# Radke v. Secretary of Health and Human Services

> United States Court of Federal Claims · July 6, 2026

URL: https://www.frixlaw.com/law-library/cases/11386151

## Case

- **Court:** United States Court of Federal Claims
- **Decided:** July 6, 2026
- **Precedential status:** Unpublished
- **Opinion:** Opinion
- **Judges:** Brian H. Corcoran
- **Cited by:** 0 later opinions in the Frix Law Library

## Citator (automated)

- No negative treatment found by the automated citator. That is not the same as a confirmation that the case is good law; read the citing cases.
- Full citator and citing cases: https://www.frixlaw.com/law-library/cases/11386151

## Opinion text

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 22-1384V

*************************
*
MARK RADKE, * Chief Special Master Corcoran
*
Petitioner, * Filed: June 8, 2026
*
v. *
*
SECRETARY OF HEALTH AND *
HUMAN SERVICES, *
*
Respondent. *
*
*************************

Amber Diane Wilson, Wilson Science Law, Washington, DC, for Petitioner.

Tyler King, U.S. Department of Justice, Washington, DC, for Respondent.

DECISION ON REMAND DENYING ENTITLEMENT 1

On September 27, 2022, Mark Radke filed a petition seeking compensation under the
National Vaccine Injury Compensation Program (the “Vaccine Program”). 2 Petitioner alleges that
he suffered polymyalgia rheumatica (“PMR”) after receipt of a pneumococcal conjugate vaccine
on September 30, 2019. Petition (ECF No. 1) at 1.

The Vaccine Program has routinely dismissed claims alleging PMR as a vaccine injury—
regardless of the vaccine involved—and I had held a trial in a PMR case featuring a highly-similar
causation theory. Because of my resulting reasoned skepticism as to the claim’s viability, I directed
the parties to brief the matter. See Petitioner’s Brief in Support of Entitlement, dated Jan. 10, 2025

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 Decision 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) (“Vaccine Act” or “the Act”).
Individual section references hereafter will be to § 300aa of the Act (but will omit that statutory prefix).
(ECF No. 36) (“Br.”); Respondent’s Opposition, dated Mar. 21, 2025 (ECF No. 39) (“Opp.”);
Petitioner’s Rebuttal Brief, dated Apr. 18, 2025 (ECF No. 41) (“Reply”).
I subsequently denied entitlement—and attempted to do so in as succinct a manner as
possible, referencing not only my prior experience with claims involving PMR (in some instances
advanced by the same current counsel and expert offered in this matter) but the fact that numerous
prior special masters had reached the same conclusion. Decision, dated Oct. 6, 2025 (ECF No. 43)
(vacated on remand). Petitioner, however, has successfully appealed the decision on review, and I
am now directed by the Court of Federal Claims to provide more detail as to the basis for my
determination. See Radke v. Sec'y of Health & Hum. Servs., No. 22-1384, 2026 WL 1132925 (Fed.
Cl. Apr. 2, 2026) (the “Remand Order”).
Herein I provide my reasoning for why I again deny entitlement in this matter. It simply
has not been demonstrated that the pneumococcal vaccine can likely cause PMR.
I. Factual Background
Pre-Vaccination Medical History
Petitioner experienced a number of treatment events in the years before the vaccination at
issue that arguably bear on his alleged injury. For example, in mid-2014, injuries to his right knee
were deemed by treaters significant enough to make him a good candidate for a knee replacement
procedure. Ex. 11 at 19–20. It was observed as early as 2015 that Petitioner had a history of lower
limb neuropathy, featuring paresthesias and reduced reflexes, that impacted his ambulation. Ex.
19 at 268–70, 306–07. These neurologic issues lead in February 2015 to a diagnosis of peripheral
neuropathy. Id. at 270. An EMG 3 performed that spring confirmed the presence of early axonal
sensorimotor neuropathy. Id. at 266. These kinds of symptoms continued to plague Petitioner in
2015, although treaters did not propose any neuropathic-specific medications or comparable
interventions. Id. at 216–17.
In 2017, Petitioner sought treatment for a worsening rash, and also reported muscle
weakness and fatigue. Ex. 19 at 271, 273. He underwent a brain MRI that August, although its
findings shed no light on possible explanations for some of his complaints. Ex. 18 at 58. He was
later treated again for neuropathic symptoms, and now reported mild progression to his upper
extremities. Ex. 20 at 3, 7. Petitioner informed some neurologists that the symptoms had existed
for several years. Ex. 14 at 1, 4. Testing did not, however, aid in identifying an etiologic
explanation for these symptoms. Id. at 6–10. In the fall of 2017, Petitioner also saw an
endocrinologist, who proposed that alcohol use might explain Petitioner’s condition. Ex. 15 at 33.

3
“Electromyography” is defined as “an electrodiagnostic technique for recording the extracellular activity (action
potentials and evoked potentials) of skeletal muscles at rest, during voluntary contradictions, and during electrical
stimulation; performed using any of a variety of surface electrodes, needle electrodes, and devices for amplifying,
transmitting, and recording the signals.” Electromyography, Dorland’s Medical Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=15854&searchterm=electromyography (last visited June 8,
2026).

2
Petitioner continued in 2018 to explore his health concerns with a variety of treaters. He
sought help in January 2018 for head pain and strange sensations, although testing identified no
explanation for the symptoms. Ex. 14 at 25, 29–31. He reported more neuropathic concerns that
summer, coupled with weakness and fatigue, but a repeat MRI revealed nothing of concern. Id. at
39, 43–45. He complained of tinnitus and hearing loss in October 2018. Ex. 13 at 45, 47. In July
2019 (two months before vaccination), he again sought treatment for tinnitus and polyneuropathy
concerns, although his symptoms were then deemed to be stable. Ex. 14 at 58. (The record also
reveals that Petitioner received a flu vaccine dose in late-August 2019. Ex. 24 at 130. Although
Petitioner’s causation theory focuses on the subsequently-received pneumococcal vaccine, that
theory at certain points attempts to bootstrap into the analysis the impact of this earlier vaccination,
as discussed below).
Vaccination and Purported Adverse Impact
Mr. Radke was sixty-seven years old when he received a pneumococcal vaccine on
September 30, 2019. Ex. 2 at 21. Two days later (October 2, 2019), Petitioner went to see his
neurologist, Dr. Terry Wimpey, for follow-up evaluation of his preexisting neuropathy symptoms.
Ex. 3 at 2. Petitioner now stated that he had been feeling increasing right leg neuropathy for the
past week (which would mean the pain began prior to the vaccination), and that he was feeling
“pain behind his calf associated with the neuropathy and muscle tightness” causing him to limp.
Id. Examination revealed nothing inconsistent from prior treatment encounters, however, and
Petitioner was referred to physical therapy (“PT”) for treatment of his symptoms. Id. at 6.

A month later (November 1, 2019), Petitioner went to orthopedist John Manfredi for
treatment of his prior, ongoing right knee pain. Ex. 11 at 16. He now stated, however, that the pain
had worsened over the past month, and he reported that he had experienced pain and swelling the
day after vaccination. Id. X-rays of Petitioner’s right knee, however, revealed only evidence of
preexisting knee concerns (severe degenerative changes in the knee and calcifications throughout
the medial femoral condyle). Id. at 17. Petitioner was provided a lidocaine injection at this visit to
treat his knee. Id.

That same November, Petitioner saw a different orthopedist for shoulder pain that he
related to falling out of bed the prior month. Ex. 4 at 2. He fell a second time in November, resulting
in an emergency room visit. Ex. 2 at 94. He claimed at this time that he had been experiencing
chronic muscle aches, weakness, and headaches following his receipt of a pneumococcal vaccine.
Id. His examination was normal, additional testing did not reveal any concerns, and he was
eventually discharged home. Id. at 95. A post-ER visit to Dr. Wimpey resulted in the same kind of
normal exam, but blood work revealed a somewhat-elevated CRP 4 and sedimentation rate—both

4
“C-reactive Protein” or “CRP” is defined as “a globulin that forms a precipitate with the somatic C-polysaccharide
of the pneumococcus in vitro; it is the most predominant of the acute-phase proteins.” C-Reactive Protein, Dorland’s
Medical Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=100489 (last visited June 8,
2026).

