SKORUPSKA v. SECRETARY OF HEALTH AND HUMAN SERVICES

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

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

BERNADETTE SKORUPSKA, *

mother and natural guardian of N.S., *

a minor, *

* No. 16-1517V

* Special Master Christian J. Moran

Petitioner, *

v. *

* Filed: February 10, 2026

SECRETARY OF HEALTH *

AND HUMAN SERVICES, *

*

Respondent. *

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

Phyllis Widman, Widman Law Firm LLC, Linwood, N.J., for petitioner;

Ryan D. Pyles, United States Dep’t of Justice, Washington, D.C., for respondent.

DECISION DENYING ENTITLEMENT TO COMPENSATION1

Bernadette Skorupska, on behalf of her minor son, N.S., claims that after

receiving the Haemophilus influenzae type b (“Hib”) vaccine on November 16,

2013, N.S. suffered infantile spasms and related seizures and neurodevelopmental

impairments, as well as a significant aggravation of his “developmental problems

characterized by motor difficulties and hypotonia.” She seeks compensation

pursuant to the National Childhood Vaccine Injury Act, 42 U.S.C. § 300aa–10

through 34. Ms. Skorupska supported her claim with reports from three experts: a

rheumatologist, Dr. Brawer; a neurologist, Dr. Ghacibeh; and a geneticist and

pediatric neurologist, Dr. Huq. She also argued her position through three briefs.

1

The E-Government Act, 44 U.S.C. § 3501 note (2012) (Federal Management and

Promotion of Electronic Government Services), requires that the Court post this decision on its

website. This posting will make the decision available to anyone with the internet. Pursuant to

Vaccine Rule 18(b), the parties have 14 days to file a motion proposing redaction of medical

information or other information described in 42 U.S.C. § 300aa-12(d)(4). Any redactions

ordered by the special master will appear in the document posted on the website.

The Secretary maintains that Ms. Skorupska is not entitled to compensation.

The Secretary relied upon opinions expressed by an expert in genetic medicine and

neurology he had retained, Dr. Raymond. The Secretary submitted a single brief

regarding entitlement.

Ms. Skorupska is not entitled to compensation. The main flaw in her case is

that she failed to present persuasive evidence that N.S. responded to the vaccine in

a way consistent with her expert’s theory. Ms. Skorupska has not shown with

preponderant evidence that the Hib vaccine harmed N.S. Moreover, N.S. was born

with a genetic mutation that made his neurologic problems nearly inevitable.

I. Facts

A. Birth and Pre-Vaccination History

1. Medical Records

N.S. was born on March 7, 2013. Exhibit 28 at 20. He did not display any

problems as a neonate. Id.

However, at the time of conception, N.S. had a mutation in a gene, known as

an SCN2A gene. Exhibit 13. This mutation was not detected until about sixteen

months after he was born.

On September 12, 2013, when he was about six months old, before the

genetic mutation was found, N.S. underwent a physical therapy evaluation “due to

concerns regarding his gross motor skills and development.” Exhibit 39 at 13.

N.S. was found to have delays in gross motor development, and was “functioning

at -2.00 standard deviations below the mean than that of his peers.” Id. at 15-16.

Dr. Selina Cali recommended that he should have an occupational therapy

evaluation. Id. at 16.

The following day, N.S. was evaluated by occupational therapist Melissa

Gianquinot using the Developmental Assessment of Young Children-Second

Edition (DAYC-2), informal observation/clinical opinion, and parent interview.

Exhibit 39 at 7. N.S. scored above average in the expressive language domain;

average in the communication and adaptive behavior domains; below average in

the cognitive, fine motor, and social-emotional domains; and poor in the physical

development domain. Id. at 9-10. Ms. Skorupska emphasizes that this evaluation

did not mention seizures or epilepsy. Pet’r’s Br. at 10.

2

During N.S.’s six-month well-child examination, his pediatrician found that

he was generally normal. However, he had not yet achieved the milestones of

looking for a dropped item or feeding himself. Exhibit 24 at 19-21 (Sep. 25,

2013).

N.S. was seen by another occupational therapist, Elizabeth Esposito, on

September 27, 2013. This therapist stated that N.S. “has not yet met any of his

developmental milestones.” Examples of the abilities typical for a six-month-old

include: rolling over, sitting up, reaching and grasping toys and tracking toys

consistently to and past midline. N.S. “made no eye contact and at times did not

seem aware of others in his environment.” Exhibit 39 at 20.

N.S. again saw his pediatrician on October 19, 2013. He did not make eye

contact, he did not follow a toy, he was not sitting, and he was not rolling over.

Exhibit 24 at 16. The doctor, Joanna B. Lis, assessed him as having hypotonia and

an unspecified delay in development. Id. at 17.

In early November 2013, N.S. had two episodes of nonstop crying. See

Exhibit 7 at 20-22 (emergency room records from November 1, 2013); Exhibit 24

at 132 (pediatrician’s follow up on November 6, 2013).

A pediatric neurologist, Steven Schwartzberg, evaluated N.S. on November

13, 2013. Exhibit 2 at 4-5. N.S. had not yet rolled over. Dr. Schwartzberg

determined that N.S. had diminished tone in all four extremities. He assessed N.S.

as having “diffuse hypotonia and developmental delay predominantly affecting

motor skills.” Id. at 5. Dr. Schwartzberg recommended that N.S. increase his

therapies. Dr. Schwartzberg also ordered an EEG and a brain MRI.

2. Expert Commentaries on N.S.’s Development before

Vaccination

The Secretary’s expert, Dr. Raymond, highlighted problems with N.S.’s

September 13, 2013 evaluation, commenting:

The major issue with this evaluation is that it is unclear

what was scored from observation and what was credited

by parental report. This becomes even more appreciable

in the discrepancy between what the evaluations found in

terms of gross motor and fine motor where one can only

be scored for actions performed. On the DAYC-2, NS

was only -1.13 SD below the mean, but when actually

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assessed during the Peabody, he was -2.40 SD below the

mean and profoundly delayed in that assessment.

Exhibit EE at 1. Dr. Raymond further opined:

This is to some extent immaterial because when seen by

pediatric neurologist Dr. Schwartzberg on November 13,

2013, at 8 months and prior to any immunization, [N.S.]

was clearly severely delayed in all domains.

Id. Dr. Raymond opined that N.S. “was severely developmental[ly] delayed prior

to the immunization.” Exhibit A at 6. He explained:

It is well-established that NS was hypotonic and not

meeting developmental milestones, so it is apparent that

the genetic disorder that he had was already affecting his

brain and had been doing so since birth. This is

concordant with what has been seen in other children

affected by early infantile epileptic encephalopathies due

to mutations in SCN2A.

Id.

Dr. Ghacibeh acknowledged that it is “evident and unquestionable” that N.S.

“was already exhibiting symptoms related to his genetic mutation” before

vaccination. Exhibit 50 at 2. However, he characterized N.S. as “showing signs of

mild developmental delay affecting primarily his motor function, most likely due

to his genetic mutation.” It was not until after vaccination, in Dr. Ghacibeh’s

analysis, that N.S. “developed infantile spasms,” and “had a severe developmental

regression which left him with profound intellectual disability and global

developmental delay.” Id. Dr. Ghacibeh summarized:

To reiterate, there is no doubt that [N.S.]’s underlying

genetic mutation was the cause of his early delay.

However, as we see from the referenced literature,

mutations on the SCN2A gene can result in a spectrum of

disorder, ranging from the mild and benign to the severe.

While it is impossible to know for sure what would have

been [N.S.]’s ultimate phenotype as related to his

mutation, the course of his development up to the day he

had received the vaccine was taking a fairly favorable

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trajectory, which suggests that he would have most

probably had mild delay. However, after receiving the

HiB vaccine, he developed refractory epilepsy and severe

developmental regression.

Id. at 3.

Dr. Raymond, in contrast, opined that N.S. was “not mildly delayed in one

domain, but rather globally delayed prior to seizure onset.” Exhibit C at 1. Dr.

Raymond noted that, when N.S. was eight months old, he was “at best meeting

two-month milestones” across various domains. Id. In summary, Dr. Raymond

stated that N.S. was “a child with a severe, generalized epilepsy with

developmental delays,” and that his genetic mutation “was the sole cause” or his

condition and “was not caused or exacerbated by the vaccination that he received.”

Id. at 3.

Dr. Ghacibeh did “not agree” with Dr. Raymond’s conclusion that N.S. had

severe delay prior to vaccination. Exhibit 59 at 2. Maintaining that N.S. “likely

suffered mild motor delay at that time,” Dr. Ghacibeh highlighted that neither Dr.

Schwartzberg’s examination nor impression indicated that N.S. had severe delay.

Id. Dr. Ghacibeh maintained this position in his next report, stating that, pre-

vaccination, N.S. “had exhibited mild delay in motor development but normal

cognitive development.” Exhibit 212 at 1. He reiterated that Dr. Schwartzberg’s

“initial evaluation clearly reports that [N.S.]’s cognitive development seemed on

track, and he only exhibited mild motor delay which was to be addressed [with]

physical therapy.” Dr. Ghacibeh again opined that N.S. “likely suffered mild

motor delay” and then “had a severe regression after the onset of his epilepsy.” Id.

Dr. Raymond maintained his position and “continue[d] to strongly disagree

with Dr. Ghacibeh’s assessment.” Exhibit K at 3. He raised the point that Dr.

