unsteady” for the past two 

days, Dr. Reiner’s impression was that “the child’s actions are normal for age.” 

The diagnosis was ataxia with a referral to a neurologist. Exhibit 5 at 25. Dr. 

Saillant saw A.F. on August 31, 2010, with continued complaints of irritability, 

constipation, and unsteadiness that had not improved. Exhibit 5 at 26. Dr. Saillant 

noted that A.F. was “markedly different from the last time I saw him a few weeks 

ago” and that his balance was “severly [sic] compromised.” Id. She confirmed the 

diagnosis of ataxia and expressed her concerns for closer neurological evaluation 

and an MRI with Dr. Coulter, scheduling an appointment for the following day. 

Id. at 26-27. 

Upon review of the past medical history and examination on September 1, 

2010, Dr. Coulter diagnosed A.F. with acute cerebellar ataxia. Exhibit 6 at 279-80. 

Dr. Coulter’s notes state that the family had reported to him that A.F. had been fine 

on August 27, 2010, with an onset of symptoms on August 28 and worsening on 

August 29. Id. at 280-82. Five days later, on September 6, 2010, A.F. was taken 

back to the emergency room due to concerns that he was “losing motor skills.” Id.

at 262. He was admitted for further evaluation. Id. at 264. 

On September 7, 2010, during the hospital stay, Kara Smith noted that A.F. 

had lost the ability to “sit independently, pull to stand and to cruise, all of which he 

had previously.” Dr. Smith diagnosed A.F. with opsoclonus myoclonus syndrome 

stating “[A.F.’s] history and exam is quite concerning and he offers opsoclonus as 

well as myoclonus.” Dr. Smith coordinated further imaging studies with A.F.’s 

neuroimmunologist, Mark Gorman, to rule out a neural crest tumor, such as a 

neuroblastoma. Exhibit 6 at 269-70, exhibit 17 at 4. A.F. was discharged the 

following day.

Under the supervision of Dr. Gorman, A.F. was readmitted on September 

14, 2010, for MRI and MIBG7 scanning. Exhibit 6 at 259. There was no evidence 

of a neuroblastoma. Id., Tr. 95-96, 160. The notes from Dr. Gorman summarized 

A.F.’s medical history including his receipt of the PCV vaccine. Dr. Gorman 

 7 An MIBG scintiscan is a type of imaging test. It uses a radioactive substance (called a 

tracer) and a scanner to find or confirm the presence of pheochromocytoma and neuroblastoma. 

These are types of tumors that affect nerve tissue. “MIBG scintiscan,” A.D.A.M. Medical 

Encyclopedia, (June 21, 2016, 10:45 AM), 

https://www.nlm.nih.gov/medlineplus/ency/article/003830.htm. 
7 

stated developmental changes began “[o]n 8/28.” Exhibit 6 at 247. Dr. Gorman 

confirmed the OMS diagnosis, stating “[t]he presentation is [entirely] consistent 

with OMS and meets 2004 Genoa criteria for the diagnosis.” Id. at 249; see 

generally exhibit 18, tab C. Dr. Gorman recommended immunosuppressive 

therapy. Exhibit 6 at 250.

A.F. returned to Dr. Gorman for a follow up visit on November 5, 2010, 

when Dr. Gorman noted that A.F. had “idiopathic OMS” being treated with 

immunosuppressive therapy that was going well. Exhibit 6 at 201-02. Dr. 

Lancaster opined that Dr. Gorman’s impression that the OMS was “idiopathic” is 

an indication that a cause or triggering event was sought, but one was not found. 

Tr. 142-43. 

Several months after Dr. Gorman’s follow up appointment, pediatric neuroophthalmologist Gena Heidary evaluated A.F. on June 2, 2011. Dr. Heidary’s 

impression of A.F.’s OMS was that while the etiology was unclear, “there is a 

question of a reaction to the pneumococcal vaccine number 13 as this was the only 

thing that antedated the onset of his symptoms.” Exhibit 6 at 143. A.F. returned to 

Dr. Heidary on September 15, 2011, and she noted that the OMS had resolved and 

he was “doing extremely well.” Id. at 119. 

II. Procedural History 

On July 12, 2013, K.O. filed a petition on behalf of her minor son, A.F., 

alleging that the PCV vaccine caused him to develop OMS. K.O. filed medical 

records, exhibits 1-12, on October 28 and 30, 2013. Affidavits were filed on 

December 17, 2013 and outstanding medical records filed on December 20, 2013. 

Exhibits 13-15. 

On January 7, 2014, the Secretary filed her report pursuant to Vaccine Rule 

4. The Secretary maintained that K.O. had failed to demonstrate causation. 

Resp’t’s Rep. at 13. The Secretary argued that K.O. did not offer reliable scientific 

evidence that demonstrated a causal relationship between the PCV vaccination and 

OMS. Although the Secretary noted that pediatric neuro-ophthalmologist Gena 

Heidary stated that she “thought” the PCV vaccination was secondary to A.F.’s 

OMS, the Secretary asserted that Dr. Heidary’s opinion was contradicted by all of 

A.F.’s treating physicians who did not mention such an association, but merely 

noted the temporal relationship. Id. at 13. 

During a January 13, 2014 status conference to discuss the Rule 4 report, 

K.O. stated that she would retain an expert to opine on her case after the parties 
8 

discussed the possibility of settlement. K.O. filed additional medical records and a 

response to the Rule 4 report on January 29, 2014. K.O. answered questions 

presented regarding medical records asserting that all requests made by respondent 

were satisfied. Pet’r’s Resp., filed Jan. 29, 2014.

On February 4, 2014, K.O. filed a status report proposing a May 5, 2014 

deadline for her expert report. The undersigned issued draft Instructions to 

Witnesses Offering Opinion Testimony (hereinafter “proposed instructions”) on 

February 12, 2014. The undersigned explained that expert reports are filed in 

advance of the hearing and provide all parties and the special master notice of the 

contents of the testimony. Therefore, the proposed instructions ordered that any

expert’s report would, most likely, constitute the expert’s testimony on direct 

examination. The undersigned further explained that the purpose of this 

requirement was two-fold: 1) to ensure a complete report that presented the 

expert’s opinions and bases for those opinions, and 2) to decrease time spent in 

hearings repeating the content of the expert report. 

The undersigned ordered K.O. to file any comments to the proposed 

instructions by February 28, 2014, and her expert report by May 5, 2014. On 

March 7, 2014, K.O. filed her Opposition to the Court's Proposed Instructions to 

Witnesses Offering Opinion Testimony. Presenting several objections to the 

proposed instructions, K.O. relied primarily upon Vaccine Rule 8. K.O. asserted 

that Rule 8(b)(2) allows petitioners to present evidence in the manner in which 

they choose and that there is no authority given to special masters to require 

evidence be presented in a specific format. Pet’r’s Opp. at 4. K.O. further asserted 

that expert reports are evidence as governed by Vaccine Rule 8(b) and therefore 

cannot be limited to the written report. Id. at 5. 

Additionally, K.O. argued that expert testimony in complex cases warranted 

oral presentation and cited two previous cases where the undersigned has stated 

that “oral testimony may be more persuasive than written records.” Id. at 6-7. 

K.O. asserted that the proposed instructions were in conflict with Federal Rules of 

Civil Procedure (“FRCP”) 26(a)(2)(B) and the role of a special master as outlined 

in Vaccine Rule 3(b)(2) because they would lead to a “more rigid, less flexible, 

and more adversarial process” contrary to Congress’s intent. Id. at 9-10. K.O. also 

made a general objection to the fairness of the proposed instructions as they 

applied to petitioners. Id. at 10-11.

