Fisher v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 20-855V

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*

CRAIG FISHER, * Chief Special Master Corcoran

*

Petitioner, * Filed: December 4, 2023

v. *

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SECRETARY OF HEALTH *

AND HUMAN SERVICES, *

*

Respondent. *

*

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Andrew D. Downing, Downing, Allison & Jorgenson, for Petitioner.

Madelyn Weeks, U.S. Dep’t of Justice, Washington, DC, for Respondent.

ENTITLEMENT DECISION 1

On July 14, 2020, Craig Fisher filed a petition for compensation under the National

Vaccine Injury Compensation Program (the “Vaccine Program”). 2 Petition (ECF No. 1) (“Pet.”).

Petitioner alleges that he suffered from brachial neuritis 3 following an influenza (“flu”) vaccine

administered on January 19, 2018. Pet. at 1. A two-day Entitlement Hearing took place on April

13–14, 2023. Now, having reviewed the record and considered the expert testimony heard at trial,

I deny entitlement, because the claimed injury has not been preponderantly established.

1

Under Vaccine Rule 18(b), each party has fourteen (14) days within which to request redaction “of any information

furnished by that party: (1) that is a trade secret or commercial or financial in substance and is privileged or

confidential; or (2) that includes medical files or similar files, the disclosure of which would constitute a clearly

unwarranted invasion of privacy.” Vaccine Rule 18(b). Otherwise, the whole Ruling will be available to the public in

its present form. Id.

2

The Vaccine Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660,

100 Stat. 3758, codified as amended at 42 U.S.C. §§ 300aa-10 through 34 (2012) [hereinafter “Vaccine Act” or “the

Act”]. Individual section references hereafter will be to Section 300aa of the Act (but will omit the statutory prefix).

3

As the experts who testified in this matter agreed, brachial neuritis can also be termed neuralgic amyotrophy or

Parsonage-Turner Syndrome, interchangeably.

I. Factual Background

Prior to vaccination, Petitioner had a past medical history significant for obesity, diabetes

mellitus with circulatory complication, acute abdominal pain syndrome, atrial fibrillation,

coronary artery disease, chronic renal disease, hypertension, and sleep apnea. Ex. 3 at 13–14.

On January 12, 2018, Petitioner presented to St. Francis Hospital for epigastric pain. Ex. 3

at 4. Petitioner underwent an abdominal CT which showed “findings consistent with small bowel

obstruction with [a] transition point in a left lower anterior abdominal wall hernia which

demonstrate[d] fat stranding indicating incarceration.” Id. at 13. The next day, Petitioner

underwent a laparotomy with release of the small bowel obstruction and a ventral hernia repair.

Id. at 15. Petitioner remained in the hospital until January 19, 2018, and was discharged with

diagnoses including acute respiratory failure, hypokalemia, and ventral hernia repair. Ex. 3 at 82,

120; Ex. 2 at 7. Before being discharged, Petitioner received a flu vaccine in his left deltoid. Ex. 2

at 5.

Two days later, on January 21, 2018, Mr. Fisher was seen by a St. Francis home health care

nurse for post-surgery aftercare. Ex. 7 at 10–73. At this time, he reported that he had not monitored

his blood sugar levels, since they had improved after losing more than two hundred pounds. Id. at

34. He also stated that he was “planning to return to work in [the] near future.” Id. at 34. However,

Petitioner did not at this time report any left shoulder or arm pain. Id.

Onset of Arm Pain and Treatment

On January 23, 2018, Mr. Fisher saw his primary care physician (“PCP”), Patrick Murphy,

M.D., at Warren Clinic South Memorial, with complaints of “severe [left] arm pain from [the] [f]lu

vaccine [four] days ago,” and noting that the “pain began [two] days after the injection.” Ex. 9 at

235. Upon examination, Petitioner exhibited “tenderness [in his] left upper arm with no redness,

warmth or firmness.” Id. at 241. Dr. Murphy’s assessment was left upper extremity pain and

recommended Petitioner begin pain relief medication. Id.

The following day (January 24, 2018), Petitioner had a second home health care visit. Ex.

7 at 41. Mr. Fisher now reported left arm pain ranging 3/10—noting that within the last twenty-

four hours, his pain had ranged from 0 to 6/10. Id. Petitioner described his pain as acute,

intermittent, and exacerbated by movement. Id. Petitioner had another home health care visit on

January 31, 2018, at which time he reiterated what he previously had reported. Id. at 60. And on

February 7, 2018, Petitioner had yet another home health care visit, at which time he stated that

“he [had] been released by the doctor to return back to work and want[ed] to be discharged, he

[wa]s no longer home-bound and no longer ha[d] a skilled need.” Id. at 73.

2

On March 30, 2018, Petitioner visited Dr. Murphy for treatment of his diabetes and

hypertension. Ex. 9 at 246. A review of systems indicated left hand numbness and the assessment

was diabetes mellitus with circulatory complication, including chronic diabetic polyneuropathy.

Id. at 254–57.

Three months later, on July 3, 2018, Petitioner saw Dr. Murphy for management of his

chronic conditions. Ex. 4 at 5–15. Petitioner’s physical exam was normal, and Dr. Murphy’s

assessment included diabetic polyneuropathy. Id. at 12. Petitioner again saw Dr. Murphy on

August 23, 2018, for urinary frequency and left arm pain. Id. at 20. At this visit, Petitioner reported

that his onset of arm pain occurred in January 2018, due to an injection reaction. Id. Petitioner

noted that the pain was in his “[l]eft upper arm to [his] fingers,” and further described the pain as

aching and moderate, with numbness in his second and third fingers. Id. A review of systems was

positive for numbness, and Dr. Murphy’s assessment included chronic polyneuropathy. Id.

Over the next ten months, Petitioner saw Dr. Murphy six times for ongoing management

of his chronic conditions plus several other complaints, including bilateral ear pain and heartburn.

Ex. 4 at 60, 70, 90, 106, 117, 126.

Subsequent Treatment

Petitioner saw neurologist Brooke McQueen, M.D., on September 24, 2019 (now more

than a year and a half since the relevant vaccination), reporting “numbness, tingling, burning, and

pins and needle sensation in the [left extremity] . . . [that] started about a year ago after the flu shot

[in January 2018] . . ..” Ex. 4 at 141. Petitioner noted numbness and tingling in his left hand,

specifically in his second and third digits, and noted that his PCP thought the flu vaccination “hit

a nerve” but that the pain would improve over time. Id. Dr. McQueen suspected that Petitioner

might have carpal tunnel syndrome (“CTS”) versus residual median sensory neuropathy from the

flu vaccine. Dr. McQueen ordered electromyography (“EMG”) 4 and nerve conduction study

(“NCS”) 5 tests—the results showing bilateral CTS and chronic cervical radiculopathy, with the

left side worse than the right for both conditions. Id. at 160; Ex. 8 at 14–16, 20–25.

Six months later, on March 24, 2020, Petitioner had a telehealth appointment with Dr.

4

“Electromyography” is defined as “an electrodiagnostic technique for recording the extracellular activity (action

potentials and evoked potentials) of skeletal muscles at rest, during voluntary contractions, and during electrical

stimulation; performed using any of a variety of surface electrodes, needle electrods, and devices for amplifying,

transmitting, and recording the signals. Electromyography,

https://www.dorlandsonline.com/dorland/definition?id=15854&searchterm=electromyography (last visited Dec. 4,

2023).

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“Nerve Conduction Study” is defined as “a diagnostic test that evaluates the function of [the] peripheral nerves. [It]

can help detect the presence and extent of peripheral nerve damage.” Nerve Conduction Study,

https://my.clevelandclinic.org/health/treatments/24821-nerve-conduction-study (last visited Dec. 4, 2023).

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McQueen, at which time he complained of continued “numbness/tingling in [his] left hand/fingers”

and noted “some numbness, tingling, burning/sharp/electrical pain,” in several of his left fingers

Ex. 4 at 163. Upon examination, Petitioner exhibited normal range of motion with mild atrophy in

the left thenar region. Id. at 174. Dr. McQueen’s assessment included: “1) Neuropathy, 2) Cervical

radiculopathy, 3) Bilateral carpel tunnel syndrome, 4) Neuropathic pain of hand, left.” Id. at 175.

Dr. McQueen also documented that Petitioner showed “mild pinched nerves in the neck; bilateral

C5 and C7 on the left, nothing to do at this time, likely age related, may consider neck imaging in

the future.” Id. at 176. It was recommended that Petitioner wear wrist splints at night to help with

his CTS. Id.

II. Witness Testimony

A. Petitioner’s Witnesses

1. Craig Fisher

Petitioner was the only fact witness to testify. See generally Tr. at 8–57. He began his

testimony addressing his pre-vaccination history, which he characterized as uneventful. Tr. at 9.

Petitioner acknowledged that he had struggled with his weight, but that in the months leading up

to his January 2018 vaccination, he had lost approximately one hundred pounds. Id. at 9–10.