Schwartzberg recommended that N.S. increase his therapies from once a week to

three times per week; gave the family instructions for hearing, feeding, and special

instructional evaluations; and planned for numerous tests and consultations. Id.

Dr. Raymond stated: “These recommendations including the significant increase in

the frequency of therapy are commensurate with the severity of this child’s delays

and not those of a ‘mild motor delay.’” Id. at 4.

When Ms. Skorupska retained Dr. Huq, he took a position similar to that of

Dr. Ghacibeh. Dr. Huq noted “concerns of mild developmental delay prior to the

Hib vaccination.” Exhibit 68 at 4. He later described N.S. as “a healthy child with

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some developmental concerns mainly in the motor domain, but he was not severely

delayed.” Id. at 27.

Just as he disagreed with Dr. Ghacibeh, Dr. Raymond disagreed with Dr.

Huq’s characterization of N.S. as “not severely delayed.” Dr. Raymond reiterated

his previous point that, at eight months of age, N.S. was “at best” meeting two-

month milestones, which he described as “a significant delay.” Exhibit T at 12.

He also again noted the treatments and recommendations N.S. received from Dr.

Schwartzberg. Id.

B. Vaccination and Next Two Weeks

N.S. returned to his pediatrician on November 16, 2013. He was assessed

with a “developmental coordination disorder.” Exhibit 24 at 4. As part of this

appointment, N.S. received the allegedly harmful Hib vaccine. Exhibit 1 at 4-5.2

On November 22, 2013 (six days after vaccination), N.S. was taken to the

emergency department at Staten Island University Hospital. The history, which

was given by N.S.’s mother and father, states that N.S. had been vomiting after

every meal and having intermittent episodes of choking for the past three days.

Exhibit 29 at 30. N.S. was also noted to be “afebrile.” Id. at 138.3 The attending

note further stated that N.S. had “been receiving extensive outpatient evaluation for

chronic vomiting and lethargy,” and had been “diagnosed with reflux and multiple

formula changes due to formula intolerance.” Id. at 31. The doctor in the

emergency department consulted N.S.’s pediatrician, who reported that N.S. “has

been not developing appropriately and was feeding poorly.” Id. at 36. A

document associated with his admission states that N.S. has a two-day history of

2

“Severe adverse events following administration of Hib vaccine are uncommon, making

it one of the safest vaccines currently available. In a study of >4000 infants, there were no

differences in the type and frequency of severe adverse events occurring among those receiving

Hib conjugate vaccine and those receiving a placebo." Exhibit F (World Health Organization,

Information Sheet: Observed Rate of Vaccine Reactions: Haemophilus Influenzae Type B (Hib)

Vaccine (2012)) at 1.

3

Ms. Skorupska asserts that N.S. started suffering from “infantile spasm type seizures

accompanied by fever.” Pet’r’s Br. at 2. The Secretary disputed this assertion. Resp’t’s Br. at

33. Ms. Skorupska did not counter the Secretary’s arguments. See Pet’r’s Reply. In the

hospital, Ms. Skorupska denied fevers. Exhibit 29 at 149 (Nov. 22, 2013).

6

spasms. Id. at 94-95. Pursuant to this history, N.S. started having spasms on

November 20, 2013 (or four days after vaccination).

In the emergency department, a doctor ordered, among other tests, a

complete blood count. Although the number of lymphocytes were reported as

higher than expected (Exhibit 29 at 173), a treating doctor said the CBC was

normal. Id. at 168.

As N.S. was stable and appeared well-hydrated, the doctors determined that

it would be appropriate to discharge N.S. and to have him follow up for an

outpatient GI workup. Exhibit 29 at 36. However, at the request of his mother,

N.S. was admitted to the hospital. Id. An initial inpatient history reported that

N.S. had “global delay.” Id. at 95. The doctor also checked the boxes on the form

to indicate that N.S. had deficits in “Gross Motor,” “Fine Motor,” and “Speech.”

Id. at 97. N.S. underwent a video EEG. See id. at 150 (report from neurology /

epilepsy attending), 167 (ordering form). He was diagnosed with spasms and

epileptic encephalopathy. Exhibit 38 at 5. A doctor ordered treatment with

adrenocorticotropic hormone (ACTH). Exhibit 29 at 153. A brain MRI was

normal. Exhibit 29 at 168-69, Exhibit 7 at 47 (Nov. 26, 2013). N.S. was

discharged on November 27, 2013. Exhibit 29 at 47. Instructions included

following up with genetics. Id. at 280.

C. Treatment and Genetic Testing

Following the diagnosis of infantile spasms, N.S. saw a variety of doctors,

who recorded his status and prescribed a variety of medications. Medications

included ACTH, topiramate (Topamax), and vigabatrin (Sabril). Because these

records are generally not relevant to determine what caused the infantile spasms,

these records are not detailed in this decision. For details, see Resp’t’s Br. at 6-7.

(Ms. Skorupska’s brief does not cite any medical records from this time.)

In short, in December 2013 and January 2014, N.S.’s doctors struggled to

get control of his seizures. See Exhibit 5 at 5 (December 12, 2013 visit during

which a neurologist added topiramate); Exhibit 15 at 1-2 (December 18, 2013 visit

during which a different neurologist (Dr. Wolf) added Sabril).

After these medications failed to control the spasms, Dr. Wolf recommended

IVIG. Exhibit 30 at 836 (Apr. 18, 2024). In May 2014, Dr. Wolf oversaw a course

of IVIG, which was administered in Beth Israel Medical Center. Exhibit 38 at 3-5;

Exhibit 30 at 800-01 (duplicate). Initially, Dr. Wolf stated the clusters of spasms

had “no improvement.” Exhibit 38 at 5. In a follow up appointment, Dr. Wolf

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reported that after the IVIG, there was a “great result of no spasms for 1.5 week

only then they returned at 1 cluster per day. But then more recently.” Exhibit 15

at 26.

The results of the genetic testing were returned on July 11, 2014. Exhibit

13. There was a mutation in the SCN2A gene. “The SCN1A and SCN2A genes

encode α subunits of the neuronal voltage-gated sodium channel.” Exhibit 193

(Dr. Huq’s second report) at 6. “Sodium channels are extremely important in

neuronal transmission and interneuronal communication and their role spans the

spectrum of early neuronal development as well as ongoing brain function in

adults. Disorders in sodium channels, referred to as channelopathies, produce a

spectrum of clinical disorders, ranging from asymptomatic carries to severe

epilepsy and developmental delays.” Exhibit 50 (Dr. Ghacibeh’s first report) at 2.

In short, N.S.’s SCN2A contained a variant that Gene Dx classified as a

“disease-causing mutation.” Exhibit 13 at 1. More specifically, in position 3631,

the amino acid was changed from guanine to adenine. This change in amino acid

meant in position 1211 there was glutamic acid, rather than lysine. Exhibit A (Dr.

Raymond’s report) at 4.

After the genetic test was returned, N.S. was seen by a clinical geneticist,

Ethylin Wang Jabs, on July 23, 2014. Exhibit 23 at 25. Dr. Jabs documented that

the infantile epilepsy panel “was significant for a heterozygous deleterious

variation in the SCN2A gene. . . . This has been reported in other patient (Ogiwara

et al., 2009) with infantile spasms that progressed to generalized epilepsy.” Id. Dr.

Jabs’s impression was that N.S. has “infantile spasms due to a known pathogenic

variant in the SCN2A gene.” Id. at 25. To support the “hypothesis” that this

mutation is a “deleterious change,” Dr. Jabs stated that the gene is “well-conserved

evolutionarily and is predicted to be deleterious from programs that analyze protein

function after mutations. It was also tested in vitro in the same paper that described

the patient with this mutation and was found to have increased activity and reduced

latent state.” Id.

The view of Dr. Jabs---that the genetic mutation was pathogenic---was at

least repeated by one other doctor. In the context of a visit to an emergency

department for lethargy in January 2015, the doctor wrote that N.S. is a “22 mo

boy with PMHx [past medical history] for significant SCN2A mutation and

resulting seizure disorder and developmental delay.” Exhibit 30 at 389 (emphasis

added).

8

As discussed extensively below, the parties differ about the role this variant

played in N.S.’s life and plays in this litigation. “Petitioner’s position is that the

variant SCN2A gene is not enough to cause [N.S.’s] current mental state. While he

may have been at an increased risk to develop some deficits due to the genetic

mutation, the vaccination (not simply the genetic mutation) is what caused his

current mental state.” Pet’r’s Br. at 4. In contrast, the Secretary argues: “It is

beyond question that N.S.’s mutation explains his entire course.” Resp’t’s Br. at

16.

II. Procedural History

Represented by Attorney Robert Krakow, Ms. Skorupska initiated this case

by filing a petition November 15, 2016. Over the next year, Ms. Skorupska

submitted various medical records. She filed an affidavit on September 18, 2017.

Exhibit 40.

The Secretary reviewed this material and determined that Ms. Skorupska

was not entitled to compensation. Resp’t’s Rep., filed pursuant to Vaccine Rule 4

on Dec. 4, 2017.

Ms. Skorupska was instructed to file a report from an expert. Order, issued

Dec. 13, 2017 (setting a deadline of March 12, 2018). For a variety of reasons, an

expert report was not filed. Ms. Skorupska was ordered to show cause why the

case should continue. Order, issued Apr. 30, 2019. It appeared that Ms.