3
of which are biomarkers for inflammation. Ex. 9 at 138–39. Later in November, Petitioner began
PT for right shoulder and knee issues (and was later discharged from PT the following winter after
reporting improvement). Ex. 16b at 1, 106.

On December 6, 2019, Mr. Radke saw rheumatologist Sana Makhdumi, M.D., with
complaints of weight loss, fever, and night sweats, which he deemed to have begun two days after
his receipt of the pneumococcal vaccine. Ex. 5 at 95. But the sole abnormality identified after
examination was “some pain” upon rotation of Petitioner’s hips. Id. at 96. Dr. Makhdumi was
unable to propose an explanation for Petitioner’s complaints, although she did express concern
that he was experiencing some form of inflammatory arthritis—PMR or rheumatoid arthritis
(“RA”) —that could have an infectious or neoplastic cause. Id. Dr. Makhdumi prescribed a steroid
taper, and also tested for two viral infections (Epstein-Barr (“EBV”) and cytomegalovirus). Id.
Petitioner tested positive for a prior/resolved EBV infection, and also again displayed an elevated
sedimentation rate (although it was deemed within a normal limit after repeat testing from the
following month). Ex. 9 at 127, 130–31.

2020 Treatment

On January 7, 2020, Petitioner returned to Dr. Makhdumi for follow up of his symptoms.
Ex. 5 at 93. He felt the prednisone was not working, and he was experiencing side temporal
headaches. Id. Examination revealed some limitations with movement of Petitioner’s spine, knees,
and hips. Id. at 94. Dr. Makhdumi’s differential diagnosis now included giant cell arteritis
(“GCA”) 5 versus PMR versus reactive arthritis, and she altered Petitioner’s steroid dose while
referring him for a temporal artery biopsy and eye exam. Id. The eye exam yielded normal results,
however, and Petitioner later decided to cancel the biopsy. Ex. 5 at 91; Ex. 12 at 10–14. Petitioner
also saw Dr. Wimpey in January, and reported a cessation of headaches and improvement in how
his shoulder felt. Ex. 14 at 89.

In February, Dr. Makhdumi reduced Petitioner’s prednisone dose, while maintaining a
differential comparable to what she had previously proposed (and keeping PMR in it). Ex. 5 at 88–
89. Petitioner again visited the ER that month, complaining of left upper extremity numbness,
heart flutters, mild left sided chest tightness, disequilibrium, and two days of mild urinary
frequency. Ex. 2 at 170. But his exam was normal and he was again discharged. Id. at 173. He had
a second ER visit later that month, reporting right calf pain and swelling. Id. at 223–24. An

5
“Giant Cell Arteritis” is defined as “a chronic vascular disease in the elderly, of unknown origin, often associated
with polymyalgia rheumatica, seen usually in the external carotid arteries but sometimes in other arteries.
Characteristics include proliferative inflammation, often with giant cells and granulomas; headache; pain with
chewing; weight loss; fever; sometimes ocular symptoms; and increased erythrocyte sedimentation rate.” Giant Cell
Arteritis, Dorland’s Medical Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=58337&searchterm=giant+cell+arteritis (last visited June 8,
2026).

4
ultrasound showed fluid collection consistent with a ruptured Baker’s cyst, and it was treated. Id.
at 227.

On March 19, 2020, Petitioner saw rheumatologist Stephen Elmore, M.D., for a second
opinion regarding his symptoms, which he felt were not being ameliorated by prednisone. Ex. 5 at
80. Examination revealed some soreness to Petitioner’s shoulders with range of movement,
slightly decreased strength, and tenderness to Petitioner’s right wrist. Id. at 82. Dr. Elmore
expressed concern for PMR versus seronegative RA, and proposed more blood tests plus different
medications. Id. at 83. Petitioner continued to see Dr. Elmore in the coming months. Ex. 5 at 74
(June visit), 75, 78 (May 2020 visit). Dr. Elmore again noted difficulty in assessing the nature of
Petitioner’s illness (while maintaining PMR in the differential), but also observed that there was
no evidence of inflammatory biomarkers, and that treatments were presuming that some kind of
rheumatic condition existed. By July, however, Petitioner informed Dr. Elmore that he felt better
overall, and Dr. Elmore directed a tapering of Petitioner’s prednisone treatments. Id. at 65. A
similar assessment was provided by Dr. Elmore in September. Id. at 24–25, 60, 63.

Treatment Beyond 2021

Petitioner has produced a large number of medical records reflecting treatment he received
from 2021 to the fall of 2022, but they shed little to no light on the issue of vaccine causation.
Petitioner continued at times to deem some of his non-orthopedic symptoms to reflect PMR, and/or
to identify them as beginning close-in-time to vaccination. And while PMR remained a fair
explanation for these symptoms, no treaters appear to have themselves proposed a vaccination-
related etiology for it. See, e.g., Ex. 5 at 5 (September 2022 visit with Dr. Elmore).

II. Expert Opinions
A. Petitioner’s Expert - Petros Efthimiou, M.D., FACR

Dr. Efthimiou, a rheumatologist, offered three written reports on behalf of Petitioner. See
Report, dated Aug. 15, 2023 (ECF No. 25-1) (“First Efthimiou Rep.”); Report, dated Apr. 19, 2024
(ECF No. 30-2) (“Second Efthimiou Rep.”); Report, dated Sept. 13, 2024 (ECF No. 35-1) (“Third
Efthimiou Rep.”). Dr. Efthimiou opined that Petitioner’s receipt of the pneumococcal vaccine
“more likely than not was a substantial factor contributing to the onset of clinical polymyalgia
rheumatica.” First Efthimiou Rep. at 1.

Dr. Efthimiou received his medical degree from the University of Ioannina Medical School
in Ioannina, Greece. Curriculum Vitae, filed as Ex. 26 (ECF No. 25-2) (“Efthimiou CV”). He then
completed an internship in Internal Medicine at the University of Iowa Hospital and Clinics,
followed by his residency in Internal Medicine at Brown University and a fellowship in
Rheumatology at the Hospital for Special Surgery and New York Presbyterian and Memorial Sloan
Kettering Cancer Center Hospital. Id. at 1–2. Dr. Efthimiou currently serves as an Associate

5
Professor of Medicine at St. George’s University School of Medicine and Ross University Medical
School. Id. at 2. He is board-certified by the American Board of Internal Medicine in
Rheumatology and has an active clinical practice. Efthimiou CV at 3; First Efthimiou Rep. at 1.
Throughout his clinical career, Dr. Efthimiou has frequently evaluated and treated individuals with
PMR, and he has spent the last twenty-one years researching inflammatory rheumatic conditions,
such as PMR and other associated inflammatory disorders. First Efthimiou Rep. at 1–2.

First Report

Dr. Efthimiou maintained at the outset of his first report that “[t]he current understanding
of the pathogenesis of PMR is a consensus model of immune-mediated disease that includes the
interaction of multiple factors, both genetic and environmental.” First Efthimiou Rep. at 15; D.
Camellino et al., Pathogenesis, Diagnosis and Management of Polymyalgia Rheumatica, 36 Drugs
& Aging 1015 (2019), filed as Ex. 28 (ECF No. 25-4) (“Camellino”). Given its understood likely
pathogenesis, Dr. Efthimiou deemed it reasonable to propose that multiple vaccine types could be
associated with triggering the onset of the disease—noting that PMR can be clinically expressed
in predisposed individuals by an environmental stimulus.