The undersigned issued an order for expert reports and addressed K.O.’s 

objections on April 17, 2014. This order mandated that the expert reports comply 

with the proposed instructions previously set forth and that the reports would 
9 

constitute direct testimony. The undersigned drew from other instances where 

written direct testimony had been used in non-jury cases by similar courts with the 

most instructive instance being the Tax Court. The undersigned analogized the 

Court of Federal Claims and the Office of Special Masters to the Tax Court in 

three ways. First, both are Article I tribunals. Second, both are devoted to one 

subject matter. Third, both hear cases without a jury. The undersigned noted that 

the Tax Court Rules of Practice and Procedure, specifically Rule 143(g), provided 

that testimony need not be presented orally. Additionally, FRCP 43(a) removed 

the oral testimony requirement. The undersigned reasoned that this was instructive 

because Court of Federal Claims Rule 43 is identical to FRCP 43. The undersigned 

cited cases in which the Court of Federal Claims and the Tax Court had received 

direct testimony from experts in the form of written reports. 

The undersigned further observed that there is no statutory restriction 

prevents the Office of Special Masters from using expert reports as direct 

testimony. In addressing K.O.’s fairness objections, the undersigned determined 

that they were unpersuasive as the order applied to both parties and was designed 

to facilitate flexibility in the presentation of evidence allowing experts weeks to 

draft comprehensive reports with assistance of counsel for development. 

K.O. filed her expert report, supporting literature, and the curriculum vitae 

from Dr. Weig on July 11, 2014. Exhibits 18-19. On July 16, 2014, K.O. filed a 

Renewed Opposition to the Court’s Orders dated February 12, 2014 and April 17, 

2014 and Motion to Vacate the Orders. K.O. renewed her objections that special 

masters lacked authority to require expert reports as direct testimony, precluding 

oral testimony was a detriment to petitioners being able to present the opinion of 

the expert fully, and that the special master had gone beyond his duties in 

mandating the instructions. See generally Pet’r’s Renewed Opp., filed July 16, 

2014. K.O. also introduced specific objections to the instructions. Id. at 10-12. 

During the ensuing status conference to discuss Dr. Weig’s report, the 

undersigned determined that most of petitioner’s outstanding motions were moot 

due to Dr. Weig answering the questions posited by the instructions in his report. 

Order, issued July 25, 2014. The Secretary filed an expert report with supporting 

literature, following the same instructions as K.O., as well as a curriculum vitae, 

from Dr. Lancaster on October 1, 2014. Exhibits A-Q. In the ensuing status 

conference to discuss Dr. Lancaster’s report, the undersigned ordered Dr. 

Lancaster to provide the basis for his assertion that “PCV contains no antigens 

expressed in a normal brain.” Reminding K.O. that Dr. Weig’s reports may 

constitute his direct testimony, the undersigned ordered a supplemental report to 

respond to Dr. Lancaster. At that time, the parties discussed exploring settlement. 
10 

The Secretary filed Dr. Lancaster’s supplemental expert report with 

supporting literature on November 5, 2014. Exhibits R-T. On December 12, 2014, 

K.O. filed Dr. Weig’s responsive expert report with supporting literature. Exhibit 

20. On January 13, 2015, the Secretary filed a status report indicating that, despite 

settlement efforts, she desired to defend the case. During a January 23, 2015 status 

conference, the undersigned questioned whether a fact hearing would be needed to 

settle the question of onset. 

The Secretary filed a supplemental expert report from Dr. Lancaster on 

February 9, 2015. Exhibit U. The parties proposed mutually convenient dates for 

an expert hearing on entitlement and a one-day hearing was set for August 13, 

2015. Pet’r’s Status Rep., filed Mar. 2, 2015. The undersigned issued a prehearing order setting the dates for pre-hearing submissions and the pre-hearing 

status conference. Order, issued Apr. 23, 2015; see also order, issued Apr. 6, 2015. 

K.O. filed her pre-hearing brief on June 24, 2015. In an order issued June 29, 

2015, the undersigned reiterated that the reports of the experts, upon careful 

review, would constitute direct testimony due to any oral direct testimony likely 

being duplicative. The undersigned allowed K.O. to submit a supplemental 

statement identifying the portions of Dr. Weig’s opinion that she believed should 

be presented orally due to her requests for oral presentation. The Secretary was 

also afforded the opportunity to submit a responsive supplemental statement from 

Dr. Lancaster.

On July 9, 2015, K.O. filed a supplemental statement asserting that oral 

direct testimony from Dr. Weig was required to present the dispute regarding onset 

of OMS symptoms, complex theories, a logical sequence of cause and effect 

showing that the vaccination was the reason for the injury, and showing a 

proximate temporal relationship between the vaccination and injury. On July 13, 

2015, the Secretary filed her pre-hearing brief. 

An expert hearing was held on August 10, 2015, in Washington, DC. Both 

Dr. Weig and Dr. Lancaster testified at the hearing. Both testified in accord with 

their reports. 

Dr. Weig testified that the onset of symptoms was late August 2010, opining 

the date to be August 25, 2010, based on K.O.’s affidavit and the August 29, 2010 

medical records from Dr. David Coulter. Tr. 74-75. He stated that K.O. noticed 

the irritability in late August which is consistent with the timing of OMS symptom 

onset. Tr. 18-19, exhibit 13 (K.O.’s affidavit) at 1-2. The medical records from 

the hospital then provided a documented parental statement of the symptoms 

presenting since three days prior to that August 28 visit. Tr. 19-20, exhibit 18 (Dr. 
11 

Weig’s report) at 7. Dr. Weig stated that the irritability noticed by the parents and 

crying at night, supported an onset date of August 25 because these behaviors were 

the early symptoms of the disease. Tr. 19-20, 23; exhibit 18 at 4. 

Dr. Weig explained that A.F.’s normal eye exam results on August 27 were 

unremarkable because, in his professional experience, a patient could be 

asymptomatic for opsoclonus and later exhibit symptoms. Tr. 38-39, 94. Dr. Weig 

ruled out constipation as the cause of A.F.’s irritability due to the duration and 

prolonged period of crying. The duration of the irritability instead pointed to a 

typical prodromal symptom of OMS. Tr. 39-41, exhibit 18 at 7. 

Dr. Weig opined that it was more likely than not that A.F.’s OMS was 

vaccine-induced because extensive testing ruled out possible alternate causes, such 

as neuroblastoma, or alternate theories. Tr. 95, 169; exhibit 18 at 9.

K.O. had approximately 30 minutes of direct examination with Dr. Weig. 

K.O. was also able to ask Dr. Weig any additional questions or gain clarification 

on re-direct examination after the Secretary cross-examined and the undersigned 

examined Dr. Weig. 

The Secretary presented the testimony of Eric Lancaster at the hearing. Dr. 

Lancaster testified that, based on the totality of the medical records, the irritability 

A.F. experienced on August 25, 2010, was due to constipation with which he was 

diagnosed and for which he was treated. Tr. 108, exhibit A at 12. He opined that 

the onset of OMS was three days later, on August 28, as confirmed by the 

contemporaneous medical records. Tr. 107, exhibit A at 13. 

Dr. Lancaster acknowledged Dr. Heidary’s records possibly linking the 

vaccination to OMS as K.O. suggested, but asserted that her notes indicated 

obscurity regarding causation and an inability to understand her thought process

fully. Tr. 141-42. In contrast to Dr. Weig’s opinion, Dr. Lancaster stated that 

A.F.’s normal eye exam was “very helpful for ruling out opsoclonus” as it would 

be “very unlikely, for any eye doctor to miss that.” The normal exam and 

physician indication that A.F. was negative of any symptoms weighed against 

onset prior to August 28. Tr. 150-51, exhibit A at 3, 12; exhibit U at 2. 

Dr. Lancaster opined that the furuncle present prior to the onset of A.F.’s 

neurological symptoms provided a better temporal fit as a potential triggering 

infection. Tr. 146-47, exhibit A at 13. He further explained that while the cause of 

A.F.’s OMS was more likely idiopathic, the furuncle was a more plausible trigger 

than the vaccination. Tr. 155-56, exhibit A at 13.
12 

Overall, the process of expert reports as direct testimony worked well. Both 

Dr. Weig and Dr. Lancaster presented their opinions (in writing and orally) 

thoughtfully. When the undersigned asked Dr. Weig his opinion regarding the 

instructions issued to him for preparing his expert reports, Dr. Weig testified that 

the instructions “helped me organize my – my thoughts, my analysis of the 

records. I didn’t think it was artificial either. I mean, I found it helpful.” Tr. 171. 

