G. v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 18-1735V

Filed: February 9, 2024

Special Master Horner

W.G.,

Petitioner,

v.

SECRETARY OF HEALTH AND

HUMAN SERVICES,

Respondent.

William E. Cochran, Jr., Black McLaren, et al., PC, Memphis TN, for petitioner.

Bridget Corridon, U.S. Department of Justice, Washington, DC, for respondent.

Decision1

On November 8, 2018, petitioner, W.G., filed a petition under the National

Childhood Vaccine Injury Act, 42 U.S.C. § 300aa-10, et seq. (2018),2 alleging that the

influenza (“flu”) vaccine and hepatitis B (“hep B”) vaccines he received on September

19, 2017 caused him to suffer “Bell’s palsy, hearing loss and neuropathy.” (ECF No. 1.)

For the reasons set forth below, I conclude that petitioner is not entitled to

compensation.

I. Applicable Statutory Scheme

Under the National Vaccine Injury Compensation Program, compensation

awards are made to individuals who have suffered injuries after receiving vaccines. In

general, to gain an award, a petitioner must make a number of factual demonstrations,

1 When this decision was originally filed the undersigned advised his intent to post it on the United States

Court of Federal Claims' website, and/or at https://www.govinfo.gov/app/collection/uscourts/national/cofc,

in accordance with the E-Government Act of 2002. 44 U.S.C. § 3501 note (2018) (Federal Management

and Promotion of Electronic Government Services). In accordance with Vaccine Rule 18(b), petitioner

filed a timely motion to redact certain information. This decision is being reissued with petitioner’s name

reduced to initials. Except for those changes and this footnote, no other substantive changes have been

made. This decision will be posted on the court’s website with no further opportunity to move for

redaction.

2

All references to “§ 300aa” below refer to the relevant section of the Vaccine Act at 42 U.S.C. § 300aa-

10-34.

1

including showing that an individual received a vaccination covered by the statute;

received it in the United States; suffered a serious, long-standing injury; and has

received no previous award or settlement on account of the injury. Finally – and the key

question in most cases under the Program – the petitioner must also establish a causal

link between the vaccination and the injury. In some cases, the petitioner may simply

demonstrate the occurrence of what has been called a “Table Injury.” That is, it may be

shown that the vaccine recipient suffered an injury of the type enumerated in the

“Vaccine Injury Table,” corresponding to the vaccination in question, within an

applicable time period following the vaccination also specified in the Table. If so, the

Table Injury is presumed to have been caused by the vaccination, and the petitioner is

automatically entitled to compensation, unless it is affirmatively shown that the injury

was caused by some factor other than the vaccination. § 300aa-13(a)(1)(A);

§ 300aa-11(c)(1)(C)(i); § 300aa-14(a); § 300aa-13(a)(1)(B).

In many cases, however, the vaccine recipient may have suffered an injury not of

the type covered in the Vaccine Injury Table. In such instances, an alternative means

exists to demonstrate entitlement to a Program award. That is, the petitioner may gain

an award by showing that the recipient’s injury was “caused-in-fact” by the vaccination

in question. § 300aa-13(a)(1)(B); § 300aa-11(c)(1)(C)(ii). In such a situation, of course,

the presumptions available under the Vaccine Injury Table are inoperative. The burden

is on the petitioner to introduce evidence demonstrating that the vaccination actually

caused the injury in question. Althen v. Sec’y of Health & Human Servs., 418 F.3d

1274, 1278 (Fed. Cir. 2005); Hines v. Sec’y of Health & Human Servs., 940 F.2d 1518,

1525 (Fed. Cir. 1991). In this case, petitioner has alleged that the flu vaccine and the

hep B vaccine caused him to suffer Bell’s palsy, hearing loss, and neuropathy. (ECF

No. 1.) Because these conditions are not listed on the Vaccine Injury Table relative to

the flu vaccine or the hep B vaccine, petitioner must establish that his injury was

“caused-in-fact” by his vaccination(s).

The showing of “causation-in-fact” must satisfy the “preponderance of the

evidence” standard, the same standard ordinarily used in tort litigation.

§ 300aa-13(a)(1)(A); see also Althen, 418 F.3d at 1279; Hines, 940 F.2d at 1525.

Under that standard, the petitioner must show that it is “more probable than not” that the

vaccination was the cause of the injury. Althen, 418 F.3d at 1279. The petitioner need

not show that the vaccination was the sole cause but must demonstrate that the

vaccination was at least a “substantial factor” in causing the condition, and was a “but

for” cause. Shyface v. Sec’y of Health & Human Servs., 165 F.3d 1344, 1352 (Fed. Cir.

1999). Thus, the petitioner must supply “proof of a logical sequence of cause and effect

showing that the vaccination was the reason for the injury[,]” with the logical sequence

being supported by “reputable medical or scientific explanation, i.e., evidence in the

form of scientific studies or expert medical testimony.” Althen, 418 F.3d at 1278; Grant

v. Sec’y of Health & Human Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992). A petitioner

may not receive a Vaccine Program award based solely on his or her assertions; rather,

the petition must be supported by either medical records or by the opinion of a

competent physician. § 300aa-13(a)(1).

2

In what has become the predominant framing of this burden of proof, the Althen

court described the “causation-in-fact” standard, as follows:

Concisely stated, Althen’s burden is to show by preponderant evidence that

the vaccination brought about her injury by providing: (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 proximate temporal relationship between

vaccination and injury. If Althen satisfies this burden, she is “entitled to

recover unless the [government] shows, also by a preponderance of the

evidence, that the injury was in fact caused by factors unrelated to the

vaccine.”

Althen, 418 F.3d at 1278 (citations omitted). The Althen court noted that a petitioner

need not necessarily supply evidence from medical literature supporting petitioner’s

causation contention, so long as the petitioner supplies the medical opinion of an

expert. Id. at 1279-80. The court indicated that, in finding causation, a Program fact-

finder may rely upon “circumstantial evidence,” which the court found to be consistent

with the “system created by Congress, in which close calls regarding causation are

resolved in favor of injured claimants.” Id. at 1280.

As with a Table Injury, respondent may ultimately prove petitioner’s injury to be

due to a factor unrelated to vaccination even if petitioner meets his initial burden of

proof. § 300aa-13(a)(1)(B). Respondent bears the burden of demonstrating the

presence of any alternative cause by preponderant evidence only if petitioner satisfies

his prima facie burden. § 300aa-13(a)(1)(B); Walther v. Sec’y of Health & Human

Servs., 485 F.3d 1146, 1150 (Fed. Cir. 2007). However, respondent may also present

evidence relating to an alternative cause to demonstrate the inadequacy of petitioner’s

evidence supporting his case in chief. Nonetheless, petitioner does not bear the burden

of eliminating alternative causes where the other evidence on causation is sufficient to

establish a prima facie case under Althen. de Bazan v. Sec’y of Health & Human

Servs., 539 F.3d 1347, 1352-53 (Fed. Cir. 2008); Walther, 485 F.3d at 1150.

II. Procedural History

Initially, this case was assigned to Special Master Christian Moran. (ECF No. 4.)

Petitioner filed medical records, an affidavit, and a statement of completion, in

December of 2018. (ECF Nos. 9-10; Exs. 1-3.) Petitioner later filed an additional

affidavit on in January of 2019. (ECF No. 13; Ex. 4.) The case was reassigned to the

undersigned on August 27, 2019, while still awaiting respondent’s medical review.

(ECF Nos. 22-24.) Thereafter, petitioner filed additional evidence, including an

immunization authorization form and additional medical records. (ECF Nos. 28, 32;

Exs. 5-6.) Petitioner filed an expert report and supporting medical literature on April 20,

2020. (ECF No. 33; Exs. 7-62.)

3

Respondent filed his Rule 4(c) Report, as well as his own expert report and

supporting medical literature, on September 29, 2020. (ECF Nos. 38-40; Exs. A

through A, Tab 4.) Respondent contended that this case is not appropriate for

compensation both because “the report provided by [petitioner’s expert] fails to meet

petitioner’s burden to demonstrate vaccine causation” and “petitioner’s diabetes alone,

is more likely than not the cause of the Bell’s palsy.” (ECF No. 38, pp. 2, 13, 14.)

Petitioner filed a responsive expert report and supporting medical literature on March

11, 2021. (ECF No. 45; Exs. 63-68.) Respondent filed a supplemental expert report on

July 29, 2021. (ECF No. 49; Ex. C.) After receiving preliminary guidance pursuant to

Vaccine Rule 5 (see ECF No. 50), petitioner filed a further expert report and supporting

medical literature in January of 2022. (ECF No. 52; Exs. 69-70.)

A one-day fact hearing was held remotely on August 25, 2022. (See ECF No.

57; Transcript of Proceedings (“Tr”), filed Sept. 19. 2022, at ECF No. 60.) Thereafter,

both parties agreed that the record should be closed. (ECF No. 62.) Petitioner filed a

Motion for Ruling on the Record on December 23, 2022. (ECF No. 64.) Respondent

responded on January 30, 2023, and additionally requested that petitioner file Walmart

pharmacy records. (ECF No. 65, p. 4, n.6.) Petitioner filed a reply and a record from

Walmart certifying that there were no additional records to be filed. (ECF Nos. 66-67;

Ex. 71.)

Petitioner argues that he was correctly diagnosed as suffering Bell’s palsy and

that he has demonstrated each of the three Althen prongs by preponderant evidence,

thereby proving his Bell’s palsy to have been caused by his flu and/or hep B vaccines.

(ECF No. 64, pp. 6-10.) Petitioner asserts that respondent has failed to present reliable

evidence explaining petitioner’s condition and that no other antecedent events are

evidenced to explain petitioner’s Bell’s palsy. (Id. at 11.) Respondent disputes that

petitioner has satisfied any of the three Althen prongs. (ECF No. 65, pp. 19-33.)

Respondent contends that the burden of proof did not shift to respondent in this case;

however, respondent stresses in the context of Althen prong two that petitioner’s

uncontrolled diabetes is the likely cause of petitioner’s Bell’s palsy. (Id. at 30-32.) In

reply, petitioner contends that respondent’s expert did not actually challenge petitioner’s

expert on any of the details of his opinion relative to the requirements of Althen, but

instead only offered petitioner’s diabetes as an alternative cause of his condition. (ECF

No. 66.)

This case is now ripe for resolution. I have concluded that the parties have had a

full and fair opportunity to develop the record and that it is appropriate to resolve this

case without an entitlement hearing. See Kreizenbeck v. Sec’y of Health & Human

Servs., 945 F.3d 1362, 1366 (Fed. Cir. 2020) (citing Simanski v. Sec’y of Health &

Human Servs., 671 F.3d 1368, 1385 (Fed. Cir. 2012); Jay v. Sec’y of Health & Human

Servs., 998 F.2d 979, 983 (Fed. Cir. 1993)); see also Vaccine Rule 8(d); Vaccine Rule

3(b)(2).

4

III. Factual History

a. As reflected in the medical records

i. Pre-vaccination

Petitioner was diagnosed with type 2 diabetes prior to 2014. (Tr. 8-9, 35.) The

medical records reflect that, throughout 2014, petitioner’s diabetes was uncontrolled

and, as a result, he suffered several injuries, including osteomyelitis in his right toe,

diabetic peripheral vascular disease, peripheral neuropathy, hypertension, benign

hyperkeratotic lesions, and diabetic retinopathy. (Ex. 2, pp. 6-153, 735-60, 813-19.)