Skorupska would wrap up her case. See Pet’r’s Status Rep., filed May 24, 2019.

However, Ms. Skorupska elected to maintain her case. Mr. Krakow was

allowed to withdraw his representation via an order issued August 7, 2019, and a

December 17, 2019 decision awarded Ms. Skorupska compensation for Mr.

Krakow’s work.

Representing herself, Ms. Skorupska submitted a report from Arthur E.

Brawer, a rheumatologist who has sometimes supported claims that a vaccine

injured a person. Dr. Brawer’s report is Exhibit 42.

In response to Dr. Brawer, the Secretary submitted a response from Gerald

Raymond, who is a medical geneticist and neurologist. Dr. Raymond generally

opined that “The pathogenic mutation in [N.S.’s] SCN2A gene is the sole cause of

his epileptic encephalopathy and was not caused or exacerbated by the

immunization that he received.” Exhibit A at 7.

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Ms. Skorupska, still appearing pro se, submitted a responsive report from

Dr. Brawer on August 5, 2020. Exhibit 46.

It appeared that this second report from Dr. Brawer completed the disclosure

of opinions from experts. Thus, the parties were directed to advocate through

briefs. Order, issued Aug. 24, 2020.

Attorney Phyllis Widman became counsel of record on September 28, 2020.

In some ways, Ms. Widman’s participation re-started the case.

A status conference was held on December 3, 2020. The Secretary asserted

that Dr. Brawer is not qualified to discuss the causes of a neurologic condition. In

this context, Ms. Widman requested an opportunity to seek a report from a

neurologist. See Order, issued Dec. 3, 2020. This December 3, 2020 order

suspended the schedule for submitting briefs.

After receiving enlargements of time, Ms. Skorupska submitted a three-page

report from Georges Ghacibeh. Exhibit 50. Dr. Ghacibeh is a neurologist. He

opined: “While it is impossible to know for sure what would have been [N.S.’s]

ultimate phenotype as related to his mutation, the course of his development up to

the day he had received the vaccine was taking a fairly favorable trajectory, which

suggests that he would have most probably had mild delay. However, after

receiving the HiB vaccine, he developed refractory epilepsy and severe

developmental regression.” Exhibit 50 at 3.

The Secretary again responded with a report from Dr. Raymond. Exhibit C.

Another round of reports followed. See Exhibit 59 (Dr. Ghacibeh’s second report)

and Exhibit K (Dr. Raymond’s third report). In this third report, Dr. Raymond

stated that N.S.’s variant has been reported in children with epilepsy seven times.

Ms. Skorupska stated that additional reports were not needed. Pet’r’s Status

Rep., filed Dec. 16, 2022. Thus, the parties were informed that an order for briefs

would be forthcoming. Order, issued Dec. 19, 2022.

Ms. Widman requested a status conference, which was held on January 12,

2023. She now realized that she should strengthen Ms. Skorupska’s case by

adding a report from a geneticist. The Secretary ultimately deferred to the special

master’s discretion, but maintained that inescapable science shows that the

mutation is pathogenic. Thus, incurring additional costs would not be justified.

However, Ms. Skorupska was given an opportunity to present the report of a

geneticist. Order, issued Jan. 16, 2023.

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Ms. Skorupska submitted a report from Mahbubul Huq on March 20, 2023.

Dr. Huq is a board-certified clinical geneticist and pediatric neurologist. His

approximately 30-page report cites approximately 90 articles. Exhibit 68.

Dr. Huq’s report kicked off another series of reports. See Exhibit T (Dr.

Raymond’s fourth report); Exhibit 193 (Dr. Huq’s second report); Exhibit EE (Dr.

Raymond’s fifth report); and Exhibit 212 (Dr. Ghacibeh’s third report). The

Secretary then advised that additional reports were not necessary. Resp’t’s Status

Rep., filed Feb. 2, 2024.

A status conference was held on February 27, 2024. The parties were

directed to file briefs as explained in the August 24, 2020 order.

For a variety of reasons, Ms. Skorupska did not submit a brief quickly.

Eventually, Ms. Skorupska argued that she was entitled to compensation. Pet’r’s

Br., filed Sep. 30, 2024. Shortly before the brief was filed, Ms. Skorupska revised

her petition. Am. Pet., filed Sep. 16, 2024. The amended petition alleges that the

Hib vaccine caused N.S. to suffer a variety of conditions, including infantile

spasms. The amended petition alternatively alleges that the Hib vaccine

significantly aggravated a pre-existing condition.

Ms. Skorupska’s September 30, 2024 brief was deficient in that it failed to

address one of the elements of compensation (timing). Thus, she was directed to

present a supplement. Order, issued Oct. 7, 2024. She did so. Pet’r’s Supp’l Br.,

filed Oct. 15, 2024.

The Secretary argued that Ms. Skorupska was not entitled to compensation

and maintained the case could be resolved without a hearing. Resp’t’s Br., filed

Dec. 2, 2024.

Ms. Skorupska attempted to answer the Secretary’s arguments in a relatively

short reply, which was filed on February 4, 2025. Upon review of this material

one question came up about a citation to evidence in the reply brief. Ms.

Skorupska provided the material in a status report, filed Sep. 17, 2025.4 The case

is ready for adjudication.

4

The September 17, 2025 status report remains slightly confusing. Although it cites to

Exhibit 148, the medical records are actually contained within Exhibit 227.

11

The case can be resolved without a hearing. Special masters possess

discretion to decide whether an evidentiary hearing will be held. 42 U.S.C. §

300aa-12(d)(3)(B)(v) (promulgated as Vaccine Rule 8(c) & (d)), which was cited

by the Federal Circuit in Kreizenbeck v. Sec’y of Health & Hum. Servs., 945 F.3d

1362, 1365 (Fed. Cir. 2018). Here, a hearing is not required because Ms.

Skorupska has had a full and fair opportunity to present her case.

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 & Hum.

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 & Hum. 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 & Hum. 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 & Hum. Servs., 219 F.3d 1357

(Fed. Cir. 2000); Hodges v. Sec’y of Health & Hum. 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).

IV. Diagnosis

In Broekelschen v. Sec’y of Health and Hum. Servs., 618 F.3d 1339, 1346

(Fed. Cir. 2010), the Federal Circuit recognized that in some circumstances, the

special master may “first determine which injury was best supported by the

evidence in the record before applying the Althen test.” Here, based upon Dr.

Raymond’s third report, the Secretary asserts that N.S. suffers from

“developmental and epileptic encephalopathy 11 (DEE11).” Resp’t’s Br. at 15,

citing Exhibit K at 5.

Dr. Huq enjoyed an opportunity to address Dr. Raymond’s opinion

regarding diagnosis. Under the heading “NS’s Diagnosis and Genetic Test

Results,” Dr. Huq stated, “NS developed epileptic spasms.” Exhibit 68 at 4. Later,

Dr. Huq wrote, “NS developed infantile spasms.” Id. at 27. However, Dr. Huq did

12

not respond to the proposal that the appropriate diagnosis is “developmental and

epileptic encephalopathy 11.” Likewise, although Ms. Skorupska enjoyed an

opportunity to address the Secretary’s argument regarding DEE11, she did not.

See Pet’r’s Reply.

Nevertheless, for the ease of analysis, this decision will proceed upon the

assumption that an appropriate diagnosis for N.S. is infantile spasms. This

assumption is made because, in part, it is not readily apparent that any difference in

nomenclature would change the analysis. See Exhibit T (Dr. Raymond’s report in

response to Dr. Huq’s first report) at 12 and 15 (apparently accepting the diagnosis

of infantile spasms).

V. Part One: Loving Analysis

Ms. Skorupska’s September 16, 2024 Amended Petition alleges both an

initial onset claim and a significant aggravation claim. In such a situation, the test

is whether the vaccinee manifested problems before the vaccination. Paluck v.

Sec’y of Health & Hum. Servs., 104 Fed. Cl. 457, 468 (2012), aff after remand on

non-relevant grounds, 786 F.3d 1373 (Fed. Cir. 2015); see also Lampe v. Sec’y of

Health & Hum. Servs., 219 F.3d 1357, 1364-65 (Fed. Cir. 2000) (ruling that the

special master did not err in reasoning that because the child-vaccinee’s seizure

disorder started after the second dose of the diphtheria-tetanus-pertussis vaccine,

the petitioners could proceed only on a theory that the third dose significantly

aggravated the seizure disorder); Childs v. Sec’y of Health & Hum. Servs., 33 Fed.

Cl. 556, 559-60 (1995) (ruling that when the vaccinee did not have a history of a

problem before the vaccination, petitioners could not proceed on a theory of

significant aggravation). Here, ample evidence shows that N.S. was experiencing

at least some neurologic problems / developmental delay before the vaccination.

Exhibit 2 at 4-5 (Dr. Schwartzberg’s Nov. 13, 2013 evaluation). Although Ms.

Skorupska’s experts (Dr. Ghacibeh and Dr. Huq) assert N.S. was only mildly

delayed, even from their perspective he was delayed pre-vaccination. Thus, it is

appropriate to categorize Ms. Skorupska’s case as presenting a significant

aggravation claim.