Petitioner also briefly discussed his hospitalization prior to receipt of the flu vaccine on

January 19, 2018. Tr. at 11–14. Around October-November 2017, he had been experiencing some

intermittent stomach pain and underwent a H. Pylori 6 test—the result of which was positive. Tr.

at 11. Petitioner’s treating physician prescribed him some antibiotics to treat the H. Pylori. Id.

Petitioner recalled getting ready to leave for an out-of-town convention when his stomach pain

became a bigger concern. Id. at 12–13. His ex-wife advised him to go to the nearby emergency

care clinic so that a CT scan could be performed to see if something more was going on—and after

receiving such a scan, he was told that he needed to go to the hospital for further evaluation and

care. Id. at 13. Once there, he was immediately prepped for surgery as it appeared he had a

herniated intestine. Id. at 13. Petitioner remained in the hospital for a week following his surgery

and was discharged on January 19, 2018. Id. at 14.

Petitioner recalled that before being discharged, he was advised to receive a flu vaccine,

since contracting the flu after intestinal surgery could cause several complications. Tr. at 14. He

had received the flu vaccine “pretty regularly” in the past, and while he had not planned to get one

6

“Helicobacter Pylori” is defined as “a species that causes gastritis and peptic ulcers and is also associated with gastric

cancer. Formerly called ‘Campylobacter pylori.’” Helicobacter Pylori, Dorland’s Medical Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=80297&searchterm=Helicobacter+pylori (last visited Dec. 4,

2023).

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that year, he decided to do so in order to avoid any potential complications. Id. at 15. Two days

after, on January 21, 2018, however, Petitioner woke up with an aching pain in his left upper arm

so severe he worried he was having a heart attack. But an exam performed during a visit from his

home health care team did not confirm this as the explanation for his pain. Id. at 16.

On January 23, 2018, Petitioner had a regularly-scheduled appointment with his PCP, Dr.

Murphy—at which time he was seeking additional treatment options for his pain, as it had gotten

to the point where it was keeping him awake at night. Tr. at 20–21. Petitioner further noted that he

had not taken any pain medication since his hernia surgery (out of concerns for avoiding

dependency on it), but that “[the pain] was more than [he] could bear,” and that he was “desperately

looking for a solution.” Id. at 21–22.

Then, on or about January 30, 2018, Petitioner began experiencing a numbness/tingling

sensation in his index finger which eventually spread to his middle finger, thumb, and half of his

left hand. Tr. at 27. He further testified that the pain in his shoulder “was horrible,” and that “the

only relief [he] found was icing it down” or scheduling massage appointments. Id. Over the course

of the next seven to eight months, Petitioner reported to Dr. Murphy on several different occasions,

since his symptoms persisted—and remain to this day. Id. at 32–33. He eventually sought a

neurology referral from Dr. Murphy at an August 2018 appointment but noted that he was unable

to schedule a consult until approximately a year later, on September 24, 2019. Id. at 34.

Petitioner concluded his testimony by briefly emphasizing that the injury had negatively

impacted his ability to work—noting that he eventually had to transition to a half-time position

approximately six months following vaccination. Tr. at 37. Although he was hoping to return to a

full-time position, it was “difficult to focus” due to the lack of sleep from the pain. Id.

2. Peter-Brian Andersson, M.D.

Dr. Andersson, a clinical neurologist, prepared two written reports for Petitioner and

testified in support of the contention that Petitioner suffered brachial neuritis caused by his receipt

of the flu vaccine. See generally Tr. at 59–179; Report, dated Feb. 18, 2022, filed as Ex. 10 (ECF

No. 26-1) (“Andersson First Rep.”); Report, dated Dec. 18, 2022, filed as Ex. 42 (ECF NO. 41-1)

(“Andersson Second Rep.”).

Dr. Andersson received his medical degree from the University of Cape Town, South

Africa, in 1986, as well as an honors degree in Medical Biochemistry in 1988. Tr. at 59–60;

Curriculum Vitae, filed as Ex. 11 (ECF NO. 26-2) (“Andersson CV”) at 1. Thereafter, Dr.

Andersson received a Ph.D. equivalent in experimental pathology from the University of Oxford,

United Kingdom in 1991. Tr. at 61; Andersson CV at 1. He later became a college lecturer in

Immunology at Christ Church, University of Oxford. Id. Dr. Andersson then completed his

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residency in neurology, followed by a fellowship in Neuroimmunology and Multiple Sclerosis at

the University of California, San Francisco. Tr. at 62; Andersson CV at 1. In addition to completing

the previously mentioned fellowship, Dr. Andersson also completed a Neuromuscular fellowship

at Oregon Health Sciences University as well as at Stanford University. Id. He is licensed to

practice medicine in California, and he is board certified by the American Board of Psychiatry and

Neurology and the American Board of Electrodiagnostic Medicine. Tr. at 62–63; Andersson CV

at 1. He has published several articles on the topic of neurology and immune-mediated diseases,

and has treated over a hundred cases of brachial neuritis, as well as thousands of cases for cervical

radiculopathy, ulnar neuropathy, and carpal tunnel syndrome. Tr. at 64; Andersson CV at 2.

Dr. Andersson began his testimony with a brief overview of Petitioner’s pre-vaccination

history—emphasizing that upon his admission to the hospital on January 12, 2018, he had not been

experiencing any numbness, arthralgias, or myalgias (making his post-vaccination condition

meaningful by contrast). Tr. at 70; Ex. 3 at 114–15. Dr. Andersson then provided an explanation

of brachial neuritis and its associated symptoms. Tr. at 71. Brachial neuritis is an inflammatory

condition with “an acute onset that affects the brachial plexus and related nerves and at times

roots.” Id. at 71–72. He identified several distinctive factors associated with brachial neuritis:

striking severity; striking distribution; striking persistence; apparent lack of cause; and associated

neurogenic features—all of which were observed in Petitioner, according to Dr. Andersson. Tr. at

72–73; Andersson First Rep. at 7–8.

Dr. Andersson analyzed each factor relevant to the diagnosis, maintaining that Petitioner’s

brachial neuritis was more likely a vaccine-induced sensory form of brachial neuritis rather than

cervical radiculopathy or CTS. Tr. at 137–38; Andersson First Rep. at 7–8. Dr. Andersson

emphasized Petitioner’s reported widespread distribution of severe pain, sudden onset, and

intractability as distinctive of brachial neuritis—further noting Petitioner’s initial concern that he

was suffering a heart attack, his inability to sleep, and the ineffectiveness of pain medication. Tr.

at 134; Andersson First Rep. at 7–8.

Dr. Andersson next explained that brachial neuritis is typically a “patchy syndrome,” but

that Petitioner exhibited “very widespread, yet very severe [pain], and brachial neuritis does that.”

Tr. at 135. Moreover, Petitioner’s pain not only began without any apparent cause, but it never

seemed to improve. Id. at 135–36. Dr. Andersson further commented on the persistence of

Petitioner’s pain—noting that “other structures that have a differential for casing pain, when they

[are] musculoskeletal, they generally exacerbate or relive, depending on your position or

movement,” but Petitioner did not experience later reduction in symptoms. Id. at 137–38.

Accordingly, Dr. Andersson opined, brachial neuritis was the only diagnosis that would unify all

of Petitioner’s presenting symptoms. Id.

Brachial neuritis can be triggered by an activation of the immune system—including, but

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not limited to, infection, vaccination, or recovery from surgery. Tr. at 75, 78–79; Anderson First

Rep. at 10; J. LJspeert et al., Neuralgic Amyotrophy, 34 Current Opinion Neurology 605, 608

(2021), filed as Ex. 15 (ECF No. 27-4) (“LJspeert”) (finding that “any immune-related factor can

trigger NA, including infection, vaccination, immunotherapy such as interferon or immune-

checkpoint inhibitors, recovery from surgery, pregnancy or childbirth, trauma or psychological

distress”); G. Suarez et al., Immune Brachial Plexus Neuropathy: Suggestive Evidence for an

Inflammatory-Immune Pathogenesis, 46 Neurology 559, 560 (1996), filed as Ex. 19 (ECF No. 27-

8). However, Dr. Andersson hesitated to endorse the opinion that surgery can be a mechanism of

injury for brachial neuritis—arguing that the literature is simply unclear as to the degree of

association. Tr. at 77–78.

To explain the mechanistic immune process that would result in brachial neuritis, Dr.

Andersson provided testimony regarding the distinctions between a primary and secondary

immune response. The primary immune response occurs in “a naïve host who [is] generating an

immune response for the first time,” whereas “in the secondary, there is a memory” or a “recall of

that original immune response in the T and the B cells [] [and] plasma cells.” Tr. at 80. An

individual’s secondary immune response would become more rapid as well as more vigorous when

an individual encountered antigens again, in subsequent exposures—and as Dr. Andersson

explained, this is not only exactly what vaccination is predicated on, but likely explains the nature

of Petitioner’s immune response to the flu vaccine he received. Id. at 81; Andersson First Rep. at

11–12.