On August 21, 2015, the undersigned issued an order for post-hearing briefs. 

While the case was still pending, K.O. filed a motion for attorneys’ fees and costs 

on an interim basis with the Secretary filing a response shortly thereafter. K.O.

filed her post-hearing brief on October 22, 2015. The Secretary submitted her 

post-hearing brief on November 18, 2015, with K.O. filing a reply on December 3, 

2015. K.O. filed an additional motion for interim fees and costs on June 20, 2016. 

The case is now ripe for a decision.

III. Standards for Adjudication

A petitioner is required to establish her case by a preponderance of the

evidence. 42 U.S.C. § 300aa–13(1)(a). The preponderance of the evidence

standard requires a “trier of fact to believe that the existence of a fact is more

probable than its nonexistence before [he] may find in favor of the party who has

the burden to persuade the judge of the fact’s existence.” Moberly v. Sec’y of

Health & Human Servs., 592 F.3d 1315, 1322 n.2 (Fed. Cir. 2010) (citations 

omitted). Proof of medical certainty is not required. Bunting v. Sec’y of Health 

&Human Servs., 931 F.2d 867, 873 (Fed. Cir. 1991).

Distinguishing between “preponderant evidence” and “medical certainty” is

important because a special master should not impose an evidentiary burden that is

too high. Andreu v. Sec’y of Health & Human Servs., 569 F.3d 1367, 1379-80

(Fed. Cir. 2009) (reversing special master’s decision that petitioners were not

entitled to compensation); see also Lampe v. Sec’y of Health & Human Servs., 

219F.3d 1357 (Fed. Cir. 2000); Hodges v. Sec’y of Health & Human Servs., 9 F.3d

958, 961 (Fed. Cir. 1993) (disagreeing with dissenting judge’s contention that the

special master confused preponderance of the evidence with medical certainty).

The elements of K.O.’s case are set forth in the often cited passage from the 

Federal Circuit’s decision in Althen: “(1) a medical theory causally connecting the 

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

the vaccination was the reason for the injury; and (3) a showing of a proximate 

temporal relationship between vaccination and injury.” Althen v. Sec’y of Health 

& Human Servs., 418 F.3d 1274, 1278 (Fed. Cir. 2005).
13 

IV. Analysis

As mentioned in the introduction of this decision, K.O.’s case fails to be 

persuasive with respect to two of the Althen prongs. First, K.O. has not presented 

evidence of sufficient quantity or quality that supports a finding that molecular 

mimicry is a reliable mechanism persuasively explaining how the PCV vaccine can 

cause OMS. This shortcoming is addressed in section A below. 

The second problem with K.O.’s case is that the timing does not fit. Both 

Dr. Weig and Dr. Lancaster opined that an acceptable interval between vaccination 

and the onset of OMS would encompass 42 days. Neither expert offered opinions 

that an onset of more than 42 days would be medically acceptable. As explained in 

section B below, the records created in August and September 2010, are much 

more consistent with a finding that A.F. started to experience OMS 45 days after 

vaccination. 

K.O.’s failure to establish either a persuasive medical theory (Althen prong 

1) or an acceptable temporal relationship (Althen prong three) resolves her case. 

Because either finding is dispositive, the analysis of the remaining Althen prong (a 

logical sequence of cause an effect) is relatively short. See section C. Finally, 

section D considers a potential cause for A.F.’s OMS that is unrelated to the PCV 

vaccine. 

A. Theory

K.O.’s burden is to present “a medical theory causally connecting the 

vaccination and the injury.” Althen, 418 F.3d 1274, 1278. 
14 

1. K.O. must prove causation by a preponderance of the evidence.

To establish the first prong of Althen, K.O. must provide “a reliable medical 

or scientific explanation.” La Londe v. Sec’y of Health & Human Servs., 110 Fed. 

Cl. 184, 201 (2013), aff’d sub nom. LaLonde v. Sec’y of Health & Human Servs., 

746 F.3d 1334, 1339-40 (Fed. Cir. 2014). A special master may require additional 

evidence supporting a theory of molecular mimicry to find that the theory is related 

to the petitioner. W.C. v. Sec’y of Health & Human Servs., 704 F.3d 1352, 1360 

(Fed. Cir. 2013); Hunt v. Sec’y of Health & Human Servs., 123 Fed. Cl. 509, 524-

25 (2015) (special master properly followed W.C. and was not arbitrary in finding 

molecular mimicry not persuasive); Crutchfield v. Sec’y of Health & Human 

Servs., 125 Fed. Cl. 251, 263 (2014) (special master was not arbitrary in finding 

that the petitioner’s expert failed to demonstrate any similarities between the 

vaccine and a relevant part of the body). 

2. Evidence relating to theory

Collectively, the parties’ evidence relating to the proposition that PCV 

vaccines can cause OMS via molecular mimicry falls into five broad categories: 

(a) literature about vaccines and OMS, (b) an article by Pranzatelli, (c) studies on 

homology, (d) an admission by Dr. Lancaster, and (e) an admission by the 

Secretary in other cases.

8

 These topics are explored below.

a. Literature 

 In support of their respective positions, the parties submitted medical articles 

discussing vaccines and disorders of the central nervous system, including OMS. 

The medical articles fall into two groups: an epidemiologic study and four case 

reports. 

Because these articles are part of the record, they must be considered. 42 

U.S.C. § 300aa−13(a); Moriarty, 2016 WL 1358616 at *9-10. An assessment of 

these articles is consistent with Terran’s endorsement of the flexible Daubert test, 

which authorizes special masters to consider, among other factors, whether an 

 8 Some of this evidence originated with the Secretary because the Secretary “is permitted 

to offer evidence to demonstrate the inadequacy of the petitioner's evidence on a requisite 

element of the petitioner's case-in-chief.” Bazan v. Sec’y of Health & Human Servs., 539 F.3d 

1347, 1353 (Fed. Cir. 2008). 
15 

expert’s opinion appears in peer review literature and whether the opinion has been 

tested. Terran v. Sec’y of Health & Human Servs., 195 F.3d 1302, 1316 (Fed. Cir. 

1999), citing Daubert v. Merrell Dow Pharmaceuticals, 509 U.S. 579, 593-94 

(1993). 

In weighing the relative value of the articles, the undersigned follows the 

guidance of the Federal Judicial Center. The Federal Judicial Center has published 

a series of guides designed “to assist judges ... in reaching an informed and 

reasoned assessment concerning the basis of expert evidence.” Jerome P. Kassirer 

and Gladys Kessler, Reference Manual on Scientific Evidence, Preface, (3d ed. 

2011). The guidance from the Federal Judicial Center translates to the Vaccine 

Program because the burden of proof in an off-Table case, like K.O.’s case, is “the 

traditional tort standard.” Moberly, 592 F.3d at 1322.

1) Epidemiology

According to the Federal Judicial Center, “[e]pidemiologic studies have 

been well received by courts deciding cases involving toxic substances.” Michael 

D. Green et al., Reference Manual on Scientific Evidence, Reference Guide on 

Epidemiology, 549 n.2 (3d ed. 2011) (citing cases). “Epidemiologic evidence 

identifies agents that are associated with an increased risk of disease in groups of 

individuals, quantifies the amount of excess disease that is associated with an 

agent, and provides a profile of the type of individual who is likely to contract a 

disease after being exposed to an agent.” Id. at 552. The authors of this guide 

from the Federal Judicial Center emphasize that “an association is not equivalent to 

causation.” Id. “In evaluating epidemiologic evidence, the key questions, then, are 

the extent to which a study’s limitations compromise its findings and permit 

inferences about causation.” Id. at 553. 

