A. v. Secretary of Health and Human Services ( 2023 )

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
Filed: January 24, 2023
Refiled in Redacted Form: March 27, 2023
*************************
E. A., * PUBLISHED
*
Petitioner, * No. 18-1587V
*
v. * Special Master Nora Beth Dorsey
*
SECRETARY OF HEALTH * Entitlement; Influenza (“Flu”) Vaccine;
AND HUMAN SERVICES, * Bell’s Palsy.
*
Respondent. *
*
*************************
Ronald C. Homer, Conway Homer, P.C., Boston, MA, for Petitioner.
Amanda Pasciuto, U.S. Department of Justice, Washington, DC, for Respondent.
RULING ON ENTITLEMENT1
I. INTRODUCTION
On October 12, 2018, E.A. (“Petitioner”) filed a petition for compensation under the
National Vaccine Injury Compensation Program (“Vaccine Act” or “the Program”), 42 U.S.C. §
300aa-10 et seq. (2012).2 Petitioner alleges that she suffered Bell’s palsy as the result of an
1
Because this Ruling 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 in accordance with
the E-Government Act of 2002. 44 U.S.C. § 3501 note (2012) (Federal Management and
Promotion of Electronic Government Services). This means the Ruling will be available to
anyone with access to the Internet. In accordance with Vaccine Rule 18(b), Petitioner has 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 (2012). All citations in this Ruling to individual sections of the
Vaccine Act are to 42 U.S.C. § 300aa.
influenza (“flu”) vaccination administered on October 19, 2015. Petition at Preamble (ECF No.
1). Respondent argued against compensation, stating that “this case is not appropriate for
compensation under the terms of the Vaccine Act.” Respondent’s Report (“Resp. Rept.”) at 2
(ECF No. 30).
After carefully analyzing and weighing the evidence presented in this case in accordance
with the applicable legal standards, the undersigned finds that Petitioner has provided
preponderant evidence that her flu vaccine caused her Bell’s palsy, satisfying Petitioner’s burden
of proof under Althen v. Secretary of Health & Human Services, 418 F.3d 1274, 1280 (Fed. Cir.
2005). Accordingly, Petitioner is entitled to compensation.
II. ISSUES TO BE DECIDED
Diagnosis is not at issue. Joint Pre-Hearing Submission, filed April 4, 2022 at 1 (ECF
No. 98). The parties stipulated that Petitioner received a flu vaccine on October 19, 2015; that
onset of her symptoms, consistent with Bell’s palsy, was November 28, 2015; and that Petitioner
experienced the residual effects of Bell’s palsy for more than six months. Id.The central issue is whether Petitioner has provided preponderant evidence of causation
for all three Althen prongs. Petitioner asserts that she has met her burden under the Althen
prongs. Petitioner’s Motion for Ruling on the Record (“Pet. Mot.”), filed Apr. 11, 2022, at 39-52
(ECF No. 107). Respondent disagrees and argues that Petitioner failed to submit preponderant
evidence that her flu vaccine more likely than not caused her Bell’s palsy. Resp. Response to
Pet. Mot. (“Resp. Response”), filed June 10, 2022, at 15-31 (ECF No. 108).
III. BACKGROUND
A. Medical Terminology
Bell’s palsy is defined as “unilateral facial paralysis of sudden onset, due to [a] lesion of
the facial nerve[,] [] resulting in characteristic distortion of the face.” Bell Palsy, Dorland’s
Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=95779 (last
visited Nov. 15, 2022).
The facial nerve, also referred to as the seventh cranial nerve, “directs the muscles on . . .
the face, including those that control eye blinking and closing and facial expressions such as
smiling.”3 Resp. Exhibit (“Ex.”) C, Tab 12 at 1.4 “The facial nerve also carries nerve impulses to
3
The large motor root “supplies the muscles of facial expression.” Nervus Facialis, Dorland’s
Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=92293 (last
visited Jan. 9, 2023).
4
Bell’s Palsy Fact Sheet, NINDS, 2018, https://www.ninds.nih.gov/bells-palsy-fact-sheet (last
modified May 13, 2020).
2
the tear glands, the saliva glands, and the muscles of a small bone in the middle of the ear.”5 Id.The facial nerve consists of three portions. Relevant here, the intratemporal portion of the facial
nerve includes three segments: labyrinthine (extending from the internal auditory canal (“IAC”)
to the geniculate ganglion), tympanic (extending horizontally from the geniculate ganglion to the
pyramidal process), and mastoid (extending vertically from the pyramidal process to the
stylomastoid foramen). See Michael Gleeson, External and Middle Ear, in Gray’s Anatomy: The
Anatomical Basis of Clinical Practice 624, 638 (Susan Standring et al. eds., 41st ed. 2016); see
also Resp. Ex. C, Tab 1 at 2.6 Due to the narrow course at which the facial nerve travels, it is
vulnerable to nerve compression and ischemia at several areas including the labyrinthine
segment. Gleeson, supra, at 639; see also Resp. Ex. A, Tab 2 at 5 (“[W]ith little room for
expansion, . . . inflammation of the nerve (due to any cause) is thought to cause compression
resulting in paralysis.”);7 Resp. Ex. C, Tab 1 at 3-4 (“[T]he facial canal’s diameter of the
labyrinthine segment is possibly an anatomical risk factor.”).
Bell’s palsy is considered an “acute idiopathic demyelinating peripheral neuropathy of
the facial nerve.” Pet. Ex. 22 at 1.8 Thus, the etiology of Bell’s palsy is unclear. Pet. Ex. 47 at
1;9 Resp. Ex. C, Tab 6 at 1.10 However, autoimmune, inflammatory, and infectious etiologies
have been postulated. Pet. Ex. 13 at 8-9; Pet. Ex. 18.11
B. Procedural History
Petitioner filed her petition on October 12, 2018, and filed medical records on February
12, 2019. Petition; Pet. Exs. 1-6. On July 12, 2019, Respondent filed a Rule 4(a) Report
offering a preliminary summary of the filed medical records but indicated that medical personnel
5
The nervus intermedius (smaller root) “contributes parasympathetic and special sensory fibers
to the facial nerve.” Nervus Intermedius, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=92313 (last visited Jan. 9, 2023).
6
Wenjuan Zhang et al., The Etiology of Bell’s Palsy: A Review, 267 J. Neurology 1896 (2020).
7
Stephen G. Reich, Bell’s Palsy, 23 Continuum 447 (2017).
8
Aharon Aviel et al., Peripheral Blood T and B Lymphocyte Subpopulations in Bell’s Palsy, 92
Annals Otology Rhinology & Laryngology 187 (1983).
9
Weigong Zhou et al., A Potential Signal of Bell’s Palsy After Parenteral Inactivated Influenza
Vaccines: Reports to the Vaccine Adverse Event Reporting System (VAERS) United States,
1991-2001, 13 Pharmacoepidemiology & Drug Safety 505 (2004).
10
Cheng-Hsiu Chou et al., Bell’s Palsy Associated with Influenza Vaccination: Two Case
Reports, 25 Vaccine 2839 (2007).
11
A. Greco et al., Bell’s Palsy and Autoimmunity, 12 Autoimmunity Rev. 323 (2012). This
article is also referenced by Respondent. Resp. Ex. A, Tab 1.
3
at the Division of Injury Compensation Programs (“DICP”) had not yet been able to review the
claim and offer an opinion as to Respondent’s position. Resp. Rule 4(a) Rept. (ECF No. 15).
Thereafter, Respondent filed a status report indicating his intent to defend the claim. Resp.
Status Rept., filed Sept. 19, 2019 (ECF No. 16).
On September 26, 2019, Chief Special Master Corcoran issued an order outlining his
preliminary impressions of Petitioner’s claim. Order dated Sept. 26, 2019, at 2 (ECF No. 17).
Chief Special Master Corcoran encouraged both parties to consider engaging in settlement
negotiations given the claim’s underlying nature. Id. The matter was subsequently transferred to
the undersigned on October 3, 2019. Notice of Reassignment, filed Oct. 3, 2019 (ECF No. 19).
Prior to retaining an expert, and at Petitioner’s request, the undersigned held a Rule 5
status conference on November 7, 2019. Rule 5 Order dated Nov. 7, 2019 (ECF No. 21); Pet.
Status Rept., filed Oct. 18, 2019 (ECF No. 20). The undersigned stated that “ample case law and
medical literature support a finding in favor of [P]etitioner in this matter.” Rule 5 Order dated
Nov. 7, 2019, at 1. “The undersigned referenced multiple cases, involving the flu vaccine and an
alleged injury of Bell’s palsy, all of which resulted in joint stipulations awarding damages to
petitioners.” Id. Nonetheless, Respondent still indicated his client was not interested in
settlement. Id. at 2. The undersigned ordered Respondent to file his Rule 4(c) Report and
recommended Petitioner strengthen her case by providing an expert report. Id.
Subsequently, on January 6, 2020, Respondent filed his Rule 4(c) Report stating that
Petitioner is not entitled to compensation for failure to meet her causation-in-fact burden of proof
under Althen, particularly, that Petitioner provided no evidence of a causal theory establishing
the flu vaccine can cause and did cause Petitioner’s Bell’s palsy. Resp. Rept. at 4-6.
On April 9, 2020, Petitioner filed an expert report from neurologist Dr. Kazim Sheikh.
Pet. Ex. 13. On July 24, 2020, Respondent filed expert reports from neurologist Dr. Dara
Jamieson and immunologist Dr. Steven Tomkins. Resp. Exs. A, C. In response, Petitioner filed
a supplemental report from Dr. Sheikh on November 2, 2020. Pet. Ex. 42.
At the request of the parties, a second Rule 5 status conference was held on December 17,
2020. Pet. Joint Status Rept., filed Sept. 18, 2020 (ECF No. 52); Rule 5 Order dated Dec. 17,
2020 (ECF No. 59). Since the Rule 5 status conference in November 2019, expert reports and
medical literature had been filed. Rule 5 Order dated Dec. 17, 2020, at 1. In addition, the
undersigned stated she had the opportunity to review “similar cases involving flu vacc[ination]
and Bell’s palsy and therefore ha[d] obtained more comprehensive knowledge of the clinical
course of Bell’s palsy, the literature, and theories behind causation of the disease.” Id. The
undersigned stated that because both parties’ experts agreed with the diagnosis of Bell’s palsy
and the onset of approximately 40 days post-vaccination, the remaining issue to be resolved was
causation. Id. The undersigned made a preliminary finding that Petitioner had provided
preponderant evidence of causation based on the Althen prongs and posited “that if this case
went to a hearing, she would probably find in favor of [P]etitioner.” Id. at 3. However, given
the risk of litigation, she recommended that “this case should be resolved by settlement.” Id.
4
The parties entertained settlement negotiations from January to July 2021. See ECF Nos.
60, 64-65, 67, 69, 7, 73. Thereafter, the parties reached an impasse in settlement discussions.
Pet. Status Rept., filed July 21, 2021 (ECF No. 73). Following a status conference on August 3,
2021, Respondent filed a supplemental report of Dr. Tompkins on October 18, 2021, and
Petitioner filed a second supplemental expert report of Dr. Sheikh on February 15, 2022. Resp.
Ex. E; Pet. Ex. 63; see Order dated Aug. 3, 2021 (ECF No. 74). Petitioner also filed updated
medical records. Pet. Exs. 62, 95.
On February 17, 2022, the parties conveyed their preference to proceed with a ruling on
the record in lieu of an entitlement hearing. Pet. Joint Status Rept., filed Feb. 17, 2022 (ECF No.
91). Petitioner filed a Motion for Ruling on the Record on April 11, 2022. Pet. Mot.
Respondent filed a response to Petitioner’s Motion for Ruling on the Record on June 6, 2022.
Resp. Response. Petitioner filed her reply on July 19, 2022. Pet. Reply to Resp. Response (“Pet.
Reply”), filed July 19, 2022 (ECF No. 111).
This matter is now ripe for adjudication.
C. Medical History
Prior to the vaccination at issue, Petitioner had a prior medical history significant for
chronic myofascial pain syndrome involving her neck and upper thoracic spine. Pet. Ex. 12 at ¶
6; Pet. Ex. 2 at 66, 231. She effectively managed this condition with trigger point injections.
Pet. Ex. 12 at ¶ 6. Petitioner had a history of degenerative spine disease. Pet. Ex. 2 at 480. She
also had a history of heart palpitations, carpal tunnel release, Dupuytren’s contractures,
fibromatosis in the feet, seasonal allergies, and several orthopedic injuries. Id. at 12-13, 187.
These were controlled with medications. Pet. Ex. 12 at ¶ 6. Regarding family history, Petitioner
reported that her half-brother is deaf due to rubella. Pet. Ex. 2 at 274.
Petitioner was 62 years old when she received the quadrivalent flu vaccine at issue in her
left deltoid on October 19, 2015. Pet. Ex. 1 at 2.
In November 2015, Petitioner traveled from her home in Virginia to Wisconsin to visit
with a large group of friends and family for the Thanksgiving holiday.12 Pet. Ex. 12 at ¶ 9.
While there, Petitioner thought she may be developing a cold and took Mucinex. Pet. Ex. 2 at
675. On November 28, 2015, 41 days after her flu vaccination, Petitioner awoke with left facial
numbness and weakness. Pet. Ex. 12 at ¶ 10. Her friend’s daughter, a physician, prescribed
Petitioner 60 mg of prednisone that she took that night. Id.; Pet. Ex. 2 at 675.
The following day, on November 29, 2015, Petitioner returned home and presented to the
emergency department (“ED”) at Walter Reed National Military Medical Center (“Walter
Reed”) for her left-sided facial complaints. Pet. Ex. 2 at 672. She reported the facial numbness
began the previous morning and quickly turned to weakness of the left cheek and the inability to
close her left eye. Id. at 672, 675. Her left eye was dry and was neither blinking nor closing
12
Thanksgiving Day was November 26, 2015.
5
completely. Id. at 673, 675. Her partner of 25 years had died the month before, and she was
very tearful. Id. at 673. A review of symptoms included “slight [upper respiratory infection]
symptoms” but no signs of infection were documented. Id. at 675. Petitioner denied difficulty
with speaking/swallowing and denied any difficulty with hearing. Id. at 673. Physical
examination showed peripheral weakness in the seventh cranial nerve (“CN VII” or “CN7”) on
the left side but bilaterally normal ears. Id. at 675. No vesicles in the ear, or elsewhere, were
noted. See id. Petitioner was diagnosed with Bell’s palsy and was prescribed Valtrex.13 Id. at
676. She was instructed to continue prednisone, to tape her eye closed, and to follow up with her
primary care provider (“PCP”). Id.