After petitioner’s appointment on August 19, 2014, there is a significant gap in

treatment until August 22, 2017, when he saw optometrist Dr. Haleh Shafa. (Ex. 2, pp.

136-53, 157-84.) During these three years, petitioner was taking “Insulin 70/30 25 units

in the mornings and 17 units in the evenings.” (Id. at 162.) At this appointment,

petitioner’s glucose was 134 mg/dL (reference range 70-140 mg/dL) and his

hemoglobin A1C was high at 11.0% (reference range 4.8-5.6%). (Id. at 169-76.)

Additionally, petitioner’s cholesterol was high at 239 mg/dL (reference range 0-199

mg/dL). (Id. at 172, 766.) During this appointment, petitioner received a pneumococcal

vaccination, as well as the first dose of a three-part hep B vaccine series. (Id. at 161,

182.) Additionally, at this appointment, petitioner underwent retinal imaging screening

for diabetic retinopathy, which found minimal diabetic retinopathy in petitioner’s right

eye. (Id. at 168-69.)

Petitioner’s next appointment was on September 14, 2017, where he was seen

by podiatrist Dr. Lisa B. Michaels. (Ex. 2, pp. 188-99.) During this appointment,

petitioner’s chief complaint was “an open lesion” on his left foot, and it was noted that

petitioner had a history of “peripheral neuropathy.” (Id. at 189.) Dr. Michaels recorded

a history of “uncontrolled” type 2 diabetes and diagnosed petitioner with a “diabetic

neuropathic ulceration.” (Id. at 189, 191.) During this appointment, Dr. Michaels

performed a selective wound debridement and removed the devitalized tissue from

petitioner’s foot. (Id. at 191.) This tissue was tested, and the results revealed a

staphylococcus infection. (Id. at 194-95, 770.) Additionally, petitioner underwent an x-

ray of this foot, which found “no fracture dislocation or osseous destruction.” (Id. at 193,

819.) At this appointment, petitioner’s glucose was high at 213 mg/dL (reference range

70-140 mg/dL). (Id. at 194, 773.) Additionally, petitioner’s urine contained high levels of

microalbumin at 47.3 mg/dL (reference range 0.0-2.0 mg/dL) and albumin at 201.5

mg/gm (reference range 0.0-30.0 mg/gm). (Id. at 771.)

On September 15, 2017, petitioner returned to Dr. Shafa for a diabetic eye exam.

(Ex. 2, pp. 203-14.) During this appointment, petitioner was diagnosed with bilateral

moderate nonproliferative retinopathy, as well as amblyopia and low visual impairment

of the left eye. (Id. at 211.)

5

ii. Vaccination and subsequent course

On September 19, 2017, petitioner saw Dr. Delphanie D. Head for a routine

follow up. (Ex. 2, pp. 218-38.) During this appointment, petitioner received the flu and

hep B vaccines that are at issue in this case. (Id. at 224-26, 236; Ex. 5, p. 6.) Petitioner

underwent a right upper quadrant ultrasound during this appointment, which found no

abnormalities. (Ex. 2, p. 225.) Petitioner’s glucose was high at 216 mg/dL (reference

range 70-140 mg/dL), his microalbumin was high at 45.3 mg/dL (reference range 0.0-

2.0 mg/dL), and his albumin was high at 251.5 (reference range 0.0-30.0 mg/gm). (Id.

at 226-28, 774, 781.) Petitioner also had a liver function test, which revealed that

petitioner’s ALT was high at 95 IU/L (reference range of 9-33 IU/L) and his AST was

high at 90 IU/L (reference range 12-41 IU/L). (Id. at 228, 779-80.)

Petitioner saw Dr. Rae A. King on September 26, 2017, for an eye exam. (Ex. 2,

pp. 242-52.) Dr. King noted that petitioner’s diagnoses included mild diabetic

retinopathy, childhood left eye trauma, left eye aphakia, and a cataract in his right eye.

(Id. at 247.) On September 29, 2017, petitioner underwent an ultrasound of his right

upper quadrant that was determined to be unremarkable. (Id. at 820-21.) Petitioner

returned to Dr. Michaels on October 3, 2017, for a follow up appointment for the ulcer

on his left foot. (Id. at 256-62.) During this appointment, petitioner underwent another

selective wound debridement to remove devitalized tissue on his left foot. (Id. at 259.)

On October 14, 2017, petitioner presented to urgent care with complaints of

facial droop on the right side; however, the physician observed that petitioner’s facial

droop was on the left, rather than the right. (Ex. 2, pp. 266-88, 733-34.) Patient

underwent an electrocardiogram (“EKG”), which was normal; a computed tomography

(“CT”) scan, which was unremarkable; and a magnetic resonance imaging (“MRI”),

which showed no acute ischemic event, no enhancing intracranial mass, and mild non-

enhancing white matter disease of the brain. (Id. at 270-73, 822-24.) At this

appointment, petitioner’s glucose was high at 129 mg/dL (reference range 70-99 mg/dL)

and his ALT and AST were high at 82 IU/L (reference range 9-33 IU/L) and 77 IU/L

(reference range 12-41 IU/L), respectively. (Id. at 271-72, 782, 784.) Petitioner’s

differential diagnosis at this appointment was between a cerebrovascular accident,

transient ischemic attack, Bell’s palsy, and electrolyte abnormalities. (Id. at 269.)

Petitioner was prescribed 20 mg of prednisone and 400 mg of acyclovir. (Id. at 268.)

Petitioner saw Dr. Head on October 17, 2017, for a follow up evaluation for Bell’s

palsy. (Ex. 2, pp. 292-306.) Petitioner described his symptoms as including light

sensitivity in his left eye, an inability to close/bling his left eye, and a protrusion of the

left eye, as well as slurred speech and twitching/paralysis of the left side of the face.

(Id. at 293.) Dr. Head decreased petitioner’s dosage of prednisone to 10 mg. (Id. at

297.) During this appointment, petitioner’s glucose was high at 155 mg/dL (reference

range 70-140 mg/dL) and his hemoglobin A1C was high at 8.90% (reference range =>

6.99%). (Id. at 300-02, 786-89.)

6

On October 24, 2017, petitioner had a follow up appointment with his

ophthalmologist, Dr. King. (Ex. 2, pp. 320-29.) Dr. King noted that petitioner was

experiencing left eye foreign bodies, redness, pain, and light sensitivity with some

tearing. (Id. at 321.) Petitioner saw his podiatrist, Dr. Michaels, on October 31, 2017,

for a follow up regarding the ulcer on his left foot. (Id. at 333-40.) Petitioner underwent

another selective wound debridement to remove devitalized tissue on his foot. (Id. at

336.)

On November 2, 2017, petitioner saw Dr. Shafa for a follow up regarding his eye

pain. (Ex. 2, pp. 344-54.) He reported feeling a foreign body sensation and upper lid

swelling. (Id. at 345.) Dr. Shafa noted that petitioner had been diagnosed with Bell’s

palsy in his left eye and has been unable to fully close his left eye. (Id.) Petitioner’s left

eye exam revealed a “capped glands upper lid, swollen lid, internal chalazion,” an

exposed cornea when blinking, a scar over his cornea, lens fragments attached to iris,

vitreous syneresis, and hazy view. (Id. at 348-49.) Petitioner saw Dr. Shafa again on

November 9, 2017, for a “follow up on chalazion.” (Id. at 359.) Dr. Shafa again noted

that petitioner had recently been diagnosed with Bell’s palsy in his left eye. (Id.) At this

encounter, petitioner was assessed as suffering from Bell’s palsy with exposure

keratopathy in his left eye. (Id. at 362-63.) He was instructed to continue using Systane

drops and Genteal nighttime ointment. (Id.)

Petitioner began seeing neurologist Dr. Joseph A. Wapenski on November 13,

2017, “for left facial paralysis” and Bell’s palsy. (Ex. 2, pp. 371-78.) Dr. Wapenski notes

that petitioner’s facial paralysis began on October 14, 2017. (Id. at 371.) He describes

petitioner’s paralysis as “moderate” with “some drooling left corner of mouth and left eye

irritation and altered taste.” (Id.) He noted that petitioner underwent a CT scan, which

was normal, and an MRI, which showed small vessel white matter disease. (Id. at 371-

72.) Dr. Wapenski acknowledged the fact of petitioner’s flu and hep B vaccinations on

September 19, 2017, but also noted petitioner’s history of uncontrolled diabetes. (Id.)

He noted that petitioner was treated with prednisone and acyclovir. (Id. at 371.)

Petitioner reported experiencing temporary paresthesia and weakness of his left leg, as

well as elevated glucose levels after starting steroids. (Id. at 372.) During petitioner’s

examination, Dr. Wapenski noted that petitioner’s face showed “asymmetry with

weakness of the face drooling left corner of mouth,” and that petitioner could “voluntarily

close and cover entire left eye with eyelid.” (Id. at 375.) Petitioner was assessed as

having left-side Bell’s palsy and a resolved transient lower left leg radiculopathy. (Id.)

On November 14, 2017, petitioner saw Dr. Michaels for another follow up for the

ulcer on his left foot. (Id. at 382-88.) At this appointment, petitioner’s diagnosis was

ulcer of the left toe and type 2 diabetes with neurological manifestation. (Id. at 385.)

Petitioner underwent another selective wound debridement and the devitalized tissue

was removed. (Id.)

On November 17, 2017, petitioner began seeing an acupuncturist to treat his

Bell’s palsy. (Ex. 3, p. 1.) The acupuncturist noted that petitioner reported symptoms “2

weeks after flu shot” and noted that petitioner experienced light sensitivity and dry eyes.

7

(Id.) The acupuncturist recommended attending appointments two times a week for

four weeks. (Id.) Petitioner thereafter attended additional acupuncture appointments on

November 18, November 20, and December 11, 2017. (Id. at 1-2.)

Petitioner had another follow up appointment with Dr. Michaels on November 28,

2017. (Ex. 2, pp. 392-98.) Petitioner underwent another selective wound debridement

to remove devitalized tissue. (Id. at 394-95.) Petitioner’s primary care physician, Dr.

Head, saw him for a routine follow up the next day on November 29, 2017. (Id. at 402-

17.) At this appointment, petitioner’s glucose was within the normal range at 124 mg/dL

(reference range 70-140 mg/dL); however, his hemoglobin A1C was high at 9.30%

(reference range <=6.99%). (Id. at 410-11, 790-91.) Dr. Head directed petitioner to

follow up with his neurologist and ophthalmologist for his left Bell’s palsy. (Id. at 407.)

Petitioner followed up with his optometrist, Dr. Shafa, on December 7, 2017, for

his keratitis and Bell’s palsy. (Ex. 2, pp. 421-32.) Dr. Shafa instructed petitioner to

continue using Systane drops and Genteal nighttime ointment. (Id. at 427.)

Additionally, Dr. Shafa noted that petitioner was experiencing “mild iritis” in his left eye,

and she was unsure of whether it was related to his Bell’s palsy. (Id.) Petitioner was

prescribed Pred Forte eye drops. (Id.) On December 12, 2017, petitioner saw Dr.

Michaels for another follow up regarding the ulcer on his left foot. (Id. at 436-41.) At

this appointment, Dr. Michaels determined that petitioner’s ulcer was healed. (Id. at

438.)

On January 5, 2018, petitioner continued his care with Dr. Shafa. (Ex. 2, pp.

445-56.) Dr. Shafa noted that petitioner’s iritis had resolved, but continued to

recommend petitioner use Systane drops and Genteal nighttime ointment to treat Bell’s

palsy. (Id. at 451.) Petitioner’s left eye exam revealed an exposed cornea, a scar

across the cornea, lens fragments, and a hazy view. (Id. at 449-50.)