As confirmed in W.C. v. Sec’y of Health & Hum. Servs., 704 F.3d 1352,

1357 (Fed. Cir. 2013), the elements of an off-Table significant aggravation case

were stated in Loving. There, the Court blended the test from Althen v. Sec’y of

Health & Hum. Servs., 418 F.3d 1274, 1279 (Fed. Cir. 2005), which defines off-

Table causation cases, with a test from Whitecotton v. Sec’y of Health & Hum.

13

Servs., 81 F.3d 1099, 1107 (Fed. Cir. 1996), which concerns on-Table significant

aggravation cases. The resulting test has six components. These 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.

In addressing a significant aggravation claim, special masters may focus

upon the last three elements in the Loving test, which correspond to the three

prongs of the well-established Althen test. Vinesar v. Sec’y of Health & Hum.

Servs., No. 18-440V, 2023 WL 5427935, at *28 (Fed. Cl. Spec. Mstr. July 28,

2023), mot. for rev. denied, 170 Fed. Cl. 681 (2024), aff’d in non-precedential op.,

No. 2024-1787, 2025 WL 2945665 (Fed. Cir. Oct. 17, 2025); Hennessey v. Sec'y

of Health & Hum. Servs., No. 01-190V, 2009 WL 1709053, at *42 (Fed. Cl. Spec.

Mstr. May 29, 2009), mot. for rev. denied, 91 Fed. Cl. 126 (2010).

Ms. Skorupska states that “Dr. Huq’s theory is that the vaccine caused

inflammation and epileptic encephalopathy. The inflammation caused altered

connectivity, which in turn, caused epilepsy.” Pet’r’s Br. at 57; accord Pet’r’s

Reply at 4. Ms. Skorupska’s assertion that Dr. Huq’s theory is based upon

inflammation is accurate. See Exhibit 68 at 73 (asserting that inflammation causes

infantile spasms). The mechanism of inflammation is through cytokines. Pet’r’s

Br. at 6-7, citing Exhibit 68 at 11-12. The Secretary, too, discussed inflammation,

challenging the theory. Thus, whether N.S. experienced inflammation is critical to

petitioner’s claim, as even if she were to prevail on the fourth Loving / first Althen

prong, she would have to establish that the theory applies to N.S.’s case. To

address this issue, this Decision evaluates the Loving / Althen prongs out of order,

beginning with the fifth Loving prong / second Althen prong.

14

A. Loving Prong 5 / Althen Prong 2

In evaluating the second Althen prong, which corresponds to the fifth

Loving prong, special masters may consider whether the vaccinee responds in a

way predicted by the expert’s theory. Hibbard v. Sec’y of Health & Hum. Servs.,

698 F.3d 1355, 1364 (Fed. Cir. 2012); La Londe v. Sec’y of Health & Hum. Servs.,

110 Fed. Cl. 184, 205 (2013), aff’d, 746 F.3d 1334 (Fed. Cir. 2014). Special

masters may also consider the views of treating doctors. Capizzano v. Sec’y of

Health & Hum. Servs., 440 F.3d 1317, 1326 (Fed. Cir. 2006). These two aspects

are considered below.5

1. Response Predicted by the Theory

As stated above, Ms. Skorupska’s theory is based upon inflammation. She

asserts that various blood tests “can be associated with inflammation.” Pet’r’s Br.

at 6.6 Later, Ms. Skorupska similarly argues that the evidence of inflammation

buttresses Dr. Huq’s theory:

Dr. Huq supports this theory of significant aggravation

based on the evidence of inflammation in N.S.’s body

post-vaccination. “One reason to think that [N.S.’s]

vaccination caused significant aggravation of effects of

the E122K variant is the evidence of interaction between

vaccine induced inflammation and SCN2A gene.”

Exhibit 193 at 5.

Pet’r’s Br. at 57.

The Secretary contends that the evidence does not support a finding that

N.S. experienced harmful inflammation. See Resp’t’s Br. at 31. After quoting the

passage from page 57 of Ms. Skorupska’s brief, the Secretary asks: “Respectfully,

what evidence?” Resp’t’s Br. at 31. Citing Dr. Raymond, the Secretary argues

that there is “no indication of inflammatory markers or MRI features in this case to

5

Arguably, another consideration in any analysis of Althen prong two / Loving prong

five could include an examination of the presence (or absence) of alternative causes. However,

the alternative cause analysis is deferred to section VI., below.

6

For the underlying blood tests, Ms. Skorupska cited Exhibit 148 at 172-73. However,

informal communications revealed that the correct citation is Exhibit 227 at 550-51 (results from

Nov. 22, 2013).

15

suggest an inflammatory event or autoimmune injury, whether vaccine-related or

not.” Id.

Ms. Skorupska answers that her primary brief “provides extensive evidence

that inflammation in N.S.’s body became evident following the Hib vaccine

administration.” Pet’r’s Reply at 5.7 She brings forward an argument based upon

N.S.’s positive response to IVIG. Id. at 5-6.

Ms. Skorupska has not persuasively established that N.S. suffered

deleterious inflammation within a relevant time of the vaccination. To start with

the last point first, IVIG is a complicated issue. Although Dr. Ghacibeh

maintained that IVIG stopped the seizures (see Exhibit 59 at 2), Dr. Raymond

raised several challenges, including the fact that N.S. was receiving other therapies

at the same time. Exhibit K at 3. Moreover, the improvement after IVIG did not

last very long. See Exhibit 15 at 26. Thus, Ms. Skorupska is oversimplifying the

question.

While Dr. Ghacibeh’s opinion regarding IVIG is not persuasive, Ms.

Skorupska does have some minimal expert support for an argument based upon

IVIG. The same cannot be said for her reliance on blood tests. In Dr. Raymond’s

second report, he stated that there was no evidence of inflammation. Exhibit C at

3. Ms. Skorupska’s experts did not refute this point. For example, Dr. Ghacibeh

reasoned the absence of inflammatory markers does not mean that N.S. did not

experience inflammation. Exhibit 59 at 2. The problem with such reasoning, as

the Secretary points out (Resp’t’s Br. at 31), is that ultimately Ms. Skorupska bears

a burden of proving her case.

With respect to the question of inflammation, the material that Ms.

Skorupska provided in her September 17, 2025 status report was reviewed. This

material does not support a finding that N.S. had information. Ms. Skorupska

attached four pages:

7

Given that Ms. Skorupska recognizes in the same paragraph of her reply that

inflammatory markers were absent, her characterization of her evidence regarding inflammation

as “extensive” appears to be an attorney’s rhetorical flourish.

16

Evidence Cited to Establish Inflammation

Pet’r’s Actual Comment

Pg in

Cite in Ex. Cite in

SR

148 Ex. 227

Intake form. Chief complaint includes

1 109 464 “involuntary muscle movements.” Inflammation

is not mentioned.

Blood tests from Nov. 26, 2013. Abnormally high

values include bun to creatinine ratio, ammonia,

and white blood cells. Ms. Skorupska has not

2 172 550

cited any evidence in which a medical professional

interpreted these results as consistent with

inflammation.

Blood tests from Nov. 22, 2013. Abnormally high

values include mean platelet value (slightly high),

percentage of lymphocytes, number of

3 173 551 lymphocytes, and number of lymphocytes. Ms.

Skorupska has not cited any evidence in which a

medical professional interpreted these results as

consistent with inflammation.

Part of medical record from N.S.’s visit to the

emergency room on Nov. 1, 2013. Medical

4 298 443

professionals did not diagnose N.S. as suffering

from inflammation.

Moreover, after N.S.’s blood tests from November 2013 were returned,

N.S.’s treating doctors did not diagnose him with or treat him for inflammation.

Similarly, neither Dr. Ghacibeh nor Dr. Huq pointed to the results of blood tests as

evidence supporting an assertion that N.S. suffered inflammation. The omission of

this type of opinion combined with Dr. Raymond’s opinion that there is no

evidence that N.S. suffered inflammation is a persuasive reason for finding that

N.S. did not experience inflammation.

17

2. Treating Doctors

The parties were directed to identify doctors who commented upon whether

the Hib vaccine could have contributed to N.S.’s medical condition. Order for

Briefs, issued Aug. 24, 2020, at 6-7. They were expected to cite relevant evidence

by exhibit number and page number.

The parties say relatively little about treating doctors. The relevant portion

of Ms. Skorupska’s brief does not discuss any statements of treating doctors. See

Pet’r’s Br. at 59-62 (discussing Dr. Huq’s, Dr. Ghacibeh’s, and Dr. Brawer’s

opinions about the logical sequence of cause and effect).

The Secretary asserts that the treating doctors do not assist Ms. Skorupska.

The Secretary argues: “no treating physician attributed N.S.’s condition in general,

or spasms and later seizures more specifically, to vaccination. Indeed, the treating

physician statements heavily weigh against causation in this case, because they did,

on aggregate, attribute N.S.’s condition – without reservation – to his SCN2A

mutation.” Resp’t’s Br. at 32.8 Strong support for the Secretary’s opinion comes

from the July 23, 20214 report from the clinical geneticist, Dr. Jabs. She wrote

that she counseled N.S.’s parents that the genetic mutation “may be causative,”

depending upon the outcome of genetic testing on N.S.’s parents. Exhibit 23 at 26.

She also characterized N.S.’s genetic mutation as “deleterious.” Id. at 25.