On December 15, 2015, Petitioner saw her PCP, Dr. Huma Chaudhery, for a follow-up
visit “on recent Bell’s palsy diagnosis.” Pet. Ex. 2 at 233. Petitioner reported she developed
left-sided facial weakness about three to four weeks prior and that her symptoms had started to
improve. Id. Her symptoms included the “inability to lift her left eye[]brow, close her left eye,
or smile on the left side.” Id. at 233, 235. These symptoms were observed upon physical
examination and “[a]bnormal diffuse left CN VII weakness” was noted. Id. at 235. Petitioner
denied vision changes or left eye pain but noted intermittent left preauricular pain. Id. at 233.
Her ear exam was normal. Id. at 234. Again, no vesicles in the ear, or elsewhere, were noted.
See id. She had been following good eye care techniques that Dr. Chaudhery instructed her to
continue including using artificial tears, wearing protective eyeglasses, and using a patch on her
eye at night while sleeping. Id. at 233, 236. Due to the “severity of dysfunction and minimal
improvement after nearly one month,” Dr. Chaudhery wanted to check for Lyme14 antibodies
and obtain a brain magnetic resonance imaging (“MRI”). Id. at 236. At this visit, Dr. Chaudhery
noted Petitioner’s chronic myofascial pain and her upcoming appointment with pain
management for trapezius and peri-scapular trigger points.15 Id. Dr. Chaudhery also noted
Petitioner’s recent loss of her partner and that she was “teary during the encounter.” Id. at 233.
13
Valtrex is trademark name for valacyclovir hydrochloride. Valtrex, Dorland’s Med.
Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=52497 (last visited
Jan. 9, 2023). Valacyclovir hydrochloride is “the hydrochloride salt of the l-valyl ester of
acyclovir, used as an antiviral agent in the treatment of genital herpes and herpes zoster in
immunocompetent adults.” Valacyclovir Hydrochloride, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=52462 (last visited Jan. 9, 2023).
14
Lyme disease is “a recurrent, multisystemic disorder caused by the spirochete Borrelia
burgdorferi; vectors for human infection are the ticks Ixodes scapularis and I. pacificus.” Lyme
Disease, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?
id=70552 (last visited Jan. 9, 2023).
15
Petitioner continued to receive trigger point injections for her chronic myofascial pain
throughout her course of treatment for Bell’s palsy. Pet. Ex. 2 at 236, 262-64, 282-83, 297-99,
311-12, 329-33, 366-69, 391-93, 431-32.
6
Petitioner underwent an MRI of the brain and IAC on December 24, 2015. Pet. Ex. 2 at
249. Dr. Robert Shih’s impression of the MRI was “[a]bnormal enhancement along the
intratemporal left CN7 is nonspecific and can be seen in the setting of Bell’s palsy.” Id. at 251.
At a follow-up visit with Dr. Chaudhery on February 16, 2016, Petitioner reported
additional improvement of symptoms in the past four to six weeks. Pet. Ex. 2 at 246. However,
she reported a new onset of left ear pressure and a “bubbling sensation/machine sound” in the
past month. Id. She denied left ear pain, drainage, hearing loss, ringing, fever, and vertigo. Id.
On physical examination, she was able to elevate her eyebrow and her frown/smile was slightly
diminished on the left. Id. at 248. Other than the onset of “ipsilateral increased
pressure/bubbling sound” in her left ear, her “left sided facial paralysis [had] slowly improv[ed]
over the past [four] months.” Id. at 251. Dr. Chaudhery recommended Petitioner resume her
previously discontinued antihistamines and nasal steroids for allergic rhinitis (seasonal allergies),
which he felt may improve her symptoms. Id. He also recommended that she follow-up with an
ear, nose, and throat (“ENT”) specialist. Id.
Petitioner was evaluated by Dr. Sally Stasio and Dr. Paula Jackson at the Walter Reed
Otolaryngology (ENT) Clinic on February 24, 2016. Pet. Ex. 2 at 255. Petitioner’s chief
complaint was “clicking in the ear.” Id. She reported that after her slow improvement at the end
of December, “she felt sharp pains in her face and twitching of her left face. Her nerve ha[d]
continued to improve, and she ha[d] noticed presence of clicking or thumping sounds in her left
ear. These [did] not match her heartbeat, and worsen[ed] when she contract[ed] her face.” Id. at
255-56. She endorsed autophonia16 and “mild sensation of fullness that does not clear with
[V]alsalva.”17 Id. at 256. Still, she denied the presence of vesicles, vertigo, and “sounds of her
eyes moving in her head.” Id. at 255-56. On examination, her hearing was functional, no
abnormalities were noted on nasal endoscopy, and her facial sensation was intact. Id. at 256.
She had mild facial weakness at the frontal and marginal branches of CN VII on the left,
16
Autophonia or autophony is the “abnormal hearing of one's own voice and respiratory
sounds.” Autophony, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/
dorland/definition?id=5016 (last visited Jan. 9, 2023).
17
Valsalva is the “forcible exhalation effort against occluded nostrils and a closed mouth causes
increased pressure in the auditory tube and middle ear, so that the tympanic membrane moves
outward.” Valsalva Maneuver, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.
com/dorland/definition?id=87881 (last visited Jan. 9, 2023).
7
classified as a House-Brackman (“HB”)18 grade two, and no synkinesis19 with animation. Id. at
256, 261. Dr. Stasio remarked that Petitioner’s “left ear thumping seems to be related to her
facial movement, suggesting [synkinesis] of CN VII innervation to the stapedius muscle.”20 Id.
at 260. Tinnitus (left ear), bilateral unspecified hearing loss, and “patulous eustachian tube[21]
(voice echoes in her head)” were also reported in Dr. Stasio’s assessment. Id. Given Petitioner’s
history, Dr. Jackson, recorded Bell’s palsy as the diagnosis, with Ramsay Hunt syndrome22 as a
differential diagnosis, but noting that the presentation of that was “not classic.” Id. at 261. Dr.
Jackson also noted Petitioner had a “near complete recovery” of the Bell’s palsy, going from HB
grade 6 (per her review of Petitioner’s video of her acute onset symptoms) to HB grade 2, and
that “time alone may result in further recovery.” Id. However, because there was a question of
enhancement in the left medial IAC, an MRI was ordered to be repeated in six to eight months.
Id.
On March 29, 2016, Petitioner returned to Dr. Chaudhery for a follow-up. Pet. Ex. 2 at
268. He reported “significant improvement” and scheduled an MRI for December 16, 2016. Id.
On April 15, 2016, Petitioner presented to the Walter Read Audiology Clinic for “left ear
problems since Bell[’]s [p]alsy on 28 November 2015.” Pet. Ex. 2 at 274. At this visit,
Petitioner reported no difficulty hearing over background noise or understanding speech. Id.
18
House-Brackmann is facial nerve scaled grading system of facial dysfunction. Pet. Ex. 18 at 2.
Grade two refers to “[s]light weakness noticeable only on close inspection. At rest: normal
symmetry of forehead, ability to close eye with minimal effort and slight asymmetry. No
synkinesis, contracture, or hemifacial spasm.” Id. at 3. Grade six refers to total paralysis. Id.
19
Synkinesis is “an unintentional movement accompanying a volitional movement, such as the
facial contortions accompanying severe exertion.” Synkinesis, Dorland’s Med. Dictionary
Online, https://www.dorlandsonline.com/dorland/definition?id=48544 (last visited Jan. 9, 2023).
20
The stapedius muscle is in the tympanic cavity (middle ear) and “attaches to the posterior
surface of the neck of the stapes.” Michael Gleeson, External and Middle Ear, in Gray’s
Anatomy: The Anatomical Basis of Clinical Practice 624, 637 (Susan Standring et al. eds., 41st
ed. 2016).
21
The eustachian tube is “a channel . . . lined with mucous membrane, that establishes
communication between the tympanic cavity and the nasopharynx and serves to adjust the
pressure of gas in the cavity to the external pressure, as well as for mucociliary clearance of the
middle ear.” Tuba Auditiva, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.
com/dorland/definition?id=115257 (last visited Jan. 9, 2023).
22
Ramsay Hunt syndrome is a “herpes zoster involving the facial and vestibulocochlear nerves,
often associated with transitory ipsilateral facial paralysis and herpetic vesicles of the external
ear or tympanic membrane; there may or may not be tinnitus, vertigo, and hearing disorders.”
Ramsay Hunt Syndrome, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/
dorland/definition?id=111266 (last visited Jan. 9, 2023).
8
However, she did report listening to the TV and radio louder since November 2015. Id. She
denied earache, ear pressure, fullness, and discharge. Id. “Tinnitus [t]riggered by Bell[’]s
[p]alsy” was noted. Id. Petitioner reported “left ear tinnitus sounds like an ocean with machine
gun sound when she talks” and that she “[h]ears herself ‘weird, it’s like banging on left ear.’” Id.
She reported her physician attributed “this ‘machine gun’ sound to facial nerve activating the
stirrup.” Id. On that date,23 an audiometric hearing test was performed and revealed “[m]ixed
conductive and sensorineural hearing loss, unilateral left ear, with unrestricted hearing on the
contralateral side: Patient has essentially normal hearing, bilaterally.” Id. at 276. Additionally, it
was noted that Petitioner would not “have difficulty understanding speech in every day listening
environments” and was not a candidate for a hearing aid. Id. Petitioner was advised that if the
tinnitus worsened, she could attend a Progressive Tinnitus Management workshop. Id. She was
to follow-up with ENT due to the conductive component in her left ear and it was recommended
to have another audiologic evaluation in one year to monitor her hearing status. Id.
Petitioner visited the Water Reed Optometry Clinic on April 19, 2016 for an annual
exam. Pet. Ex. 2 at 278. Petitioner did not report any vision problems. Id. She was diagnosed
with bilateral dry eyes syndrome. Id. at 280.
At a follow-up visit with Dr. Chaudhery on June 28, 2016, Petitioner had “recovered
most of her function” but felt that her “progress has plateaued.” Pet. Ex. 2 at 292. Her tinnitus
was still “moderately bothersome.” Id. at 289. Physical examination found “facial sensation to
light touch decreased on the left, left sided ptosis.” Id. at 290. She was advised to follow up
with ENT for her tinnitus and she was referred to physical therapy for facial rehabilitation. Id. at
292.
On July 6, 2016, Petitioner followed-up with the Otolaryngology Clinic for Bell’s palsy
and tinnitus. Pet. Ex. 2 at 293. She was seen by Dr. Joseph F. Goodman. Id. Her main concern
was the tinnitus and described a “repetitive thumping/knocking (like a machine gun)” sound in
her left ear that was brought on by “smiling, grimacing, and tilting her head down.” Id. She
reported continued difficulty hearing out of her left ear and her recent audiogram showing mild
10dB hearing loss in her left ear was noted. Id. She also complained of continued difficulty with
dry eyes, which was controlled by eye drops, and dry mouth, which was controlled by a mouth
rinse and lozenges. Id. Petitioner reported increased nasal congestion and “ear fullness” since
stopping Flonase. Id. She denied postnasal drip, reflux, and sore throat. Id. There was no
“middle ear effusion” evident on examination but Petitioner reported “sensation of fluid in ears
on [V]alsalva.” Id. at 294. Facial sensation to light touch was symmetric bilaterally. Id. Facial
strength was HB 3/6 on the left with “weakness of marginal branch and some asymmetry at rest,
but complete eye closure.” Id. Dr. Goodman noted residual weakness primarily in the marginal
and cervical branches of the facial nerve.” Id. at 295.
Given her history and the sensation of fluid in her ears, Dr. Goodman recommended
starting her on a nasal regimen of oxymetazoline for five days, Flonase daily, and saline rinses.
23
A hearing test was performed in 2013 but those results are not available. Pet. Ex. 2 at 274; see
also Resp. Ex. A at 5, 5 n.2.
9
Pet. Ex. 2 at 294. Dr. Goodman’s assessment was “[t]innitus likely caused by stapedius
myoclonus[24] and synkinesis after the recovery from [Bell’s palsy]. If extremely bothered by
this and no relief from nasal spray regimen to open the Eustachian tube may refer to Dr. Gupta to
assess for possible laser ablation of stapedius tendon.” Id. Petitioner indicated she was not
interested in that option at the time. Id. Dr. Goodman also stated the tinnitus had “not improved
and worsens with smiling, grimacing, and looking down.” Id. at 295. He determined “given
history of CN 7 injury her symptoms are likely 2/2 synkinesis of stapedius muscle or tensor
tympani muscle.”25 Id. He added that Petitioner “may have had an atypical presentation of
Ramsey-Hunt given the severe ear pain she experienced about one week after the onset of facial
paralysis, also given her mild middle ear symptoms.” Id.
On July 13, 2016, Petitioner had her first physical therapy session at the Jackson Clinics
with Deborah Gilpin. Pet. Ex. 3 at 1. Petitioner presented with complaints of facial weakness
and asymmetry following her “acute onset of [left] sided Bell’s palsy.” Id. She reported waking
up with left-sided facial paralysis on November 28, 2015, went to the ED and started medication,
and that three weeks later she started to regain facial movement but then got tinnitus in her left
ear. Id. She noticed improvement in the following months but was still having numbness along
the left side of her face. Id. at 2. She still had difficulty eating and drinking “due to weakness
and motor control” and would have “involuntary twitching along upper lip and eyelid.” Id. She
expressed wanting to be able “to smile and open and close her [left] eye symmetrically to her
[right eye].” Id. Petitioner also reported feeling like she “slurr[ed] her words occasionally” and
that she was found to have some “mid[-]range” hearing loss. Id. On evaluation, Ms. Gilpin
noted that Petitioner demonstrated “some volitionary use of her [left] facial muscles—just end
range weakness and tight scalenes[26] and [sternocleidomastoid muscle (“SCM”)][27] that may be
24
Myoclonus are “shocklike contractions of a portion of a muscle, an entire muscle, or a group
of muscles, restricted to one area of the body or appearing synchronously or asynchronously in
several areas.” Myoclonus, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com
/dorland/definition?id=32802 (last visited Jan. 9, 2023).
25
The tensor tympani and stapedius muscles are located in the tympanic cavity (middle ear).
Gleeson, supra note 20, at 637. “When noises are loud, and immediately before speaking, a
reflex contraction of stapedius and tensor tympani takes place that helps dampen down the
movement of the ossicular chain before vibrations reach the ear.” Id.
26
Scalenes are lateral vertebral (neck) muscles. John C. Watkinson & Michael Gleeson, Neck,
in Gray’s Anatomy: The Anatomical Basis of Clinical Practice, supra note 20, at 442, 451.
“Scaleni anterior, medius and posterior extend obliquely between the upper two ribs and the
cervical transverse process.” Id. Scalene muscles help elevate the first or second ribs and bend
the cervical portion of the vertebral column forward and/or laterally and rotate it towards the
opposite side. Id.
27
The sternocleidomastoid muscle (“SCM”) “descends obliquely across the side of the neck and
forms a prominent surface landmark, especially when contracted.” Watkinson & Gleeson, supra
note 26, at 448-49. The SCM rotates the head upward and to the opposite side. Id.