Consistent with the instruction from the Federal Judicial Center, the Federal 

Circuit has long endorsed special masters’ consideration of epidemiologic 

evidence. W.C., 704 F.3d at 1361; Grant v. Sec’y of Health & Human Servs., 956 

F.2d 1144, 1149 (Fed. Cir. 1992) (“epidemiological studies are probative evidence 

relevant to causation”). However, special masters may not go so far as to require 

petitioners in off-Table cases to present epidemiologic evidence to establish that a 
16 

particular vaccine can cause a particular injury. Capizzano v. Sec’y of Health & 

Human Servs., 440 F.3d 1317, 1325 (Fed. Cir. 2006).9 

Here, the record contains one epidemiologic study. Exhibit K (Hung Fu 

Tseng et al., Postlicensure surveillance for pre-specified adverse events following 

the 13-valent pneumococcal vaccine in children, 31 Vaccine 2578 (2013)). The 

researchers relied upon information held in the Vaccine Safety Datalink.10 The 

authors compared the number of adverse events following approximately 600,000 

doses of the PCV-13 vaccine with the number of adverse events following 

administration of PCV-7. After reviewing medical records, the researchers found 

that PCV-13 was not associated with an increased risk of encephalopathy. Id. at 

2580. 

In their reports, first Dr. Lancaster and then Dr. Weig commented on the 

Tseng study.11 Based on Tseng, Dr. Lancaster concluded that the “medical 

literature therefore does not support any association between PCV13 and OMS.” 

Exhibit A at 10. Dr. Weig challenged Dr. Lancaster’s reliance on the Tseng study. 

Dr. Weig’s starting points were that the incidence of OMS is approximately one 

case per five million children and that the non-neuroblastoma incidence is 

approximately one case per ten million children. From here, Dr. Weig argued: “In 

a sample size of 500,000, we would only expect to see .1 child (1/10 of a child) 

with OMS. Given the incredibly low incidence rate of OMS, the sample size of 

[the] Tseng study is underpowered to detect even one incidence of OMS.” Exhibit 

20 at 2. 

 9 If a petitioner presented reliable epidemiologic evidence that a vaccine is associated 

with a statistically significant increased risk of developing a disease, the Secretary would likely 

agree to resolve the case. See National Injury Compensation Program: Revisions to the Vaccine 

Injury Table, 80 Fed. Reg. 45132-01 (proposed July 29, 2015) (to be codified at 42 C.F.R. 

§ 100.3) (discussing epidemiological studies supporting modifications to the list of injuries 

presumptively caused by vaccines).

10 For more information regarding the Vaccine Safety Datalink, see Parsley v. Sec’y of 

Health & Human Servs., No. 08-781V, 2011 WL 2463539, at *10 n.33 (Fed. Cl. Spec. Mstr. 

May 27, 2011); Werderitsh v. Secʼy of Health & Human Servs., No. 99-319V, 2005 WL 

3320041 (Fed. Cl. Spec. Mstr. Nov. 10, 2005) (denying motion for production of documents). 

11 Dr. Weig has no training or experience in epidemiology. Tr. 12. Dr. Lancaster has 

taken one course on epidemiology and biostatistics while obtaining his medical degree. Tr. 103. 
17 

At hearing, Dr. Lancaster changed his position. He stated “Dr. Weig has a 

good point, that the disease is very rare, which makes it very hard to fully power to 

detect it.” Tr. 133-34. Nevertheless, without citing any authority, the Secretary 

argued that the Tseng study remains “evidence to be considered.” Resp’t’s Posth’g 

Br. at 11 n.3. In contrast, K.O. contended that the only value of the Tseng study is 

to call into question Dr. Lancaster’s credibility. Pet’r’s Resp. at 8-9. 

It is important to remember that K.O. has the burden to show that the PCV 

vaccine can cause OMS. Pafford v. Sec’y of Health & Human Servs., 451 F.3d 

1352, 1355 (Fed. Cir. 2006). In finding no increased risk of OMS after PCV-13, 

the Tseng study does not help K.O. meet her burden. Whether the Tseng study 

would be a reliable basis for an opinion that PCV vaccinations cannot cause OMS 

is another question and a question that is not germane to this case’s outcome. The 

Secretary does not bear the burden of establishing that it is impossible for PCV 

vaccinations to cause OMS.

2) Case Reports

Unlike Tseng, which the Secretary’s expert introduced, K.O. relied upon a 

set of four case reports. See Pet’r’s Preh’g Br. at 14, 20; Pet’r’s Posth’g Br. at 25-

28; Pet’r’s Resp. at 9-10. In her view, “case reports . . . supplement and bolster her 

other evidence of causation.” Pet’r’s Resp. at 10. 

Again, the undersigned follows the lead of the Federal Judicial Center. A 

pertinent guide states “[a]necdotal evidence usually amounts to reports that events 

of one kind are followed by events of another kind. Typically, the reports are not 

even sufficient to show association, because there is no comparison group.” David 

H. Kaye and David A. Freedman, Reference Manual on Scientific Evidence, 

Reference Guide on Statistics, at 218. These authors also state “some courts have 

suggested that attempts to infer causation from anecdotal reports are inadmissible 

as unsound methodology under Daubert.” Id. at 217 n. 14 (citing cases).

The only Federal Circuit case to discuss the value of case reports in the 

Vaccine Program found no error in a special master’s giving the case reports little 

weight. In a series of five cases involving auto-immune hepatitis, the undersigned 

special master rejected case reports as evidence of causation. Porter v. Sec’y of 

Health & Human Servs., No. 99–639, 2008 WL 4483740, at *13 (Fed. Cl. Spec. 

Mstr. Oct. 2, 2008). Under the caption of a different case, a judge at the Court of 

Federal Claims disagreed with this weighing of evidence. Rotoli v. Sec’y of 

Health & Human Servs., 89 Fed. Cl. 71, 86-87 (2009).
18 

When the Federal Circuit reviewed the special master’s decision, the Federal 

Circuit stated that “[t]he special master found that the remaining two articles, both 

describing single case studies, did not contain any meaningful analysis about 

causation.” Porter v. Sec’y of Health & Human Servs., 663 F.3d 1242, 1253 (Fed. 

Cir. 2012). The Federal Circuit also stated that the “decision reveals a thorough 

and careful evaluation of all the evidence including ... medical literature.” Id. at 

1254. Admittedly, the discourse on case reports in Porter is indirect and there may 

come a time when the Federal Circuit addresses the evidentiary value of case 

reports in the Vaccine Program more directly. Until that future Federal Circuit 

case, the undersigned relies upon Porter, which endorsed a view that single case 

studies did not contain any meaningful analysis of causation. 

It is interesting to juxtapose case reports with epidemiologic studies. Case 

reports are generally seen as holding less evidentiary value than epidemiologic 

studies. Campbell v. Sec’y of Health & Human Servs., 97 Fed. Cl. 660, 668 

(2011).12 Here, what is more useful — an observational study involving more than 

a half million people or a handful of anecdotes? As discussed above, K.O. and Dr. 

Weig present an insightful criticism of the Tseng study: it was not sufficiently 

powered to detect increases in OMS. Yet, with regard to the case reports, K.O. and 

Dr. Weig have not presented any persuasive argument why the case reports rise 

even to the level of circumstantial indicia of causation. Tr. 44-45; exhibit 18. As 

the Court of Appeals for the Eleventh Circuit stated, case reports “do not offer the 

underlying toxicological data in a scientifically reliable form to satisfy Daubert.” 

McClain v. Metabolife Int’l, Inc., 401 F.3d 1233, 1253-54 (11th Cir. 2005). 