There is generally a broad spectrum for inflammatory rheumatic diseases, and that
spectrum includes autoinflammatory and autoimmune diseases. First Efthimiou Rep. at 17.
“Autoinflammatory” would mean “an aberrant activation of the innate immune response without
autoantibody production,” while “autoimmune” refers to “a dysregulated adaptive immune
response and by the presence of organ-specific (pathogenic) antibodies.” Id. PMR, he proposed,
falls between these two possible pathogenic etiologies. E. Hysa et al., Immune System Activation
in Polymyalgia Rheumatica: Which Balance between Autoinflammation and Autoimmunity? A
Systemic Review, 21 Autoimmunity Reviews 1, 7 (2022), filed as Ex. 30 (ECF No. 25-6) (“Hysa”)
(suggesting that “the balance of [PMR] between autoinflammation and autoimmunity seems to lie
halfway … by considering both ends of the pathophysiological spectrum of immune-mediated
rheumatic disease, PMR might be regarded as an inflammatory immune-mediated disease with
mixed mechanisms”). As a result, Dr. Efthimiou opined, it did not matter where PMR fit on that
spectrum, since “the vaccines administered can reliably explain clinical onset of either subtype of
immune mediated response.” First Efthimiou Rep. at 17.

Dr. Efthimiou maintained that PMR likely clinically presents due to an environmental
trigger, such as infection or vaccination, which then dysregulates an individual’s T-cell response.
First Efthimiou Rep. at 17. In support, he referenced government publications about how vaccine-
caused adverse events can occur. Committee to Review Adverse Effects of Vaccines: Evidence and
Causality 59–60 (K. Stratton et al., eds., 2012), filed as Ex. 33 (ECF No. 25-9) (the “IOM Rep.”)
(listing T-cells as contributing to the development of adverse events after vaccination). T-cells, he
contended, are integral to an individual’s maintenance of the immune system and self-tolerance.
First Efthimiou Rep. at 18. But PMR is understood to mechanistically arise as a result of the
disruption of one’s self-tolerance by certain T-cells and their inability to prevent autoreactivity. Id.

6
Components in a particular vaccine could initiate autoreactive T-cells that in turn attack
the body while providing aberrant immune signals leading to dysregulation and clinical disease
onset. First Efthimiou Rep. at 18. Here, Petitioner may have already possessed these autoreactive
cells due to previous vaccine exposure or some different environmental exposure. Id. Because a
vaccine has the potential to trigger “already present” immune cells” in an individual, Dr. Efthimiou
argued, the vaccine “could be” triggering a non-specific immune signal which adversely activates
another immune signal and leads to disease onset. Id. at 18–19; IOM Rep. at 82 (explaining that
both epidemiological and mechanistic research has recognized that individuals experiencing an
adverse reaction to vaccine administration have a predisposition that can exists for several reasons,
including genetics, intervening illness, or prior immunological and environmental exposures).

Medical literature has recognized an association between the seasonal flu and/or Tdap
vaccine, on the one hand, and PMR, and in Dr. Efthimiou’s view such evidence bore on Mr.
Radke’s circumstances. In support, Dr. Efthimiou referenced a number of case reports and/or case
series observing a temporal association between vaccination and PMR. See generally A. Soriano
et al., Giant Cell Arteritis and Polymyalgia Rheumatica After Influenza Vaccination: Report of 10
Cases and Review of the Literature, 21 Lupus 153 (2012), filed as Ex. 27 (ECF No. 25-3)
(“Soriano”); E. Liozon et al., Giant Cell Arteritis or Polymyalgia Rheumatica after Influenza
Vaccination: A Study of 12 Patients and a Literature Review, 20 Autoimmunity Rev. 1 (2021),
filed as Ex. 32 (ECF No. 25-8) (“Liozon”); P. Falsetti et al., Polymyalgia Rheumatica following
Infective Triggers or Vaccinations: A Different Subset of Disease?, 58 Rheumatologia 76 (2020),
filed as Ex. 29 (ECF No. 25-5) (“Falsetti”).

Although the vaccine involved in this case is different, Dr. Efthimiou maintained that “a
mechanism common to both vaccines [flu versus pneumococcal] was discovered as both vaccines
shared profiles related to myeloid lineage and inflammation,” making them equivalent in their
respective capacities to spur an aberrant immune reaction. First Efthimiou Rep. at 20–21; G.
Obermoser et al., Systems Scale Interactive Exploration Reveals Quantitative and Qualitative
Differences in Response to Influenza and Pneumococcal Vaccines, 38 Immun. 4:831 (2013), filed
as Ex. 34 (ECF No. 26-1) (“Obermoser”), at 2 (a comparison of the flu vaccine with the
pneumococcal vaccine demonstrated that the two vaccines “elicit common, as well as distinct,
transcriptional signatures, both early (innate immunity) and late (adaptive immunity), that
eventually lead to the development of protective antibody responses”).

Dr. Efthimiou further attempted to link the version of the pneumococcal vaccine covered
by the Program and other vaccines, in particular Tdap. The covered pneumococcal vaccine
includes bacterial components conjugated to a carrier protein, CRM197 6—thus, making any
reported associations with the Tdap vaccine (which Dr. Efthimiou alleged contain the same

6
CRM197 is a genetically detoxified mutant of diphtheria toxin. Because it is naturally non-toxic but highly
immunogenic, it is widely used as a carrier protein in conjugate vaccines like the pneumococcal vaccine, in order to
boost the body's immune response against the polysaccharide bacterial components. see Deshler v. Sec'y of Health &
Hum. Servs., No. 16-1070V, 2020 WL 4593162, at *11, 19 (Fed. Cl. Spec. Mstr. July 1, 2020).

7
diphtheria proteins) relevant when analyzing Petitioner’s case. First Efthimiou Rep. at 20. Because
these vaccines share the diphtheria toxoid component, they are equally capable of eliciting B-cell
responses in a T-cell dependent manner, making it reasonable to conclude that Petitioner’s immune
response post-vaccination became more susceptible to triggering cross-reactive immune memory
cells, and hence causing PMR. Id.

Dr. Efthimiou also endeavored to demonstrate that Petitioner’s receipt of a flu vaccine dose
the month before the vaccination at issue could have played a role in development of PMR. First
Efthimiou Rep. at 19, 20. In support, he noted the literature he had offered that associated this
vaccine with PMR. Id. at 19; Soriano; Liozon. He also emphasized Obemoser’s findings that the
flu vaccine elicited the same kinds of cytokines and immune cell response as pneumococcal, even
if the two vaccines were distinguishable. First Efthimiou Rep. at 20. And other evidence
established that the immune response to the flu vaccine would peak within four to six weeks of
administration—consistent with the time Petitioner received the pneumococcal vaccine
approximately a month later. S. Rastogi et al., Time to Peak Serum Antibody Response to Influenza
Vaccine, 2 Clin. & Diag. Lab. Immunol. 1:120 (1995), filed as Ex. 35 (ECF No. 26-2) (“Rastogi”).
Thus, Dr. Efthimiou suggested the two vaccines could have somehow contributed to Petitioner’s
PMR (although he did not explicitly set forth in his first report how this could have occurred).

Second Report

Dr. Efthimiou’s second report responded to comments made by Respondent’s diagnostic
expert, Dr. Chester Oddis. He first addressed Dr. Oddis’s opinion that Petitioner’s more likely
diagnosis was an “exaggerated pain response,” evidenced by interactions with his surgeon
following his knee replacement surgery. Second Efthimiou Rep. at 1. Dr. Efthimiou maintained in
reaction that studies have reported that “peripheral arthritis has been described in up to 50% of
patients with PMR with knee involvement present in the majority.” Id. (citing M. Cimmino et al.,
High Frequency of Capsular Knee Involvement in Polymyalgia Rheumatica/Giant Cell Arteritis
Patients Studied by Positron Emission Tomography, 52 Rheumatology 1865 (2013), filed as Ex.
40 (ECF No. 30-3) (“Cimmino”). Moreover, recent research on the pathophysiology of PMR has
confirmed the frequency of knee involvement. See K. Kobayashi et al., Ultrasound of Shoulder
and Knee Improves the Accuracy of the 2012 EULAR/ACR Provisional Classification Criteria for
Polymyalgia Rheumatica, 61 Rheumatology 1185, 1180 (2022), filed as Ex. 41 (ECF No. 30-4)
(“Kobayashi”) (finding that the data revealed not only the shoulder but also the knee [as] the joint
where [ultrasound] abnormalities are frequently detected … 95% of patients with definite PMR
had some [ultrasound] abnormalities in the knee, whereas 77% and 10% had tenderness and
swelling, respectively.”).