10
contributing to impingement of the facial nerve. She also demonstrate[d] impaired balance
which speaks to some involvement of the vestibular nerve as well.” Id. Ms. Gilpin indicated
Petitioner’s “excellent” rehab potential to “strengthen those muscles and normalize her motor
ability” on the left side of her face and recommended one to two physical therapy sessions per
week. Id. at 1-2.
By August 12, 2016, Petitioner had attended four physical therapy sessions “focusing on
facial motor learning, myofascial release[,] and progressing a home exercise program of facial
exercises to restore symmetry and movement to the [left] side of her face” for her “sudden onset
on 11/28/15” of Bell’s palsy. Pet. Ex. 3 at 17. In addition to her home exercise program, a
protocol to use her “portable electrical stimulation machine”28 was implemented for Petitioner
“to improve recruitment of the muscles innervated by the facial nerve.” Id. at 8, 17. During this
time of treatment, Petitioner reported “some improvement in her ability to smile on the [left
side], open her eye, and to blow a feather. Muscles still fatigue significantly by the end of the
day and she is still having some difficulty with eating and drinking.” Id. at 17. Continued
physical therapy was recommended. Id.
On August 17, 2016, Petitioner returned to the Otolaryngology Clinic for a follow-up on
her Bell’s palsy and tinnitus. Pet. Ex. 2 at 300. “[R]esidula synkinesis after left sided Bell’s
palsy, as well as some tinnitus and stapedial muscle spasm” was noted. Id. at 305. Petitioner
expressed concern about the transcutaneous electrical nerve stimulation (“TENS”) unit
“worsening her synkinesis.” Id. at 300. It was explained that she may continue using it if it
provides symptomatic relief but that it would “likely not help or hurt her synkinesis.” Id. at 304.
She was to continue with physical therapy. Id. at 305. Petitioner again did not wish to pursue
surgical options at this time. Id. at 304. A hearing aid to “help mask her underlying tinnitus was
discussed and Petitioner requested a referral to audiology to discuss it further. Id. Botox was
also discussed as a potential way to improve facial symmetry in the future. Id.
Petitioner presented to the Audiology Clinic at Walter Reed on October 24, 2016. Pet.
Ex. 2 at 316. Petitioner reported hearing loss and tinnitus in her left ear that comes and goes and
described as an “ocean sound.” Id. She also reported the “machine gun” noise which was
“intermittent in the left ear associated with talking, chewing[,] and/or smiling.” Id. It was noted
that this was “secondary to recovered Bell’s palsy episode on 28 Nov[ember] 2015. Recent ENT
eval[uation] suggests that this sound/sensation is likely secondary to stapedius myoclonus.” Id.
A hearing test was performed and revealed “no significant change in hearing” since her last visit.
Id. at 316-17. An amplification hearing aid, which would not help the intermittent “machine
gun” noise but could help with the “ocean” sounding tinnitus, was discussed. Id. at 317.
Petitioner did not want to try the hearing aid at that time. Id.
Petitioner saw Dr. Chaudhery again on February 28, 2017. Pet. Ex. 2 at 398. She stated
she felt her recovery had “plateaued.” Id. Dr. Chaudhery noted she had tried physical therapy
28
The portable electrical stimulation machine is referred to in Petitioner’s declaration and future
medical records as a “TENS” unit, short for transcutaneous electrical nerve stimulation. See,
e.g., Pet. Ex. 12 at 23; Pet. Ex. 2 at 300.
11
but it was “without benefit.” Id. Petitioner mentioned she would be retiring soon and requested
a referral to Johns Hopkins Facial Paralysis and Pain Treatment Center. Id.
On March 27, 2017, Petitioner presented to the Optometry Clinic for a comprehensive
eye exam. Pet. Ex. 2 at 409. Reason for visit was “residual dryness from Bell’s palsy November
2015.” Id. at 407. Petitioner reported she felt “like there is a tightening across the eyelid that
decreases her fissure width.” Id. Bilateral dermatochalasis29 and dry eyes were noted. Id. at
409. She was interested in a therapy referral to improve her facial nerve function. Id. at 407.
On March 28, 2017, at the Hearing Conservation Clinic, Petitioner reported her tinnitus
was “mildly bothersome.” Pet. Ex 2 at 419. No hearing loss was noted, and her automated pure
tone threshold audiogram was normal. Id.
Petitioner had a consultation with Dr. Amir Hossein Dorafshar at the Johns Hopkins
Plastic Surgery Clinic on April 6, 2017. Pet. Ex. 5 at 6. Petitioner presented with concern of
facial asymmetry, twitching, and synkinesis. Id. On examination, Dr. Dorafshar noted
“excessive skin and hooding of the left upper eyelid. She has ptosis of the left upper eyelid. Her
left nasolabial fold is pronounced. She has hypertrophy of her neck platysmal muscles. There is
twitching of her upper and lower lips and chin.” Id. Prognosis and treatment options discussed
included Botox for the twitching, upper eyelid ptosis and removal of the excess skin, tissue
rearrangement to improve facial symmetry, and removal of platysmal bands on the left side. Id.
Petitioner was to consider her options and attend physical therapy. Id.
An MRI of the brain and IAC was performed on April 7, 2017 due to “left facial nerve
paresis with incomplete recovery.” Pet. Ex. 2 at 710. The results were normal. Id. The
enhancement of the left facial nerve seen on the MRI of December 24, 2015 was no longer
present. Id.
On April 26, 2017, Petitioner presented to the Ophthalmology Clinic at Walter Reed for
“evaluation of synkinesis follow[ing] left Bell’s palsy.” Pet. Ex. 2 at 444. Her chief complaint
was “left upper eyelid ‘pulling’ closed.” Id. “When she yawns, sneezes, or coughs, her left eye
completely closes. She also bites the left side of her mouth frequently.” Id. Ophthalmologist
Dr. Eva Chou evaluated her and noted that Petitioner had not yet seen an ophthalmologist or
neurologist since developing Bell’s palsy. Id. Dr. Chou discussed with Petitioner that “her
periorbital symptoms and left upper eyelid relative ptosis could most likely be lessened with
Botox treatments.” Id. at 445. Two days later, on April 28, Petitioner had her first periorbital
Botox treatment at nine injection sites. Id. at 455.
Petitioner presented with her referral from Dr. Dorafshar to her first physical therapy
appointment at Johns Hopkins on May 9, 2017. Pet. Ex. 5 at 30. She had five physical therapy
sessions for “management of residual facial synkinesis” from May to December 2017. Id. at 30-
29
Dermatochalasis is a “disorder[] of the elastic fiber network in which the skin lacks elasticity
and resilience.” Cutis Laxa, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.
com/dorland/definition?id=68177 (last visited Jan. 9, 2023).
12
105. At her subsequent appointments in June, August, and December, she reported improvement
in facial synkinesis since starting the Botox treatment. Id. at 68, 81, 94.
Dr. Kevin Cannard, a neurologist at the Walter Reed Neurology Clinic, evaluated
Petitioner for “left facial synkinesis following recovery from Bell’s palsy” on June 27, 2017.
Pet. Ex. 2 at 480. Petitioner was sent to Dr. Cannard to expand Botox injections to the lower
muscles of her facial expression. Id. Dr. Cannard’s assessment was left hemifacial spasm with
associated synkinesis as a residual effect of Bell’s palsy. Id. Dr. Cannard said Petitioner had
“obtained excellent results of the involuntary contractions of her obicularis oculi muscles”
following her first Botox injection in Ophthalmology. Id. He noticed the spasms were less
apparent that day because she was “currently at the peak effect of her first Botox injection”
administered on April 28. Id. Dr. Cannard’s assessment also included palsy of the seventh
cranial nerve “with subtle residual weakness; onset 28 November 2015.” Id. He discussed with
Petitioner that the “asymmetry secondary to the weakness [would] not be compensated for with
Botox injections and may even become more pronounced. . . . Fortunately, the effects of Botox
[would] be transient.” Id. Dr. Cannard planned to expand the injection pattern established by
Dr. Chou as well as “inject some of her lower muscles of facial expression in hopes of achieving
a more comprehensive suppression of her symptoms.” Id. at 481.
On August 17, 2017, Petitioner received her first Botox injection from Dr. Cannard for
“control of left hemifacial spasm and synkinesis.” Pet. Ex. 2 at 512. On this date Dr. Cannard
noted “[i]t [was] clear . . . that the patient does indeed have some persistent weakness as a
residual effect of her Bell’s palsy back in 2015.” Id. at 511.
Petitioner continued to receive these injections approximately every three to four months.
Pet. Ex. 2 at 562 (November 30, 2017); Pet. Ex. 2 at 590 (March 15, 2018); Pet. Ex. 2 at 612
(July 23, 2018); Pet. Ex. 2 at 645 (October 24, 2018); Pet. Ex. 10 at 6 (March 4, 2019); Pet. Ex.
10 at 37 (June 17, 2019); Pet. Ex. 10 at 60 (October 16, 2019); Pet. Ex. 60 at 53 (January 28,
2020). Dr. Cannard noted “[e]ach time we inject the patient she is getting [a] slightly better
response with [the] minor adjustments we are making.” Pet. Ex. 10 at 50. Due to the Covid-19
pandemic, Petitioner’s regular Botox injections were delayed. Pet. Ex. 60 at 28. Petitioner
resumed injections on July 6, 2020. Id.; Pet. Ex. 60 at 9 (October 5, 2020); Pet. Ex. 61 at 68
(January 28, 2021); Pet. Ex. 61 at 34 (June 7, 2021); Pet. Ex. 61 at 11 (October 5, 2021).
While receiving the periodic Botox treatments, Petitioner sought additional consultations
regarding her facial asymmetry. On February 27, 2019, Petitioner presented to the Johns
Hopkins Facial Plastic & Reconstructive Surgery Clinic. Pet. Ex. 11 at 14. Dr. Patrick Joseph
Byrne noted Petitioner presented for the diagnosis of facial paralysis. Id. In addition to the
facial paralysis and asymmetry, Petitioner had continued complaints of “tinnitus with smile, eye
closure when talking[,] and tightness of her left chin.” Id. Facial injections were performed at
this visit. Id. at 15. Dr. Byrne’s assessment was “incomplete left facial paralysis following
Bell’s palsy in [November] 2015.” Id. He discussed with Petitioner injectable treatments,
platysmectomy (facial retraining), and surgical interventions. Id.
Petitioner presented to Dr. Michael Timothy Gocke at Virginia Oral, Facial & Implant
Surgery on October 4, 2019. Pet. Ex. 8 at 3. Petitioner reported that the “[B]otox ha[d] been
13
helpful with [spasms,] opening up of left eye[,] and [synkinesis,] but ha[d] not helped with smile
and lower part of face.” Id. Surgical options were discussed. Id. Dr. Gocke recommended
Botox or collagen lift threads. Id. at 5.
Seeking a facial nerve expert, on May 11, 2021, Petitioner had a telehealth consultation
with plastic surgeon, Dr. Babak Azizzadeh, of Beverly Hills, California. Pet. Ex. 62 at 1. Dr.
Azizzadeh recommended reconstruction surgery. Id. At a follow-up with Dr. Cannard,
Petitioner discussed her consultation with Dr. Azizzadah. Pet. Ex. 61 at 35. Dr. Cannard
advised against surgical intervention as it could “make her response to Botox therapy more
challenging and because she has very little disfiguration as a result of the residual weakness from
her Bell’s palsy.” Id.
Petitioner followed-up with Dr. Azizzadeh for an in-person evaluation on January 24,
2022. Pet. Ex. 62 at 1. Her main goal was improving her smile. Dr. Azizzadeh’s surgical plan
including selective neurectomy, symmetrical facial repositioning, chin augmentation, and
bilateral eye lifts, was further discussed. Id. at 1, 4-5.
No further records have been filed.
D. Petitioner’s Declaration30
In her declaration, Petitioner stated she worked as a registered nurse (“RN”), served as a
Commissioned Officer in the U.S. Public Health Service (“USPHS”), and worked as an attorney
for the U.S. Department of Health and Human Services (“HHS”), Office of General Counsel
(“OGC”). Pet. Ex. 12 at ¶¶ 1-2, 5. She retained her status as an active-duty nurse officer in the
USPHS for thirty years until her retirement from HHS, OGC in 2017. Id. at ¶ 5.
Prior to her Bell’s palsy, Petitioner stated her “main ongoing health issue was chronic
upper back and neck myofascial pain syndrome.” Pet. Ex. 12 at ¶ 6. She effectively managed
this issue with “trigger point injections, foam rolling, stretching, regular exercise, and occasional
pain medications and muscle relaxants.” Id. She has degenerative changes in her spine, and has
had periodic musculoskeletal and joint problems, such as wrist and ankle fractures that required
surgical repair. Id. She also stated a “history of seasonal allergy symptoms and heart
palpitations that are controlled for the most part with medications.” Id. With these conditions
under control, she considered herself to be “generally very healthy and active.” Id. at ¶ 7. She
attributed this to healthy eating and vigorous fitness classes she “participated in 3-5 times weekly
since 2011, except for the periods when [she] was recovering from ankle surgery.” Id.
Petitioner received the flu vaccine at a USPHS Federal Occupational Health Center on
October 19, 2015. Pet. Ex. 12 at ¶ 8. As an active duty USPHS nurse officer, she was required
to get the annual flu vaccine. Id.
30
This exhibit is titled “Affidavit” but it is not notarized, and therefore, the undersigned
references it as a declaration.
14
The following month, Petitioner travelled to Milwaukee, Wisconsin to visit friends for
the Thanksgiving holiday. Pet. Ex. 12 at ¶ 9. On November 26, 2015, she had dinner at her
friend’s house with over 20 people in attendance. Id. The next day, the day before the onset of
her Bell’s palsy, she went to a Pilates class and out shopping with a friend. Id. She asserted she
“was feeling so good, so [she] was shocked when [she] woke up with facial paralysis the next
day.” Id.
Shortly after waking up on November 28, 2015, Petitioner discovered the left side of her
face “seemed paralyzed.” Pet. Ex. 12 at ¶ 10. She was getting ready to go to a Pilates class like
the day before, when she noticed that “the left side of [her] face was drooping and felt numb.
When [she] tried to brush [her] teeth, [she] could not keep the toothpaste in [her] mouth. [She]
could not move any facial muscles on [her] left side, and [she] could not close [her] left eye.” Id.
Petitioner did a self-assessment to rule out a stroke, then realized she “might be experiencing
Bell’s palsy.” Id. She was otherwise feeling fine, but because of the facial paralysis she skipped
the Pilates class. Id. Her friend’s daughter, a physician, gave her a prescription for Prednisone
which she started taking immediately. Id. She also bought eyedrops because she recalled her
“left eye became dry and irritated from not spontaneously blinking.” Id. “[She] had difficultly
drinking and eating due to [her] my facial paralysis. [She] had to hold [her] lips closed while
drinking and chewing, and use [her] finger to manually extract food that got stuck in [her] left
cheek.”
