# HARGROVE v. SECRETARY OF HEALTH AND HUMAN SERVICES

> United States Court of Federal Claims · November 21, 2023

URL: https://www.frixlaw.com/law-library/cases/10736964

## Case

- **Court:** United States Court of Federal Claims
- **Decided:** November 21, 2023
- **Precedential status:** Unpublished
- **Opinion:** Opinion
- **Judges:** Nora Beth Dorsey
- **Cited by:** 0 later opinions in the Frix Law Library

## Citator (automated)

- No negative treatment found by the automated citator. That is not the same as a confirmation that the case is good law; read the citing cases.
- Full citator and citing cases: https://www.frixlaw.com/law-library/cases/10736964

## How later opinions describe it (automated extraction)

- noting that “close calls” are resolved in Petitioner’s favor
- noting that special masters are bound by both § 13(b)(1) and Vaccine Rule 8(b)(1) to consider only evidence that is both “relevant” and “reliable”

## Opinion text

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
Filed: October 27, 2023

* * * * * * * * * * * * * * *
DESTANIE HARGROVE, as Mother *
on behalf of A.F.M., *
*
Petitioner, * No. 17-233V
*
v. * Special Master Dorsey
*
SECRETARY OF HEALTH * Entitlement; Diphtheria-Tetanus-Acellular-
AND HUMAN SERVICES, * Pertussis (“DTaP”) Vaccine; Epilepsy;
* Seizures; Encephalopathy.
Respondent. *
*
* * * * * * * * * * * * * * *

Rick Alan Cory, Danks & Danks, Evansville, IN, for Petitioner.
Colleen Clemons Hartley, U.S. Department of Justice, Washington, DC, for Respondent.

DECISION1

I. INTRODUCTION

On February 17, 2017, Destanie Hargrove, as Mother, on behalf of A.F.M., (“Petitioner”)
filed a petition under the National Vaccine Injury Compensation Program (“Vaccine Act” or “the
Program”), 42 U.S.C. § 300aa-10 et seq. (2018).2 Petitioner alleges A.F.M. suffered “table[]

1
Because this Decision contains a reasoned explanation for the action in this case, the
undersigned is required to post it on the United States Court of Federal Claims’ website and/or at
https://www.govinfo.gov/app/collection/uscourts/national/cofc in accordance with the E-
Government Act of 2002. 44 U.S.C. § 3501 note (2018) (Federal Management and Promotion of
Electronic Government Services). This means the Decision will be available to anyone with
access to the Internet. In accordance with Vaccine Rule 18(b), Petitioners have 14 days to
identify and move to redact medical or other information, the disclosure of which would
constitute an unwarranted invasion of privacy. If, upon review, the undersigned agrees that the
identified material fits within this definition, the undersigned will redact such material from
public access.
2
The National Vaccine Injury Compensation Program is set forth in Part 2 of the National
Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755, codified as amended,
42 U.S.C. §§ 300aa-10 to -34 (2018) (“Vaccine Act” or “the Act”). All citations in this Decision
to individual sections of the Vaccine Act are to 42 U.S.C.A. § 300aa.
injuries, including, but not limited to, severe static epileptic encephalopathy and permanent brain
damage resulting from adverse effects of one or more . . . vaccinations received on May 7,
2014,” including diphtheria-tetanus-acellular-pertussis (“DTaP”), hepatitis B (“Hep B”),
inactivated polio vaccine (“IPV”), Haemophilus influenzae type b (“Hib”), and Rotavirus.
Petition at 1 (ECF No. 1).3 Respondent argued against compensation, stating that “this case is
not appropriate for compensation under the terms of the Act.” Respondent’s Report (“Resp.
Rept.”) at 2 (ECF No. 38).

After carefully analyzing and weighing the evidence presented in this case in accordance
with the applicable legal standards,4 the undersigned finds that Petitioner has failed to provide
preponderant evidence that A.F.M.’s DTaP vaccine caused her condition. Thus, Petitioner has
failed to satisfy her burden of proof under Althen v. Secretary of Health & Human Services, 418
F.3d 1274, 1280 (Fed. Cir. 2005). Accordingly, the petition must be dismissed.

II. ISSUES IN DISPUTE

First, the parties dispute whether the initial event experienced by A.F.M. on May 8, 2014
was a seizure or an apparent life-threatening event (“ALTE”). See Joint Prehearing Statement of
Facts and Issues (“Joint Prehearing Submissions”), filed Apr. 10, 2022 (ECF No. 99).

The next issue is whether A.F.M. suffered a Table injury. Petitioner’s Motion for Ruling
on the Record (“Pet. Mot.”), filed Apr. 23, 2021, at 1, 12 (ECF No. 80). As acknowledged by
Respondent, the alleged Table injury is based on the question of whether A.F.M. suffered an
“encephalopathy.” Resp. Response to Pet. Mot. (“Resp. Response”), filed Aug. 13, 2021, at 21
(ECF No. 83) (citing 42 C.F.R § 100.3(a)(II)(B)). In the alternative, Petitioner asserts a
causation-in-fact claim in which Petitioner may be entitled to compensation if she shows by
preponderant evidence that A.F.M.’s injury was caused-in-fact by the DTaP vaccination she
received on May 7, 2014. Pet. Mot. at 1. The parties disagree about whether Petitioner has
provided preponderant evidence of causation for all three Althen prongs. See Joint Prehearing

3
Petitioner subsequently narrowed her allegation to assert Table and causation-in-fact claims for
injuries caused by the DTaP vaccination on May 7, 2014, and not the other vaccinations A.F.M.
received that day. See Petitioner’s Motion for Ruling on the Record (“Pet. Mot.”), filed Apr. 23,
2021, at 1, 12 (ECF No. 80). Therefore, the undersigned references only the DTaP vaccination
going forward except when describing the opinions of Dr. Holmes when he uses the term
“vaccinations.”
4
Although this Decision discusses some but not all of the medical literature in detail, the
undersigned reviewed and considered all of the medical records and all of the medical literature
submitted in this matter. See Moriarty v. Sec’y of Health & Hum. Servs., 844 F.3d 1322, 1328
(Fed. Cir. 2016) (“We generally presume that a special master considered the relevant record
evidence even though [s]he does not explicitly reference such evidence in h[er] decision.”);
Simanski v. Sec’y of Health & Hum. Servs., 115 Fed. Cl. 407, 436 (2014) (“[A] Special Master
is ‘not required to discuss every piece of evidence or testimony in her decision.’” (citation
omitted)), aff’d, 601 F. App’x 982 (Fed. Cir. 2015).

2
Submissions at 1; Pet. Mot. at 6, 25; Resp. Response at 21-26; Althen, 418 F.3d at 1280.

III. BACKGROUND

A. Procedural History

Petitioner filed her petition on February 17, 2017, and filed medical records in the
following months.5 Petition; Pet. Exhibits (“Exs.”) 1-36. Respondent filed his Rule 4(c) Report
arguing against compensation on December 11, 2017. Resp. Rept. at 2.

On March 15, 2018, Petitioner filed an expert report from Dr. Marcel Kinsbourne. Pet.
Ex. 37. Respondent filed an expert report from Dr. Gregory Holmes on June 7, 2018. Resp. Ex.
A. In October 2018 and February 2019, the parties filed supplemental expert reports from Dr.
Kinsbourne and Dr. Holmes, respectively. Pet. Ex. 39; Resp. Ex. C. At a status conference held
on May 1, 2019, the special master assigned to the case presented additional questions for the
experts to opine on. Order dated May 6, 2019 (ECF No. 51). From June 2019 to January 2021,
the parties filed responsive expert reports from Dr. Kinsbourne and Dr. Holmes. Pet. Exs. 40-44;
Resp. Exs. D-G.

Throughout this time, the parties entertained settlement discussions but ultimately
requested a ruling on the record. See ECF Nos. 57, 72, 71. On April 23, 2021, Petitioner filed
her motion for a ruling on the record. Pet. Mot. Respondent filed a response on August 13,
2021, and Petitioner filed a reply on September 13, 2021. Resp. Response; Pet. Reply to Resp.
Response (“Pet. Reply”), filed Sept. 13, 2021 (ECF No. 84).

Upon reassignment of the case to the undersigned, a status conference was held on
February 10, 2022. See Notice of Reassignment dated Feb. 7, 2022 (ECF No. 87); Order dated
Feb. 10, 2022 (ECF No. 88). The undersigned acknowledged the case was ripe for a ruling on
the record; however, after review of the evidence, she opined that given the complexity of the
issues with this case, a hearing would be very helpful. Order dated Feb. 10, 2022, at 2. The
parties agreed to a remote hearing. Id. Prior to the hearing, Respondent confirmed that he
wished to defend the case and was not interested in settlement discussions. Resp. Status Rept.,
filed Apr. 18, 2022 (ECF No. 106).

An entitlement hearing was held via videoconference on May 17, 2022. See Order dated
May 18, 2022 (ECF No. 112); Transcript (“Tr.”) 1. Dr. Kinsbourne and Dr. Holmes testified at
the hearing. Tr. 3. On October 31, 2022, Petitioner filed a post-hearing brief. Pet. Post-Hearing
Brief (“Pet. Br.”), filed Oct. 31, 2022 (ECF No. 122). Respondent filed a post-hearing brief on
March 3, 2023, and Petitioner filed a reply on March 23, 2023. Resp. Post-Hearing Submission
(“Resp. Br.”), filed Mar. 3, 2023 (ECF No. 125); Pet. Reply to Br. in Further Support of
Compensability of Pet. Claim (“Pet. Reply Br.”), filed Mar. 23, 2023 (ECF No. 126).

This matter is now ripe for adjudication.

5
Petitioner continued to file medical records throughout the course of litigation.

3
B. Factual History

1. Summary of Medical Records6

A.F.M., a female, was born full-term on October 24, 2013, by a vaginal delivery. Pet.
Ex. 8 at 18.7 She weighed seven pounds, three ounces at birth. Id. Her newborn screening was
normal. Pet. Ex. 7 at 1.8 A.F.M. received a Hep B vaccination on the date of her birth. Pet. Ex.
8 at 17.

Following A.F.M.’s birth, Petitioner presented A.F.M. for regular pediatric well-child
visits at eight-days old, one-month old, and two-months old with her pediatrician, Dr. Larry
Crick. See Pet. Ex. 7 at 2-12. The assessments on these dates were normal. Id. On January 27,
2014, A.F.M. received the Pediatrix (DTaP, Hep B, IPV), Hib, and Rotavirus vaccinations. Id. at
13.

On May 7, 2014, A.F.M. returned to Dr. Crick’s office for her six-month physical
examination. Pet. Ex. 7 at 15-19. A.F.M. was examined that day by Sharon Shields, advanced
practice registered nurse (“APRN”). Id. A.F.M. presented with a cough and runny nose, but was
developmentally appropriate and her examination was normal. Id. In connection with the visit,
A.F.M. received the subject vaccinations—Pediatrix (DTaP, Hep B, IPV), Hib, and Rotavirus.
Id. at 17.

The next day, on May 8, 2014, A.F.M. was taken by ambulance to Methodist Hospital
emergency department (“ED”), as she was reportedly “limp and staring off at ceiling” and was
“not responsive initially.” Pet. Ex. 8 at 47-110. The emergency medical responders (“EMS”)
indicated that A.F.M. was not responding appropriately upon their arrival, but she became more
alert during transport. Id. It was noted that A.F.M. received routine vaccinations the day before.
Id.

6
The medical record summary is taken directly from Respondent’s Rule 4(c) Report, which the
undersigned finds fairly and accurately depicts the events described in the medical records.
Resp. Rept. at 2-14. For an additional detailed summary of the medical records, see Dr. Holmes’
initial expert report. Resp. Ex. A at 1-19.
7
Exhibit 8 (ECF No. 6-9) as outlined in Petitioner’s exhibit list is the “Birth records and Post-
Injury records from Methodist Hospital.” These records were Bates-stamped as “Exhibit 4.”
Hereinafter, the undersigned, like Respondent, will refer to the birth records and post-injury
records from Methodist Hospital as “Exhibit 8.” ECF No. 6-9.
8
Exhibit 7 (ECF No. 6-8) as outlined in Petitioner’s exhibit list is the “Vaccine, Pre-Injury and
Post-Injury records from Dr. Larry Crick.” These records were Bates-stamped as “Exhibit 5.”
Hereinafter, the undersigned, like Respondent, will refer to Dr. Crick’s records as “Exhibit 7.”
ECF No. 6-8.

4
At the ED, A.F.M. was alert and in no distress. Pet. Ex. 8 at 47-110. A.F.M.’s physical
examination was normal. Id. A.F.M. was admitted overnight for observation for upper
respiratory infection (“URI”), an episode of altered mental status (“suspect possibly secondary to
a reflux or chocking episode, but she did not have any cyanosis”),9 and possible urinary tract
infection (“UTI”). Id. at 67-68.

During her overnight observation,10 A.F.M.’s lab results displayed an abnormal liver
function test with a mildly elevated serum glutamic-oxaloacetic transaminase (“SGOT”) and an
alkaline phosphatase of 247 (normal 50-136). Pet. Ex. 8 at 56-57. A.F.M. had an elevated white
count on complete blood count (“CBC”) of 15.19 (normal 4.8-10.8), elevated platelet count of
542,000 (normal up to 400,000), and an increase in the percentage of bands to 24 (normal 0-11).
Id. A.F.M.’s urinalysis was abnormal with positive nitrite and leukoesterase and 2+ bacteria. Id.
A.F.M.’s chest X-ray was negative. Id. at 88. A.F.M.’s urine culture was positive for
Escherichia coli (“E. coli”). Id. at 86. On May 9, 2014, A.F.M.’s discharge diagnoses included
a UTI and URI. Id. at 47. A.F.M.’s physical examination was normal at the time and the
hospitalist recommended that A.F.M. have an outpatient electroencephalogram (“EEG”) to rule
out a seizure. Id. at 83.

On May 13, 2014, A.F.M. presented for an EEG which displayed normal results. Pet. Ex.
8 at 111. On May 15, 2014, A.F.M. returned to her pediatrician, Dr. Crick, for follow-up from
her hospital discharge and EEG. Pet. Ex. 7 at 23-27. Dr. Crick noted that A.F.M. had
experienced no problems since her hospital discharge and that she continued to take antibiotics
because her urine culture grew E. coli. Id. A.F.M.’s physical examination was normal, and she
was assessed with a UTI. Id.

On May 22, 2014, A.F.M. experienced another episode of “altered mental status” and
presented to Dr. Crick. Pet. Ex. 7 at 28-31. Petitioner reported that A.F.M. “stared upward with
[her] mouth open and her face was red” and then her behavior normalized within five minutes.
Id. Dr. Crick assessed A.F.M. with gastroesophageal reflux (“GERD”), he noted that her cystitis
(UTI) was resolved, and he wanted to “[rule out] [s]eizures.” Id. Dr. Crick prescribed
Ranitidine for GERD. Id. at 5.

