Williams v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 19-1307V

Filed: December 18, 2025

Special Master Horner

TIMOTHY WILLIAMS,

Petitioner,

v.

SECRETARY OF HEALTH AND

HUMAN SERVICES,

Respondent.

Emily Beth Ashe, Anapol Weiss, Philadelphia, PA, for petitioner.

Meghan Murphy, U.S. Department of Justice, Washington, DC, for respondent.

DECISION1

On August 28, 2019, petitioner, Timothy Williams, filed a petition under the

National Childhood Vaccine Injury Act, 42 U.S.C. § 300aa-10, et seq. (2012),2 alleging

that he suffered myasthenia gravis (“MG”) and chronic inflammatory demyelinating

polyneuropathy (“CIDP”)3 caused-in-fact by an influenza (“flu”) vaccination that he

received on September 16, 2016. (ECF No. 1, p. 1.) On March 29, 2021, petitioner

filed an amended petition to additionally allege inflammatory polyradiculopathy. (ECF

1

Because this document contains a reasoned explanation for the action taken in this case, it must be

made publicly accessible and will be posted on the United States Court of Federal Claims' website, and/or

at https://www.govinfo.gov/app/collection/uscourts/national/cofc, in accordance with the E-Government

Act of 2002. 44 U.S.C. § 3501 note (2018) (Federal Management and Promotion of Electronic

Government Services). This means the document 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, I agree that the identified material fits within this definition, I will redact such material from

public access.

2

Within this decision, all citation to § 300aa will be the relevant sections of the Vaccine Act at 42 U.S.C.

§ 300aa-10-34.

3

Although this decision consistently uses the acronym CIDP, in some instances varying terms were used

to refer to this condition. The petition refers to CIDP as being a polyneuritis and Dr. Steinman made

some references to “chronic inflammatory neuropathy” or “chronic demyelinating neuropathy” while Dr.

Price at one point referenced “chronic inflammatory demyelinating polyradiculoneuropathy.”

1

No. 44, p. 1.) For the reasons set forth below, I conclude that petitioner is not entitled to

an award of 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,

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); § 300 aa-

11(c)(1)(C)(i); § 300aa-14(a).

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 ex rel. Sevier v. Sec’y of Health & Human Servs.,

940 F.2d 1518, 1525 (Fed. Cir. 1991).

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 1278-79; Hines, 940 F.2d at 1525.

Under that standard, 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. He 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 at issue and was a “but for” cause.

Shyface v. Sec’y of Health & Human Servs., 165 F.3d 1344, 1352 (Fed. Cir. 1999).

Thus, petitioner must supply “proof of a logical sequence of cause and effect showing

that the vaccination was the reason for the injury[.]” Althen, 418 F.3d at 1278 (quoting

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

Ultimately, petitioner must satisfy what has come to be known as the Althen test, which

requires: (1) a medical theory causally connecting the vaccination and the injury; (2) a

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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.4 Id.

Because the Vaccine Act requires a petitioner to present a claim for

compensation for a “vaccine-related injury or death,” § 300aa-11(c); § 300aa-

13(a)(1)(A); Stillwell v. Sec’y of Health & Human Servs., 118 Fed. Cl. 47, 56 (2014),

aff’d per curiam, 607 F. App’x 997 (Fed. Cir. 2015), a petitioner “must specify his

vaccine-related injury and shoulder the burden of proof on causation.” Broekelschen v.

Sec’y of Health & Human Servs., 618 F.3d 1339, 1346 (Fed. Cir. 2010). Accordingly,

where the identity and nature of the vaccine-related injury is in dispute, the Federal

Circuit has held that it is “appropriate for the special master to first determine what

injury, if any, [is] supported by the evidence presented in the record before applying the

Althen test to determine causation. Lombardi v. Sec’y of Health & Human Servs., 656

F.3d 1343, 1352-53 (Fed. Cir. 2011). However, “the function of a special master is not

to ‘diagnose’ vaccine-related injuries.” Andreu v. Sec’y of Health & Human Servs., 569

F.3d 1367, 1382 (Fed. Cir. 2009). Instead, special masters shall determine “based on

the record evidence as a whole and the totality of the case, whether it has been shown

by a preponderance of the evidence that a vaccine caused the [petitioner’s] injury.” Id.

(quoting Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 549 (Fed. Cir.

1994)).

Ultimately, 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). Medical records

are generally viewed as particularly trustworthy evidence because they are created

contemporaneously with the treatment of the patient. 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 to adopt

the conclusions of such an individual, even if they must be considered and carefully

evaluated. § 300aa-13(b)(1). A petitioner may rely upon circumstantial evidence. See

Althen, 418 F.3d at 1280. Moreover, 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

4

The Vaccine Act also permits petitioners to recover damages for any vaccine-caused “significant

aggravation” of a pre-existing condition. The Act defines significant aggravation as “any change for the

worse in a preexisting condition which results in markedly greater disability, pain, or illness accompanied

by substantial deterioration of health.” § 300aa-33(4). Where a petitioner in an off-Table case is seeking

to prove that a vaccination aggravated a pre-existing injury, petitioners must establish three additional

factors. See Loving v. Sec’y of Health & Human Servs., 86 Fed. Cl. 135, 144 (2009) (combining the first

three Whitecotton factors for claims regarding aggravation of a Table Injury with the three Althen factors

for off-Table Injury claims to create a six-part test for off-Table significant aggravation claims); see also

W.C. v. Sec’y of Health & Human Servs., 704 F.3d 1352, 1357 (Fed. Cir. 2013) (applying the six-part

Loving test.). The additional Loving factors require petitioners to demonstrate significant aggravation by

showing: (1) the vaccinee’s condition prior to the administration of the vaccine, (2) the vaccinee’s current

condition, and (3) whether the vaccinee’s current condition constitutes a “significant aggravation” of the

condition prior to the vaccination. Loving, 86 Fed. Cl. at 144.

3

1279-80. While scientific certainty is not required, that expert’s opinion must be based

on “sound and reliable” medical or scientific explanation. Boatmon v. Sec’y of Health &

Human Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019).

Cases in the Vaccine Program are assigned to special masters who are

responsible for “conducting all proceedings, including taking such evidence as may be

appropriate, making the requisite findings of fact and conclusions of law, preparing a

decision, and determining the amount of compensation, if any, to be awarded.” Vaccine

Rule 3(b)(1). Special masters must ensure each party has had a “full and fair

opportunity” to develop the record but are empowered to determine the format for taking

evidence based on the circumstances of each case, including having the discretion to

decide cases without an evidentiary hearing. Vaccine Rule 3(b)(2); Vaccine Rule 8(a);

Vaccine Rule 8(d). Special masters are not bound by common law or statutory rules of

evidence but must consider all relevant and reliable evidence in keeping with

fundamental fairness to both parties. Vaccine Rule 8(b)(1). The special master is

required to consider “all . . . relevant medical and scientific evidence contained in the

record,” including “any diagnosis, conclusion, medical judgment, or autopsy or coroner’s

report which is contained in the record regarding the nature, causation, and aggravation

of the petitioner’s illness, disability, injury, condition, or death,” as well as the “results of

any diagnostic or evaluative test which are contained in the record and the summaries

and conclusions.” § 300aa-13(b)(1). The special master is required to consider the

entirety of the evidentiary record, draw plausible inferences, and articulate a rational

basis for the decision. Winkler v. Sec’y of Health & Human Servs., 88 F.4th 958, 963

(Fed. Cir. 2023) (citing Hines, 940 F.2d at 1528).

II. Procedural History

As noted above, the initial petition alleged either MG or CIDP caused-in-fact by

petitioner’s vaccination. (ECF No. 1.) In September of 2019, petitioner filed initial

medical records and an affidavit in support of his claim. (ECF Nos. 7-8; Exs. P1-P9.)

Throughout the rest of 2019 and the beginning of 2020, petitioner filed additional

medical records and a statement of completion. (ECF Nos. 10, 12, 14, 16-17, 19-21;

Exs. P10-P18.)

Respondent filed a Rule 4(c) Report on August 7, 2020. (ECF No. 26.)

Respondent contended that petitioner failed to support his allegation of vaccine injury

with preponderant evidence, stressing that petitioner had not submitted an expert

report, petitioner’s symptoms preceded vaccination by between six months to five years,

and the lack of reliable evidence showing a causal association between the flu vaccine

and MG and/or CIDP in the existing medical literature. (Id. at 9-10.) Thereafter,

petitioner filed additional medical records and another statement of completion by the

end of 2020. (ECF Nos. 35-36; Exs. P19-P20.)

In March of 2021, petitioner filed additional medical records and another

statement of completion. (ECF Nos. 41-42; Exs. P21-P23.) Petitioner filed an expert

report by neurologist and neuroimmunologist Lawrence Steinman, M.D., with supporting

4

medical literature, on March 29, 2021. (ECF Nos. 43; Ex. P24.) Dr. Steinman opined

that petitioner’s condition represented an inflammatory polyradiculopathy, rather than

either CIDP or MG. (Ex. P24, p. 6.) Thereafter, petitioner filed an amended petition,

alleging inflammatory polyradiculopathy in addition to the previously alleged MG and

CIDP. (ECF No. 44.)

Respondent then filed responsive expert reports by neurologist Raymond S.

Price, M.D., and immunologist John T. Bates, Ph.D., along with supporting medical

literature. (ECF Nos. 47-48; Exs. A-D.) Dr. Price opined that petitioner suffered MG,

but not CIDP or inflammatory polyradiculopathy. (Ex. A, pp. 9-13.) Dr. Bates’s opinion

contested Dr. Steinman’s theory of vaccine causation vis-à-vis inflammatory

polyradiculopathy. (Ex. C.) The parties then exchanged further reports by their experts.

(ECF Nos. 50, 52, 54-55; Exs.P25-P26; Exs. E-F.)

An entitlement hearing was scheduled to commence on July 23, 2024. (ECF No.

59.) Before the hearing, petitioner filed additional medical records and medical

literature. (ECF Nos. 60, 62-64; Exs. P27-P36.) In a joint pre-hearing submission, the

parties agreed that petitioner did not suffer CIDP, narrowing the diagnostic dispute to

MG versus inflammatory polyradiculopathy. (ECF No. 69.)

The two-day entitlement hearing commenced on July 23, 2024. (See Transcript

of Proceedings (“Tr.”), at ECF Nos. 80-81.) At the close of the hearing, the parties

confirmed that the evidentiary record was complete. (ECF No. 76.) However, I advised

the parties that, although petitioner had initially pleaded a vaccine-caused MG, I felt that

petitioner had effectively abandoned any prosecution of such a claim. (Tr. 333-34.) I

instructed petitioner to explain in post-hearing briefing what basis, if any, he had for

continuing to assert a claim for vaccine-caused MG. (Id. at 334-35.) Thereafter, on July

26, 2024, petitioner filed a status report indicating that he was “releasing his claim” that

his flu vaccine caused MG. (ECF No. 77.)

Petitioner filed his post-hearing brief on October 7, 2024 (ECF No. 83);

respondent filed his responsive post-hearing brief on November 2, 2024 (ECF No. 84);

and petitioner filed his reply on November 18, 2024 (ECF No. 85). Accordingly, this

case is now ripe for resolution of entitlement.

Petitioner argues that he has met his burden of proof with respect to a vaccine-

caused inflammatory polyradiculopathy regardless of whether he additionally suffered

MG. (ECF Nos. 83, 85.) Respondent argues, however, that petitioner only ever

suffered MG and not inflammatory polyradiculopathy. (ECF No. 84, pp. 15-18.)

Because I agree with respondent, and because petitioner did not pursue any claim that

his vaccine caused or aggravated MG, it is not necessary to reach any Althen or Loving

analysis in this case.

5

III. Factual History

a. Medical Records

Before receiving the vaccine at issue in this case, petitioner had a medical history

significant for sinus problems, coronary artery disease, and hypertension. (E.g., Ex. P2,

p. 158; Ex. P13, p. 11.) Additionally, he suffered from chronic low back pain with

radiculopathy and was treated with Depo-Medrol injections. (E.g., Ex. P2, p. 165; Ex.

P11, pp. 311-23.) On December 8, 2014, petitioner reported that, despite conservative

treatment with pain and anti-inflammatory medication, his back pain was so severe that

he was unable to walk more than 100 feet before having to stop. (Ex. P8, pp. 250-52.)

He additionally reported numbness in his right thigh that caused his leg to give way,

interfering with his ability to work. (Id. at 252.) Petitioner was treated with Depo-Medrol

injections and NSAIDs for hip and back pain up until the vaccination at issue in this

case. (Ex. P8, pp. 186-93, 201, 205-08, 211-13, 228-30.) Petitioner also received

annual flu vaccinations in 2013, 2014, and 2015. (Ex. P2, pp. 94, 172.)

On September 16, 2016, petitioner followed up with his primary care physician,

William Pickard, M.D., for back pain and sinus problems. (Ex. P2, pp. 93-96.) Dr.

Pickard noted that petitioner’s back pain, which was associated with his lumbar

radiculopathy, was improved and stable at that time. (Id. at 93.) However, during this

appointment, petitioner reported back and joint pain, as well as sinus pressure. (Id. at

95.) His physical exam was positive for low back pain, as well as sinus congestion pain

and pharyngitis. (Id. at 95-96.) Petitioner received the flu vaccination at issue at this

appointment. (Id. at 94; Ex. P1, p. 1.)

On September 20, 2016, petitioner returned to Dr. Pickard with reports of

excessive fatigue, which he suspected could be due to Lyme disease as he had

recently spent time in the woods. (Ex. P2, p. 90.) However, he denied a rash and

subsequent Lyme disease testing was negative. (Id. at 90, 182.) His physical exam

continued to show pharyngitis and low back pain but was otherwise normal. (Id. at 92-

93.)

The next day, September 21, 2016, petitioner presented to neurologist

Mohammad Sadeghi, M.D. (Ex. P3, pp. 1-8.) On his intake form, petitioner indicated

that he presented for evaluation of possible multiple sclerosis symptoms. (Id. at 25.)

He reported a five-year history of intermittent, aching pain that “starts in my arm and

wrist on left side, then goes to the left hip with a burning sensation and then from calf

down to foot on left side.” (Id. at 25-26.) His pain intensified when sitting but improved

when walking. (Id. at 26.) Petitioner also reported back pain, numbness and weakness

in his arm and leg, tingling in hands and feet, limping, facial weakness and tremors,

difficulties with speech and swallowing, cough, extreme fatigue, decreased

concentration, double or blurry vision, and lightheadedness. (Id. at 27-29.) He noted

that he experiences his back pain “[q]uite a bit.” (Id. at 28.) Petitioner described his leg

numbness, weakness, and pain as moderate, while noting that his arm weakness was

moderate with only minimal pain and numbness. (Id.)

6

At his appointment with Dr. Sadeghi, petitioner reported a history of insomnia

with worsening fatigue over the past four years. (Ex. P3, pp. 5, 7.) Petitioner indicated

that he was started on testosterone injections to address his fatigue, which helped for a

time, but he noticed worsening fatigue about six months prior, followed by new onset of

blurry vision. (Id.) He described one “major” episode at night, as well as frequent

episodes while watching television. (Id.) He also reported intermittent numbness of the

left side of his face, arm, and leg; increased phonation; difficulty swallowing; and slurred

speech. (Id.) On physical exam, petitioner’s speech was “somewhat slurred” and nasal

but coherent, and his sensory exam, coordination, and gait were normal. (Id. at 6, 8.)

Petitioner’s strength was normal and intact in his bilateral upper and lower extremities,

with the exception of some mild fatigability in petitioner’s right upper extremity. (Id.) Dr.

Sadeghi ordered testing for myasthenia gravis (“MG”) and prescribed Mestinon. (Id.)

Petitioner underwent an MRI of his brain on September 28, 2016. (Ex. P4, p.

14.) The study showed no acute intracranial abnormality and mild nonspecific white

matter changes most commonly secondary to chronic small vessel ischemia. (Id.) On

October 6, 2016, petitioner presented to Dr. Sadeghi for a review of his MRI and follow

up for possible MG. (Ex. P3, p. 46.) He reported improvement in his symptoms since

he began taking Mestinon. (Id.) Specifically, he reported that he did not feel as fatigued

and denied further episodes of diplopia and ptosis. (Id.) However, petitioner did note

that he “takes up to 3 or 4 tablets” of Mestinon when working the night shift as his

symptoms recur at the end of the day. (Id.) On physical exam, petitioner had diplopia

and fatigability upon sustained upward gaze. (Id. at 47.) However, strength in his

bilateral upper and lower extremities was normal with no appreciable fatigability. (Id.)

Petitioner’s sensory examination, gait, and coordination were normal. (Id.)

Petitioner had a follow up appointment with his primary care provider on October

14, 2016. (Ex. P2, p. 87.) Dr. Pickard noted that petitioner had recently been

diagnosed with MG but was doing much better after starting Mestinon. (Id. at 89.)

Petitioner reported joint and back pain, as well as sinus problems. (Id.) Petitioner’s low

back pain, sinus congestion pain, and pharyngitis were confirmed on physical exam.

(Id. at 90.) However, his exam was otherwise unremarkable. (Id.)

On October 27, 2016, petitioner presented to gastroenterologist Dr. Nezar

Shobassy. (Ex. P5, p. 2.) Petitioner reported his MG diagnosis and explained that he

was having indigestion and difficulty swallowing. (Id.) His physical examination was

normal. (Id.) Dr. Shobassy scheduled petitioner for an abdominal ultrasound, an

esophagogastroduodenoscopy (“EGD”), and a colonoscopy. (Id.) Petitioner’s EGD was

suggestive of Barrett’s esophagus; however, a biopsy was performed which was

negative for Barrett’s esophagus with no evidence of dysplasia or malignancy. (Ex. P5,

pp. 1, 3-4, 6.)