Petitioner changed her flight to return home early to seek evaluation from Walter Reed,
where she had received medical care from for decades. Pet. Ex. 12 at ¶ 11. She always travels
with 12-hour Mucinex. Id. She takes is whenever she has allergy symptoms such as post-nasal
drip and excess mucus. Id. She also uses Flonase for allergies which she stated can sometimes
cause nosebleeds. Id. On the flight home, Petitioner was upset. Id. Her partner of 25 years
recently passed away. Id. She was “dealing with sudden paralysis on the left side of [her] face
while simultaneously grieving [her] partner’s recent death.” Id.
Petitioner reported to the Walter Reed ED on Sunday, November 29, 2015. Pet. Ex. 12 at
¶ 12. Petitioner recalled feeling overwhelmed in the ED waiting room; she was tearful,
emotional, and blowing her nose. Id. After examination, she was diagnosed with Bell’s palsy.
Id. She received anti-viral medication, eye care materials, and was instructed to continue the
Prednisone. Id. She was advised that most people with Bell’s palsy fully recover within three to
six months. Id.
Petitioner felt “very self-conscious about [her] appearance and had some uncomfortable
physical symptoms.” Pet. Ex. 12 at ¶ 13. But because there were no limitations on her physical
activity, she resumed her usual daily routine (early morning fitness classes followed by a full day
in the office). Id. at ¶¶ 12-13. She had an “extremely dry” mouth, impaired speech, and
“difficulty enunciating and was slurring [her] words at times.” Id. at ¶ 13. Her left eye was
“very dry.” Id. She had blurry vision and working on the computer for “extended periods of
time per usual was difficult and uncomfortable.” Id. She developed intermittent pain around her
left ear and toward the back of [her] head.” Id.
15
According to Petitioner, approximately two to three weeks after the onset of her Bell’s
palsy, she was “able to initiate some minimal voluntary movements on the left side of [her] face.
[Her] lips moved slightly on the left side when [she] tried to smile, and [she] could raise [her]
left eyebrow a bit.” Pet. Ex. 12 at ¶ 14.
She saw her PCP, Dr. Chaudhery, on December 15, 2015, and had the recommended
MRI on December 24. Pet. Ex. 12 at ¶¶ 15-16. The MRI “results were consistent with Bell’s
palsy.” Id. at ¶ 16.
Approximately one month after the onset of her Bell’s palsy, the left side of her face
“was less droopy although [her] lower face was still shifted toward the left.” Pet. Ex. 12 at ¶ 17.
The left side of her lips “moved outward a bit more when [she] tried to smile, but they did not
move well or in sync with the right side when [she] spoke.” Id. She could voluntarily close her
left eye “about halfway” and eventually “fully . . . with some effort.” Id. “[H]owever, it did not
fully close with spontaneous blinking.” Id.
While her facial paralysis symptoms gradually improved, she started to develop new
symptoms. Pet. Ex. 12 at ¶ 18. She “felt pressure and a gurgling/bubbling sensation in [her] left
ear at rest.” Id. Petitioner also had “an ocean-like sound in [her] left ear while at rest and [her]
voice seemed to echo within [her] head” when speaking. Id. She noticed a “rapid thumping
tinnitus (a machine-gun sound) with facial movements, such as smiling or talking.” Id.
Petitioner recalled the sounds were distracting and that she “had an embarrassing tendency to
raise [her] voice while talking in an attempt to mask them and concentrate on what [she] was
saying.” Id. Her left naval passage “felt partially collapsed” and she had difficulties inhaling
through that nostril. Id. When she “pulled [her] left nasal passage open with [her] finger,” she
could breathe better. Id.
Petitioner developed synkinesis. Pet. Ex. 12 at ¶ 19. She explained that her “droopy left
eye would close more, and [her] left eyelids would twitch when [she] talked or chewed food.
[Her] left eye would also close more when [she] smiled, swallowed, yawned, opened [her] mouth
wide, or pursed [her] lips.” Id. Additionally, her left cheek, chin, and lips would “pull upward
and outward when [she] closed [her] eyes, opened [her] eyes wide, or raised [her] eyebrows.” Id.
Her chin “remained cockeyed toward the left side of [her] face and was dimpling.” Id. She had
involuntary twitching and developed “painful tightness and pulling sensations” around her left
eye and from her left cheek to chin. Id. She also noticed “bulging” of her left neck muscles. Id.
Petitioner was told by ENT physicians at Walter Reed that she had “mild hearing loss in
her left ear.” Pet. Ex. 12 at ¶ 20. She was advised of treatment that may alleviate the “machine-
gun sound” including surgery and a hearing aid. Id. She attempted several nasal remedies to
improve her ability to clearly inhale through her left nostril, but they did not help. Id.
Six months after the onset of her Bell’s palsy, she was referred to physical therapy. Pet.
Ex. 12 at ¶ 21. She continued to have difficulty drinking, eating, and occasional slurring of her
words. Id. From July to August 2016, she had four physical therapy treatment sessions where
she practiced facial exercises focused on restoring muscle strength, movement, and symmetry.
Id. at ¶ 22. She noticed improvement in her ability to raise her left eyelid “(although it fatigued
16
quickly and drifted back down),” and in her ability to lift the left corner of her lips when smiling
“(although [her] smile was still lopsided/asymmetrical).” Id. She still had synkinesis, twitching,
and difficulty eating and drinking. Id. Self-massage on her cheek and neck muscles provided
temporary relief. Id. at ¶ 23. After using the TENS unit for about a week, she became concerned
that it was making her synkinesis worse. Id. She discontinued use of the TENS unit. Id.
Petitioner requested a referral to the Johns Hopkins Facial Paralysis and Pain Treatment
center. Pet. Ex. 12 at ¶ 24. She had a consult with Dr. Dorafshar in early April 2017. Pet. Ex.
12 at ¶ 25. Botox and reconstructive surgery were recommended. Id. Because Petitioner had
already scheduled a Botox appointment at Walter Reed, she wanted to wait to see how Botox
would help before considering surgical innervation. Id.
Dr. Chou administered Botox injections around Petitioner’s left eye in late April 2017.
Pet. Ex. 12 at ¶ 26. She was pleased with the results because it “opened up [her] droopy eye, and
reduced the pain, synkinesis, and twitching.” Id. Because Dr. Chou could not administer Botox
to other areas of her face, Petitioner was referred to Dr. Cannard. Id.
From May to December 2017, Petitioner had four physical therapy sessions. Pet. Ex. 12
at ¶ 27. She was instructed on facial retraining exercises and massage therapy. Id. While
Petitioner “diligently adhered” to the home exercise program, she did not notice “much
improvement” in her residual effects during that time. Id. “As time progressed, it also seemed
as if [her] full smile was worse with little lip parting, and fewer teeth showing, on [her] left
side.” Id.
Following an initial neurology evaluation with Dr. Cannard in June 2017, Dr. Cannard
administered Botox injections around Petitioner’s left eye and other areas of her face in August
2017. Pet. Ex. 12 at ¶¶ 28-29. Petitioner continued to receive Botox injections for the next three
to four months. Id. at ¶ 29. She received some beneficial results that were most noticeable about
five days after injections, up until about two months later, when the Botox “[wore] off.” Id. at ¶
30.
E. Expert Reports
1. Petitioner’s Expert, Dr. Kazim A. Sheikh31
a. Background and Qualifications
Dr. Sheikh is a board-certified neurologist who specializes in neuromuscular and
peripheral nervous system disorders. Pet. Ex. 13 at 1. Dr. Sheikh received his medical degree
from King Edward Medical College in Pakistan. Id. Thereafter, he completed a neurology
residency at the Neurological Institute at Columbia University in New York and was a
postdoctoral fellow in peripheral nerve disorders at Johns Hopkins in Baltimore, Maryland. Id.;
Pet. Ex. 14 at 1. Dr. Sheikh is currently both a physician and a professor. Pet. Ex. 14 at 1.
31
Dr. Sheikh submitted three expert reports in this matter. Pet. Ex. 13, 42, 63.
17
Dr. Sheikh is a tenured Professor of Neurology and the Director of the Neuromuscular
Program at the University of Texas (“UT”) Medical School. Pet. Ex. 14 at 1. He also serves as
the Director of the Neuromuscular Disorders Center at the Mischer Neuroscience Institute at
Memorial Hermann-Texas Medical Center and the Director of the Muscle and Nerve Laboratory.
Id. He has authored or co-authored over 150 publications related to immune neuropathies and
has served on numerous review panels related to immune and inflammatory neuropathies. Pet.
Ex. 13 at 1. As a neurologist and neuromuscular and peripheral nerve specialist, Dr. Sheikh has
an active inpatient and outpatient clinical practice at the UT Medical School at Houston and
affiliated hospitals. Id. He has seen and managed over 150 cases of Bell’s palsy throughout his
career. Id. at 2.
b. Opinion
Dr. Sheikh opined that approximately 40 days after receiving the flu vaccine, Petitioner
developed left Bell’s palsy and to a “reasonable degree of medical probability,” the flu vaccine
was the etiology of her Bell’s palsy by an autoimmune response. Pet. Ex. 13 at 1, 7.
i. Althen Prong One
Dr. Sheikh opined the flu vaccine can cause Bell’s palsy either through an autoimmune
process or an infectious process. Pet. Ex. 13 at 8, 10. Here, Dr. Sheikh favored the theory of
autoimmunity. Pet. Ex. 42 at 1-2; Pet. Ex. 13 at 8 (noting a “cell-mediated autoimmune
mechanism has been suggested as the pathogenesis of Bell’s palsy” (quoting Pet. Ex. 18 at 4)).
Regarding infectious etiologies, Dr. Sheikh stated that both Borrelia burgdorferi and
herpes zoster have been “well documented to result in Bell’s palsy.” Pet. Ex. 13 at 8. Dr. Sheikh
explained that in the case of herpes zoster, there is a direct infection of geniculate ganglion.32 Id.
In some cases, herpes simplex virus (“HSV”) “is the cause of Bell’s palsy and reflects virus
reactivation from latency in the geniculate ganglion rather than primary infection.” Id. He
referred to several studies indicating that the flu vaccine can reactivate different strains of HSV
in the nervous system. Id. (citing Pet. Ex. 15;33 Pet. Ex. 16;34 Pet. Ex. 17).35 However, Dr.
32
The geniculate ganglion is “the sensory ganglion of the facial nerve, situated on the geniculum
of the facial nerve.” Ganglion Geniculi Nervi Facialis, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=78055 (last visited Jan. 9, 2023).
33
L.M. Hassman & D.A. DiLoreto, Immunologic Factors May Play a Role in Herpes Simplex
Virus 1 Reactivation in the Brain and Retina After Influenza Vaccination, 6 ID Cases 47 (2016).
34
Allan Lieberman & Luke Curtis, HSV2 Reactivation and Myelitis Following Influenza
Vaccination, 13 Hum. Vaccines & Immunotherapeutics 572 (2017).
35
J.-F. Chen et al., Pityriasis Rosea Following Influenza (H1N1) Vaccination, 74 J. Chinese
Med. Assoc. 280 (2011).
18
Sheikh noted several shortcomings to the infectious theory. For example, “Bell’s palsy is almost
exclusively motor in nature without any mucocutaneous manifestations typically seen with
herpes viral reactivation.” Pet. Ex. 42 at 5-6. Additionally, “HSV-1 causes recurrent
reactivations, which raises the question of why Bell’s palsy is an isolated episode in the
overwhelming majority of cases.” Id. at 5-6 (quoting Pet. Ex. 18 at 4). Therefore, Dr. Sheikh
focused on the autoimmunity theory. Id. at 1-2.
Dr. Sheikh first explained that autoimmune conditions are “characterized by an aberrant
activation of the adaptive immune response with T and/or B cells reacting to tissue specific self-
antigens,” here, in the seventh cranial nerve. Pet. Ex. 42 at 1. Dr. Sheikh explained that the
stimulation of the immune system from a triggering event such as vaccination “disrupt[s] the
balance needed to maintain immunologic homeostasis” thus “making the host susceptible to
autoimmune diseases.” Id. at 2. This “provides the potential basis for rarity with which Bell’s
palsy develops in an individual after exposure to triggers such as vaccines.” Id.
Dr. Sheikh described the cell-mediated autoimmune process, otherwise known as
molecular mimicry: “If the antigens present on the vaccine share any homology with host
antigens, then the immune response will be directed at both the injected antigens and host
antigens, leading to an autoimmune response.” Pet. Ex. 13 at 10; see generally Pet. Ex. 34.36
Particularly, he stated that vaccines have been recognized to “lead to autoimmune responses
directed against antigens on peripheral nerves, such as the facial nerve,” triggering
demyelination, and “resulting in inflammatory polyneuropathies.” Pet. Ex. 13 at 10; see also Pet.
Ex. 35.37 Dr. Sheikh stated that this suggests the importance of cell-mediated autoimmune
mechanisms in the pathogenesis of Bell’s palsy. Pet. Ex. 13 at 9.
Dr. Sheikh opined that flu vaccines “can induce autoimmunity by molecular mimicry by
more than one mechanism.” Pet. Ex. 42 at 4. He explained that mimicry can involve T and/or B
cells and can occur at sequential or structural levels.38 Id. at 5. He also discussed non-
homologous molecular mimicry. Id. He primarily focused on the mimic of myelin basic protein
and anti-ganglioside responses.
36
M.B.A Oldstone, Molecular Mimicry, Microbial Infection, and Autoimmune Disease:
Evolution of the Concept, 296 Current Topics Microbiology & Immunology 1 (2005).
37
Lawrence Schonberger et al., Guillain-Barre Syndrome Following Vaccination in the
National Influenza Immunization Program, 110 Am. J. Epidemiology 105 (1979).
38
He described autoimmune responses through the reactivation of B and T cell receptors, as well
as decreased T cells documented in the acute phase of Bell’s palsy. Pet. Ex. 13 at 10; Pet. Ex. 37
at 1; Pet. Ex. 24 at 2.
19
In support of molecular mimicry generally, Dr. Sheikh analogized Bell’s palsy with
Guillain-Barré syndrome (“GBS”).39 Pet. Ex. 13 at 9. While he acknowledged that Bell’s palsy
and GBS “represent two extremes on the spectrum of clinical syndromes,” Dr. Sheikh
highlighted that Bell’s palsy, like GBS, is an acute demyelinating disease of the peripheral
nervous system. Id. (citing Pet. Ex. 18 at 4). He further emphasized their immunological
similarities40 suggest that Bell’s palsy is autoimmune by nature, that Bell’s palsy is often
considered a mononeuritic variant of GBS, and that Bell’s palsy and GBS “may share a similar
etiology and pathogenesis.” Id. (citing Pet. Ex. 18 at 4, 9); see also Pet. Ex. 22 at 1, 3.
Accordingly, Dr. Sheikh intermittently referred to GBS literature in support of molecular
mimicry, a well-established causal theory for GBS.