The foregoing assessment describes the limited value of case reports 

generally. Here, the case reports K.O. and Dr. Weig identify have even less value 

because they report a sequence in which a vaccine, but not a vaccine against 

pneumococcus, precede the onset of OMS. Exhibit 18, tab B (Kinsbourne); 

Exhibit 18, tab L (Nicholas Christoff, Myoclonic encephalopathy of infants: A 

report of two cases and observations on related disorders, 21 Arch Neurol. 229 

(1969)); Exhibit 18, tab N (James McCarthy & James Filiano, Opsoclonus 

myoclonus after human papilloma virus vaccine in a pediatric patient, 15 

Parkinsonism and Related Disorders 792 (2009)); Exhibit 18, tab M (F. Lapenna et 

 12 Although Campbell recognized that case reports have less value, Campbell continued: 

“Nevertheless, the fact that case reports can by their nature only present indicia of causation does 

not deprive them of all evidentiary weight. See, e.g., Rotoli, 89 Fed. Cl. 86-87.” After Campbell

was issued, the Federal Circuit reversed Rotoli. Porter, 663 F.3d at 1245. 
19 

al., Post-vaccinic opsoclonus- myoclonus syndrome: a case report, 6 Parkinsonism 

and Related Disorders 241 (2000)).

An expert may “extrapolate from existing data,” Snyder v. Sec’y of Health 

& Human Servs., 88 Fed. Cl. 706, 743 (2009), and use “circumstantial evidence,” 

Althen, 418 F.3d at 1280. But, the reasons for the extrapolation should be 

transparent and persuasive. Here, Dr. Weig did not offer any persuasive reasons 

for extrapolating from the rubella vaccine, HPV vaccine, DTP vaccine, and polio 

vaccine, to the PCV vaccine. 

After considering the case reports, the testimony about the case reports, and 

the briefs containing arguments about the case reports, the undersigned chooses to 

give the four case reports negligible weight. See Whitecotton v. Sec’y of Health & 

Human Servs., 81 F.3d 1099, 1108 (Fed. Cir. 1996) (“Congress desired the special 

masters to have very wide discretion with respect to the evidence they would 

consider and the weight to be assigned that evidence”). They are not a reliable 

basis for finding causation. Consequently, the evidence relating to the reliability of 

the theory of molecular mimicry will be explored in detail. The following three 

sections (the Pranzatelli article, homology, and Dr. Lancaster’s admission) concern 

molecular mimicry. 

b. Pranzatelli article

Dr. Michael Pranzatelli is considered one of the leading researchers for 

OMS. Tr. 24. When Dr. Weig was asked to identify the articles that most strongly 

supported his opinion regarding molecular mimicry, Dr. Weig cited a review 

article that Dr. Pranzatelli wrote in 1996. Tr. 53, citing exhibit 18, tab G (Michael 

R. Pranzatelli, The immunopharmacology of the opsoclonus-myoclonus syndrome, 

19 Clin. Neuropharmacology 1 (1996)). 

In that lengthy article, Dr. Pranzatelli proposes molecular mimicry as one 

among several possible etiologic theories. Exhibit 18, tab G at 21-22. In this 

context, Dr. Pranzatelli states that “Cross-reactivity between neural crest-derived 

tumors and brain antigens...in paraneoplastic cases is also very plausible, given 

their shared embryology.” Id. at 22.13 Dr. Pranzatelli returns to molecular 

mimicry in his conclusion. “A peripheral induction mechanism involving 

 13 K.O. frequently cited these pages of the Pranzatelli article. Pet’r’s Preh’g Br., filed 

July 9, 2015, at 12, 19; Pet’r’s Posth’g Br. at 19; Pet’r’s Posth’g Resp. at 8; see also Tr. 25. 
20 

molecular mimicry or one of several other possible mechanisms leads to immune 

system dysregulation, which transiently allows otherwise for hidden 

autoaggression against cross-reactive brain antigens. Although immunizations are 

logical candidates for costimulation in peripheral induction in children, if there is 

an adult counterpart, it is unknown.” Id. at 36. Dr. Weig interpreted this passage 

as indicating that Dr. Pranzatelli was “certainly... open to the idea of immunization 

as a potential initiating factor in children.” Tr. 26.

Dr. Weig’s assessment that Dr. Pranzatelli was “open” to the idea that 

immunizations may contribute to the onset of OMS appears accurate. Dr. 

Pranzatelli also discussed vaccinations in another part of his long article. Dr. 

Pranzatelli’s list of environmental factors that are “likely to be very important in 

OMS” includes viruses, bacteria, and immunizations. Yet, Dr. Pranzatelli 

recognized that “Assessment of the potential effects of immunization on the onset 

of OMS is not simple.” Id. at 18-19. Dr. Weig understood Dr. Pranzatelli as 

wanting to avoid the logical pitfall known as “post hoc ergo propter hoc.” In other 

words, it is wrong to conclude that because a second event occurs after a first 

event, the first event caused the second event. Tr. 60. In his article, Dr. Pranzatelli 

recommended an epidemiologic study. Exhibit 18, tab G at 19. 

At hearing, K.O. referenced Dr. Pranzatelli’s statement that a reaction to a 

tumor and virus producing OMS “presented both a puzzle and a clue.” Dr. Weig 

explained that the puzzle is determining what a virus or bacterium have in common 

with a form of cancer. The clue would be that the body responds to fight a tumor 

in the same manner it responds to fight a virus or bacterium. Tr. 57-58. 

Dr. Pranzatelli made this statement as part of his thesis for his research into 

the mechanism of action of current therapy. Exhibit 18, tab G at 2. Dr. Pranzatelli 

ultimately stated that the virus was not directly encephalogenic in OMS cases 

associated with viral infection. Id. at 4. Specifically on vaccinations, he states that 

molecular mimicry is a “possible mechanism.” Id. at 21, 36.

In the Secretary’s post-hearing brief, she challenged K.O.’s reliance on the 

Pranzatelli article in several respects. First, the Secretary observes that Dr. 

Pranzatelli did not state “that vaccines in general (let alone the PCV vaccine 

specifically) can cause OMS” via molecular mimicry. Second, Dr. Weig’s 

conclusion that Dr. Pranzatelli was “open” to vaccines as a causative factor “is 

insufficient for petitioner to meet her burden.” Third, the Secretary argues that the 

lack of validation of molecular mimicry outside the context of a neuroblastoma in 

the 20 years since Dr. Pranzatelli wrote the article is “telling.” Resp’t’s Posth’g 
21 

Br., filed Nov. 18, 2015, at 12. K.O.’s reply brief did not answer these specific 

criticisms of the Pranzatelli article. 

Whether developments in the last two decades have supported the proposal 

that vaccines can cause OMS via molecular mimicry is considered next.

c. Homology

A premise for molecular mimicry is that a particular antigen (say, a vaccine) 

shares that molecular structure with some part of the human body such that the 

immune system’s attack on the antigen is misdirected to the host’s own tissue. 

Exhibit 18, tab G (Pranzatelli) at 21. The medical term for similarity in structure is 

homology. Dorland’s at 868. 

The degree of homology between two proteins can be determined using a 

method known as blast sequencing according to an article Dr. Weig submitted. 

Exhibit 18, tab H (Paul M. Candler et al., Post-streptococcal opsoclonusmyoclonus syndrome associated with anti-neuroleukin antibodies, J. Neurol. 

Neurosurgery Psychiatry 507 (2006)) at 509; see also Wirt v. Secʼy of Health & 

Human Servs., No. 11-118V, 2014 WL 1911421, *8 (Fed. Cl. Spec. Mstr. April 

18, 2014). The article cites to a website maintained by the National Institutes of 

Health. 

The Secretary’s expert, Dr. Lancaster, explained the experiment the Candler 

group conducted. Dr. Lancaster also criticized the experiment in certain respects, 

but these perceived flaws are not particularly important to the outcome of K.O.’s 

case. Tr. 118-22. More significantly, K.O.’s expert, Dr. Weig, struggled to 

explain the Candler experiment. Tr. 53-55. When asked to explain what a blast 

sequence is and whether it could be used on the pneumococcal vaccine, Dr. Weig 

said that he did not have the background to answer those questions. Tr. 55-56.

On cross-examination, Dr. Weig was asked whether he was aware of any 

homology between the PCV vaccine and brain cells. Dr. Weig stated that he did 

not know. Dr. Weig was also asked whether he knew of any homology between 

the pneumococcal bacteria (the target of the PCV vaccine) and brain cells, Dr. 