Overall, Ms. Skorupska has not presented a logical sequence of cause and

effect connecting the Hib vaccination to the change in N.S.’s health in November

2013 (regardless of whether this change is categorized as a new injury for Althen

or the significant aggravation of a pre-existing problem for Loving). The Federal

Circuit has clarified that “to require identification and proof of specific biological

mechanisms would be inconsistent with the purpose and nature of the vaccine

compensation program.” Knudsen v. Sec’y of Health & Hum. Servs., 35 F.3d 543,

549 (Fed. Cir. 1994). However, “notation of absence is not requirement of

presence.” Howard v. United States, No. 16-1592V, 2023 WL 4117370, at *7

(Fed. Cl. May 18, 2023) (denying motion for review and commenting that,

“Because Petitioner's theory relied on the pathogenetic role of certain antibodies,

Petitioner cannot then fault the Decision for noting the absence of evidence

8

The Secretary’s argument would have been stronger if the Secretary supported his

assertion by citing exhibit numbers and page numbers for the medical records in which treating

doctors linked N.S.’s genetic mutation to his neurologic problems. See Resp’t’s Br. at 32.

18

preponderantly indicating their presence”), aff'd, No. 2023-1816, 2024 WL

2873301 (Fed. Cir. June 7, 2024). Here, Ms. Skorupska’s theory relied on the

presence of cytokine-driven inflammation. Without a showing that this

inflammation did occur, she cannot establish a logical sequence of cause and effect

under the fifth Loving prong / second Althen prong. Ms. Skorupska’s failure to

meet her burden of proof on this element means that she is not entitled to

compensation.

B. Loving Prong 6 / Althen Prong 3

The timing prong actually contains two parts. A petitioner must show the

“timeframe for which it is medically acceptable to infer causation” and that the

onset of the disease occurred in this period. Shapiro v. Secʼy of Health & Hum.

Servs., 101 Fed. Cl. 532, 542-43 (2011), recons. denied after remand on other

grounds, 105 Fed. Cl. 353 (2012), aff’d without op., 503 F. App’x 952 (Fed. Cir.

2013).

Ms. Skorupska’s position regarding timing is not clear. Part of the lack of

clarity may derive from an inconsistency in Dr. Huq’s first report. Dr. Huq wrote:

“As the initial brain injury occurred due to activation of the innate immunity by

[the] Hib vaccine, the timing of epileptic spasms 5 days after the vaccination is

appropriate.” Exhibit 68 at 7-8. He repeats this sentence on page 28. But, in this

context, Dr. Huq stated, “NS developed infantile spasms seven days after Hib

vaccination.” Id. at 28.

The relevant portion of Ms. Skorupska’s original brief did not engage with

timing. See Pet’r’s Br. at 63-64. She did not identify a period for which an

inference of aggravation is appropriate, and she did not state when N.S.’s pre-

existing condition was first aggravated. She was, accordingly, directed to clarify

her position. Order, issued Oct. 7, 2024.

Ms. Skorupska presented more fulsome arguments. As to the interval for

which an inference of aggravation is appropriate, Ms. Skorupska stated that the

appropriate range of time would be “within the first 72 hours – six days.” Pet’r’s

Supp’l Br., filed Oct. 15, 2024, at 1. Although Ms. Skorupska cited two medical

articles, they do not propose six days. The first is by Tro-Baumann, which found

that the majority of children with Dravet’s syndrome experienced febrile seizures

19

within 72 hours of a vaccination against diphtheria-tetanus-pertussis. Exhibit 224.9

The second is by Verbeek, which found febrile seizures within 24 hours of a

vaccination in children with Dravet’s syndrome. Exhibit 225.10

Next, to fit N.S.’s initial aggravation within these periods, Ms. Skorupska

relies upon her September 18, 2017 affidavit. There, she averred that during the

night after the vaccination, N.S. developed a “mild fever.” Exhibit 40 ¶ 5. She

added that in the emergency room, she realized that N.S. “had been having spasms

for at least two days, maybe more.” Id. at 8. At least one medical record from this

time corroborates Ms. Skorupska’s account, at least in respect to the two days of

trouble. See Exhibit 29 at 94-95 (report dated November 22, 2013 and stating Ms.

Skorupska “reports a 2 day history of new onset spasms”).

The Secretary challenges Ms. Skorupska’s arguments regarding timing in at

least two respects. First, the Secretary disagrees with Ms. Skorupska’s reliance

upon the Tro-Baumann and Verbeek articles because those articles were written

about children experiencing febrile seizures in the context of Dravet’s syndrome.

In the Secretary’s view, because N.S. did not have a febrile seizure, “data

concerning febrile seizures are completely irrelevant to establish an appropriate

temporal relationship between the Hib vaccine in this case and the onset of

infantile spasms.” Resp’t’s Br. at 34. Second, the Secretary points out another

mismatch: “Even if febrile seizure data were relevant here, N.S.’s spasms were

first observed four days after vaccination, outside the time frame of within three

days cited in Tro-Baumann, or within a day cited in Verbeek.” Id.11

Ms. Skorupska largely fails to answer these arguments. She maintains that

she “provided evidence of a clear temporal relationship between the administration

of the Hib vaccine and the onset of N.S.'s seizures.” Pet’r’s Reply at 5. However,

she did not address the Secretary’s arguments about (the lack of relevance for)

9Blanca Tro-Baumann et al., A retrospective study of the relation between vaccination

and occurrence of seizures in Dravet syndrome, 52 EPILEPSIA 175 (2011). Filed as Exhibit 224.

10

Neinke E. Verbeek et al., Prevalence of SCN1A-related dravet syndrome among

children reported with seizures following vaccination: a population-based ten-year cohort study,

8 PLOS ONE 1 (2013). Filed as Exhibit 225.

11

A third potential argument is that N.S. was having infantile spasms before his mother

observed them, possibly before the vaccination. See Resp’t’s Br. at 33 n.14. However,

preponderant evidence does not establish that N.S. was experiencing infantile spasms before the

vaccination.

20

febrile seizures or the development of infantile spasms after the period predicted

by the Tro-Baumann article.

Under these circumstances, crediting Ms. Skorupska’s proof regarding

timing is difficult. If it is assumed that Tro-Baumann and Verbeek, two articles

about febrile seizures, provide information about the time that afebrile seizures

develop after vaccination, then preponderant evidence favors a finding that the

seizures would manifest within about 72 hours of the vaccination. But, the

evidence does not support a conclusion that N.S. displayed symptoms of a seizure

within the first 72 hours post-vaccination. In an affidavit written in 2017, Ms.

Skorupska averred that N.S. “had been having spasms for at least two days, maybe

more” as of November 22, 2013, placing the onset at four days after vaccination,

“maybe” sooner. Exhibit 40 at 2. Ms. Skorupska also states that N.S. had a fever

the night of vaccination, and, “in retrospect, she felt as though N.S. had been

having seizures possibly for the ‘entire week,’ meaning from the first day, or two,

of the vaccination.” Pet’r’s Supp’l Br. at 3.

Ms. Skorupska’s account does not overcome the medical records created

when N.S. went to the hospital in November 2013. These medical records, which

were generated contemporaneously with N.S.’s illness, note only a two-day history

of spasms, i.e., four-days post-vaccination. This is not to indicate that Ms.

Skorupska is presenting a false narrative; special masters have often refrained from

crediting accounts presented years later because of a faulty memory, not

dishonesty. See Hodge v. Sec'y of Health & Hum. Servs., No. 09-453V, 2023 WL

4186513, at *71 (Fed. Cl. Spec. Mstr. May 24, 2023), mot. for rev. denied, 168

Fed. Cl. 117 (2023); Barnett v. Sec'y of Health & Hum. Servs., No. 19-1578V,

2021 WL 6211590, at *6 (Fed. Cl. Spec. Mstr. Dec. 10, 2021); Duda v. Sec'y of

Health & Hum. Servs., No. 19-31V, 2021 WL 4735857, at *8 (Fed. Cl. Spec. Mstr.

Aug. 10, 2021); Mueller v. Sec'y of Health & Hum. Servs., No. 06-775V, 2011

WL 1467938, at *9 (Fed. Cl. Spec. Mstr. Mar. 16, 2011); Velchek v. Sec’y of

Health & Hum. Servs., No. 02-1479, 2005 WL 2847451, at *17 (Fed. Cl. Spec.

Mstr. Oct. 28, 2005). Here, Ms. Skorupska’s affidavit—written nearly four years

after N.S.’s vaccination and, additionally, phrased in uncertain terms—is too far-

removed and too speculative to be credited over the medical records.

Ms. Skorupska argued that the two events (vaccination and onset of infantile

spasms) could not simply be viewed as a “coincidence.” Pet’r’s Br. at 64.

However, in several cases, special masters have found that a sequence of events in

which a child-vaccinee’s febrile seizure occurred within one day of a vaccination

21

did not mean that the vaccine caused the child’s epilepsy. Vinesar, 2023 WL

5427935 at *32.

In sum, Ms. Skorupska has not presented any persuasive evidence to justify

a timeframe of up to six days. After 72 hours is credited as an acceptable

timeframe, Ms. Skorupska has not demonstrated that N.S. developed symptoms

within this time. Accordingly, Ms. Skorupska has failed to meet her burden

regarding timing. Regardless, if Ms. Skorupska were found to have prevailed on

the timing element, she would still not be entitled to compensation due to

deficiencies in other parts of her case. Grant v. Sec’y of Health & Hum. Servs.,

956 F.2d 1144 (Fed. Cir. 1992) (“Temporal association is not sufficient, however,

to establish causation in fact.”).