For example, Dr. Sheikh cited an article by Abramsky et al.,41 which supported a cell-
mediated autoimmune mechanism in Bell’s palsy. Pet. Ex. 13 at 9; Pet. Ex. 19 at 1. The study
“demonstrated a defined in vitro response to a human basic protein (P1L) of peripheral nerve
myelin in patients with Bell’s palsy” resulting in immunologic lymphocyte alterations. Pet. Ex.
19 at 5. This response suggests that the sensitization of lymphocytes to the self-protein “may be
an important factor in the pathogenesis of the paralysis.” Id. at 7. Moreover, Jahnke et al.42 and
Lucchese et al.43 provide evidence of sequence peptide mimicry with a number of myelin and
neuronal peptides. Pet. Ex. 42 at 4 (citing Pet. Ex. 48; Pet. Ex. 49).
39
GBS is a “rapidly progressive ascending motor neuron paralysis of unknown etiology,
frequently seen after an enteric or respiratory infection. An autoimmune mechanism following
viral infection has been postulated. . . . Variant forms include acute autonomic neuropathy,
Miller-Fisher syndrome, acute motor axonal neuropathy, and acute motor-sensory axonal
neuropathy.” Guillain-Barré Syndrome, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=110689 (last visited Jan. 9, 2023).
40
Dr. Sheikh discussed similarities among GBS and Bell’s palsy patients such as lymphocyte
sensitization to the same P1L protein of peripheral nerve myelin, the percentage of reduced T
lymphocytes, and the changes in peripheral blood leukocyte numbers. Pet. Ex. 13 at 9 (citing
Pet. Ex. 19 at 6; Pet. Ex. 29 at 1; Pet. Ex. 18 at 4; Pet. Ex. 22 at 3; Pet. Ex. 30 at 1).
41
O. Abramsky et al., Cellular Immune Response to Peripheral Nerve Basic Protein in Idiopathic
Facial Paralysis (Bell’s Palsy), 26 J. Neurological Sci. 13 (1975).
42
Ulrike Jahnke et al., Sequence Homology Between Certain Viral Proteins and Proteins Related
to Encephalomyelitis and Neuritis, 229 Science 282 (1985).
43
Guglielmo Lucchese et al., Peptide Sharing Between Influenza A H1N1 Hemagglutinin and
Human Axon Guidance Proteins, 40 Schizophrenia Bulletin 362 (2014). Lucchese et al.
discussed H1N1 viral peptides. Id. The flu vaccine Petitioner received contained an H1N1
strain. Resp. Ex. E, Tab 5 at 11.
20
Dr. Sheikh then turned to Nachamkin et al.,44 which looked at whether flu vaccines can
elicit anti-ganglioside (anti-GM1)45 responses absent Campylobacter jejuni (“C. jejuni”)
contamination. Pet. Ex. 50 at 1. Nachamkin et al. found that each flu vaccine used46 induced
antibodies to anti-GM1 but not to C. jejuni. Id. at 5. They also found antibody responses to
hemagglutinin, a viral surface glycoprotein found in the flu vaccine. Id. Therefore, they
determined hemagglutinin could bind to cellular gangliosides and mimic an anti-ganglioside
antibody. Id.
Accordingly, Dr. Sheikh opined that “it can be postulated that either the [flu] vaccine can
induce anti-ganglioside responses either through GM1-like epitopes it contains or through the
components of the vaccine (hemagglutinin protein) that can bind to host’s own antigens to
overcome self-tolerance.” Pet. Ex. 42 at 4. Importantly, he explained that gangliosides are
“enriched in peripheral and cranial nerves,” and that “anti-GM1 antibodies are associated with
motor neuropathic disorders.” Id. (citing Pet. Ex. 51 at 1;47 Pet. Ex. 52 at 1).48
In support of his opinions, Dr. Sheikh cited several studies and case reports on the
association between the flu vaccine and Bell’s palsy.
Zhou et al.,49 found a signal or “possible association between [flu] vaccines and an
increased risk of Bell’s palsy.” Pet. Ex. 47 at 5. Zhou et al. reviewed and analyzed reports from
the Vaccine Adverse Event Reporting System (“VAERS”) to evaluate the risk of Bell’s palsy
following the administration of flu vaccines given by the parenteral route (intramuscular
injection) from 1991 to 2001. Id. at 1. Of the 197 reports, a Bell’s palsy diagnosis was verified
in 154, and among those, 145 cases received the flu vaccine alone. Id. The authors noted that
while the etiology and pathogenesis of Bell’s palsy is not clear, “[i]mmune response mechanisms
44
Irving Nachamkin et al., Anti-Ganglioside Antibody Induction by Swine (A/NJ/1976/H1N1)
and Other Influenza Vaccines: Insights into Vaccine-Associated Guillain-Barré Syndrome, 198 J.
Infectious Diseases 226 (2008).
45
Ganglioside GM-1 is “one of several gangliosides considered a target antigen in the
pathogenesis of GBS.” Pet. Ex. 50 at 5.
46
They used surviving samples of the 1976 “swine flu” vaccine and vaccines from the 1991-92
and 2004-05 flu seasons to immunize mice. Pet. Ex. 50 at 1.
47
Ortwin Rott et al., Influenza A Virus Hemagglutinin is a B Cell-Superstimulatory Lectin, 184
Med. Microbiology & Immunology 185 (1996).
48
Vladimir A. Slepshukin et al., Interaction of Influenza Virus with Gangliosides and Liposomes
Containing Gangliosides, 173 Eur. J. Biochemistry 599 (1988).
49
Weigong Zhou et al., A Potential Signal of Bell’s Palsy After Parenteral Inactivated Influenza
Vaccines: Reports to the Vaccine Adverse Event Reporting System (VAERS)-United States
1991-2001, 13 Pharmacoepidemiological Drug Safety 505 (2004).
21
have . . . been considered,” and concluded that this “study provided multiple lines of evidence for
a signal that Bell’s palsy may be associated with the [flu] vaccine[].” Id. at 4-5.
Mutsch et al.,50 reported 46 cases of Bell’s palsy associated with the inactivated
intranasal flu vaccine administered over a seven-month period in Switzerland. Pet. Ex. 40 at 1-2.
The risk of Bell’s palsy after intranasal vaccination was 19 times higher than the risk seen in
control subjects. Id. at 2. Of the 412 patients, the authors identified 91 patients who developed
Bell’s palsy following the flu vaccine and found “[t]he risk was highest during the second month
after intranasal vaccination.” Id. at 5-6. There were also reports of Bell’s palsy in those who
received the vaccine parenterally (by injection).51 Id. at 5. The authors concluded “the intranasal
[flu] vaccine used in Switzerland during the 2000–2001 [flu] season greatly increased the risk of
Bell’s palsy among vaccinees,” and they described the association as “strong, temporal, and
specific.” Id. at 6.
Dr. Tompkins, Respondent’s expert, opined that the intranasal vaccine contained
Escherichia coli (“E. coli”) heat-labile enterotoxin and that itself caused the increased incidence
of post-vaccinal Bell’s palsy. Resp. Ex. C at 5. However, referencing Couch,52 which was
written responsive to Mutsch et al., Dr. Sheikh stated “there are no direct anatomical connections
that would explain transfer of E. coli heat-labile enterotoxin to facial nerve motor axons or
neurons (facial motor nucleus) after intranasal administration.” Pet. Ex. 63 at 1-2 (Couch
“concluded that indirect mechanisms rather than direct toxicity [were] involved in post-vaccinal
Bell’s palsy cases.”); Pet. Ex. 66 at 2. In contrast, molecular mimicry between bacterial
glycoconjugates and peripheral nerve gangliosides has been implicated. See Pet. Ex 42 at 4-5;
Pet. Ex. 63 at 3-5.
Moreover, Dr. Sheikh stated that the post-vaccinal interval of developing Bell’s palsy is
inconsistent with the E. coli heat-labile enterotoxin hypothesis. Pet. Ex. 63 at 2. He referenced
literature that concluded “direct toxicity of E. coli heat-labile enterotoxin in post-vaccinal cases
was not relevant due to interval between vaccination and onset of Bell’s palsy.” Id. For
example, the risk period identified in Mutsch et al. was spread from one to 91 days with the
50
Margot Mutsch et al., Use of the Inactivated Intranasal Influenza Vaccine and the Risk of
Bell’s Palsy in Switzerland, 350 New Eng. J. Med. 896 (2004).
51
The authors stated that “27 of the 182 patients with Bell’s palsy (14.8%) . . . had been
immunized with [the] parenteral [flu] vaccine.” Pet. Ex. 40 at 4. With regard to this data, the
authors stated that “there was essentially no risk of Bell’s palsy after receipt of the traditional,
parenteral vaccine.” Id. However, these findings were commented on in the Stowe et al. paper
as follows: “Although [the Mutsch et al.] study showed no association very few patients had
received the parenteral vaccine and the study design had a number of limitations and biases that
may have led to missing a true association.” Resp. Ex. C, Tab 8 at 1. Julia Stowe et al., Bell’s
Palsy and Parenteral Inactivated Influenza Vaccine, 2 Hum. Vaccines 110 (2006).
52
Robert B. Couch, Nasal Vaccination, Escherichia coli Enterotoxin, and Bell’s Palsy, 350 New
Eng. J. Med. 860 (2004).
22
highest number of cases seen within 31-60 days post-vaccination. Pet. Ex. 40 at 1. Ronthal &
Greenstein53 commented that “[t]he peak occurrence of Bell’s palsy was between 31 and 60 days
after intranasal vaccination, suggesting that the palsy was not due to a direct toxic response but
rather an induced immune response.” Pet. Ex. 65 at 3.
Finally, a study by Bardage et al.,54 which examined the risk of neurological and
autoimmune adverse events to people vaccinated with the 2009 pandemic H1N1 flu vaccine
compared to unvaccinated people, found that the relative risk of developing Bell’s palsy was
significantly increased within 45 days of vaccination. Pet. Ex. 41 at 1. Dr. Sheikh cited several
other case reports supporting the immunological theory. Pet. Ex. 13 at 10 (see, e.g., Pet. Ex. 38
(describing a child that suffered Bell’s palsy following diphtheria-pertussis-tetanus (“DPT”) and
polio vaccines);55 Pet. Ex. 39 (describing a child who suffered Bell’s palsy and brachial neuritis
following a DPT vaccine)).56
Dr. Sheikh acknowledged, to Dr. Jamieson’s, Respondent’s expert’s, credit that the
epidemiologic evidence of the current flu vaccine to an increased incidence of Bell’s palsy is not
well-established. Pet. Ex. 42 at 4. He stated that if such “definite epidemiologic evidence for
increased incidence of Bell’s palsy with any vaccine (including [flu] vaccine) was available, then
that particular vaccine would not be in widespread use.” Id. at 3. Thus, Dr. Sheikh noted that
studies showing an association of flu vaccination and Bell’s palsy are more meaningful than
epidemiological studies that did not find an increased incidence of Bell’s palsy after flu
vaccination. Id. at 3.57
He reasoned “[o]ne of the central tenets of epidemiology . . . is that a rare event cannot be
ruled out using statistical tools applied to a population,” therefore, “a study that finds no
association between two variables does not rule out the possibility that a rare association could
still exist.” Pet. Ex. 42 at 3. Accordingly, he stated, “our argument is biologic and not
epidemiologic as epidemiologic studies do not take into account the heterogeneity and
comorbidities of each individual” like Petitioner. Id.53
Michael Ronthal & Patricia Greenstein, Bell’s Palsy: Pathogenesis, Clinical Features, and
Diagnosis in Adults, UpToDate, https://www.uptodate.com/contents/bells-palsy-pathogenesis-
clinical-features-and-diagnosis-in-adults (last updated May 11, 2020).
54
Carola Bardage et al., Neurological and Autoimmune Disorders After Vaccination Against
Pandemic Influenza A (H1N1) with a Monovalent Adjuvanted Vaccine: Population Based
Cohort Study in Stockholm, Sweden, 343 BMJ 1 (2011).
55
John J. Manning & Kedar K. Adour, Facial Paralysis in Children, 49 Pediatrics 102 (1972).
Gilbert I. Martin & Michael I. Weintraub, Brachial Neuritis and Seventh Nerve Palsy – A Rare
56
Hazard of DPT Vaccination, 12 Clinical Pediatrics 506 (1973).
57
Dr. Sheikh noted that Respondent’s experts only presented evidence of increased incidence,
not of association like he did. Pet. Ex. 42 at 3.
23
ii. Althen Prongs Two and Three
Dr. Sheikh opined that Petitioner’s flu vaccine caused her Bell’s palsy through an
autoimmune mechanism described above. Pet. Ex. 42 at 7. Dr. Sheikh opined that “vaccine
induced autoimmunity and related tissue (facial nerve) injury is plausible in this case.” Id. at 3.
Dr. Sheikh stated “it is notable that her examination [on November 29, 2015] showed
facial nerve palsy and normal ear examination and there were no vesicles in auditory canals to
suggest Ramsay-Hunt syndrome. Further, the ED evaluation mentioned cold symptoms, but no
signs of infection were documented on physical examination.” Pet. Ex. 13 at 2. Again, he
pointed out that an ear examination on December 15, 2015 was normal. Id. at 3.
Dr. Sheikh included in his review of Petitioner’s medical history her MRI on December
24, 2015 that showed “[a]bnormal enhancement along the intratemporal left CN7” that is “seen
in the setting of Bell’s palsy.” Pet. Ex. 13 at 3 (quoting Pet. Ex. 2 at 260). The Greco et al.
article, referenced by Dr. Sheikh, discussed that the most common abnormality observed on
MRIs indicative of Bell’s palsy is the “enhancement of the distal intracanalicular and
labyrinthine segments of the facial nerve. The geniculate ganglion may also be involved.”58 Pet.
Ex. 18 at 2.
Dr. Sheikh opined that Petitioner’s left facial weakness began on November 28, 2015,
approximately 40 days, or less than six weeks, after her flu vaccination. Pet. Ex. 13 at 7. He
found this onset to be “well within the biologic window in which post-[flu] vaccination [Bell’s]
palsy has been documented.” Pet. Ex. 42 at 7.
Based on the explanation above that Bell’s palsy is considered a variant of GBS, Dr.
Sheikh reasoned the timing of post-vaccination GBS literature is applicable here. Pet. Ex. 13 at
10. For the onset of inflammatory demyelinating polyneuropathies following the flu vaccine,
“the period of increased risk was concentrated within the 5-6 week period after vaccination but
lasted for approximately 9 or 10 weeks.” Id. (citing Pet. Ex. 35). The Institute of Medicine
(“IOM”),59 now the National Academy of Medicine, determined that six weeks is the period
“during which post-vaccination adverse autoimmune complications can arise.” Pet. Ex. 42 at 6;
see generally Resp. Ex. A, Tab 13. Therefore, Dr. Sheikh stated that because “[Petitioner’s]
symptoms started 40 days following a[] [flu] vaccination, [that] timing [] would be within the
biologic window (3-42 days) of an autoimmune event triggered by a vaccine.” Pet. Ex. 13 at 10.