On November 2, 2016, petitioner had a follow up appointment with his primary

care physician for his lumbar radiculopathy. (Ex. P2, p. 84.) While physical exam

continued to show joint and back pain, Dr. Pickard noted that petitioner’s back pain was

7

somewhat improved. (Id. at 86-87.) At this appointment, petitioner requested a

neurology referral for a second opinion. (Id. at 84, 87.) Additionally, Dr. Pickard

ordered MG antibody panels after documenting that petitioner’s neurologist “lost” his

prior laboratory results. (Id. at 87.) During a follow up encounter on November 18,

2016, Dr. Pickard noted that petitioner was still undergoing a neurology workup. (Id. at

81.) That same day, petitioner’s lab results, including an MG panel and testing for

acetylcholine receptor binding antibodies and muscle-specific kinase (“MuSK”)

antibodies, returned negative. (Id. at 178-81.) However, it is noted in the record that a

negative result does not conclusively rule out MG. (Id. at 179.)

On November 28, 2016, petitioner presented for further evaluation by

neurologist, Robert Glenn Smith, M.D. (Ex. P6, p. 3.) Dr. Smith noted petitioner’s MG

diagnosis and description of “2 different types of problems” involving weakness. (Id. at

4.) Petitioner reported “many years” of severe fatigue “when he has overworked

himself,” with a recovery period of hours to overnight before returning to his baseline.

(Id.) This problem was compounded by his chronic low back pain and history of

radicular pain, and he noted an increase in the severity of his symptoms over the past

two years. (Id.) However, petitioner’s “more recent severe activity dependent fatigue”

appeared to be a separate issue. (Id.) He documented an episode of weakness and

difficulty breathing, requiring up to two days of sleep before he felt normal. (Id.)

Petitioner reported that his arms and legs “feel like lead” and become very fatigued with

activity. (Id.) He described another episode, during which petitioner experienced leg

cramps from climbing stairs or ladders and low back pain without radicular pain. (Id.)

He also reported bilateral ptosis with episodic muscle twitching, and worsening choking

on foods and liquids, especially when fatigued. (Id.) Petitioner reported further

weakness in his shoulders and neck. (Id.) Although petitioner reported diplopia, Dr.

Smith opined that this could be related to petitioner’s cataracts, rather than actual

binocular diplopia. (Id.) Petitioner reported improvement in his ptosis, diplopia, and

fatigue with Mestinon, as well as a reduction in pain with Celebrex. (Id.) While Dr.

Smith did not have petitioner’s lab results to review, he recorded that, according to

petitioner, the initial and repeat MG panels were both negative. (Id.) Dr. Smith further

recorded that petitioner “has a history of sciatica, possibly most affecting dermatome L5,

and S1,” as well as “a history of singultus, associated with his increase in episodic

choking.” (Id.)

Physical exam revealed mild, bilateral ptosis affecting the right more than the left;

mild atrophy of the tongue; and minimally reduced strength in petitioner’s left hip flexor,

knee extensor, and ankle evertor. (Ex. P6, pp. 6-7.) His reflexes were normal and

intact, with the exception of reduced reflexes in petitioner’s knees bilaterally. (Id. at 7-

8.) Petitioner’s sensory exam, coordination, and gait were all normal. (Id. at 8.)

Petitioner’s differential diagnosis was MG, though Dr. Smith observed that additional

testing was necessary to verify the diagnosis. (Id. at 9.) He therefore ordered an EMG,

CT of the chest with contrast, and basic metabolic panel. (Id.)

Petitioner underwent an EMG/nerve conduction study on December 7, 2016.

(Ex. P19, p. 2.) There was no evidence of decrement on repetitive nerve stimulation.

8

(Ex. P19, p. 8.) The EMG revealed evidence of “inactive, mild to moderate severity

denervation with partial reinnervation of muscles normally in functional contact with

motor neurons at multiple lumbar levels, consistent with an inactive polyradiculopathy.”

(Ex. P19, p. 8.) The upper extremity muscles tested were “much less affected

electrically, with denervation changes noted mostly in C7 and possible C8 innervated

muscles.” (Id.) The nerve conduction study revealed normal distal latencies and

conduction velocities in the tested upper and lower extremity motor nerves with the

exception of right ulnar distal latency and mild slowing of the left median motor velocity.

(Id.) F-wave latencies were essentially normal. (Id.) Dr. Smith’s impression of

petitioner’s EMG/nerve conduction study findings was

[w]idespread inactive motor denervation with partial reinnervation in the

tested lower extremity, with significantly less denervation reinnervation

changes observed in the tested upper extremity. Likewise, reduction in

recruitment was observed in both upper and lower extremities tested.

Inactive denervation changes were observed in the thoracic paraspinal

muscles and in the genioglossus muscles.

Relatively normal nerve conduction studies, though early demyelination

changes possibly may be observed in right median and ulnar nerve

responses.

(Id. at 10.) These findings suggested the presence of a “longstanding, progressive,

relatively inactive, polyradiculopathy” without significant neuropathy. (Id.) Although the

differential diagnosis was broad and included inflammatory, infectious, paraneoplastic,

POEMS, MUGAS, vascular, metabolic, or genetic etiologies, it was noted that many of

these etiologies had been excluded and that petitioner’s upper motor neuron findings

were not consistent or present in most of these diseases. (Id.) Additionally, petitioner’s

chest CT showed “[a] couple of lung nodules bilaterally likely post inflammatory.” (Ex.

P23, p. 1.)

On January 17, 2017, petitioner followed up with Dr. Smith to review his test

results. (Ex. P6, pp. 22-23.) Dr. Smith recorded that petitioner presented with a

symptom complex suggestive of a neuromuscular junction disorder with improvement of

ptosis and weakness with Mestinon. (Id. at 23.) In documenting petitioner’s history, Dr.

Smith recorded:

Since last seen, he [has] undergone EMG, which did not confirm decrement

on repetitive stimulation, but noted the presence of a polyradiculopathy.

While no obvious neuropathic findings were observed, the patient did have

significant side-to-side variation in his left versus right median nerve, with

slight slowing in conduction velocity noted on the tested left side. Similar

observation was noted in comparing the left and right sensory median

results. Other than prolonged motor distal latency of the ulnar nerve on the

left, without sensory latency abnormality, no other significant abnormalities

were noted on nerve conduction studies.

9

(Id.) Petitioner reported that he was able to stay off Mestinon for 36 hours prior to his

EMG study. (Id. at 23-24.) However, his weakness and fatigue had worsened since his

last visit. (Id. at 23.) Although his symptoms improved with Mestinon, Dr. Smith

documented that petitioner was unable to completely control his activity dependent

weakness. (Id.)

Petitioner’s physical examination again showed mild, bilateral ptosis affecting the

right more than the left, mild tongue atrophy, minimally reduced strength in the left lower

extremity, as well as mild tenderness over the cervical spine without reduced range of

motion or muscle spasm and tenderness over the lumbosacral spine with mildly

reduced range of motion. (Ex. P6, pp. 26-27.) His sensory exam, coordination, and gait

were all again normal, and his reflexes were normal and intact with the exception of

reduced reflexes in his knees, bilaterally. (Id. at 28.) X-ray of the thoracic and cervical

spine both showed degenerative changes. (Ex. P23, pp. 2-3.) Dr. Smith documented

that the x-ray of petitioner’s cervical spine revealed “C6/C7 degenerative/spondylitic

changes” with minimal changes observed in the thoracic spine. (Ex. P6, p. 29.) Dr.

Smith’s assessment was MG with exacerbation, CIDP, bilateral lumbar radiculopathy,

chronic bilateral low back pain without sciatica, polyradiculopathy, and a possible

cervical radiculopathy at C7/C8. (Id. at 29-31.) In addition to continuing with Mestinon,

petitioner was started on prednisone and CellCept, and further testing was ordered. (Id.

at 25, 29-31.)

On January 25, 2017, petitioner underwent a successful lumbar puncture, which

revealed no abnormalities. (Ex. P23, p. 4; Ex. P29, p. 389.) Given that there was no

evidence of any significant brachial blood brain barrier or CSF inflammation, Dr. Smith

opined that most of the differential diagnoses for polyradiculopathy could be excluded

on the basis of the lumbar puncture results. (Ex. P6, p. 31.)

Petitioner’s next follow up appointment with Dr. Smith was on March 30, 2017.

(Ex. P6, pp. 44, 47-48.) Since his last visit, petitioner reported improvement in his

generalized weakness, fatigue, ptosis, double vision, and beathing. (Id.) His response

to Mestinon was described as “variable.” (Id.) Dr. Smith noted that petitioner called the

office in January of 2017 to report persistent muscle weakness that continued to

progress. (Id.) At that time, petitioner’s work was significantly limited by weakness and

associated shortness of breath. (Id.) However, petitioner reported “significant

improvement” after introducing prednisone and CellCept. (Id.) Petitioner also reported

continued episodic difficulty swallowing and “choking spells,” though it was noted that

“symptom onset predates the onset of other myasthenic symptoms.” (Id.) He described

his fatigue and weakness as constant. (Id.) Although he experienced an erratic sleep

pattern due to his shift work, he reported “feeling excessively fatigued even after full

night/day sleep.” (Id.) He also reported occasional transient double vision at the end of

his workday. (Id.) However, he denied shortness of breath after day-to-day activities,

focal weakness in arms and legs, or a limitation of his activity at work or at home due to

weakness. (Id.)

10

Petitioner’s physical exam showed mild ptosis, affecting the right more than the

left; mildly reduced range of motion in his lumbar spine; slightly reduced strength in his

left deltoid, bicep, hip flexor, and knee extensor; and reduced strength in the left ankle

evertor. (Ex. P6, pp. 51-52.) Petitioner’s reflexes were normal with the exception of

reduced reflexes in his triceps, bilaterally. (Id. at 52.) Petitioner’s sensory examination,

coordination, and gait were all normal. (Id. at 53.)

Dr. Smith continued to list MG as a diagnosis. (Ex. P6, p. 55.) However, CIDP

was removed from petitioner’s problem list. (Id. at 44.) Dr. Smith noted that, although

petitioner’s EMG showed no evidence of decrement on repetitive nerve stimulation and

his antibody testing was negative, petitioner has had “significant response” to his

treatment regimen. (Id. at 55.) Dr. Smith suggested a reevalution for MG antibodies.

(Id.) Additionally, Dr. Smith noted petitioner’s long shifts that alternated between day

and night shifts, highlighting that petitioner had finished his night shift early that morning

but had not yet slept by the time he presented for his afternoon appointment, and that

petitioner reported significant fatigue, despite normal strength testing that was stable

when compared to his prior testing. (Id.) Dr. Smith prescribed modafinil on a trial basis

for “shift work sleep disorder.” (Id.) He also documented concern for undiagnosed

obstructive sleep apnea and advised petitioner to undergo a sleep study. (Id.)

To evaluate for a clinical diagnosis of vertebrobasilar insufficiency, Dr. Smith

recommended that petitioner undergo an MRA of the head and neck. (Ex. P6, p. 55.)

Petitioner’s subsequent MRA on April 7, 2017, was unremarkable. (Ex. P23, pp. 5-6.)

Petitioner followed up with his primary care physician on April 26, 2017, and May 26,

2017. (Ex. P2, pp. 62-68.) At both encounters, petitioner reported low back pain. (Id.

at 65, 68.) Additionally, his primary care provider noted that petitioner’s energy levels

were improving on his current medication regimen and that his insomnia was also

better. (Id. at 68.)

On June 14, 2017, petitioner had a follow up appointment with Dr. Smith. (Ex.

P6, p. 67.) Although petitioner reported experiencing both good and bad days, he

described fewer episodes of swallowing problems. (Id. at 70.) He also could not recall

when he last experienced double vision, but continued to report occasional blurred

vision when fatigued. (Id.) Petitioner continued to take CellCept, Mestinon, and

prednisone. (Id.) He denied fluctuating weakness, despite taking prednisone on

alternating days. (Id.) Additionally, petitioner reported experiencing significant

improvement in function when taking modafinil to address his shift work sleep disorder.

(Id. at 67, 77.) Dr. Smith documented that petitioner’s symptoms of double vision,

ptosis, and shortness of breath had largely resolved. (Id. at 77.) Additionally, he

recorded that petitioner was negative for the acetylcholine receptor and the MuSK

antibodies and without evidence of decrement on repetitive nerve stimulation. (Id.)

However, Dr. Smith noted that petitioner had a polyradiculopathy on needle exam and

that the possibility of a distal inflammatory motor polyneuropathy producing symptoms

similar to MG could not be ruled out. (Id.) Dr. Smith assessed petitioner with MG,

cervical radiculopathy at C7, polyradiculopathy, and bilateral lumbar radiculopathy, as

11

well as insomnia and shift work sleep disorder. (Id.) Petitioner continued to follow up

with his primary care physician throughout the rest of the year. (Ex. P2, pp. 44-62.)

Petitioner’s next follow up appointment with Dr. Smith was on December 20,

2017. (Ex. P6, p. 90.) Petitioner reported that “he continues to have more good days

than bad with function continuing to improve, though in a more limited fashion.” (Id.)

He described difficulty with endurance, despite apparently normal immediate strength,

and increased fatigue when walking or standing for extended periods. (Id.) Specifically,

petitioner was only able to walk about 50 yards and could stand for no more than 5

minutes before needing to rest. (Id.) Dr. Smith documented that petitioner had

“previously been noted to have a polyradiculopathy superimposed upon his myasthenia

gravis, with clinical findings suggestive of the C7 and/or C6 radiculopathy affecting the

upper extremities (C7/C8 by EMG).” (Id.) He also noted that “[s]econdary to

[petitioner’s] polyradiculopathy and proximal weakness, our concern about CIDP as a

component of his overall process (with additional involvement of the neuromuscular

junction) is increasing.” (Id. at 97.)

On physical exam, petitioner had minimal ptosis in the right side only, mildly

reduced range of motion in his lumbar spine, and normal strength in his extremities with

the exception of 4+/5 strength in his left ankle evertor. (Ex. P6, pp. 94-95.) Petitioner’s

reflexes were normal and intact with the exception of reduced reflexes in his triceps,

bilaterally. (Id. at 95.) His sensory examination, coordination, and gait were normal.

(Id.) Dr. Smith assessed petitioner with CIDP, MG with exacerbation, bulbar MG,

chronic bilateral low back pain without sciatica, cervical radiculopathy at C7, and

vertebrobasilar TIAs. (Id. at 97.)

Dr. Smith ordered a repeat EMG, which petitioner underwent on January 17,

2018. (Ex. P6, p. 97; Ex. P20, p. 1.) The repeat EMG revealed:

Inactive, chronic polyradiculopathy, affecting all tested extremities on

needle exam. The patient’s denervation disease does not appear to have

progressed significantly since last visit; there may be some mild evidence

of improvement proximally in the upper extremities and thoracic paraspinal

muscles.

Nerve conduction studies no longer document evidence of demyelination,

with improvement in previously noted slowing of several motor distal

latencies and/or conduction velocities.

(Ex. P20, p. 7.) Dr. Smith remarked that these findings were consistent with an

“inactive, demyelinating motor polyradiculopathy,” and that the possible etiologies

remained “broad.” (Id. at 8.)

Petitioner continued to see his primary care physician throughout 2018. (Ex. P2,

pp. 6-44; Ex. P8, pp. 82-95.) On June 14, 2018, petitioner had a follow up appointment

with Dr. Smith for fatigable weakness and MG. (Ex. P6, p. 131.) Dr. Smith explained

12

that petitioner’s “neuromuscular junction abnormality has been complicated by the

presence of an additional polyradiculopathy, a component of which appears not to have

a structural basis.” (Id.) Since his last encounter, petitioner’s insurance had denied

treatment of his MG with either IVIG or rituximab. (Id.) While petitioner noted that his

weakness was better controlled after increasing his prednisone dosage, he reported

that he continued to experience intermittent weakness, shortness of breath, and

paroxysmal nocturnal dyspnea-like episodes. (Id.) Additionally, petitioner noted fatigue

at the end of the day with episodes of tremulousness in his legs after showering and

hand tremors. (Id.) Despite evidence that treatment with steroids and Mestinon was

“aiding his level of function,” petitioner reported that he did not believe CellCept was

offering any symptomatic relief for his MG and requested a different medication. (Id.)

Petitioner’s physical exam was consistent with prior exams except for a 6 Hz tremor that

was previously described as an essential tremor. (Id. at 136.) Dr. Smith recommended

reassessing petitioner’s acetylcholine receptor and MuSK antibody titers. (Id. at 131.)

Petitioner was assessed in pertinent part with acetylcholine receptor antibody double

negative bulbar MG, lumbosacral radiculitis, CIDP, cervical radiculopathy at C7, bilateral

lumbar radiculopathy, and shift work sleep disorder. (Id. at 140.) Dr. Smith noted that a

significant portion of the appointment was spent discussing whether petitioner’s

polyradiculopathy was playing a role in his fatigable weakness. (Id.)

Petitioner continued to see his primary care provider throughout 2019. (Ex. P8,

pp. 45-82; Ex. P11, pp. 150-170.) Additionally, petitioner underwent physical therapy

from January 2019 to February 2019 and from June 2019 to August 2019 to improve his

generalized weakness. (See Ex. P7.)