On June 16, 2014, A.F.M. returned to Dr. Crick’s office for a seven-month, well-child
visit. Pet. Ex. 7 at 32-36. A.F.M. was “pulling at her left ear” on arrival. Id. On examination,
A.F.M. achieved all expected developmental milestones. Id. A.F.M. was taking Ranitidine,
ibuprofen, and hydroxyzine (as needed for nasal congestion). Id. Nurse Shields noted that
“A.F.M.’s parents are very concerned the Pertussis component of her combination immunization

9
Cyanosis is “a bluish discoloration, especially of the skin and mucous membranes due to
excessive concentration of deoxyhemoglobin in the blood.” Cyanosis, Dorland’s Med.
Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=12098 (last visited
Oct. 16, 2023).
10
During the observation period, A.F.M.’s grandmother inquired as the “contents of vaccination
from a couple days before.” Pet. Ex. 8 at 83.

5
may have caused a perceived seizure in May of 2014.” Id. Further, Nurse Shields noted that
“[w]hile the EEG was negative and there was a greater concern for a choking episode related to
Reflux[,] the pertussis vaccine will be eliminated for the time being and dosing for vaccines will
be administered on an alternative schedule.” Id. A.F.M. received Rotavirus and diphtheria
tetanus (“DT”) vaccinations at this visit. Id.

Six days later, on June 22, 2014, A.F.M. presented to the ED at Union County Methodist
Hospital for a seizure. Pet. Ex. 10 at 1-15.11 En route to the ED, A.F.M. became unresponsive.
Id. at 6. On arrival to the ED, A.F.M. was responding to touch and slightly crying. Id.
Petitioner reported that A.F.M. had a history of seizures for three months. Id. Petitioner further
reported that A.F.M. “received the TDAP [three] months ago and had a seizure about [one] week
later” and that A.F.M. “had TD immunization on Monday and seizure today.” Id. at 5. A.F.M.’s
initial white count on CBC was elevated at 17.49 (4-10 nl), and she was transferred to St. Mary’s
Medical Center (“SMMC”) pediatric intensive care unit (“ICU”) for a higher level of care. Id.

From June 22 to June 25, 2014, A.F.M. was hospitalized at SMMC for new onset
seizures and a UTI.12 Pet. Ex. 9 at 1-5.13 On arrival at SMMC, A.F.M. was “completely at her
baseline.” Id. at 3. She was “alert, happy, responsive[,] and completely nontoxic on exam.” Id.
A.F.M. did not have a fever. Id. The hospital physician, Dr. Taveepong Terayanont pursued a
seizure work-up, as it was reported that this was the third episode. Id. at 7. A head
computerized tomography (“CT”) and chest X-ray were normal. Id. at 3. A.F.M.’s brain
magnetic resonance imaging (“MRI”) was also normal. Id. While A.F.M.’s EEG during the
hospitalization did not display frank epileptiform discharges, it was noted that “in the correct
clinical context may be associated with a predisposition towards partial seizures or partial
seizures with secondary generalization, but this must be carefully correlated clinically.” Id. at 3.

Following the EEG, a physician at SMMC consulted with a neurologist at Kosair
Children’s Hospital (“Kosair”). Pet. Ex. 9 at 3. The Kosair neurologist recommended that
A.F.M. start Keppra. Id. A.F.M.’s urine culture was positive for E. coli, and she was started on
amoxicillin. Pet. Ex. 9 at 36. A renal ultrasound was ordered, which displayed a probable right
extrarenal pelvis and thickening of the urinary bladder wall, probable cystitis. Id. at 40-42. At
discharge, Petitioner was instructed to have A.F.M. follow-up with Kosair pediatric neurology

11
Exhibit 10 (ECF No. 6-11) as outlined in Petitioner’s exhibit list is the “Post-Injury records
from Union County Methodist Hospital.” These records were Bates-stamped as “Exhibit 7.”
Hereinafter, the undersigned, like Respondent, will refer to the post-injury records from Union
County Methodist Hospital as “Exhibit 10.” ECF No. 6-11.
12
It was noted during this hospitalization that A.F.M.’s grandmother believed that “A.F.M. [was]
having seizures after vaccines and is possibly allergic to something in the shot.” Pet. Ex. 9 at 63.
13
Exhibit 9 (ECF No. 6-10) as outlined in Petitioner’s exhibit list is the “Post-Injury records
from St. Mary’s Medical Center.” These records were Bates-stamped as “Exhibit 6.”
Hereinafter, the undersigned, like Respondent, will refer to the post-injury records from St.
Mary’s Medical Center as “Exhibit 9.” ECF No. 6-10.

6
and her pediatrician. Id. at 5.

On June 29, 2014, A.F.M. experienced a seizure episode and presented to Methodist
Hospital Union County ED. Pet. Ex. 10 at 16-19. A.F.M. was transferred to Kosair for further
work-up. Pet. Ex. 11 at 1-253.14

On admission to Kosair, A.F.M.’s Keppra dosage was increased, she was treated for her
UTI, and a video EEG was completed. See Pet. Ex. 11 at 1-253. The video EEG documented a
25-minute focal seizure, during which time A.F.M. was interactive. Id. at 3-9. A.F.M. also had
a four-minute generalized tonic-clonic seizure associated with desaturation, requiring Ativan and
a bag-valve-mask ventilation for recovery. Id. The neurology service noted that A.F.M.’s
“family [was] very concerned these ‘seizures’ [were] a result of her DTaP vaccine that she
received one day prior to initial onset of symptoms.” Id. at 30. The neurology service diagnosed
A.F.M. with focal epilepsy, recommended a further increase of Keppra, and ordered Diastat as
needed. Id. at 35. A.F.M. was discharged on July 2, 2014. Id.

Later the same day, A.F.M. presented to Methodist Hospital ED due to two reported
seizures since her discharge from Kosair. Pet. Ex. 8 at 115-42. A.F.M. was tearful and irritable,
and she was transported by ambulance to the pediatric ICU at SMMC. Id.

On admission to SMMC, it was noted that A.F.M. had a history of a seizure disorder that
had been “detected roughly [two] weeks ago.” Pet. Ex. 9 at 76-77. A.F.M. displayed daily
seizures at SMMC that initially responded to increased Keppra. Id. Then, A.F.M. required
endotracheal intubation for airway protection and the hospitalist believed that her condition
required transfer to a tertiary care center with an inpatient pediatric neurology team. Id. On July
5, 2014, A.F.M. was transferred to Vanderbilt Children’s Hospital (“Vanderbilt”) for further
treatment. Id.

From July 5 to September 12, 2014, A.F.M. was hospitalized at Vanderbilt and
underwent an extensive work-up. Pet. Ex. 12 at 16-22.15 Upon arrival to Vanderbilt, A.F.M.
was alert, but ten minutes later, she suffered a seizure lasting 140 minutes. Id. at 1045-49.
Thereafter, A.F.M. was placed in a pentobarbital coma. Id. A.F.M.’s genetics work-up for
epilepsy was unrevealing. Id. at 16. On August 27, 2014, a gastric tube (“G-tube”) was placed
following reduced oxygen saturations with feeding and aspiration. Id. A.F.M.’s brain MRI
displayed “restricted diffusion involving bilateral hippocampi with mild surrounding edema.”

14
Exhibit 11 as outlined in Petitioner’s exhibit list is the “Post-Injury records from Kosair
Children’s Hospital.” These records were Bates-stamped as “Exhibit 8.” Hereinafter, the
undersigned, like Respondent, will refer to the birth records and post-injury records from Kosair
Children’s Hospital as “Exhibit 11.”

Exhibit 12 as outlined in Petitioner’s exhibit list is the “Post-Injury records from Vanderbilt
15

Monroe Carell Jr. Children’s Hospital.” These records were Bates-stamped as “Exhibit 9.”
Hereinafter, the undersigned, like Respondent, will refer to the post-injury records from
Vanderbilt Monroe Carell Jr. Children’s Hospital as “Exhibit 12.”

7
Id. From September 4 to September 6, 2014, A.F.M. underwent a two-day EEG, which
displayed “seizures involving right parieto-temporo-occipital region.” Id. at 1075. At the time
of discharge on September 12, 2014, A.F.M.’s primary diagnosis was epilepsy and secondary
diagnosis was hypoxemia. Id. at 16.

Following discharge, A.F.M. was admitted to Cardinal Hill Rehabilitation from
September 12 to September 18, 2014. Pet. Ex. 13 at 2-7.16 On admission, A.F.M.’s history was
noted as “beginning around June 2014 patient started having seizures that became increasingly
frequent.” Id. During rehabilitation, A.F.M. had two to three seizures a day without
desaturations below 80%, and all resolved in less than four minutes without medications. Id.
Thereafter, Petitioner and her mother requested that A.F.M. be transferred to University of
Kentucky Children’s Hospital (“UK”) for continuous EEG monitoring. Id. A.F.M. was stable at
the time of discharge. Id.

Accordingly, on September 18, 2014, A.F.M. was transferred to UK and remained
inpatient until September 25, 2014. Pet. Ex. 11 at 683-715. Without the results of the genetic
testing from Vanderbilt, neurologist Dr. Kimberley Jones noted that the most likely explanation
for A.F.M.’s seizures and neurocognitive decline was an “underlying genetic disorder, either a
channelopathy or mitochondrial disorder.” Id. at 715. Likewise, Dr. Donita Lightner noted
concern about a metabolic or genetic disease during the hospitalization. Id. at 704-05. On
September 25, 2014, the discharge diagnoses included “intractable multifocal epilepsy” with
“[s]uspected West syndrome[,] infantile spasms [and] hypsarrhythmia on EEG,”
“[e]ncephalopathy,” and “[b]ehavioral regression . . . [l]ikely secondary to intractable epileptic
seizures compounded by [medications].” Id. at 695.17

On October 1, 2014, A.F.M. presented to SMMC by ambulance, having reportedly
suffered 22 seizures that day. Pet. Ex. 9 at 408. The ED physician noted that A.F.M.’s
neurologic baseline was declining and she recently had a G-tube placed for feeds. Id. at 404.
A.F.M. was then transferred to Kosair by air ambulance for further evaluation. Id.

A.F.M. remained inpatient at Kosair from October 2 to October 9, 2014. Pet. Ex. 11 at
256-60. Following an extensive examination, pediatric neurologist Dr. Vinay Puri’s impression
was that A.F.M. was suffering from infantile spasms and cryptogenic epilepsy with malignant
migrating seizures of infancy. Id. at 275-77. Dr. Puri noted that A.F.M. likely had an
“underlying epilepsy of unidentified etiology that progressed and now likely has post-seizure
encephalopathy due to prolonged seizures (140 minute seizure on 7/5/2014).” Id. at 275. Dr.

16
Exhibit 13 as outlined in Petitioner’s exhibit list is the “Post-Injury records from Cardinal Hill
Rehabilitation.” These records were Bates-stamped as “Exhibit 10.” Hereinafter, the
undersigned, like Respondent, will refer to the post-injury records from Cardinal Hill
Rehabilitation as “Exhibit 13.”
17
Again, A.F.M.’s grandmother noted concerns that vaccines caused her seizures and she also
questioned molds and parasites. Pet. Ex. 11 at 683. The family noted that they were upset with
the treatment at Vanderbilt and think they are responsible for her current neurologic status. Id.

8
Puri also noted that A.F.M.’s genetic work-up had been unrevealing as to a genetic cause for her
epilepsy. Id. Moreover, Dr. Puri reviewed the genetic test (EpiSEEK) gene analysis from
Vanderbilt, which displayed two genetic variants18 of uncertain clinical significance, as neither
was associated with severe epilepsy or matched her clinical picture. Id. at 275, 659-61. On
October 9, 2014, A.F.M.’s discharge diagnosis was infantile spasms and partial complex seizure
disorder. Id. at 256.

Following her hospitalization, on October 13, 2014, A.F.M. had a repeat EEG, which
displayed tracing consistent with hypsarrhythmia.19 Pet. Ex. 11 at 916-17. The same day,
A.F.M.’s mitochondrial whole genome sequencing testing results were reported. Pet. Ex. 32 at
5-6. A.F.M.’s testing revealed that “no large deletions or known deleterious mutations were
detected.” Id. The diagnosis of a mitochondrial DNA disorder could not be confirmed. Id.

Two days later, on October 15, 2014, A.F.M. presented to Methodist Hospital by
emergency transport for respiratory distress. Pet. Ex. 8 at 143-67. A.F.M.’s chest X-ray
displayed evidence of right lower lobe pneumonia, and she was transferred to SMMC. Id. at
164; Pet. Ex. 9 at 415-19. On admission, Dr. Puri, from Kosair, was consulted as it was noted
that they were having problems controlling her airway due to severe encephalopathy and chronic
intractable seizure disorder. Pet. Ex. 9 at 415-19. At that time, Dr. Puri and the SMMC
hospitalist believed that palliative care would be in the best interest of the child, but the family
wanted everything done, including “very aggressive care.” Id. at 419. Thereafter, A.F.M. was
transferred to Kosair for further treatment and the potential placement of a trach. Pet. Ex. 11 at
1027-33.

A.F.M. remained inpatient at Kosair from October 16 to October 31, 2014. Pet. Ex. 11 at
928-32. A trach was not placed. Id. A.F.M.’s discharge diagnoses included aspiration
pneumonia, infantile spasms, and cryptogenic epilepsy. Id.

Following discharge from Kosair, A.F.M. returned to her pediatrician, Dr. Crick, on
November 3, 2014. Pet. Ex. 7 at 37-41. Petitioner reported that A.F.M. continued to experience
seizures and that A.F.M. had fluid on her liver. Id. On examination, A.F.M. had poor eye
contact, non-purposeful movements, and weakness in all extremities. Id. Dr. Crick’s assessment
was global developmental delay, infantile spasms with intractable epilepsy, and hypotonic
cerebral palsy. Id. Dr. Crick recommended a hearing examination and ophthalmology
consultation with Dr. Craig Douglas. Id.

In November 2014, A.F.M. began physical therapy through First Steps. Pet. Ex. 14 at 1-

18
The two genetic variants reviewed were RAF1 and SCN4A. Pet. Ex. 11 at 659-60.
19
Hypsarrhythmia refers to “an electroencephalographic abnormality sometimes observed in
infants, with random, high-voltage slow waves and spikes that arise from multiple foci and
spread to all cortical areas. It is seen most commonly in cases of jackknife seizures.”
Hypsarrhythmia, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/
definition?id=24469 (last visited Oct. 16, 2023).

9
2.20 On December 24, 2014, A.F.M. returned to the Methodist Hospital ED for seizures. Pet.
Ex. 16 at 9-21.

On January 21, 2015, A.F.M. had a repeat EEG, on which “no normal activity was seen,”
and the results were interpreted as “likely consistent with a transitional state between
hypsarrhythmia and the slow spike and wave of Lennox-Gastaut syndrome.”21 Pet. Ex. 18 at 4-
5.

On February 5, 2015, A.F.M. underwent an asthma evaluation with pediatric
pulmonologist, Dr. Ronald Morton. Pet. Ex. 27 at 5-7. Dr. Morton’s assessment was chronic
lung disease, chronic pulmonary aspiration, and restrictive lung disease. Id.

A.F.M. returned to Dr. Puri on August 10, 2015 for a follow-up pediatric neurology
evaluation. Pet. Ex. 31 at 27-33. At that time, Dr. Puri indicated that A.F.M.’s conditions were
of an “unclear etiology.” Id. An EEG study on the same date was consistent with epileptic
encephalopathy, but no longer displayed findings suggestive of hypsarrhythmia. Id. at 34-35.

From September 1 to September 9, 2015, A.F.M. was hospitalized at Kosair for
aspiration pneumonia, and she was treated with antibiotics. Pet. Ex. 18 at 75-84.