In support of his opinion that Petitioner’s brachial neuritis was likely mediated by a

secondary/adaptive immune process, Dr. Andersson offered several items of literature. Tr. at 83;

Andersson First Rep. at 11–12; See, e.g., F. Vriesendorp et al., Anti-Peripheral Nerve Myelin

Antibodies and Terminal Activation Products of Complement in Serum of Patients with Acute

Brachial Plexus Neuropathy, 50 Arch. Neurology 1301, 1303 (1993), filed as Ex. 23 (ECF No.

28-2) (“Vriesendrop”) (supporting the notion that complement-dependent, antibody-mediated

demyelination may participate in the initial peripheral nerve damage or augment an ongoing

process based on the detection of anti-PNM antibodies and complement activation products in

three patients with brachial plexus neuropathy). Some items were case reports. A. Hamati-Haddad

& F. Fenichel, Brachial Neuritis following Routine Childhood Immunization for Diphtheria,

Tetanus, and Pertussis (DTP): Report of Two Cases and Review of the Literature, 99 Pediatrics

602 (1997), filed as Ex. 32 (ECF No. 29-1) (reporting two cases of brachial neuritis following

receipt of the tetanus toxoid vaccination in adults); S. Queler et al., Parsonage-Turner Syndrome

following COVID-19 Vaccination: MR Neurography, 302 Radiology 84, 85 (2022), filed as Ex.

33 (ECF No. 29-2) (“Queler”) (reporting onset of Parsonage-Turner syndrome post-vaccination

within 28 days and as early as the same day as immunization).

Dr. Andersson also opined that the timeframe in which Petitioner’s brachial neuritis began

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was consistent with an adaptive/secondary immune-mediated process. He noted that when an

individual is exposed to viral antigenic material to which he or she has previously been exposed,

an immune-mediated process can occur more rapidly. Tr. at 93. As Dr. Andersson explained, an

individual will “have a host who has an immune system primed and ready to go, . . . and now they

have an antigenic trigger from a vaccination that will generate a response to this vaccine.” Id. In

so responding, the immune system has also “activated clones of cells that were memory cells, []

so the effect is now to generate a host attack . . . and this attack is going to be severe [and rapid]

because the immune response is secondary.” Id. P. Tsairis et al., Natural History of Brachial Plexus

Neuropathy, 27 Arch Neurology 109, 111 (1972), filed as Ex. 16 (ECF No. 27-5) (“Tsairis”)

(finding that “the most striking feature of this disease was the rapid onset of pain usually followed

by muscle weakness or paralysis”). Thus, he deemed an onset of two to three days post-vaccination

to be medically acceptable.

B. Respondent’s Witnesses

1. Brian Callaghan, M.D.

Dr. Callaghan, a neuromuscular specialist in treatment of neuropathies like brachial

neuritis, prepared two written reports for Respondent and testified for Respondent in support of

the contention that there is not a causal association between the flu vaccine and brachial neuritis.

See generally Tr. at 181–281; Report, dated June 2, 2022, filed as Ex. A (ECF No. 31-1)

(“Callaghan First Rep.”); Report, dated Feb. 19, 2023, filed as Ex. E (ECF No. 44-1) (“Callaghan

Second Rep.”).

Dr. Callaghan received his undergraduate degree from the University of Michigan in 1999,

his medical degree from the University of Pennsylvania in 2004, and his Masters in Science from

the University of Michigan in 2011. Curriculum Vitae, filed as Ex. B (ECF No. 31-2) (“Callaghan

CV”) at 1; Tr. at 183–84. He became a clinical lecturer at the University of Michigan Health

System’s Department of Neurology in 2009 and has been an Associate Professor of Neurology

there since 2018. Callaghan CV at 1; Tr. at 182. He is licensed to practice medicine in Michigan,

and he is board certified by the American Board of Psychiatry and Neurology and the American

Board of Electrodiagnostic Medicine. Id. Dr. Callaghan has published mover than 120 articles and

medical book chapters, with a majority focusing on neuropathy, and including the appropriate

diagnostic evaluation and treatment of neuropathy. Callaghan CV at 14–24; Callaghan First Rep.

at 1; Tr. at 186. Dr. Callaghan has averred that he has treated more than 50 patients with brachial

neuritis. Callaghan Rep. at 1.

Dr. Callaghan began his testimony addressing the rarity of both brachial neuritis and pure

sensory brachial neuritis—noting that in his fifteen years as a neurologist, he has treated only a

handful of cases for brachial neuritis, but has never seen a case of pure sensory brachial neuritis.

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Tr. at 189. He defined brachial neuritis to be “a syndrome characterized by pain, followed by

weakness and atrophy, that usually occurs in one limb and evolves over a series of months.” Id.

He then briefly addressed the diagnostic criteria for brachial neuritis—emphasizing that “in the

absence of neurographic studies, [diagnosis] requires weakness in [the] muscles supplied by more

than one peripheral nerve, and then EMG and nerve conduction studies need to localize injury to

the brachial plexus.” Id. at 191; Callaghan First Rep. at 4–5. This kind of testing was in fact critical

to the diagnosis. Tr. at 206.

Dr. Callaghan testified that he agreed with Petitioner’s treating physicians: Petitioner

neither suffered from brachial neuritis nor from a pure sensory form of the condition, but instead

more likely suffered from diabetic neuropathy, cervical radiculopathy, and/or CTS. Id. at 194.

Indeed, there was no mention, even as part of a differential diagnosis, of brachial neuritis in treater

records, and he was never formally so diagnosed. Id. at 195. Rather, Petitioner’s diagnosis was

consistent with the symptoms he had reported to his treating physicians, and Dr. Callaghan

emphasized that the nature of those symptoms, as well as the pain involved, were common to

diabetic neuropathy, cervical radiculopathy, or CTS. 7 Id. at 197–98. He would have made the same

diagnoses as Petitioner’s treating physicians did, and would not have considered a pure sensory

form of brachial neuritis as explanatory, given the record. Id. at 209.

Dr. Callaghan went on to identify why Petitioner’s reported symptoms plus exam and

testing findings did not satisfy the diagnostic criteria for brachial neuritis. Tr. at 215; Callaghan

First Rep. at 5. For example, Petitioner never reported weakness in the affected arm, nor was it

demonstrated on exam—thus not meeting criterion two. Id. Additionally, Petitioner did not display

motor, sensory, and reflex deficiencies upon examination. The degree of pain Petitioner was

reporting was not a factor favoring a brachial neuritis diagnosis, since actual severity of these

conditions often did not correlate with complained-of pain levels. Id. Moreover, Petitioner’s

symptoms did not appear to be widespread, but instead were isolated to his left upper extremity

and three left hand fingers. Id. at 221–22. According to Dr. Callaghan, patients suffering from

brachial plexus injuries typically experience more widespread symptoms. Id.

The EMG/NCS testing performed in this case was also not confirmatory for a brachial

neuritis diagnosis, in Dr. Callaghan’s view. The relevant testing revealed “things that are super

common and completely describe the patient’s symptoms, and so cervical radiculopathy at those

levels and a carpal tunnel syndrome would be exactly expected to give the symptoms that

[Petitioner] presented with.” Tr. at 206, 216. The results did not confirm the existence of the kind

of dysfunction that could be attributed to the brachial plexus. Callaghan First Rep. at 5. Petitioner’s

EMG/NCS results were also consistent with some bilateral injuries, specifically on the left side,

as well as cervical radiculopathy at C5 and C7 spine levels. Id. at 206–07.

7

Dr. Callaghan defined CTS as “a mechanical injury of the median nerve in the carpal tunnel itself,” deeming it not

only the most common neuropathy, but particularly prevalent for patients with diabetes. Tr. at 200.

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Petitioner’s past medical history, Dr. Callaghan opined, suggested a credible alternative

explanation for Petitioner’s symptoms. That history was significant for diabetes, making Petitioner

more prone to “every peripheral nerve manifestation.” Tr. at 196 (emphasis added). Diabetes, Dr.

Callaghan explained, can often cause a form of polyneuropathy or increase an individual’s risk of

radiculopathy, and can even lead to an increased chance of developing mononeuropathies,

including carpal tunnel syndrome. Id. There was even other evidence consistent with the

conclusion that such processes were already under way. Petitioner suffered from C5/C7

radiculopathy, which Dr. Callaghan described as an “injury to the nerve roots in the neck”—noting

that C5 typically causes pain that travels down the arm, and oftentimes involves the shoulder and

the first few digits whereas C7 usually involves the middle finger. Id. at 196–97. Petitioner’s

diagnosis was consistent with the symptoms Petitioner reported to his treating physicians—and in

fact, in Dr. Callaghan’s opinion the pain Petitioner described could equally implicate the existence

of a diabetic neuropathy, cervical radiculopathy, or CTS. Id. at 197–98.