Petitioner’s next follow up appointment with Dr. Smith was on March 20, 2019.

(Ex. P29, p. 374.) In documenting petitioner’s history, Dr. Smith noted that petitioner

was previously diagnosed with acetylcholine receptor and MuSK antibody negative MG,

although petitioner’s clinical symptoms were more typical for acetylcholine receptor

antibody positive disease. (Id.) He also noted that petitioner had “evidence on EMG of

a superimposed neuropathic process, initially recognized as a demyelinating

polyradiculoneuropathy.” (Id.) Based on repeat EMG findings, Dr. Smith explained that

petitioner’s polyradiculoneuropathy had been stable on Mestinon, CellCept, and

prednisone. (Id.) However, petitioner’s fatigable weakness worsened, and he was

started on methotrexate to help stabilize his motor function. (Id.) At the time of the

encounter, petitioner reported that he was still experiencing significant problems with

fatigable weakness, noting that he typically was unable to function after a day of work,

as well as episodes of blurred vision and shortness of breath. (Id.) Petitioner’s

shortness of breath primarily occurred at night when he was lying flat and resolved after

several minutes of standing. (Id.) That said, Dr. Smith also noted that petitioner

experienced shortness of breath almost exclusively on days that he does not take

prednisone, suggesting that he may be experiencing diaphragmatic weakness when his

medication wears off. (Id.) Additionally, petitioner’s visual blurring would be present

when he woke up in the morning prior to taking his first dose of medication. (Id.) Dr.

Smith noted that petitioner’s undiagnosed sleep apnea was superimposed on these two

issues. (Id.) Petitioner also reported experiencing radicular and allodynic pain affecting

13

his shoulders and neck, as well as occasional difficulty maintaining a grip on objects.

(Id.) Dr. Smith documented that petitioner was suffering from distal peripheral

neuropathy and noted that his severe allodynic pain occurred mainly at night limiting

petitioner’s sleep. (Id.) Finally, Dr. Smith noted that petitioner was also suffering from

“shiftwork disorder with mental clouding” and experienced incomplete improvement with

medication. (Id.)

Based on these findings, Dr. Smith concluded that (1) petitioner still had

substantial problems with his MG, and that the condition was not yet adequately

controlled on the days that he takes prednisone; (2) that petitioner’s radiculopathy and

distal, painful neuropathy were both negatively impacting his life and affecting his ability

to complete activities of daily living; and (3) that petitioner’s shift work sleep disorder,

presumably superimposed on his other problems, was making it more difficult for

petitioner to function throughout the day. (Ex. P29, p. 374.) On physical exam,

petitioner had minimal ptosis on the right side only, a 6 Hz tremor, slightly decreased

strength in the hip flexors and left ankle evertor, and reduced reflexes in the triceps,

knees, and ankles. (Id. at 379-80.) Petitioner’s sensory examination was abnormal with

decreased pinprick sensation in the bilateral upper and lower extremities and decreased

vibration sensation in the bilateral lower extremities. (Id. at 381.) Additionally, petitioner

had a positive Baylor and lateral Adson’s tests, bilaterally. (Id. at 380.) Although his

request for IVIG treatment for petitioner was denied the year prior, Dr. Smith planned to

request IVIG again. (Id. at 375, 384.) Petitioner began his IVIG treatment in June of

2019. (See Ex. P18.)

Petitioner began seeing pulmonologist Sujatha Goli, M.D., on August 15, 2019,

for evaluation of symptoms related to his MG, including shortness of breath and

choking, as well as treatment for sleep apnea. (Ex. P15, p. 1.) Dr. Goli ordered a

pulmonary function test, arterial blood gas test, a chest x-ray, and a swallow study. (Id.

at 2.) Petitioner’s labs and chest x-ray were largely unremarkable, and the swallow

study did not reveal any evidence of aspirations. (Id. at 4.) However, a home sleep

study showed severe sleep apnea. (Id. at 4, 12.)

On September 22, 2019, petitioner was admitted to the hospital after presenting

to the emergency department with reports of a sudden onset of palpitations, which he

described as feeling like his heart was racing, and associated shortness of breath. (Ex.

P12, pp. 6, 8.) What was likely a new onset of atrial fibrillation was detected, and

petitioner was treated with a Cardizem drip. (Id.) He was discharged on September 24,

2019. (Id. at 6.)

Petitioner followed up with Dr. Smith on May 28, 2020. (Ex. P28, p. 438.) Dr.

Smith summarized petitioner’s history as “acetylcholine receptor antibody negative,

[M]u[SK] antibody negative, LR P4 antibody? [MG] (with clinical symptoms more typical

for acetylcholine receptor antibody positive disease) and evidence o[n] EMG of a

superimposed neuropathic process, initially recognized as a demyelinating

polyradiculoneuropathy.” (Id.) He noted that petitioner was responding well to IVIG and

had experienced an improvement in overall motor function; however, despite petitioner’s

14

improvement with IVIG therapy, Dr. Smith documented that petitioner continued to take

Mestinon, methotrexate, and steroids, in combination with IVIG. (Id.) Additionally, Dr.

Smith explained that petitioner had developed acute lower back pain on January 27,

2020, and had participated in aquatic therapy through March of 2020. (Id.) At the time

of the visit, petitioner reported that his “back pain is still relatively severe and continues

to be a problem,” as well as some residual balance problems. (Id.)

At this encounter, Dr. Smith assessed petitioner with MG and CIDP, among other

conditions, such as lumbosacral radiculitis, bilateral lumbar radiculopathy, chronic

bilateral low back pain, cervical radiculopathy at C7, and shift work sleep disorder. (Ex.

P28, p. 450.) He documented that petitioner “has multiple problems, caused by

different diseases.” (Id.) Dr. Smith noted that petitioner’s MG was finally improving with

IVIG therapy but indicated that petitioner needed to increase the frequency of his

treatments to maintain better control. (Id.) Additionally, Dr. Smith remarked that while

treatment with steroids had helped petitioner control his neuromuscular disorder

symptoms, his distal symmetric polyneuropathy had worsened with steroid use. (Id.)

Further, Dr. Smith documented that “[t]he fact that his previous neuropathic findings in

ulnar and median nerve is actually improved on immunomodulatory therapy has

suggested that his EMG quantitated and clinically identified motor neuropathic findings

[that] are likely inflammatory in nature.” (Id.) However, he noted that a marker antibody

to explain petitioner’s myasthenic signs and symptoms had not yet been detected. (Id.)

Dr. Smith instructed petitioner to determine if his insurance would cover testing for

LRP4 antibodies and indicated that petitioner may still need a cell-based assay for

acetylcholine receptor antibody testing. (Id.)

To address petitioner’s low back pain, Dr. Smith ordered an MRI of the

lumbosacral spine. (Ex. P28, pp. 450-51.) He also noted that petitioner had not

experienced further episodes of left neck pain. (Id. at 451.) Petitioner was instructed to

consider restarting aquatic therapy and advised on back exercises for older individuals

with radiculopathies that he could do at home. (Id.) Petitioner began physical therapy

in September of 2020 and continued to pursue treatment until September 2023. (Ex.

P27; Ex. P31.) During some of these visits, petitioner reported being diagnosed with

Guillain-Barré Syndrome (“GBS”). (Ex. P31.)

On November 9, 2020, petitioner underwent an MRI of the lumbar spine, which

revealed “no acute osseous lesion,” normal spinal contents and paraspinal structures,

“[m]oderate compromise of the spinal canal at L3-4 [that] is secondary to ligamentous

hypertrophy and spondylotic change without disc herniation or compromise of the neural

foramina,” and “[m]oderately severe compromise of the spinal canal at L4-5 . . . due to

ligamentous hypertrophy, spondylotic change and a central, 7 mm disc herniation which

compresses the thecal sac and does not affect the neural foramina.” (Ex. P28, pp. 453-

54.) Petitioner had another follow up appointment with Dr. Smith on November 19,

2020. (Id. at 423.) Dr. Smith reviewed petitioner’s MRI and explained that petitioner’s

“newest clinical symptoms are suggestive of lumbosacral stenosis with neurogenic

claudication.” (Id.) Petitioner continued to report back pain and fatigable weakness

upon walking and standing. (Id.) Dr. Smith suggested that, “[g]iven that his aquatic

15

therapy only provided transient benefits, and that his white count [when] most recently

checked was elevated with mild left shift, assessment by his [primary care physician]

would be appropriate to verify lack of an infectious process coincident with his current

low back symptoms.” (Id.) Additionally, Dr. Smith noted that surgical intervention was

likely necessary, given the severity of his lumbosacral canal stenosis. (Id. at 423, 436-

37.) While petitioner could undergo a repeat EMG, Dr. Smith advised that petitioner’s

canal stenosis would be affecting multiple roots, and thus the EMG would basically just

reveal worsening of his polyradiculopathy. (Id. at 437.) With respect to petitioner’s MG,

Dr. Smith documented that petitioner’s condition was well-controlled after increasing the

frequency of his IVIG treatments and expressed his intent to pursue LRP4 antibody

testing if covered by petitioner’s insurance. (Id. at 427, 436.)

Petitioner’s next follow up appointment was on April 1, 2021. (Ex. P28, p. 708.)

Dr. Smith reported that petitioner had “symptoms of CIDP, but additional fatigable

weakness complaints previously diagnosed as acetylcholine receptor antibody negative,

[M]u[SK] negative, LRP4 [antibody]? [MG].” (Id.) He explained that petitioner continued

to be treated with steroids, methotrexate, Mestinon, and IVIG. (Id.) Dr. Smith continued

to stress that petitioner needed to undergo LRP4 antibody testing, if possible. (Id. at

721.) He also indicated that petitioner would need to continue with his current therapy

for treatment of CIDP. (Id.)

On September 13, 2021, petitioner returned to Dr. Smith. (Ex. P28, p. 832.)

Petitioner reported experiencing significant life stressors since his last visit, including his

wife being ill and his daughter unexpectedly passing away. (Id.) He indicated that he

had to take a few days off in early June after experiencing a flare of dyspnea,

weakness, and fatigue. (Id.) Additionally, petitioner reported that he resumed aquatic

therapy in mid-June, but that he had to end at least one session early due to weakness,

and that his physical therapy evaluation confirmed significant leg weakness. (Id.)

Petitioner’s diltiazem dose was reduced, which helped with the dyspnea but did not

improve his weakness. (Id.) However, at the time of the encounter, petitioner reported

that he was feeling stronger. (Id. at 833.) Dr. Smith documented that petitioner’s “[l]ast

EMG actually suggested stabilization of the disease and possible slight improvement at

least in demyelinating features. However, if he fails to improve, we will need to

readdress at least markers that are potentially involved in this process.” (Id. at 832.)

He noted that LRP4 antibody testing should be more affordable as it was now available

through multiple laboratories. (Id.) No diagnosis was listed for this appointment;

however, it was noted that petitioner would be reevaluated in March of 2022. (Id. at

846.)

Petitioner saw Dr. Smith again on March 14, 2022. (Ex. P28, p. 1012.) Dr. Smith

documented that petitioner had

fatiguable weakness associated with radicular pain and other problems

suggestive of overwork, previously followed by Dr. Sadeghi for myasthenia

gravis, which she diagnosed in 2016. On [Mestinon], the patient has noted

improvement in fatigable weakness and diplopia. However, he has been

16

negative for any markers of myasthenia gravis. Further, EMG-tested in

2016-showed no evidence of decrement on repetitive stimulation. In fact,

there was no evidence of neuropathy, although there was a

polyradiculopathy noted on testing. Subsequent studies in 2017 [and] 2018

did not show any significant progression in neuro changes, again only

documenting evidence of a polyradiculopathy.

(Id.) With respect to petitioner’s underlying disease, Dr. Smith explained that petitioner

“does not meet criteria” for either MG or CIDP, but noted that petitioner has “a

polyradiculopathy and fatigable weakness that appears to respond to IVIG.” (Id.) He

noted that petitioner had not experienced any significant worsening in his strength

except in the most proximal muscles. (Id. at 1026.) While possibly indicative of a

progression of petitioner’s underlying disease, Dr. Smith documented that petitioner

experienced a worsening in clinical symptoms around the time he became due for his

next IVIG treatment, which suggested that any progression was likely due to the

treatment wearing off. (Id. at 1012, 1026.) However, petitioner declined to increase the

frequency of his IVIG treatments and indicated his preference to increase his Mestinon

dose as needed in the event of worsening fatigue. (Id. at 1012.) Dr. Smith listed MG,

CIDP, neurogenic claudication due to lumbar spinal stenosis, bilateral lumbar

radiculopathy, cervical radiculopathy at C7, and shift work sleep diagnoses among the

diagnoses for the encounter. (Id. at 1026.)

On October 31, 2022, petitioner had his next follow up appointment with Dr.

Smith for “CIDP MG overlap,” as well as fatigable weakness associated with radicular

pain and other problems suggestive of overwork. (Ex. P29, p. 126.) Petitioner reported

occasionally feeling weak before his IVIG infusion, but his symptoms were otherwise

essentially stable and controlled on Mestinon, methotrexate, and IVIG. (Id. at 126-27,

141.) Petitioner also reported that he occasionally experiences “right hand tingling and

‘shock’ like pain from the wrist down.” (Id. at 127.) Dr. Smith noted that these

symptoms were consistent with a right median neuropathy, specifically carpal tunnel

syndrome. (Id. at 126, 141.) Petitioner’s positive right Phalen’s sign and prior EMG

also supported a finding of carpal tunnel syndrome. (Id.) Given the mildness of his

symptoms, petitioner was advised to treat conservatively with acetaminophen and a

splint. (Id.) MG and CIDP were listed as petitioner’s diagnoses for the encounter. (Id.

at 141.)

Petitioner’s next appointment with Dr. Smith was on March 27, 2023, for fatigable

weakness and CIDP MG overlap. (Ex. P28, p. 1479.) In recording petitioner’s history,

Dr. Smtih continued to stress that, despite his prior MG diagnosis and improvement on

Mestinon, petitioner had tested negative for antibody markers for MG and his EMG

showed no evidence of decrement on repetitive stimulation. (Id.) However, Dr. Smith

noted that petitioner’s Mestinon “may not have been completely ‘out of his system’ with

his ingestion of the medication within 24 hours of his [EMG] testing.” (Id.) He also

documented that petitioner’s polyradiculopathy and evidence of demyelination revealed

by his initial EMG had somewhat improved by the time of his most recent needle exam

assessment in early 2018. (Id.) Petitioner continued to report experiencing weakness

17

prior to his next IVIG therapy session. (Id.) Accordingly, Dr. Smith concluded that, “[a]t

present, his polyradiculopathy with fatigable weakness is therefore adequately but

incompletely controlled by current IVIG treatments.” (Id.) Additionally, Dr. Smith noted

that once petitioner started therapy, petitioner’s “demyelinating polyneuropathy

‘resolved’ with normalization of the previously demyelinating neuropathic features,

indicating improvement on therapy.” (Id.) Petitioner again refused to increase the

frequency of his IVIG therapy. (Id.) CIDP, MG, bilateral lumbar radiculopathy,

neurogenic claudication due to lumbar spinal stenosis, sensory polyneuropathy, and

shift work sleep disorder were listed among petitioner’s diagnoses for the encounter.

(Id. at 1493.)

In April of 2023, petitioner presented for chiropractic care, with major complaints

of cervical, thoracic, and lumbo pelvic pain, which petitioner indicated first occurred after

his flu vaccination in 2016. (Ex. P32, p. 3.) Petitioner reported that he was

subsequently diagnosed with GBS, MG, and CIDP. (Id.) He explained that he

experiences periodic flares of varying intensity that last anywhere from a day to a week.

(Id.) Petitioner described his discomfort as an ache in the cervical, thoracic, and lumbo

pelvic areas with tingling in his left hand and a burning sensation in his thighs, as well

as weakness in his left arm and thigh. (Id.) The chiropractic provider described

petitioner’s gait as abnormal, noting that he tended to drag his left foot, and observed

that he had difficulty breathing. (Id.) Petitioner reported that his pain is aggravated by

standing for more than hour and is less bothersome when he is seated or laying down.

(Id.) On physical exam, petitioner’s left ilium appeared higher than his right, and his

right shoulder was higher than his left. (Id.) Additionally, he had reduced cervical range

of motion with discomfort during testing, as well as reduced thoraco-lumbar range of

motion with discomfort along the entire spine on flexion and pain in the lumbo pelvic,

lower thoracic, and scapular areas on lateral flexion. (Id.) Petitioner was diagnosed

with “[c]hronic severe cervical sprain and strain with associated cervical subluxation

complex, accompanied by moderate to severe myalgia and cervicalgia,” “[c]hronic

severe thoracic sprain and strain with associated thoracic subluxation complex,

accompanied by moderate to severe thoracic and costal myalgia and pain;” “[c]hronic

severe lumbo pelvic sprain and strain with associated lumbo pelvic subluxation

complex, accompanied by severe myalgia and lumbo pelvic pain;” and “[c]hronic mild to

moderate sprain/strain in left shoulder and arm with associated upper extremity

subluxation complex accompanied by weakness and tingling.” (Id. at 3-4.) After

petitioner initiated regular chiropractic care in November of 2023, he was able to

maintain “an overall decrease in his pain levels.” (Id. at 4.) Petitioner continued

chiropractic treatment through June of 2024. (Ex. P32.)