C. Loving Prong 4 / Althen Prong 1

The first Althen prong, which corresponds to the fourth Loving prong,

requires a petitioner to present a reliable and persuasive medical theory. Boatmon

v. Sec'y of Health & Hum. Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019) (citing

Knudsen v. Sec'y of Health & Hum. Servs., 35 F.3d 543, 548 (Fed. Cir. 1994)).

Ms. Skorupska presents the theory that the Hib vaccine caused inflammation,

which “caused altered connectivity, which in turn, caused epilepsy.” Pet’r’s Br. at

57. Ms. Skorupska further states that N.S.’s genetic mutation made him more

susceptible to the inflammatory response, but that his “genetic mutation alone is

not a sound explanation for [his] infantile spasms,” as his “genetic variant would

typically cause something different than infantile spasms” such as delays or

autism. Id. at 57-58. Ms. Skorupska summarizes, “The theory is that [N.S.]’s

susceptible genetic mutation made him more likely to have the particular reaction

to the vaccine,” and that she “has set forth his medical theory causally connecting

his injury of infantile spasms and the sequelae to the Hib vaccination that he

received in 2013.” However, while Ms. Skorupska may theorize that the vaccine

caused N.S.’s condition, she does not actually describe in her briefs the underlying

mechanism to explain how the vaccine could have done so. Instead, she simply

states that she is relying on all of her experts’ reports. Pet’r’s Br. at 58.

Citing various cases, the Secretary asserts that a theory based upon cytokines

is too general to be persuasive. The Secretary argues that “there is an utter lack of

evidence in this case that the Hib vaccine can cause proinflammatory cytokines

that ultimately, and deleteriously, affect voltage-gated sodium channels encoded by

SCN2A.” Resp’t’s Br. at 24. Additionally, the Secretary notes that vaccines are

meant to stimulate the immune system, and so invocation of an innate immune

22

response is not sufficient to explain causation, as it would mean that all vaccines

and pathogens could cause N.S.’s condition. Id. at 26. Finally, the Secretary

argues that Ms. Skorupska and Dr. Huq’s assertion of molecular mimicry is

“unwarranted,” as no treating doctor “even suspected that N.S. had an autoimmune

condition.” Id. at 27. The Secretary further notes that generalized theories of

molecular mimicry are frequently invoked and rejected in the program. Id. at 27-

28.

A finding that a petitioner has not met one element of the Althen prongs

justifies a denial of compensation. Ms. Skorupska has not carried her burden under

the other Loving / Althen prongs. As discussed more thoroughly in the previous

sections, the evidence does not preponderate in a finding that N.S. experienced

cytokine-driven inflammation, nor did he exhibit inflammatory symptoms within

the relevant timeframe. Without a showing that N.S. experienced cytokine-driven

inflammation, Ms. Skorupska cannot prevail with a theory relying on such

inflammation, regardless of whether she has met her burden under this prong.

Additionally, neither party discussed Ms. Skorupska’s theory in great detail in their

briefs. See Pet’r’s Br. at 57-58; Resp’t’s Br. at 24-28; Pet’r’s Reply at 3.12 Thus, a

fulsome analysis of the theory is not necessary.

VI. Part Two: Alternative Cause

The foregoing analysis is a basis for determining that Ms. Skorupska failed

to meet her burden of proving with preponderant evidence that the Hib vaccine

significantly aggravated N.S.’s neurologic problems. See Osenbach v. Sec’y of

Health & Hum. Servs., No. 16-419V, 2023 WL 5714809, at *29-32 (Fed. Cl. Spec.

Mstr. Aug. 8, 2023) (finding Dr. Huq’s theory of inflammation unpersuasive), mot.

for rev. denied, unpublished op., aff’d, No. 2024-1663, 2025 WL 2387944 (Fed.

Cir. Aug. 18, 2025). To a degree, the analysis has been incomplete because it has

12

Although Ms. Skorupska cites three articles about molecular mimicry (see Pet’r’s Br.

at 41-42), she does not present any detailed argument. Rather, the parties devoted more

discussion to inflammation. Likewise, this Decision focuses on cytokine-driven inflammation.

Importantly, Ms. Skorupska has not adequately established that N.S. suffered from an

autoimmune condition. See Exhibit C at 3; Resp’t’s Br. at 27, 31. Thus, even if it were assumed

that molecular mimicry was a reliable theory to explain how the Hib vaccine can cause infantile

spasms, Ms. Skorupska would remain not entitled to compensation because N.S.’s medical

history does not align with the theory. See Hibbard v. Sec’y of Health & Hum. Servs., 698 F.3d

1355, 1364 (Fed. Cir. 2012). For these reasons, this Decision does not elaborately evaluate

molecular mimicry.

23

largely not addressed the “elephant in the room,” which is N.S.’s genetic variation.

See Stone v. Sec'y of Health & Hum. Servs., 676 F.3d 1373, 1380 (Fed. Cir. 2012).

If, for the sake of argument, it were assumed that Ms. Skorupska had met her

burden of proof, then the Secretary may show N.S.’s “condition . . . is due to

factors unrelated to the administration of the vaccine.” 42 U.S.C. § 300aa–

13(1)(B). “If a petitioner successfully satisfies the Loving inquiry, the burden

shifts to the government to prove by a preponderance of the evidence that a ‘factor

unrelated’ to the vaccine caused the petitioner’s injuries.” Sharpe v. Sec’y of

Health & Hum. Servs., 964 F.3d 1072, 1080 (Fed. Cir. 2020). As stated earlier, the

parties differ widely about the significance of the genetic variation. Ms. Skorupska

maintains that the genetic mutation “primed N.S. to have the adverse reaction to

the Hib vaccine.” Pet’r’s Br. at 3. Her “position is that the variant SCN2A gene is

not enough to cause Petitioner’s current mental state. While he may have been at

an increased risk to develop some deficits due to the genetic mutation, the

vaccination (not simply the genetic mutation) is what caused his current mental

state." Id. at 4. In contrast, the Secretary maintains: “It is beyond question that

N.S.’s mutation amply explains his entire course.” Resp’t’s Br. at 16.

A. Method of Analysis / Precedent Cases

Special masters may consider the method of analysis and outcome of similar

cases, although those outcomes are not binding. Oliver v. Sec’y of Health & Hum.

Servs., 900 F.3d 1357, 1363-64 (Fed. Cir. 2018); Nunez v. Sec’y of Health &

Hum. Servs., 144 Fed. Cl. 540, 548 (2019), aff’d on non-related grounds, 825 F.

App'x 816 (Fed. Cir. 2020).

The topic of genetic variants and their potential to cause harm has been

discussed in multiple cases that reached the Federal Circuit. As recounted

extensively, the first four opinions from the Federal Circuit ruled that special

masters were not arbitrary in finding that a genetic mutation in an SCN1A gene

was the sole basis for a child’s condition. Vinesar, 2023 WL 5427935, at *1-20

(citing cases). But, then, the tide may have shifted. The Federal Circuit vacated an

opinion in which the special master found a genetic mutation explained the child-

vaccinee’s worsening. Sharpe, 964 F.3d 1072; see also Vinesar, 2023 WL

5427935, at *14-18. Then, the Federal Circuit went a step further and reversed the

(undersigned) special master’s finding of genetic causation. Sanchez v. Sec’y of

24

Health & Hum. Servs., 34 F.4th 1350 (Fed. Cir. 2022); see also Vinesar, 2023 WL

5427935, at *18-20.13

The Secretary argues that Ms. Skorupska’s case “is analytically no different

from the Dravet syndrome cases in which respondent has uniformly prevailed

through Federal Circuit review.” Resp’t’s Br. at 16. The Secretary also attempts

to distinguish Sharpe. Id. at 17-19. However, the Secretary omits any discussion

of Sanchez.

The omission of Sanchez from the Secretary’s brief can be excused because

Ms. Skorupska cites no Federal Circuit cases about vaccines and genetics. See

Pet’r’s Br. The omission of Federal Circuit genetic cases, especially Sanchez,

from Ms. Skorupska’s brief is less easily justified.

The lack of argument based upon Sanchez from Ms. Skorupska is

regrettable. As stated in Vinesar, 2023 WL 5427935, at *45-47, the Federal

Circuit’s opinion in Sanchez has introduced questions about how special masters

(at least the undersigned special master) should approach cases with genetic issues.

For example, the Federal Circuit’s opinion in Sanchez could be interpreted as

requiring evidence from the Secretary about a genetic variant that is stronger than

the evidence previously credited in cases such as Hammitt v. Sec'y of Health &

Hum. Servs., 98 Fed. Cl. 719 (2011), aff'd sub nom. Stone v. Sec'y of Health &

Hum. Servs., 676 F.3d 1373 (Fed. Cir. 2012). Future precedential opinions from

the Federal Circuit may provide additional guidance. See Strickland v. United

States, 423 F.3d 1335, 1338 & n. 3 (Fed. Cir. 2005) (stating that if a trial court

thinks Federal Circuit opinions are inconsistent with Supreme Court precedent, the

trial court may note the conflict and urge en banc consideration).

B. Evidence

Several pieces of overlapping evidence support a finding that the E1211K

variant is the sole cause of N.S.’s medical condition.