58
As referenced earlier, the labyrinthine segment (which extends from the IAC to the geniculate
ganglion) is part of the intratemporal portion of the facial nerve. See Gleeson, supra note 20, at
638; Resp. Ex. C, Tab 1 at 2.
59
Inst. of Med., Influenza Vaccine, in Adverse Effects of Vaccines: Evidence and Causality 293
(Kathleen Stratton et al. eds., 2012).
24
Further, Zhou et al., which demonstrated association of Bell’s palsy with parenteral
inactivated flu vaccines in VAERS over a ten-year period, found that more than 5% of patients
developed Bell’s palsy between 31-60 days after vaccination. Pet. Ex. 47 at 4.
Dr. Sheikh concluded that in Petitioner’s case, “not only is the timing appropriate, . . . but
there is also a reasonable sequence of cause and effect.” Pet. Ex. 13 at 10.
2. Respondent’s Expert, Dr. Dara G. Jamieson60
a. Background and Qualifications
Dr. Jamieson is a board-certified neurologist licensed in New York. Resp. Ex. B at 2.
She received her medical degree from the University of Pennsylvania, followed by a neurology
residency and a cerebrovascular fellowship at the University of Pennsylvania Hospital. Resp.
Ex. A. at 1. Dr. Jamieson was a practicing neurologist for 32 years before transitioning to a
voluntary faculty appointment in 2018. Id. She is currently a Clinical Associate Professor of
Neurology at Weill Cornell Medicine, where she teaches medical students in neurology courses
and clinical inpatient clerkships, as well as lectures to residents and fellows. Id. She has also
lectured extensively nationally and internationally on neurological topics. Id. at 2; Resp. Ex. B
at 4-10. Dr. Jamieson serves on several editorial boards, including the Journal of
Neuroimmunology, Current Treatment Opinions in Neurology, and Neurology Alert. Resp. Ex.
A. at 2. She has authored or co-authored numerous publications in peer reviewed journals as
well as authored books and book chapters on various neurological topics. Id.; Resp. Ex. B at 13-
14.
b. Opinion
Dr. Jamieson opined to a “reasonable degree of medical probability” that Petitioner’s
“Bell’s palsy with incomplete recovery was unrelated to her flu vaccine.” Resp. Ex. A at 17.
i. Althen Prong One
Dr. Jamieson opined that an autoimmune theory is not supported by “data associating
Bell’s palsy with parenteral [flu] vaccinations.” Resp. Ex. A at 10. Dr. Jamieson first noted
there are significant differences between GBS and Bell’s palsy. Id. at 9. Namely, “GBS is a cell
mediated, autoimmune neuropathy involving multiple, bilateral peripheral nerves,” whereas
Bell’s palsy involves “injury to a single unilateral cranial nerve.” Id. However, she
acknowledged “[c]ombining the viral and immunological theories has led to a suggestion that
Bell’s palsy could be an autoimmune, post-viral disease.” Id.
Dr. Jamieson explained that while older studies have postulated an association between
the flu vaccine and Bell’s palsy, epidemiologic evidence is lacking in recent data. Resp. Ex. A at
13. Dr. Jamieson criticized Dr. Sheikh for relying on older literature evaluating Bell’s palsy
60
Dr. Jamieson submitted one expert report in this matter. Resp. Ex. A.
25
following vaccinations. Id. at 10. She stated that Dr. Sheikh merely “conflated older data,
related to an intranasal, adjuvanted [flu] vaccine that is no longer in clinical use, with more
current data from the parenteral vaccine used on [Petitioner].” Id.
Dr. Jamieson stated that “the cause of Bell’s palsy is still unknown.” Resp. Ex. A at 12.
Nonetheless, she concluded there is no autoimmune mechanism to explain a causal association
between the flu vaccine and Bell’s palsy, and no epidemiological data that links the flu vaccine
to Bell’s palsy. Id. at 17. In support of her opinions, Dr. Jamieson cited several works of
medical literature that she claimed, “discredit a causal association between parenteral [flu]
vaccinees and Bell’s palsy.” Resp. Ex. A at 15.
Stowe et al. conducted a population-based study of 2,128 individuals who developed
Bell’s palsy from 1992 to 2005 and found “no evidence of an increased risk [of Bell’s palsy] in
the three months following parenteral inactivated [flu] vaccine.” Resp. Ex. C, Tab 8 at 1-2. The
highest incidence rate Stowe et al. found was during the risk period of 1 to 30 days. Id. at 2. The
authors wrote, “[t]his study suggests that the association seen with the inactivated intranasal [flu]
vaccine may be specific to the administration of the intranasal vaccine and the association
observed cannot be extrapolated to the parenteral inactivated vaccine.” Id. at 3.
Rowhani-Rahbar et al.61 examined the association between Bell’s palsy and vaccines in
children from 2001 to 2006. Resp. Ex. A, Tab 17 at 1-2. Of the 822 children in the study, 233
received at least one vaccine in the 12 months prior to onset. Id. at 4. The authors found no
association between vaccination (flu (trivalent), hepatitis B, or any vaccine) and Bell’s palsy
during their risk intervals of 1-14 days, 1-28 days, and 29-56 days. Id.
Dr. Jamieson cited to Wijnans et al., a self-controlled case series from the United
Kingdom aimed “to determine whether there was an increased risk of Bell’s palsy following
vaccination with any [flu] vaccine containing A/California/7/2009 (H1N1)-like viral strains.”62
Resp. Ex. A, Tab 19 at 1. The study population was comprised of all Bell’s palsy cases using a
primary health care database in the United Kingdom from 2009 to 2013. Id. at 1-2. They found
a relative incidence rate of Bell’s palsy between one and 42 days post-flu vaccination to be 0.88.
Id. at 5. When adjusted for confounders, the relative incidence rate decreased to 0.85. Id. The
authors did not find “evidence of an increased risk of Bell’s palsy following vaccination with any
[flu] vaccine containing A/California/7/2009 (H1N1)-like viral strains, either pandemic or
seasonal vaccines.” Id. at 8. Additionally, they found “no evidence of an increased incidence of
Bell’s palsy consultations following seasonal [flu] vaccination overall, nor for monovalent
pandemic [flu] vaccine in 2009.” Id. at 7.
Ali Rowhani-Rahbar et al., Immunization and Bell’s Palsy in Children: A Case-Centered
61
Analysis, 175 Am. J. Epidemiology 878 (2012).
62
Petitioner’s flu vaccine contained a similar strain. Resp. Ex. E, Tab 5 at 11.
26
Dr. Jamieson also cited to Greene et al.,63 a study for adverse events, such as Bell’s palsy,
among individuals who received seasonal trivalent inactivated flu vaccines during specified flu
seasons. Resp. Ex. A, Tab 15 at 1, 3. The risk of adverse events, including GBS and Bell’s
palsy, following flu vaccination was compared in each season with that in previous seasons. Id.
at 1. After administration of 1,195,552 doses to children and 4,773,956 doses to adults, the
authors found “no evidence of elevated risk following [flu vaccination] for any of [the]
predefined adverse event categories.” Id. at 9. Similarly, a 2014 study by Vaughn et al.64 did not
find a “statistically significant” association between vaccines and the reporting of adverse events,
including facial paralysis. Resp. Ex. A, Tab 16 at 1, 13. However, Vaughn et al. noted that
“small increases in the risk of such events cannot be ruled out” and identified Bell’s palsy as an
adverse event of special interest “considered worthy of closer safety monitoring” following
administration of flu vaccination. Id. at 13-14.
Finally, Dr. Jamieson noted that IOM published a report in 2012 concluding that “[t]he
evidence favors rejection of a causal relationship between inactivated [flu] vaccine and Bell’s
palsy.” Resp. Ex. A, Tab 13 at 366. However, in coming to this conclusion, they only reviewed
Stowe et al. and Greene et al. Id.
ii. Althen Prongs Two and Three
Dr. Jamieson agreed that Petitioner developed Bell’s palsy on November 28, 2015. Resp.
Ex. A at 11. However, she opined that Petitioner’s development of symptoms were
“coincidental[]” to the flu shot she received about 40 days, or six weeks, earlier on October 19,
2015. Id. at 17.
Dr. Jamieson believed that “the extent of [Petitioner’s] facial weakness and her
incomplete recovery [could be] suggestive of Ramsay Hunt syndrome, a varicella zoster virus
(VZV infection).” Resp. Ex. A at 11. She reasoned that “[p]atients with Ramsay Hunt syndrome
often have more severe facial paralysis at onset and are less likely to recover completely.” Id.
Dr. Jamieson explained that Ramsey Hunt Syndrome is a peripheral facial nerve palsy
“associated with a[] vesicular rash on the ear ([herpes] zoster oticus) or in the mouth.” Id.
Importantly, “Ramsey Hunt Syndrome is caused by a VZV infection.” Id. (citing Resp. Ex. A,
Tab 2 at 12 (Ramsey Hunt Syndrome is “due to reactivation of [VZV] in the geniculate
ganglion.”)).
However, Dr. Jamieson stated that on Petitioner’s physical examination on November 29,
2015, “[n]o skin lesions were identified that indicated an overt viral infection as a cause of the
facial nerve injury.” Resp. Ex. A at 11. Further, she acknowledged that “[t]his alternative
63
Sharon K. Greene et al., Near Real-Time Surveillance for Influenza Vaccine Safety: Proof-of-
Concept in the Vaccine Safety Datalink Project, 171 Am. J. Epidemiology 177 (2010).
64
David Vaughn et al., Safety Of AS03-Adjuvanted Inactivated Split Virion A(H1N1)Pdm09
and H5N1 Influenza Virus Vaccines Administered to Adults: Pooled Analysis Of 28 Clinical
Trials, 10 Hum. Vaccines & Immunotherapeutics 2942 (2014).
27
diagnosis cannot be proven because acute VZV titers were not obtained at the time of the onset
of [Petitioner’s] weakness.” Id. Instead, Dr. Jamieson opined that Petitioner had “Bell’s palsy
with incomplete recovery” and developed residual synkinesis. Id. at 17.65
Dr. Jamieson conceded that “[b]y the definition of the syndrome [“facial weakness of
unknown cause”], there is no alternative cause of Bell’s palsy that is identified in a person’s
medical history.” Resp. Ex. A at 11. In fact, she stated that “[i]f a specific cause is found, such
as Lyme disease . . . , it should not be referred to as Bell’s palsy.” Id. (quoting Resp. Ex. A, Tab
2 at 1). She added, “[i]f the cause of the facial weakness is known, then the entity is known as
facial weakness due to that specific causative disease [or Ramsey Hunt Syndrome] and is not
called a Bell’s palsy.” Id. at 12. While Dr. Jamieson acknowledged that “[r]eactivation of a
latent herpes viral infection has been postulated as a [pathogenetic] mechanism, leading to the
weak suggestion for acute treatment with antiviral medication,” she stated that “the cause of
Bell’s palsy is still unknown with empiric steroid treatment used in a supposed effort to hasten
facial reinnervation and decrease the incidence of synkinesis.” Id. at 12. Reich et al. noted that
“[t]he use of steroids and antivirals to improve the recovery of Bell’s palsy is based on the . . .
observations about the possible role[] of HSV type 1 in the . . . etiology” of Bell’s palsy. Resp.
Ex. A, Tab 2 at 13. However, the authors concluded that “adding an antiviral does not
significantly improve the likelihood of recovery.” Id. at 17. Here, Dr. Jamieson acknowledged
that “[d]espite appropriate treatment with steroids and antivirals, [Petitioner’s] return of facial
symmetry was incomplete.” Resp. Ex. A at 17.
Of note, while Dr. Jamieson stated that “[c]onditions associated with an increased risk of
developing idiopathic facial weakness include diabetes, pregnancy, stress[,] and acute respiratory
tract infections,” Dr. Jamieson did not opine that Petitioner’s Bell’s palsy was caused by an
upper respiratory infection. Resp. Ex. A at 12.
3. Respondent’s Expert, S. Mark Tompkins, Ph.D.66
a. Background and Qualifications
Dr. Tompkins is an immunologist. Resp. Ex. C at 1. He received his Ph.D. in
Immunology and Molecular Pathogenesis from Emory University in Atlanta, Georgia. Id.; Resp.
Ex. D at 1. He does not hold a medical degree. Resp. Ex. D at 1. Dr. Tompkins’ postdoctoral
training focused on “immunologic mechanisms of induction of autoimmune disease, specifically
interrogating antigen- and virus-induced models of experimental autoimmune encephalomyelitis;
models for the neurologic autoimmune disease, multiple sclerosis.” Resp. Ex. C at 1. His
second postdoctoral fellowship focused on “understanding the immune response to [flu]
infection and vaccination.” Id. Dr. Tomkins is currently a Full Professor at the Center for
Vaccines and Immunology and the Department of Infectious Diseases, both at the University of
65
Moreover, the parties stipulated that Petitioner’s diagnosis was Bell’s palsy, thus it cannot be
Ramsey Hunt syndrome. Joint Pre-Hearing Submission at 1.
66
Dr. Tompkins submitted two expert reports in this matter. Resp. Exs. C, E.
28
Georgia (“UGA”) College of Veterinary Medicine. Resp. Ex. D at 2. He also serves as the
Assistant Department Head and Curriculum Coordinator of the Department of Infectious
Diseases at the UGA College of Veterinary Medicine. Id. As a faculty member, Dr. Tompkins
teaches immunology and virology to graduate students and trains doctoral fellows. Resp. Ex. C
at 1. His research interest is on understanding the interactions of the flu virus and the flu vaccine
with the host, or more generally, in the etiology of immune-mediated disease. Id.; Resp. Ex. D at
15-16. Dr. Tomkins explained that while “aspects of [his] research entail zoonotic [flu] viruses
and understanding the determinants of infection, transmission, and pathogenesis, the core of [his]
research remains understanding the immune response to viral infection and vaccination.” Resp.
Ex. C at 1. Dr. Tomkins has authored or co-authored numerous peer-reviewed papers, book
chapters, and articles on immunology and virology. Id.; Resp. Ex. D at 29-40.
b. Opinion
Because Dr. Tompkins does not hold a medical degree and thus is not qualified to
diagnose or treat patients, he did not dispute Petitioner’s diagnosis of Bell’s palsy or her
development of symptoms approximately 40 days after her flu vaccination. Resp. Ex. C at 2.
Instead, he focused on the potential association between the flu vaccine and the onset of Bell’s
palsy. Id.; Resp. Ex. E at 1. As such, his opinions are generally limited to Althen Prong One.
i. Althen Prong One
Dr. Tompkins first stated that the etiology of Bell’s palsy is unclear. Resp. Ex. C at 2-3.
He noted that Zhang et al. “summarized five major hypotheses including anatomical, viral
infection, ischemia, inflammation, and cold stimulation.” Id. (quoting Resp. Ex. C, Tab 1)
(internal quotations omitted). But he opined there is no evidence that flu vaccination elicits
Bell’s palsy. Id. at 7; Resp. Ex. E at 7. Instead, Dr. Tompkins suggested “infection[] or viral
reactivation due to stress and infection” as potential explanations for Petitioner’s Bell’s palsy.