Based on the records submitted in this case, petitioner continued to receive IVIG

through April of 2024. (Ex. P30.)

b. Testimony

Petitioner filed a sworn affidavit and provided testimony during the entitlement

hearing. (Ex. P9; Tr. 7-34.) Petitioner avers that, prior to the subject vaccination, he

18

“had no history of neurological disorders.” (Ex. P9, ¶ 3.) He maintains that he received

the flu vaccine at issue in this case on September 16, 2016. (Id. ¶ 4; Tr. 13.)

During the hearing, petitioner provided testimony regarding the nature of his

employment at an oil refinery. (Tr. 8-12, 31.) He describes the intense physical

demands of his job, explaining, for example, that some tasks involved climbing towers in

excess of 200 feet via ladder and noting that he was sometimes required to “work

endless days of 12-hour shifts.” (Id. at 9-12, 31.) Petitioner admits that, prior to

receiving the flu vaccination at issue, he suffered from low back pain. (Id. at 13-14, 29-

34.) He recalls receiving some injections for his low back pain and concedes that he

followed up with his primary care provider, Dr. Pickard, for continuing low back pain.

(Id. at 14, 29-31.) However, petitioner states that he was able to work through it and

avers that his low back pain did not prevent him from doing his job or any of his

hobbies. (Id. at 14, 32-34.)

Petitioner summarizes his medical course as contained in his medical records.

(Ex. 9, ¶¶10-28; Tr. 16-28.) He maintains that he started experiencing fatigue and

weakness approximately three days after receiving his flu vaccine. (Tr. 14-16.)

Petitioner states that he followed up with Dr. Pickard the next day and requested to be

tested for Lyme disease as he had spent the prior weekend at his lake house. (Id. at

16-17; Ex. 9, ¶ 10.) He recalls his neurology appointment with Dr. Sadeghi on

September 21, 2016, stating that he remembers experiencing fatigue, weakness,

blurred vision, trouble swallowing, slurred speech, tingling from his head to his foot, and

left sided pain at the time of that encounter. (Tr. 18; Ex. 9, ¶ 11.) Petitioner avers that

prior to receiving his flu vaccine on September 16, 2016, he had never experienced

blurred or double vision, difficulty speaking or swallowing, or tingling from his face down

to his foot. (Tr. 18-19, 21-22.) Dr. Sadeghi prescribed Mestinon and ordered blood

tests for myasthenia gravis (“MG”), which came back negative. (Id. at 23.) After

becoming frustrated with Dr. Sadeghi’s office, petitioner explains that he sought a

second opinion from Dr. Smith in November of 2016. (Id. at 24.) Petitioner avers that

Dr. Smith eventually diagnosed him with polyradiculopathy. (Id. at 24-26.) However, he

also states that Dr. Smith thought petitioner had MG, kept him on the treatment, and

tested him for MG again, which came back negative. (Id. at 25.) Throughout the course

of his care, Dr. Smith continued to prescribe petitioner Mestinon and started him on

prednisone, CellCept, physical therapy, and eventually IVIG treatment. (Ex. 9, ¶¶ 19,

22; Tr. 26.) As of the date of the hearing, he was still taking Mestinon and prednisone,

undergoing IVIG therapy, and attending physical therapy. (Tr. 26-28.) He avers that

prior to his flu vaccine, he had not taken prednisone or any other steroids and had never

undergone IVIG treatment. (Id. at 27-28.)

Petitioner describes how he continues to suffer from constant and severe pain,

fatigue, weakness, and numbness. (Ex. 9, ¶ 29.) These symptoms have limited his

ability to walk, work, perform many activities of daily living, and participate in many

activities he previously enjoyed, such as fishing and hunting. (Id. ¶¶ 29-30.)

19

IV. Expert Opinions and Qualifications5

a. Petitioner’s Expert, Lawrence Steinman, M.D.6

Dr. Steinman submitted three expert reports and testified during the entitlement

hearing. (Exs. P24-P26; Tr. 35-122, 321-33.) He was proffered, without objection, as

an expert in neurology and neuroimmunology. (Tr. 6-7, 38.)

According to Dr. Steinman, the three most likely diagnoses considered by

petitioner’s treating physicians’ included MG, CIDP, and inflammatory

polyradiculopathy. (Ex. P24, p. 6.) However, Dr. Steinman notes that he and Dr. Price

agree that petitioner does not suffer from CIDP. (Ex. P24, p. 6; Ex. P26, p. 2; Tr. 102.)

Therefore, the two competing diagnoses in this case are MG and inflammatory

polyradiculopathy. (Tr. 44-45.) Dr. Steinman states that it is possible for inflammatory

polyradiculopathy and MG to exist as comorbid diagnoses in rare cases. (Ex. P24, pp.

1, 6 (citing Saskia Bolz et al., CIDP, Myasthenia Gravis, and Membranous

Glomerulonephritis – Three Autoimmune Disorders in One Patient: A Case Report, 18

BMC NEUROLOGY 1 (2018) (Ex. P24, Tab 4)); see also Tr. 119-20.) However, he

maintains that in this case, it is more likely than not that petitioner suffers from one or

the other, rather than both conditions. (Tr. 119-20.) While he concedes that a

diagnosis of MG cannot be definitively ruled out and notes that this is a complex case,

Dr. Steinman opines that inflammatory polyradiculopathy is more likely than not the

correct diagnosis in this case. (Tr. 44-45; Ex. P24, pp. 1, 6; Ex. P26, p. 2.)

Dr. Steinman contends that petitioner does not suffer from MG. (Tr. 46; Ex. P24,

p. 1.) To support his opinion, he points to petitioner’s antibody and electrodiagnostic

testing results. (Tr. 45, 100.) He stresses that petitioner tested negative for the

acetylcholine receptor and muscle-specific kinases (“MuSK”) antibodies, which he

maintains are “rarely” negative “in people who actually still have myasthenia gravis.”

(Id. at 45.) Additionally, Dr. Steinman emphasizes that petitioner’s treating neurologist,

Dr. Smith, conducted comprehensive EMG studies which revealed no evidence of

decrement on repetitive nerve stimulation. (Id. at 54, 100; Ex. P24, p. 6.) While he

5

Because I have concluded, for the reasons discussed below, that the diagnostic issue presented by the

parties is dispositive, summaries of the experts’ opinions are limited to their views regarding diagnosis

and do not address their opinions relative to whether the flu vaccine at issue in this case can or did cause

an inflammatory polyradiculopathy.

6

Dr. Lawrence Steinman received his medical degree from Harvard University. (Ex. P24, Tab 1, p. 1.)

He completed a surgery internship and two residencies, one in pediatrics and one in pediatric and adult

neurology, at Stanford University Hospital. (Id.; Tr. 36.) He also completed fellowships at the Weizmann

Institute of Science, the Aharon Katzir-Katchalsky Center, and the National Institutes of Health. (Ex. P24,

Tab 1, p. 1.) He currently works at Stanford University as a professor of Neurology and Neurological

Sciences, Pediatrics, and Genetics. (Id.) He is board certified in psychiatry and neurology. (Id. at 2.) Dr.

Steinman was elected to the Institute of Medicine of the National Academy of Sciences in 2009. (Ex.

P24, pp. 2-3; Tr. 40-41.) He has cared for hundreds of patients with neuroinflammatory diseases,

including inflammatory polyradiculoneuropathy and MG, and he has written several papers on MG. (Ex.

P24, pp. 1-2; Tr. 36.) He has published roughly 600 journal articles. (Ex. P24, Tab 1, pp. 5-49.)

20

concedes that it is possible for an individual to suffer from “double antibody negative,

EMG negative” MG, he opines that he puts “[v]ery low weight” on that possibility in

petitioner’s case. (Tr. 100.)

While he notes that petitioner does not satisfy the antibody or electrodiagnostic

tests to support a diagnosis of MG, Dr. Steinman opines that petitioner “was treated with

the appropriate drugs.” (Ex. P25, p. 12.) Dr. Steinman acknowledges that petitioner

was started on Mestinon, an effective and approved treatment for MG. (Tr. 45.)

Although he concedes that Mestinon is not a medication prescribed to treat

inflammatory polyradiculopathy, Dr. Steinman emphasizes that Dr. Smith “escalated”

petitioner’s therapy by prescribing steroids and CellCept to suppress inflammation,

which he suggests favors a diagnosis of inflammatory polyradiculopathy. (Id. at 45-46.)

However, Dr. Steinman acknowledges that medications, such as prednisone and

CellCept, would also benefit patients suffering from MG. (Id. at 46, 53.) Dr. Steinman

argues that the fact that Dr. Smith added four “highly impactful” medications to

petitioner’s regimen over the course of his treatment indicates that petitioner was not

responding well to Mestinon, which cuts against a finding that MG is the most

appropriate diagnosis. (Id. at 323-24.)

Moreover, Dr. Steinman stresses that Dr. Smith, an expert on neuromuscular

disease, “weighed all of the evidence and cast aside a diagnosis of myasthenia gravis in

favor of inflammatory polyradiculopathy.” (Tr. 45.) He places high value on the opinion

of Dr. Smith as the treating physician and agrees with Dr. Smith that inflammatory

polyradiculopathy, rather than MG, is the correct diagnosis. (Id. at 46, 99.) Specifically,

Dr. Steinman opines that “abandoning the diagnosis of myasthenia gravis is the best

course of action” in this case. (Id. at 53.) While he acknowledges that he cannot point

to a record where Dr. Smith explicitly used the word “inflammatory” when diagnosing

petitioner with a polyradiculopathy, Dr. Steinman contends that based on the context,

particularly his decision to treat petitioner with potent anti-inflammatory medications,

such as prednisone and CellCept, Dr. Smith thinks petitioner has an inflammatory

polyradiculopathy. (Id. at 104-05, 117.) He concedes that Dr. Smith continued to list

MG as a diagnosis in the record for petitioner’s most recent neurology encounter;

however, Dr. Steinman states that he thinks it is very clear that Dr. Smith does not

believe petitioner suffers from MG and argues that just because MG is listed as a

diagnosis within an electronic medical record does not mean that Dr. Smith endorses

MG as an appropriate diagnosis. (Id. at 101.)

In addition, Dr. Steinman opines that petitioner does not suffer from CIDP. (Ex.

P24, p. 6; Ex. P25, p. 13; Tr. 90, 102, 105, 108.) He explains that petitioner does not

have evidence of a demyelinating neuropathy. (Ex. P24, p. 6; Tr. 103.) Specifically, Dr.

Steinman stated that petitioner’s electrodiagnostic studies did not reveal evidence of

demyelination, which would be expected for an individual suffering from CIDP. (Tr. 102,

112.) Again, while he acknowledges that Dr. Smith continues to list CIDP as a

diagnosis in petitioner’s most recent medical records, Dr. Steinman indicates it is very

clear that Dr. Smith does not think petitioner has CIDP. (Id. at 56, 101-02, 108.)

21

According to Dr. Steinman, inflammatory polyradiculopathy has been described

with an autoimmune response to a paranodal protein called contactin-1. (Ex. P24, p. 6

(citing Kathrin Doppler et al., Destruction of Paranodal Architecture in Inflammatory

Neuropathy with Anti-Contactin-1 Autoantibodies, 86 J. NEUROLOGY NEUROSURGERY &

PSYCHIATRY 720 (2015) (Ex. P24, Tab 6)); Ex. P26, p. 2.) Additionally, he notes that

antibodies to another paranodal protein, neurofascin, have been reported in patients

with inflammatory polyradiculopathy. (Ex. P25, pp. 12-13 (citing Atay Vural et al.,

Autoantibodies Against the Node of Ranvier in Seropositive Chronic Inflammatory

Demyelinating Polyneuropathy: Diagnostic, Pathogenic, and Therapeutic Relevance, 9

FRONTIERS IMMUNOLOGY 1 (2018) (Ex. P25, Tab 5); Masato Kadoya et al., IgG4 Anti-

Neurofascin155 Antibodies in Chronic Inflammatory Demyelinating

Polyradiculoneuropathy: Clinical Significance and Diagnostic Utility of a Conventional

Assay, 301 J. NEUROIMMUNOLOGY 16 (2016) (Ex. P25, Tab 6)); Ex. P26, p. 2.)

Relying on a study by Doppler et al., he explains that contactin-1, an antigen at

the node of Ranvier, is targeted in inflammatory polyradiculopathy. (Tr. 62, 66

(discussing Doppler et al., supra, at Ex. P24, Tab 6).) He states that inflammatory

polyradiculopathy does not involve demyelination because contactin-1 is at the node of

Ranvier, not in the myelin. (Id. at 103 (discussing Doppler et al., supra, at Ex. P24, Tab

6).) Dr. Steinman explains that inflammatory polyradiculopathy involves axonal damage

and potentially axonal loss. (Id. at 108.) Because contactin-1 is not limited to nerve

roots and is found in the central and peripheral nervous systems, Dr. Steinman opines

that it is difficult to determine whether inflammatory polyradiculopathy involves a

generalized process affecting the whole spine or discrete lesions at various points on

the spine. (Id. at 116-17.)

In Doppler et al., high reactivity to contactin-1 by enzyme-linked immunosorbent

assay (“ELISA”) was observed in four patients with chronic inflammatory demyelinating

polyradiculopathy and in none of the patients with GBS. (Ex. P24, p. 6 (citing Doppler

et al., supra, at Ex. P24, Tab 6).) Dr. Steinman notes that the four patients in Doppler et

al. presented with a typical clinical picture, namely acute onset of disease and severe

motor symptoms, and three patients developed an action tremor. (Id. (citing Doppler et

al., supra, at Ex. P24, Tab 6).) In these four patients, disruption of paranodal

architecture was observed via immunofluorescence-labelling of paranodal proteins of

dermal myelinated fibers, and histology testing revealed axonal damage with no

classical signs of demyelination. (Id. (citing Doppler et al., supra, at Ex. P24, Tab 6).)

Therefore, the authors of the Doppler et al. study concluded that “anti-contactin-1-

related neuropathy constitutes a presumably autoantibody-mediated form of

inflammatory neuropathy with distinct clinical symptoms and disruption of paranodal

architecture as a pathological correlate. Anti-contactin-1-associated neuropathy does

not meet morphological criteria of demyelinating neuropathy and therefore, might rather

be termed a ‘paranodopathy’ rather than a subtype of demyelinating inflammatory

neuropathy.” (Id. at 7 (citing Doppler et al., supra, at Ex. P24, Tab 6).)

Dr. Steinman opines that the clinical picture of the four patients examined in

Doppler et al. is closest to petitioner’s clinical picture. (Ex. P24, p. 6; Tr. 116 (citing

22

Doppler et al., supra, at Ex. P24, Tab 6).) He states that the four patients examined in

Doppler et al. were found to have a non-demyelinating inflammatory polyradiculopathy.

(Tr. 66, 103-05.) Dr. Steinman opines that petitioner did not suffer from demyelination

and agrees underlying pathophysiology at petitioner’s nerve root is not demyelinating.

(Id. at 103, 111-13.) Therefore, Dr. Steinman contends the diagnosis in Doppler et al.

supports his opinion that inflammatory polyradiculopathy is the diagnosis that fits best in

this case. (Ex. P24, p. 6, Tr. 104-05, 116 (citing Doppler et al., supra, at Ex. P24, Tab

6).)

Specifically, Dr. Steinman opines that petitioner suffered from a significant

aggravation of an inflammatory polyradiculopathy on the weekend he received the flu

vaccine. (Ex. P24, p. 6; Tr. 39, 114-15.) He argues that petitioner’s symptoms following

vaccination, specifically the symptoms in his face, numbness and tingling, and his

difficulty swallowing and speaking, are more likely than not a manifestation of a new

radiculopathy that developed after he received the flu vaccination at issue. (Tr. 50.) Dr.

Steinman explains that petitioner’s preexisting radiculopathy seemed amplified post-

vaccination with new areas of the nervous system, specifically cervical and bulbar nerve

roots, being implicated. (Id. at 43-44, 50.)

Although Dr. Steinman concedes that he would expect an individual suffering

from inflammatory polyradiculopathy to have elevated cerebrospinal fluid (“CSF”)

protein, he explains that petitioner was on anti-inflammatories at the time the CSF

testing was completed which could have kept his CSF albumin levels within normal

range. (Tr. 117-18.) He argues that all of the symptoms that petitioner presented with

post-vaccination can be explained by inflammatory polyradiculopathy. (Id. at 118.)

Furthermore, Dr. Steinman opines that the EMG and nerve conduction study results and

the antibody testing results reinforce his preferred diagnosis of inflammatory

polyradiculopathy because these tests are negative for CIDP and MG. (Id. at 111-12,

118-19.) Accordingly, he agrees that the diagnosis of inflammatory polyradiculopathy is

arrived at in this case by process of elimination. (Id. at 118.) Additionally, Dr. Steinman

agrees that inflammatory polyradiculopathy is an umbrella term for a variety of different

conditions, such as CIDP and GBS, as opposed to a specific clinical entity with strict

diagnostic criteria. (Id. at 115-16.)

While the medical records indicate that petitioner suffered from lumbar

radiculopathy prior to receiving the flu vaccine at issue, Dr. Steinman emphasizes that

there is no reference to any cervical radiculopathy in the pre-vaccination records. (Tr.