Weig again stated that he did not know. Tr. 85. Dr. Weig’s lack of knowledge 

creates a considerable gap in K.O.’s case. 

Special masters may consider whether the expert’s opinion can be and has 

been tested. Terran, 195 F.3d at 1316, citing Daubert, 509 U.S. at 593-94. Here, 

Dr. Weig is assuming that there is homology between the PCV vaccine and brain 
22 

tissue. However, Dr. Weig lacks a background to determine the accuracy of his 

assumption. This lack of testing constitutes a reason for finding Dr. Weig 

unpersuasive. See Caves v. Sec’y of Health & Human Servs., 100 Fed. Cl. 119, 

135 (2011) (“Without any empirical evidence that the theory [of molecular 

mimicry] actually applies to the influenza vaccine and [transverse myelitis], the 

first prong of Althen would be rendered meaningless”), aff’d without opinion, 463 

F. App’x 932 (Fed. Cir. 2012).

d. Admission by Dr. Lancaster

K.O. argued that a showing of homology between the PCV vaccine and 

brain tissue is not needed because Dr. Lancaster has accepted molecular mimicry 

as a theory to explain how neuroblastomas can lead to OMS. Pet’r’s Posth’g Br., 

filed Oct. 22, 2015, at 20; Pet’r’s Posth’g Resp., filed Dec. 3, 2015, at 7. To 

review, a neuroblastoma is a tumor of embryonic cells that develop into a nerve 

cell or neuron. See Dorland’s at 1263 (defining neuroblast and neuroblastoma), 

1668 (defining sarcoma). Neuroblastomas are found in approximately 50 percent 

of OMS cases.

The frequency of cases in which neuroblastomas precede OMS has led to a 

conclusion that neuroblastomas cause OMS. How neuroblastomas cause OMS has 

not been elucidated. Tr. 42-44, 112. Dr. Pranzatelli’s 1996 article proposes that: 

“While the initial immune response is appropriately directed to eradicating virus or 

tumor, the immune response becomes secondarily pathological.” Exhibit 18, tab G 

at 21. Dr. Pranzatelli, as discussed above, suggested molecular mimicry as one 

theory to explain the harmful response of the immune system.

Dr. Lancaster stated, “in the case of patients with neuroblastoma, [I think] 

that molecular mimicry is – is close to the correct concept.” Tr. 116. Later, Dr. 

Lancaster clarified that molecular mimicry in cases with a neuroblastoma is “not 

yet firmly established because we don’t have the specific antigen.” Tr. 135.

While Dr. Lancaster accepted molecular mimicry as a “highly likely” link 

between neuroblastomas and OMS, Dr. Lancaster distinguished viruses as a 

potential source of cross-reactivity. “Given how very different viruses are from 

human beings, it would be unusual for some component of the virus to very closely 

resemble some component of the brain.” Tr. 117. Dr. Lancaster’s opinion was 

that viruses might cause OMS through some process other than molecular 

mimicry. Tr. 117-18, 135.
23 

K.O. charges Dr. Lancaster with being inconsistent in two respects. First, 

K.O. argues that Dr. Pranzatelli proposed molecular mimicry as a theory by which 

neuroblastomas (tumors) and infections could lead to OMS. Pet’r’s Posth’g Br. at 

20; Pet’r’s Posth’g Resp. at 7. In this respect, K.O. is only partially correct. It is 

true that Dr. Pranzatelli suggested molecular mimicry for tumors as well as 

infections. Exhibit 18, tab G at 21. However, molecular mimicry is not the only 

theory that Dr. Pranzatelli proposed. Id. at 16 (“Response to Viruses”), 19-22. 

Thus, Dr. Pranzatelli’s article can accommodate molecular mimicry for 

neuroblastomas and some other theory for infectious agents. 

Second, K.O. argues that Dr. Lancaster is being inconsistent because science

has not found the pathway for either neuroblastomas or infections. Under K.O.’s 

logic, because the lack of knowledge about the target antigen does not prevent Dr. 

Lancaster from accepting molecular mimicry as a method to explain the connection 

between neuroblastomas and OMS, this same lack of knowledge should not 

prevent Dr. Lancaster from accepting molecular mimicry as a method to connect 

infections and OMS. Pet’r’s Preh’g Br. at 22; Pet’r’s Posth’g Resp. at 7.

Here, too, K.O.’s argument misses its mark. Because neuroblastomas are 

essentially malignant nerve cells, it is easy to see how the immune system’s 

response to neuroblastomas could be misdirected against other nerve cells, such as 

those found in the brain. See Tr. 51 (Dr. Weig). That step is relatively short. In 

contrast, the PCV vaccine does not contain nerve cells. Thus, an attempt to join 

the PCV vaccine and brain cells affected in OMS requires a much longer jump.14 

In short, K.O. is not persuasive in arguing that because molecular mimicry 

may be valid in some situations not involving vaccines, molecular mimicry also 

should be accepted as a reliable theory in a situation involving vaccines.

 14 K.O. could have shortened the gap between the PCV vaccine and brain cells by 

presenting evidence that they are homologous. However, as discussed above, K.O. did not 

narrow the gap. 
24 

e. Admission by the Secretary

Finally, K.O. argues that her theory is reliable because the Secretary has 

agreed to settle other cases involving OMS. Pet’r’s Resp. at 3-4. Procedurally, the 

argument was raised too late. K.O. could have offered this same argument in 

either her pre-hearing brief or her initial post-hearing brief. But, she did not. Nonjurisdictional arguments that are raised for the first time in a reply brief are 

typically considered waived. See Demodulation, Inc. v. United States, 103 Fed. 

Cl. 794, 808 (2012). As attorneys experienced in the Vaccine Program, K.O.’s 

counsel should have known that raising an argument this late is improper. 

More significantly, settlements are not considered admissions that can be 

used to establish a fact based upon a settlement. See Woods v. Sec’y of Health & 

Human Servs., 105 Fed. Cl. 148, (2012) (settlement of cases cannot equate to the 

finding of reasonable basis); R.V. and E.V. v. Secʼy of Health & Human Servs., 

No. 08-504V, 2015 WL 1396357 (Fed. Cl. Spec. Mstr. March 6, 2015) (rejecting 

argument that the Secretary was judicially estopped from litigating an argument 

based upon a settlement of another case), mot. for rev. denied, 127 Fed. Cl. 136 

(2016). Thus, the resolution of other cases involving OMS does not meaningfully 

change the analysis of the evidence K.O. and the Secretary presented in this case.

f. Synopsis

Through Dr. Weig, K.O. has presented a theory to explain how the PCV 

vaccine can cause OMS. However, K.O. has not presented a reliable basis for 

finding this theory persuasive. Consequently, K.O. has not established her burden 

of proof regarding Althen prong one.

B. Timing

K.O. must establish a “proximate temporal relationship” between the PCV 

vaccination and the onset of A.F.’s opsoclonus myoclonus. Bazan, 539 F.3d at 

1352. This formulation implies that the third prong from Althen actually contains 

two parts. First, there must be a showing that a range of time is “acceptable” to 

infer causation. Second, there must be a showing that the vaccinee’s disease arose 

in this acceptable time. Shapiro v. Sec’y of Health & Human Servs., 101 Fed. Cl. 

532, 542-43 (2011), recons. denied after remand on other grounds, 105 Fed. Cl. 

353 (2012), aff’d per curiam, 503 F. App’x 952 (Fed. Cir. 2013).
25 

1. Medically Acceptable Interval

The first part of the third prong of Althen requires K.O. to show a time 

which is “medically acceptable” for an injury to appear after a vaccination, 

assuming that the vaccination caused the injury. Bazan 539 F.3d at 1352. 

Here, the parties generally agree that an interval from which inferring 

causation is acceptable is from one to six weeks. Dr. Weig provided this estimate 

in his report, exhibit 18 at 7, and based his estimate on a 1994 report from the 

Institute of Medicine (“IOM”) that considered whether vaccines against tetanus, 

diphtheria, and pertussis could cause demyelinating diseases. When asked during 

the hearing if he could explain the 42 day limit, Dr. Weig stated: “I don’t know. 