Petitioner saw his neurologist, Dr. Wapenski, on January 8, 2018 for another

follow up regarding his Bell’s palsy. (Ex. 2, pp. 460-66.) Dr. Wapenski described

petitioner’s “mild left face residua” as “much better,” and noted that he continued to

suffer from “left eye exposure keratitis.” (Id. at 461.) Dr. Wapenski’s impression

described petitioner’s condition as “Neuropathy diabetic,” “Resolving Bell’s Left,” and

“Old left eye injury.” (Id. at 462.) Additionally, petitioner noted distorted hearing in his

left ear. (Id.) On January 10, 2018, petitioner saw Dr. Head for a routine follow up. (Id.

at 470-85.) At this appointment, petitioner’s hemoglobin A1C was high at 8.80%

(reference range <=6.99%), and his ALT and AST were high at 49 IU/L (reference range

9-33 IU/L) and 51 IU/L (reference range 12-41 IU/L), respectively. (Id. at 476-77, 794,

796-97.) Petitioner saw Dr. Michaels on January 29, 2018, for a follow up regarding the

ulcer on his left foot. (Id. at 489-95.) Petitioner’s ulcer remained healed. (Id. at 492.)

On February 5, 2018, petitioner saw Dr. Wapenski again. (Ex. 2, pp. 496-508.)

Dr. Wapenski noted that petitioner’s Bell’s palsy “is showing very good recovery” and

“[h]e can almost completely cover his left eye.” (Id. at 500.) Petitioner was still

8

experiencing “mild weakness of the left face,” “left ear hearing distortion,” and

“paresthesia of the chest,” left abdomen, and left leg. (Id.)

Petitioner saw his primary care physician on February 12, 2018, for a routine

follow up. (Ex. 2, pp. 512-23.) During this visit, petitioner’s glucose was high at 194

mg/dL (reference range 70-140 mg/dL), and his hemoglobin A1C was high at 8.80%

(reference range <=6.99%). (Id. at 517-19, 798-99.)

On February 16, 2018, petitioner saw Dr. Dennis L. Frew regarding “hearing

issues in [his] left ear.” (Ex. 2, pp. 527-32.) Dr. Frew noted that petitioner “presents for

left sided Bell’s palsy with onset October 2017 and treated with steroids and has a past

medical history of [uncontrolled type 2 diabetes, hypertension, hyperlipidemia, left

aphakia, left Bell’s palsy, and left eye trauma].” (Id. at 527-28.) Petitioner underwent a

CT, which came back as normal. (Id. at 529-30, 825-26.) Roughly three weeks later,

on March 8, 2018, petitioner saw Dr. Frew again for a follow up on his audio exams.

(Id. at 536-44.) Dr. Frew noted that petitioner had “left moderate sensorineural hearing

loss.” (Id. at 536.) Thereafter, petitioner underwent a brain MRI that revealed “[n]o

significant abnormality . . . in either facial nerve,” and “[n]o areas of abnormal

enhancement in either IAC.” (Id. at 540, 827-28.)

On March 12, 2018, petitioner had an appointment with ophthalmologist Dr.

Seongmu Lee for an eyelid evaluation. (Ex. 2, pp. 548-58.) Dr. Lee found that

petitioner’s facial function was improving and recommended “aggressive ocular surface

lubrication.” (Id. at 554.) Additionally, Dr. Lee discussed implanting gold weights or

tarsorrhaphy surgery to close petitioner’s eyelid if his symptoms got worse. (Id.)

Petitioner had a follow up appointment with Dr. Michaels for the ulcer on his left foot.

(Id. at 562-69.) Dr. Michaels noted that petitioner’s ulcer remained healed. (Id. at 563.)

On April 3, 2018, petitioner had a follow up appointment with Dr. Head. (Ex. 2,

pp. 573-86.) Petitioner’s glucose was slightly elevated at 144 mg/dL (reference range

70-140 mg/dL), his hemoglobin A1C was high at 8.80% (reference range <=6.99%), his

cholesterol was high at 206 mg/dL (reference range 0-199 mg/dL), and his ALT and

AST were high at 45 IU/L (reference range 9-33 IU/L) and 55 IU/L (reference range 12-

41 IU/L), respectively. (Id. at 579-82, 803-10.) On April 16, 2018, petitioner presented

to Dr. Michaels for a follow up regarding the ulcer on his left foot. (Id. at 590-97.) There

were no significant changes during this appointment. (Id.)

On May 21, 2018, petitioner had a follow up appointment with Dr. Lee regarding

his eyelid. (Ex. 2, pp. 601-10.) Petitioner reported “dryness and tearing on/off.” (Id. at

602.) Dr. Lee again noted that petitioner should continue “aggressive ocular surface

lubrication,” and discussed the surgical options to help close petitioner’s eyelid. (Id. at

606.) Petitioner “elect[ed] [the] nonsurgical plan.” (Id.) On May 24, 2018, petitioner

had a follow up appointment with his neurologist, Dr. Wapenski, for paresthesia in his

chest and left facial palsy. (Id. at 614-27.) After reviewing petitioner’s old MRI and CT

scan, Dr. Wapenski ordered an MRI of petitioner’s neck, as well as an electromyogram

and nerve conduction study (EMG/NCV) to documents neuropathy in petitioner’s left

9

extremities. (Id. at 619-27.) On June 15, 2018, petitioner underwent an MRI of the

cervical spine that showed “left paracentral disc protrusion with minimal effacement of

the left ventral aspect of the spinal cord contributing to his mild spinal canal stenosis,”

and “[d]isc osteophyte complexes which appear predominately osteophytic . . .

contributing to mild spinal canal stenosis.” (Id. at 623-25, 829-30.) Petitioner had a

follow up appointment with Dr. Michaels on May 29, 2018, during which it was

determined that the ulcer on his left foot remained healed. (Id. at 631-38.)

Petitioner saw Dr. Frew on June 22, 2018, for a follow up regarding his Bell’s

palsy and hearing loss. (Ex. 2, pp. 642-46.) Petitioner noted that he had “no

improvement from initial exam.” (Id. at 642.) Dr. Frew ordered a repeat audio exam

and requested that petitioner follow up after the exam. (Id.) On June 28, 2018,

petitioner saw Dr. Lee for a follow up regarding his left eye. (Id. at 650-59.) During this

appointment, petitioner’s left eye was “very red and irritated.” (Id. at 651.) Petitioner

reported using Genteal gel, which had been working well until that week. (Id.) Dr. Lee

recommended continuing “aggressive ocular surface lubrication.” (Id. at 656.)

Petitioner was prescribed Maxitrol for his irritation. (Id. at 658.) At his follow up

appointment on July 9, 2018, petitioner reported that his eye was “[n]o longer irritated.”

(Id. at 664.) On July 11, 2018, petitioner underwent an EMG/NCV that showed

“electrophysiological evidence for severe, ongoing and chronic, generalized

polyneuropathy with axonal>demyelinating features,” as well as “a superimposed left S1

radiculopathy and a mild median neuropathy at the left wrist.” (Id. at 676-98.)

On July 20, 2018, petitioner saw an ophthalmologist Dr. Essence C. Bell for a

follow up regarding his glaucoma. (Ex. 2, pp. 702-13.) Petitioner complained of right

eye pain and swelling. (Id. at 703.) Petitioner noted that he had been applying Maxitrol,

which helped. (Id.) Petitioner was diagnosed with an age related cataract and

proliferative retinopathy in his right eye. (Id. at 707.) Petitioner had a follow up

appointment with ophthalmologist Azad Mansouri, M.D., on August 3, 2018, for a

diabetic retinal evaluation. (Id. at 717-29; Ex. 6, pp. 4-20.) Petitioner was diagnosed

with severe nonproliferative diabetic retinopathy. (Ex. 2, p. 723; Ex. 6, p. 14, 46-47.)

Petitioner underwent an intravitreal injection of Avastin into his right eye and cataract

surgery in his left eye. (Ex. 2, p. 724; Ex. 6, pp. 16, 18.) Additionally, petitioner

underwent an ocular coherence tomographic study, which confirmed petitioner’s

diagnosis. (Ex. 6, pp. 24-26.)

On August 19, 2018, petitioner saw Dr. Head for a diabetic screening. (Ex. 6, pp.

29-31.) Petitioner had a follow up appointment with Dr. Lee on August 20, 2018. (Id. at

34-36.) Petitioner had another appointment with Dr. Lee on October 8, 2018. (Id. at 83-

98.) Petitioner reported feeling a foreign object sensation and dryness in his left eye.

(Id. at 85.) Dr. Lee recommended petitioner “continue aggressive ocular surface

lubrication.” (Id. at 89.)

Petitioner began participating in a diabetes and hypertension panel management

program on October 15, 2018. (Ex 6, pp. 107-10.) At that time, petitioner was overdue

10

for a hemoglobin A1C test, a foot exam, flu and hep B immunizations, and a

microalbumin test. (Id. at 109.)

On November 12, 2018, petitioner followed up with Dr. Lee regarding his Bell’s

palsy. (Ex. 6, pp. 129-44.) Petitioner reported that he noticed numbness and tightness

in his face. (Id. at 131.) There were no significant changes during this appointment.

(Id. at 127-44.) Petitioner had a follow up neurology appointment with Dr. Sonal R.

Hazariwala on November 15, 2018. (Id. at 159-79.) Dr. Hazariwala noted that

petitioner had previously been diagnosed and treated for facial tingling and paresthesias

and has since developed “numbness along the inside of the jaw/cheek.” (Id. at 160.)

During this appointment, petitioner underwent a magnetic resonance angiography

(“MRA”) of his head and neck, which showed no acute intracranial abnormality and no

cervical abnormality; however, there was evidence of an intracranial aneurysm. (Id. at

170.) Dr. Hazariwala diagnosed petitioner with “[l]eft facial numbness” of “unclear

etiology.” (Id. at 167.) He noted that, although petitioner’s tightness may be related to

his Bell’s palsy, the “numbness is concerning.” (Id.) Additionally, he discussed

petitioner’s EMG/NCS results and diagnosed petitioner with polyneuropathy. (Id.)

Petitioner’s labs during this appointment showed high microalbumin at 46.0 mg/dL

(reference range 0.0-2.0 mg/dL) and high albumin at 384.9 mg/gm (reference range 0.0-

30.0 mg/gm). (Id. at 189.)

On February 11, 2019, petitioner called to schedule a podiatry appointment

regarding a potential ulcer on his left foot. (Ex. 6, pp. 290-92.) He saw Dr. Michaels on

February 12, 2019, who confirmed that petitioner had an ulcer on his left foot. (Id. at

308-11.) During this appointment, petitioner underwent an x-ray that showed no

evidence of osteomyelitis and an excisional wound debridement. (Id. at 311-15, 328-

29.) At this appointment, petitioner’s hemoglobin A1C was high at 10.3% (reference

range <=7.0%). (Id. at 341-42.) On March 5, 2019, petitioner called his doctor’s office

and noted that he had an allergic reaction to medication. (Id. at 374-81.) Petitioner saw

Dr. Michaels the next day to address these side effects. (Id. at 385-96.) During this

appointment, petitioner underwent a selective wound debridement. (Id. at 389.)

Petitioner’s labs showed that his red blood cell count was low at 3.92 10*6 uL (reference

range 4.06-5.69 10*6 uL), his HGB was low at 11.6 g/dL (reference range 13.0-17.0

g/dL), and his hematocrit was low at 35.9% (reference range 38.8-50.0%). (Id. at 420.)