42-43.) He places the onset of petitioner’s nerve pain and dysfunction in his cervical

spine after the flu vaccination at issue. (Id. at 43.) Dr. Steinman distinguishes

petitioner’s preexisting lumbar radiculopathy from his post-vaccination clinical

presentation, stating that the anatomy of petitioner’s preexisting radiculopathy was

confined to the lumbar area and extended, at most, into the thoracic area with no

evidence of cervical or bulbar involvement. (Id. at 43-44, 49-50.) He notes that

petitioner’s lumbar radiculopathy primarily manifested as back pain, and that petitioner’s

pre-vaccination records do not reference many of the symptoms that petitioner

complained of after vaccination, including tingling in his face and double vision. (Id. at

23

44.) While acknowledging that petitioner had fatigue prior to vaccination, Dr. Steinman

contends that petitioner complained of fatigue “much more vigorously” post-vaccination.

(Id. at 43-44.)

Dr. Steinman disagrees with Dr. Price’s opinion that the evidence of chronic

polyradiculopathies observed on petitioner’s first EMG indicates that petitioner

sustained a nerve root axonal injury prior to receiving the flu vaccination at issue, with

some of the lumbar radiculopathies being secondary to his preexisting low back pain

experienced in late 2014. (Ex. P25, pp. 12-13; Tr. 47-51.) He fails to understand how

Dr. Price can assert that petitioner’s EMG could pinpoint pathology back to two years

prior. (Ex. P25, p. 13; Tr. 51.) Dr. Steinman explains that an EMG captures one point

in time. (Tr. 49.) Accordingly, there is no way to substantiate Dr. Price’s theory that,

had petitioner undergone an EMG in late 2014 or early 2015, it would have

demonstrated chronic polyradiculopathies with axon loss. (Id.) Dr. Steinman stresses

petitioner’s complaints following vaccination go above the lumbar and thoracic areas,

while his complaints pre-vaccination never went above his low back. (Id. at 49, 52.)

Specifically, he states that post-vaccination, petitioner had complaints of new

symptoms, including blurry vision, double vision, difficulty swallowing, and numbness

and tingling in the face and arm, and contends that these symptoms could not be

attributed to a lumbar radiculopathy. (Id. at 52; Ex. P25, p. 13; Ex. P26, p. 1.)

b. Respondent’s Expert, Raymond S. Price, M.D.7

Dr. Price submitted two expert reports and provided testimony during the

entitlement hearing in this case. (Exs. A, E; Tr. 123-273.) He was proffered as an

expert in neurology without objection. (Tr. 6-7.)

Dr. Price provided an extensive review of petitioner’s medical course. (Ex. A, pp.

2-9.) He notes that petitioner’s pre-vaccination medical history was significant for

chronic low back pain with a lumbar radiculopathy. (Ex. A, p. 2; Tr. 140-41, 249-50.)

Specifically, Dr. Price stresses petitioner’s encounter with his primary care doctor in

December of 2014, at which time petitioner reported that his back pain had not

improved with pain medication and anti-inflammatories, complained of numbness in his

right thigh causing his leg to give out, and noted that he could not walk for more than

100 feet without stopping and was thus not able to work. (Tr. 140-41 (discussing Ex. 8,

p. 252).) He opines that petitioner’s reported history and complaints are certainly

7

Dr. Raymond S. Price received his medical degree from the University of Pennsylvania in 2004, before

going on to complete an internship in internal medicine, a residency in neurology, and a fellowship in

clinical neurophysiology with a neuromuscular focus at the University of Pennsylvania. (Ex. B, p. 1.) He

is board certified in psychiatry and neurology, electrodiagnostic medicine, and neuromuscular medicine,

and he maintains an active medical license in Pennsylvania. (Id. at 2.) He currently works as an

associate professor in Clinical Neurology at the University of Pennsylvania School of Medicine, and as

both the Neurology Residency Director and the Neurohospitalist Division Co-Director in the Department of

Neurology at the University of Pennsylvania. (Id. at 1.) He has published 16 peer-reviewed research

articles and reviews; 41 editorials, reviews, and chapters; and one book. (Id. at 11-15.) Additionally, he

has cared for hundreds of patients with radiculopathies, neuropathies, and neuromuscular junction

diseases, including patients with both CIDP and MG. (Ex. A, p. 1.)

24

suggestive of underlying lumbar spine disease. (Id. at 140.) Given the intense and

physically demanding nature of petitioner’s job and his reported symptomology, Dr.

Price opines “[i]t’s more likely than not by 99.9 percent that” petitioner’s chronic back

pain, leg numbness, and difficulty walking were “secondary to spine degenerative

changes as opposed to some latent inflammatory polyradiculopathy.” (Id. at 140-41.)

Additionally, Dr. Price emphasizes that later records indicate that petitioner’s chronic

back pain with radicular pain improved with physical therapy and chiropractic

maneuvers, which are treatments very commonly used to treat degenerative spine

disease but are not treatments for a preexisting inflammatory polyradiculopathy. (Id. at

153, 155-56 (discussing Ex. P2, p. 192).)

Like Dr. Steinman, Dr. Price addresses the three diagnoses potentially at issue:

MG, CIDP, and inflammatory polyradiculopathy. (Ex. A, pp. 9-13.) However, he opines

that only MG is implicated in this case. (Id.) He explains that autoimmune MG8 is a

disease affecting the neuromuscular junction. (Ex. A, p. 9; Tr. 127.) Dr. Price explains

that MG can be classified based on the presenting clinical symptoms, noting that ocular

MG symptoms are localized to the eye whereas generalized MG can impact the eye, as

well as other muscular components in the body, such as the throat and extremities. (Tr.

127-28.) Additionally, MG can be subdivided based on the presence or absence of

certain antibodies. (Id. at 128; see also Ex. A, p. 9.) Most patients affected by MG have

antibodies against the acetylcholine receptor or the muscle-specific tyrosine kinase

(“MuSK”); however, some individuals have seronegative MG, meaning they test

negative for both known antibodies. (Ex. A, p. 9 (citing Emma Ciafaloni, Myasthenia

Gravis and Congenital Myasthenic Syndromes, 25 CONTINUUM: MUSCLE &

NEUROMUSCULAR DISORDERS 1767 (2019) (Ex. A, Tab 1)); Tr. 128-29, 132-33.)

Therefore, the fact that an individual may test negative for a “known” MG antibody does

not rule out the possibility of autoimmune MG. (Tr. 129.)

Ptosis, frequently asymmetric, and binocular diplopia are the most common

presenting symptoms of MG. (Ex. A, p. 9 (citing Ciafaloni, supra, at Ex. A, Tab 1); see

also Tr. 130.) Other classic symptoms of generalized MG include blurred vision;

dysphagia; jaw closure weakness; facial weakness; speech that is slurred, nasal, or of

reduced volume; and weakness of big muscles. (Ex. A, p. 9 (citing Ciafaloni, supra, at

Ex. A, Tab 1); Tr. 130-31.) Dr. Price emphasizes that MG typically does not involve

weakness in distal muscles, such as muscles in the hands, fingers, toes, and feet. (Tr.

131.) Rather, MG typically involves weakness in proximal muscles and tends to be

localized to the shoulder and pelvic area. (Id.) Limb weakness often results in difficulty

performing tasks, such as getting up from a seated position, walking prolonged

distances, climbing stairs, and tasks that involve raising the arms above the head. (Ex.

A, p. 9 (citing Ciafalonia, supra, at Ex. A, Tab 1); Tr. 131.)

8

Dr. Price explained that in addition to autoimmune myasthenia gravis, there is also a genetic myasthenia

referred to as congenital myasthenic syndrome, which is not associated with antibodies. (Tr. 128-29.)

However, congenital myasthenic syndrome is not at issue in this case. (Tr. 127.) Therefore, all

references to myasthenia gravis (“MG”) in this decision refer to autoimmune MG.

25

Fluctuating and fatigable weakness of muscle groups that worsens with activity

and improves with rest is the core clinical feature of MG. (Ex. A, p. 9 (citing Ciafaloni,

supra, at Ex. A, Tab 1); Tr. 135-36.) Therefore, it is very common for individuals with

MG to describe their symptoms getting worse at the end of the day. (Tr. 135.)

Additionally, similar to individuals with other neurologic conditions such as CIDP,

patients with MG can have a “relapsing-remitting course,” meaning they can experience

flare ups where their symptoms are worse or severe and periods where they experience

low to no symptomology. (Id. at 136.)

Dr. Price explains that there are various approaches to diagnosing an individual

with MG. (Tr. 131-35.) One method involves placing patients on an

acetylcholinesterase inhibitor, such as Mestinon,9 which is a medication that blocks the

breakdown of acetylcholine in the neuromuscular junction. (Id. at 131-32.)

Improvement on an acetylcholinesterase inhibitor is highly suggestive of a

neuromuscular disease, such as MG. (Id. at 132.) Another method is serologic testing,

which involves testing patients for known antibodies. (Id.) Approximately 70-80% of

individuals with generalized MG will test positive for an acetylcholine receptor antibody.

(Id.) Of the population of patients with generalized MG who are negative for the

acetylcholine receptor antibody, around 5-10% are positive for the MuSK antibody. (Id.)

However, approximately 15-20% of individuals with generalized MG test negative for

both known antibodies, and are found to have seronegative MG. (Id. at 129, 133.) In

the case of seronegative MG, Dr. Price notes that some physicians hypothesize that

those cases involve different antibodies, such as the low-density lipoprotein c-receptor

related protein 4 (“LRP4”). (Ex. A, p. 9; Tr. 133.) Providers can also try to diagnose

generalized MG electrophysiologically via repetitive nerve stimulation. (Tr. 133.) If a

reduction in the amplitude (“decrement”) is observed when you repetitively stimulate the

nerve within one second, that is suggestive of a neuromuscular disease, such as MG.

(Id.) However, Dr. Price emphasizes that a decrement on repetitive nerve stimulation is

only observed in approximately 60-70% of patients with MG. (Id. at 133-34, 168.)

Lastly, providers can perform a single-fiber EMG of a weak muscle, which is the most

sensitive diagnostic tool used to confirm the diagnosis of MG and is positive in

approximately 97% of affected patients. (Ex. A, p. 9 (citing Ciafalonia, supra, at Ex. A,

Tab 1)); Tr. 134, 222.) If a single-fiber EMG is normal in a clinically affected muscle, the

diagnosis of MG is excluded. (Ex. A, p. 9 (citing Ciafalonia, supra, at Ex. A, Tab 1)); Tr.

134.) Dr. Price stresses that in his practice, it is not uncommon for him to see patients

who are seronegative with no evidence of decrement on EMG and are only found to

have MG based on a single-fiber EMG. (Tr. 134-35.)

In this case, Dr. Price opines that petitioner was correctly diagnosed with MG.

(Ex. A, p. 9-11.) He emphasizes that when petitioner presented for his first neurology

encounter on September 21, 2016, he reported symptoms consistent with generalized

9

Mestinon is brand name preparation of pyridostigmine bromide, which acts by inhibiting destruction of

acetylcholine to facilitate transmission of impulses across the neuromuscular junction and is used for

symptomatic treatment of myasthenia gravis. Mestinon, DORLAND’S MEDICAL DICTIONARY ONLINE,

https://www.dorlandsonline.com/dorland/definition?id=30704 (last visited Dec. 10, 2025); Pyridostigmine

bromide, DORLAND’S MEDICAL DICTIONARY ONLINE,

https://www.dorlandsonline.com/dorland/definition?id=42398 (last visited Dec. 10, 2025).

26

MG, including fatigue, difficulty with swallowing and speech, and episodic blurred vision

that is associated with fatigue and happens at night. (Tr. 141-44; Ex. A, pp. 9-10

(discussing Ex. P3, p. 5).) Additionally, Dr. Price stresses that petitioner’s physical

examination revealed nasal, slurred speech and mild fatigability of the right upper

extremity with repetitive effort despite normal strength, which are findings also

consistent with generalized MG. (Tr. 144-45; Ex. A, pp. 9-10 (discussing Ex. P3, p. 6).)

At that encounter, Dr. Sadeghi noted that petitioner reported that “[h]e was started on

testosterone injections which did help with fatigue until 6 months ago when he noticed

worsening fatigue then new onset blurred vision.” (Ex. P3, pp. 5, 7.) Dr. Price opines

that this documentation places the onset of petitioner’s worsening fatigue and episodic

blurred vision before September 16, 2016, which suggests that petitioner developed

generalized MG prior to receiving the flu vaccination at issue. (Ex. A, p. 10; Tr. 142-44.)

Dr. Price concedes that some of the symptoms that petitioner reported at this

encounter cannot be attributed to MG. (Ex. A, pp. 9, 11.) These symptoms include pain

when lifting heavy weights, pain when walking more than half of a mile, left-sided

burning pain, and intermittent numbness of the left face, arm, and leg. (Id. at 9-10.)

However, Dr. Price attributes some of these symptoms to petitioner’s preexisting lumbar

radiculopathy. (Id. at 10.) Moreover, Dr. Price stresses that petitioner’s sensory

examination was normal, revealing no objective evidence of his reported sensory

symptoms of facial tremor and numbness in his hands and feet. (Tr. 144-45.)

At his follow up appointment with Dr. Sadeghi on October 6, 2016, petitioner

reported significant improvement in his symptoms since starting Mestinon, noting that

he does not feel as fatigued and denying further episodes of double vision and ptosis.

(Ex. A, p. 10; Tr. 148-49 (discussing Ex. P3, p. 46).) Diplopia and fatigability upon

sustained upward gaze were observed on physical examination. (Ex. A, p. 10; Tr. 148-

50 (discussing Ex. P3, p. 47).) These symptoms are all consistent with MG. (Ex. A, p.

10; Tr. 150.) Dr. Price states that petitioner’s response to Mestinon is exactly what he

would expect to see in a patient with MG. (Ex. A, p. 10; Tr. 148-49, 230.) He notes that

petitioner reported taking more Mestinon when working long shifts to counterbalance

the fact that his symptoms worsen as the day progresses. (Tr. 150.) Again, Dr. Price

opines that this fluctuation in symptoms and fatigability as the day progresses is

indicative of MG. (Id.) He explains that Mestinon is a medication that is specific to

symptomatic treatment of MG, and stresses that “[i]t is not used in the treatment of

virtually any other neurologic conditions.” (Id. at 149; see also id. at 157, 217-18.)

Specifically, Dr. Price emphasizes that Mestinon is not used to treat inflammatory

polyradiculopathy or CIDP, and that he would not expect to see an improvement in a

patient suffering from those conditions on Mestinon alone. (Id. at 149, 151.)

When petitioner first presented to Dr. Smith on November 28, 2016, he reported

a history of symptoms consistent with generalized MG, including bilateral ptosis,

choking on foods and liquids, neck weakness, weakness in his arms and legs with

activity, shortness of breath, and diplopia. (Ex. A, p. 10; Tr. 153-56 (discussing Ex. 2, p.

192).) Dr. Price describes this history as “almost textbook for myasthenia gravis.” (Tr.

156.) He also notes that petitioner’s reported multi-year history of severe fatigue with

27

overexertion is also consistent with MG, which again suggests the possibility that

petitioner developed MG prior to the vaccination at issue. (Id. at 153, 156.) Dr. Price

also concludes that Dr. Smith’s finding of bilateral, asymmetrical ptosis on exam is

again consistent with MG. (Ex. A, p. 10; Tr. 157.) Moreover, Dr. Price stresses that his

opinion that petitioner was correctly diagnosed with MG aligns with the opinions of his

treating neurologists, Dr. Sadeghi and Dr. Smith, because MG was consistently listed as

a diagnosis throughout the course of petitioner’s treatment. (Ex. A, p. 10.)

Dr. Price recognizes that petitioner tested negative for both acetylcholine

receptor binding antibody and MuSK antibody. (Ex. A, p. 10; Tr. 151-53 (discussing Ex.

2, pp. 179-80).) However, as Dr. Price explained, 20% of patients with generalized MG

are seronegative. (Ex. A, p. 10; Tr. 128-29, 216, 224-25, 266-67.) While he concedes

that petitioner’s EMG studies were normal with no evidence of decrement on repetitive

nerve stimulation, Dr. Price stresses that a decrement is only observed in 60-70% of

patients with MG. (Tr. 168, 204.) Moreover, he notes that petitioner had been on

Mestinon at the time of the study, which could have impacted sensitivity of the test. (Id.

at 168.) Petitioner was also never tested for low density lipoprotein c receptor-related

protein 4 antibodies (“LRP4”), nor did he ever undergo single fiber EMG testing, which

is the most sensitive test for diagnosing MG. (Ex. A, p. 10; Tr. 133, 241.)

While Dr. Price stresses that petitioner’s initial marked improvement on Mestinon,

especially with respect to his bulbar symptoms, is indicative of MG (Ex. A, pp. 10, 13-

14; Tr. 149-50, 157, 230), he acknowledges that petitioner subsequently experienced a

regression in the management of some of his symptoms, specifically fatigue and

weakness (Tr. 193-94, 196). He explains that generalized MG is typically not controlled

indefinitely with symptomatic treatment alone. (Id. at 150-51, 193.) While a patient may

experience an initial improvement in their symptoms after initiating Mestinon, the

underlying problem in generalized MG is the immune system. (Id. at 150, 193.)

Therefore, effective treatment requires symptomatic therapy with medications like

Mestinon in combination with medications like prednisone, CellCept, methotrexate, and

IVIG, that suppress or attempt to suppress the antibody production in MG, even if the

specific antibody cannot be identified. (Id. at 150-51, 193-94.) Accordingly, he states

that it is typically standard practice to start a patient with generalized MG on prednisone

and a prednisone-sparing agent, such as CellCept, in addition to Mestinon. (Id. at 193-

94.) Given petitioner’s delay in starting prednisone, Dr. Price opines that it is not

surprising that petitioner, after experiencing a period of initial improvement, started to

notice that some of his symptoms were not responding as well to Mestinon and required

immunosuppression. (Id. at 194.)