Dr. Callaghan then briefly discussed several post-vaccination visits with Petitioner’s

treating physicians—but focused specifically on his visits with Dr. McQueen in 2019-20. Tr. at

203. By this time (18-plus months post-vaccination), Petitioner was describing pain in the left

upper arm that traveled down into his fingers and hand accompanied by numbness in his second

and third fingers. But in Dr. Callaghan’s view, such symptoms were fully consistent with

Petitioner’s prior diagnosis of C5/C7 radiculopathy and carpal tunnel syndrome. Id.

In addition to disputing the propriety of a brachial neuritis diagnosis, Dr. Callaghan denied

that the flu vaccine could likely cause the condition. Callaghan First Rep. at 5–6. In so doing, he

addressed Dr. Andersson’s effort to analogize the autoimmune process deemed to be possibly

triggered by the flu vaccine, resulting in GBS. In Dr. Callaghan’s view, GBS and brachial neuritis

were wholly-distinct illnesses (even if both are peripheral nerve injuries), since GBS affects “the

myelin or covering of the nerve,” whereas brachial neuritis is “an injury to the blood vessels that

supply the nerve.” Tr. at 222 (emphasis added). They otherwise have different underlying

pathologies, require different forms of treatment, and result in separate kinds of impacts to the

body. Id. As a result, Dr. Callaghan deemed Dr. Andersson’s assertion that brachial neuritis

essentially operates the same way as GBS to amount to a be “huge leap of faith.” Id. at 223. Dr.

Callaghan further maintained that he could find no reliable literature support establishing a likely

causal link between the flu vaccine and brachial neuritis. Id. at 223–24.

2. Andrew MacGinnitie, M.D.

Dr. MacGinnitie, an allergist/immunologist, prepared two written reports for Respondent

and testified for Respondent, opining that there is no causal connection between the flu vaccine

and the neurologic problems Petitioner suffered (however they are defined). See generally Tr. at

280–342; Report, dated May 31, 2022, filed as Ex. C (ECF No. 31-3) (“MacGinnitie First Rep.”);

Report, dated Feb. 15, 2023, filed as Ex. F (ECF No. 44-2) (“MacGinnitie Second Rep.”).

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Dr. MacGinnitie received his bachelor’s degree from Yale University and then attended

the University of Chicago, Pritzker School of Medicine, where he received both an M.D. and a

Ph.D. from the Department of Pathology. Curriculum Vitae, filed as Ex. D (ECF No. 31-4)

(“MacGinnitie CV”) at 1; Tr. at 281–82. Thereafter, he completed a residency in pediatrics in the

Boston Combined Residency Program, a joint venture of Boston Children’s Hospital and Boston

Medica Center, followed by an Allergy/Immunology fellowship at Boston Children’s Hospital.

Id.; MacGinnitie First Rep. at 1–2. Dr. MacGinnitie is an Associate Professor Pediatrics at Harvard

Medical School, as well as the Clinical Chief for the Division of Immunology at Boston Children’s

Hospital where he directs clinical operations for Allergy/Immunology, Rheumatology and

Dermatology. MacGinnitie CV at 1–2; MacGinnitie First Rep. at 1; Tr. at 283–84. He is board

certified in both Pediatrics and Allery and Clinical Immunology. MacGinnitie CV at 11; Tr. at

281. Dr. MacGinnitie has averred that he treats approximately 1,700 patients annually, and has

extensive experience in caring for both children and adults with a variety of immunologic diseases,

such as reactions to vaccines. MacGinnitie First Rep. at 2.

Dr. MacGinnitie began his testimony by noting that he would not be offering an opinion

on the diagnosis of brachial neuritis, deferring on that issue to Dr. Callaghan. Tr. at 286–87.

Instead, Dr. MacGinnitie provided his view as to whether there likely exists a reasonable

mechanism by which the flu vaccine could trigger brachial neuritis (and finding that there was

not). Id. at 287.

In so opining, Dr. MacGinnitie provided an explanation for the concept of molecular

mimicry (which Dr. Andersson’s theory appeared to rely upon). Tr. at 287–89. He explained that

the immune system has two responsive “arms”: the innate response, which immediately responds

to antigenic exposure, sometimes involving or promoting inflammation, and then the second,

adaptive response—i.e., the targeting of specific epitopes, typically proteins, on infections such as

bacteria or viruses. Tr. at 288. Dr. MacGinnitie allowed that Petitioner’s receipt of the flu vaccine

would implicate the secondary, adaptive response, since the immune system would likely

recognize the flu antigens from prior vaccine exposures (despite differences in the vaccine from

year to year). Tr. at 302–03.

Dr. MacGinnitie agreed with Dr. Andersson’s explanation of molecular mimicry as

involving the secondary/adaptive response, and occurring where “there’s some immune stimulus,

typically thought of to be an infection—but could be vaccination or environmental exposure—and

there is an antigen or epitope [that is] recognized by [the] immune system [and] is similar in

structure to a human protein,” later resulting in the production of antibodies that recognize, and

attack, both the foreign antigen as well as the similar human protein. Tr. at 287–88. In Dr.

MacGinnitie’s experience, four criteria must be demonstrated 8 if molecular mimicry is to be

8

I note that the criteria Dr. MacGinnitie discusses do not constitute elements of the legal test Petitioner must satisfy

to meet his burden of proof. But they do stand as the kinds of factors that the scientific community would consider

significant in whether molecular mimicry deserves explanatory weight, and I therefore evaluate them only in that

11

credibly invoked as an explanatory mechanism for a disease process. L. Peterson & R. Fujinami,

Molecular Mimicry, 13 (Yehuda Shoenfeld et al. eds., 2nd ed. 2007) (“Peterson and Fujinami”).

These are the “similarity between a host epitope and an epitope of a microorganism or

environmental agent; detection of antibodies or T cells cross-reactive with both epitopes in patients

with the autoimmune disease; epidemiological link between exposure to the environmental agent

or microbe and development of autoimmune disease; and reproducibility of autoimmunity in an

animal model following sensitization with the epitopes, infection with the microbe or exposure to

the environmental agent.” Tr. at 290; MacGinnitie Second Rep. at 1. Peterson Fujinami at 13.

In this case, molecular mimicry could not be demonstrated to be a reliable explanation for

how the flu vaccine could cause brachial neuritis. In particular, Dr. MacGinnitie noted, the first

and second criteria for deeming molecular mimicry an apt explanation for an immune-mediated

process were absent. Tr. at 16. Thus, Dr. Andersson had failed to identify any homology between

flu vaccine antigenic amino acid sequences and the human nerve proteins which would presumably

be targeted. Id. at 288–89. Without establishing a specific basis for an errant cross-attack through

the identification of some homology one could essentially maintain that “really anything that

stimulates [an individual’s] immune system could cause any autoimmune disease”—which he

maintained is not a very robust and convincing application. Id. at 295. Moreover, Dr. Andersson

had not specified whether the immune response elicited B cells or T cells in carrying out its

disease-causing process. Id. at 289, 292. And no cross-reactive antibodies or T cells that might

theoretically drive an autoimmune process had been identified. Dr. MacGinnitie also felt it

significant that little medical literature supported a causal relationship between the flu vaccine and

brachial neuritis. Tr. at 296. He noted that, in conducting his own research for purposes of this

hearing, he had found nothing so supportive except for a “handful of case reports [for] influenza

and other vaccines but no epidemiologic studies that show a connection.” Id.

There was otherwise, Dr. MacGinnitie maintained, no reason to deem the vaccine

Petitioner received as more likely causal than several other potential explanations for Petitioner’s

symptoms evident from the medical record. He noted, for example, that “some infections could

trigger inflammation in an organ leading to autoimmunity without any evidence of molecular

mimicry.” Tr. at 309. Although there are “significant safeguards in the immune system to protect

against autoimmunity,” such mechanisms can be breached either through genetic mutations or

other mechanisms. Tr. at 309. Surgery is another common preceding event for brachial neuritis,

“roughly on the order of magnitude [as] vaccination.” Id. at 310. Here, eight to nine days prior to

development of symptoms argued to reflect brachial neuritis, Petitioner had undergone surgery to

repair an incarcerated hernia—which “would make that a much more plausible trigger of brachial

neuritis than vaccination.” Id. In fact, Dr. MacGinnitie stressed, surgery is a “significant immune

stimulus”—noting that damage-associated molecular patterns are released by damaged cells, and

regard (since they provide some insight into why an expert might not deem molecular mimicry to stand as a persuasive

explanation for an immune-mediated injury).

12

that when an individual undergoes any type of surgery or experiences trauma, “patients have a

significant inflammatory response.” Id. at 311.

Dr. MacGinnitie also opined that Petitioner’s onset date was inconsistent with Dr.

Andersson’s proposed theory, and its reliance on molecular mimicry. An onset of 40 hours post-

vaccination “is too fast for an adaptive immune response, which would be required for molecular

mimicry.” Tr. at 289–90. This was true in his view even though he agreed that Petitioner (having

been exposed to prior versions of the flu vaccine) would likely have a shorter adaptive response.