Based on these labs, petitioner’s doctor expressed concern that he was developing an

infection. (Id. at 406.) Petitioner underwent an MRI of his foot that found no evidence

of osteomyelitis or abscess; however, it did find cellulitis. (Id. at 426-27, 436-38.)

Petitioner saw Dr. Michaels for another follow up appointment on March 15, 2019. (Id.

at 464-73.) Dr. Michaels noted that petitioner’s ulcer had healed. (Id. at 467.)

Petitioner had two more follow up appointments regarding his foot: one on March 22,

2019, and the other on March 29, 2019. (Id. at 502-11, 525-34.) Petitioner’s foot

remained healed. (Id.)

b. As reflected in petitioner’s testimony

In addition to submitting two written statements, petitioner testified at a fact

hearing on August 25, 2022. (ECF Nos. 59-60; Exs. 1, 4.) He noted that prior to

11

September 2017, he had never experienced facial paralysis. (Tr. 8.) Though he

experienced a gap in treatment from 2014 to 2017, he explained that prior to his

vaccination, he had been seeking treatment for diabetes and peripheral neuropathy and

saw a doctor regularly. (Id. at 9, 34.) Additionally, petitioner testified that he injured his

left eye when he was six years old. (Id. at 9-10, 52.) This injury has affected his vision

in that eye. (Id. at 10.) Petitioner also had a toe infection, which petitioner claimed was

due to running, but is also a symptom of diabetes. (Id. at 33, 47-48, 53-56.) In 2017,

petitioner was also diagnosed with hypertension. (Id. at 35.)

Petitioner explained that he did not seek treatment from September 2014 through

July of 2017. (Tr. 11.) He was unemployed during those years and he could not afford

to see a doctor. (Id.) During this time, petitioner explained that he managed his

diabetes through diet and exercise and monitored his blood sugar using a monitor and

urinary strips. (Id. at 12, 39-41.) However, when we went to the doctor, his A1C was

still high and noted that his diabetes was not under control until he began seeing a

doctor in 2017. (Id. at 12, 39.)

Petitioner testified that he received the flu and hep B vaccines on September 19,

2017. (Tr. 13.) He testified that he did not notice anything different until around

October 19, 2017, when he “woke up that morning and [his] face was twisted.” (Id. at

13, 50.) He explained that, at that time, he believed he was having a stroke and went to

the emergency room. (Id. at 13.) In the emergency room, petitioner was diagnosed

with Bell’s palsy and was prescribed prednisone and acyclovir. (Id. at 14-15.) However,

his primary care physician decreased his prednisone because it impacted his blood

pressure and blood sugar. (Id.) At this time, petitioner was taking Lisinopril to help with

his blood pressure and kidneys and was only monitoring his glucose levels “to a

degree.” (Id. at 15, 51.)

Petitioner noted that even when he was able to take prednisone and acyclovir, he

was still experiencing symptoms of his Bell’s palsy. (Tr. 15.) He explained that his

symptoms included problems speaking, twisted facial features, light sensitivity, hearing

issues, and a tingling sensation on the left side of his face. (Id. at 16.) Additionally,

petitioner explained that his eye does not close all the way and he often slurs his words

and drools. (Id. at 17.) He noted that his doctor had recommended surgery on his left

eye. (Id.) He explained that the Bell’s palsy primarily impacted the left side of his face.

(Id.) Petitioner also testified that he experienced severe pain in his abdomen which was

diagnosed as a “neuropathy episode.” (Id. at 20.)

Petitioner testified that the last time he sought treatment for his Bell’s palsy was

July 2018. (Tr. 21-22.) He explained that he had not sought treatment since then

because he was functioning well and the pandemic made it more difficult to seek care.

(Id. at 22.) He testified that he wanted to follow up with a neurologist but the soonest

appointment was for February 2023. (Id.) He explained that he continued to do facial

exercises, use ointment on his eye, and massage his face. (Id. at 23.)

12

Petitioner testified that his current symptoms include tearing, facial twitching,

sensitivity to sunlight, hearing issues, and drooling. (Tr. 23.) Petitioner testified that he

has to wear sunglasses when he is outside due to his eye sensitivity and goggles in the

shower because he cannot close his eye all the way. (Id. 19-20.) He explained that his

ophthalmologist recommended surgery options to help him close his eye. (Id. at 21.)

Additionally, he testified to how his condition has impacted him psychologically. He

explained that his confidence is low and that it has impacted his personal life as a

mentor through his church. (Id. at 23-24, 27-29.)

Petitioner testified that he discussed the possible causes of his Bell’s palsy with

his treating physicians. (Tr. 25.) He noted that none of his doctors “said exactly what

caused it;” however, he describes three times that his doctors mentioned potential

causes. (Id.) First, he described how the doctors in the emergency room asked if

petitioner had been out of the country or “around any viruses or anyone with a virus.”

(Id.) He explained that he told the doctor that he had not been out of the country, but

had been vaccinated and the doctor had said it was possible those vaccinations could

have caused his Bell’s palsy. (Id.) Second, he described how his first neurologist

explained to him that the type of vaccine he had received was associated with Bell’s

palsy. (Id.) And finally, his second neurologist told him that Bell’s palsy is usually

caused by a virus and tested him for HIV, which came back negative. (Id. at 25-26.) He

noted that his doctors never told him that his diabetes could have caused his Bell’s

palsy. (Id. at 26-27.)

IV. Expert Opinions

a. Petitioner’s Expert, Dr. M. Eric Gershwin, M.D.3

Petitioner’s expert, Dr. M. Eric Gershwin, submitted three expert reports in this

case. (Exs. 7, 63, 69.) In his first report, Dr. Gershwin begins by noting that the

molecular mechanisms of Bell’s palsy “have not been dissected.” (Ex. 7, p. 2.) He goes

on to explain the current state of the mechanistic research and notes that “[t]he

mechanism of Bell’s palsy is thought to be due to an abnormal immune response and

likely has more than [one] mechanism.” (Id. at 5.) One such mechanism, which

according to Dr. Gershwin is most relevant to this case, is a “T cell mediated

inflammatory process, including a localized inflammatory reaction within the facial

nerve.” (Id.) In support of this conclusion, Dr. Gershwin cites two studies that

determined that:

3 Dr. Gershwin received his medical degree from Stanford University. (Ex. 62, p. 1.) He is board certified

in Internal Medicine, Internal Medicine with a subspeciality of Rheumatology, and Allergy and Clinical

Immunology. (Id. at 2.) He is currently a Professor of Medicine in the Division of Rheumatology/Allergy

and Clinical Immunology and Director of the Allergy-Clinical Immunology Program at the University of

California School of Medicine in Davis, California. (Id. at 1.) He has written 69 books and monographs,

938 experimental papers, and 208 book chapters, and he has participated in 38 guest editorials and book

reviews. (Id. at 8-125.)

13

[H]istologic changes in the facial nerve can be summarized as follows: 1)

The nerve was infiltrated by small, round inflammatory cells from the internal

acoustic meatus to the stylomastoid foramen. 2) There was a breakdown

of the neuron myelin sheaths that involved the macrophages. 3) There was

an increase in the spaces between the neurons, which was interpreted as

edema. 4) The bony fallopian canal was normal, and there was no sign of

facial nerve compression by the bone of the fallopian canal. The small

round cells of lymphocytic nature and the breakdown of myelin sheaths

probably are the histologic expression of an autoimmune response.

(Id. (quoting A. Greco et al., Bell’s Palsy and Autoimmunity, 12 AUTOIMMUNITY REVS.

323, 325 (2012) (Ex. 38, p. 3) (discus Stephen L. Liston & M. Stephen Kleid,

Histopathology of Bell’s Palsy, 99 LARYNGOSCOPE 23, 24 (1989) (Ex. 39, p. 3))).)

Dr. Gershwin cites several studies that suggest “[a] cell-mediated autoimmune

mechanism has been suggested as the pathogenesis of Bell’s palsy.” (Ex. 7, p. 5 (citing

O. Abramsky et al., Cellular Immune Response to Peripheral Nerve Basic Protein in

Idiopathic Facial Paralysis (Bell’s Palsy), 26 J. NEUROLOGICAL SCIS. 13 (1975) (Ex. 40);

Francis H. McGovern et al., Immunological Concept for Bell’s Palsy: Further

Experimental Study, 86 ANNALS OTOLOGY RHINOLOGY & LARYNGOLOGY 300 (1977) (Ex.

41); P. S. J. Z. Mulkens et al., Acute Facial Paralysis: A Virological Study, 5 CLINICAL

OTOLARYNGOLOGY 303 (1980) (Ex. 42)).) Specifically, Dr. Gershwin notes that a clinical

study found “some alterations in the lymphocyte subsets of the peripheral blood during

the acute stage of” Bell’s palsy. (Id. (citing Aharon Aviel et al., Peripheral Blood T and B

Lymphocyte Subpopulations in Bell’s Palsy, 92 ANNALS OTOLOGY RHINOLOGY &

LARYNGOLOGY 187 (1983) (Ex. 43)).) Yet another study found “cellular and humoral

immunologic alterations” in patients with Bell’s palsy. (Id. (citing M. Mañós-Pujol et al.,

Cellular Immunity Abnormalities in Patients with Recurrent Bell’s Palsy, 12 CLINICAL

OTOLARYNGOLOGY 283 (1987) (Ex. 44)).) Additionally, Dr. Gershwin notes that

“[d]ecreased percentages of total T cells (CD3) and T helper/inducer cells (CD4) have

been documented in the acute phase of disease compared with control patients.” (Id.

(citing Clara Gorodezky et al., The HLA System and T-Cell Subsets in Bell’s Palsy, 111

ACTA OTO-LARYNGOLOGICA (STOCKHOLM) 1070 (1991) (Ex. 45)).)

Dr. Gershwin also notes that there is an association between facial paralysis and

Guillain-Barré syndrome (GBS), a “cell mediated, autoimmune neuritis,” which

continues to support the theory that the mechanism that causes Bell’s palsy is immune

mediated. (Ex. 7, p. 6 (citing Donald I. Charous & Bruce I. Saxe, The Landry-Guillain-

Barré Syndrome, 267 NEW ENG. J. MED. 1334 (1962) (Ex. 46); Oded Abramsky et al.,

Cell-Mediated Immunity to Neural Antigens in Idiopathic Polyneuritis and

Myeloradiculitis: Clinical-Immunologic Classification of Several Autoimmune

Demyelinating Disorders, 25 NEUROLOGY 1154 (1975) (Ex. 47)).) Dr. Gershwin explains

that patients with Bell’s palsy and GBS have been shown to respond to a human basic

protein (P1L) of peripheral nerve myelin. (Id. (citing Abramsky et al., supra, at Ex. 40;

Christian A. Vedeler et al., Antibodies to Peripheral Nerve Tissue in Sera from Patients

with Acute Guillain-Barré Syndrome Demonstrated by a Mixed Haemagglutination

14

Technique, 2 J. NEUROIMMUNOLOGY 209 (1982) (Ex. 48)).) Additionally, Dr. Gershwin

notes that patients with Bell’s palsy and GBS had decreased T lymphocytes, specifically

T suppressor cells. (Id. (citing Christian A. Vedeler et al., Immunoglobulins,

Complement Components and Lymphocyte Subpopulations in Bell’s Palsy, 25 EUR.