Moreover, Dr. Price opines that petitioner’s persistent and excessive fatigue is

likely multifactorial, and points to documentation in the medical records to support this

contention. (Tr. 196-98, 208-09, 214-15, 223, 230.) While MG would contribute to

petitioner’s fatigue, Dr. Price notes that MG would not be expected to cause brain

fogginess, and neither would inflammatory polyradiculopathy. (Id. at 197.) He stresses

that Dr. Smith was concerned that petitioner was suffering from undiagnosed

obstructive sleep apnea, which was ultimately later confirmed via a sleep study. (Id. at

28

197-98; Ex. A, p. 11.) Dr. Smith also diagnosed petitioner with work shift sleep disorder.

(Tr. 198; Ex. A, p. 11.) Given that both of these sleep disorders are not autoimmune in

nature, they would not respond to Mestinon, anti-inflammatories, or steroids. (Tr. 198.)

Accordingly, Dr. Price opines that these untreated sleep disorders likely contributed to

petitioner’s persistent and excessive fatigue. (Id.) He also notes that Dr. Smith

diagnosed petitioner with a distal symmetrical neuropathy in 2019, highlighting that his

neuropathy included a severe pain component that limited petitioner’s sleep thereby

contributing to his fatigue. (Id. at 213-14.)

Dr. Price opines that petitioner does not suffer from CIDP. (Ex. A, pp. 11-12; Tr.

138, 159.) Dr. Price opines that petitioner’s clinical presentation is not indicative of

CIDP, noting that petitioner’s “prominent bulbar symptoms” are not characteristic of

CIDP. (Ex. A, p. 12.) Typically, a loss of reflexes is one of the first symptoms observed

in a demyelinating polyneuropathy. (Tr. 159.) Dr. Price notes that petitioner’s reflexes

were symmetrical and intact throughout 2016, 2017, and 2018, and therefore not

suggestive of CIDP. (Id. at 159 (discussing Ex. P2, p. 196), 236-37.) Furthermore, Dr.

Price indicates that the brief episodic nature of petitioner’s symptoms is inconsistent

with CIDP. (Ex. A, p. 12.) Additionally, petitioner’s lumbar puncture did not reveal

albuminocytologic dissociation, which is typically seen in individuals with CIDP involving

the nerve roots. (Id.)

Moreover, Dr. Price opines that petitioner’s electrodiagnostic testing does not

support a diagnosis of CIDP. (Ex. A, pp. 11-12.) While he recognizes that Dr. Smith

found evidence of demyelination on petitioner’s first EMG and considered a diagnosis of

CIDP, Dr. Price stresses that petitioner did not satisfy any of the electrodiagnostic

criteria for a diagnosis of CIDP on either of his two EMG studies. (Id. at 7, 11-12; Tr.

163-64, 204, 207, 209.) He notes that petitioner’s nerve conduction studies were

“mostly normal” with some “very minimal abnormalities.” (Tr. 162.) Dr. Price disagrees

with Dr. Smith’s finding of possible early demyelinating changes on petitioner’s initial

EMG. (Id. at 162-64, 204.) Although he acknowledges that petitioner’s distal latencies

in his right ulnar nerve and some of his sensory nerves were slightly longer than

expected, Dr. Price explains that the distal latencies were not prolonged enough to meet

formal, definitive criteria for demyelination. (Id. at 163-64.) Therefore, he contends that

Dr. Smith’s finding of evidence of demyelination on petitioner’s first EMG that showed

signs of improvement on his second EMG represents an “overinterpretation” of

petitioner’s nerve conduction studies. (Id. at 209.) Dr. Price stresses that there were no

demyelinating features on either of petitioner’s nerve conduction studies. (Id. at 204.)

He also notes that petitioner’s F wave studies were normal with no evidence of proximal

demyelination or axonal loss. (Id. at 164-65.)

Dr. Price also opines that petitioner’s condition is inconsistent with inflammatory

polyradiculopathy. (Ex. A, pp. 12-13.) He explains that inflammatory polyradiculopathy,

a condition distinct from MG, is a disease involving multiple nerve root injuries. (Tr.

137.) The most common cause of a radiculopathy or polyradiculopathy is degenerative

changes to the spine. (Id. at 137-38.) Other causes include infections and

inflammatory processes, meaning “more of an autoimmune-type condition.” (Id. at 138.)

29

Dr. Prices agrees that inflammatory polyradiculopathy represents a large umbrella

category of various conditions, including CIDP and acute inflammatory demyelinating

polyradiculopathy (“AIDP”). (Id.) Typical symptoms depend on which nerve roots and

cranial nerves are impacted, as well as the cause of the inflammatory polyradiculopathy.

(Id. at 139.) Dr. Price acknowledges that an individual can develop a cranial neuropathy

that causes double vision, dysphagia, or weakness or numbness in particular areas.

(Id.) However, he notes that those symptoms are usually “relatively fixed” with an

inflammatory polyradiculopathy, and therefore likely would not fluctuate as the day

progresses. (Id. at 139-40, 195.)

Dr. Price emphasizes that petitioner’s brief episodes of predominantly bulbar

symptoms and fatigable weakness on examination are not consistent with a diagnosis

of inflammatory polyradiculopathy. (Ex. A, p. 12.) For example, he discusses notations

in petitioner’s medical records that indicate his symptoms would emerge or worsen at

the end of his work shift. (E.g., Tr. 195 (discussing Ex. P6, p. 48).) Dr. Price notes that

these subjective reports demonstrate fatigability within the day, which is very typical for

MG but atypical and not expected in patients with inflammatory polyradiculopathy. (Id.)

He also stresses that petitioner’s sensory examinations were normal. (E.g., id. at 144-

45.) Although petitioner reported some sensory symptoms at his first neurology

encounter on September 21, 2016, including a facial tremor and numbness and tingling

in his face, arm, and leg, Dr. Price highlights that there was no objective evidence of

these sensory symptoms on exam. (Id. at 144-45, 159-60, 195, 229-30, 235, 264-66.)

While he acknowledges that later medical records indicate that petitioner had objective

evidence of a tremor, Dr. Price notes that the tremor was said to be an essential tremor,

which is an inherited tremor unrelated to inflammatory polyradiculopathy. (Id. at 268-

70.) Additionally, Dr. Price stresses that petitioner’s lumbar puncture was normal and

showed no evidence of pleocytosis or elevated cerebrospinal fluid protein, which would

be inconsistent with inflammatory polyradiculopathy. (Ex. A, p. 12; Tr. 190-92, 230-31.)

While Dr. Price recognizes that petitioner’s EMG conducted on December 7,

2016, did show “chronic denervation with increased motor unit amplitude and duration

of the bilateral lower extremity muscles and C7/C8 muscles, with preservation of

sensory responses consistent with lumbar radiculopathies and a C7/8 radiculopathy,” he

opines that the needle EMG findings are not consistent with an inflammatory

radiculopathy beginning after September 16, 2016. (Ex. A, p. 12; see also Ex. E, p. 3;

Tr. 173.) He maintains that the needle EMG findings suggest that petitioner had mild to

moderate nerve root axonal injury prior to receiving his flu vaccination on September 16,

2016. (Ex. A, p. 12; Ex. E, p. 3; Tr. 173.) Dr. Price states that axonal loss has “a very

predictable pattern of changes” demonstrated on needle EMG examination. (Tr. 170.)

He notes that “[w]ith acute motor axonal loss from a radiculopathy of any cause, there

will be denervation of muscle cells that were supplied by the injured axons.” (Ex. E, p.

4.) When a muscle cell is denervated, “meaning it no longer has a neuromuscular

junction or a nerve controlling it,” the muscle cell will start turning itself on after about

two to three weeks from when the injury occurred. (Tr. 170; see also Ex. A, p. 13; Ex.

E, p. 4.) This spontaneous electrical activity is referred to as fibrillation potentials or

positive sharp waves. (Tr. 170.) With a needle EMG examination, Dr. Price explains

30

that, when you put a needle close to a muscle that is denervated, these spontaneous

electrical activities will be observed when the patient is asked not to move. (Id. at 171.)

The denervated muscle cell will continue to electrically turn itself on for at least two

years if it never gets reinnervated, or until collateral reinnervation is complete. (Id.; Ex.

A, p. 13; Ex. E, p. 4.)

When a denervated muscle cell undergoes collateral reinnervation, meaning the

muscle cell is now controlled by a remaining motor axon, the motor unit amplitude and

duration will increase on EMG. (Ex. E, p. 4; Tr. 171-72.) Dr. Price explains that this

finding typically begins to develop three to six months after the acute denervation. (Ex.

E, p. 4; Tr. 172.) During the early stages of reinnervation, the motor units may have

prolonged durations with normal amplitudes. (Ex. E, p. 4.) Therefore, if petitioner had

developed inflammatory polyradiculopathy with axon loss beginning on September 16,

2016, his EMG on December 7, 2016 should have shown “fibrillation potentials or

positive sharp waves without increased motor unit amplitudes.” (Ex. A, p. 13; see also

Ex. E, p. 4.)

Dr. Price stresses that petitioner’s EMG study on December 7, 2016,

demonstrated increased motor unit amplitude and duration, which are findings that

indicate complete reinnervation of the denervated muscle and typically develop three to

six months after the acute denervation. (Ex. A, pp. 12-13; Ex. E, p. 4; Tr. 172.)

Furthermore, he emphasizes that petitioner’s needle examination did not reveal

fibrillation potentials or positive sharp waves, which are signs of subacute denervation.

(Ex. A, p. 13; Ex. E, p. 4; Tr. 174-75.) Accordingly, Dr. Price opines that petitioner’s

EMG findings are consistent with chronic denervation and complete reinnervation

occurring at least three to six months prior. (Ex. E, p. 4; Tr. 173-75; Ex. A, pp. 12-13.)

Thus, Dr. Price argues that the findings of petitioner’s EMG conducted on December 7,

2016, evidence that his radiculopathies predate petitioner’s flu vaccine that he received

on September 16, 2016. (Ex. A, p. 12; Ex. E, p. 3; Tr. 173-75.) He also emphasizes

that Dr. Smith described petitioner’s polyradiculopathy as longstanding and inactive,

rather than subacute or recent, which he argues is consistent with his opinion that

petitioner’s polyradiculopathy clearly predates vaccination. (Tr. 182-83.) Dr. Price also

opines that petitioner’ second EMG/never conduction study is consistent with a chronic,

more than six-month old polyradiculopathy without significant progression or evidence

of worsening injury. (Id. at 203-06 (discussing Ex. P29, pp. 395-96).)

Dr. Price dismisses Dr. Steinman’s reliance on Doppler et al. as evidence of

diagnosis in this case. (Ex. A, p. 13; Tr. 233-39 (discussing Doppler et al., supra, at Ex.

P24, Tab 6).) Specifically, Dr. Price argues that petitioner’s clinical picture is not similar

to the clinical picture of the four patients with anti-contaction-1-associated neuropathy in

Doppler et al. (Ex. A, p. 13; Tr. 233-39.) In Doppler et al., the four patients were all

initially diagnosed with GBS after presenting with an acute onset of rapidly progressing

proximal and distal weakness and distal sensory symptoms. (Ex. A, p. 13; Tr. 234-35.)

Dr. Price acknowledges that petitioner experienced some proximal weakness; however,

he stresses that petitioner did not have progressive distal weakness. (Ex. A, p. 13; Tr.

235.) Additionally, while petitioner reported some numbness and tingling in his hands

31

and feet, Dr. Price observes that those symptoms were never objectively corroborated

on physical exam. (Tr. 235.) Moreover, Dr. Price explains that GBS typically involves

an acute presentation of severe ascending weakness with absent reflexes. (Id. at 236-

37.) He argues that petitioner’s reflexes were intact on exam when he first sought care

in 2016 and 2017, and notes that petitioner never had severe weakness. (Id. at 237.)

The four patients in Doppler experienced initial improvement with IVIG treatment,

whereas petitioner experienced initial improvement on Mestinon. (Id. at 236.) Dr. Price

highlights that there is no evidence in the medical records to suggest that petitioner’s

treating providers initially suspected he was suffering from GBS, nor do the authors in

Doppler et al. suggest that myasthenia gravis was considered as an initial diagnosis for

any of the four patients. (Id. at 238.)

Dr. Price also explains that petitioner’s clinical course differs from the patients in

Doppler et al. from an electrophysiological perspective. (Ex. A, p. 13; Tr. 237.) Prior to

the detection of contactin-1 autoantibodies, the diagnosis for the four patients in Doppler

et al. was modified from GBS to CIDP, a condition that Dr. Price and Dr. Steinman

agree petitioner does not suffer from. (Ex. A, pp. 12-13.) Nerve conduction studies for

all four patients revealed prolonged distal latencies, decreased nerve conduction

velocity, and prolonged F wave latencies, supporting their modified diagnosis of CIDP.

(Id. at 13; Tr. 237.) Dr. Price opines that petitioner’s nerve conduction studies were

normal with no evidence of demyelination. (Ex. A, p.13; Tr. 237.) Lastly, Dr. Price

emphasizes that, while all four patients in Doppler et al. had elevated protein in their

cerebrospinal fluid, petitioner’s lumbar puncture was normal. (Ex. A, p. 13; Tr. 238.)

Dr. Price further notes that Kadoya et al. studied patients with CIDP; however,

because petitioner does not suffer from a CIDP, a conclusion Dr. Steinman agrees with,

Dr. Price opines that this study has no relevance to this case. (Id. (citing Kadoya et al.,

supra, at P25, Tab 6).) Additionally, both Vural et al. and Kadoya et al. studied patients

with antibodies against human neurofascin155. (Id. at 2 (discussing Kadoya et al.,

supra, at P25, Tab 6; Vural et al., supra, at Ex. P25, Tab 5).) However, there is no

evidence in the medical records that suggests petitioner was ever assessed for human

neurofascin155 antibodies. (Id.) Moreover, Dr. Price stresses that petitioner’s clinical

presentation is not consistent with the patients in Kadoya et al. and Vural et al., which

suggests that petitioner does not have antibodies against human neurofascin155. (Id.

at 2-3.) Specifically, petitioner “did not have loss of proprioception sensation, or diffuse

areflexia, or hyporeflexia as seen with a peripheral cause of a sensory ataxia or tremor.”

(Id. at 3.) Nor did the medical records show elevated cerebrospinal fluid protein,

prolonged distal motor or f-wave latencies, or enhancement or enlargement of the spinal

root on MRI. (Id.) Lastly, petitioner was treated with IVIG, not Rituximab. (Id.)

Considering patients with human nuerofascin155 antibodies typically respond poorly to

IVIG treatment, Dr. Price contends that petitioner’s treating physicians were clearly not

considering a nuerofascin155 antibody mediated condition. (Id.)

In sum, Dr. Price contends that it is “exceedingly more likely than not” that

petitioner suffers from autoimmune, seronegative MG based on his clinical presentation.

(Tr. 228, 241.) Based on documentation in the medical records, Dr. Price opines that

32

the onset of petitioner’s MG was likely before petitioner received his flu vaccination on

September 16, 2016. (Id. at 142-44, 153, 156.) In addition to MG, Dr. Price states that,

based on his review of the medical records, petitioner also has bilateral lumbar

radiculopathies caused by his spinal stenosis, sensory polyneuropathy likely secondary

to prolonged steroid use, shift work sleep disorder, obstructive sleep apnea, and a

chronic, longstanding, inactive polyradiculopathy that likely predates petitioner’s flu

vaccine at issue. (Id. at 228.) He maintains that petitioner’s clinical presentation is not

consistent with inflammatory polyradiculopathy or a contactin-1 mediated disease. (Id.

at 232-33, 242.) Lastly, Dr. Price agrees with Dr. Steinman that petitioner does not

suffer from CIDP as his EMG studies did not reveal evidence of demyelination. (Id. at

228, 231.)

c. Respondent’s Expert, John T. Bates, Ph.D.10

Respondent’s second expert, Dr. Bates, submitted two expert reports in this case

and testified at the entitlement hearing. (Exs. C, F; Tr. 274-320.) He was proffered as

an expert in immunology without objection. (Tr. 6-7.) Dr. Bates defers to Dr. Price on

the issue of petitioner’s diagnosis and addresses Dr. Steinman’s theory of causation as

it relates to inflammatory polyradiculopathy, the diagnosis endorsed by Dr. Steinman.

(Ex. C, p. 3; Tr. 312-13.) Accordingly, his opinion is not further summarized.

V. Analysis

In this case, petitioner initially alleged that the flu vaccine at issue caused him to

develop MG and CIDP. (ECF No. 1.) Following his expert’s assessment, petitioner filed

an amended petition alleging that the flu vaccine caused him to suffer MG, CIDP, and/or

inflammatory polyradiculopathy. (ECF No. 44.) In their prehearing submissions, the

parties indicated that they agree that petitioner’s injury is not CIDP. (ECF No. 69, p. 1;

ECF No. 70, p. 16, n.4; ECF No. 72, p. 15, n.5.) Additionally, both Dr. Steinman and Dr.

Price testified that petitioner does not suffer from CIDP. (Tr. 108, 159.) However, the

parties dispute whether MG or inflammatory polyradiculopathy is the best supported

diagnosis in this case.