Here, between October and November 2019 (and hence after the September vaccination),
Mr. Radke reported that his chronic right knee pain had worsened, and he noticed an acute change
in pain over the past month. Second Efthimiou Rep. at 1; Ex. 24 and 139. Petitioner consistently
reported a difference in his knee pain to his primary care physician, Dr. Young, as well as pain

8
that occurred suddenly. Because, Dr. Efthimiou argued, “PMR arthritis is an inflammatory arthritis
that is known to occur suddenly, and joint “warmth” is a hallmark of inflammatory arthritis”—
both of which were reported and documented in Petitioner’s medical records—the onset of these
problems was consistent with a PMR diagnosis. Second Efthimiou Rep. at 3.

Dr. Efthimiou then described “atypical” PMR, and how that descriptor best fit Petitioner’s
clinical presentation. Second Efthimiou Rep. at 3. While patients with “classic” PMR present more
commonly with bilateral shoulder abnormalities (such as bursitis or bicep tenosynovitis), patients
with an atypical clinical presentation commonly report a history of pain and swelling in the knee,
symptoms of carpal tunnel syndrome, or pain localized to both knees with radiation. Id. at 4; M.
Fitzcharles & J. Esadile, Atypical Presentation of Polymyalgia Rheumatica, 33 Arthritis & Rheum
403, 406 (1990), filed as Ex. 42 (ECF No. 30-5) (“Fitzcharles & Esadile”) (describing six patients
that did not present with any symptoms referable to the limb girdles, and where five out of the six
patients developed a more typical presentation of PMR over the course of two to twelve months).
Dr. Efthimiou noted, however, that “the differential diagnosis of PMR can have overlapping
symptoms,” and that “[t]he most challenging mimicking disorder” is seronegative RA. Second
Efthimiou Rep. at 4. Concurring with Dr. Oddis, Dr. Efthimiou maintained that seronegative RA,
along with other mimicking PMR disease, had properly been ruled out by Petitioner’s treating
physicians. Id.

Regarding Petitioner’s inflammatory markers throughout his treatment course, Dr.
Efthimiou noted that Mr. Radke had two documented inflammatory increases—on May 5, 2020,
and then on February 21, 2022. Id. Although Dr. Oddis argued that Petitioner’s inflammatory
markers were not consistent, Dr. Efthimiou responded that “[s]ymptoms and ESR/CRP levels 7 are
often not concordant”—stating that “[p]atients with PMR can present with normal ESR values and
in patients with relapse, ESR levels have been observed in 68% of cases and CRP levels normal
in 62% of cases.” Id. at 5 (referencing M. Florescu et al., Polymyalgia Rheumatica: An Update
(Review), 26 Experimental & Therapeutic Medicine 1, 4 (2023), filed as Ex. 44 (ECF No. 30-7)
(“Florescu”). Despite the medical records demonstrating multiple instances of normal labs over
the course of Petitioner’s treatment course, Dr. Efthimiou opined that Petitioner exhibited a
“relapsing course [of PMR] that requires longer treatment.” Second Efthimiou Rep. at 5
(emphasizing Dr. Oddis’ citation to literature discussing slower response times to treatment with
low-dose glucocorticoids).

7
ESR stands for “erythrocyte sedimentation rate,” and is defined as “the rate at which erythrocytes precipitate out
from a well-mixed specimen of venous blood, measured by the distance the top of the column of erythrocytes falls in
a given time interval under specified conditions; an increase in rate is usually due to elevated levels of plasma proteins,
especially fibrinogen and immunoglobulins, which decrease the zeta potential on erythrocytes by dielectric shielding
and thus promote rouleau formation. It is increased in monoclonal gammopathy, hypergammaglobulinemia due to
inflammatory disease, hyperfibrinogenemia, active inflammatory disease, and anemia.” Erythrocyte Sedimentation
Rate, Dorland’s Medical Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=102146 (last
visited June 8, 2026).

9
Dr. Efthimiou concluded his second report reiterating his overarching opinion—that
Petitioner’s development of PMR was likely triggered by his receipt of the pneumococcal vaccine,
and that his clinical presentation and course was most representative of a probable post-vaccination
cause. Id. at 6.

Third Report

In his final report, Dr. Efthimiou addressed the assertion of Respondent’s causation expert,
Dr. Stephen Jameson, that it is essential to consider whether there is a likely link between a specific
vaccine and a given autoinflammatory disease in the medical literature before proposing an
association. Third Efthimiou Rep. at 2. In response, Dr. Efthimiou instead maintained that his own
analysis “focused on reliably explaining why the vaccines administered and [Petitioner’s]
sequence of immunological events is supported by both the clinical evidence and a biologically
plausible mechanistic explanation …” Id. Moreover, Dr. Efthimiou reiterated that his medical
theory causally linking Petitioner’s receipt of the vaccine and his development of PMR was based
on reliable medical and scientific information. Id.

Dr. Efthimiou briefly acknowledged his disagreement with Dr. Jameson’s understanding
of the level of support needed to confirm a medical theory causally connecting the pneumococcal
vaccine and PMR. Third Efthimiou Rep. at 3. He explained that both “scientific” and “medical”
literature are necessary when evaluating Petitioner’s overall clinical sequence—and here, Dr.
Efthimiou argued, the literature supported a finding that Petitioner’s vaccination and subsequent
development of PMR represents a vaccine-associated cause. Id. at 3–4. In his own analysis, Dr.
Efthimiou stated, he examined “the totality of th[e] clinical information that supports how a
biologically plausible mechanistic link connects the pneumococcal vaccination to being capable
of initiating the understood adverse pathology of PMR illness.” Id. at 4.

Dr. Efthimiou then addressed criticisms that he had generalized outcomes of other case
studies or reports involving different vaccines as supporting the capacity of the pneumococcal
vaccine to trigger the onset of PMR. He asserted that “at least 21” instances of PMR after receipt
of a pneumococcal vaccine had been reported in the “Vaccine Adverse Event Reporting System,”
or “VAERS.” Third Efthimiou Rep. at 5. 8 And while case reports pertaining to other vaccines also
being associated with PMR are “not intended, especially in isolation, to provide general
conclusions” about vaccine association (especially since the risk was low), they still had
evidentiary value. Clinical associations between PMR and different types of vaccine antigens, did
not, according to Dr. Efthimiou, “equate to different adverse biological mechanisms explaining
how a patient’s PMR illness can reliably be pathologically caused within a few days.” Id. at 7. And
he discounted the absence of epidemiologic evidence, noting that “if epidemiological studies
observed an increased risk of PMR illness in association with receiving pneumococcal vaccines,
administration of the vaccine would not be recommended.” Third Efthimiou Rep. at 5 (citing T.

8
The source for this contention is not evident from any items filed in conjunction with any of Dr. Efthimiou’s reports.

10
Shimabukuro et al., Safety Monitoring in the Vaccine Adverse Event Reporting System (VAERS),
33 Vaccine 4398 (2015), filed as Ex. 47) (ECF No. 35-2) (“Shimabukuro”).

Dr. Efthimiou also attempted in his third report to explain in greater detail how the flu
vaccine dose Petitioner received the month before administration of the pneumococcal vaccine
could have also played a role in the development of PMR. Third Efthimiou Rep. at 7–9. He
contended that both vaccines had been shown to have the capacity to “directly activate” an
immediate, innate response—and that this was meaningful given that (a) Petitioner had received
the pneumococcal vaccine before, and (b) the impact of the flu vaccine administration would still
be present as of late September 2019. Id. at 7–8. In addition, the medical record evidence
established that Petitioner was experiencing a flare-up of preexisting peripheral neuropathy
symptoms by early October 2019, and by November the impact of the pneumococcal vaccine
would peak as well. Id. at 8. Thus, “[t]he evidence supporting that the flu vaccines are associated
with initiating the same innate immune responses as pneumococcal vaccinations biologically links
the clinical data associating the onset of PMR illness with both the flu vaccine and the tetanus
toxin containing vaccine.” Id. at 8–9.