Resp. Ex. C at 6.
Like Dr. Jamieson, Dr. Tompkins took issue with Dr. Sheikh’s comparison of GBS and
Bell’s palsy. He stated Zhang et al. and Greco et al., relied on by Dr. Sheikh, “use a circular
argument that [Bell’s palsy] and GBS may be related because the diseases share [these]
hypothetical etiologies.” Resp. Ex. C at 3. Dr. Tompkins acknowledged the similarities of GBS
and Bell’s palsy including changes in lymphocyte frequencies and potential responses to nervous
tissue antigens, but opined that the conditions do not have a shared etiology. Id. He explained,
however, it is “not surprising both diseases could have evidence of humoral or cellular immune
responses to peripheral nerve antigens” as both “GBS and [Bell’s palsy] may involve nervous
tissue damage, which may elicit immune responses to self-antigens.” Id. But Dr. Tompkins
opined “this does not support the supposition by Dr. Sheikh that [Bell’s palsy] is a variant of
GBS.” Id.
Dr. Tompkins acknowledged that molecular mimicry is a “well-established
immunological concept” but opined there is no support for Dr. Sheikh’s statement that “vaccines
have been recognized to trigger autoimmune responses . . . directed against antigens on
peripheral nerves, such as the facial nerve, resulting in inflammatory polyneuropathies.” Resp.
29
Ex. C at 4 (quoting Pet. Ex. 13 at 10). He opined “there is no evidence that vaccination with
current [flu] vaccines initiates immune responses to self-antigens through molecular mimicry.”
Id. at 7.
Additionally, Dr. Tompkins criticized Dr. Sheikh’s literature on GBS and the potential
antibody-mediated molecular mimicry. Resp. Ex. E at 6-7. Dr. Tompkins explained that “over
time, human [flu] viruses accumulate glycosylation sites on the hemagglutinin protein,” which he
claimed “would increase the number of available carbohydrates to potentially elicit
antiganglioside antibodies.” Id. at 6. Yet he opined “the only vaccine associated with GBS is
the A/NJ/1976 (H1N1) vaccine that contained limited glycosylation sites, undermining the
persuasiveness of this hypothesis.” Id. Dr. Tompkins cited to Wang et al.67 and Lei et al.68 to
support his hypothesis that there is no correlation with flu vaccination and the induction of
antiganglioside antibodies. Id. at 6-7. However, Wang et al. found that “both GM-1 and GM-2
antiganglioside [] antibodies cross-reacted with multiple H1N1 and H3N2 [flu] strains,” and
while that reaction varied among the strains it was “directly associated with the glycosylation of
[hemagglutinin].” Resp. Ex. E, Tab 15 at 3. Additionally, they found that “[a]s the number of
potential glycosylation sites increased on the [hemagglutinin], the reactivity of the virus with the
antiganglioside antibody also increased.” Id. Moreover, Lei et al “could not exclude the
possibility that anti-GM1 antibodies might be generated rarely in [flu] vaccinees.” Resp. Ex. E,
Tab 16 at 5.
Regarding Mutsch et al., which found an increased risk of developing Bell’s palsy after
an intranasal flu vaccine (Nasalflu), Dr. Tompkins stated that Petitioner did not receive an
intranasal vaccine, but instead received a parenteral vaccine (FluArix). Resp. Ex. C at 4; Resp.
Ex. E at 2; Resp. Ex. E, Tab 5 at 1. He explained that besides the methods of delivery, the most
significant difference between the two flu vaccines is that Nasalflu contained a potent adjuvant
(E. coli heat-labile enterotoxin). Resp. Ex. C at 4. Dr. Tompkins opined “the association of the
Nasalflu vaccine with [Bell’s palsy] is due to the adjuvant and is unrelated to the [flu] antigens.”
Id. at 5. For support, Dr. Tompkins cited Lewis et al.69 and Halsey et al.70 Resp. Ex. E at 2.
Lewis et al. discussed the risks of E. coli enterotoxins as adjuvants in intranasal vaccines. Resp.
Ex. E, Tab 3 at 1. They found Bell’s palsy occurred only where the individual received a heat-
67
David J. Wang et al., No Evidence of a Link Between Influenza Vaccines and Guillain–Barre
Syndrome–Associated Antiganglioside Antibodies, 6 Influenza & Other Respiratory Viruses 159
(2011).
68
Ting Lei et al., Anti-ganglioside Antibodies Were Not Detected in Human Subjects Infected
with or Vaccinated Against 2009 Pandemic Influenza A (H1N1) Virus, 30 Vaccine 2605 (2012).
69
David J. Lewis et al., Transient Facial Nerve Paralysis (Bell’s Palsy) Following Intranasal
Delivery of a Genetically Detoxified Mutant of Escherichia Coli Heat Labile Toxin, 4 PLoS One
e6999 (2009). This article is also cited by Petitioner. Pet. Ex. 67.
70
Neal A. Halsey et al., The Safety of Influenza Vaccines in Children: An Institute for Vaccine
Safety White Paper, 33 Vaccine F1 (2015).
30
labile enterotoxin adjuvant and not a vaccine antigen. Id. at 3; see also Resp. Ex. A, Tab 18 at
23-24. However, Lewis et al. was conducted using only the human immunodeficiency virus
(“HIV”) and tuberculosis vaccines, not a flu vaccine. Resp. Ex. E, Tab 3 at 1. Nonetheless, the
clinical course and the timing of onset of post-vaccination Bell’s palsy in the cases presented in
Lewis et al. suggested an immune mediated response. Halsey et al., which discussed Mutsch et
al. and Lewis et al., concluded that “[t]he most likely hypothesis for the association with . . .
vaccines and Bell’s palsy is that the E. coli enterotoxin resulted in inflammation and entrapment
of the facial nerve in the facial canal.” Resp. Ex. A, Tab 18 at 24. Dr. Tompkins therefore
opined that “[t]he onset of [Bell’s palsy] in three different vaccines containing the enterotoxin
suggested the adjuvant was associated with [Bell’s palsy], not the vaccine antigens.” Resp. Ex.
C at 5. However, Halsey et al. did find a signal of Bell’s palsy in adults following the 2009
inactivated flu vaccine. Resp. Ex. A, Tab 18 at 24.
Dr. Tompkins then referenced case reports about the onset of Bell’s palsy after flu
vaccination. He particularly pointed out Stowe et al., which assessed the overall incidence of
Bell’s palsy at defined intervals after vaccination. Resp. Ex. C at 5. “They found no increase in
[Bell’s palsy] between 1-30, 31-60, 61-91, or 1-91 days after [flu] vaccination.” Id. (citing Resp.
Ex. C, Tab 8). Similarly, the IOM found no evidence of increased risk of Bell’s palsy after
inactivated flu vaccination. Id. at 5-6 (citing Resp. Ex. A, Tab 13 at 366).
Ultimately, Dr. Tompkins found no evidence of association between the parenteral flu
vaccine and the risk of Bell’s palsy. Resp. Ex. E at 4.
ii. Althen Prongs Two and Three
Dr. Tomkins agreed that Petitioner’s onset of symptoms was approximately 40 days, or
six weeks, after administration of the flu vaccine. Resp. Ex. C at 5. But he hypothesized
“infection[] or viral reactivation due to stress and infection” are “possibilities here” for the
etiology of Petitioner’s Bell’s palsy. Id. at 6. He opined that her Bell’s palsy resulted from a
mild respiratory infection she had hours or days before. Id. “The stress and acute viral infection
noted in the medical records, along with seasonal cold temperatures at the time of [P]etitioner’s
onset [were] the most likely triggers of her [Bell’s palsy].” Resp. Ex. E at 8. However, he
acknowledged he is not a clinician. Resp. Ex. C at 2.
Dr. Tompkins noted that the medical records show a “day before the symptoms[,]
[Petitioner] thought she might be developing a cold and took some [M]ucinex.” Resp. Ex. C at 6
(quoting Pet. Ex. 2 at 675). Dr. Tompkins averred that “[w]hile this medical note was not further
discussed, it is highly relevant as infections are associated with [Bell’s palsy].” Id.
The National Institute of Neurological Disorders and Stroke (“NINDS”) reported that
“[m]ost scientists believe that reactivation of an existing (dormant) viral infection may cause the
disorder. Impaired immunity from stress, sleep deprivation, physical trauma, minor illness[,] or
autoimmune syndromes are suggested as the most likely triggers.” Resp. Ex. C, Tab 12 at 1.
31
Moreover, Dr. Tompkins cited Mathew et al.,71 which noted a seasonality of Bell’s palsy that
overlaps with several respiratory infections. Resp. Ex. C at 6 (citing Pet. Ex. 27 at 1). He also
noted that Halsey et al. and Zhang et al. discussed herpesvirus reactivation as a potential etiology
of Bell’s palsy. See id. (citing Resp. Ex. A, Tab 18 at 23; Resp. Ex. C, Tab 1 at 2). However,
Zhang et al. noted that “the behavior of patients with [Bell’s palsy] is unusual compared to that
of patients with other diseases more commonly associated with HSV” and “clinical evidence of
HSV-1 infection in the geniculate ganglion remains elusive.” Resp. Ex. C, Tab 1 at 5.
Nonetheless, Dr. Tompkins concluded that this “evidence provide[s] a plausible explanation for
the cause of [Petitioner’s] [Bell’s palsy].” Resp. Ex. C at 7.
He reasoned that because Petitioner “was traveling, visiting at least 20 people and
shopping/dining during the Thanksgiving holiday, it is highly plausible that she was exposed to a
common human respiratory pathogen, resulting in a respiratory infection, eliciting [Bell’s
palsy].” Resp. Ex. C at 6. Additionally, he noted Petitioner’s recent loss of her partner. Id. He
concluded “[t]his stress, combined with travel and a possible respiratory infection[,] could have
enabled the reactivation of a latent herpesvirus infection, triggering the [Bell’s palsy].” Id.
While Dr. Tomkins acknowledged literature on immune responses to flu vaccination, he
explained that such literature “generally focus[es] on time points between 7 and 28 days post-
vaccination.” Resp. Ex. C at 6. For example, Dolfi et al.72 found a peak in CD4 T cell responses
in elderly persons 7 to 14 days post-vaccination that returned to baseline levels 28 to 60 days
post-vaccination. Resp. Ex. C, Tab 9 at 3. Co et al.73 found small increases in CD8 T cell
responses that waned by two months post-vaccination. Resp. Ex. C, Tab 10 at 5 tbl.1. Finally,
Nougarede et al.74 found increases in vaccine-specific antibody responses at days 14 and 21 but
waned by day 180 post-vaccination. Resp. Ex. C, Tab 11 at 3 fig.1D.
Accordingly, while Dr. Thompkins agreed that the flu vaccine can elicit vaccine-specific
antibody responses, and that those responses vary, they tend to wane as early as 14 days post-
vaccination. Resp. Ex. C at 6. “So, while there is no evidence that [flu]-specific T cell responses
are associated with [Bell’s palsy],” he opined “the decreasing post-vaccine response further
argues against potential involvement with [Petitioner’s Bell’s palsy] 40 days after vaccination.”
Id.
71
Thomas Mathew et al., Bell’s Palsy and Guillain–Barré Syndrome May Be 2 Ends of the Same
Spectrum, 59 Muscle & Nerve E48 (2019)
72
Douglas V. Dolfi et al., Vaccine-Induced Boosting of Influenza Virus-Specific CD4 T Cells in
Younger and Aged Humans, 8 PLoS e77164 (2013).
73
Mary Dawn T. Co et al., Discordance Between Antibody and T Cell Responses in Recipients
of Trivalent Inactivated Influenza Vaccine, 26 Vaccine 1990 (2008).
74
Nolwenn Nougarede et al., Nine μg Intradermal Influenza Vaccine and 15 μg Intramuscular
Influenza Vaccine Induce Similar Cellular and Humoral Immune Responses in Adults, 10 Hum.
Vaccines & Immunotherapeutics 2713 (2014).
32
Additionally, and in support of his alternative theory, Dr. Tompkins added that the onset
of Bell’s palsy in children “usually occurs hours to days after an upper respiratory tract
infection.” Resp. Ex. C at 6 (quoting Resp. Ex. A, Tab 18 at 23). He averred this timing
supports his hypothesis of Petitioner developing Bell’s palsy hours or days after recognizing she
might be sick. Id. at 7. However, Dr. Tomkins left out that Halsey et al. went on to add that the
onset of Bell’s palsy symptoms hours to days after infection “resolves spontaneously without
treatment.” Resp. Ex. A, Tab 18 at 23.
IV. DISCUSSION
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
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). Petitioner need not make a specific type of
evidentiary showing, i.e., “epidemiologic studies, rechallenge, the presence of pathological
markers or genetic predisposition, or general acceptance in the scientific or medical communities
to establish a logical sequence of cause and effect.” Capizzano v. Sec’y of Health & Hum.
Servs., 440 F.3d 1317, 1325 (Fed. Cir. 2006). Instead, Petitioner may satisfy her burden by
presenting circumstantial evidence and reliable medical opinions. Id. at 1325-26.
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). The
received vaccine, however, need not be the predominant cause of the injury. Shyface, 165 F.3d
at 1351. 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 respondent 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.
33
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.”).
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.
B. Causation
To receive compensation through the Program, Petitioner must prove either (1) that she
suffered a “Table Injury”—i.e., an injury listed on the Vaccine Injury Table—corresponding to a
vaccine that she received, or (2) that she suffered an injury that was actually caused by a
vaccination. See §§ 11(c)(1), 13(a)(1)(A); Capizzano, 440 F.3d at 1319-20. Because Petitioner
does not allege she suffered a Table Injury, she must prove a vaccine she received caused her
injury. To do so, Petitioner must establish, by preponderant evidence: “(1) a medical theory
causally connecting the vaccination and the injury; (2) a logical sequence of cause and effect
showing that the vaccination was the reason for the injury; and (3) a showing of a proximate
temporal relationship between vaccination and injury.” Althen, 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 v.
Sec’y of Health & Hum. Servs., 35 F.3d 543, 548-49 (Fed. Cir. 1994). 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
34
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).
V. ANALYSIS
A. Althen Prong One
Under Althen Prong One, Petitioner must set forth a medical theory explaining how the
received vaccine could have caused the sustained injury. Andreu v. Sec’y of Health & Hum.