It’s just there.” Tr. 65. 

Dr. Lancaster also relied upon the 1994 IOM report but stated that the IOM 

report states that onset is more likely to occur within seven to 21 days of 

vaccination. Tr. 137-38; exhibit A at 12. Thus, Dr. Lancaster explained that while 

the IOM provides 42 days within the range for onset, it is the upper limit of 

plausibility. Tr. 140. 

Based upon entire record, the undersigned finds that an acceptable interval 

extends to 42 days. The record does not contain any persuasive basis for extending 

this period past 42 days. As Dr. Lancaster explained, the IOM found that vaccines 

might produce a demyelinating disease within seven to 21 days. The IOM, then, 

further extended the 21 days to 42 days to account for any outliers. Tr. 140; 

exhibit Q (Institute of Medicine, Adverse Events of Vaccines Evidence and 

Causality (Kathleen Stratton et al. eds. (2011))) at 535; exhibit P (Institute of 

Medicine, Adverse Events of Vaccines Evidence and Causality (Kathleen Stratton 

et al. eds. (1994))) at 26. 

Therefore, to establish the third prong of Althen, K.O. must establish that 

A.F.’s OMS developed within 42 days of his PCV 13 vaccination.15

 15 Although a finding of 42 days (and not 43) may appear arbitrary, the persuasive 

evidence does not go further than 42 days. “At the margins of any judgment call, reasonable 

minds may differ as to the judgment reached. Such is the natural consequence of regulatory linedrawing, much as the natural consequence of judicial line-drawing will permit of marginal 

dispute. But that is not to say that the line-drawing exercise lacks reason or is arbitrary.” Haggar 

Apparel Co. v. United States, 222 F.3d 1337, 1342 (Fed. Cir. 2000). 
26 

2. Onset of OMS

Unlike the agreeing opinions that an acceptable interval was up to 42 days, 

the parties have considerable dispute about when A.F. first began to manifest 

problems of his OMS. As previously discussed, the onset of OMS is sometimes 

marked by the presentation of prodromal symptoms such as irritability, behavioral 

disturbances, and ataxia. K.O. asserts that the prodromal symptoms were present 

on August 25, 2010 (42 days after vaccination). The Secretary disagrees and 

proposes August 28, 2010, as the onset date (45 days after vaccination).

16 

Dr. Weig first opined an onset date as far back as August 20, 2010. Exhibit 

18 at 7. When asked how he determined this date, he answered “Well, not directly 

in the medical record. That was working backwards from...K.O.’s report of late 

August and then knowing, in my mind, that the symptoms began on the -- you 

know, the first mention we have in there is August 25th, that I thought it was 

probably started a few days earlier.” Tr. 73. Dr. Weig agreed that the medical 

records did not support this onset date. Id. K.O. recalled that in “late August 

2010” A.F. experienced difficulty sleeping and sensitivity to light. Exhibit 13 ¶ 3. 

She stated on August 25, 2010, A.F. was constipated but this improved with after 

giving him prune juice. Id. at ¶4. 

In the absence of a reliable foundation for his opinion that A.F. started to 

experience OMS on August 20, 2010, Dr. Weig came up with another date. He 

proposed August 25, 2010. Tr. 19-20. The medical records show A.F. was 

irritable and constipated. Exhibit 4 at 8-9, 12-13, 15; see also Tr. 18. Dr. Weig 

agreed that A.F. was constipated, but contended that the degree of irritability 

described made it prodromal. Tr. 39-40. K.O. did not address the constipation 

otherwise.

 In K.O.’s post-hearing brief, she asserts that determining the onset of OMS 

in children of A.F.’s age is difficult. For this argument, she relies on her expert, 

Dr. Weig, who stated that behavioral issues, which can be prodromal symptoms of 

OMS, are more difficult to assess in a child one-year to two-years old. Pet’r’s 

Posth’g Br. at 16; Tr. 17. Dr. Weig states that while “exact timing of onset of 

symptomatology is frequently quite difficult to ascertain with absolute precision,” 

the sleep disturbances and irritability that A.F. experienced made it “evident that 

 16 This difference of three days is significant because it changes the onset from 42 to 45 

days, which then falls outside of the accepted range as established by the IOM report.
27 

by 8/25/2010” these were symptoms consistent with the onset of OMS. Exhibit 18 

at 7. 

The Secretary’s expert, Dr. Lancaster, stated that A.F. was experiencing 

constipation based on the totality of the medical records on August 25, 2010. He 

stated that K.O. reported several times in the record that the symptoms of 

irritability subsided once A.F. passed a hard stool. Tr. 107-08. The resolution of 

A.F.’s irritability after he moved his bowels suggested that constipation was 

causing the irritability. If a brain-based neurologic disorder had been causing 

A.F.’s irritability, then the irritability would have continued after the bowel 

movement. Thus, August 25, 2010 is not the date of onset of A.F.’s OMS. 

Here, the persuasive evidence indicates that the onset of A.F.’s OMS was on 

August 28, 2010. Dr. Lancaster provided an onset date of August 28 based on the 

medical records. Exhibit A at 13; Tr. 150. Several medical records point to an 

onset of August 28, 2010. These include: exhibit 6 at 282-86 (Dr. Shrivastava’s 

notes on August 29, 2010, stating “Mom noted his coordination seemed to be off a 

little yesterday.”); exhibit 6 at 286-89 (Dr. Coulter’s notes on August 29, 2010, 

stating “[A.F.]...presents today with a one day [history] of ‘wobbliness and 

floppiness’... Of note: five days prior to presentation, when he was ‘constipated’ 

with mom noting that he had increased straining, and needed prunes to pass a hard 

stool.”); exhibit 6 at 290-91 (Dr. Viccari’s notes on August 29, 2010, stating “The 

patient is a 13-month-old male crying inconsolably on and off since yesterday. 

History of being constipated.”); exhibit 5 at 25 (Dr. Reiner’s notes on August 30, 

2010, stating “Unsteady, different sense of balance, past 2 days.”); exhibit 5 at 26-

7 (Dr. Saillant’s notes on August 31, 2010, stating “3 days ago was irritable and 

had some constipation and thought to have imbalance/dizziness.”); exhibit 6 at 

279-80 (Dr. Coulter’s notes on September 1, 2010, stating “When I saw [A.F.] on 

September 1st, his parents again noted that [A.F.] had been pretty normal on 

Friday, August 27th, and in fact had seen the eye doctor that day and had a normal 

examination.”); exhibit 8 at 4 (phone call from A.F.’s father to Bennet Family Eye 

care stating “since after appt [A.F.’s] leg’s wobbly, trouble sitting more clumsy”).

This abundant evidence, which K.O. did not address in her reply brief, 

supports a finding that the onset of OMS was August 28, 2010. This finding 

means that 45 days elapsed after the vaccination. Because K.O. offered no basis 

for extending the accepted interval past 42 days (see Pet’r’s Posth’g Br. at 37), the 

timing for A.F. does not work. See Bazan, 539 F.3d 1352 (a petitioner fails to 

satisfy the third prong of Althen when too much time elapses between vaccination 

and onset). 
28 

C. Logical Sequence of Cause and Effect

The remaining prong from Althen is “a logical sequence of cause and effect 

showing that the vaccination was the reason for the injury.” Althen, 418 F.3d at 

1278. Evidence particularly relevant to this inquiry is the view of any treating 

doctor. Capizzano, 440 F.3d at 1326. 

Here, the parties rely upon different views expressed by two doctors. K.O.

cites pediatric neuro-ophthalmologist Gena Heidary’s June 2, 2011 report. Pet’r’s 

Posth’g Br. at 32-33. Dr. Heidary wrote: while the etiology was unclear, “there is 

a question of a reaction to the pneumococcal vaccine number 13 as this was the 

only thing that antedated the onset of his symptoms.” Exhibit 6 at 143. 