B. Respondent’s Experts

1. Chester V. Oddis, M.D.

Dr. Oddis, a rheumatologist, offered one written report on behalf of Respondent. See
Report, dated Dec. 26, 2023 (ECF No. 29-1) (“Oddis Rep.”). Based on his years of experience in
the practice of clinical inpatient and outpatient rheumatology, Dr. Oddis opined that Petitioner did
not have PMR, and that he also did not suffer from vaccine-induced PMR. Oddis Rep. at 12.

Dr. Oddis received his undergraduate degree from the University of Pittsburgh, and his
medical degree from Pennsylvania State University College of Medicine. He is board-certified in
both Internal Medicine and Rheumatology. Oddis Rep. at 1. Dr. Oddis is currently Professor of
Medicine in the Division of Rheumatology and Clinical Immunology and the Director of the
Myositis Center in the School of Medicine at the University of Pittsburgh. Id. His primary area of
research and clinical care is in the clinical, epidemiologic, serologic and treatment aspects of
myositis and autoimmune interstitial lung disease. Id. Dr. Oddis has also published numerous
journal articles on these subjects. Id. at 2. Over the course of his clinical career, Dr. Oddis has
diagnosed, treated, and managed the care of many individuals with PMR and other
rheumatological disease. Id.

Dr. Oddis summarized the pertinent medical facts before discussing PMR in general. See
generally Oddis Rep. at 2–8. PMR is understood as a common inflammatory rheumatic condition,
oftentimes characterized by prominent morning stiffness of the shoulder, hip girdle, and neck. Id.
at 8; C. Salvarani & F. Muratore, Clinical Manifestations and Diagnosis of Polymyalgia
Rheumatica, UpToDate (Oct. 2023), filed as Ex. A Tab 1 (ECF No. 29-2) (“Salvarani &
Muratore”) at 1. PMR is found in individuals almost exclusively over the age of 50, and with a

11
peak incidence occurring between the ages of 70 and 80. Oddis Rep. at 8; Salvarani & Muratore
at 2. Dr. Oddis further explained that the clinical manifestations of PMR include an abrupt onset
of symmetrical aching and stiffness of the shoulders, hip girdle, neck and torso, with pain being
the worst in the morning. Oddis Rep. at 8; Salvarani & Muratore at 4. Approximately 70–95% of
patients with PMR will exhibit bilateral shoulder pain as the presenting clinical manifestation, with
about 50% exhibiting lower extremity symptoms. Salvarani & Muratore at 4. Patients with PMR,
however, can also present with non-specific signs or symptoms, such as malaise, fatigue,
depression, weight-loss or low-grade fever. Id. at 5; Oddis Rep. at 8.

Dr. Oddis then discussed the common laboratory findings in PMR—emphasizing the
significance of the diagnostic value of inflammatory biomarkers like ESR and CRP. Oddis Rep. at
9. ESR, the “traditional laboratory finding in PRM,” typically ranges from mildly to markedly
increased, whereas CRP is “nearly always elevated.” Salvarani & Muratore at 5 (stating that “in
two reports, an elevated ESR (greater than 30 mm/hour) was noted in 92 to 94 percent of patients
at the time of diagnosis of PMR, while 99 percent of such patients had an increased serum CRP
level (greater than 5mg/L).”). Here, Petitioner’s inflammatory markers, specifically ESR and CRP,
were not “consistently concordant with either an improvement or an exacerbation of PMR
symptoms.” Oddis Rep. at 10. Similarly, during a follow-up with Dr. Young on June 15, 2021,
Petitioner reported “constant morning stiffness” but his inflammatory markers at that time were
noted as within the normal range. Ex. 5 at 46, 49. Dr. Oddis stated that this instance, among others
noted in the medical records, indicates an inconsistency between Petitioner’s symptoms and lab
results and proposed diagnosis. Oddis Rep. at 10.

The initial treatment course for PMR typically involves the use of low-dose glucocorticoids
(i.e., Prednisone) and the therapeutic response is understood to be brisk and complete. Oddis Rep.
at 9. Patients oftentimes start with a suggested dose of 15mg/day; however, lower dosages may be
more appropriate for certain individuals. Id. On the other hand, chronic management of PMR
involves the gradual tapering of the Prednisone dosage, of which the duration of treatment can
vary among individuals (i.e., some patents can wean off treatment in 1 to 2 years, while others
require longer). Id. Dr. Oddis emphasized not only how unusual it was that Petitioner’s Prednisone
dosage fluctuated greatly throughout his treatment course, but that the dosage often exceeded
20mg/day—a level that generally aids in alleviating symptoms of PMR quickly and completely.
Id. at 11; C. Salvarani & F. Muratore, Treatment of Polymyalgia Rheumatica, UpToDate (Oct.
2023), filed as Ex. A Tab 2 (ECF No. 29-3) at 1–2.

Based on the medical records and literature, Dr. Oddis opined that Petitioner more than
likely did not have PMR. Oddis Rep. at 11. Petitioner’s symptoms did not feature the classical
presentation of bilateral shoulder pain and hip stiffness that improves throughout the day and
responds well steroid treatment. Id. at 10. Moreover, Petitioner’s treating physicians were not
confident that his overall signs and symptoms were consistent for a diagnosis of PMR—and Dr.
Oddis referenced a note from an April 2, 2020, visit with Dr. Young that stated “[w]e discussed
that [Petitioner’s] presentation has not been classic for PMR … the doses of prednisone which
12
have relieved [Petitioner’s] symptoms are higher than which would normally be used in PMR.”
Id. at 11 (citing Ex. 24 at 186). In addition, Petitioner’s treating physicians ruled out other
inflammatory and non-inflammatory diseases that can sometimes mimic PMR, such as elderly
onset RA, late-onset spondyloarthropathy, inflammatory myopathy, lupus, various forms of
vasculitis, calcium pyrophosphate deposition disease, or infection. Oddis Rep. at 9.

2. Stephen C. Jameson, Ph.D.

Dr. Jameson, an immunologist, offered one written report on behalf of Respondent. See
Report, dated June 25, 2024 (ECF No. 34-1) (“Jameson Rep.”). Dr. Jameson opined that it is more
likely than not Petitioner’s receipt of the pneumococcal vaccine on September 20, 2019, did not
cause his development of PMR. Jameson Rep. at 5.

Dr. Jameson attended the University of Bristol, England for his undergraduate degree in
Cellular Pathology, and the University of Cambridge, England for his Ph.D. in Physiology and
Genetics Research. Curriculum Vitae, filed as Ex. C (ECF No. 34-4) (“Jameson CV”) at 1. He then
completed a post-doctoral fellowship in Immunology at the Scripps Research Institute, La Jolla,
California, and the University of Washington, Seattle, before establishing his own laboratory at
the University of Minnesota in 1995. Id.; Jameson Rep. at 1. Dr. Jameson is currently a Professor
in the Center for Immunology, Masonic Cancer Center and Department of Laboratory Medicine
and Pathology, at the University of Minnesota Medical School. Jameson Rep. at 1–2. He has
published over 130 primary research papers, as well as over 50 review articles—nearly all focusing
on various topics in immunology and on the immune response to pathogens. Id. at 2. Dr. Jameson’s
primary research focus is the study of cellular immune response against pathogens and vaccines
via animal models, and the impact the studied immune responses have on protective immunity,
immunopathology, and autoimmunity. Id.

Dr. Jameson primarily focused his short report on responding to Dr. Efthimiou’s
proposition that Petitioner’s immune response to his receipt of the pneumococcal vaccine
subsequently led to the development of PMR. The innate immune response, Dr. Jameson
explained, can be considered as “the acute response to infection, vaccination or tissue damage”
that typically features the induction of inflammatory responses. Jameson Rep. at 3. This response
involves several different cell types—predominantly myeloid cells, such as macrophages. Id.