NEUROLOGY 177 (1986) (Ex. 49); H. Nyland & A. Næss, Lymphocyte Subpopulations in

Blood and Cerebrospinal Fluid from Patients with Acute Guillain-Barré Syndrome, 17

EUR. NEUROLOGY 247 (1978) (Ex. 50); R. A. C. Hughes et al., Lymphocyte

Subpopulations and Suppressor Cell Activity in Acute Polyradiculoneuritis (Guillain-

Barré Syndrome), 51 CLINICAL EXPERIMENTAL IMMUNOLOGY 448 (1983) (Ex. 51); Aviel et

al., supra, at Ex. 43)).) Dr. Gershwin also notes that “similar changes in peripheral

blood lymphocyte subpopulations were also described in the course of several

demyelinating diseases, such as in acute exacerbations of multiple sclerosis and during

the acute stage of [GBS].” (Id. (citing Mulkens et al., supra, at Ex. 42; Nyland & Næss,

supra, at Ex. 50; R. P. Lisak et al., T and B Lymphocytes in Multiple Sclerosis, 22

CLINICAL EXPERIMENTAL IMMUNOLOGY 30 (1975) (Ex. 52)).) Based on these similarities,

Dr. Gershwin concludes that GBS and Bell’s palsy “may share a similar etiology and

pathogenesis,” and even notes that, in some cases, Bell’s palsy is considered “a

mononeuritic variant of [GBS],” or alternatively a polyneuropathy specific to the cranial

nerves. (Id. (citing Aviel et al., supra, at Ex. 43; J. Chaco, Subclinical Peripheral Nerve

Involvement in Unilateral Bell’s Palsy, 52 AM. J. PHYSICAL MED. 195 (1973) (Ex. 53);

Kedar K. Adour et al., The True Nature of Bell’s Palsy: Analysis of 1,000 Consecutive

Patients, 88 LARYNGOSCOPE 787 (1978) (Ex. 12); Leslie P. Weiner et al., Medical

Progress: Viral Infections and Demyelinating Diseases, 288 NEW ENG. J. MED. 1103

(1973) (Ex. 54); Peter W. Lampert, Autoimmune and Virus-Induced Demyelinating

Diseases: A Review, 91 AM. J. PATHOLOGY 176 (1978) (Ex. 55)).) Nonetheless, Dr.

Gershwin acknowledges that “Bell’s palsy is a clinical syndrome, and it is entirely

possible that more than one disease entity can produce an idiopathic facial palsy.” (Id.

at 5.)

In addition to the similarities between Bell’s palsy and GBS, Dr. Gershwin also

relies on the fact that “viruses and immune mechanisms involvement have also been

proposed in Bell’s palsy,” which he notes supports the theory that it is caused by “an

autoimmune postviral disease.” (Ex. 7, p. 6 (citing Abramsky et al., supra, at Ex. 40).)

Dr. Gershwin explains that the mechanism leading to this potential causal association is

not clear. (Id. (citing Aviel et al., supra, at Ex. 43).) However, he then explains some

potential theories that have been considered. (Id. at 6-7.) Specifically, Dr. Gershwin

notes that patients with Bell’s palsy have “elevated concentrations of the cytokines

interleukin-1 (IL-1), IL-6, and tumor necrosis factor-alpha (TNF-alpha),” which,

according to Dr. Gershwin, is evidence of an activation of cell-mediated effectors. (Id. at

6 (citing Mustafa Yilmaz et al., Serum Cytokine Levels in Bell’s Palsy, 197 J.

NEUROLOGICAL SCIS. 69 (2002) (Ex. 57)).) Dr. Gershwin supports this conclusion by

noting that some studies have “proposed that a breakdown of peripheral tolerance

occurred in patients with hepatitis C virus infection as a consequence of interferon

(IFN)-alpha therapy.” (Id. at 6-7 (citing Matthew Hoare et al., Bell’s Palsy Associated

with IFN-α and Ribavirin Therapy for Hepatitis C Virus Infection, 25 J. INTERFERON &

CYTOKINE RSCH. 174 (2005) (Ex. 58)).) Dr. Gershwin suggests these issues exist in the

15

myelin sheath because most patients with Bell’s palsy do recover quickly. (Id. at 7

(citing Abramsky et al., supra, Ex. 40).)

Dr. Gershwin posits that the evidence that Bell’s palsy is cell-mediated and its

association with viruses is also evidence that Bell’s palsy can be caused by vaccines.

(Ex. 7, pp. 2-3, 7.) Specifically, Dr. Gershwin notes that “[i]ntranasal administration of

influenza vaccines may reduce the transmission of influenza more efficiently than

parenteral administration because it stimulates both mucosal and systemic immune

responses.” (Id. at 7 (citing Edel A. McNeela & Kingston H.G. Mills, Manipulating the

Immune System: Humoral Versus Cell-Mediated Immunity, 51 ADVANCED DRUG

DELIVERY REVS. 43 (2001) (Ex. 61)).) In support of this conclusion, Dr. Gershwin

submitted several case studies, reports, and research studies. (Id. at 2-3 (citing

Barbara Rath et al., “All that Palsies is not Bell’s [1]” – The Need to Define Bell’s Palsy

as an Adverse Event Following Immunization, 26 VACCINE 1 (2007) (Ex. 13)

(comprehensive literature review regarding classifying Bell’s palsy as an adverse event

following immunization, which specifically notes that Bell’s palsy has been studied

following various vaccines); 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) (Ex. 15) (case-control study and a case-series analysis finding that there is a

“strong association between the inactivated intranasal influenza vaccine used in

Switzerland and Bell’s palsy,” however, this vaccine is no longer used); 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) (Ex. 16) (study

revealing a “possible association between influenza vaccines and an increased risk of

Bell’s palsy”)).)4

Dr. Gershwin also acknowledges the association between diabetes and Bell’s

palsy. (Ex. 7, pp. 3-4.) He notes that “approximately 5-10% of patients” with Bell’s

palsy also have diabetes. (Id. at 2 (citing Raymond L. Hilsinger, Jr. & Kedar Karim

Adour, Idiopathic Facial Paralysis, Pregnancy, and the Menstrual Cycle, 84 ANNALS OF

OTOLOGY RHINOLOGY & LARYNGOLOGY 433 (1975) (Ex. 8); Mark May & Susan R. Klein,

4 However, Dr. Gershwin acknowledges that some studies have found no association between

vaccination and Bell’s palsy. (Ex. 7, pp. 2-3 (citing Leonoor Wijnans et al., Bell’s Palsy and Influenza

(H1N1)pdm09 Containing Vaccines: A Self-Controlled Case Series, 12 PLOS ONE 1 (2017) (Ex. 20)

(finding “no evidence of increased incidence of Bell’s palsy following seasonal influenza vaccination

overall, nor for monovalent pandemic influenza vaccine in 2009); Ali Rowhani-Rahbar et al., Immunization

and Bell’s Palsy in Children: A Case-Centered Analysis, 175 AM. J. EPIDEMIOLOGY 878 (2012) (Ex. 14)

(finding no association between immunization and Bell’s palsy in children); Sharon K. Greene et al., Near

Real-Time Surveillance for Influenza Vaccine Safety: Proof-of-Concept in the Vaccine Safety Datalink

Project, 171 AM. J. EPIDEMIOLOGY 177 (2010) (Ex. 17) (study looking at several adverse events associated

with vaccination and not finding a statistically significant relationship between seasonal trivalent

inactivated influenza vaccine and Bell’s palsy); Julia Stowe et al., Bell’s Palsy and Parental Inactivate

Influenza Vaccine, 2 HUM. VACCINES 110 (2006) (Ex. 18) (study found “no evidence of an increased risk of

Bell’s palsy in the three months following parenteral inactivated influenza vaccine”). But see Samuel

Shapiro, Invited Commentary: Immunization and Bell’s Palsy in Children, 175 AM. J. EPIDEMIOLOGY 886

(2012) (Ex. 19) (identifying some issues with how the study in Ex. 18 was conducted)).)

16

Differential Diagnosis of Facial Nerve Palsy, 24 OTOLARYNGOLOGIC CLINICS N. AM. 613

(1991) (Ex. 9); Erik Peitersen, The Natural History of Bell’s Palsy, 4 AM. J. OTOLOGY 107

(1982) (Ex. 10); R.E. Mountain et al., The Edinburgh Facial Palsy Clinic: A Review of

Three Years’ Activity, 39 J. ROYAL COLL. SURGEONS EDINBURGH 275 (1994) (Ex. 11);

Adour et al., supra, at Ex. 12).) However, Dr. Gershwin also notes that the magnitude

of the association between diabetes and Bell’s palsy is controversial. (Id. at 3 (citing

Ru-Lan Hsieh et al., Correlates of Degree of Nerve Involvement in Early Bell’s Palsy, 9

BMC NEUROLOGY 1 (2009) (Ex. 21); I.M. Smith et al., Idiopathic Facial (Bell’s) Palsy: A

clinical Survey of Prognostic Factors, 13 CLINICAL OTOLARYNGOLOGY 17 (1988) (Ex. 22);

Luzy Abraham-Inpijn & Pieter P. Devriese, Hypertension and Diabetes Mellitus in Bell’s

Palsy, in DISORDERS OF THE FACIAL NERVE: ANATOMY, DIAGNOSIS, AND MANAGEMENT 251

(Malcomn D. Graham & William F House eds., 1982) (Ex. 23); Akira Takahashi & Itsuro

Sobue, Concurrence of Facial Paralysis and Diabetes Mellitus: Prevalence, Clinical

Features and Prednisolone Treatment, in DIABETIC NEUROPATHY: CLINICAL MANAGEMENT

173 (Aristidis Veves & Rayaz Malik eds., 2nd ed. 1982) (Ex. 24)).) Specifically, he

quotes a paragraph from a study critical of research that found an association between

Bell’s palsy and diabetes because the literature is older and the studies used tests not

common in clinical practice. (Id. at 3-4 (quoting Maria Riga et al., The Role of Diabetes

Mellitus in the Clinical Presentation and Prognosis of Bell Palsy, 25 J AM. BOARD FAM.

MED. 819, 821-24 (2012) (Ex. 25, pp. 3-6)).)

Instead, Dr. Gershwin opines that petitioner’s diabetes merely left petitioner more

susceptible to Bell’s palsy because “diabetics already have some degree of nerve

ischemia.” (Ex. 7, p. 4 (citing Riga et al., supra, at Ex. 25).) Dr. Gershwin opines that

after petitioner received his vaccination, he “develop[ed] immune response as expected

from any vaccination,” and that, “[i]n the absence of any other etiological events that can

be associated with Bell’s palsy, [petitioner] would have a localized T cell mediated

inflammatory response based upon a molecular mimicry with either the influenza or the

hepatitis B vaccine.” (Id. at 7.) He concludes that, instead of causing his Bell’s palsy,

petitioner’s diabetes instead “suggests that his facial nerve was already damaged from

his diabetic neuropathy and therefore any further inflammatory response would

compromise the nerve further.” (Id.)

In his second report, Dr. Gershwin addresses the etiology of Bell’s palsy and

goes into further detail regarding the T cell reaction caused by petitioner’s vaccination

and the temporal association between petitioner’s vaccination and development of Bell’s

palsy. (Ex. 63.) First, Dr. Gershwin notes that the etiology of Bell’s palsy has been

summarized as: (1) anatomical structure, (2) viral infections, (3) ischemia, (4) immune

inflammatory, and (5) acute cold exposure. (Id. at 1 (citing Wenjuan Zhang et al., The

Etiology of Bell’s Palsy: A Review, 267 J. NEUROLOGY 1896 (2020) (Ex. 64)).) He notes

that the authors of that study additionally point out that the clinical and immunological

data “‘suggests activation of cell-mediated effectors and the involvement of immune

mechanisms in Bell’s palsy.’” (Id. (quoting Zhang et al., supra, at Ex. 64, p. 6).)