Petitioner asserts that he suffers from inflammatory polyradiculopathy, stressing

that all of the documentation from his treating physicians and Dr. Steinman’s expert

opinion support the diagnosis. (ECF No. 70, pp. 16-19.) In his prehearing submissions,

petitioner emphasizes that Dr. Steinman and his treating neurologist, Dr. Smith, agree

that MG is not an appropriate diagnosis, and that they both opine that he is

experiencing polyradiculopathy. (Id.; ECF No. 74, p. 2.) After the conclusion of the

entitlement hearing, petitioner released any claim that he suffered vaccine-caused MG.

10

Dr. John T. Bates received his Ph.D. in microbiology from the University of Alabama at Birmingham in

2005, before going on to complete two post-doctoral fellowships, one in the Department of Microbiology

and Immunology at Wake Forest University School of Medicine in 2010 and another in the Vanderbilt

Vaccine Center at Vanderbilt University School of Medicine in 2014. (Ex. D, p. 1.) He currently works as

an assistant professor at the University of Mississippi Medical Center in both the Department of Medicine

and the Department of Microbiology and Immunology. (Id. at 2.) He has authored 19 publications. (Id. at

2-4.)

33

(ECF No. 77.) In his post-hearing briefing, petitioner argues that his flu vaccination

caused significant aggravation of his preexisting lumbar spine radiculopathy which he

alleges developed into polyradiculopathy involving his cervical spine. (ECF No. 83, p. 2;

ECF No. 85, p. 2.) Petitioner acknowledges that his treating neurologist diagnosed him

with both MG and polyradiculopathy and maintains that an individual can suffer from

both conditions. (ECF No. 85, pp. 2-3.)

Respondent asserts that petitioner was correctly diagnosed with MG, which is the

best supported diagnosis in this case. (ECF No. 72, pp. 15-17; ECF No. 84, pp. 15-18.)

He contends that petitioner’s clinical presentation is inconsistent with inflammatory

polyradiculopathy and thus cannot be preponderantly supported given the record

evidence. (ECF No. 72, pp. 16-17; ECF No. 84, pp. 17-18.) Therefore, respondent

maintains that, because petitioner cannot demonstrate that he suffers from inflammatory

polyradiculopathy by a preponderance of the evidence, petitioner’s claim fails as his

proposed causal theory is based only on a diagnosis of inflammatory polyradiculopathy.

(ECF No. 84, p. 18.)

For the reasons discussed below, I find that there is preponderant evidence that

petitioner suffers from MG rather than an inflammatory polyradiculopathy.

a. Petitioner’s symptoms are consistent with MG

Dr. Price emphasized that petitioner’s symptoms were primarily bulbar with some

proximal weakness which is “perfectly consistent” with MG. (Tr. 229; see also id. at

201, 267; Ex. A, pp. 13-14.) Specifically, he noted that petitioner’s symptoms of

worsening fatigue, ptosis, dysphagia, diplopia, blurred vision, slurred nasal speech,

shortness of breath, and fatigable weakness with activity, support a diagnosis of MG.

(Ex. A, pp. 9-11,13-14 (citing Ciafaloni, supra, at Ex. A, Tab 1); Tr. 141-45, 148-50, 153-

57, 267.) While petitioner experienced some proximal weakness throughout his clinical

course (e.g., Tr. 196 (discussing Ex. P6, p. 52)), Dr. Price stressed that there was not

much evidence of distal weakness in the medical records, which is consistent with MG

(Id. at 229, 235). Moreover, throughout the hearing, Dr. Price testified that even when

Dr. Smith started to suspect that petitioner suffered from CIDP, petitioner’s clinical

presentation remained consistent with MG. (E.g., id. at 218-19, 221-23, 226.) While Dr.

Price acknowledged that some of petitioner’s subjective sensory complaints cannot be

explained by MG, all of petitioner’s objective findings are consistent with MG. (Id. at

265-66.)

Moreover, Dr. Price stressed that fluctuating and fatigable weakness of muscle

groups that worsens with activity and improves with rest is the core clinical feature of

MG. (Ex. A, p. 9 (citing Ciafaloni, supra, at Ex. A, Tab 1); Tr. 135-36.) As pointed out

by Dr. Price, there are several notations in the medical records indicating that

petitioner’s symptoms fluctuated, worsening as the day progressed and with repetitive

use. For example, at his initial neurology encounter on September 21, 2016, petitioner

reported experiencing episodic blurred vision that was associated with fatigue and

occurred at night. (Ex. P3, p. 5.) Additionally, at his encounter with Dr. Sadeghi on

34

October 6, 2016, petitioner reported needing to take an increased dose of Mestinon

when he is working long shifts to counterbalance the fact that his symptoms recur at the

end of the day. (Id. at 46.) This fluctuating and fatigable weakness was also objectively

demonstrated on physical exam, with instances of diplopia and fatigability being

observed with sustained upward gaze and mild fatigability of the right upper extremity

with repetitive effort. (Id. at 6, 47.)

Ultimately, Dr. Price is persuasive in opining that petitioner’s clinical presentation

is consistent with a diagnosis of MG. (Tr. 267.) Dr. Steinman likewise agreed that

petitioner’s presenting symptoms post-vaccination were predominantly bulbar in nature.

(Id. at 118.) He also acknowledged that petitioner’s presenting symptoms, specifically

double vision and trouble chewing and swallowing, are symptoms typically observed in

patients with MG. (Id.) Moreover, petitioner’s treating neurologist, Dr. Smith, classified

many of the symptoms identified above as “myasthenic symptoms.” (E.g., Ex. P6, p.

48.) Therefore, both experts and petitioner’s treating physician appear to agree that

petitioner’s presentation is consistent with MG.

b. Petitioner’s antibody and electrodiagnostic testing results are not

inconsistent with a diagnosis of MG

Petitioner points to his antibody and EMG testing as support for his argument

that MG is not the most appropriate diagnosis in this case. (Tr. 45-46, 100, 118, 323;

ECF No. 70, pp. 17-19; Ex. P24, p. 5.) Dr. Steinman testified that individuals who have

MG “rarely” test negative for both the acetylcholine receptor and MuSK antibodies. (Tr.

45.) He also stressed that Dr. Smith conducted a comprehensive electrodiagnostic

study, which was negative for MG. (Id. at 100.) While he conceded that there is “a

small chance” that petitioner could have seronegative, EMG negative MG, he stated he

would put “[v]ery low weight” on that. (Id.)

However, Dr. Price explained that a sizeable minority of individuals with

autoimmune MG will lack a known antibody and have no evidence of decrement on

repetitive nerve stimulation. (Tr. 128-29, 133-35, 241.) Specifically, Dr. Price testified

that seronegative MG, meaning an individual is negative for both the acetylcholine

receptor and MuSK antibodies, is observed in approximately 15-20% of cases of

autoimmune MG. (Id. at 128-29, 216, 224-25, 266-67; Ex. A., pp. 9-10 (citing Caifaloni,

supra, at Ex. A, Tab 1).) Additionally, Dr. Price explained that a decrement on repetitive

nerve stimulation is only observed in about 60-70% of individuals with MG. (Tr. 133-34,

165-68.) He noted that the sensitivity of repetitive nerve stimulation depends upon the

muscle being tested, indicating that if the muscle is not a weak muscle, then the

sensitivity of the test declines. (Id. at 133-34.)

Moreover, petitioner was already on Mestinon at the time of his EMGs (Ex. P6,

pp. 9, 91-92, 111-12), which may have impacted the sensitivity and quality of the

testing. (Tr. 232.) Although petitioner was instructed to hold his Mestinon for 36 hours

prior to his EMG (Ex. P6, p. 9), his treating neurologist, Dr. Smith, raised the possibility

of a false negative in a later treatment record, noting that Mestinon may not have been

35

“completely ‘out of [petitioner’s] system’” at the time of his EMG testing (Ex. P28, p.

1479). Dr. Price explained that

if you are trying to stress the neuromuscular junction with multiple repetitive

stimulations within a second and the patient is able to keep more

acetylcholine in the neuromuscular junction because of the presence of

Mestinon, then you are not stressing it as much as you think and therefore

you will have a false negative test.

(Tr. 232.)

Dr. Price testified that it is not uncommon for neurologists at academic medical

centers to see patients who are seronegative and had a normal repetitive nerve

stimulation who are only found to have MG by a single-fiber EMG of a weak muscle.

(Tr. 134-34; see also Ex. A, p. 9.) A single-fiber EMG, the diagnostic test for MG with

the highest sensitivity, and is positive in 97% of affected patients. (Ex. A, p. 9 (citing

Caifaloni, supra, at Ex. A, Tab 1).) A normal single-fiber EMG in an affected muscle

excludes MG as a possible diagnosis. (Id. (citing Caifaloni, supra, at Ex. A, Tab 1).)

However, petitioner never underwent a single-fiber EMG. (Id. at 9-10; Tr. 222, 241.)

Dr. Price is persuasive in explaining why petitioner’s antibody and

electrodiagnostic testing results do not rule out MG as a likely diagnosis.

c. Petitioner’s improvement on Mestinon supports a diagnosis of MG

Both parties acknowledge that petitioner reported experiencing “significant”

improvement in his symptoms after starting Mestinon. (ECF No. 70, p. 2; ECF No. 72,

p. 4 (citing Ex. P3, pp. 46-47).) At his neurology follow-up visit on October 6, 2016,

petitioner reported that since initiating Mestinon, his fatigability improved, noting that he

was able to perform most of his duties at work without issue, and he also denied further

episodes of double vision and ptosis (Ex. P3, p. 46), which are all symptoms consistent

with MG (Tr. 150). When asked whether this marked improvement in petitioner’s

symptoms after starting Mestinon is what he would expect to see in an individual with

MG, Dr. Price testified, “Yes, a hundred precent.” (Id. at 230.) Additionally, he

emphasized that taking Mestinon alone would not provide any symptomatic relief in an

individual suffering from inflammatory polyradiculopathy. (Id. at 151.)

Dr. Price explained that Mestinon, as an acetylcholinesterase inhibitor, is a

medication specific to the symptomatic treatment of MG. (Tr. 149.) He stressed that

“[i]t is not used in the treatment of virtually any other neurologic conditions[,]” including

GBS, CIDP, sarcoidosis, or radiculopathies, and would therefore not be expected to

provide any symptomatic relief in individuals with those diseases. (Id.) Moreover, Dr.

Steinman agreed that Mestinon is an effective treatment for MG and conceded that it is

not a medication used to treat inflammatory polyradiculopathy. (Id. at 45, 98.) He also

opined that petitioner “was treated with the appropriate drugs.” (Ex. P25, p. 12.) Given

his concession that Mestinon is a drug that provides effective treatment for MG and not

36

a medication prescribed to treat inflammatory polyradiculopathy, Dr. Steinman failed to

explain why petitioner was appropriately treated with Mestinon if he does not suffer from

MG. Instead, Dr. Price is persuasive in opining that symptomatic improvement in an

individual on Mestinon “would be highly suggestive of a neuromuscular junction

disease,” such as MG. (Tr. 132.)

During the hearing, Dr. Steinman emphasized that Dr. Smith added prednisone,

IVIG, CellCept, and methotrexate to petitioner’s medication regimen throughout the

course of petitioner’s treatment. (Tr. 323-24.) He argued that the fact that Dr. Smith

added these “highly impactful” medications on top of Mestinon suggests that petitioner

was not responding as well to Mestinon as respondent claims, thereby casting doubt on

MG as the appropriate diagnosis. (Id.) However, Dr. Steinman also conceded that

additional medications prescribed by Dr. Smith, specifically prednisone and CellCept,

would benefit an individual suffering from MG. (Id. at 45-46.) During the hearing, Dr.

Price persuasively testified that, because the underlying problem in autoimmune MG is

the immune system, effective treatment often requires medications that address the

underlying immune component in addition to symptomatic therapy like Mestinon. (Id. at

150-51.) Therefore, he explained that it is not uncommon for patients with MG to be

prescribed medications such as prednisone, CellCept, methotrexate, and IVIG in

combination with Mestinon. (Id. at 150-51, 262.) While Dr. Smith did add these

medications due to a suspicion of CIDP, he never removed MG from petitioner’s list of

diagnoses or stopped Mestinon. Moreover, the fact that Dr. Smith noted that petitioner

responded to IVIG treatment is not informative for the reasons discussed by Dr. Price.

Additionally, Dr. Price explained that generalized MG is not typically controlled

indefinitely with symptomatic management alone. (Tr. 193.) While an individual with

MG may initially show signs of improvement after starting symptomatic treatment like

Mestinon, the individual’s symptoms will typically worsen over time or respond less to

Mestinon if the underlying autoimmune activity that is causing the MG is not treated.

(Tr. 193-94.) Accordingly, Dr. Price emphasized that individuals with generalized MG

are typically started on prednisone in addition to Mestinon. (Id.) However, in this case,

petitioner did not start taking prednisone and CellCept until January of 2017,

approximately 3 months after initiating Mestinon. (Ex. P6, pp. 22-25.) Given petitioner’s

delay in starting on an immunosuppressant, Dr. Price is persuasive in opining that it is

not surprising that petitioner’s symptoms worsened after initially showing signs of

improvement after starting Mestinon.11 (Tr. 194.)

11

When petitioner reported experiencing significant fatigue and brain fog despite remaining on Mestinon

in March of 2017, Dr. Smith diagnosed petitioner with shift work sleep disorder and expressed concern for

obstructive sleep apnea, which petitioner was subsequently diagnosed with. (Ex. P6, p. 55; Ex. P15, p.

12.) Dr. Price testified that while MG certainly could have contributed to some of petitioner’s fatigue, it

would not explain his entire clinical presentation as MG does not cause brain fog. (Tr. 197.) Critically, he

stressed that inflammatory polyradiculopathy also does not cause brain fog. (Id.) Therefore, Dr. Price

explained that petitioner’s two different sleep disorders were likely contributing, at least in part, to

petitioner’s extreme fatigue. (Id. at 197-98, 209.) Because these sleep disorders are not autoimmune

conditions, they would not respond to Mestinon or immunosuppressants. (Id. at 198.) Petitioner failed to

address these non-neurologic causes of fatigue when assessing petitioner’s response to Mestinon.

Accordingly, the symptomatic flares petitioner experienced, particularly with his fatigue, do not evidence

that petitioner was not responding effectively to Mestinon.

37

In sum, petitioner’s response to Mesitnon is strong evidence supporting a

diagnosis of MG. Petitioner has not offered any compelling explanation for why he

would have experienced this symptomatic improvement after starting Mestinon if his

presentation was primarily due to inflammatory polyradiculopathy.

d. Petitioner mischaracterizes Dr. Smith’s opinion regarding the most

appropriate diagnosis in this case

As a treating provider, petitioner argues that Dr. Smith’s findings should carry

significant weight as to the appropriate diagnosis in this case. (ECF No. 70, pp. 17-19

(citing Andreu, 569 F.3d at 1375); see also ECF No. 83, pp. 6-7.) Petitioner contends

that Dr. Smith “did not agree” that he was suffering from MG and diagnosed petitioner

with polyradiculopathy. (ECF No. 70, p. 17.) Dr. Steinman testified that it is very clear

that Dr. Smith does not think petitioner suffers from MG, and he agrees with him. (Tr.

98.) He stated that Dr. Smith weighed all the evidence and abandoned a diagnosis of

MG in favor of inflammatory polyradiculopathy. (Id. at 45, 53.) Petitioner stresses the

importance of the record for his follow-up encounter on March 14, 2022, in which Dr.

Smith documented that, “[w]ith regards to his underlying disease, [petitioner] does not

meet criteria either for myasthenia gravis or CIDP, but does have a polyradiculopathy

and fatigable weakness that appears to respond to IVIG.” (ECF No. 70, pp. 18-19

(emphasis omitted) (citing Ex. P28, p. 1012).)

Dr. Price suggested, however, that Dr. Smith’s comment that petitioner did not

meet the criteria for MG simply reflects that petitioner tested negative for MG-associated

antibodies and had no decrement on repetitive nerve stimulation (Tr. 222-24), points

addressed separately above as not being dispositive of diagnosis. Indeed, there are

several records that include documentation by Dr. Smith expressing his frustration with

the lack of antibody and electrodiagnostic evidence to confirm a diagnosis of MG. (See,

e.g., Ex. P6, pp. 77, 97, 131; Ex. P28, p. 438; Ex. P29, p. 374.) However, this does not

actually indicate that Dr. Smith had concluded that MG is not an appropriate diagnosis.

Dr. Smith also repeatedly documented that petitioner should consider undergoing

testing for low density lipoprotein c receptor-related protein 4 antibodies (“LRP4”) (Ex.

P28, pp. 436, 721, 832), which, as explained by Dr. Price, demonstrates that Dr. Smith

was still considering the involvement of a rare antibody for MG (Tr. 224-25). Moreover,

despite his remark about petitioner not meeting the criteria, Dr. Smith still listed MG as

one of petitioner’s diagnoses on March 14, 2022. (Ex. P28, p. 1026.) In fact, Dr. Smith

continued to include MG as a diagnosis through March 27, 2023, and no records for

subsequent neurology encounters were filed in this case.12 (Id. at 1493.) Indeed,

petitioner testified that Dr. Smith continued to prescribe him Mestinon, noting that he

was still taking the medication as of the date of the hearing. (Tr. 27.) As explained

12

Notably, Dr. Steinman did not accept that ongoing inclusion of MG as a listed diagnosis in petitioner’s

electronic medical record is meaningful as to Dr. Smith’s thinking. (Tr. 101.) I have considered this point

but conclude that the continued presence of MG as a listed diagnosis does provide some evidence of Dr.

Smith’s thinking when viewed in the context of the record as a whole.