When an individual has an immune response to a trigger such as an infection or vaccination,
however, it is the secondary, adaptive immune response (involving primarily T- and B-cells) that
takes over. Jameson Rep. at 3. This is because macrophages are usually insufficient in containing
an individual’s immune response to infection or vaccination. Id. Specifically, T-helper cells
promote the activation of B-cells, which then lead to the production of “potent high-affinity
antibodies, capable of neutralizing the pathogen or its toxins.” Id. When a cooperative response
exists between T-cells and B-cells, their populations of cells can persist long-term, thus, creating
immunological memory. Id. Therefore, any future exposure to the same or related pathogens will

13
essentially trigger a faster and more effective adaptive immune response, Dr. Jameson opined. Id.
But because vaccines (like the pneumococcal vaccine) are “attenuated compared to an infection”
(which would have significantly more impact on the human immune response), “effective immune
memory [due to vaccination] is typically generated without excessive or prolonged inflammation.”
Id.

Dr. Jameson briefly responded to Dr. Efthimiou’s assertion that aspects of the innate and
adaptive immune response have been observed in immunopathological responses, such as
autoimmunity and autoinflammatory diseases—thus establishing that PMR may involve both
autoimmune and autoinflammatory characteristics. Jameson Rep. at 3. Dr. Jameson, however,
argued that simply because protective immune responses share pathways with autoimmune and/or
autoinflammatory disease, this did not also suggest that activation of the pathway likely leads to
illness. Id. If this were true, every infection or vaccination would result in “damaging
autoinflammatory diseases and multiorgan autoimmunity,” even though that is not the case. Id.
Instead, Dr. Jameson maintained that the similarity between the types of pathways involved in
protective and damaging inflammatory/immune responses can exist without both being equally
capable of sparking a disease process. Id.

When considering whether a causal link exists between a given infection or vaccination
and a specific autoimmune/autoinflammatory disease, Dr. Jameson maintained, the scientific
community looks for reliable evidence such as epidemiological and mechanistic studies (although
he admitted that establishing sound bases for concluding causality under such circumstances was
difficult). Jameson Rep. at 3, 4. But here, there was very little in the way of medical literature
suggesting the existence of a causal link between infections and/or vaccination and PMR. Id. at 4.
At most, Dr. Efthimiou had offered articles that discuss a possible connection between PMR and
different vaccines, like the flu or Tdap vaccines—neither of which were relevant to Mr. Radke’s
case. Indeed, one such article ultimately concluded that “a causal association between [influenza
vaccination] and GCA or PMR is not supported by adequate evidence.” Id.; Liozon at 5 (emphasis
added).

Dr. Efthimiou also proposed “a somewhat tortuous link” for a causal association, Dr.
Jameson argued. Jameson Rep. at 5. Dr. Efthimiou had attempted to demonstrate an association
between pneumococcal vaccine and PMR based upon the fact that the Tdap and pneumococcal
vaccines arguably share a component—diphtheria toxoid, which Dr. Efthimiou analogized to the
conjugate CRM197 component in the pneumococcal vaccine—and therefore the pneumococcal
vaccine could also provoke the onset of PMR in a manner comparable to the Tdap vaccine. Id.;
see also Falsetti at 3 (two out of six PMR patients had received a Tdap-like vaccine prior to the
onset of PMR). Dr. Jameson, however, took issue with Dr. Efthimiou’s reliance on Falsetti—
arguing that “all [one] can glean from [the] report is that those patients received tetanus toxoid
vaccines—and since tetanus toxoid is not a component of the Prevnar 13 pneumococcal conjugate
vaccine received by [Petitioner], this undercuts Dr. Efthimiou’s argument that the presence of

14
diphtheria toxin in Prevnar 13 provides a mechanistic basis by which it could induce PMR, based
on the literature.” Jameson Rep. at 5.

Dr. Jameson ultimately maintained that Dr. Efthimiou’s generalization that the “elements
of the immune system that are involved in the response to vaccines are also involved in
autoimmune response” is “not pertinent” when analyzing whether Petitioner’s receipt of the
pneumococcal vaccine on September 13, 2019, most likely led to his development of PMR.
Jameson Rep. at 5. He opined instead that based on Petitioner’s clinical presentation and course,
as well as the medical literature, it was more likely than not that Petitioner’s receipt of the vaccine
at issue did not cause his alleged injury. Id.

III. Literature Overview

Petitioner filed 17 items of literature. 9 Special masters are not obligated to address in their
written decision every single medical or scientific article filed in a case (and it is not presumed
they did not consider a particular item just because it is not mentioned). 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”).
Nevertheless, in order to fully meet the terms of the Remand Order, I shall herein address each
item Petitioner filed 10—and explain my construction of it and/or the weight I deem it merits.

A. Soriano

Soriano is a case series discussing ten instances (out of a cohort of 95 patients, which only
included 22 actual PMR diagnoses) in which an individual reported receipt of a flu vaccine within
two weeks to three months of receipt of a flu vaccine. Soriano at 154 Table 1. Of the ten, only five
were diagnosed with PMR wholly or partially (with the related condition of GCA being the other
diagnosis). The earliest an individual experienced onset was three weeks post-vaccination (with
one patient experiencing a PMR relapse within two weeks). Id. The authors proposed the flu
vaccine could trigger PMR in individuals with a genetic propensity, but admitted that they had

9
I also permitted Petitioner the opportunity to file any “newly-published” materials (which I defined as published in
2025 or later, given that briefing on the claim was originally completed in the spring of 2025) relevant to causation.
See Scheduling Order, dated Apr. 9, 2026 (ECF No. 52). But he filed two articles that were published in 2024, with
no effort to explain how their submission comported with my Order. Moreover, these same two articles had already
been offered in the course of resolving the Motion for Review, but rejected by the Court as untimely-submitted. Order
Denying Motion, dated Jan. 8, 2026 (ECF No. 50). I therefore struck them from the record. Order, dated May 12, 2026
(ECF No. 55).
10
I do not, however, include herein a detailed review of the items filed by Respondent. Respondent does not bear the
burden of proof in Vaccine Act cases, and (based upon my review of Petitioner’s evidence) I deem Petitioner to have
failed to carry his prima facie case—based solely on what Petitioner filed.

15
relied on a small sample, and that the incidence for the sample (one of two patients experiencing
PMR or GCA after vaccination) was less than predicted by other studies. Id. at 155.

Soriano is generally inapposite to this case, as it does not involve the pneumococcal
vaccine. In addition, it based its conclusions upon an extremely small sample, and (as noted above
and below) case reports deserve the lowest level of evidentiary weight in Vaccine Program cases.
(I also observe that Soriano has been offered in prior cases that rejected causation arguments
attempting to link covered vaccines to PMR—and hence its evidentiary strength has repeatedly
been found inadequate, consistent with my own reading of the article).

B. Camellino

Camellino is a general review article discussing PMR’s characteristics, with some
commentary on its suspected pathogenesis. It notes that PMR tends to impact women more than
men, and most often in cohorts older than 50. Camellino at 2. It usually presents with shoulder
and/or hip pain, spreading to the limbs and appearing both abruptly and progressively, with worse
pain the night and early morning hours. Id. As far as cause, Camellino’s authors noted that “we do
not have a clear understanding of the etiology and pathogenesis of PMR,” adding that it likely has
a “multifaceted pathogenesis,” and that possession of a particular gene complex may increase
susceptibility to it.

Camellino makes no mention of vaccine causation—suspected, proposed, or
investigated—of PMR. At most, its authors allow for the possibility of infectious agents as triggers,
but linked PMR only to three (mycoplasma, parvovirus B19, and parainfluenza virus)—none of
which are strong analogs for the pneumococcal vaccine. Camellino at 2. Its authors did discuss the
role that an aberrant T cell response might play in PMR’s pathogenesis, with T helper cells in
particular, but did not propose how this dysregulated environment would come to be. Id. at 2–3.