Id. at 302–03. The adaptive response would take three days or more to manifest antibodies capable

of the kind of cross-reaction implicated by molecular mimicry. Tr. at 298.

III. Post-Hearing Reports

After the hearing, I informed the parties that although it appeared Petitioner primarily relied

on a theory involving an adaptive immune response as mediating the alleged brachial neuritis, it

seemed as if Dr. Andersson had allowed for an innate response as also potentially driving brachial

neuritis (and that this might be more consistent with the fast, post-vaccination onset of Petitioner’s

symptoms). Thus, the parties were afforded a final opportunity to submit a single supplemental

report addressing whether brachial neuritis can be caused by an innate immune response. Both

sides offered a report from one expert. See Dr. Andersson Report, dated June 15, 2023, (ECF No.

67-1) (“Andersson Supp. Rep.”); Dr. MacGinnitie Report, dated June 13, 2023 (ECF No 66-1)

(“MacGinnitie Supp. Rep.”).

Dr. Andersson’s Post-Hearing Report

Dr. Andersson first acknowledged that although he had referred to the innate immune

response as pathogenic at hearing, he did not use that specific term in his reports. He nevertheless

emphasized that “brachial neuritis is an immune mediated condition and as such it has two

potential pathogenic mechanisms by which it is affected”—the adaptive and innate responses.

Andersson Supp. Rep. at 1. In this report, Dr. Andersson addressed each system and discussed

their respective relevance to Petitioner’s alleged injury and claim. Id.

As Dr. Andersson noted, “[t]he pathophysiology of NA remains uncertain, although it often

suggests an auto-immune origin such as in Guillain-Barré syndrome.” Andersson Supp. Rep. at 1;

P. Seror, Neuralgic Amyotrophy: An Update, 84 Joint Bone Spine 153, 156 (2017), filed as Ex. 43

(ECF No. 38-1). He further noted that even if the timing of onset from vaccination to injury in this

case (two days) was relatively rapid for an adaptive immune response, such timing did not rule out

an adaptive-mediated path. Andersson Supp. Rep. at 1. Indeed, because Petitioner had previously

been exposed to the flu vaccine, an immune memory-oriented response had likely occurred, and it

would happen in a shorter timeframe. Id.

However, Dr. Andersson also opined that brachial neuritis could be the result of an aberrant

innate immune response. The innate response “is the body’s first line of defense against pathogens

13

entering the body and it responds in the same way to all foreign substances.” Andersson Supp.

Rep. at 2. Studies discussing histopathologic evidence relevant to brachial neuritis had observed

“[i]ncreased levels of complement 9 C5-C9 and decreased levels of C3,” as well the “presence of

“local inflammatory infiltrates, severe pain caused by the release of inflammatory mediators and

ischemia of the nervi nervorum, and acute damage to the paranodal regions of large nerve fibers.’”

Id.; J. Van Eijk et al., Neuralgic Amyotrophy: An Update on Diagnosis, Pathophysiology, and

Treatment, 53 Muscle & Nerve 337, 340 (2016), filed as Ex. 18 (ECF No. 27-7); LJspeert at 4.

Additionally, Dr. Andersson relied on statements made in the LJspeert article, which argued that

essentially any factor that provokes the innate immune response can constitute an immunological

trigger. Andersson Second Supp. Rep. at 2; LJspeert at 4.

In fact, it might be difficult to differentiate the contributions of the innate versus adaptive

immune response in attempting to identify the primary impetus for brachial neuritis. As Dr.

Andersson noted, “the histopathology of brachial plexitis as inflammatory and the deposition of

complement that is the [contribution of the] innate immune system” meant that the innate arm was

likely also important to the disease process. Andersson Supp. Rep. at 2; Andersson Second Rep.

at 11. The evidence of complement activation in brachial neuritis was “further evidence that an

acute onset of symptoms within just a couple of days following a trigger is due to an innate

immune-mediated response.” Id. Dr. Andersson thus maintained that an innate immune response

could lead to the development of brachial neuritis through an “acute, nonspecific, immune-

mediated inflammatory response triggered by localized inflammation, complement cascade, and

localized lymphocytic infiltration”—all present in Petitioner’s case. Id. at 3.

Dr. Andersson concluded his final report with a comment on whether Petitioner’s pre-

vaccination hernia surgery could explain his injury. Although he could not dispute the fact of the

surgery, Dr. Andersson maintained that there was a lack of an explanatory mechanism by which

the surgery could have caused his brachial neuritis, adding that an interval of eight days post-

surgery (January 13-21) would exclude the possibility that immune stimulation due to surgery was

explanatory.

Dr. MacGinnitie’s Post-Hearing Report

Dr. MacGinnitie began his supplemental report with a brief overview of the nature of the

innate and adaptive immune responses—noting that “innate immunity involves defense

mechanisms that are not specific for any single pathogen, while the adaptive immune response can

generate a near infinite number of receptors, capable of recognizing almost any protein or other

molecules.” MacGinnitie Supp. Rep. at 2–6. Although the two arms of the immune response might

work together to cause brachial neuritis, the adaptive arm better “explained” the disease’s

9

“Complement” is defined as “the entire functionally related system comprising at least 20 distinct serum proteins,

their cellular receptors, and related regulatory proteins that is the effector not only of immune cytolysis but also of

other biologic functions including anaphylaxis, phagocytosis, opsonization, and hemolysis.” Complement, Dorland’s

Medical Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=10705&searchterm=complement

(last visited on Dec. 4, 2023).

14

pathogenic process, even if the innate arm also played a role. Id. at 6. 10 Indeed, although

complement is released via the innate immune response, the articles Dr. Andersson relied on also

discussed the presence of both anti-myelin antibodies and complement activation—suggesting that

an innate response might only occur after the adaptive immune response produces autoantibodies

that instigate the disease initially. Id.; Vriesendrop at 1303. Other, more recent literature also

illustrated the coordinated role the innate and adaptive immune responses play in the development

of autoimmune diseases. MacGinnitie Supp. Rep. at 9; G. Wigerbald et al., Neutrophil

Extracellular Traps in Systemic Autoimmune and Autoinflammatory Diseases, 23 Nat. Rev.

Immunology 274 (2023). 11

Dr. MacGinnitie therefore denied that an innate immune response alone could cause

brachial neuritis. MacGinnitie Supp. Rep. at 10. Because the innate response is not antigen-

specific, it is unlikely that “generalized inflammation could trigger the organ-specific

autoimmunity seen in [brachial neuritis] (or pure sensory BN).” Id. Dr. MacGinnitie acknowledged

one case report cited by Dr. Andersson involving a patient who developed symptoms of brachial

neuritis within approximately 13 hours after receiving the Covid-19 vaccine, but emphasized the

limitations of relying on such case reports. Id.; Queler at 1. In addition, the flu vaccine is generally

not a strong stimulus for the innate immune response, especially since “the majority of influenza

vaccines administered in the US are unadjuvanted, including the one [Petitioner] received, where

adjuvants are materials added to vaccines specifically to trigger the innate immune system.”

MacGinnitie Supp. Rep. at 11.

An innate response also could not explain a purely sensory form of brachial neuritis.

MacGinnitie Supp. Rep. at 11. In almost all of the literature discussing an immune mediated

pathology for brachial neuritis, the adaptive immune response was discussed. Id. Moreover, innate

immunity is not antigen-specific, and thus “innate immune activation would not explain symptoms

limited to the peripheral nervous system.” Id. He concluded by reiterating his prior point that the

timeframe for Petitioner’s onset was too rapid to be attributed to an adaptive response. Id.

IV. Procedural History

As noted above, this claim was initiated in July 2020, and the matter was originally

designated as a “Special Processing Unit” (the “SPU”) case, based on anticipation that the claim

was likely to settle. ECF Nos. 1, 4. All medical records with and an amended Statement of

Completion were filed by December 2020. ECF No. 14. Respondent filed his Rule 4(c) Report

contesting Petitioner’s right to compensation on June 16, 2021. ECF No. 21, and the matter was

subsequently transferred out of SPU to my regular docket. Thereafter, expert reports were filed,

10

Dr. MacGinnitie disagreed with Dr. Andersson’s contention, however, that macrophages are only involved in the

innate immune response. As a result, Dr. Andersson’s point about histopathology findings relating to brachial neuritis

was supportive of both arms playing a role. MacGinnitie Supp. Rep. at 6.

11

I note, however, that Respondent did not file this item of literature.

15

and a two-day entitlement hearing was held on April 13-14, 2023. The parties have filed their

supplemental expert reports addressing whether brachial neuritis can be caused by an innate

immune response, and the matter is now ripe for resolution.