At 22 months of age, on September 17, 2015, A.F.M. underwent a developmental
evaluation. Pet. Ex. 14 at 5-7. A.F.M.’s fine and gross motor skills were in the two-month
range, her communication skills were in the three-month range, her cognitive skills were in the
two-to-three-month range, and her social skills were in the three-month range. Id.

Due to feeding intolerance, A.F.M. returned to Kosair for a Nissen fundoplication with a
G-tube exchange from December 14 to December 16, 2015. Pet. Ex. 18 at 472-73. While in the
hospital, she was seen by pediatric urology for her neurogenic bladder with associated urinary
retention. Id. at 510-15.

On July 18, 2016, A.F.M. had an initial asthma and allergy evaluation with Dr. Kelly
Brauer. Pet. Ex. 23 at 4-7. Petitioner reported in A.F.M.’s “past immunization history” that she
had “reaction to shots – very bad seizures.” Id. Food allergy testing was completed that day and
Petitioner was instructed to return with A.F.M. when the test results were available. Id.

20
Exhibit 14 as outlined in Petitioner’s exhibit list is the “Post-Injury records from First Steps.”
These records were Bates-stamped as “Exhibit 12.” Hereinafter, the undersigned, like
Respondent, will refer to the post-injury records from First Steps as “Exhibit 14.”
21
Lennox-Gastaut syndrome is “an atypical form of absence epilepsy characterized by diffuse
slow spike waves, often with atonic, tonic, or clonic seizures and intellectual disability; there
may also be other neurologic abnormalities or multiple seizure types.” Lennox Syndrome,
Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=
110889 (last visited Oct. 16, 2023).

10
On July 25, 2016, A.F.M. was admitted to Kosair for seizures with secondary diagnoses
of viral illness (unspecified), metabolic acidosis, and hypernatremia. Pet. Ex. 18 at 865-69. A
repeat EEG completed the same day was suggestive of a moderate diffuse encephalopathy and
“may be seen in children with global developmental delays.” Id. at 900. It was also suggestive
of an ongoing potential towards a multifocal epilepsy disorder. Id. There was no
hypsarrhythmia noted. Id. A.F.M. was discharged the next day. Id.

On August 24, 2016, A.F.M. was evaluated by pediatric ophthalmologist, Dr. Craig
Douglas. Pet. Ex. 30 at 2-5. Dr. Douglas diagnosed her with cortical visual impairment and
recommended follow-up in two years. Id. Dr. Douglas noted that while her vision may improve
somewhat, her prognosis was extremely guarded. Id.

On September 2, 2016, A.F.M. returned to Dr. Brauer for results of her food allergy
testing. Pet. Ex. 23 at 8-10. Petitioner inquired about “potential immune problems.” Id.
A.F.M.’s immunoglobulin (“Ig”) E testing was negative for common foods. Id. Moreover, she
had reassuring immunoglobulins for her age, but no appreciable pneumococcal or diphtheria
titers. Id.

A.F.M. returned for a pediatric neurology evaluation with Dr. Puri on September 12,
2016. Pet. Ex. 31 at 12-18. In connection with the follow-up, Dr. Puri noted his impression that
A.F.M. “had a genetic abnormality that predisposed her to having seizures after having
immunizations, and that she definitely developed epilepsy encephalopathy.” Id.

A.F.M. again returned to Dr. Puri on December 13, 2016, and Dr. Puri noted that “[t]he
etiology of her epilepsy is likely genetic. She would benefit from more expansive genetic
testing.”22 Pet. Ex. 31 at 11.

On December 19, 2016, Petitioner presented with A.F.M. to Pediatric Health Group to
establish new pediatric care. See Pet. Ex. 29 at 2-8. Petitioner reported that she “believe[d]
vaccine[s] cause[d] [A.F.M.’s] medical problems.” Id. at 2. A.F.M. was wheelchair bound at
that time. Id.

In April 2017, A.F.M. was hospitalized at St. Vincent Hospital for chronic constipation.
Pet. Ex. 35 at 1-3. In addition, A.F.M. had a repeat EEG on April 27, 2017, which showed
slowing of the background consistent with generalized encephalopathy and the presence of
epileptiform discharges. Id. at 21-22.

2. Summary of Additional Records23

22
It is not clear whether this recommended testing was done as no results were filed.
23
This section includes a brief summary of specific records relevant to the factual issue or to the
undersigned’s Decision.

11
A.F.M.’s medical records establish that on May 7, 2014, the day of her DTaP
vaccination, she was examined by a nurse practitioner, and noted to have a cough and runny
nose, but otherwise was normal and developmentally appropriate. Pet. Ex. 7 at 15-19. The
following morning, May 8, 2014, a call was placed for an ambulance at 5:34 a.m. Pet. Ex. 38 at
2. The ambulance arrived on the scene at 5:46 a.m. Id. Upon arrival, EMS found A.F.M. in her
“grandmother’s lap, unresponsive” with “respirations irregular and labored.” Id. Lung sounds
were clear, pulse was regular, and her skin was pale. Id. Pupils were dilated and non-reactive.
Id. EMS did not document that A.F.M. was having seizure activity when they arrived. EMS
records show that at 5:48 a.m., A.F.M. had a pulse of 140, respiratory rate of 20, and oxygen
saturation of 88% on room air.24 Id. at 1. Oxygen was administered and A.F.M.’s oxygen
saturation improved to 92%. Id. At 5:54 a.m., A.F.M. was noted to be “improved.” Id.
Assessment documented at 5:48 a.m. revealed no mental abnormalities, no abnormalities of the
head, face, eyes, or airway, and no abnormalities of lung sounds. Id. EMS departed the home at
5:59 a.m. and arrived at the ED at 6:22 a.m. Id. Again, A.F.M.’s condition was noted to be
improved. Id. In their narrative notes for the event, EMS documented that A.F.M.’s “condition
gradually improved to normal response for age” and remained stable for the “duration of the
trip.” Id.

The ED records on May 8, 2014, at 6:30 a.m. document that A.F.M.’s condition on
arrival was stable, and she was alert and playful. Pet. Ex. 8 at 51, 53, 68. Her eyes were open;
she was babbling and obeying commands. Id. at 52. The emergency physician (Dr. Eric Ervin)
was at the bedside at 6:40 a.m. to examine A.F.M. Id. at 55. At 6:50 a.m., A.F.M. was again
noted to be “awake, happy, [and] playing.” Id. at 49. Neurological examination revealed that
she was oriented and had no motor or sensory deficit. Id. At 10:48 a.m., A.F.M.’s condition was
“good stable.” Id. at 59. Dr. Ervin’s impression was “[URI], episode of altered mental status,
suspect possibly secondary to a reflux or choking episode, but she did not have any cyanosis.
Possible [UTI].” Id. at 69.

Nursing neurological system assessment performed on May 8, 2014, at 11:35 a.m.
documented that A.F.M. was alert, that her behavior was appropriate, and that her assessment
was within defined neurological parameters. Pet. Ex. 8 at 90. A.F.M. was noted to be awake,
cooperative, and smiling at 12:14 p.m. Id. at 93. Progress notes at 1:13 p.m., note that A.F.M.
was “awake and alert, baby appear[ed] appropriate for age. Pleasant affect. No acute distress.”
Id. at 81. During nursing rounds at 6:29 p.m., A.F.M. was again noted to be awake and
cooperative, and smiling. Id. at 94. Throughout the evening and overnight, A.F.M.’s
assessments remained stable with no indication of abnormal neurological behavior. See id. at
93-100. On May 9, 2014, at 5:16 a.m., A.F.M. was “awake” and “cooperative.” Id. at 89.

A.F.M. was discharged on May 9, 2014, at 9:46 a.m., and her physical examination prior
to discharge was normal. Pet. Ex. 8 at 65, 71, 83. There is no indication that A.F.M. had any
decreased or abnormal level of consciousness during her hospitalization. See id. On May 13,
2014, A.F.M. had an EEG, which was normal. Id. at 111. There is no indication that she had a
decreased or abnormal level of consciousness at that time. See id. A.F.M. was seen by her

24
Normal oxygen saturation is ≥ 95%; ≤ 75% is critical. Kathleen D. Pagana & Timothy J.
Pagana, Mosby’s Manual of Diagnostic and Laboratory Tests, 1061-62 (6th ed. 2018).

12
pediatrician, Dr. Crick, on May 15, 2014. Pet. Ex. 7 at 23-27. Dr. Crick documented that
A.F.M. had no problems following her hospital discharge; her physical examination was normal.
Id.

No recent medical records have been filed.

C. Expert Reports

1. Petitioner’s Expert, Dr. Marcel Kinsbourne25

a. Background and Qualifications

Dr. Kinsbourne earned his B.A. from Christ Church at Oxford University in 1952, his
Bachelor of Medicine (B.M.) and Bachelor of Surgery (B.Ch.) from Oxford University Medical
School in 1955, his M.A. and Doctor of Medicine (D.M.) from Oxford University in 1956 and
1963, and his M.D. from State of North Carolina in 1967. Pet. Ex. 40 at 1. From 1955 to the
early 1990s, he regularly treated patients. Id. at 1-2; Tr. 7. Throughout his career, Dr.
Kinsbourne has also held teaching positions at various institutions. Pet. Ex. 40 at 2-3. Dr.
Kinsbourne has held medical licenses in the United Kingdom, Canada, North Carolina,
Massachusetts, and Virginia. Id. at 2. He has been bestowed numerous honors and awards, has
served and is currently serving on a number of editorial boards, and has authored or co-authored
more than 400 publications. Id. at 3-39.

Dr. Kinsbourne has not practiced pediatric neurology in over forty years. Tr. 30.

b. Opinions

Dr. Kinsbourne offered opinions related to the factual issue, whether A.F.M. experienced
a seizure or an ALTE the day after vaccination. He also opined as to causation.

i. Initial Event May 8, 2014—Seizure vs. ALTE

At the hearing, Dr. Kinsbourne summarized the events of May 8, 2014, the day after
vaccination, and concluded A.F.M. had a seizure. Tr. 10-15. A.F.M.’s medical records show
that at approximately 6:30 a.m., Petitioner “saw her daughter unresponsive with [her] eyes turned
up . . . and mouth open, limp, and [] struggling for breath.” Tr. 10. A.F.M. was taken by
ambulance to Methodist Hospital, and the “ambulance record reflected that they thought [] she []
was having a seizure.” Tr. 11. Dr. Kinsbourne stated that when A.F.M. arrived at the hospital,
“she had spontaneously recovered without treatment.” Id. Dr. Kinsbourne testified that the
physicians were “unclear as to what had happened,” and they questioned whether she had
choked, regurgitated, or had a seizure. Id. An EEG was ordered, and it was normal. Id. He
acknowledged that A.F.M. was afebrile before the event. See Pet. Ex. 39 at 6; Tr. 53.

25
Dr. Kinsbourne submitted six expert reports and testified at the entitlement hearing on May 17,
2022. Pet. Exs. 37, 39, 41-44; Tr. 3.

13
Dr. Kinsbourne agreed that when A.F.M. was discharged from the hospital, after her
admission on May 8, 2014, her discharge diagnosis did not include seizure. Tr. 44. He opined
that at the time, the physicians did not know what had happened, whether A.F.M.’s episode was
caused by choking, apnea,26 or infection. Id.

According to Dr. Kinsbourne, A.F.M. had a seizure on May 8, 2014, presenting as
“behavioral arrest,” since “the child [] stopped doing anything whatever – stopped moving,
stopped making any noise – and [was] fixed in one position.” Tr. 15. Dr. Kinsbourne described
A.F.M. as being in a “static limbo,” while having “very brief focal attacks lasting [] a minute or
two or three at a time, coming in . . . [a] cluster, one after the other . . . without the child retaining
full awareness or full behavior in between.” Tr. 15-16. Dr. Kinsbourne also opined there was
“continuous status epilepticus, which is a seizure lasting more than 30 minutes.” Tr. 16.

Dr. Kinsbourne disagreed with Respondent’s expert Dr. Holmes’ opinion that A.F.M.’s
initial event on May 8, 2014 was an ALTE. Tr. 17. According to Dr. Kinsbourne, ALTE is “not
a diagnosis,” but a condition that can have many different causes, including seizures. Id.; see
also Pet. Ex. 42 at 1-2. He cited several articles that describe ALTE, including one by
Aminiahidashti,27 who defined it as “as an episode that is frightening to the observer . . .
characterized by some combination of apnea, color change, marked change in muscle tone,
choking, gagging, or coughing.” Pet. Ex. 42 at 1 (quoting Pet. Ex. 42A at 1).28 Dr. Kinsbourne
disagreed that A.F.M. had “gagging, choking, coughing[,] or an obstructed airway.” Id. at 2.

1. Type and Duration of Event on May 8, 2014

At the hearing, Dr. Kinsbourne testified that A.F.M.’s initial seizure on May 8, 2014, was
a focal or “hypomotor seizure.” Tr. 13-14. Prior to the hearing, however, his opinions were
different and changed over the course of his six reports.

In his first expert report, Dr. Kinsbourne opined that A.F.M.’s initial seizure was an
“absence seizure.” Pet. Ex. 37 at 3. He defined absence seizures as “seizures that [] last just a
few seconds, and are characterized by a blank or ‘absent’ stare.” Id. (internal citation omitted).
They “involve brief, sudden lapses of consciousness. . . . [and] are more common in children

26
Apnea is the “cessation of breathing.” Apnea, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=3758 (last visited Oct. 16, 2023).
27
Hamed Aminiahidashti, Infantile Apparent Life-Threatening Events, an Educational Review, 3
Emergency 8 (2015). This is also cited as Resp. Ex. F, Tab 18.
28
Aminiahidashti stated that ALTE is not a diagnosis, and it may be associated with various
conditions, including GERD, “respiratory infections, and seizures.” Pet. Ex. 42A at 2. For
“reported final diagnoses for patients with apparent life-threatening events,” see Pet. Ex. 42A at
2 tbl.1.

14
than adults.” Id. (internal citation omitted). Riviello29 explained that the “peak age of childhood
absence epilepsy is from 6 to 7 [years].” Pet. Ex. 37L at 4. “The seizures consist of an abrupt
cessation of ongoing activity, with a change of facial expression and a blank gaze. The duration
is short, rarely lasting longer than 30 [seconds], there is no preceding aura or subsequent
postictal depression, and there may be frequent automatisms.” Id.

In his second expert report, Dr. Kinsbourne opined that A.F.M.’s first seizure was
“nonconvulsive status epilepticus (NCSE),”30 or in the alternative, “a complex partial status
epilepticus.”31 Pet. Ex. 39 at 1. In support of this opinion, Dr. Kinsbourne cited an abstract (not
the full article) by Chang and Shinnar.32 See Pet. Ex. 39B. They defined status epilepticus as a
“medical emergency” requiring “prompt recognition and treatment.” Id. at 1. And they
described nonconvulsive status epilepticus as a “heterogeneous disorder with varied causes and
several subtypes” but there is “no universally accepted definition.” Id. The two most common
subtypes are absence status epilepticus and complex partial status epilepticus. Id. “The degree
of mental status alteration can vary from mild confusion all the way to coma.” Id. Chang and
Shinnar further stated that NCSE “should be suspected in patients who fail to wake up after a
convulsive seizure and in those with coma of undetermined cause.” Id.