C. Falsetti

Falsetti’s authors began with a group of 58 PMR patients, and from that cohort identified
15 patients who reported some environmental pre-onset stimulus (six vaccines (four flu versus two
with tetanus toxoid) versus nine recalling some form of prior infection). Falsetti at 78. They went
on to emphasize that it was “well known” that the flu vaccine was associated with PMR, but
otherwise the focus of the paper was on the clinical features of environmentally-triggered PMR
(including what certain inflammatory biomarkers were more likely to be seen in its context), as
well as the general effectiveness of glucocorticoid treatments under such circumstances. Id. at 77–
79 (finding “[t]hese data suggest that PMR triggered by an environmental factor could constitute
a different subset of milder disease, as they have a more rapid response to GC therapy with a higher
[form of inflammatory biomarker] at diagnosis). But the authors admitted that their “retrospective”
data could not “provide information about the endocrinologic, immunological and genetic state of
our PMR patients.” Id. at 79.

16
Falsetti does mention two instances of PMR occurring after receipt of tetanus toxoid-
containing vaccines, but such factual circumstances are not all that comparable to the
pneumococcal vaccine’s diphtheria conjugate component (as explained below). Moreover,
Falsetti’s authors relied on self-reporting from their patient sample of pre-onset vaccination, and
focused far more on the flu vaccine as a potential environmental trigger.

D. Hysa

Hysa is a review article that relied on a search of prior published studies involving PMR.
Hysa at 1. It concludes (consistent with Dr. Efthimiou’s contention) that PMR is mediated through
some mix of autoinflammatory and autoimmune processes. Id. at 2, 7 (“PMR might be regarded
as an inflammatory immune-mediated disease with mixed mechanisms in a background of genetic
and epigenetic factors together with immunological and endocrine senescence”). Hysa does not,
however, opine as to possible triggers of the mixed process it proposes leads to PMR (including
vaccines). At most, it notes that

despite the interesting role of B cells in active PMR, the titre of different
autoantibodies does not appear to correlate with active disease and nor
their pathogenetic role is supported by the literature. Therefore, their
positivity has been interpreted as a consequence of hyper-inflammation
or as cross-reactive phenomena triggered by environmental causes (e.g.,
infections) and antigenic release from damaged tissue/cells.

Id. at 7. In other words, autoantibodies may appear in the context of PMR and contribute to a
disease process, but they are not understood to initiate the disease itself (and since vaccines are
largely intended to promote antibody production as a first order goal, this further diminishes the
possibility of vaccine causation). Id. (“[a]lthough the evidence supporting the role of
autoantibodies pathogenicity seems lacking in PMR, their detection might provide indirect hints
of its underlying immune-mediated mechanisms”).

E. I. Lundberg et al., An Update on Polymyalgia Rheumatica, 292 J. Int. Med. 717
(2022), filed as Ex. 31 (ECF No. 25-7) (“Lundberg”).

Lundberg is a general review article discussing the diagnostic tools used to assess PMR,
and treatment recommendations and issues. It includes the observation that PMR has been
proposed to be possibly triggered by the flu vaccine (referencing in support Liozon (Lundberg at
718 n.20), which is discussed below), and that “a potential safety signal” in connection to a
COVID-19 vaccine was observed in passive surveillance data obtained from a pharmacovigilance
database (although the reference, which was not filed in this case, is explained by Lundberg’s
authors to deem the risk observed was less than what was true for the flu vaccine). Lundberg at
718. It also notes that PMR “is a disease of elderly people” (and hence its pathogenesis might have
something to do with immune system senescence), and that no specific autoantibody is known to
be associated with it. Id. at 719.

17
F. Liozon

As Dr. Jameson noted in his report, Liozon does not stand as particularly strong support
for the contention that the flu vaccine could trigger PMR. Liozon at 5. Liozon’s authors began
with an initial patient pool of 358 patients with GCA or GCA/PMR (diagnosed between 2002-
2020), narrowing the sample to 10 patients (approximately three percent of the sample) who had
received a flu vaccine prior to onset and developed GCA, with two additional individuals who
developed PMR. Liozon at 3, 5. Both PMR patients manifested symptoms within 10 days of
vaccination. Id. at 3. Thus, the sample relied upon to establish a vaccine link was exceedingly
small.

Moreover, there are several other reasons to give Liozon little weight (ignoring the fact
that it does not involve any of the vaccines at issue in this case—and its authors themselves
discounted the strength of the causation showing their study proposed). 11 For example, Liozon’s
authors proposed that a specific form of HMC allele found in some humans was likely associated
with GCA/PMR triggered by the flu vaccine (Liozon at 5)—something the Petitioner in this case
has not been shown to possess. The authors also discuss the possibility that a “vigorous vaccine-
induced immune reaction” in elderly patients may play a role in encouraging PMR triggering,
invoking a concept (“autoimmune syndrome induced by adjuvants,” or “ASIA”) that has been
consistently found to lack merit in numerous prior Vaccine Program cases. Id. at 1, 5, 6. 12

G. IOM Report

Petitioner filed the entirety of the IOM Report—all 131 pages of it. See generally Ex.33.
This plainly exceeds what the occasion calls for (claimants would not need to file the entire
dictionary if they wished to establish the spelling or meaning of a particular word), and the
indiscriminate filing of such a lengthy article only obscures the pinpoint aspects of the document
relevant to the causation theory at issue. The portions of this exhibit that have been highlighted do,
however, set forth some general points claimants like to stress—for example, that epidemiologic
evidence cannot preclude the possibility of a vaccine cause (IOM Report at IX–X, 39–47), that
conclusions about vaccine-associated adverse events are not certain (Id. at XI), and (as Dr.
Efthimiou maintained) that adverse events may not always be specific to a vaccine, but could
reflect generalized immune system dysregulation (Id. at 82). However, the IOM Report is

11
In fact, Liozon’s authors specifically stated that 60 patients from the initial 358 sample of individuals reported “other
potential triggers,” such as infections or intercurrent illnesses, but “[n]o GCA onset after vaccination other than [flu]
(especially pneumococcal vaccination) was reported by any patient.” Liozon at 3 (emphasis added).
12
J.F. v. Sec’y of Health & Hum. Servs., No. 13-799V, 2022 WL 5434214, at *32 (Fed. Cl. Spec. Mstr. Sept. 9, 2022)
(discussing weaknesses of ASIA as causation theory/injury); Rowan v. Sec’y of Health & Hum. Servs., No. 10-272V,
2014 WL 7465661, at *12 (Fed. Cl. Spec. Mstr. Dec. 8, 2014) (rejecting the ASIA theory because it “is not a proven
theory,” and no “persuasive or reliable evidence” supports it), aff’d, 2015 WL 3562409 (Fed. Cl. 2015).

18
completely silent on adverse events associated with the pneumococcal vaccine, and also does not
identify PMR as an adverse event associated with any of the vaccines it does consider.

H. Obermoser

Obermoser aimed to evaluate the similarities and differences in the immune response
(innate as well as adaptive) to the flu and a form of pneumococcal vaccine not covered in the
Program, “Pneumovax 23”). 13 Both were found to provoke similar activation of an innate response,
with evidence of different cytokine (immune cell messengers) upregulation within hours of
administration. Obermoser at 5. However, the subsequent adaptive responses were not temporally
the same, with the response to the pneumococcal vaccine lasting longer. Id. at 6. The authors also
observed that although the two vaccines had some common immune response mechanisms, the
fact that the vaccines have distinguishable components meant that “different vaccines might lead
to development of adaptive immunity through different innate immune pathways.” Id. at 7.

At best, Obermoser stands for the proposition that vaccines can have a rapid impact on the
initial, innate immune response, and that their subsequent effectiveness/temporality (when the
adaptive leg begins) will depend on the specific nature of the bacterial/viral components of the
vaccine. But this does not mean that what is known about the flu vaccine (here, that some studies
arguably link it to PMR) applies with the same force to the pneumococcal vaccine. Obermoser
comments not at all on PMR or other possible vaccine adverse events.