V. Applicable Legal Standards

A. Petitioner’s Overall Burden in Vaccine Program Cases

To receive compensation in the Vaccine Program, a petitioner must prove either: (1) that

he suffered a “Table Injury”—i.e., an injury falling within the Vaccine Injury Table—

corresponding to one of the vaccinations in question within a statutorily prescribed period of time

or, in the alternative, (2) that his illnesses were actually caused by a vaccine (a “Non-Table

Injury”). See Sections 13(a)(1)(A), 11(c)(1), and 14(a), as amended by 42 C.F.R. § 100.3; §

11(c)(1)(C)(ii)(I); see also Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1321 (Fed.

Cir. 2010); Capizzano v. Sec’y of Health & Hum. Servs., 440 F.3d 1317, 1320 (Fed. Cir. 2006). 12

Petitioner does not herein assert a Table claim—nor could he, since the only Table claim for

brachial neuritis involves tetanus-containing vaccines.

For both Table and Non-Table claims, Vaccine Program petitioners bear a “preponderance

of the evidence” burden of proof. Section 13(1)(a). That is, a petitioner must offer evidence that

leads the “trier of fact to believe that the existence of a fact is more probable than its nonexistence

before [he] may find in favor of the party who has the burden to persuade the judge of the fact’s

existence.” Moberly, 592 F.3d at 1322 n.2; see also Snowbank Enter. v. United States, 6 Cl. Ct.

476, 486 (1984) (mere conjecture or speculation is insufficient under a preponderance standard).

Proof of medical certainty is not required. Bunting v. Sec’y of Health & Hum. Servs., 931 F.2d

867, 873 (Fed. Cir. 1991). In particular, a petitioner must demonstrate that the vaccine was “not

only [the] but-for cause of the injury but also a substantial factor in bringing about the injury.”

Moberly, 592 F.3d at 1321 (quoting Shyface v. Sec’y of Health & Hum. Servs., 165 F.3d 1344,

1352–53 (Fed. Cir. 1999)); Pafford v. Sec’y of Health & Hum. Servs., 451 F.3d 1352, 1355 (Fed.

Cir. 2006). A petitioner may not receive a Vaccine Program award based solely on his assertions;

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

physician. Section 13(a)(1).

In attempting to establish entitlement to a Vaccine Program award of compensation for a

Non-Table claim, a petitioner must satisfy all three of the elements established by the Federal

Circuit in Althen v. Sec'y of Health and Hum. Servs., 418 F.3d 1274, 1278 (Fed. Cir. 2005): “(1) a

12

Decisions of special masters (some of which I reference in this ruling) constitute persuasive but not binding

authority. Hanlon v. Sec’y of Health & Hum. Servs., 40 Fed. Cl. 625, 630 (1998). By contrast, Federal Circuit rulings

concerning legal issues are binding on special masters. Guillory v. Sec’y of Health & Hum. Servs., 59 Fed. Cl. 121,

124 (2003), aff’d 104 F. App’x. 712 (Fed. Cir. 2004); see also Spooner v. Sec’y of Health & Hum. Servs., No. 13-

159V, 2014 WL 504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014).

16

medical theory causally connecting the vaccination and the injury; (2) a logical sequence of cause

and effect showing that the vaccination was the reason for the injury; and (3) a showing of

proximate temporal relationship between vaccination and injury.”

Each Althen prong requires a different showing. Under Althen prong one, petitioners must

provide a “reputable medical theory,” demonstrating that the vaccine received can cause the type

of injury alleged. Pafford, 451 F.3d at 1355–56 (citations omitted). To satisfy this prong, a

petitioner’s theory must be based on a “sound and reliable medical or scientific explanation.”

Knudsen v. Sec’y of Health & Hum. Servs., 35 F.3d 543, 548 (Fed. Cir. 1994). Such a theory must

only be “legally probable, not medically or scientifically certain.” Id. at 549.

Petitioners may satisfy the first Althen prong without resort to medical literature,

epidemiological studies, demonstration of a specific mechanism, or a generally accepted medical

theory. Andreu v. Sec’y of Health & Hum. Servs., 569 F.3d 1367, 1378–79 (Fed. Cir. 2009) (citing

Capizzano, 440 F.3d at 1325–26). Special masters, despite their expertise, are not empowered by

statute to conclusively resolve what are essentially thorny scientific and medical questions, and

thus scientific evidence offered to establish Althen prong one is viewed “not through the lens of

the laboratorian, but instead from the vantage point of the Vaccine Act’s preponderant evidence

standard.” Id. at 1380. Accordingly, special masters must take care not to increase the burden

placed on petitioners in offering a scientific theory linking vaccine to injury. Contreras, 121 Fed.

Cl. at 245 (“[p]lausibility . . . in many cases may be enough to satisfy Althen prong one” (emphasis

in original)).

In discussing the evidentiary standard applicable to the first Althen prong, the Federal

Circuit has consistently rejected the contention that it can be satisfied merely by establishing the

proposed causal theory’s scientific or medical plausibility. See Boatmon v. Sec’y of Health & Hum.

Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019); LaLonde v. Sec’y of Health & Hum. Servs., 746 F.3d

1334, 1339 (Fed. Cir. 2014) (“[h]owever, in the past we have made clear that simply identifying a

‘plausible’ theory of causation is insufficient for a petitioner to meet her burden of proof.” (citing

Moberly, 592 F.3d at 1322)); see also Howard v. Sec'y of Health & Hum. Servs., 2023 WL

4117370, at *4 (Fed. Cl. May 18, 2023) (“[t]he standard has been preponderance for nearly four

decades”), appeal docketed, No. 23-1816 (Fed. Cir. Apr. 28, 2023). And petitioners always have

the ultimate burden of establishing their overall Vaccine Act claim with preponderant evidence.

W.C. v. Sec’y of Health & Hum. Servs., 704 F.3d 1352, 1356 (Fed. Cir. 2013) (citations omitted);

Tarsell v. United States, 133 Fed. Cl. 782, 793 (2017) (noting that Moberly “addresses the

petitioner’s overall burden of proving causation-in-fact under the Vaccine Act” by a

preponderance standard).

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

supported by facts derived from a petitioner’s medical records. Althen, 418 F.3d at 1278; Andreu,

17

569 F.3d at 1375–77; Capizzano, 440 F.3d at 1326; Grant v. Sec’y of Health & Hum. Servs., 956

F.2d 1144, 1148 (Fed. Cir. 1992). In establishing that a vaccine “did cause” injury, the opinions

and views of the injured party’s treating physicians are entitled to some weight. Andreu, 569 F.3d

at 1367; Capizzano, 440 F.3d at 1326 (“medical records and medical opinion testimony are favored

in vaccine cases, as treating physicians are likely to be in the best position to determine whether a

‘logical sequence of cause and effect show[s] that the vaccination was the reason for the injury’”)

(quoting Althen, 418 F.3d at 1280). Medical records are generally viewed as particularly

trustworthy evidence, since they are created contemporaneously with the treatment of the patient.

Cucuras v. Sec’y of Health & Hum. Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993).

Medical records and statements of a treating physician, however, 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. Section 13(b)(1) (providing that “[a]ny such diagnosis, conclusion, judgment,

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

of Health & Hum. Servs., 88 Fed. Cl. 706, 746 n.67 (2009) (“there is nothing . . . that mandates

that the testimony of a treating physician is sacrosanct—that it must be accepted in its entirety and

cannot be rebutted”). As with expert testimony offered to establish a theory of causation, the

opinions or diagnoses of treating physicians are only as trustworthy as the reasonableness of their

suppositions or bases. The views of treating physicians should be weighed against other, contrary

evidence also present in the record—including conflicting opinions among such individuals.

Hibbard v. Sec’y of Health & Hum. Servs., 100 Fed. Cl. 742, 749 (2011) (not arbitrary or capricious

for special master to weigh competing treating physicians’ conclusions against each other), aff’d,

698 F.3d 1355 (Fed. Cir. 2012); Veryzer v. Sec’y of Dept. of Health & Hum. Servs., No. 06-522V,

2011 WL 1935813, at *17 (Fed. Cl. Spec. Mstr. Apr. 29, 2011), mot. for review den’d, 100 Fed.

Cl. 344, 356 (2011), aff’d without opinion, 475 F. Appx. 765 (Fed. Cir. 2012).

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

the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been equated to the

phrase “medically-acceptable temporal relationship.” Id. A petitioner must offer “preponderant

proof that the onset of symptoms occurred within a timeframe which, given the medical

understanding of the disorder’s etiology, it is medically acceptable to infer causation.” de Bazan

v. Sec’y of Health & Hum. Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for what

is a medically acceptable timeframe must align with the theory of how the relevant vaccine can

cause an injury (Althen prong one’s requirement). Id. at 1352; Shapiro v. Sec’y of Health & Hum.

Servs., 101 Fed. Cl. 532, 542 (2011), recons. den’d after remand, 105 Fed. Cl. 353 (2012), aff’d

mem., 503 F. Appx. 952 (Fed. Cir. 2013); Koehn v. Sec’y of Health & Hum. Servs., No. 11-355V,

2013 WL 3214877 (Fed. Cl. Spec. Mstr. May 30, 2013), mot. for rev. den’d (Fed. Cl. Dec. 3,

2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).