In his third and fifth expert reports, Dr. Kinsbourne again opined that A.F.M.’s first
seizure was a NCSE, and stated it was a “prolonged absence seizure [that] exceeded 30 minutes
in duration.” Pet. Ex. 41 at 1; see also Pet. Ex. 43 at 1. Dr. Kinsbourne also clarified the
definition of NCSE: “Strictly speaking, [NCSE] is only used when the seizure activity is
corroborated by concurrent [EEG].” Pet. Ex. 41 at 1. A.F.M. did not have an EEG done during
her episode on May 8, 2014. Pet. Ex. 43 at 2.

29
James Riviello, Pediatric EEG Abnormalities, in The Clinical Neurophysiology Primer 178
(A.S. Blum & S.B. Rutkove eds., 2007).
30
NCSE is a “status epilepticus that does not include generalized tonic-clonic seizures.”
Nonconvulsive Status Epilepticus, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=108328 (last visited Oct. 10, 2023).
31
Dr. Holmes opined that “complex partial status epilepticus” is a “term that is no longer used.”
Resp. Ex. F at 2.
32
Andrew K. Chang & Shlomo Shinnar, Nonconvulsive Status Epilepticus, 29 Emergency Med.
Clinics N. Am. 65 (2011).

15
In his fifth report, Dr. Kinsbourne opined that A.F.M.’s initial seizure was “atypical” for
an absence seizure. Pet. Ex. 43 at 1.33 He stated that “[e]ach individual [absence] seizure lasts
no more than a few seconds” and typically “occur in clusters.” Id. He further opined that
because A.F.M. was limp during the initial event, it was “atypical for absence seizures.” Id. He
then opined that A.F.M.’s initial seizure was an “absence status” seizure, which according to Dr.
Kinsbourne, is “the most common type of [NCSE].” Id. at 2 (citing Pet. Ex. 43E).34

Grin and DiMario stated that absence status epilepticus is “characterized by a prolonged
confusional state of variable duration and severity produced by a diagnostic [EEG] spike and
wave pattern.” Pet. Ex. 43E at 1. Dr. Kinsbourne also cited Andermann and Robb,35 stating that
“absence status is a clearly recognizable seizure pattern but by no means a uniform one. The
essential feature is a prolonged confusional state of varying severity.” Pet. Ex. 43 at 2 (quoting
Pet. Ex. 43A at 2). While the diagnosis is “possible on the basis of a detailed history,” even
without EEG, Andermann and Robb explained that the diagnosis “must be supported by the
presence of generalized interictal spike and wave discharges.” Pet. Ex. 43A at 2. They also
found that absence status epilepticus before age 10 was rare. Id. at 5. The duration of these
seizures varies; Andermann and Robb reported “episodes may last from half an hour to [two]
days.” Id.

Lastly, in his sixth expert report, Dr. Kinsbourne, responding to statements made by Dr.
Holmes, denied that he ever opined that A.F.M. had an “absence seizure disorder.” Pet. Ex. 44 at
3. Instead, he said he was describing A.F.M.’s “prolonged onset seizure,” to involve “behavioral

33
Dr. Kinsbourne cited an article by Nolan et al., regarding atypical absence seizures. Pet. Ex.
43G (Melinda Nolan et al., Clinical and Neurophysiologic Spectrum Associated with Atypical
Absence Seizures in Children with Intractable Epilepsy, 20 J. Child Neurology 404 (2005)). It
stated that atypical absence seizures “present with a gradual clinical behavioral change in onset
and offset.” Id. at 2. During the seizures “children can retain some ability for purposeful
movement and speech.” Id. There may be “limpness, arrest of activity, but with retention or
only ‘fogging’ of consciousness.” Id.
34
Jennifer M. Grin & Francis J. DiMario , Absence Status Epilepticus Causing a Prolonged
Acute Confusional State, 37 Clinical Pediatrics 37 (1998).
35
F. Andermann & J.P. Robb, Absence Status: Reappraisal Following Review of Thirty-Eight
Patients, 13 Epilepsia 177 (1972).

16
arrest without motor concomitants, which is one of the three ways in which [migrating focal
seizures in infancy (“MFSI”)]36 begins.” Id.

Regarding the duration of the initial seizure, in his first report, Dr. Kinsbourne opined
that A.F.M. had an “absence seizure,” and that absence seizures generally last a few seconds and
no longer than 30 seconds. Pet. Ex. 37 at 3. In his third report, he opined that A.F.M.’s first
seizure was 41 minutes in duration, based on his interpretation of the EMS report. Pet. Ex. 41 at
3. In his third and fifth expert reports, Dr. Kinsbourne opined that A.F.M. had a “prolonged
absence seizure [that] exceeded 30 minutes in duration.” Pet. Ex. 41 at 1; see also Pet. Ex. 43 at
1. In his fifth report, Dr. Kinsbourne pulled back from his earlier opinion that A.F.M.’s initial
seizure was 41 minutes, and instead he opined that A.F.M. was “unresponsive for 30 minutes or
more.” Pet. Ex. 43 at 1.

ii. Table Claim

In his first expert report, Dr. Kinsbourne specifically stated that his opinion was “as to
causation-in-fact.” Pet. Ex. 37 at 6. He did not offer opinions to support a Table claim or
suggest that A.F.M. had acute encephalopathy demonstrated by a “significantly decreased level
of consciousness that last[ed] at least 24 hours.” 42 C.F.R. § 100.3(c)(2)(i)(A)(1). He did not
appear to offer any opinions supporting a Table claim thereafter, in his expert reports, or at the
hearing.

iii. Causation-in-Fact

Dr. Kinsbourne opined, “to a reasonable degree of medical probability, that [A.F.M.’s]
six-month vaccinations, most likely the DTaP, caused [her] epilepsy, leading into epileptic
encephalopathy.” Pet. Ex. 37 at 6. His specific opinions are set forth below.

36
This type of epilepsy is also referred to as migrating partial seizures of infancy (“MPSI”). See
Pet. Ex. 41B (Amy McTague et al., Migrating Partial Seizures of Infancy: Expansion of the
Electroclinical, Radiological and Pathological Disease Spectrum, 136 Brain 1578 (2013)). In his
second expert report, Dr. Kinsbourne referred to A.F.M.’s diagnosis as “malignant migrating
partial seizures of infancy (MMPSI).” Pet. Ex. 39 at 2. And in his sixth report, Dr. Kinsbourne
referred to AFM’s disorder as “migrating focal seizures in infancy (MFSI).” Pet. Ex. 44 at 1.
Respondent’s expert, Dr. Holmes, referred to A.F.M.’s disorder as “malignant migrating partial
seizures of infancy.” Resp. Ex. A at 20. He also referred to it as “migrating focal epilepsy,”
“malignant migrating focal epilepsy,” and “multifocal migrating epilepsy.” Resp. Ex. F at 4;
Resp. Ex. G at 1. The medical literature also uses different names, including “migrating focal
seizures in infancy” and “malignant migrating partial seizures in infancy.” Pet. Ex. 44a (Robert
Horacio Caraballo, Migrating Focal Seizures in Infancy: Analysis of the Electroclinical Patterns
in 17 Patients, 23 J. Child Neurology 497 (2008)); Resp. Ex. A, Tab 1 (Giangennaro Coppola,
Malignant Migrating Partial Seizures in Infancy: An Epilepsy Syndrome of Unknown Etiology,
50 Epilepsia 49 (2009)). For the sake of simplicity, the undersigned will use the acronym of
MFEI (migrating focal epilepsy of infancy) throughout this Decision, unless quoting a medical
record, expert report, medical article, or testimony.

17
1. Althen Prong One

At the hearing, Dr. Kinsbourne explained that his opinions were specific to the DTaP
vaccine administered on May 7, 2014. Tr. 38. He opined that the DTaP vaccination37 is known
to carry a risk for causing seizures within three days of administration. Tr. 18; see also Pet. Ex.
37 at 4. He posited that the vaccination activates the innate immune system the same way that
infection does, leading to the release of proinflammatory cytokines that cause inflammation of
the brain. Tr. 18. This leads to overactivity or excitation of neurons, disrupting the balance, and
manifesting as seizures. Tr. 18-19. The onset or first seizure “renders the brain more excitable”
due to the production of proinflammatory cytokines, and momentum gathers to lead to devasting
results. Tr. 22. More specifically, Dr. Kinsbourne opined that the acellular pertussis component
of the vaccine led to secretion of proinflammatory cytokines which affect the microglia in the
cerebral cortex, which put out more proinflammatory cytokines, which overactivated neurons,
causing seizures. Tr. 54.

According to Dr. Kinsbourne, epilepsy is a “hyperexcitability condition” of the brain. Tr.
38. He explained that in the “normal brain, the different neurons are acting differently
depending on the circumstances, but if all the neurons . . . fire together, then an epileptic seizure
is likely to occur.” Tr. 45. The process by which a single afebrile seizure evolves into epilepsy
was described by Dr. Kinsbourne as follows: Cytokines lower the seizure threshold, and when
the seizure occurs the next time, the threshold lowers, and over time, the brain is modified so that
seizures occur without fever or other provocation, which is epilepsy. Tr. 58.

Dr. Kinsbourne conceded that vaccine-related “isolated seizures” can occur that do not
cause harm. Tr. 22. But he did not agree that was the case here. Id. He asserted that the first
seizure was followed by a second one, with behavioral arrest, followed by a third seizure, where
there was also behavioral arrest. Id.

He also discussed his opinions about whether seizures can only occur in the context of
fever. Dr. Kinsbourne opined that when seizures occur without fever, they are called afebrile
seizures. Tr. 22. He explained that in “special circumstance[s] . . . if the child already has a
lower seizure threshold, [] an afebrile seizure is much more likely.” Tr. 23. He asserted that
vaccines lower the seizure threshold and release the inherent tendency in a child with a genetic
susceptibility. Tr. 24-25. And he testified that this process could occur in the absence of fever.
Tr. 23; see also Pet. Ex. 39 at 4.

37
Dr. Kinsbourne acknowledged that use of the acellular pertussis vaccination, as compared to
the former whole-cell pertussis vaccine, has “radically reduced the frequency of pertussis-
vaccine related seizures,” but he asserted that “seizures still occur.” Pet. Ex. 37 at 3-4; see also
Pet. Ex. 39 at 3.

18
Dr. Kinsbourne referenced several articles to support his opinions that proinflammatory
cytokines can lead to seizures and epilepsy. Tr. 39. Vezzani and Baram38 explored the
mechanisms “that transform a normal brain to an epileptic one,” acknowledging that these
processes “are not fully understood.” Pet. Ex. 37N at 1. They presented “the hypothesis that
[the cytokine] IL-1β may contribute to the development of epilepsy” through several pathways.
Id. One of these proposed mechanisms is that cytokines “release[d] during the inciting insult
may directly contribute to hyperexcitability.”39 Id. The phenomenon of hyperexcitability is
“particularly well defined in temporal lobe epilepsy,” however this type of epilepsy is not at
issue in this case. Id. Further, the authors explained that the “formation of a hyperexcitable
circuit may depend on a “functional . . . abnormality in the case of epilepsies involving genetic
causes.” Id. Lastly, the authors discussed the role of IL-1β in the context of fever and febrile
seizures. See id. at 3. Vaccinations were not discussed.

Another paper cited by Dr. Kinsbourne was published by Dr. Holmes and Ben-Ari40 and
stated that “seizures in the developing brain can result in irreversible alterations in neuronal
connectivity.” Pet. Ex. 37E at 1.41 The authors explained that the “core physiologic feature of
epileptic seizures is hyperexcitability of [central nervous system (“CNS”)] neurons. When a
sufficient number of neurons synchronously depolarize and generate action potentials, a seizure
begins.” Id. at 2. Although “children are at higher risk for seizures than adults,” the “developing
neurons [in children] are less vulnerable [to] neuronal damages and cell loss.” Id. at 3.
However, “prolonged or recurrent seizure activity . . . can irreversibly alter the way the immature
brain develops . . . [and] alterations in normal neuronal connectivity can result in long-term
consequences in seizure susceptibility, learning and memory, and risk for subsequent seizure-
induced injury.” Id. at 5.

Next, Dr. Kinsbourne testified that when infections trigger seizures, they do so by innate
immune system activation, which stimulates production of proinflammatory cytokines and
lowers the seizure threshold. Tr. 41. He asserted that vaccines trigger the innate immune system
in the same way as infections. Tr. 43; Pet. Ex. 37 at 5. Further, he opined that whether a seizure
caused by the DTaP vaccination leads to a seizure that “proceeds to epilepsy depends on other

38
Annamaria Vezzani & Tallie Z. Baram, New Roles for Interleukin-1 Beta in the Mechanisms
of Epilepsy, 7 Current Rev. Basic Sci. 45 (2007).
39
For further discussion of Dr. Kinsbourne’s opinions about inflammation and its effect on
excitability and the excitation-inhabitation ratio, see Pet. Ex. 37 at 5.
40
Gregory L. Holmes & Yehezkiel Ben-Ari, The Neurobiology and Consequences of Epilepsy in
the Developing Brain, 49 Pediatric Rsch. 320 (2001).
41
Dr. Kinsbourne also cited Chen et al., which discussed an animal study suggesting the
pertussis toxin can “promote the generation of IL-17 producing CD4 cells through a
proinflammatory cytokine pathway.” Pet. Ex. 39C at 8 (Xin Chen et al., Pertussis Toxin by
Inducing IL-6 Promotes the Generation of IL-17-Producing CD4 Cells, 178 J. Immunology 6123
(2007)). The authors did not discuss the acellular pertussis vaccine at issue here.

19
factors to do with the patient, not with the vaccination. Some seizures lead to epilepsy; some
don’t.” Tr. 44. Dr. Kinsbourne cited Wang et al.42 for “insight” as to how “seizures engender
seizures.” Pet. Ex. 37 at 6 (citing Pet. Ex. 50).

Wang et al. studied the relationship between cytokine levels and severe epilepsy by
sampling serum cytokine levels from 1,218 patients with temporal lobe epilepsy, extra-temporal
lobe epilepsy, and idiopathic generalized epilepsy. Pet. Ex. 50 at 1, 12.43 Interictal44 serum
levels of six cytokines, including Il-1β,45 were “associated with seizure severity” and three
cytokines were “significant biomarkers for patients with severe epilepsy.” Id. at 12. The authors
concluded that “among 14 cytokines, four independent biomarkers (Il-6, IFNγ, IL-17a, and
IFNλ3) for severe seizures in three different types of epilepsy were identified.” Id. They stated
that “[i]mportant roles of these cytokines in the development of severe seizure[s] could be
speculated, and they may be used as potential markers to identify severe epilepsy.” Id.
However, the authors did not conclude that vaccination in general, or the DTaP vaccination
specifically, induced cytokine release that caused severe epilepsy.

In further support of his opinions, Dr. Kinsbourne cited a study by Sun et al.46 examining
the risk of febrile seizures and epilepsy after DTaP, IPV, and Hib vaccinations in Denmark. Pet.
Ex. 47. Vaccinations were “associated with an increased risk of febrile seizures on the day of the
first [two] vaccinations given at [three] and [five] months.” Id. However, vaccination “was not
associated with an increased risk of epilepsy.” Id. Febrile seizures are not at issue here.

On cross-examination, Dr. Kinsbourne conceded that there are no animal models to show
that activation of the immune system causes epilepsy. Tr. 38-39.