Additionally, Dr. Gershwin notes that petitioner developed Bell’s palsy “within a month of

vaccination,” which “is consistent with the production of T cell immunity after influenza

vaccination.” (Id. at 2 (citing Tina Schmidt et al., CD4+ T-Cell Immunity After Pandemic

17

Influenza Vaccination Cross-Reacts with Seasonal Antigens and Functionally Differs

from Active Influenza Infection, 42 EUR. J. IMMUNOLOGY 1755 (2012) (Ex. 66) (finding

increases in T cell production up to 10 weeks post-vaccination with influenza); Ulrik

Stervbo et al., Age Dependent Differences in the Kinetics of ỿδ T Cells After Influenza

Vaccination, 12 PLOS ONE 1 (2017) (Ex. 67)).) Dr. Gershwin notes that there is a

similar timeline for an immunological response to the hep B vaccine. (Id. (citing I.

Desombere et al., Characterization of the T Cell Recognition of Hepatitis B Surface

Antigen (HBsAg) by Good and Poor Responders to Hepatitis B Vaccines, 122 CLINICAL

& EXPERIMENTAL IMMUNOLOGY 390 (2000) (Ex. 68)).) Dr. Gershwin acknowledges that

petitioner “has had diabetes for more than a decade;” however, he notes that petitioner

did not develop Bell’s palsy until after he was vaccinated. (Id.) Dr. Gershwin concluded

that “[t]he acute T cell-mediated immunity expected after his seasonal influenza and

second Hepatitis B vaccination was the final insult that led to further ischemic changes

and his development of Bell’s palsy.” (Id.)

In his third report, Dr. Gershwin addresses whether, in his opinion, petitioner’s

Bell’s palsy was a result of his diabetes alone. (Ex. 69.) For this report, Dr. Gershwin

reviewed a study, which found that “‘[a]ll the clinical and immunological data . . .

suggests activation of cell-mediated effectors and the involvement of immune

mechanisms in Bell’s palsy.’” (Id. (quoting Zhang et al., supra, at Ex. 64, p. 6).)

Additionally, Dr. Gershwin notes that “[n]ot all studies have demonstrated an association

of diabetes and Bell’s palsy,” and “[t]he relationship between Bell’s [p]alsy and diabetes

is not clearly related to diabetes control (hyperglycemia) and they suggest further

studies are warranted.” (Id. (citing Riga et al., supra, at Ex. 25).)

b. Respondent’s Expert, Dr. Thomas P. Leist, M.D., Ph.D.5

Respondent’s expert, Dr. Thomas P. Leist, submitted two reports in this case.

(Exs. A; C.) In his first report, Dr. Leist opined that “diabetes related microvascular

injury is the likely cause of [petitioner’s] Bell’s palsy.” (Ex. A, p. 5.) In support of this

opinion, Dr. Leist cites a study done by Pecket and Schattner, which found that “‘in a

series of 126 patients with Bell’s palsy, chemical or overt diabetes was found in 39% of

cases.’” (Id. (quoting P. Pecket & A. Schattner, Concurrent Bell’s Palsy and Diabetes

Mellitus: A Diabetic Mononeuropathy?, 45 J. NEUROLOGY NEUROSURGERY & PSYCHIATRY

652 (1982) (Ex. A, Tab 2)).) In another study of 684 patients with Bell’s palsy, 11.4%

had diabetes. (Id. (citing Kedar K. Adour et al., Prevalence of Concurrent Diabetes

Mellitus and Idiopathic Facial Paralysis (Bell’s Palsy), 24 DIABETES 449 (1975) (Ex. A,

Tab 1)).) Additionally, relying on one of the studies cited by Dr. Gershwin, Dr. Leist

explains that “‘Bell’s palsy is considered to be an entrapment neuropathy resulting from

inflammation, edema, and strangulation. Diabetes, hypertension, and

5 Dr. Leist is board certified in Psychiatry and Neurology. (Ex. B, p. 1.) He received his medical degree

from the University of Miami and his Ph.D. in Biochemistry from the University of Zurich. (Id.) He

currently works as a Professor of Neurology at Thomas Jefferson University, Chief of the Division of

Clinical Neuroimmunology and Director of the Comprehensive Multiple Sclerosis Center, a neurology

consultant at the Inglis Foundation, and Director of Hospital-Based Neurology Infusion Service. (Id.) He

has published 61 peer-reviewed papers, 12 review and invited publications, editorials, commentaries, and

book chapters, and participated in 47 clinical trials. (Id. at 5-14.)

18

hypercholesterolemia have all been related to microangiopathies.’” (Id. (quoting Riga et

al., supra, at Ex. 25, p. 1).)

Dr. Leist notes that petitioner’s diabetes was “poorly controlled from at least

2007.” (Ex. A, p. 4.) Additionally, Dr. Leist opines that “[t]here was clinical evidence

microvascular/microcirculatory compromise in [petitioner’s] case prior to the

administration of vaccines on September 19, 2017.” (Id. at 5.) Dr. Leist opines that

these “preexisting microvascular/microcirculatory compromise included diabetic

neuropathy indicative of microvascular compromise/microvascular injury of the

peripheral nerves, diabetic retinopathy and macular edema suggestive of microvascular

changes/injury in the eyes, microalbuminuria – suggesting microvascular injury in the

kidneys, and skin ulcers indicating peripheral vascular compromise.” (Id.) Additionally,

Dr. Leist noted that “elevated hemoglobin A1c values correlated significantly with severe

Bell’s palsy.” (Id. (citing Riga et al., supra, at Ex. 25).) Therefore, Dr. Leist opines “that

association between Bell’s palsy and diabetes and severity of Bell’s palsy and elevated

hemoglobin A1c is well established.” (Id.)

Finally, Dr. Leist rejects the opinion that vaccines can cause Bell’s palsy. (Ex. A,

p. 5.) He noted that “[t]he Institute of Medicine has reviewed the question of an

association of inactivated influenza vaccine and Bell’s palsy and concluded that the

evidence favored rejection of a causal relationship.” (Id. (citing IOM Report 2012 (Ex. A,

Tab 4)).)

In his second report, Dr. Leist reiterates his opinion that “[t]he association of

diabetes and Bell’s palsy is well documented.” (Ex. C, p. 1 (citing Pecket & Schattner,

supra, at Ex. A, Tab 2; Adour et al., supra, at Ex. A, Tab 1).) Dr. Liest further quotes an

article by Zhang et al, which states that “in certain clinical conditions, such as diabetes

mellitus, primary ischemic neuropathy is likely to occur,” and “after transient ischemia

and reperfusion, acute inflammation of the diabetic nerve is seen.” (Id. (quoting Zhang

et al., supra, Ex. 64, p. 5.) Dr. Leist notes that Dr. Gershwin acknowledged this when

he admitted that petitioner’s diabetes left him more susceptible to Bell’s palsy. (Id. at 2

(citing Ex. 63, p. 2).)

Additionally, Dr. Leist opines that “Dr. Gershwin does not provide any evidence

that influenza vaccine causes inflammation essentially restricted to the facial nerve and

does not explain why the two-step process of injury he proposes as having occurred is

the more likely cause of Bell’s palsy in [petitioner’s] case than poorly controlled diabetes

alone.” (Ex. C, p. 2.) Dr. Leist acknowledges that diabetes can lead to inflammation in

the facial nerve; however, he noted that “Dr. Gershwin does not provide any insights

how to distinguish reactive inflammation of the facial [nerve] following transient ischemia

due to diabetes . . . from vaccine induced inflammation of the facial nerve which he

alleges occurred but for which he has not provided any evidence.” (Id. (citing Zhang et

al., supra, at Ex. 64).)

19

V. Discussion

a. Althen prongs one and three

Under Althen prong one, petitioners must provide a “reputable medical theory,”

demonstrating that the vaccine received can cause the type of injury alleged. Pafford,

451 F.3d at 1355-56 (quoting Pafford v. Sec’y of Health & Human Servs., No. 01-

0165V, 2004WL 171359, at *4 (Fed. Cl. Spec. Mstr. July 16, 2004), aff’d, 64 Fed. Cl. 19

(2005), aff’d, 451 F.3d 1352 (Fed. Cir. 2006)). Scientific evidence offered to establish

Althen prong one is viewed “not through the lens of the laboratorian, but instead from

the vantage point of the Vaccine Act’s preponderant evidence standard.” Andreu ex rel.

Andreu v. Sec’y of Health & Human Servs., 569 F.3d 1367, 1380 (Fed. Cir. 2009). In

this case, petitioner relies on Dr. Gershwin’s assertion that his Bell’s palsy was caused

by “a localized T cell mediated inflammatory response based upon a molecular mimicry

with either the influenza or the hepatitis B vaccine.” (ECF No. 64, p. 6 (citing Ex. 7, p.

7); ECF No. 66, p. 1.) According to Dr. Gershwin, this immune reaction caused

inflammation in the facial nerve, which led to paralysis of the facial muscles. (ECF No.

64, pp. 6-7 (citing Ex. 7, pp. 1-2, 5).)

The third Althen prong requires establishing a “proximate temporal relationship”

between the vaccination and the injury alleged. Althen, 418 F.3d at 1278. A petitioner

must offer “preponderant proof that the onset of symptoms occurred within a timeframe

for which, given the medical understanding of the disorder’s etiology, it is medically

acceptable to infer causation-in-fact.” de Bazan, 539 F.3d at 1352. Petitioner contends

that he “developed Bell’s palsy within a month of vaccination,” which “is consistent with

the production of T cell immunity after influenza vaccination.” (ECF No. 64, p. 10 (citing

Ex. 63, p. 2 (relying on Schmidt et al., supra, at Ex. 66)).) Petitioner relied on Dr.

Gershwin’s assertion that “T cells are activated after a flu vaccination within 3.5 weeks,”

and that similar data exists for the hep B vaccine. (Id. (citing Ex. 63 (relying on Exs. 66-

68).) Therefore, petitioner notes that he developed Bell’s palsy within 3.5 weeks

following vaccination, “which is within the period expected given the proposed

mechanism.” (Id.)

Petitioner argues that respondent has not actually challenged his showing with

respect to either Althen prongs one or three. (ECF No. 66, pp. 1-2, 4.) This is not

accurate. (See ECF No. 65.) However, the analysis below does confirm that

petitioner’s claim fails under Althen prong two regardless of the outcome of prongs one

or three. Accordingly, in the interest of brevity, this decision will assume, but not decide,

that petitioner has satisfied Althen prongs one and three in order to reach the dispositive

issues in this case relating to whether there is a logical sequence of cause and effect

implicating petitioner’s vaccination in his own course of Bell’s palsy.6 Accord Winkler v.

6 Though not resolving Althen prongs one and three in this case, I do note that another special master

has determined that there are reputable medical theories supporting the conclusion that the flu vaccine

and the hep B vaccine can cause Bell’s palsy up to 40 days post-vaccination depending on the theory

proffered. E.g., Sturdevant v. Sec’y of Health & Human Servs., No. 17-172V, 2022 WL 3369716 (Fed. Cl.

Spec. Mstr. July 19, 2022); Beraki v. Sec’y of Health & Human Servs., No. 17-243V, 2021 WL 4891119

(Fed. Cl. Spec. Mstr. Sept. 20, 2021); E.A. v. Sec’y of Health & Human Servs., No. 18-1587V, 2023 WL

20

Sec’y of Health & Human Servs., No. 18-203V, 2021 WL 6276203, at *23 (Fed. Cl.