The Secretary, in contrast, mentions the November 5, 2010 report of 

pediatric neuro-immunologist Mark Gorman. Dr. Gorman’s early history showed 

that he was aware of A.F.’s receipt of the PCV vaccine. Exhibit 6 at 247. Yet, on 

November 5, 2010, Dr. Gorman described A.F.’s OMS as “idiopathic,” meaning 

Dr. Gorman did not know the cause of the OMS. Exhibit 6 at 201-02. 

Dr. Heidary’s report does not assist K.O. in any significant way. Dr. 

Heidary received a history that A.F. had received that PCV vaccination three 

weeks prior to symptom development. Exhibit 6 at 143. But, this history is 

erroneous. The actual interval between vaccination and onset was longer than Dr. 

Heidary understood. When a treating doctor receives an inaccurate history, the 

special master is not required to defer to that doctor’s opinion regarding causation. 

Dobrydnev v. Sec’y of Health & Human Servs., 566 F. App’x 976, 992-83, reh’g 

denied, (Fed. Cir. 2014), cert. denied, 135 S. Ct. 1560, 191 L. Ed. 2d 639 (2015). 

Moreover, Dr. Heidary’s actual words are “there is a question of a reaction.” 

This wording does not indicate that Dr. Heidary believes, on a more-likely-thannot basis, that the vaccination caused A.F.’s OMS. See Paterek v. Sec’y of Health 

& Human Servs., 527 F. App’x 875 (Fed. Cir. 2013) (indicating that a treating 

doctor’s statement that vaccine-causation was “not impossible” does not establish 

causation). 

In addition to the problems with Dr. Heidary’s report, other evidence 

suggests that there is not a logical sequence between A.F.’s vaccination and his 

OMS. As discussed above, K.O. has not presented a reliable basis for crediting the 

theory that PCV vaccine can cause OMS. As a matter of logic, if there is no 

showing that the vaccine can cause an injury, there cannot be a basis for finding 

the vaccine did cause the injury. Similarly, K.O. has not established an acceptable
29 

temporal relationship. Again, as a matter of logic, if the injury occurs outside of 

the time expected, then a finding of causation would not be logical. 

D. Alternate Causes

Finally, some precedent suggests that special masters, in considering 

whether petitioners have met their burden regarding prong two, should consider 

whether petitioners have ruled out any other potential causes for the injury. See

Doe 11 v. Sec’y of Health & Human Servs., 601 F.3d 1349, 1358 (Fed. Cir. 2010); 

Contreras v. Sec’y of Health & Human Servs., 107 Fed. Cl. 280, 296 (2012), mot. 

for rev. granted after remand, 116 Fed. Cl. 472 (2014), mot. for rev. denied after 

third remand, 121 Fed. Cl. 230 (2015), appeal docketed, No. 15-5097 (Fed. Cir. 

June 15, 2015). 

Here, Dr. Lancaster proposed that A.F.’s OMS was “idiopathic.” Exhibit A 

at 13; Tr. 156. Alternatively, between the two factors that were considered as 

possible causes (the furuncle and the vaccination), Dr. Lancaster ranked the 

furuncle as more likely than the vaccination. In Dr. Lancaster’s opinion, the 

furuncle was a stronger candidate than the vaccination (but still less likely than an 

unknown cause) because A.F. experienced the furuncle in closer temporal 

proximity than the vaccination. Tr. 147. 

K.O.’s brief addresses only the Secretary’s contention that the most likely 

cause of A.F.’s OMS was an unknown cause. K.O. makes a creditable argument 

that assuming she has met her burden of proof regarding the three Althen prongs, 

the Secretary cannot rely upon an idiopathic cause to defeat the claim for 

compensation. Pet’r’s Posth’g Br. at 42-43, citing Knudsen v. Sec’y of Health & 

Human Servs., 35 F.3d 543, 547-48 (Fed. Cir. 1994). However, the predicate of 

this argument — that K.O. established the three Althen prongs with preponderant 

evidence — is not correct for the reasons explained above. Therefore, the burden 

of proof did not shift to the Secretary. LaLonde, 746 F.3d at 1340. 

To the extent that the presence of potential alternative causes bears on the 

petitioner’s burden regarding Althen prong two, K.O. errs when she states 

“respondent has offered no evidence of an alternative cause leading to the onset of 

A.F.’s OMS.” Pet’r’s Reply at 19 (emphasis in original). As just mentioned, Dr. 

Lancaster proposed that the furuncle was a more likely cause than the vaccination. 

Thus, it is not correct to say the Secretary has “no evidence.” Similarly, K.O.

argues “Respondent’s ‘ranking’ of the potential causes from most likely to least 

likely as 1) idiopathic, 2) skin infection and 3) PCV vaccine is baseless.” Pet’r’s 
30 

Reply at 20. The Secretary’s argument is not “baseless” because it is based on Dr. 

Lancaster’s opinion. 

For the furuncle, K.O. essentially places all her eggs in one basket — an 

argument that because Dr. Lancaster could not say that the furuncle was the likely 

cause of the injury, his opinion is “wholly irrelevant.” Pet’r’s Reply at 20. 

However, K.O. has not cited any precedent that the Secretary must establish an 

alternative cause as more likely than not before a petitioner must address the 

proposed alternative cause.17 The case law seems to be heading in the opposite 

direction. See Stone v. Sec’y of Health & Human Servs., 676 F.3d 1373, 1380 

(Fed. Cir. 2012) (causation cannot be evaluated without addressing the “elephant in 

the room” of evidence indicating a separate cause for the injury). Once the 

argument about relevancy is passed, K.O. says nothing about the furuncle. She 

cannot challenge the fact that A.F. had a furuncle on August 11, 2010, which is 17 

days before August 28, 2010. 

K.O.’s expert, Dr. Weig, offers little assistance to her. (K.O. did not cite any 

testimony about the furuncle from him in her post-hearing briefs.) At hearing, 

when asked why the bacteria that is the source of the furuncle was not a trigger for 

molecular mimicry leading to A.F.’s OMS, Dr. Weig stated that “it’s more likely 

than not that the vaccine would be the cause.” He went on to state that he 

discounted the bacteria because he knew of no known associations between skin 

infections and opsoclonus myoclonus syndrome. Tr. 169-70. This argument 

essentially undercuts K.O.’s assertion that the PCV vaccine caused A.F.’s OMS as 

she presented no evidence of known associations between the PCV vaccine and 

OMS. 

Thus, the analysis has come full circle. The first problem with K.O.’s case 

is that she has not demonstrated, at a preponderance of the evidence level, that the 

PCV vaccine can cause OMS. As discussed at length above, the cause of OMS is 

not known in approximately 50 percent of the cases. In these non-neuroblastoma 

cases, there is a lack of supporting evidence for any proposed causes, including 

viruses, bacteria, and vaccines. The fact that bacteria have not been established as 

a cause of OMS is analytically distinct from whether the PCV vaccine can cause 

OMS. See Caves, 100 Fed. Cl. at 140-41. The second problem with K.O.’s case is 

 17 Knudsen’s comments arose in a case in which the petitioners had established their child 

suffered an on-Table injury, meaning the petitioners were presumptively entitled to 

compensation. Here, K.O. has not met her burden of proof. 
31 

that the timing between A.F.’s vaccination and the onset of OMS is not a match. 

The timing problem is also completely independent of the furuncle. Thus, the 

outcome of K.O.’s case would be the same regardless of whether Dr. Lancaster had 

mentioned the furuncle. Overall, K.O.’s case is not persuasive. 

V. Conclusion

K.O. claimed that the PCV vaccine caused A.F. to develop OMS. The 

evidence was not sufficient to establish the causal relationship between the 

vaccination and OMS. Consequently, K.O. is not entitled to compensation on 

behalf of her minor son, A.F. 

The Clerk’s Office is instructed to enter judgment in accord with this 

decision.

IT IS SO ORDERED. 

 s/Christian J. Moran 

 Christian J. Moran 

 Special Master