13

In two recent non-precedential opinions, the Federal Circuit affirmed judgments

denying compensation in cases in which the child-vaccinee had a genetic mutation without

discussing genetics. See Vinesar v. Sec’y of Health & Hum. Servs., No. 2024-1787, 2025 WL

2945665 (Fed. Cir. Oct. 17, 2025); Osenbach v. Sec’y of Health & Hum. Servs., No. 2024-1663,

2025 WL 2387944 (Fed. Cir. Aug. 18, 2025).

25

An important and foundational article is by Ogiwara and colleagues.14

These researchers discovered an SCN2A-E1211K mutation in a person who

suffered from infantile spasms. He was born with mild asphyxia. Ogiwara at

1051. His seizures began at age 11 months. Ogiwara at 1047. The researchers

compared the genetic mutation (c3613G>A) to a cohort of approximately 300

individuals. This genetic mutation was found “only in affected individuals.” Id. at

1048. The researchers then conducted “whole-cell patch-clamp recordings” and

other tests. (“Patch clamps” allow researchers to measure the flow of current

through ion channels. Dorland’s Illus. Med. Dict. at 362 (33rd ed.).) The

researchers determined that E1211K is “evolutionarily conserved among vertebrae

and invertebrae VGSC [voltage gated sodium channel] α subunits.” Id. at 1049.

The researchers also tested how the E1211K variant affected a cell’s

electrophysiologic property. They found “E1211K . . . markedly altered the

voltage-dependence of Nav1.2 indicating high pathologic potential[] of E1211K.”

Id. The researchers concluded: “our present study and others’ provide solid

genetic evidence implicating SCN2A in the etiology of human epilepsies.” Id. at

1052.

In 2014, when analyzing the results of N.S.’s genetic testing, Dr. Jabs cited

the Ogiwara article. She noted that the Ogiwara researchers tested the mutation

and they found the mutation changed the functioning of the protein. This testing

supported Dr. Jabs’s opinion that N.S.’s genetic mutation was a “deleterious

change.” Exhibit 23 at 25.

Dr. Raymond cited the 2009 Ogiwara article in his first report. Exhibit A at

5. In his view, Ogiwara and colleagues “clearly demonstrated that this mutation

seriously impairs the normal gating actions of the channel.” Id. at 6.

Dr. Huq’s response to Ogiwara was underwhelming. Dr. Huq stated that:

“Only one other individual with SCN2A E1211K variant has been reported but that

individual also had birth asphyxia which likely contributed to or modified the

pathogenesis of his epilepsy.” Exhibit 68 at 4; accord Id. at 7, 10, 28.15 Although

14

I. Ogiwara et al., De novo mutations of voltage-gated sodium channel alpha II gene

SCN2A in intractable epilepsies, 73 NEUROLOGY 1046 (2009). Filed as Exhibit A-2.

15

As discussed below, by the time Dr. Huq wrote his first report, Dr. Raymond had

identified other cases in which individuals had the same genetic mutation. See Exhibit C at 1-2.

Thus, the evidentiary basis for Dr. Huq’s assertion that “only one other individual” is not readily

apparent.

26

he highlighted the potential importance of asphyxia, Dr. Huq did not engage with

other meaningful parts of Ogiwara. Dr. Huq did not contest Ogiwara’s assertion

that E1211K is evolutionarily conserved. Dr. Huq also did not contest the

electrophysiologic consequences to an alteration in E1211K.

The electrophysiologic testing carries great weight because this testing

shows that the genetic variant interferes with how the sodium channel is supposed

to function. See Exhibit C at 2 (Dr. Raymond’s second report: “E1211K produced

severely affected channels with electrophysiologic properties very different than

the normal functioning voltage gated sodium channel”). In other words, the gene

directed the creation of a protein that does not act as it should. Oligawa’s finding

regarding the electrophysiologic dysfunction appears to be confirmed by other

researchers. Exhibit E (Lauxmann).16 Due to this variation in how the sodium

channel was created in N.S., N.S.’s sodium channel had a deficiency. It is difficult

to see how the vaccination affected N.S.’s anatomy.17

Ogiwara also lays a foundation for an answer to another potential challenge

to the significance of N.S.’s genetic variant. Dr. Huq acknowledges that the

“E1211K variant has not been detected in healthy individuals.” Exhibit 193 at 2.

Although Dr. Huq does not cite a basis for this assertion, Ogiwara did not find the

16

Stephan Lauxmann et al., Relationship of electrophysiological dysfunction and clinical

severity in SCN2A-related epilepsie, 12 HUM. MUTAT. 1942 (2018). Filed as Exhibit E.

17

Although the electrophysiologic properties are important to the undersigned (see

Whitecotton v. Sec’y of Health & Hum. Servs., 81 F.3d 1099, 1108 (Fed. Cir. 1996) (stating that

special masters have discretion in how they weigh evidence)), conceivably, the undersigned is

overvaluing this testing. In Sanchez, in one of the critical articles about the significance of the

genetic mutation in that case (the Parfait article), “the researchers used fibroblasts to see how the

gene performed in tissue cultures. . . . Their experiment ‘confirm[ed] the deleterious effect of this

mutation.’” Sanchez, 2020 WL 5641872, at *59. Based upon this work, the petitioners’

geneticist (Dr. Niyazov) conceded that the genetic mutation was “an ‘altered function’

mutation.” Id. at *60. However, upon an appeal, the Federal Circuit stated that “There is no

evidence . . . that [the child-vaccinee’s] mutations would have resulted in the same progression

and severity of his [disease], absent the vaccine.” Sanchez, 34 F.3d at 1356. The Federal Circuit

did not discuss the fibroblast testing.

This discussion about whether the Federal Circuit’s precedential opinion in Sanchez bars

the consideration of the electrophysiologic testing is academic in the sense that Ms. Skorupska

has made no argument about Sanchez. Ms. Skorupska also did not discuss the Ogiwara’s

electrophysiologic testing. See Pet’r’s Reply.

27

mutation when they looked for it among approximately 300 healthy individuals.

Ogiwara at 1048. Dr. Huq’s response is that “population databases contain DNA

sequence information of only a tiny percentage of healthy population.” Exhibit

193 at 2. Dr. Raymond persuasively refutes a concern about population databases.

Exhibit EE at 2 (relying, in part, on the gnomAD database). Special masters have

rejected concerns that population databases are unlikely to detect healthy

individuals with the potentially harmful genetic mutation. See Harris v. Sec’y of

Health & Hum. Servs., No. 07-60V, 2011 WL 2446321, at *15 (Fed. Cl. Spec.

Mstr. May 27, 2011), mot. for rev. granted, 102 Fed. Cl. 282 (2011), reinstated sub

nom., Snyder v. Sec’y of Health & Hum. Servs., 553 Fed. App’x 994 (Fed. Cir.

2014); Stone v. Sec’y of Health & Hum. Servs., No. 04-1041V, 2010 WL

1848220, at *25 (Fed. Cl. Spec. Mstr. Apr. 15, 2010), mot. for rev. denied after

remand, 99 Fed. Cl. 187 (2011), aff’d, 676 F.3d 1373 (Fed. Cir. 2012).

The lack of unaffected individuals contrasts with the number of examples in

the literature of children with the same mutation and who developed neurologic

problems similar to N.S.’s problems. Dr. Raymond cited Ogiwara in his first

report. Exhibit A at 5. In his second report, Dr. Raymond cited two more articles

(Wolff and Wong).18 Exhibit C at 1-2. In his third report, Dr. Raymond

emphasized that these people had the “exact same variant.” Exhibit K at 5. Then,

after Dr. Huq mistakenly asserted that there was only one case in the literature, Dr.

Raymond found more cases and presented them in his fourth report. Exhibit T at

14. Finally, in the fifth report, Dr. Raymond brought forward two more examples.

Exhibit EE at 4.

The Secretary aptly summarizes this evidence:

(Case No. 1) Ex. A, Tab 1: Marcus Wolff et al., Genetic

and phenotypic heterogeneity suggest therapeutic

implications in SCN2A-related disorders, 140 BRAIN

1316-36 (2017). The subject with an E1211K mutation is

listed as subject number 49 in Table 3. Id. at 11. The

subject had West syndrome (WS) (see page 6 for

abbreviation, WS) with seizure outcome noted to be

18

Markus Wolff et al., Genetic and phenotypic heterogeneity suggest therapeutic

implications in SCN2A-related disorders, 140 BRAIN 1316 (2017). Filed as Exhibit 55.

Virginia C. N. Wong et al., SCN2A mutation in a Chinese boy with infantile spasm -

response to Modified Atkins Diet, 37 BRAIN DEV. 729 (2015). Filed as Exhibit D.

28

intractable. Id. (last followed at 4 years of age).

Cognition at both onset and follow-up was “severe

intellectual disability” (SD) (see page 12 for

abbreviation, SD). Id.

(Case No. 2) Ex. A, Tab 2: I. Ogiwara et al., De novo

mutations of voltage-gated sodium channel [alpha II]

gene SCN2A in intractable epilepsies, 73 NEUROLOGY

1046-53 (2009). This article supports Dr. Raymond’s

statement that “the glutamine at position 1211 is highly

evolutionarily conserved among vertebrate and

invertebrate voltage gated sodium channels and [the

authors] went on to demonstrate that significantly altered

the functional properties of the channel.” Ex. A at 5

(citing Ex. A, Tab 2, at 4-5); see also Ex. T at 13 (Dr.

Raymond). With regard to the E1211K subject discussed

in the article, the authors state: “One de novo mutation,

E1211K, was identified in a patient with sporadic

infantile spasms that progressed into severe symptomatic

generalized epilepsy.” Ex. A, Tab 2, at 6.

