# SKORUPSKA v. SECRETARY OF HEALTH AND HUMAN SERVICES

> United States Court of Federal Claims · March 6, 2026

URL: https://www.frixlaw.com/law-library/cases/11273335

## Case

- **Court:** United States Court of Federal Claims
- **Decided:** March 6, 2026
- **Precedential status:** Unpublished
- **Opinion:** Opinion
- **Judges:** Christian J. Moran
- **Cited by:** 0 later opinions in the Frix Law Library

## Citator (automated)

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- Full citator and citing cases: https://www.frixlaw.com/law-library/cases/11273335

## How later opinions describe it (automated extraction)

- 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
- stating that special masters have discretion in how they weigh evidence
- reversing special master's decision that petitioners were not entitled to compensation

## Opinion text

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

3
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
4
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

5
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
7
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.

9
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.

10
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

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Source: Frix Law Library, https://www.frixlaw.com/law-library/cases/11273335. Public record. Not legal advice.