42
Ye Wang et al., Interictal Cytokine Levels Were Correlated to Seizure Severity of Epileptic
Patients: A Retrospective Study on 1218 Epileptic Patients, 13 J. Translational Med. 378 (2015).
43
Dr. Kinsbounre also cited another article which discussed the role of cytokines in epilepsy.
See Pet. Ex. 37J (Gang Li et al., Cytokines and Epilepsy, 20 Seizure 249 (2011)) (summarizing
three different cytokines and their role in epilepsy).
44
Interictal refers to “occurring between attacks or paroxysms.” Interictal, Dorland’s Med.
Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=25576 (last visited
Oct. 16, 2023).
45
Only the cytokine Il-6, however, was associated with seizure severity in three types of epilepsy
studied. Pet. Ex. 50 at 13.
46
Yuelian Sun et al., Risk of Febrile Seizures and Epilepsy After Vaccination with Diphtheria,
Tetanus, Acellular Pertussis, Inactivated Poliovirus, and Haemophilus Influenzae Type B, 307
JAMA 823 (2012). This is also cited as Resp. Ex. A, Tab 8.

20
2. Althen Prong Two47

Dr. Kinsbourne opined that the incident on May 8, 2014 was A.F.M.’s “onset seizure”
and that it triggered her epileptic encephalopathy. Tr. 21. A.F.M. had a genetic susceptibility
and her vaccinations triggered the onset of her epileptic encephalopathy. Tr. 10. He testified
that once epilepsy is set in motion, “it keeps going, [and] the genetic flaw wreaks its devasting
effect on the individual’s brain.” Tr. 21.

He further opined that A.F.M. “suffers from a rare epileptic encephalopathy called
migrating focal or partial epilepsy of infancy or MFEI.” Tr. 8. Dr. Kinsbourne described MFEI
as “a condition in which the cerebral cortex is hyperstimulated, [and] hyperexcitable.” Id.
“[F]ocal locations in the cortex [] send out paroxysmal waves, which are epileptic.” Id. In
A.F.M.’s case, there “is an exchange of focal epilepsy from one hemisphere to the other” and
back and forth across the cortex. Id. The “focus . . . changes and changes . . . over time.” Id.
MFEI is “a very serious disorder,” and “an epileptic encephalopathy” with “seizures [that] have
detrimental effects on the development of the child.” Tr. 9. Dr. Kinsbourne opined that the
“seizures are so damaging that in some cases the child loses almost all [] prospective skills.” Id.
He added, it is more than epilepsy, since it is “also a disorder of the brain, which retards
development.” Id. He further opined that the illness usually appears before six months of age.
Id.

At the hearing, Dr. Kinsbourne testified that A.F.M.’s initial seizure was “very
consistent” with seizures seen in MFEI. Tr. 13. He opined that the seizure was “focal,”
characterized by a “state of behavioral interruption,” difficulty with breathing, limpness, and an
abnormal position. Tr. 12. A.F.M. also had abnormal color, described “both as pallor and . . .
looking red.” Id. In addition to describing the onset seizure as consistent with MFEI, Dr.
Kinsbourne also opined that an appropriate characterization was “hypomotor seizure,” a
description used by Dr. Holmes.48 Tr. 13-14. He agreed that A.F.M. was afebrile before the
event. See Pet. Ex. 39 at 6; Tr. 53.

Regarding A.F.M.’s diagnosis of MFEI, Dr. Kinsbourne cited Caraballo et al., who
described three types of onset in MFEI. Pet. Ex. 44 at 2 (citing Pet. Ex. 44A at 1). Dr.
Kinsbourne opined that type two is descriptive of A.F.M.’s seizure type. Id. Type two seizures
are “focal complex seizures characterized by behavioral arrest with lip cyanosis and oro-

47
Some of Dr. Kinsbourne’s opinions related to prong two are covered in the section above
related to diagnosis and are not repeated here.
48
Dr. Holmes first used the term “hypomotor seizure” in his sixth expert report. Resp. Ex. G at
4.

21
alimentary automatism[49] without obvious motor manifestations.” Id. (quoting Pet. Ex. 44A at 2,
9). Caraballo et al. described the course of 17 infants with MFEI seizure disorders and explained
the EEG features, therapy, and long-term outcome. Pet. Ex. 44A at 1. The mean age of seizure
onset was 40 days of age, with a median of 31 days. Id. at 2. Seizures became progressively
frequent over a period of 10 to 60 days. Id. In nine patients with type two (as described by Dr.
Kinsbourne), the first seizures were “characterized by behavioral arrest, [and] autonomic
manifestations (such as apnea, flushing, or cyanosis).” Id.; see also Pet. Ex. 44 at 2. “Soon after
onset, the daily seizures became very frequent in all 17 patients, evolving into a status epilepticus
in 15.” Pet. Ex. 44A at 2. The children were “generally refractory to antiepileptic drugs and
[had] severe psychomotor delay . . . before the age of [five] months.” Id. at 7. Vaccines were
not discussed or identified as a trigger or cause in any of the patients.

Regarding A.F.M.’s EEG findings, Dr. Kinsbourne agreed that A.F.M.’s first EEG (May
13, 2014) was normal, her second EEG was abnormal, and her third EEG clearly showed
epileptic encephalopathy. Tr. 17. He opined that the first EEG does not have to be abnormal.
Tr. 25; Pet. Ex. 41 at 1. When asked why an EEG would be normal in a child with symptomatic
epilepsy, Dr. Kinsbourne opined that experts are unable to explain this finding. Tr. 54.

But in attempts to support his opinion that EEGs may be normal, he again cited Caraballo
et al., who described EEG findings in children with MFEI. See Pet. Ex. 42 at 2-3 (citing Pet. Ex.
44A).50 They described the “characteristic ictal [EEG] pattern consisting of seizures that arise
independently and sequentially from both hemispheres[] that are refractory to antiepileptic
drugs.” Pet. Ex. 44A at 1. The authors also reported that the “interictal EEG at onset showed
normal background activity even during sleep in all patients.” Id. at 2.

The second article cited by Dr. Kinsbourne about MFEI was authored by McTague et al.
which reported on a British study involving 14 children. Pet. Ex. 41B at 1. The authors
described the condition as a “rare early infantile epileptic encephalopathy with poor prognosis,
presenting with focal seizures in the first year of life.” Id. Most of the infants had focal seizures
that “were clearly migratory in [eight] of 14 cases.” Id. at 4. Some infants had “aversive
seizures with head turning and involvement of the eyes with eye flickering or rolling.” Id. Most
had facial flushing followed by drooling or pupil changes. Id. Frequent seizures occurred in 14
patients. Id. McTague et al. observed 14 children with the condition and noted that the initial
EEG was normal in three out of the 14. Id. at 5. But by six months, most infants were abnormal,
showing “diffuse background slowing and multifocal epileptogenic foci.” Id. The cause was
attributable to “multiple genetic, structural[,] and metabolic causes similar to that seen in other

49
Automatisms “refer to purposeful or quasipurposeful movements that occur without the
patients’ awareness and with subsequent amnesia concerning the episode.” Resp. Ex. A, Tab 12
at 3 (G.L. Holmes, Absence (Petit Mal) Seizures, in Diagnosis and Management of Seizures in
Children 173 (1987) (also cited as Resp. Ex. F, Tab 11)). For example, automatic behavior may
consist of licking the lips, chewing, grimacing, etc. Id.
50
Dr. Kinsbourne also referenced articles about Dravet syndrome, that reported infants with this
condition may have normal EEGs early in the clinical course. See Pet. Ex. 42 at 2-3.

22
early infantile epileptic encephalopathy syndromes.” Id. at 12. Vaccines were not discussed or
identified as playing a role in causation.

Further, Dr. Kinsbourne explained that EEGs are done in the “quiet period” between
seizures, called the interictal period. Tr. 55. He concluded that while an interictal EEG is often
abnormal in epilepsy, it is not always abnormal. Id.

Moving to the progression of A.F.M.’s seizure disorder, Dr. Kinsbourne explained how
the event on May 8, 2014 caused A.F.M.’s subsequently diagnosed seizure disorder. He opined
that the seizure on May 8 “initiated an innate immune reaction that through the action of
proinflammatory cytokines lowered the seizure threshold.” Pet. Ex. 44 at 2. “[I]f the child’s
seizure threshold [had] already been lowered by a genetic abnormality,” he opined that “even a
usually harmless proinflammatory response can suffice to lower seizure threshold even further,
to the point at which a triggered seizure occurs.” Id. at 3.

Dr. Kinsbourne acknowledged that the cause of A.F.M.’s epilepsy is genetic. Tr. 9; Pet.
Ex. 44 at 1.51 “Although A.F.M.’s underlying genetic susceptibility . . . has not been identified,
it is clear from the medical literature that she must harbor a severe underlying genetic flaw.” Pet.
Ex. 44 at 1. There is “no one particular genetic flaw” that causes the disorder, and the genetic
basis is not yet known. Tr. 9. According to Dr. Kinsbourne, A.F.M. had a “very serious
susceptibility, which was inherited” and present from birth, and “the vaccination [] triggered the
onset of its clinical manifestations.” Id. “In the absence of such a genetic predisposing factor,
A.F.M. would most likely have developed quite normally, vaccination or not.” Pet. Ex. 44 at 1.

Although Dr. Kinsbourne recognized the genetic etiology of A.F.M.’s epilepsy, he opined
that A.F.M.’s vaccination “was the trigger that launched the clinical onset” of her seizure
disorder. Pet. Ex. 44 at 1. As explained by Dr. Kinsbourne, A.F.M.’s underlying genetic
abnormality acted to reduce her seizure threshold, and so her seizures occurred even without the
presence of a fever. Id.; Tr. 23-24. He testified that “[a]ll vaccines do is to lower the seizure
threshold.” Tr. 24. He further opined vaccines “don’t cause a disease like A.F.M. has. It was
inherent in her, and . . . [vaccines] released it.” Tr. 24-25. Dr. Kinsbourne opined that on May 8,
A.F.M. did not have a fever, and therefore, her seizure would be classified as afebrile. Tr. 53.
Also, since she did not have a fever, Dr. Kinsbourne conceded there was no evidence that A.F.M.
had inflammatory cytokines, other than the fact that she had seizures. Tr. 60-61.

After acknowledging that MFEI is associated with genetic abnormalities, Dr. Kinsbourne
reviewed several articles that discussed the prognosis of children with this type of epilepsy. He
concluded that if A.F.M. had not received the vaccination at issue, she “would have had the

51
In his second expert report, Dr. Kinsbourne opined that A.F.M. did “not necessarily” have a
genetic cause for her seizures.” Pet. Ex. 39 at 4. But if she did, he agreed that it “might explain
her susceptibility to epileptogenesis,” but “it would not counteract the fact,” that he believed her
vaccination triggered her “onset seizure.” Id. In a subsequent expert report, however, Dr.
Kinsbourne acknowledged that migrating focal epilepsies have been associated with several
different genetic abnormalities, including SCN2A variants. See Pet. Ex. 42 at 3.

23
benefit of a longer period of uninterrupted psychomotor development before the onset of her
epilepsy had it not been triggered by vaccinations.” Pet. Ex. 42 at 4. He concluded that the
vaccinations “deprived her of the chance to achieve further normal mental development pending
any ultimate seizure onset.” Id. But at the hearing, Dr. Kinsbourne took the position that if
A.F.M. had not been vaccinated, her condition might not have been triggered or might “not have
been as severe.” Tr. 26. But he agreed that most children who have migrating focal epilepsy of
infancy are “severely damaged.” Id. And he agreed that A.F.M. had a severe course consistent
with most children. Id.52

He cited animal studies on SCN1A mutation seizure disorders to support his opinion that
genetic abnormalities make a child “more susceptible than normal to the detrimental effects of
the seizures.” Pet. Ex. 43 at 2. But he disagreed with the methodology and statistical analysis of
studies53 that purported to conclude that earlier seizure onset (in the context of the SCNIA
genetic mutation) in children with vaccine proximate seizures did not affect outcome. Id. at 3.
He argued that there is “no evidence to support the view that developmental history is unrelated
to the age at seizure onset.” Id. at 4. He cited several papers to support his opinion that age at
seizure onset could affect outcome.

The first paper was by Dutton et al.54 Pet. Ex. 43B. The animal studies reported by
Dutton et al. examined two models of complex early-life febrile seizures in a mouse line that
expressed a SCN1A mutation to examinate the role of complex febrile seizures in “long-term
disease progression.” Id. at 10. The first model induced prolonged febrile seizures and the
second induced acute febrile seizures followed the next day by an induced prolonged febrile
seizure. Id. The research showed that “complex early-life [febrile seizures] lead to increased
seizure susceptibility, more severe spontaneous seizures,” impairments in behavior and memory,
and more severe adult SCN1A epilepsy. Id. The results, however, were limited to febrile
seizures and their effects on adults with epilepsy with the SCN1A mutations. The authors did
not discuss a model characterized by only one afebrile seizure.

52
Dr. Kinsbourne argued that MFEI does not always result in “severe intellectual disability.”
Pet. Ex. 42 at 3. He opined that developmental outcome is “attributable to the cumulative impact
of the seizures once they begin.” Id.
53
Specifically, Dr. Kinsbourne disagreed with McIntosh et al., who determined that while
vaccination “might trigger earlier onset of Dravet syndrome in children who, because of an
SCN1A mutation, are destined to develop the disease,” but found “no evidence that vaccinations
before or after disease onset affect[ed] outcome.” Pet. Ex. 42G at 1 (Anne M. McIntosh et al.,
Effects of Vaccination on Onset and Outcome of Dravet Syndrome: a Retrospective Study, 9
Lance Neurology 592 (2020)). This is also cited as Resp. Ex. G, Tab 12.
54
Stacey B.B. Dutton et al., Early-Life Febrile Seizures Worsen Adult Phenotypes in SCN1A
Mutants, 293 Experimental Neurology 159 (2017).

24
The second article cited by Dr. Kinsbourne, by Salgueiro-Pereira et al.55 reported on an
animal study done on mice carrying an SCN1A mutation where short seizures were induced
daily for 10 days using hyperthermia or a chemical that induces seizures (Flurothyl.) Pet. Ex.
43H at 2. The research demonstrated that the mice with an asymptomatic or mild phenotype
were transformed into a “severe [Dravet syndrome-like] phenotype,” with increased seizures and
“cognitive/behavior deficits.” Id. The authors did not study the effects of one afebrile seizure.

Moreover, Dr. Kinsbourne recognized the speculative nature of hypothetical “what if”
questions about what would have happened if A.F.M. had not received her DTaP vaccination.
See Tr. 26. He stated, “[t]he whole point is that we don’t know what would have happened if the
vaccination hadn’t been given and the disease hadn’t been triggered.” Id.

3. Althen Prong Three

Dr. Kinsbourne opined that A.F.M.’s condition began “16 hours after the vaccinations”
which “places the situation in the . . . risk period of seizure onset after DTaP.” Tr. 11. Dr.
Kinsbourne opined that the risk period of seizures with DTaP is the first three days after
vaccination, although the first day and earlier is most notable. Tr. 18. A.F.M. had her seizure at
approximately 16 to 17 hours after her DTaP vaccination, which is within the known risk period.
Tr. 26-27. He further opined that the vaccination given on May 7, 2018 triggered A.F.M.’s
“epileptic encephalopathy.” Tr. 10.