(Case No. 3) Ex. D: Virginia C.N. Wong et al., SCN2A

mutation in a Chinese boy with infantile spasm –

response to Modified Atkins Diet, 37 BRAIN & DEV.

729-32 (2015). This is a case report of the same E1211K

mutation. The subject “had developmental delay since

birth. He developed flexor spasm of his upper limbs

occurring in clusters since 15 months. … He had

developmental regression and autistic features later

during subsequent follow up. Electroencephalography

(EEG) showed modified hypsarrhythmia.” Id. at 2

(noting “severe intellectual disability” at age 6).

Characterizing the nature of the mutation, the authors

state, “this mutation affected highly conserved amino

acid … and the mutation was predicted to be deleterious

to protein function and pathogenic by PolyPhen-2, SIFT

and Align-GVGD analysis. This mutation has been

reported previously in a patient with sporadic IS, marked

29

developmental delay and severe intellectual disability.”

Id. (citing Ogiwara (Ex. A, Tab 2)).

(Case No. 4) Ex. Q: Hane Lee et al., Clinical Exome

Sequencing for Genetic Identification of Rare Mendelian

Disorders, 312(18) JAMA 1880-87 (2014) (including

relevant Supplementary Online Content). On page 27, the

authors report a case of “p.Glu1211Lys” like in this case.

The clinical indications are listed as “developmental

delay, epilepsy, seizures, spasms, autism, [m]icrocephaly,

wide palpebral fissures, hypertonia, mitochondrial [sic],

complex IV, cytochrome c oxidase deficiency, Rett

syndrome, Lennox Gastaut.” Id.

(Cases No. 5-7) Ex. R: Qi Zeng et al., SCN2A-Related

Epilepsy: The Phenotypic Spectrum, Treatment and

Prognosis, 15(809951) FRONTIERS MOLECULAR

NEUROSCIENCE (2022). This is a report of three cases

overall. On page 5, the authors report 2 cases of E1211K,

both with commensurately severe outcomes as the

current case, one subject noted to be unable to sit alone

or speak (last follow-up at age 6 years, 11 months), the

other with delay before seizure onset, walking at 4 years,

8 months, and unable to speak (last follow-up at age 5).

On page 7, the third subject was also delayed before

seizure onset and could not walk or speak.

(Cases No. 8-9) Ex. V: Géza Berecki et al., Functional

correlates of clinical phenotype and severity in recurrent

SCN2A variants, 5(1) COMMUNICATIONS BIOLOGY

1-13 (2022) (Article No. 515) (doi: 10.1038/s42003-022-

03454-1) (including Supplementary Data 1: Phenotypic

data of 179 individuals with 38 recurrent SCN2A

variants, and 2 individuals with unique variants (Ex. V at

14)). The authors reported two previously-unreported

cases of E1211K mutation both with moderate delays

prior to seizure development, like in the current case, and

both with severe delay “at last review,” like in the current

case. Id. at 14 (also listing the cases cited in Ogiwara

30

(Ex. A, Tab 2), Wong (Ex. D), and Wolff (Ex. A, Tab

1)).

(Case No. 10) Ex. HH: Balamurugan Nagarajan et al.,

Landscape of genetic infantile epileptic spasms

syndrome—A multicenter cohort of 124 children from

India, 00 EPILEPSIA OPEN 1-22 (2023)

(doi:10.1002/epi4.12811). In Table 1, a subject is listed

as having the c.3631G>A variation, like in the current

case. Id. at 5. All the subjects had “infantile-onset (2

months-2 years) epileptic spasms and classical or

modified hypsarrhythmia on EEG with or without

developmental delay or regression.” Id. at 3 (defining

Infantile Epileptic Spasms Syndrome for the purpose of

the report). The subject with variation c.3631G>A is

coded as “Serial no. 16.” Id. at 5. In the outcomes table

(Table 4) on page 13, that patient had generalized tonic

(GT) seizures at 6 months and epileptic spasms (ES) at 7

months. At 14 months, she developed stereotypies, and

her phenotypic characteristics included central hypotonia

(C HYP) and clinodactyly (CLDY). By 81 months of

age, she was non-ambulatory (NAMB) and autistic (AU).

Id. at 13 (see page 19 for explanation of abbreviations).

The authors note that “the longterm neurodevelopmental

outcome was poor in most children with SCN2A (5/6

non-ambulatory, 4/7 autistic, one progressed to LGS

[Lennox-Gastaut syndrome]).” Id. at 10.

(Case No. 11) Ex. II (Eye, Eye): Sylvia Vidal et al., The

utility of Next Generation Sequencing for molecular

diagnostics in Rett syndrome, 7:12288 SCIENTIFIC

REPORTS 1-11 (2017) (doi:10.1038/s41598-017-11620-

3). The patient with the same mutation as N.S. is

highlighted on page 4. That study evaluated Rett

syndrome-like patients, “an early-onset

neurodevelopmental disorder that almost exclusively

affects girls and is totally disabling.” Id. at 1 (emphasis

added) (noting characteristics to be “a period of

apparently normal development (up to the age of 6–18

31

months), followed by a regression characterized by loss

of speech and purposeful hand use and motor apraxia that

may be associated with epilepsy and dysautonomic

features”). Contextually, the patient with the same

missense mutation as N.S. had a severe disorder. See also

Id. at 5 (“we detected 2 SNVs [single nucleotide variants]

… in SCN2A genes, which are associated with mental

retardation, stereotypic movements, epilepsy, and/or

cerebral malformations”).

Resp’t’s Br. at 13-15.

This consistency of outcomes contributes to finding that the E1211K variant

causes neurologic problems. The consistency of outcomes for this variant further

weakens an argument that variations among SCN2A genes produces a variety of

outcomes. See Exhibit 50 at 2, Exhibit 68 at 8, Exhibit 212 at 2; see also Pet’r’s

Br. at 57. Dr. Raymond agrees that some SCN2A genetic variants lead to different

results. See Exhibit T at 4. But, those other genetic variants are not N.S.’s variant.

From the evidence presented, N.S.’s variant, the E1211K variant, appears to lead to

neurologic problems always.

For all these reasons, a preponderance of the evidence supports the finding

that N.S.’s genetic variant caused and was the sole cause of his neurologic

problem. Dr. Raymond’s opinion regarding the sole cause is persuasive. See

Exhibit A at 7 (“The pathogenic mutation in [N.S.’s] SCN2A gene is the sole cause

of his epileptic encephalopathy"); Exhibit C at 3 (N.S.’s “pathogenic mutation in

SCN2A . . . is the sole cause of his early infantile epileptic encephalopathy”);

Exhibit EE at 6 (same).

The finding that the E12111K variant impaired N.S.’s neurologic

development should not be controversial. Even Dr. Huq stated the “missense

variant in SCN2A gene E1211K . . . is considered to be pathogenic.” Exhibit 68 at

6.19 Dr. Huq’s opinion that this “pathogenic variant” merely meant that he was

19

To reinforce the conclusion that the E1211K variant is pathologic, Dr. Raymond’s final

report cites an article with guidelines in how to interpret variants. Exhibit EE at 2-3, citing

Exhibit BB (Sue Richards et al., “Standards and Guidelines for the Interpretation of Sequence

Variants: A Joint Consensus Recommendation of the American College of Medical Genetics and

Genomics and the Association for Molecular Pathology,” 17(5) Genet Med. 405 (2015)).

However, these Guidelines are relatively complicated and difficult to understand. Thus, the

32

“predisposed to having seizures” is not in line with the multiple researchers who

have identified the mutation as causative. See Terran v. Sec’y of Health & Hum.

Servs., 195 F.3d 1302, 1316 (Fed. Cir. 1999) (authorizing special masters to

consider, among other factors, whether an opinion “enjoys general acceptance

within a relevant scientific community”).

For these reasons, the evidence preponderates in favor of finding that N.S.’s

genetic variant was the sole cause of his neurologic problems, including the

infantile spasms and developmental delay. Thus, even if it were found that Ms.

Skorupska met her burden of presenting a persuasive case for each of the Loving

prongs, she would remain not entitled to compensation because the Secretary

would have met his burden to present a factor unrelated to the vaccination caused

N.S.’s condition.

VII. Conclusion

Ms. Skorupska has consistently maintained that the Hib vaccine harmed her

son. She has persevered during this litigation, even representing herself for a time.

Her dedication and love for her son is admirable. However, these traits cannot be a

basis for awarding compensation. Congress requires that special masters evaluate

claims based upon the evidence.

Here, Ms. Skorupska’s evidence is lacking. The primary flaw is that she did

not establish that N.S. developed inflammation as her experts’ theory predicted. In

addition, it is more likely than not that N.S.’s variant in the E1211K gene was the

sole cause of his neurologic problems. Thus, Ms. Skorupska is not entitled to

compensation.

The Clerk's Office is instructed to enter judgment in accord with this

decision unless a motion for review is filed. Information about filing a motion for

review, including the deadline, can be found in the Vaccine Rules, which are

available on the website for the Court of Federal Claims.

Guidelines do not affect the outcome of Ms. Skorupska’s case. In the future, Dr. Raymond may

wish to proceed through the Guidelines step-by-step.

33

IT IS SO ORDERED.

s/Christian J. Moran

Christian J. Moran

Special Master

34