38

above, both parties’ experts recognize that Mestinon is an effective treatment for MG

and is not a medication used to treat inflammatory polyradiculopathy. (Id. at 45, 98,

149, 151.)

Accordingly, petitioner is not persuasive in arguing that Dr. Smith abandoned a

diagnosis of MG.

e. The medical records do not preponderantly support a diagnosis of

inflammatory polyradiculopathy

Petitioner argues that “[a]ll of the documentation from Petitioner’s treating

physicians, in the weeks and months after vaccination, support the diagnosis of

inflammatory polyradiculopathy.” (ECF No. 70, p. 16.) In that regard, the record for

petitioner’s initial EMG on December 7, 2016, does indicate that Dr. Smith interpreted

petitioner’s EMG findings to be consistent with a “longstanding, progressive, relatively

inactive, polyradiculopathy.” (Ex. P19, p. 10.) Moreover, both Dr. Steinman and Dr.

Price agree that petitioner’s EMG reveals evidence of a polyradiculopathy. However, a

finding of a polyradiculopathy on EMG does not automatically warrant a conclusion that

the polyradiculopathy is inflammatory. Dr. Price testified that a polyradiculopathy can

develop from a variety of different causes, with the most common cause being

degenerative spine disease. (Tr. 137-38.) Regarding petitioner’s own

polyradiculopathy, Dr. Price explained that petitioner’s EMG results, history of back

pain, and negative lumbar puncture, are consistent with a mechanical explanation. (Id.

at 137-41, 190-92, 205-06.)

Dr. Steinman repeatedly testified that petitioner’s treating neurologist, Dr. Smith,

diagnosed petitioner with inflammatory polyradiculopathy. (E.g., Tr. 45-46, 53.)

However, after extensively reviewing the medical records filed in this case, the

undersigned was unable to locate any record in which Dr. Smith specifically diagnosed

petitioner with an inflammatory, non-demyelinating polyradiculopathy. Rather, careful

review of the medical records reveals that Dr. Smith diagnosed petitioner with a

polyradiculopathy without ever explicitly specifying that petitioner’s polyradiculopathy

was inflammatory, as conceded by petitioner in his post-hearing briefing. (ECF No. 83,

p. 9.) Moreover, when questioned by the undersigned, Dr. Steinman was unable to

point to a record in which Dr. Smith specifically employed the terminology “inflammatory

polyradiculopathy.” (Tr. 104-05.) Instead, Dr. Smith identified a broad list of possible

etiologies for petitioner’s polyradiculopathy, including structural, inflammatory,

infectious, neoplastic, vascular, metabolic, and genetic etiologies. (Ex. P19, p. 10.)

Nonetheless, Dr. Steinman testified that, even if Dr. Smith never explicitly used

the terminology “inflammatory polyradiculopathy,” it is clear that he felt petitioner’s

polyradiculopathy was inflammatory in nature. (Tr. 105.) This is informed two additional

points. First, Dr. Steinman points to the fact that Dr. Smith had petitioner on two anti-

inflammatory drugs, a steroid and CellCept. (Id.) He contends that Dr. Smith’s decision

to prescribe petitioner these medications demonstrates that he thinks petitioner’s

polyradiculopathy is inflammatory. (Id.) Second, in the record for petitioner’s encounter

39

on November 19, 2020, Dr. Smith noted that “[t]he fact that [petitioner’s] previous

neuropathic findings in his ulnar and median nerve is actually improved on

immunomodulatory therapy has suggested that his EMG quantitated and clinically

identified motor neuropathic findings are likely inflammatory in nature (CIDP).” (Ex.

P28, p. 436.)

However, as discussed separately above, Dr. Steinman’s observation regarding

anti-inflammatory medications is undercut by his testimony acknowledging that steroids

and CellCept are medications that would also benefit an individual suffering from MG.

(Tr. 45-46.) Therefore, the fact that petitioner was prescribed anti-inflammatories is not

compelling evidence that petitioner was suffering from an inflammatory

polyradiculopathy. Additionally, Dr. Smith’s specific reference to a likely inflammatory

process is inextricably linked to his interpretation of petitioner’s second EMG study as

showing an improvement in demyelination. (Id. at 219-20.) Yet, both Dr. Steinman and

Dr. Price disagree with Dr. Smith’s finding of evidence of demyelination on EMG and

clearly opined that petitioner did not ever suffer from demyelination. (Tr. 102-03, 110-

11, 113, 116, 138, 163-64, 201, 209, 216-17, 232.) Therefore, these points do not lend

any support to petitioner’s argument that inflammatory polyradiculopathy is the most

appropriate diagnosis in this case.

Ultimately, Dr. Steinman indicated that his preferred diagnosis of inflammatory

polyradiculopathy is arrived at by a process of elimination. (Tr. 118.) He stressed that

petitioner’s EMG and nerve conduction study results and the antibody testing results

reinforce his preferred diagnosis of inflammatory polyradiculopathy because these tests

are negative for MG. (Id. at 111-12, 118-19.) However, as explained above, petitioner’s

antibody testing results and EMG findings do not rule out a diagnosis of MG. Moreover,

Dr. Steinman agreed that inflammatory polyradiculopathy is an umbrella term for a

variety of conditions, such as CIDP. (Id. at 115-16.) However, especially because both

parties agree that petitioner does not suffer from CIDP, Dr. Steinman is unable to point

to any specific diagnosis under that umbrella, instead relying broadly on the concept of

inflammatory polyradiculopathy as a non-specific umbrella diagnosis with no real

diagnostic criteria. Dr. Steinman has not pointed to any significant objective evidence in

the medical records that affirmatively supports his argument that inflammatory

polyradiculopathy is the most likely diagnosis in this case.

f. Petitioner is not persuasive in arguing that his clinical presentation is

most consistent with inflammatory polyradiculopathy

Dr. Steinman testified that all of petitioner’s presenting symptoms could be

explained by a diagnosis of inflammatory polyradiculopathy. (Tr. 118.) Because

petitioner’s presenting symptoms were predominantly bulbar, Dr. Steiman explains that

petitioner’s inflammatory polyradiculopathy would involve the “nerve roots that come off

the central nervous system and innervate the extraocular muscles and the swallowing

muscles.” (Id.) Dr. Price acknowledged that an individual can develop a cranial

radiculopathy that causes symptoms similar to those experienced by petitioner,

including dysphagia, double vision, weakness, and numbness. (Id. at 139.) However,

40

the fact that a polyradiculopathy implicating cranial nerves is possible, does not

necessarily demonstrate that inflammatory polyradiculopathy is the best supported

diagnosis in this case.

Dr. Price opined that with inflammatory polyradiculopathy, symptoms are

relatively fixed and therefore likely would not fluctuate as the day progresses. (Tr. 139-

40, 195.) As explained above, there are several notations within the medical records

indicating that petitioner reported his symptoms worsened with fatigue and as the day

progressed, as well as documentation of fatigable weakness with repetitive use

observed on physical exam. Petitioner has not offered any explanation of how the

fluctuating fatigability of petitioner’s symptoms is consistent with inflammatory

polyradiculopathy. While Dr. Steinman cited literature in which patients who were found

to have an anti-contactin-1-associated neuropathy experienced a relapsing and

remitting course of disease (Doppler et al., supra, at Ex. P24, Tab 6, p. 6), there is no

evidence in that article that suggests those patients experienced fluctuations in their

symptoms as the day progressed. Moreover, Dr. Price distinguished a relapsing and

remitting course from the fluctuating fatigability within the course of a day that is

frequently observed in patients with MG. (Tr. 135-36.) Therefore, petitioner has not

explained how his fluctuating fatigability is consistent with a diagnosis of inflammatory

polyradiculopathy.

To support his opinion that inflammatory polyradiculopathy is the most likely

diagnosis in this case, Dr. Steinman placed significant emphasis on the Doppler et al.

paper. (Ex. P24, pp. 6-7; Tr. 104-08, 110, 116, 120 (discussing Doppler et al., supra, at

Ex. P24, Tab 6).) In Doppler et al., the authors tested the serum of patients diagnosed

with either GBS or CIDP for autoantibodies against contaction-1. (Doppler et al., supra,

at Ex. P24, Tab 6, pp. 1, 3; Tr. 234.) The authors noted that autoantibodies directed

against nodal and paranodal proteins, such as contactin-1, had recently been detected

in patients with GBS and CIDP. (Doppler et al., supra, at Ex. P24, Tab 6, p. 1.) High

reactivity to contactin-1 by ELISA was observed in four of the patients studied, all of

whom had CIDP. (Id. at 1, 3.) While all four patients had electrodiagnostic studies

indicative of demyelination and therefore consistent with a diagnosis of CIDP, sural

nerve biopsies were performed and semithin sections demonstrated axonal loss and

degeneration of nerve fibers without typical features of demyelination, such as onion

bulbs or numerous thinly myelinated fibers. (Id. at 4-5, 8.) Analysis of myelinated fibers

in skin biopsies revealed disruption of paranodal architecture. (Id. at 1, 6, 8.)

Accordingly, the authors state that these histopathological findings support the theory

that damage to the paranodes, rather than the myelin sheath, causes impairment of

nerve conduction in the anti-contactin-1-associated neuropathy subtype of CIDP. (Id. at

8.)

Dr. Steinman opined that petitioner’s clinical presentation is most consistent with

the clinical picture of the four patients discussed in Doppler et al., stating that the

diagnosis of inflammatory polyradiculopathy in Doppler et al. is the diagnosis that fits

best in this case. (Tr. 116, 120; Ex. P24, p. 6 (discussing Doppler et al., supra, at Ex.

P24, Tab 6).) However, Dr. Steinman did not further explain or specifically elaborate on

41

how petitioner’s clinical presentation was similar or consistent with the four patients in

Doppler et al. Moreover, Dr. Price persuasively described how petitioner’s clinical

presentation does not resemble those four patients from a clinical or

electrophysiological perspective. (Tr. 233-39; Ex. A, p. 13.)

In Doppler et al., the authors summarized the clinical picture of each of the four

patients. (Doppler et al., supra, at Ex. P24, Tab 6, pp. 3-4.) All four patients were

initially diagnosed with GBS due to their acute and rapidly progressive distal and

proximal weakness, as well as their distal sensory symptoms. (Doppler et al., supra, at

Ex. P24, Tab 6, p. 3; Tr 234-35.) However, the diagnosis for all four of the patients was

modified to CIDP when their symptoms progressed after experiencing a short period of

initial improvement. (Doppler et al., supra, at Ex. P24, Tab 6, p. 3.) Additionally, all four

of the patients in Doppler et al. experienced initial improvement with IVIG treatment.

(Id.) The nerve conduction studies of all four patients showed prolonged distal

latencies, decreased nerve conduction velocity, and prolonged F-wave latencies, which

worsened throughout the course of the disease. (Tr. 237-38; Doppler et al., supra, at

Ex. P24, Tab 6, p. 4.) Total cerebrospinal fluid protein was elevated in all four patients.

(Tr. 238; Doppler et al., supra, at Ex. P24, Tab 6, p. 4).

As explained by Dr. Price, petitioner’s clinical presentation is distinguishable from

the four patients in Doppler et al. (Tr. 233-39; Ex. A, p. 13.) There is no record

evidence indicating that petitioner’s treating providers diagnosed him with GBS, and

both experts agree that petitioner does not suffer from CIDP. Dr. Price emphasized

that, in contrast to the four patients in Doppler et al., the onset of petitioner’s disease

was not characterized by rapidly progressive distal and proximal weakness and distal

sensory symptoms. (Tr. 235.) As explained above, petitioner’s symptoms were

predominantly bulbar with some proximal weakness. While he complained of sensory

symptoms at his initial neurology encounter, Dr. Price highlighted that those symptoms

were never objectively corroborated on physical exam. (Tr. 235.) Additionally,

petitioner experienced initial improvement on Mestinon, not IVIG, and there is nothing in

the Doppler et al. paper that suggests that treating providers for any of the four patients

suspected MG as a potential diagnosis. Moreover, both parties agree that petitioner did

not have elevated protein in his cerebrospinal fluid. (Id. at 117, 238.) There is also no

evidence in the medical records indicating that petitioner was ever tested for contactin-1

antibodies or that his treating providers suspected that petitioner suffered from a

contactin-1 mediated disease.

Most notably, both Dr. Steinman and Dr. Price agree that petitioner’s nerve

conduction studies were relatively normal and did not show any evidence of

demyelination. (Tr. 111, 160-65, 237.) Therefore, petitioner’s electrodiagnostic studies

stand in stark contrast to the progressively worsening prolonged distal and F-wave

latencies and decreased nerve conduction velocity observed in the four patients in

Doppler et al. Importantly, the authors in Doppler et al. emphasized that anti-contactin-

1-associated neuropathy is associated with a reduction of nerve conduction velocity.

(Doppler et al., supra, Ex. P24, Tab 6, p. 8.) Based on their findings, the authors

suggested that reduced nerve conduction velocities and increased distal latencies, as

42

observed in the four patients at issue, could be indicative of disruption to the paranodal

architecture caused by autoantibodies against contactin-1. (Id.) Therefore, I find Dr.

Price’s testimony regarding the relevance of Doppler et al. persuasive. While Doppler

et al. demonstrates that a contacted-1-mediated autoantibody disease is possible, it is

not evidence that inflammatory polyradiculopathy is more likely than not the most

appropriate diagnosis in petitioner’s case.

In sum, petitioner has not offered preponderant evidence that his clinical

presentation is most consistent with a diagnosis of inflammatory polyradiculopathy.

g. Petitioner is not persuasive in suggesting that petitioner suffers from

both MG and inflammatory polyradiculopathy

In his prehearing briefing, petitioner states that petitioner’s treating neurologist,

Dr. Smith, “did not agree that he was experiencing MG but rather his diagnosis was that

[petitioner] was experiencing polyradiculopathy.” (ECF No. 70, p. 17.) He emphasizes

that Dr. Smith documented that petitioner “does not meet criteria” for a diagnosis of MG,

stressing that petitioner’s EMG studies did not reveal evidence of decrement on

repetitive nerve stimulation and that petitioner tested negative for any antibody markers

for MG. (ECF No. 70, pp. 18-19 (emphasis omitted) (citing Ex. P28, pp. 1012, 1479; Ex.

P26, pp. 126-27).) Additionally, throughout the hearing, Dr. Steinman repeatedly

testified that petitioner does not suffer from MG. (E.g., Tr. 46, 53-54, 95, 98,100, 104-

05, 109, 120.)

However, in his post-hearing reply brief, petitioner stresses that Dr. Smith

diagnosed him with both MG and polyradiculopathy. (ECF No. 85, p. 2.) He argues

that finding MG is an appropriate diagnosis does not warrant a conclusion that

inflammatory polyradiculopathy is not also an appropriate diagnosis in this case. (Id. at

2-3.) Petitioner emphasizes that both Dr. Steinman and Dr. Price agreed that an

individual could suffer from both MG and inflammatory polyradiculopathy. (Id. at 3

(citing Tr. 119-20, 240).)

While both experts did agree that it is possible that an individual could have both

MG and inflammatory polyradiculopathy, petitioner ignores the fact that Dr. Steinman

explicitly testified that it is far more likely in this particular case that the petitioner suffers

from one or the other. (Tr. 119-20.) Accordingly, given the undersigned’s conclusion

that petitioner more likely than not suffers from MG, Dr. Steinman has effectively agreed

that his preferred diagnosis of inflammatory polyradiculopathy is unlikely. Even if the

undersigned were to overlook Dr. Steinman’s testimony on this point, the analysis

above explains why petitioner likely does suffer MG and likely does not suffer an

inflammatory polyradiculopathy. Therefore, petitioner’s suggestion that he suffers from

both MG and inflammatory polyradiculopathy is unpersuasive.

43

h. Althen Analysis is Unnecessary

Petitioner did not offer any causal theory or argument implicating his flu vaccine

as a cause of his MG. In fact, petitioner ultimately released his claim that his flu vaccine

caused MG. (ECF No. 77.) Accordingly, no Althen analysis is necessary in this case.

Lombardi, 656 F.3d at 1352-53. However, even if petitioner had continued to pursue his

MG claim, it is unlikely he would have succeeded in preponderantly showing that his flu

vaccine caused his condition. Prior petitioners have been unsuccessful in seeking to

provide theories of causation establishing that the flu vaccine can cause or significantly

aggravate MG. E.g., Kelly v. Sec’y of Health & Human Servs., No. 16-1548V, 2023 WL

3274159 (Fed. Cl. Spec. Mstr. May 5, 2023) (undersigned); Smilo v. Sec’y of Health &

Human Servs., No. 18-1585V, 2023 WL 3918397 (Fed. Cl. Spec. Mstr. May 15, 2023)

(Dorsey); Demore v. Sec’y of Health & Human Servs., No. 20-1265V, 2024 WL

4542934 (Fed. Cl. Spec. Mstr. Sep. 26, 2024) (Moran), aff’d, 175 Fed. Cl. 756 (2025).

VI. Conclusion

There is no question that petitioner has suffered. He has my sympathy, and I do

not question his sincerity in bringing this claim. However, for all the reasons discussed

above, I find that petitioner has not met his burden of proof in this case. Therefore,

pursuant to § 300aa-12(d)(3)(A) and Vaccine Rule 10, this decision concludes that

petitioner is not entitled to an award of compensation. Absent a timely motion for

review, the Clerk is directed to enter judgment dismissing this case for insufficient proof

in accordance with Vaccine Rule 11(a).

IT IS SO ORDERED.

s/Daniel T. Horner

Daniel T. Horner

Special Master

44