2. Respondent’s Expert, Dr. Gregory Lawrence Holmes56

a. Background and Qualifications

Dr. Holmes earned his B.S. from Washington and Lee University in 1970, and his M.D.
from University of Virginia School of Medicine in 1974. Resp. Ex. H at 1. He is a licensed
physician with board certifications in pediatrics, neurology, and neurophysiology. Id.; Resp. Ex.
A at 1; Tr. 72. Dr. Holmes is currently a Professor of Neurological Sciences and Pediatrics and
Chair of the Department of Neurological Sciences at the University of Vermont College of
Medicine. Resp. Ex. A at 1; Resp. Ex. H. at 1-2; Tr. 73. As Chair of the Department, he is
responsible for the physicians, the research, and the educators, and is heavily involved in clinical
care. Tr. 73-75. Dr. Holmes mainly sees patients of pediatric neurological disorders. Tr. 74.
His primary research interest is epilepsy. Tr. 80. Dr. Holmes has authored numerous

55
Ana Rita Salgueiro-Pereira et al., A Two-Hit Story: Seizures and Genetic Mutation Interaction
Sets Phenotype Severity in SCN1A Epilepsies, 125 Neurobiology Disease 31 (2019).
56
Dr. Holmes submitted six expert reports and testified at the entitlement hearing on May 17,
2022. Resp. Exs. A, C-G; Tr. 3.

25
publications, including a number of medical articles that have been filed here.57 See Resp. Ex. H
at 36-82; Tr. 82-83. He has reviewed a number of cases and testified in the Vaccine Program
many times but has never found a vaccine-related injury. Tr. 150-51.

b. Opinions

Like Dr. Kinsbourne, Dr. Holmes offered opinions about what happened to A.F.M. on
May 8, as well as causation.

i. Initial Event May 8, 2014—Seizure vs. ALTE

Dr. Holmes opined that A.F.M.’s event on May 8, 2014 was an “apparent life-threatening
event” or ALTE. Tr. 94. He agreed with the characterization of an ALTE described by
Aminiahidashti. Resp. Ex. F at 3. Dr. Holmes noted that ALTE is a “concern in the neonatal
period” up to the first year of life, including the age of A.F.M. at the time of her initial event. Id.
Aminiahidashti described ALTE as “an episode that is frightening to the observer, and is
characterized by some combination of apnea, color change, marked change in muscle tone,
choking, gagging, or coughing.” Pet. Ex. 42A at 1. The underlying cause “varies.” Id. at 2.
“The most frequent problems associated with ALTE are gastrointestinal (50%), neurologic
(30%), respiratory (20%), cardiovascular (5%), metabolic and endocrine (<5%), or others.” Id.

One reason for Dr. Holmes’ opinion included the medical record noting that A.F.M. had
“some degree of apnea,” her color was “pallid,” she was “very limp and hypotonic,” and when
suctioned, she had “a lot of saliva and mucus.” Tr. 95. When asked to respond to Dr.
Kinsbourne’s opinion that A.F.M. had a seizure, Dr. Holmes opined that it was “very, very
difficult based on the medical records to be so definitive” as to conclude that A.F.M. had a
seizure. Id. Instead of a seizure, Dr. Holmes believed it was more likely that A.F.M. had reflux,
a vasovagal attack, or laryngospasm, causing choking and decrease blood flow to the brain. Tr.
98. He agreed that ALTE encompassed seizure activity. Tr. 141. Dr. Holmes also
acknowledged that A.F.M. was afebrile before the event. See Resp. Ex. A at 21; Tr. 126, 180.

Although Dr. Holmes opined that A.F.M. had an ALTE on May 8, he agreed that the
EMS providers who transported A.F.M. to the hospital thought that she had a seizure. Tr. 140

57
See Pet. Exs. 37E, 37F (Gregory L. Holmes & Pierre-Pascal Lenck-Santini, Role of Interictal
Epileptiorm Abnormalities in Cognitive Impairment, 8 Epilepsy & Behavior 504 (2006)); Resp.
Ex. A, Tabs 12, 16, 28 (Gregory L. Holmes, Seizure-Induced Damage in the Developing Human:
Relevance of Experimental Models, in 135 Progress in Brain Research 321 (T. Situla & A.
Pitkanen eds., 2002)); Resp. Ex. F, Tab 14 (Gregory L. Holmes et al., Maturation of EEG
Oscillations in Children with Sodium Channel Mutations, 34 Brain & Development 469 (2012)
(also cited as Resp. Ex. G, Tab 17)).

26
(citing Pet. Ex. 38 at 2). During the hearing, after reviewing the EMS trip report,58 Dr. Holmes
agreed A.F.M.’s respirations were noted to be irregular, and that this could be consistent with a
seizure. Tr. 154. He also acknowledged that A.F.M.’s pupils were described as dilated and her
eyes rolled back, and these abnormalities can be seen with seizures. Tr. 154-55. Even after
reviewing the EMS report, however, Dr. Holmes remained skeptical that A.F.M. had a seizure.
Tr. 165.

Dr. Holmes noted that the ED physician’s (Dr. Ervin’s) impression was “6-month-old
with an [URI]; episode of altered mental status, suspect possibly secondary to a reflux or a
choking episode, but she did not have any cyanosis; and a possible [UTI].” Resp. Ex. E at 1
(citing Pet. Ex. 7 at 22). A.F.M. was admitted for observation; antibiotics and intravenous fluids
were administered, and medication for congestion was ordered. Id. Dr. Holmes observed that
Dr. Ervin did not diagnose a seizure. Id.

According to Dr. Holmes, ALTE “is a basket-term,” to describe events when there is
insufficient information upon which to discern a specific diagnosis. Tr. 96. In contrast, he
testified the diagnosis of a seizure requires enough information so that it can be classified using
the International Classification of Seizures in Epilepsy (most recently updated in 2017).59 Id.

Regarding the fact that A.F.M.’s initial EEG was normal, Dr. Holmes agreed with Dr.
Kinsbourne that “a normal EEG or MRI does not rule out the possibility of a seizure.” Resp. Ex.
D at 1. He further opined that an “EEG [] done six days after the event on May 8 [] cannot be
used to determine if the [] event was a seizure.” Id. If the EEG had been abnormal, and shown
epileptiform activity, Dr. Holmes opined then it would have been more likely that A.F.M.’s
initial event was a seizure. Id.

On cross-examination, Dr. Holmes was asked questions about a note written by Dr.
Terayanont documenting a history of A.F.M.’s illness after she was admitted to the hospital for
seizure activity on June 22, 2014. See Tr. 168. Dr. Terayanont took a history from Petitioner
and her mother who reported that the event on June 22 was “the third time” that she had “this
particular symptom.” Pet. Ex. 9 at 7. The “symptoms started with eye staring and eventually
eyes rolled to the left and [she had] slightly jerking movement of both upper extremities which
last[ed] for about a few seconds. There is no history of cyanotic spell” and “the patient

58
Chief complaint was “possible seizure like activity.” Pet. Ex. 38 at 1. A.F.M. was found
“unresponsive; respirations irregular and labored; lung sound clear; pulse reg[ular]; skin pale;
pupils dilated non reactive.” Id. at 2. A.F.M. was found “with arms extended out; eyes rolled
back; not breathing; skin color was normal.” Id. A.F.M.’s condition gradually improved
throughout the duration of the trip. Id.; see also Pet. Ex. 8 at 53 (ED noted indicating A.F.M.
“arrived per EMS with report of suspected seizure activity”).
59
It does not appear that Dr. Holmes filed a reference or provided a citation for this text. He did,
however, file an article on the definition and classification of status epilepticus. See Resp. Ex.
D, Tab 2 (Eugen Trinka et al., A Definition and Classification of Status Epilepticus – Report of
the ILAE Task Force on Classification of Status Epilepticus, 56 Epilepsia 1515 (2015)).

27
recover[ed] by herself.” Id. After reviewing this note, Dr. Holmes still disagreed that there was
sufficient evidence to conclude that A.F.M. had a seizure on May 8 (which would have been the
first time A.F.M. had the symptoms reported to Dr. Terayanont as documented). Tr. 168-69.

While Dr. Holmes did not agree that A.F.M. had a seizure, he did agree that she had an
altered state of consciousness during the event. Tr. 143. Based on the times documented in the
ambulance trip report, Dr. Holmes opined that A.F.M. was unresponsive for approximately 16 to
20 minutes. Tr. 157-58.60

1. Type and Duration of Event on May 8, 2014

While Dr. Holmes disagreed that A.F.M. has a seizure, regarding seizure type, Dr.
Holmes strongly disagreed with Dr. Kinsbourne’s opinion that A.F.M. had an absence seizure61
or absence status epilepticus62 on May 8, 2014. Tr. 99-100; Resp. Ex. G at 1. He defined an
absence seizure as a “generalized seizure[] [that] involve[s] widespread areas of the brain from
the onset.” Resp. Ex. D at 2. Further, he explained that absence seizures are “common in
children and typically don’t cause long term problems.” Resp. Ex. A at 21. Dr. Holmes also
noted that absence seizures usually occur in older children, ages four to 14 years. Id. Lastly, he
opined that a normal EEG in a child with a suspected absence seizure is “extremely unusual and
almost rules out typical absence seizures.” Resp. Ex. G at 2 (citing Resp. Ex. G, Tab 5 at 3-4, 7-
8, 14 (explaining that typical and atypical absences seizures are characterized by abnormal EEGs
and “[a] normal EEG in a young child with recent appearance of suspect absences is extremely
unusual and almost rules out typical absences if adequate hyperventilation[63] was performed”).64

He further explained that absence status epilepticus is “very rare” and “typically seen in
adolescents.” Resp. Ex. F at 1. Moreover, this type of seizure usually occurs in patients with

60
Dr. Holmes testified that the record reflects a period of 16 minutes, but he noted that this did
not account for the time it took for the family to place the call. Tr. 158.
61
For a more detailed explanation of the reasons that Dr. Holmes disagreed that A.F.M. had
absence seizures, see Resp. Ex. A at 21; Resp. Ex. F at 2. Dr. Holmes authored an article on
absence seizures in children. See Resp. Ex. A, Tab 16 (Gregory L. Holmes et al., Absence
Seizures in Children: Clinical and Electroencephalographic Features, 21 Annals Neurology 268
(1982) (also cited as Resp. Ex. F, Tab 12; Resp. Ex. G, Tab 1)).
62
For a more detailed explanation of the reasons that Dr. Holmes disagreed that A.F.M. had
absence status epilepticus, see Resp. Ex. F at 1.
63
According to Dr. Holmes, hyperventilation was not performed on A.F.M. due to her age, but
she was asleep during her first EEG, and he opined that “sleep is a powerful activator of
epileptiform discharges in epilepsy, including absence epilepsy.” Resp. Ex. G at 2.
64
Jean Aicardi, Epilepsy in Children, in 2 The International Review of Child Neurology (Isabelle
Rapin ed., 1994).

28
“idiopathic generalized epilepsy and has an excellent prognosis” and “absence status epilepticus
has not been shown to occur in the first year of life.” Id. Dr. Holmes further disagreed with Dr.
Kinsbourne that the paper by Grin and DiMario supported the idea that A.F.M. had absence
status epilepticus. Resp. Ex. G at 2 (citing Pet. Ex. 43E). There the patient had a “long episode
of a flat affect, decreased but not absent speech, confusion, and an EEG showing generalized
spike and wave activity.” Id. (citing Pet. Ex. 43E). A.F.M. did not have a similar presentation,
thus Dr. Holmes opined the description “does not fit” what happened here.65 Id.

If A.F.M. had either an absence seizure or absence status epilepticus, Dr. Holmes testified
it would have been very unlikely that her initial EEG (done May 13, 2014) would have been
normal. Tr. 100. Also, one week after her event, when seen by her physician on May 15,
A.F.M. was described as doing well, and her motor skills were good. Tr. 102. Therefore, Dr.
Holmes opined there is “no basis whatsoever” to conclude that A.F.M. had status epilepticus on
May 8. Tr. 100. Further, once A.F.M. was diagnosed with epilepsy, Dr. Holmes noted that her
seizures were not unusual. Tr. 101. She became “rigid, [with] eye deviation, [and] stiffening of
the body.” Id. For these reasons, Dr. Holmes concluded that A.F.M.’s event on May 8, 2014,
was not an absence seizure or absence status epilepticus. Id.; see also Resp. Ex. G at 2.

Dr. Holmes also disagreed with Dr. Kinsbourne’s opinion that A.F.M.’s initial event was
a NCSE. Resp. Ex. C at 1; Resp. Ex. D at 2; Resp. Ex. F at 2. He defined NCSE as “a change in
mental status from baseline of at least 30-minute duration without convulsive activity, associated
with continuous or near continuous EEG ictal discharges that consist of generalized or focal
spikes, spike-waves or slow activity with intermixed spikes.” Resp. Ex. D at 2 (citing Resp. Ex.
F, Tab 13 at 3-4).66 He opined that NCSE is associated with “severe brain insults, such as
hypoxia,[67] intracranial hemorrhage, [and] with abnormal MRI scans.” Resp. Ex. C at 1. Dr.
Holmes explained that it is “implausible that A.F.M. had NCSE and awoke in the ambulance,
arriving in the [ED] alert and playful.” Id. Moreover, he noted that none of the treating
physicians considered NCSE as a possible diagnosis. Id. Dr. Holmes also opined that if

65
In the case report, the exact length of time the patient was disoriented was not noted.
However, she was disoriented and confused upon awakening, and returned to bed, and fell asleep
for one hour. Pet. Ex. 43E at 1-2. When she awoke, she was coherent, but later enroute to the
hospital, she became confused again. Id.
66
Stacey K.H. Tay et al., Nonconvulsive Status Epilepticus in Children: Clinical and EEG
Characteristics, 47 Epilepsia 1504 (2006). The patients studied by Tay et al. had EEG
abnormalities ranging from “typical and atypical spike and wave discharges” to “multiple or
polyspike discharges and rhythmic sharp delta activity with evolution.” Resp. Ex. F, Tab 13 at 3.
“Interictal abnormalities were present in all the patients in EEGs obtain after the resolution of
NCSE.” Id. at 4.
67
Hypoxia is the “reduction of oxygen supply to tissue below physiologic levels despite
adequate perfusion of the tissue by blood.” Hypoxia, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=24462 (last visited Oct. 16, 2023).

29
A.F.M.’s initial seizure had been NCSE, her initial EEG would likely have been abnormal.
Resp. Ex. D at 1; Resp. Ex. F at 2.