Servs., 569 F.3d 1367, 1375 (Fed. Cir. 2009); Pafford, 451 F.3d at 1355-56. Petitioner’s theory
of causation need not be medically or scientifically certain, but it must be informed by a “sound
and reliable” medical or scientific explanation. Boatmon v. Sec’y of Health & Hum. Servs., 941
F.3d 1351, 1359 (Fed. Cir. 2019); see also Knudsen, 35 F.3d at 548; Veryzer v. Sec’y of Health
& Hum. Servs., 98 Fed. Cl. 214, 223 (2011) (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”). If Petitioner relies upon a medical opinion to support her theory, the basis for the
opinion and the reliability of that basis must be considered in the determination of how much
weight to afford the offered opinion. See Broekelschen v. Sec’y of Health & Hum. Servs., 618
F.3d 1339, 1347 (Fed. Cir. 2010) (“The special master’s decision often times is based on the
credibility of the experts and the relative persuasiveness of their competing theories.”); Perreira
v. Sec’y of Health & Hum. Servs., 33 F.3d 1375, 1377 n.6 (Fed. Cir. 1994) (stating that an
“expert opinion is no better than the soundness of the reasons supporting it” (citing Fehrs v.
United States, 620 F.2d 255, 265 (Ct. Cl. 1980))).
The undersigned finds Petitioner has set forth a sound and reliable medical theory,
molecular mimicry, to explain how the flu vaccine can cause Bell’s palsy. The medical literature
shows persuasive evidence of the similarity between GBS and Bell’s palsy, that molecular
mimicry is an appropriate causal mechanism of GBS, and therefore by analogy, is sound and
reliable here.
The preferred theory proposed by Dr. Sheikh is an autoimmune or immune-mediated
75
theory, the most popular of which is that the same mechanism involved in the etiology of GBS
is present for Bell’s palsy—a post-vaccination monovariant polyneuropathy. In support of this
theory, Dr. Sheikh provided persuasive literature.
The Greco et al. article provides a comprehensive analysis of the relevant immunological
theories of causation, specifically molecular mimicry. The authors state, “[s]ome evidence
implicates the involvement of immune mechanisms in Bell’s palsy. Many reports have indicated
75
While Dr. Sheikh also mentioned the possibility of an infectious theory, and Dr. Tompkins
suggested an infectious theory instead of molecular mimicry, the undersigned focuses her
discussion on the immune-mediated (molecular mimicry) theory as it is the preferred theory by
Dr. Sheikh. Moreover, Dr. Tompkins acknowledged molecular mimicry as an immunological
concept.
35
the association between facial paralysis and [GBS], a condition that was recently shown to be a
cell mediated, autoimmune neuritis.” Pet. Ex. 18 at 4. The authors go on to discuss the
Abramsky et al. article, which found a “defined in vitro response to a human basic protein (P1L)
of peripheral nerve myelin in patients with Bell’s palsy. They suggested that cell-mediated
autoimmune mechanisms may be of importance in the pathogenesis of Bell’s palsy.” Id.; see
also Pet. Ex. 19 at 1. The literature also discusses the similarity between GBS and Bell’s palsy
with regard to lymphocyte sensitization to the same P1L protein. Bell’s palsy, like GBS, is an
acute demyelinating disease of the peripheral nervous system. This all suggests that Bell’s palsy
is a mononeuritic variant of GBS. There is a body of evidence showing there is an immune
mediated, or autoimmunity causal theory that is sound and reliable, and the most likely of those
mechanisms would be molecular mimicry.
The experts agree, and many of the medical articles filed, establish that GBS is known to
be an autoimmune condition, and that molecular mimicry is a likely causal mechanism.
Petitioner provided sound and reliable reasons for extending the application of molecular
mimicry to Bell’s palsy. Petitioner provided preponderant evidence, by expert opinion and
medical literature, of an association between the flu vaccine and Bell’s palsy, including
numerous case studies reporting the development of Bell’s palsy following the flu vaccine. For
example, Zhou et al. concluded there “may be a signal of possible association between [flu]
vaccines and an increased risk of Bell’s palsy.” Pet. Ex. 47 at 5. Bardage et al. found “a
significantly increased risk for Bell’s palsy” in “those vaccinated in the early phase of the
vaccination campaign (≤ 45 days), when high risk groups predominated.” Pet. Ex. 41 at 4.
While the authors of these studies did not reach any conclusions as to the pathogenesis of Bell’s
palsy, some hypothesized an immune-mediated response mechanism to be at play. Additionally,
studies cited by Respondent’s experts noted that an immune-mediated response is thought to play
a part in the development of demyelinating polyneuropathies.
The lack of epidemiological evidence is not dispositive. It is difficult to use
epidemiology to determine whether a vaccine is implicated in causation. Because while adverse
reactions like this do not appear in the epidemiological evidence cited by Respondent’s experts,
it may be that events are too rare to be captured. Moreover, “[r]equiring epidemiologic studies . .
. or general acceptance in the scientific or medical communities . . . impermissibly raises a
claimant’s burden under the Vaccine Act and hinders the system created by Congress, in which
close calls regarding causation are resolved in favor of injured claimants.” Andreu, 569 F.3d at
1378 (quoting Capizzano, 440 F.3d at 132-26); see also Althen, 418 F.3d at 1280 (noting that
“close calls” are resolved in Petitioner’s favor). The undersigned does not find the
epidemiological literature to be definitive or determinative in this regard.
For these reasons, the undersigned finds that Petitioner has provided preponderant
evidence of a sound and reliable causal theory, satisfying Althen Prong One.
B. Althen Prong Two
Under Althen Prong Two, Petitioner must prove by a preponderance of the evidence that
there is a “logical sequence of cause and effect showing that the vaccination was the reason for
the injury.” Capizzano, 440 F.3d at 1324 (quoting Althen, 418 F.3d at 1278). “Petitioner must
36
show that the vaccine was the ‘but for’ cause of the harm . . . or in other words, that the vaccine
was the ‘reason for the injury.’” Pafford, 451 F.3d at 1356 (internal citations omitted).
In evaluating whether this prong is satisfied, the opinions and views of the vaccinee’s
treating physicians are entitled to some weight. Andreu, 569 F.3d at 1367; Capizzano, 440 F.3d
at 1326 (“[M]edical records and medical opinion testimony are favored in vaccine cases, as
treating physicians are likely to be in the best position to determine whether a ‘logical sequence
of cause and effect show[s] that the vaccination was the reason for the injury.’” (quoting Althen,
418 F.3d at 1280)). Medical records are generally viewed as trustworthy evidence, since they are
created contemporaneously with the treatment of the vaccinee. Cucuras v. Sec’y of Health &
Hum. Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993). The Petitioner need not make a specific
type of evidentiary showing, i.e., “epidemiologic studies, rechallenge, the presence of
pathological markers or genetic predisposition, or general acceptance in the scientific or medical
communities to establish a logical sequence of cause and effect.” Capizzano, 440 F.3d at 1325.
Instead, Petitioner may satisfy her burden by presenting circumstantial evidence and reliable
medical opinions. Id. at 1325-26.
In regard to Althen Prong Two, the undersigned finds Petitioner provided preponderant
evidence of a logical sequence of cause and effect showing that her vaccination was the cause of
her Bell’s palsy. First, Petitioner’s clinical course is consistent with the medical literature and
case reports of Bell’s palsy following vaccination.
Petitioner received the flu vaccine on October 19, 2015, and approximately 40 days later,
she reported facial paralysis. Petitioner’s MRI showed enhancement of the seventh cranial
nerve, which can be seen in Bell’s palsy, and suggests a demyelinating process. Petitioner’s
MRI also showed a questionable enhancement in the medial left IAC, or internal auditory canal
nerve, again suggestive of Bell’s palsy. Petitioner’s follow up MRI showed no enhancement.
These diagnostic findings are consistent with the clinical course of this condition as supported by
medical literature provided by Petitioner and Dr. Sheikh.
Next, the undersigned finds Petitioner’s clinical course is consistent with the proposed
causal mechanism. The MRI finding, suggesting a demyelinating process, supports the current
understanding that Bell’s palsy is mononeuropathy variant of GBS, which supports the theory of
molecular mimicry. Dr. Sheikh explained that for onset of inflammatory demyelinating
polyneuropathies following the flu vaccine, “the period of increased risk was concentrated within
the 5-6 week period.” Pet. Ex. 13 at 10 (internal citation omitted). Importantly, Petitioner’s
onset of symptoms was 40 days after vaccination which is less than six weeks.
Further, the undersigned finds no evidence of any alternative cause, and Dr. Jamieson
concedes there is no such evidence. Dr. Jamieson stated, “[b]y the definition of the syndrome
[“facial weakness of unknown cause”], there is no alternative cause of Bell’s palsy that is
identified in a person’s medical history.” Resp. Ex. A at 11. There was a suggestion by a
treating physician that Petitioner could have had an atypical presentation of Ramsey Hunt
syndrome, but there is no evidence in the record to suggest that Petitioner had VZV or HSV.
Moreover, she did not have vesicles, a rash, or lesions. She also did not test positive for Lyme
disease.
37
While Dr. Tompkins proposes that infection and/or stress caused Petitioner to develop
Bell’s palsy, Dr. Sheikh highlighted that there were no signs of infection documented on
Petitioner’s ED physical examination. Therefore, Dr. Tompkins’ theory is merely speculative.
It is important to note that Dr. Tompkins is not a medical doctor, but a Ph.D., and based
on the undersigned’s review of his curriculum vitae, he does not have the requisite training,
education, experience, or qualifications to diagnosis or treat patients who have neurological
illnesses, like Bell’s palsy. In other words, he has not diagnosed a patient with Bell’s palsy. And
he has not determined whether a patient’s Bell’s palsy was caused by infection or stress as
opposed to a vaccine. While Dr. Tompkins is imminently qualified to opine in the area of his
expertise—immunology and molecular pathogenesis—the undersigned finds that his opinions as
to diagnosis and/or alternate cause carry less weight in this particular case, especially given the
statement in his expert report, where Dr. Tompkins states that he “will not dispute whether
[Petitioner] was suffering from [Bell’s palsy]. This is outside my expertise.” Resp. Ex. C at 2.
Dr. Jamieson, who is a medical doctor (neurologist), did not offer an opinion that
infection or stress caused Petitioner’s condition. Because Dr. Jamieson is well qualified to opine
on diagnosis and the etiology of that diagnosis by virtue of her training, experience, and
qualifications, the undersigned finds her opinions more persuasive. “In weighing the
persuasiveness of opinion testimony, special masters may consider the relative expertise of the
witness.” Koehn v. Sec’y of Health & Hum. Servs., No. 11-355V, 2013 WL 3214877, at *32
(Fed. Cl. Spec. Mstr. May 30, 2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014); see also Dwyer v.
Sec’y of Health & Hum. Servs., No. 03-1202V, 2010 WL 892250, at *64 (Fed. Cl. Spec. Mstr.
Mar. 12, 2010) (giving greater weight to M.D. epidemiologists’ opinions on medical issues than
to Ph.D. epidemiologist’s opinion); Pafford, 451 F.3d at 1359 (affirming the special master’s
rejection of expert’s testimony because he lacked proper qualifications in the specialty areas in
which he testified). While the undersigned acknowledges the Circuit Court’s directive in Koehn,
here, Dr. Tompkins has explained that the question of diagnosis is specifically outside of his
expertise. Koehn, 773 F.3d at 1244. Like diagnosis, the question of whether Petitioner’s Bell’s
palsy was caused by infection, stress, or vaccination involves the practice of medicine, which
requires specific training, experience, and qualifications, and in general, experience in caring for
patients. Thus, the relative specialties of the experts here are more proscribed and defined.
Moreover, Dr. Tompkins failed to state his opinion as to alternate cause to a reasonable
degree of probability. He opined infection and/or stress “provide a plausible explanation” for
both “the onset of [Bell’s palsy]” and for “the cause of [Petitioner’s] [Bell’s palsy].” Resp. Ex. C
at 6-7. He also stated that infection and/or stress are “the most likely triggers” and are “both
possibilities here” regarding the etiology of onset. Id. at 6; Resp. Ex. E at 8. But he used the
words “most likely” and “possibilities” which are inconsistent standards. Further, possibilities
are insufficient to establish an alternative cause for Petitioner’s Bell’s palsy. 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);
Waterman, 123 Fed. Cl. at 573-74 (denying Petitioner’s motion for review and noting that a
possible causal link was not sufficient to meet the preponderance standard); Boatmon, 941 F.3d
at 1359-60; Paterek v. Sec’y of Health & Hum. Servs., 527 F. App’x 875, 883 (Fed. Cir. 2013).
38
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. Accordingly,
because Dr. Tompkins’ opinions are inconsistent with regard to the applicable standard, the
undersigned finds that they do not rise to the level required by the Vaccine Act, as such, they do
not carry sufficient weight to support alternative causation.
Thus, the undersigned finds that Petitioner provided preponderant evidence of a logical
sequence of cause and effect, satisfying Althen Prong Two.
C. Althen Prong Three
Althen Prong Three requires Petitioner to establish a “proximate temporal relationship”
between the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been
defined as a “medically acceptable temporal relationship.” Id. The Petitioner must offer
“preponderant proof that the onset of symptoms occurred within a timeframe which, given the
medical understanding of the disease’s etiology, it is medically acceptable to infer causation-in-
fact.” de Bazan, 539 F.3d at 1352. The explanation for what is a medically acceptable time
frame must also coincide with the theory of how the relevant vaccine can cause the injury alleged
(under Althen Prong One). Id.; Koehn, 773 F.3d at 1243; Shapiro v. Sec’y of Health & Hum.
Servs., 101 Fed. Cl. 532, 542 (2011), recons. den’d after remand, 105 Fed. Cl. 353 (2012), aff’d
mem., 503 F. App’x 952 (Fed. Cir. 2013).
The parties stipulated, and the experts agree, that Petitioner received a flu vaccine on
October 19, 2015, and approximately 40 days later, on November 28, 2015, she developed Bell’s
palsy. This onset timeframe is appropriate given the purported autoimmune mechanism of
molecular mimicry. Therefore, Petitioner has provided preponderant evidence satisfying Althen
Prong Three.
D. Alternative Causation
Because the undersigned concludes that Petitioner established a prima facie case,
Petitioner is entitled to compensation unless Respondent can put forth preponderant evidence
“that Petitioner’s injury was in fact caused by factors unrelated to the vaccine.” Whitecotton v.
Sec’y of Health & Hum. Servs., 17 F.3d 374, 376 (Fed. Cir. 1994), rev’d on other grounds sub
nom., Shalala v. Whitecotton, 514 U.S. 268 (1995); see also Walther v. Sec’y of Health & Hum.
Servs., 485 F.3d 1146, 1151 (Fed. Cir. 2007). As discussed above in the Althen Prong Two
analysis, the undersigned found Respondent failed to establish evidence to show that Petitioner’s
Bell’s palsy was caused by a source other than vaccination. Thus, Respondent did not prove by a
preponderance of evidence that Petitioner’s injury is “due to factors unrelated to the
administration of the vaccine.” § 13(a)(1)(B).
VI. CONCLUSION
For the reasons discussed above, the undersigned finds that Petitioner has established by
preponderant evidence that her flu vaccine caused her Bell’s palsy. Therefore, Petitioner is
entitled to compensation. A separate damages order will issue.
39
IT IS SO ORDERED.
s/Nora Beth Dorsey
Nora Beth Dorsey
Special Master
40