Spec. Mstr. Dec. 10, 2021) (citing Vaughan ex rel. A.H. v. Sec’y of Health & Human

Servs., 107 Fed. Cl. 212, 221-22 (2012); Hibbard v. Sec’y of Health & Human Servs.,

698 F.3d 1355, 1364 (Fed. Cir. 2012)), aff’d, 88 F.4th 958 (Fed. Cir. 2023) (finding no

abuse of discretion where the special master “assumed” Althen prong one was met

before concluding Althen prong two was dispositive).

b. Althen prong two

The second Althen prong requires proof of a logical sequence of cause and

effect, usually supported by facts derived from a petitioner’s medical records. Althen,

418 F.3d at 1278; Andreu, 569 F.3d at 1375-77; Capizzano v. Sec’y of Health & Human

Servs., 440 F.3d 1317, 1326 (Fed. Cir. 2006); Grant, 956 F.2d at 1148. Medical records

are generally viewed as particularly trustworthy evidence. Cucuras v. Sec’y of Health &

Human Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993). However, medical records and/or

statements of a treating physician’s views do not per se bind the special master. See

§ 300aa-13(b)(1) (providing that “[a]ny such diagnosis, conclusion, judgment, test result,

report, or summary shall not be binding on the special master or court”); Snyder v. Sec’y

of Health & Human Servs., 88 Fed. Cl. 706, 746 n.67 (2009) (“[T]here is nothing . . . that

mandates that the testimony of a treating physician is sacrosanct—that it must be

accepted in its entirety and cannot be rebutted.”). A petitioner may support a cause-in-

fact claim through either medical records or expert medical opinion. § 300aa-13(a).

The special master is required to consider all the relevant evidence of record, draw

plausible inferences, and articulate a rational basis for the decision. Winkler, 88 F.4th at

963 (citing Hines, 940 F.2d at 1528). Petitioner need not prove his vaccination was the

sole cause of his injury, but he must show that it was a substantial contributing factor

and a “but for” cause. Shyface, 165 F.3d at 1352. Although petitioners do not bear a

burden of eliminating other causes of injury, evidence of other possible sources of injury

can be relevant to determining whether a prima facie showing has been made as to

vaccine causation. Winkler, 88 F.4th at 963 (citing Stone v. Sec’y of Health & Human

Servs., 676 F.3d 1373, 1379 (Fed. Cir. 2012).)

On petitioner’s behalf, Dr. Gershwin presents a “cell-mediated immune response

following vaccination” as the “final insult” that “further compromised [petitioner]’s

ischemia” and led to his Bell’s palsy. (Ex. 63, p. 2; Ex. 69, p. 1.) Dr. Gershwin’s search

for an inciting immune event may be a natural extension of his own proposed theory of

causation, however, he acknowledges that his theory is only one possible etiologic

explanation for Bell’s palsy. He explains that studies are lacking that “would help define

the mechanisms” of injury in Bell’s palsy and that it “likely has more than [one]

mechanism.” (Ex. 7, pp. 2, 5.) He specifically states that “Bell’s palsy is a clinical

syndrome, and it is entirely possible that more than one disease entity can produce an

idiopathic facial palsy.” (Id. at 5.) He explains that while the “key evidence” for the

etiology of Bell’s palsy includes immune inflammation, it also includes anatomical

structures, viral infections, acute cold exposure, and, importantly, ischemia. (Ex. 63, p.

2640710 (Fed. Cl. Spec. Mstr. Jan. 24, 2023); Arredondo v. Sec’y of Health & Human Servs., No. 18-

1782V, 2023 WL 8181138 (Fed. Cl. Spec. Mstr. Oct. 31, 2023).

21

1.) Dr. Gershwin posits that there are no other “etiological events” that could explain

petitioner’s condition. (Ex. 7, p. 7.) However, he contradicts himself by acknowledging

that “facial nerves get their vascular supply by a multitude of vessels and when they are

obstructed, it will lead to ischemia. Since patients with diabetes may already have

nerve ischemia, the pre-existing microangiopathy may facilitate the natural history of

Bell’s palsy.” (Id. at 4.) Further to this, Dr. Gershwin agrees that petitioner “has chronic

insulin-dependent Type II diabetes, and has a previous history of polyneuropathies

secondary to the vascular/ischemia associated with diabetes.” (Ex. 69, p. 1.) Dr.

Gershwin explicitly opines that petitioner “was already compromised based upon his

underlying ischemia from the diabetes.” (Ex. 63, p. 2.)

Thus, both parties’ experts opine that petitioner’s diabetes is at minimum a

significant part of the explanation for petitioner’s Bell’s palsy. Further to which,

respondent’s expert, Dr. Leist, is persuasive in observing that Dr. Gershwin has little to

no basis for additionally invoking an immune mechanism of injury.7 (Ex. A, p. 5; Ex. C,

p. 2.) Dr. Leist correctly explains that on this record “Dr. Gershwin does not provide any

insights how to distinguish reactive inflammation of the facial [nerve] following transient

ischemia due to diabetes, which he opines was present, from vaccine induced

inflammation of the facial nerve which he alleges occurred but for which he has not

provided any evidence.” (Ex. C, p. 2.) In contrast to the lack of any clinical indicators of

injurious post-vaccination inflammation, the medical records very clearly establish not

merely that petitioner had coincidental diabetes, but that his diabetes was not under

control at the time of his Bell’s palsy and that it was otherwise manifesting similar

complications pre-dating the vaccinations at issue. Specifically, Dr. Leist explains that

[t]here was clinical evidence [of] microvascular/microcirculatory

compromise in [petitioner]’s case prior to the administration of vaccines on

September 19, 2017. Preexisting findings that indicated preexisting

microvascular/microcirculatory compromise included diabetic neuropathy

indicative of microvascular compromise/microvascular injury of the

peripheral nerves, diabetic retinopathy and macular edema suggestive of

microvascular changes/injury in the eyes, microalbuminuria – suggesting

7 Petitioner contends that respondent’s expert “does not dispute that [petitioner]’s vaccines caused harm.”

(ECF No. 66, p. 2.) But this is not accurate. Petitioner focuses on the phrasing of the conclusion to Dr.

Leist’s two reports in which he stated that petitioner “did not suffer an enduring injury” as a consequence

of his vaccinations. (Ex. A, p. 6; Ex. C, p. 2.) Petitioner interprets Dr. Leist’s reports as implying that

petitioner may have suffered a short-term harm. (ECF No. 66, pp. 2-3.) While Dr. Leist’s use of the word

“enduring” is a bit confusing, it is apparent when examining his opinion as a whole that Dr. Leist does, in

fact, challenge petitioner’s contention that petitioner suffered any vaccine caused injury at all. In his first

report, Dr. Leist stressed that petitioner “did not report any immediate or delayed side effects of the

vaccinations in the minutes, hours, and days following administration.” (Ex. A, p. 4.) Instead, he stated,

“It is my opinion that diabetes related microvascular injury is the likely cause of [petitioner]’s Bell’s palsy.”

(Id. at 5.) In his second report, Dr. Leist further indicated that “Dr. Gershwin does not provide any

evidence that influenza vaccine causes inflammation essentially restricted to the facial nerve and does

not explain why the two-step process of injury he proposes as having occurred is the more likely cause of

Bell’s palsy in [petitioner]’s case than poorly controlled diabetes alone.” (Ex. C, p. 2.)

22

microvascular injury in the kidneys, and skin ulcers indicating peripheral

vascular compromise.

(Ex. A, p. 5.) Dr. Gershwin has not challenged this assessment. In fact,

notwithstanding his search for an additional final straw, Dr. Gershwin agrees not only

that petitioner was suffering diabetes-related ischemia sufficient to induce neurologic

damage but further that the relevant facial nerve was likely already damaged by

petitioner’s diabetes prior to vaccination. (Ex. 7, p. 7 (stating that “[t]he presence of

diabetes in [petitioner] suggests that his facial nerve was already damaged from his

diabetic neuropathy”); Ex. 63, p. 2 (submitting “that he was already compromised based

upon his underlying ischemia from diabetes”).)

Dr. Gershwin opines that all of this left petitioner merely susceptible to Bell’s

palsy and stresses that petitioner’s history of diabetic ischemic polyneuropathy “does

not make [him] immune from a secondary insult.” (Ex. 69, p. 1.) The latter point may be

true as far as it goes, but it is not evidence that a secondary insult is implicated. Apart

from a post-vaccination onset, petitioner has not pointed to any clinical evidence that

supports Dr. Gershwin’s opinion. Even while assuming the onset of petitioner’s Bell’s

palsy could be compatible with Dr. Gershwin’s theory, Dr. Leist is correct to stress that

petitioner did not report any immediate or delayed side effects of the vaccinations in the

days following vaccination. (Ex. A, p. 4.) Especially in the context of petitioner’s

chronic, ongoing, and uncontrolled diabetes, the three-and-a-half week latency in this

case, even if generally plausible under petitioner’s theory, is not compelling on its own

as any kind of clear indicator of vaccine causation.8 Nor does petitioner point to any

medical opinion by any treating physician favoring his assertion of vaccine causation.9

(ECF No. 64, pp. 8-10; ECF No. 66, pp. 2-4.) Moreover, Dr. Leist correctly observes

that Dr. Gershwin “does not explain why the two-step process of injury he proposes as

having occurred is the more likely cause of Bell’s palsy in [petitioner]’s case than poorly

controlled diabetes alone.” 10 (Ex. C, p. 2.)

8 In some cases, post-vaccination Bell’s palsy has been alleged based on an innate immune response

that created an onset occurring within days of vaccination. See, e.g., Sturdevant, 2022 WL 3369716;

Beraki, 2021 WL 4891119. In such cases, it is easier to see how the timing of onset could potentially be

viewed as suspicious for a sequence of cause and effect whereby an acute event led directly, and more

or less immediately, to the Bell’s palsy. But, in any event, the Federal Circuit has explained that

“[a]lthough probative, neither a mere showing of a proximate temporal relationship between vaccination

and injury, nor a simplistic elimination of other potential causes of the injury suffices, without more, to

meet the burden of showing actual causation.” Althen, 418 F.3d at 1278 (citing Grant, 956 F.2d at 1149).

9 Though petitioner testified that his doctors discussed the possibility of vaccine causation with him (Tr.

25-27), this is not reflected in any of his medical records. In any event, petitioner confirmed in his

testimony that none of his physicians actually concluded his Bell’s palsy was vaccine caused,

acknowledging that none of his doctors “said exactly what caused it.” (Id. at 25.)

10 Though the idea of an immune trigger may be consistent with Dr. Gershwin’s theory, his assertion of

that trigger in this specific case, based on no clinical evidence apart from petitioner’s very manifestation of

the allegedly vaccine-caused injury, amounts to a circular logic that has been rejected in prior cases.

Accord Dodd v. Sec’y of Health & Human Servs., No. 09-0585V, 2013 WL 3233210, at *14 (Fed. Cl.