When asked to assume hypothetically that A.F.M.’s event was a seizure, and asked to
describe the seizure type, Dr. Holmes testified that he would have categorized it as a “hypomotor
seizure.” Tr. 97. He defined hypomotor seizures as those “characterized by decreased behavior
activity with indeterminate level of consciousness.” Resp. Ex. G at 4.68 He opined that the
“majority of hypomotor seizures are partial (focal) in nature, rather than generalized” and the
“focal EEG abnormalit[ies] . . . usually involve the temporal or temporoparietal brain regions
resulting in a diminution of behavioral motor activity.” Id. As it relates to A.F.M., however,
characterizing A.F.M.’s initial event as a hypomotor seizure was not satisfactory to Dr. Holmes
because A.F.M. was described as limp, and he has never seen a seizure “documented with EEG
in which the child was totally limp and floppy.” Tr. 98.

ii. Table Claim

Dr. Holmes opined that A.F.M. did not suffer vaccine-induced epileptic encephalopathy.
These opinions are integrated below.

iii. Causation-in-Fact

1. Althen Prong One

Dr. Holmes opined that Dr. Kinsbourne’s mechanistic opinion is not reliable. Tr. 110.
Specifically, Dr. Holmes disagreed that “a single vaccine given in the thigh [could produce]
enough cytokines to lead to seizure” or “irreparable changes in the brain that lead [] to epilepsy,”
when there is “no evidence of inflammation in the brain.” Id. There was no fever, no “abnormal
neurological signs,” no “alteration in consciousness,” no encephalopathy, a normal EEG, and a
normal MRI. Id.69 Given these facts, Dr. Holmes opined the May 8, 2014 event did not cause a
“vaccine-induced epileptic encephalopathy.” Id.

As explained by Dr. Holmes, the support that the DTaP vaccination can cause an afebrile
seizure is very weak. Tr. 112. He noted that the articles cited by Dr. Kinsbourne do not support
the idea that there is an increased risk of afebrile seizures after the DTaP vaccination. See id.
For example, Conrad and Jensen70 concluded “that the risk of seizures is lower with the acellular
pertussis than the whole-cell pertussis.” Resp. Ex. A at 21 (citing Pet. Ex. 37D at 5 (Table 4

68
For Dr. Holmes’ complete description of hypomotor seizures, see Resp. Ex. G at 4.
69
Dr. Holmes also testified that an MRI would show inflammation if the vaccinations increased
cytokines in the brain. Tr. 149-50.
70
Dennis A. Conrad & Hal B. Jenson, Using Acellular Pertussis Vaccines for Childhood
Immunization Potential Benefits Far Outweigh Potential Risks, 105 Postgraduate Med. 165
(1999). This is also cited as Resp. Ex. A, Tab 19.

30
shows the incidence of fever, and Table 5 shows the estimated rates of moderate to severe
adverse reactions of diphtheria-tetanus-pertussis (“DTP”) as compared with DTaP, and vastly
reduced rates of seizures, particularly for two types of vaccines, Certiva and Tripedia)).
Moreover, Dr. Holmes testified that the study published by Le Saux et al.,71 cited by Dr.
Kinsbourne, did not show an increased risk of afebrile seizures after vaccination with DTaP. Id.
(citing Pet. Ex. 37I at 1, 4-5 (noting “risks of febrile seizures and [hypotonic-hyporesponsive
episodes] . . . declined significantly with the introduction of acellular pertussis vaccine”)).

Regarding Dr. Kinsbourne’s reliance on the paper by Chen et al., Dr. Holmes noted that it
was a study about the pertussis toxin and not the pertussis vaccination and its effect on the
proinflammatory cytokine pathway. Resp. Ex. C at 2 (citing Pet. Ex. 39C). Additionally, Dr.
Holmes cited Sun et al., which evaluated febrile seizures after childhood vaccinations (including
DTaP) given at three, five, and 12 months, and found that while the vaccinations were
“associated with an increased risk of febrile seizures on the day of the first [two] vaccinations
given at 3 and 5 months,” that “vaccination with DTaP-IPV-Hib was not associated with an
increased risk of epilepsy.” Tr. 122 (citing Pet. Ex. 47 at 1).

Dr. Holmes opined that there is a condition characterized by afebrile seizures, but it is
related to a specific epileptic syndrome, Dravet syndrome. Tr. 112. He explained that some
studies have shown that some children with Dravet syndrome have seizures after the DTaP
vaccination, but studies have also shown the post-vaccination seizure does not alter the child’s
course. Tr. 113-16; Resp. Ex. F at 3-4; see Resp. Ex. G, Tab 12; Pet. Ex. 37M at 10.72

In support of his opinion regarding the role of genetics in the etiology of epilepsy, Dr.
Holmes cited a study by Verbeek et al. (also cited by Dr. Kinsbourne), of 990 children who had
seizures after vaccination within the first two years. Tr. 117 (citing Pet. Ex. 37M at 1). The
study showed that “in most cases genetic or structural defects [were] the underlying cause of
epilepsy with onset after vaccination.” Id. (citing Pet. Ex. 37M at 1, 10). Dr. Holmes
emphasized that vaccination is not the cause of the epilepsy, but the genetic defect is the cause.
Id. Similarly, he explained that the article cited by Dr. Kinsbourne, authored by von Spiczak et
al.,73 does not provide evidence that vaccines are the cause of seizures; instead, the underlying
cause of the epilepsy is the reason for seizures. Tr. 118 (citing Pet. Ex. 39L).

71
Nicole Le Saux et al., Decrease in Hospital Admissions for Febrile Seizures and Reports of
Hypotonic-Hyporesponsive Episodes Presenting to Hospital Emergency Departments Since
Switching to Acellular Pertussis Vaccine in Canada: A Report From IMPACT, 112 Pediatrics
e348 (2003). This is also cited as Resp. Ex. A, Tab 20.
72
Nienke E. Verbeek et al., Etiologies for Seizures Around the Time of Vaccination, 134
Pediatrics 658 (2014). This is also cited as Resp. Ex. A, Tab 22.
73
Sarah von Spiczak, A Retrospective Population-Based Study on Seizures Related to Childhood
Vaccination, 52 Epilepsia 1506 (2011).

31
von Spiczak et al. studied seizure types and epilepsy syndromes in infants who presented
with seizures after vaccination. Pet. Ex. 39L at 1. They identified clinical information and
genetic factors related to Dravet syndrome, West syndrome, as well as other seizure types and
syndromes that occurred in temporal association with vaccination. Id. at 11. They concluded
that “severe childhood epilepsies comprise a notable subset of these cases,” and recommended
genetic counseling and “early diagnosis by clinical recognition and confirmation of the
underlying etiology.” Id.

Dr. Holmes then turned to the issue of whether a single afebrile seizure can cause
excitatory changes in the brain that then leads to epileptic encephalopathy, as proposed by Dr.
Kinsbourne. Tr. 118. Dr. Holmes strongly disagreed that a single afebrile seizure could cause
epileptic encephalopathy. Id. While he did agree that after many seizures, “the brain can
become more excitable,” he opined that one cannot “equate excitability with epilepsy.” Id. He
also disagreed that the article he co-authored with Dr. Ben-Ari, proposed that “changes in
excitability lead to epilepsy.” Tr. 134. The authors explained that “the immature brain is more
prone to seizures than the mature brain because of a developmental mismatch between the
delicate balance of excitation and inhibition.” Resp. Ex. A, Tab 26, at 5. Nothing in the article
suggests that a single afebrile seizure can cause epilepsy, instead, “prolonged or recurrent seizure
activity, through activity-dependent mechanisms, can irreversibly alter the way the immature
brain develops and forms synapses. There alteration in normal neuronal connectivity can result
in long-term consequences in seizure susceptibility, learning and memory, and risk for
subsequent seizure-induced injury.” Id. at 5.

Next, Dr. Holmes reviewed additional medical literature referenced by Dr. Kinsbourne
and provided opinions about whether it supported vaccine causation. He explained the Li et al.
paper discussed the role of cytokines in epilepsy, but Dr. Holmes opined that there was nothing
in the paper relevant to vaccinations. Tr. 129-30 (citing Pet. Ex. 37J). Dr. Holmes agreed that
“seizures can lead to increased cytokines,” but he disagreed that a “single seizure” can increase
cytokines so as to cause epilepsy. Tr. 130. He had similar comments about the Wang et al.
paper, regarding the question of whether higher cytokine levels are present in those with frequent
seizures and more severe epilepsy. Tr. 137 (citing Pet. Ex. 50). He noted Wang et al. did not
relate to vaccination. Id. Likewise, he testified that the article by Braun et al.74 did not provide
evidence that the acellular pertussis vaccine (DTaP) caused epilepsy. Tr. 129 (citing Pet. Ex.
37A).

Dr. Holmes also discussed the Vezzani and Baram papers and agreed that they showed
that cytokines in the brain “can be associated with seizures and can be a result of seizures.” Tr.
130 (citing Pet. Exs. 37N, 39K). But he explained that they “had not studied vaccines,” and
specifically vaccines administered peripherally, to determine if they increase the production of

74
M. Miles Braun et al., Infant Immunization with Acellular Pertussis Vaccines in the United
States: Assessment of the First Two Years’ Data From the Vaccine Adverse Event Reporting
System (VAERS), 106 Pediatrics e51 (2000).

32
cytokines, or if so, whether this leads to epilepsy. Tr. 130 (citing Pet. Ex. 39K;75 Pet. Ex. 37N).
While he agreed that cytokines “play a role in epilepsy,” he opined it is too simplistic to focus
only on cytokines when there are other factors that play a role in epileptogenesis. Id. In
summary, Dr. Holmes testified that none of the articles about the acellular pertussis vaccine
reported a causal association between the vaccine and seizures or epileptic encephalopathy. Tr.
135.

Finally, regarding Dr. Kinsbourne’s opinion that a child with MFEI can have a normal
EEG, Dr. Holmes agreed. Tr. 123. By way of example, Dr. Holmes opined that children with
Dravet syndrome may initially have a normal EEG, but he explained that this is in the context of
genetic epilepsy. Id. Dr. Holmes disagreed that the mechanistic theory proposed by Dr.
Kinsbourne, resulting in “an encephalopathic process due to cytokines in the brain,” would result
in a normal EEG. Tr. 124. He explained that if there were sufficient cytokines to result in
inflammation in the brain, there should be functional and/or EEG abnormalities. Id.

2. Althen Prong Two

Dr. Holmes opined that the vaccination at issue did not play a role in A.F.M.’s
neurological condition. Tr. 110. He testified that there is no evidence that A.F.M.’s epilepsy is
related to her vaccination. Id. Instead, it “is related to her genetic defect.” Id. Moreover, he
opined that the vaccination did not cause A.F.M.’s event on May 8, which he opined was not a
seizure, but an ALTE. Tr. 111.

Further, Dr. Holmes opined that there was not a logical sequence of cause and effect
between vaccination and A.F.M.’s epilepsy. Tr. 125. There was no evidence of an inflammatory
response to the DTaP vaccination. Id. He agreed she was afebrile before the event. See Resp.
Ex. A at 21; Tr. 126, 180. Dr. Holmes explained that A.F.M. did not have encephalitis76 or
meningitis,77 or alterations in awareness, alertness, or behavior. Tr. 125. When A.F.M. was seen
on May 8, 2014 after the event, she “respond[ed] normally” except for “congestion which had
begun a week prior to immunizations.” Resp. Ex. A at 20. Dr. Holmes stated that she was
diagnosed with an URI, treated with antibiotic, and discharged home.78 Id. She had no
weakness, sleep disturbance, or fever. Tr. 125-26. She had a normal EEG and normal

75
Annamaria Vezzani et al., The Role of Inflammation in Epilepsy, 7 Nat’l Rev. Neurology 31
(2011).
76
Encephalitis is the “inflammation of the brain.” Encephalitis, Dorland’s Med. Dictionary
Online, https://www.dorlandsonline.com/dorland/definition?id=16168 (last visited Oct. 16,
2023).
77
Meningitis is the “inflammation of the meninges, usually by either a bacterium . . . or a virus.”
Meningitis, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/
definition?id=30340 (last visited Oct. 16, 2023).
78
Dr. Holmes testified that A.F.M.’s infection was not significant to his opinions. Tr. 180.

33
neurological examination on May 13th, several days after the event. Id. Her MRI was also
normal. Id. Based on all these facts, Dr. Holmes testified that it was “inconceivable” that
A.F.M. had inflammation of the brain. Tr. 126; see also Resp. Ex. A at 20 (opining that there is
no evidence that any injury occurred following A.F.M.’s vaccinations on May 7, 2014).

Conversely, Dr. Holmes opined that on June 22, 2014, A.F.M. did have a seizure.79 Tr.
103; Resp. Ex. D at 1. She was “rigid and fixed to the right” when she arrived at the hospital and
required diazepam intravenously. Tr. 103. Dr. Holmes characterized the event as a “focal
seizure with secondary generalization.” Tr. 173. An EEG done the next day, June 23, 2014,
confirmed “focal seizures [] with secondary generalization.” Tr. 104. The EEG findings were
consistent with “epileptic interictal discharges involving both hemispheres.” Tr. 105. Based on
A.F.M.’s seizure on June 22, and her EEG results on June 23, Dr. Holmes agreed that the
diagnosis of epilepsy was appropriate. Tr. 167.

After she was diagnosed with epilepsy, Dr. Holmes briefly described A.F.M.’s
subsequent course. See Tr. 106-09. On June 29, 2014, video EEG showed a 25-minute seizure
and a four-minute tonic-clonic seizure with oxygen desaturation. Tr. 106-07. EEG monitoring
from June 30 to July 1, 2014 was markedly abnormal, showing many seizures. Tr. 107. From
July 5 to September 12, 2014, A.F.M. was hospitalized at Vanderbilt Hospital. Id. She had a
seizure that lasted 140 minutes and required a phenobarbital coma. Id. After that, A.F.M. had an
abnormal MRI and clinical deterioration. Tr. 108. Her seizures were very refractory to
medication. Id. Dr. Holmes concluded that A.F.M. had a course of continued seizures and
cognitive decline. Tr. 109.

Regarding the type of seizures A.F.M. developed in June 2014, Dr. Holmes opined that
A.F.M.’s seizure disorder (MFEI) is “a rare, age-specific epileptic encephalopathy.” Resp. Ex. A
at 20. He explained that onset of the illness occurs by six months of age and is characterized by
“frequent multifocal seizures with ictal [EEG] activity shifting from one hemisphere to the other,
no identifiable immediate or remote causes, intractability to antiepileptic drugs, profound
developmental arrest, hypotonia[,] and often abnormal movements.” Id. Although genetic
mutations have been found in some patients, other patients do not have identifiable genetic
markers. Id.80 Dr. Holmes believed that A.F.M.’s epilepsy is genetic, although no specific
mutation has been identified. Id.

79
On May 22, 2014, A.F.M. had another event, described by Dr. Holmes as staring “upward
with her mouth open, [and her] face was red.” Tr. 103. A.F.M.’s mother reported that her
daughter returned to baseline in five minutes. Id. When A.F.M. was seen by Dr. Crick, she was
described as “alert, and [in] no acute distress.” Id. Dr. Holmes explained that Dr. Crick’s
assessment was reflux and rule out seizures. Id. Dr. Holmes viewed this second incident as “an
usual movement disorder.” Tr. 143. He opined that there was not enough information to
determine whether A.F.M. had an altered state of consciousness during this second event. Id.
80
For more details about the genetic mutations that have been associated with A.F.M.’s type of
epilepsy, see Resp. Ex. A at 20. Dr. Holmes explained that A.F.M.’s genetic testing
“demonstrated a gene variant in SCN4A,” but “at this point it is unclear whether the SCN4A
mutation has any role in A.F.M.’s current condition.” Id.

34
Dr. Holmes noted that Caraballo et al. and McTague et al., who described MFEI, do not
implicate vaccinations as a trigger for seizures or epilepsy. Tr. 132-33 (citing Pet. Exs. 41C,
41B). Dr. Holmes explained that the type of seizures that A.F.M. developed were “quite
different than the event on [May 8, 2014].” Id. He also opined that there is no evidence that
MFEI is “triggered by vaccination.” Id. Lastly, he opined that A.F.M.’s presentation of MFEI
was within the upper age limit known for this epileptic disorder. Id.