18

B. Legal Standards Governing Factual Determinations

The process for making determinations in Vaccine Program cases regarding factual issues

begins with consideration of the medical records. Section 11(c)(2). 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.” Section 13(b)(1)(A). The special

master is then required to weigh the evidence presented, including contemporaneous medical

records and testimony. See Burns v. Sec'y of Health & Hum. Servs., 3 F.3d 415, 417 (Fed. Cir.

1993) (determining that it is within the special master's discretion to determine whether to afford

greater weight to contemporaneous medical records than to other evidence, such as oral testimony

surrounding the events in question that was given at a later date, provided that such determination

is evidenced by a rational determination).

As noted by the Federal Circuit, “[m]edical records, in general, warrant consideration as

trustworthy evidence.” Cucuras, 993 F.2d at 1528; Doe/70 v. Sec'y of Health & Hum. Servs., 95

Fed. Cl. 598, 608 (2010) (“[g]iven the inconsistencies between petitioner's testimony and his

contemporaneous medical records, the special master's decision to rely on petitioner's medical

records was rational and consistent with applicable law”), aff'd, Rickett v. Sec'y of Health & Hum.

Servs., 468 F. App’x 952 (Fed. Cir. 2011) (non-precedential opinion). A series of linked

propositions explains why such records deserve some weight: (i) sick people visit medical

professionals; (ii) sick people attempt to honestly report their health problems to those

professionals; and (iii) medical professionals record what they are told or observe when examining

their patients in as accurate a manner as possible, so that they are aware of enough relevant facts

to make appropriate treatment decisions. Sanchez v. Sec'y of Health & Hum. Servs., No. 11–685V,

2013 WL 1880825, at *2 (Fed. Cl. Spec. Mstr. Apr. 10, 2013); Cucuras v. Sec'y of Health & Hum.

Servs., 26 Cl. Ct. 537, 543 (1992), aff'd, 993 F.2d at 1525 (Fed. Cir. 1993) (“[i]t strains reason to

conclude that petitioners would fail to accurately report the onset of their daughter's symptoms”).

Accordingly, if the medical records are clear, consistent, and complete, then they should

be afforded substantial weight. Lowrie v. Sec'y of Health & Hum. Servs., No. 03–1585V, 2005 WL

6117475, at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed, contemporaneous medical records

are often found to be deserving of greater evidentiary weight than oral testimony—especially

where such testimony conflicts with the record evidence. Cucuras, 993 F.2d at 1528; see also

Murphy v. Sec'y of Health & Hum. Servs., 23 Cl. Ct. 726, 733 (1991), aff'd per curiam, 968 F.2d

1226 (Fed. Cir. 1992), cert. den'd, Murphy v. Sullivan, 506 U.S. 974 (1992) (citing United States

v. United States Gypsum Co., 333 U.S. 364, 396 (1947) (“[i]t has generally been held that oral

testimony which is in conflict with contemporaneous documents is entitled to little evidentiary

19

weight.”)).

However, the Federal Circuit has also noted that there is no formal “presumption” that

records are accurate or superior on their face to other forms of evidence. Kirby v. Sec’y of Health

& Hum. Servs., 997 F.3d 1378, 1383 (Fed. Cir. 2021). There are certainly situations in which

compelling oral or written testimony (provided in the form of an affidavit or declaration) may be

more persuasive than written records, such as where records are deemed to be incomplete or

inaccurate. Campbell v. Sec'y of Health & Hum. Servs., 69 Fed. Cl. 775, 779 (2006) (“like any

norm based upon common sense and experience, this rule should not be treated as an absolute and

must yield where the factual predicates for its application are weak or lacking”); Lowrie, 2005 WL

6117475, at *19 (“[w]ritten records which are, themselves, inconsistent, should be accorded less

deference than those which are internally consistent”) (quoting Murphy, 23 Cl. Ct. at 733)).

Ultimately, a determination regarding a witness's credibility is needed when determining the

weight that such testimony should be afforded. Andreu, 569 F.3d at 1379; Bradley v. Sec'y of

Health & Hum. Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).

When witness testimony is offered to overcome the presumption of accuracy afforded to

contemporaneous medical records, such testimony must be “consistent, clear, cogent, and

compelling.” Sanchez, 2013 WL 1880825, at *3 (citing Blutstein v. Sec'y of Health & Hum. Servs.,

No. 90–2808V, 1998 WL 408611, at *5 (Fed. Cl. Spec. Mstr. June 30, 1998)). In determining the

accuracy and completeness of medical records, the Court of Federal Claims has listed four possible

explanations for inconsistencies between contemporaneously created medical records and later

testimony: (1) a person's failure to recount to the medical professional everything that happened

during the relevant time period; (2) the medical professional's failure to document everything

reported to her or him; (3) a person's faulty recollection of the events when presenting testimony;

or (4) a person's purposeful recounting of symptoms that did not exist. La Londe v. Sec'y of Health

& Hum. Servs., 110 Fed. Cl. 184, 203–04 (2013), aff'd, 746 F.3d 1334 (Fed. Cir. 2014). In making

a determination regarding whether to afford greater weight to contemporaneous medical records

or other evidence, such as testimony at hearing, there must be evidence that this decision was the

result of a rational determination. Burns, 3 F.3d at 417.

C. Analysis of Expert Testimony

Establishing a sound and reliable medical theory often requires a petitioner to present

expert testimony in support of his claim. Lampe v. Sec’y of Health & Hum. Servs., 219 F.3d 1357,

1361 (Fed. Cir. 2000). Vaccine Program expert testimony is usually evaluated according to the

factors for analyzing scientific reliability set forth in Daubert v. Merrell Dow Pharm., Inc., 509

U.S. 579, 594–96 (1993). See Cedillo v. Sec’y of Health & Hum. Servs., 617 F.3d 1328, 1339 (Fed.

Cir. 2010) (citing Terran v. Sec’y of Health & Hum. Servs., 195 F.3d 1302, 1316 (Fed. Cir. 1999).

Under Daubert, the factors for analyzing the reliability of testimony are:

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(1) whether a theory or technique can be (and has been) tested; (2) whether the

theory or technique has been subjected to peer review and publication; (3) whether

there is a known or potential rate of error and whether there are standards for

controlling the error; and (4) whether the theory or technique enjoys general

acceptance within a relevant scientific community.

Terran, 195 F.3d at 1316 n.2 (citing Daubert, 509 U.S. at 592–95).

In the Vaccine Program the Daubert factors play a slightly different role than they do when

applied in other federal judicial settings, like the district courts. Typically, Daubert factors are

employed by judges (in the performance of their evidentiary gatekeeper roles) to exclude evidence

that is unreliable or could confuse a jury. By contrast, in Vaccine Program cases these factors are

used in the weighing of the reliability of scientific evidence proffered. Davis v. Sec'y of Health &

Hum. Servs., 94 Fed. Cl. 53, 66–67 (2010) (“uniquely in this Circuit, the Daubert factors have

been employed also as an acceptable evidentiary-gauging tool with respect to persuasiveness of

expert testimony already admitted”). The flexible use of the Daubert factors to evaluate the

persuasiveness and reliability of expert testimony has routinely been upheld. See, e.g., Snyder, 88

Fed. Cl. at 742–45. In this matter (as in numerous other Vaccine Program cases), Daubert has not

been employed at the threshold, to determine what evidence should be admitted, but instead to

determine whether expert testimony offered is reliable and/or persuasive.

Respondent frequently offers one or more experts in order to rebut a petitioner’s case.

Where both sides offer expert testimony, a special master's decision may be “based on the

credibility of the experts and the relative persuasiveness of their competing theories.”

Broekelschen v. Sec'y of Health & Hum. Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (citing

Lampe, 219 F.3d at 1362). However, nothing requires the acceptance of an expert's conclusion

“connected to existing data only by the ipse dixit of the expert,” especially if “there is simply too

great an analytical gap between the data and the opinion proffered.” Snyder, 88 Fed. Cl. at 743

(quoting Gen. Elec. Co. v. Joiner, 522 U.S. 146 (1997)); see also Isaac v. Sec'y of Health & Hum.

Servs., No. 08–601V, 2012 WL 3609993, at *17 (Fed. Cl. Spec. Mstr. July 30, 2012), mot. for

review den'd, 108 Fed. Cl. 743 (2013), aff'd, 540 F. App’x. 999 (Fed. Cir. 2013) (citing Cedillo,

617 F.3d at 1339). Weighing the relative persuasiveness of competing expert testimony, based on

a particular expert's credibility, is part of the overall reliability analysis to which special masters

must subject expert testimony in Vaccine Program cases. Moberly, 592 F.3d at 1325–26

(“[a]ssessments as to the reliability of expert testimony often turn on credibility determinations”);

see also Porter v. Sec'y of Health & Hum. Servs., 663 F.3d 1242, 1250 (Fed. Cir. 2011) (“this court

has unambiguously explained that special masters are expected to consider the credibility of expert

witnesses in evaluating petitions for compensation under the Vaccine Act”).