Spec. Mstr. June 5, 2013) (explaining that “Dr. Kinsbourne’s circular logic, that one event was caused by

another simply because the second event occurred, is also unavailing”), aff’d, 114 Fed. Cl. 43 (2013);

23

Even granting petitioner the assumption that he has satisfied Althen prongs one

and three, the Federal Circuit has cautioned that the second Althen prong “is not without

meaning.” Capizzano, 440 F.3d at 1327. Satisfying Althen prongs one and three

generally serves largely as a threshold demonstration that a petitioner’s claim is even

possible. The Court explained that

[t]here may well be a circumstance where it is found that a vaccine can

cause the injury at issue and where the injury was temporally proximate to

the vaccination, but it is illogical to conclude that the injury was actually

caused by the vaccine. A claimant could satisfy the first and third prongs

without satisfying the second prong when medical records and medical

opinions do not suggest that the vaccine caused the injury, or where the

probability of coincidence or another cause prevents the claimant from

proving that the vaccine caused the injury by preponderant evidence.

Id.

That is precisely the scenario presented in this case. Given the lack of either

treating physician support or meaningful clinical evidence and the undisputed presence

of uncontrolled diabetes, Dr. Gershwin’s mere ipse dixit assertion that petitioner’s

vaccination was a factor additional to his diabetes in bringing about his own Bell’s palsy

does not carry petitioner’s burden of proof under Althen prong two. Moreover, Dr.

Gershwin’s own concessions regarding the important role of diabetes in bringing about

petitioner’s own injury dramatically undercut the assertion. This is not a question of

petitioner disproving any role for his diabetes in causing his injury. As explained above,

petitioner need not show his vaccination to have been the sole cause of his injury.

Shyface, 165 F.3d at 1352. Instead, Dr. Gershwin’s opinion is inadequate to

preponderantly demonstrate that petitioner’s vaccinations played any role, as a

substantial contributing factor or a but for cause additional to his diabetes, in the

development of his Bell’s palsy.

c. Factor unrelated to vaccination

In this case, both parties addressed their arguments to the question of whether

petitioner has met his burden of proof under the Althen test in the face of respondent’s

opposition, which is based primarily on diabetes as the cause of petitioner’s condition.

(ECF Nos. 64-65.) Importantly, however, as noted above, petitioner is not obligated as

part of his prima facie burden of proof to eliminate alternative causes of his condition.

de Bazan, 539 F.3d at 1352-53; Winkler, 88 F.4th at 962-63. Instead, once a petitioner

has satisfied his own burden pursuant to the Althen test, the burden shifts to respondent

Morgan v. Sec’y of Health & Human Servs., No. 12-77V, 2017 WL 6893079, at *22 (Fed. Cl. Spec. Mstr.

Dec. 6, 2017) (concluding, “Petitioner’s experts assumed that the very fact she experienced a rare injury

at all was circumstantial proof of her ‘unique genetic repertoire.’ This kind of circular logic (the injury is

itself proof of causation) does not meet the preponderant evidentiary standard set for a vaccine injury

claim.” (internal citation omitted)).

24

to demonstrate that his injury was caused by factors unrelated to vaccination. § 300aa-

13(a)(1)(B); Deribeaux v. Sec’y of Health & Human Servs., 717 F.3d 1363, 1367 (Fed.

Cir. 2013).

Consistent with the parties’ framing of the issue, I have concluded that petitioner

did not meet his burden of proof under Althen for the reasons discussed above. Accord

Winkler, 88 F.4th at 962 (quoting Doe v. Sec’y of Health & Human Servs., 601 F.3d

1349, 1356-58 (Fed. Cir. 2010), for the proposition that “a ‘petitioner’s failure to meet his

burden of proof as to the cause of an injury or condition is different from a requirement

that he affirmatively disprove an alternative cause”). However, in the interest of

completeness, I additionally note that, even assuming arguendo that petitioner did meet

his initial burden under Althen, I would still conclude that respondent has put forward

sufficient evidence to preponderantly demonstrate that petitioner’s Bell’s palsy was

more likely than not caused by his diabetes, rather than his vaccination(s). Although

respondent has argued that the burden of proof never shifted to him, he is clear in

contending that his expert has established diabetes as a more likely cause of

petitioner’s Bell’s palsy to the exclusion of his vaccinations. (ECF No. 65, p. 32; ECF

No. 38, p. 14.)

In order to meet his shifted burden of proof, respondent must demonstrate by

preponderant evidence “that a particular agent or condition (or multiple

agents/conditions) unrelated to the vaccine was in fact the sole cause (thus excluding

the vaccine as a substantial factor).” de Bazan, 539 F.3d at 1354 (emphasis omitted).

As with petitioner’s burden under Althen, respondent must show a logical sequence of

cause and effect linking the injury to the proposed factor unrelated. Deribeaux, 717

F.3d at 1368-69. It need not be scientifically certain but must be legally probable. Id.

Conditions or other factors that are “idiopathic, unexplained, unknown, hypothetical, or

undocumentable” cannot defeat a petitioner’s claim. § 300aa-13(a)(2); Knudsen ex rel.

Knudsen, 35 F.3d 543, 548 (Fed. Cir. 1994).

First, there is no meaningful dispute in this case that diabetes can cause Bell’s

palsy. Both parties’ experts agree that the medical literature supports an association

between diabetes and Bell’s palsy, even as petitioner’s expert, Dr. Gershwin, cautions

that the magnitude of the association is unsettled. (Ex. A, p. 5; Ex .7, pp. 3-4.) Despite

cautioning that not all available studies have confirmed an association between

diabetes and Bell’s palsy (Ex. 69, p. 1), Dr. Gershwin agrees on petitioner’s behalf that

“the role of diabetes in the development of Bell’s palsy is well known” (Ex. 7, p. 3).

Respondent’s expert, Dr. Leist, further explains that Bell’s palsy is an entrapment

neuropathy that can result from, inter alia, primary ischemic neuropathy due to diabetes.

(Ex. A, p. 5; Ex. C, p. 1.) Dr. Gershwin does not disagree. (Ex. 7, p. 4; Ex. 63, p. 1.)

Although Dr. Gershwin asserts on petitioner’s behalf that Bell’s palsy can also have an

immune etiology, he acknowledges that there are likely multiple pathophysiologic

pathways and multiple disease entities that lead to Bell’s palsy and/or facial paralysis.

(Ex. 7, p. 5.) Consistent with Dr. Leist’s opinion, he further agrees that diabetes-related

ischemia can cause nerve damage, including damage to the nerve implicated in Bell’s

palsy. (Ex. 7, p. 4; Ex. 63, p. 1.)

25

Regarding a logical sequence of cause and effect, Dr. Leist is persuasive in

contending that petitioner’s diabetes alone is a sufficient explanation for his condition.

(Ex. A, p. 5.) There is no question that petitioner had a longstanding history of

uncontrolled diabetes. (E.g., Ex. 63, p. 2 (Dr. Gershwin acknowledging petitioner “had

diabetes for more than a decade, preceding his September 2017 influenza vaccination.

His diabetes has been poorly controlled throughout much of that time.”) Additionally,

Dr. Leist cites literature reflecting a correlation between elevated hemoglobin A1c (as

seen in uncontrolled diabetes) and severity of Bell’s palsy (though not ultimate

prognosis).11 (Ex. A, p. 5 (citing Riga et al., supra, at Ex. 25, p. 6).) And, although

petitioner asserts that he was attempting to manage his diabetes, he acknowledged in

his testimony that his diabetes was not controlled around the time of the onset of his

Bell’s palsy.12 (Tr. 11-13, 39-40, 45-46.) This is confirmed by his medical treatment

records as discussed in the factual summary above, which show his ongoing elevations

in blood glucose and hemoglobin A1C. Moreover, as Dr. Leist observes, there is no

question that petitioner experienced preexisting microvascular compromise leading to

neurologic complications attributable to his diabetes. (Ex. A, p. 5.) Petitioner has

offered no argument that these complications were due to anything other than his

diabetes. In fact, petitioner’s own expert concedes that his Bell’s palsy is at least partly

explained by diabetic nerve damage. (Ex. 7, p. 7 (stating that “[t]he presence of

diabetes in [petitioner] suggests that his facial nerve was already damaged from his

diabetic neuropathy”); Ex. 63, p. 2 (submitting that petitioner “was already compromised

based upon his underlying ischemia from diabetes”).) Dr. Leist is also persuasive in

contending that Dr. Gershwin has no basis for distinguishing inflammatory damage

purportedly due to vaccination from the otherwise undisputed ischemic nerve damages

resulting from petitioner’s diabetes. (Ex. C, p. 2.) Thus, based on all of this, Dr. Leist is

persuasive in opining “that diabetes related microvascular injury is the likely cause of

[petitioner]’s Bell’s palsy.” (Ex. A, p. 5 (emphasis added).)

While Dr. Gershwin is well qualified to discuss the potential immunologic causes

of a clinical syndrome such as Bell’s palsy, Bell’s palsy itself is a form of neuropathy,

which places the condition more firmly in Dr. Leist’s area of clinical expertise with

respect to the spectrum of patient presentations and etiologies for the condition.

Neither expert’s curriculum vitae discloses any specific prior experience with either

Bell’s palsy or diabetes in particular. (Ex. 62; Ex. B.) However, Dr. Leist does represent

that his clinical experience as a board-certified neurologist has included treatment of

11 Dr. Gershwin urges caution regarding the clarity of the relationship observed by Riga et al., given the

limitations noted by the authors (Ex. 69, p. 1; Ex. 7, p. 4), but does not seek to refute the study. In fact,

Dr. Gershwin cited the study approvingly in his first report. (Ex. 7, pp. 3-4.)

12 Specifically, petitioner testified that his diabetes was uncontrolled at the time he first saw Dr. Head, but

that “I would say I began controlling it once I got under her care.” (Tr. 39-40.) Petitioner’s first encounter

with Dr. Head on September 19, 2017, is the same encounter at which he received the subject

vaccinations. (Ex. 2, pp. 218-38; Ex. 5, p. 6.) Petitioner separately testified, however, that he only

subsequently (around 2021) learned of the need to reduce his carbohydrate intake to control his diabetes,

suggesting his earlier efforts to control his diabetes were not fully effective. (Tr. 12-14, 46.)

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patients with Bell’s palsy. (Ex. A, p. 1.) Dr. Gershwin makes no similar representation

and it is not readily apparent that his experience as a rheumatologist/immunologist

would include any experience with patients presenting for Bell’s palsy. Accordingly,

even if all else were equal, Dr. Leist’s opinion would still be entitled to greater weight

with respect to his assessment of petitioner’s clinical history vis-à-vis the underlying

cause of his Bell’s palsy. Where both parties offer expert testimony, a special master's

decision may be “based on the credibility of the experts and the relative persuasiveness

of their competing theories.” Broekelschen v. Sec’y of Health & Human Servs., 618

F.3d 1339, 1347 (Fed. Cir. 2010) (citing Lampe v. Sec’y of Health & Human Servs., 219

F.3d 1357, 1362 (Fed. Cir. 2000)). In determining whether a particular expert’s

testimony was reliable or credible, a special master may consider whether the expert is

offering an opinion that exceeds the expert’s training or competence. E.g., Walton v.

Sec’y of Health & Human Servs., No. 04-503V, 2007 WL 1467307, at *17-18 (Fed. Cl.

Spec. Mstr. Apr. 30, 2007) (finding that an otolaryngologist was not well suited to testify

about disciplines other than his own specialty).

VI. Conclusion

Petitioner has clearly suffered and he has my sympathy. However, for all the

reasons discussed herein, petitioner has not preponderantly demonstrated that he

actually suffered a vaccine-caused injury and is therefore not entitled to compensation.

Accordingly, this case is dismissed.13

IT IS SO ORDERED.

s/Daniel T. Horner

Daniel T. Horner

Special Master

13 In the absence of a timely-filed motion for review of this Decision, the Clerk of the Court shall enter

judgment accordingly.

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