He disagreed with Dr. Kinsbourne’s opinion that the “vaccines received by A.F.M.
resulted in the early onset of migrating focal epilepsy.” Resp. Ex. F at 4. Even assuming that
A.F.M. had a seizure on May 8, 2014, and that the seizure marked the beginning of her epilepsy,
Dr. Holmes did not agree that she would have had a better outcome if the onset of her epilepsy
had been delayed. Resp. Ex. G at 3. Citing studies about children with Dravet syndrome, Dr.
Holmes opined that age of onset is not correlated to outcome. Id. Instead, he explained that
disease severity is more likely associated with the severity of a child’s genetic phenotype. Id.

Moreover, Dr. Holmes testified that none of A.F.M.’s treating physicians attributed her
epilepsy to vaccination. Tr. 127. Instead, they believed there was a genetic or metabolic cause.
Id. Genetic testing was done but it did not reveal the specific genetic condition. Id.

In conclusion, Dr. Holmes opined that there is no evidence that the vaccinations
“precipitated the onset of [A.F.M.’s] epilepsy or had any effect [] on her eventual outcome.”
Resp. Ex. F at 4.

3. Althen Prong Three

Dr. Holmes opined that there was not a medically appropriate temporal relationship
between A.F.M.’s DTaP vaccination and her epilepsy. Tr. 128. He opined that from the time of
A.F.M.’s initial event on May 8, 2014, it was 46 days before she had “what clearly was a
seizure” and the development of epilepsy. Id. Dr. Holmes testified that Dr. Kinsbourne did not
provide any mechanism that would explain how the initial event (seizure or ALTE) could lead to
the development of epilepsy after 46 days. Id.

IV. LEGAL STANDARDS

A. Standards for Adjudication

The Vaccine Act was established to compensate vaccine-related injuries and deaths.
§ 10(a). “Congress designed the Vaccine Program to supplement the state law civil tort system
as a simple, fair and expeditious means for compensating vaccine-related injured persons. The
Program was established to award ‘vaccine-injured persons quickly, easily, and with certainty
and generosity.’” Rooks v. Sec’y of Health & Hum. Servs., 35 Fed. Cl. 1, 7 (1996) (quoting
H.R. Rep. No. 908 at 3, reprinted in 1986 U.S.C.C.A.N. at 6287, 6344).

Petitioner’s burden of proof is by a preponderance of the evidence. § 13(a)(1). The
preponderance standard requires a petitioner to demonstrate that it is more likely than not that the

35
vaccine at issue caused the injury. Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315,
1322 n.2 (Fed. Cir. 2010). Proof of medical certainty is not required. Bunting v. Sec’y of Health
& Hum. Servs., 931 F.2d 867, 873 (Fed. Cir. 1991). In particular, Petitioner must prove that the
vaccine was “not only [the] but-for cause of the injury but also a substantial factor in bringing
about the injury.” Moberly, 592 F.3d at 1321 (quoting Shyface v. Sec’y of Health & Hum.
Servs., 165 F.3d 1344, 1352-53 (Fed. Cir. 1999)); see also Pafford v. Sec’y of Health & Hum.
Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006). A petitioner who satisfies this burden is entitled to
compensation unless respondent can prove, by a preponderance of the evidence, that the
vaccinee’s injury is “due to factors unrelated to the administration of the vaccine.” §
13(a)(1)(B). However, if a petitioner fails to establish a prima facie case, the burden does not
shift. Bradley v. Sec’y of Health & Hum. Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).

“Regardless of whether the burden ever shifts to the [R]espondent, the special master
may consider the evidence presented by the [R]espondent in determining whether the [P]etitioner
has established a prima facie case.” Flores v. Sec’y of Health & Hum. Servs., 115 Fed. Cl. 157,
162-63 (2014); see also Stone v. Sec’y of Health & Hum. Servs., 676 F.3d 1373, 1379 (Fed. Cir.
2012) (“[E]vidence of other possible sources of injury can be relevant not only to the ‘factors
unrelated’ defense, but also to whether a prima facie showing has been made that the vaccine
was a substantial factor in causing the injury in question.”); de Bazan v. Sec’y of Health & Hum.
Servs., 539 F.3d 1347, 1353 (Fed. Cir. 2008) (“The government, like any defendant, is permitted
to offer evidence to demonstrate the inadequacy of the [P]etitioner’s evidence on a requisite
element of the [P]etitioner's case-in-chief.”); Pafford, 451 F.3d at 1358-59 (“[T]he presence of
multiple potential causative agents makes it difficult to attribute ‘but for’ causation to the
vaccination. . . . [T]he Special Master properly introduced the presence of the other unrelated
contemporaneous events as just as likely to have been the triggering event as the vaccinations.”).

B. Factual Issues

Petitioner must prove, by a preponderance of the evidence, the factual circumstances
surrounding her claim. § 13(a)(1)(A). To resolve factual issues, the special master must weigh
the evidence presented, which may include contemporaneous medical records and testimony.
See Burns v. Sec’y of Health & Hum. Servs., 3 F.3d 415, 417 (Fed. Cir. 1993) (explaining that a
special master must decide what weight to give evidence including oral testimony and
contemporaneous medical records).

Medical records, specifically contemporaneous medical records, are presumed to be
accurate and generally “warrant consideration as trustworthy evidence.” Cucuras v. Sec’y of
Health & Hum. Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993). But see Kirby v. Sec’y of Health
& Hum. Servs., 997 F.3d 1378, 1382 (Fed. Cir. 2021) (rejecting the presumption that “medical
records are accurate and complete as to all the patient’s physical conditions”); Shapiro v. Sec’y
of Health & Hum. Servs., 101 Fed. Cl. 532, 538 (2011) (“[T]he absence of a reference to a
condition or circumstance is much less significant than a reference which negates the existence
of the condition or circumstance.” (quoting Murphy v. Sec’y of Health & Hum. Servs., 23 Cl. Ct.
726, 733 (1991), aff’d per curiam, 968 F.2d 1226 (Fed. Cir. 1992))), recons. den’d after remand,
105 Fed. Cl. 353 (2012), aff’d mem., 503 F. App’x 952 (Fed. Cir. 2013). The weight afforded to
contemporaneous records is due to the fact that they “contain information supplied to or by

36
health professionals to facilitate diagnosis and treatment of medical conditions. With proper
treatment hanging in the balance, accuracy has an extra premium.” Id. To overcome the
presumptive accuracy of medical records, a petitioner may present testimony which is
“consistent, clear, cogent, and compelling.” Sanchez v. Sec’y of Health & Hum. Servs., No. 11–
685V, 2013 WL 1880825, at *3 (Fed. Cl. Spec. Mstr. Apr. 10, 2013) (citing Blutstein v. Sec’y of
Health & Hum. Servs., No. 90–2808V, 1998 WL 408611, at *5 (Fed. Cl. Spec. Mstr. June 30,
1998)), mot. for rev. denied, 142 Fed. Cl. 247 (2019), vacated on other grounds & remanded, 809
F. App’x 843 (Fed Cir. 2020).

There are situations in which compelling testimony may be more persuasive than written
records, such as where records are deemed to be incomplete or inaccurate. Campbell v. Sec’y of
Health & Hum. Servs., 69 Fed. Cl. 775, 779 (2006) (“[L]ike any norm based upon common
sense and experience, this rule should not be treated as an absolute and must yield where the
factual predicates for its application are weak or lacking.”); Lowrie v. Sec’y of Health & Hum.
Servs., No. 03–1585V, 2005 WL 6117475, at *19 (Fed. Cl. Spec. Mstr. Dec. 12, 2005)
(“[W]ritten records which are, themselves, inconsistent, should be accorded less deference than
those which are internally consistent.” (quoting Murphy, 23 Cl. Ct. at 733). Ultimately, a
determination regarding a witness’s credibility is needed when determining the weight that such
testimony should be afforded. Andreu v. Sec’y of Health & Hum. Servs., 569 F.3d 1367, 1379
(Fed. Cir. 2009); Bradley, 991 F.2d at 1575.

Despite the weight afforded medical records, special masters are not bound rigidly by
those records in determining onset of a petitioner’s symptoms. Valenzuela v. Sec’y of Health &
Hum. Servs., No. 90–1002V, 1991 WL 182241, at *3 (Fed. Cl. Spec. Mstr. Aug. 30, 1991); see
also Eng v. Sec’y of Health & Hum. Servs., No. 90–1754V, 1994 WL 67704, at *3 (Fed. Cl.
Spec. Mstr. Feb. 18, 1994) (Section 13(b)(2) “must be construed so as to give effect also to §
13(b)(1) which directs the special master or court to consider the medical records (reports,
diagnosis, conclusions, medical judgment, test reports, etc.), but does not require the special
master or court to be bound by them”).

C. Table Claim

To receive compensation through the Program, Petitioner must prove either (1) that
A.F.M. suffered a “Table Injury”—i.e., an injury listed on the Vaccine Injury Table—
corresponding to a vaccine that she received, or (2) that A.F.M. suffered an injury that was
actually caused by a vaccination. See §§ 11(c)(1), 13(a)(1)(A); Capizzano v. Sec’y of Health &
Hum. Servs., 440 F.3d 1317, 1319-20 (Fed. Cir. 2006). Here, Petitioner alleges both a Table
injury and a causation-in-fact injury. Pet. Mot. at 1. As acknowledged by Respondent, the
alleged Table injury is based on the question of whether A.F.M. suffered an “encephalopathy.”
See Resp. Rept. at 16 (citing 42 C.F.R § 100.3(a)(II)(B)).

The Vaccine Injury Table provides that encephalopathy is a recognized injury for DTaP
vaccinations if the first symptom or manifestation of onset occurs within 72 hours of vaccine
administration. 42 C.F.R. § 100.3(a)(II)(B). A “vaccine recipient shall be considered to have
suffered an encephalopathy if an injury meeting the description of acute encephalopathy occurs
within the applicable time period and results in a chronic encephalopathy.” Id. at § 100.3(c)(2).

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Acute encephalopathy, for children less than 18 months of age, that presents without a seizure “is
indicated by a significantly decreased level of consciousness that lasts at least 24 hours.” Id. at §
100.3(c)(2)(i)(A)(1). Acute encephalopathy following a seizure “is demonstrated by a
significantly decreased level of consciousness that lasts at least 24 hours and cannot be attributed
to a postictal state—from a seizure or a medication.” Id. at § 100.3(c)(2)(i)(A)(2). “Clinical
features” that do not in themselves “demonstrate an acute encephalopathy or a significant change
in either mental status or level of consciousness” include “sleepiness, irritability (fussiness),
high-pitched and unusual screaming, poor feeding, persistent inconsolable crying, bulging
fontanelle, or symptoms of dementia.” Id. at § 100.3(c)(2)(i)(C). Moreover, “[s]eizures in
themselves are not sufficient to constitute a diagnosis of encephalopathy and in the absence of
other evidence of an acute encephalopathy, seizures shall not be viewed as the first symptom or
manifestation of an acute encephalopathy.” Id. at § 100.3(c)(2)(i)(D).

Exclusionary criteria for encephalopathy include, “[a]n underlying condition or systemic
disease shown to be unrelated to the vaccine (such as malignancy, structural lesion, psychiatric
illness, dementia, genetic disorder, prenatal or perinatal central nervous system (CNS) injury).”
42 C.F.R. § 100.3(c)(2)(ii)(A). The time period for first symptom or manifestation of onset of
encephalopathy is less than or equal to 72 hours after DTaP vaccine administration. Id. §
100.3(a)(II)(B).

D. Causation

In the alternative, Petitioner alleges a causation-in-fact claim. To prevail on this claim,
Petitioner must prove that a vaccine A.F.M. received caused her injury. To do so, Petitioner
must establish, by preponderant evidence: (1) a medical theory causally connecting the vaccine
and A.F.M.’s injury (“Althen Prong One”); (2) a logical sequence of cause and effect showing
that the vaccine was the reason for A.F.M.’s injury (“Althen Prong Two”); and (3) a showing of
a proximate temporal relationship between the vaccine and A.F.M.’s injury (“Althen Prong
Three”). § 13(a)(1); Althen, 418 F.3d at 1278.

The causation theory must relate to the injury alleged. Petitioner must provide a sound
and reliable medical or scientific explanation that pertains specifically to this case, although the
explanation need only be “legally probable, not medically or scientifically certain.” Knudsen, 35
F.3d at 548-49. Petitioner cannot establish entitlement to compensation based solely on her
assertions; rather, a vaccine claim must be supported either by medical records or by the opinion
of a medical doctor. § 13(a)(1). In determining whether Petitioner is entitled to compensation,
the special master shall consider all material in the record, including “any . . . conclusion, [or]
medical judgment . . . which is contained in the record regarding . . . causation.” § 13(b)(1)(A).
The undersigned must weigh the submitted evidence and the testimony of the parties’ proffered
experts and rule in Petitioner’s favor when the evidence weighs in her favor. See Moberly, 592
F.3d at 1325-26 (“Finders of fact are entitled—indeed, expected—to make determinations as to
the reliability of the evidence presented to them and, if appropriate, as to the credibility of the
persons presenting that evidence.”); Althen, 418 F.3d at 1280 (noting that “close calls” are
resolved in Petitioner’s favor).

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Testimony that merely expresses the possibility—not the probability—is insufficient, by
itself, to substantiate a claim that such an injury occurred. See Waterman v. Sec’y of Health &
Hum. Servs., 123 Fed. Cl. 564, 573-74 (2015) (denying Petitioner’s motion for review and
noting that a possible causal link was not sufficient to meet the preponderance standard). The
Federal Circuit has made clear that the mere possibility of a link between a vaccination and a
petitioner’s injury is not sufficient to satisfy the preponderance standard. Moberly, 592 F.3d at
1322 (emphasizing that “proof of a ‘plausible’ or ‘possible’ causal link between the vaccine and
the injury” does not equate to proof of causation by a preponderance of the evidence); Boatmon
v. Sec’y of Health & Hum. Servs., 941 F.3d 1351, 1359-60 (Fed. Cir. 2019). While certainty is
by no means required, a possible mechanism does not rise to the level of preponderance.
Moberly, 592 F.3d at 1322; see also de Bazan, 539 F.3d at 1351.

V. ANALYSIS

A. Initial Event May 8, 2014—Seizure or ALTE

As Federal Circuit precedent establishes, in certain cases it is appropriate to determine
the nature of an injury before engaging in the Althen analysis. Broekelschen v. Sec’y of Health
& Hum. Servs., 618 F.3d 1339, 1346 (Fed. Cir. 2010). Since “each prong of the Althen test is
decided relative to the injury[,]” determining facts relating to the claimed injury can be
significant. Id. Here, the factual issue is whether A.F.M. had a seizure or an ALTE on May 8,
2014. Thus, before determining if Petitioner has met each prong of Althen, the undersigned
addresses whether Petitioner has established, by a preponderance of the evidence, that A.F.M.
suffered from a seizure on May 8, 2014, as alleged by Petitioner, or an ALTE, as suggested by
Respondent.

The EMS records are the earliest-in-time documents about what happened the morning
of May 8, 2014. They state that primary

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Source: Frix Law Library, https://www.frixlaw.com/law-library/cases/10736964. Public record. Not legal advice.