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.
2

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). 
3

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.
4

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.
5

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. 
6

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.
7

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). 
8

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). 
9

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. 
10

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.
11

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. 
12

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). 
13

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 
14

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.
15

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.
16

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 “machinegun 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 
17

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.
18

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).
19

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 selfantigens,” 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 nonhomologous 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. 
20

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 cellmediated 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. 
21

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). 
22

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). 
23

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-pathogenesisclinical-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). 

56 Gilbert I. Martin & Michael I. Weintraub, Brachial Neuritis and Seventh Nerve Palsy – A Rare 

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. 
24

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). 
25

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.
26

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.

61 Ali Rowhani-Rahbar et al., Immunization and Bell’s Palsy in Children: A Case-Centered 

Analysis, 175 Am. J. Epidemiology 878 (2012). 

62 Petitioner’s flu vaccine contained a similar strain. Resp. Ex. E, Tab 5 at 11.
27

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-ofConcept 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). 
28

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.
29

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. 
30

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 heat67 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). 
31

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. 
32

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 postvaccination.” 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 postvaccination. 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).
33

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. 
34

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 
35

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 

theory,75 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. 
36

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 
37

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.
38

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). 
39

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-infact.” 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.
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IT IS SO ORDERED.

s/Nora Beth Dorsey

Nora Beth Dorsey

Special Master