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D. Consideration of Medical Literature

Both parties filed medical and scientific literature in this case, but not all such items factor

into the outcome of this decision. While I have reviewed all the medical literature submitted, I

discuss only those articles that are most relevant to my determination and/or are central to

Petitioner’s case—just as I have not exhaustively discussed every individual medical record filed.

Moriarty v. Sec’y of Health & Hum. Servs., No. 2015–5072, 2016 WL 1358616, at *5 (Fed. Cir.

Apr. 6, 2016) (“[w]e generally presume that a special master considered the relevant record

evidence even though he does not explicitly reference such evidence in his decision”) (citation

omitted); see also Paterek v. Sec’y of Health & Hum. Servs., 527 F. App’x 875, 884 (Fed. Cir.

2013) (“[f]inding certain information not relevant does not lead to—and likely undermines—the

conclusion that it was not considered”).

ANALYSIS

I. Treatment of Brachial Neuritis Claims

Although the Vaccine Injury Table only provides for a claim of brachial neuritis after

receipt of the tetanus vaccine, special masters have on many occasions found that other vaccines—

including the flu vaccine—might also be causal of the condition. Morgan v. Sec’y of Health &

Hum. Servs., No. 16-269V, 2023 WL 3984415 (Fed. Cl. Spec. Mstr. June 12. 2023) (finding two

to three days post-intradermal influenza vaccination and the progression of pain and weakness

over several days to be an acceptable temporal association); Abels v. Sec’y of Health & Hum.

Servs., No. 18-558V, 2022 WL 2036101 (Fed. Cl. Spec. Mstr. May 6, 2022) (flu vaccine deemed

causal of brachial neuritis).

When adjudicating comparable claims, my decisions have turned less on whether the

vaccine at issue could cause brachial neuritis, and more on whether onset occurred in a medically

acceptable timeframe. See, e.g., Greene v. Sec’y of Health & Hum. Servs., No. 11-631V, 2019 WL

4072110 (Fed. Cl. Spec. Mstr. Aug. 2, 2019) (41-day onset after tetanus vaccine too long to be

causal in Table claim), mot. for rev. den’d, 146 Fed. Cl. 655 (Fed. Cl. 2020), aff’d, 841 Fed. App’x.

195 (Fed. Cir. 2020); Garner v. Sec’y of Health & Human Servs., No. 15-063V, 2017 WL 1713184

(Fed. Cl. Mar. 24, 2017), mot. for rev. den’d, 2017 WL 3483352 (Fed. Cl. July 31, 2017)

(dismissing claim that the Hepatitis A and B vaccines caused brachial neuritis, where claimant

reported arm or shoulder pain 45 days post-vaccination).

II. Petitioner has Not Preponderantly Established Brachial Neuritis as His Injury

Here, as in many cases, disposition of the claim turns on its proper, evidence-supported

characterization. Broekelschen, 618 F.3d at1350. Petitioner solely seeks to establish brachial

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neuritis as his injury, and thus disposition of the case depends on the finding that this injury has

preponderant evidentiary support. Unfortunately, the record does not support that conclusion. 13

Dr. Callaghan made a number of reasonable and persuasive points suggesting a brachial

neuritis diagnosis was not reflected by the medical record. First, he correctly observed that the

proposed diagnosis was not corroborated by record evidence of contemporaneous treater support.

In fact, arguably the best treater diagnostic opinion for the alleged brachial neuritis injury comes

from Dr. McQueen’s exams of Petitioner—which occurred in September 2019 and then March

2020, and thus significantly after the vaccination and onset. And even the findings from those

visits are more supportive of the diagnoses embraced by Dr. Callaghan.

Second, Respondent successfully demonstrated that the criteria for brachial neuritis are not

ultimately met given the facts of Petitioner’s medical history. Dr. Callaghan referred to the Table

criteria in advancing this aspect of his opinion (see Callaghan First Rep. at 5), and although those

elements are not controlling for this non-Table claim, they provide useful guidance for brachial

neuritis’s elements. The criteria establishing a Table claim for brachial neuritis include:

(i) Pain in the affected arm and shoulder is a presenting symptom and occurs

within the specified time-frame;

(ii) Weakness;

a. Clinical diagnosis in the absence of nerve conduction and

electromyographic studies requires weakness in muscles supplied by more

than one peripheral nerve.

b. Nerve conductions studies (NCS) and electromyographic (EMG) studies

localizing the injury to the brachial plexus are required before the

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Because the alleged injury lacks preponderant support, I need not conduct an Althen analysis. Lombardi v. Sec’y of

Health & Hum. Servs., 656 F.3d 1343, 1353 (Fed. Cir. 2011). I note, however, that I would not have trouble finding

on this record that the flu vaccine “can cause” brachial neuritis. Despite the reasonable objections made to the theory

by Dr. MacGinnitie, the evidence offered was sufficiently preponderant on the question of vaccine causality for an

Althen prong one finding in Petitioner’s favor. The timeframe prong under Althen presents a more difficult question,

since onset occurred fairly close in time to vaccination, and thus is not consistent with an adaptive immune-mediated

response. However, the immune memory arguments posited by Dr. Andersson have some persuasive value in the

context of a brachial neuritis injury. In addition, although Respondent did effectively note the strong possibility that

Petitioner’s surgery was a “factor unrelated” explanation for brachial neuritis (and I did not find persuasive Petitioner’s

argument that surgery is only a risk due to positional effects—rather, surgery clearly could trigger an immune response

as well), Respondent did not exclude the possibility of the vaccine as a substantial factor. Stone v. Sec'y of Health &

Hum. Servs., 95 Fed. Cl. 233, 237 n.5 (2010).

Of course, not establishing the alleged injury in this case is equivalent to failing to prove that the flu vaccine “did

cause” it (meaning the second Althen prong is not established). The evidence—both from the record and based on

expert submissions—heavily preponderates against the finding that Petitioner’s injury is best characterized as brachial

neuritis.

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diagnosis can be made if weakness is limited to muscles supplied by a

single peripheral nerve.

(iii) Motor, sensory, and reflex findings on physical examination and the

results of NCS and EMG studies, if performed, must be consistent in

confirming that dysfunction is attributable to the brachial plexus; and

(iv) No other condition or abnormality is present that would explain the

vaccine recipient’s symptoms.

42 C.F.R.§ 100.3(a), (c)(6).

As Dr. Callaghan noted, Petitioner never exhibited symptoms or examination findings

indicating weakness in the left arm compared to the right arm despite two visits to his neurologists

and several to his PCP. Callaghan First Rep. at 5; Tr. at 206–209; 220–21. Weakness is a central

feature of brachial neuritis, yet evidence of it is absent in this medical record. See, e.g., Tsairis at

111.

The record also lacked evidence of “motor, sensory, reflexes findings, and EMG/NCS

studies confirming dysfunction in the brachial plexus.” Callaghan First Rep. at 5. Rather, EMG

and NCS testing were supportive of CTS and radiculopathy. Id. These conditions were all

explanatory for Petitioner’s complaints. Id. at 7; Callaghan Second Rep. at 2 (“Petitioner’s

symptoms of left shoulder pain and numbness, tingling, and burning in the 1-3 digits of the left

hand are exactly the type of symptoms one would expect from a left C5 radiculopathy as

demonstrated on the EMG/NCS”). That diagnostic testing was not supportive of brachial neuritis,

as the contemporaneous record established. See Ex. 8 at 14-16 (EMG confirming bilateral CTS

and chronic cervical radiculopathy).

Finally, the characterization of Petitioner’s injury as an especially uncommon, pure sensory

form of brachial neuritis was effectively rebutted by Dr. Callaghan as lacking record evidence

substantiation. Callaghan Second Rep. at 1. No treater so diagnosed Petitioner. In addition, the

EMG/NCS testing did not reveal injury to sensory nerves (as would be expected in a pure sensory

form of brachial neuritis), but instead was (again) fully consistent with CTS, cervical

radiculopathy, and neuropathy (all of which were the diagnoses made by Petitioner’s treating

physicians).

Dr. Andersson was a qualified and competent expert, fully capable of offering an opinion

on the neurologic issues in dispute, and he made many credible points in Petitioner’s favor. The

case was certainly reasonably disputed. But his contentions about the appropriateness of a brachial

neuritis diagnosis were ultimately lacking in sufficient record support.

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CONCLUSION

Petitioner has not established the alleged brachial neuritis injury with sufficient

preponderant evidence, and therefore is not entitled to an award of compensation. In the absence

of a motion for review filed pursuant to RCFC Appendix B, the Clerk of the Court SHALL

ENTER JUDGMENT in accordance with the terms of this Decision. 14

IT IS SO ORDERED.

/s/ Brian H. Corcoran

Brian H. Corcoran

Chief Special Master

14

Pursuant to Vaccine Rule 11(a), the parties may expedite entry of judgment if (jointly or separately) they file notices

renouncing their right to seek review.

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