I. Rastogi

Rastogi is a 31-year-old article that aimed to determine (based on a sample of 118 elderly
patients) the timeframe it would take from the date of receipt of a trivalent form of flu vaccine to
result in peak antibody response, determining that the general peak occurred within four to six
weeks after vaccination, with no statistically significant difference in the interval. Rastogi at 120.
It also notes that peaks could occur sooner, or later (when adjuvants are included in the vaccine).
Id. at 121.

Dr. Efthimiou cited Rastogi to support his contentions about the timeframe in which
Petitioner’s receipt of a flu vaccine prior to receipt of the pneumococcal vaccine would peak in
terms of immune response, thus lending support to the possibility that both vaccines played a role
in his PMR. First Efthimiou Rep. at 21. Rastogi makes no mention of the pneumococcal vaccine
or vaccine adverse events, however, and thus does not itself establish peak antibody timeframes
for recipients of the pneumococcal vaccine.

13
Edwards v. Sec’y of Health & Hum. Servs., No. 20-1682V, 2023 WL 3775021, at *1 (Fed. Cl. Spec. Mstr. June 2,
2023 (quoting Bundy v. Sec’y of Health & Hum. Servs., No. 12-769V, 2014 WL 348852, at *1 (Fed. Cl. Spec. Mstr.
Jan. 8, 2024)). “But only pneumococcal conjugate vaccines, routinely administered to children, and covered by the
Vaccine Program.” Id. Pneumovax 23 is considered a polysaccharide vaccine, and therefore, is not a covered vaccine.

19
J. S. Mori & Y. Koga, Glucocorticoid-Resistant Polymyalgia Rheumatica:
Pretreatment Characteristics and Tocilizumab Therapy, 35 Clin. Rheumatol. 1367
(2016), filed as Ex. 36 (ECF No. 26-3) (“Mori & Koga”).

Mori & Koga discusses some PMR patients who in treatment proved resistant to the most
common modality used for it (glucocorticoids), and what efforts were then tested on their treatment
to identify “alternative immunosuppressive agents” that could be helpful. Mori & Koga at 1374.
Dr. Efthimiou referenced this article in the section of his opinion addressing his embrace of PMR
as the proper diagnosis, noting that the treatment Petitioner had been receiving was recognized in
Mori & Koga. First Efthimiou Rep. at 15. This article does not appreciably relate to, or advance,
Petitioner’s causation arguments (and while it may bulwark Petitioner’s diagnosis arguments, my
disposition of the claim does not turn on whether he did or did not have PMR).

K. Cimmino

Cimmino (observing that PMR patients frequently also experienced peripheral arthritis–in
particular featuring knee involvement) sought to evaluate the utility and effectiveness of PET/CT
imaging of the knee, in order to “determine the frequency of knee inflammation and to evaluate its
anatomical localization.” Cimmino at 1865. Dr. Efthimiou referenced Cimmino mainly for its
statement that “up to 50%” of PMR patients also experienced knee-oriented peripheral arthritis
(although Petitioner did not file the citation from Cimmino underlying this assertion—an article
from 1984). Id. at 1865 n.3. Otherwise, Cimmino is offered not for purposes of supporting
causation (and indeed, it says nothing about PMR’s suspected or speculated causes), but on the
disputed issue of diagnosis.

L. Kobayashi

Like Cimmino, Kobayashi focuses on knee-oriented symptomatic issues seen in the context
of PMR, and whether testing aimed at the status of the knee or shoulder would lead to greater
certainty in diagnosis. Its authors sought to test (in a sample of 60 patients) whether “the
examination of the knee [via certain imaging procedures] for the pathologies beyond bursitis and
synovitis would increase the accuracy of PMR classification and obviate the need for the hip
assessment,” concluding that diagnostic accuracy for PMR was heightened if imaging/testing was
focused on the knee or shoulder rather than the hip. Kobayashi at 1186, 1189. Kobayashi says little
to nothing about possible PMR causation, however; in fact, its authors specifically acknowledge
(consistent with Camellino or Salvarani & Muratore) that “[t]he diagnosis of PMR can be
challenging because the pathogenesis of PMR remains largely unknown and there are no specific
serologic or imaging biomarkers”). Id. at 1185.

M. Fitzcharles & Esdaile

Fitzcharles & Esdaile is a 36-year-old case series report discussing six PMR patients (seen
in the mid-1980s) who presented “without the typical limb girdle features associated with PMR.”

20
Fitzcharles & Esdaile at 302. Its authors deemed the evaluated cases to fit the diagnosis for PMR
despite their atypical features, and they also proposed that a subset of PMR patients might see
evolution from “clinical or subclinical synovitis of nonproximal joints” to the more commonly-
seen PMR symptoms. Id. at 406. Fitzcharles & Esdaile appears to have been referenced by Dr.
Efthimiou to support his interpretation of the medical records as supportive of the PMR diagnosis,
despite the discrepancies observed by Dr. Oddis.

N. S. Ahmed et al., Case Report and Literature Review of an Atypical Polymyalgia
Rheumatica and Its Management, 16 Int. Med. Case Rep. J. 873 (2023), filed as
Ex. 43 (ECF No. 30-6) (“Ahmed”).

Ahmed is a case report involving a single elderly individual whose initial presentation for
treatment was deemed inconsistent with PMR as commonly understood, since he complained
initially of leg weakness and pain plus impaired mobility, rather than the usual complaints of
morning stiffness or hip and shoulder issues. Ahmed at 873, 878. Ahmed says nothing about
possible causes of PMR, however, and at most noted the possibility that some kind of prior
infectious trigger was to blame (although Ahmed’s authors also observed that such an explanation
was undercut by the individual’s “afebrile condition with mild leukocytosis” was inconsistent with
an infection leading to sepsis). Id. at 878. Ahmed may have relevance herein to disputes about the
evidentiary basis for the proposed PMR diagnosis, but it is not even a case report in which a
vaccination was identified as predating symptoms onset.

O. Florescu

Florescu is a review article that seeks to “to depict the current pathogenic hypothesis,
diagnostic and treatment approach for patients with PMR,” taking into account existing diagnostic
criteria. Florescu at 1. It reiterates what is known about PMR observed in other filed items of
literature in this matter, including hypotheses about immune system response features, mentioning
(a) innate response cytokines as possibly increasing or encouraging inflammation, and (b) the role
of T-helper cells, and/or immune system tolerance deregulation. Id. at 2–3. It also briefly highlights
some proposed environmental triggers, including certain infections (none of which are specifically
analogous to the components of the pneumococcal vaccine—although some mentioned are
bacterial). Florescu was otherwise referenced by Dr. Efthimiou more to support his diagnostic
contentions than as bulwarking causation.

P. S. Muller et al., Long-Term Use of Glucocorticoids for Polymyalgia Rheumatica:
Follow-Up of the PMR Cohort Study, Rheum. Advances in Practice 1 (2022), filed as Ex.
45 (ECF No. 30-8) (“Muller”).

Muller was another article offered by Dr. Efthimiou to defend his embrace of PMR as the
proper diagnosis. He deemed it supportive of the notion that some individual PMR patients will
experience a more prolonged course, with a concomitant need for different kinds of treatment.

21
Second Efthimiou Rep. at 5–6. But because my determination does not turn on whether Petitioner
did likely experience PMR, I do not include a summary of Muller’s findings.

Q. Shimabukuro

Shimabukuro discusses the VAERS passive surveillance system that permits individuals
in the U.S. to voluntarily report what they believe was an adverse event potentially associated with
receipt of a particular vaccine. Shimabukuro at 3–4. Importantly, the reported adverse events are
not confirmed medically by VAERS, and the system is understood to provide only evidence of
potential “safety signals” warranting additional research or evaluation. Id. at 4, 6. Because of its
nature, VAERS is clearly “subject to reporting bias,” as well as potential under or over-reporting
of a putative adverse event due to public awareness of a possible concern, and VAERS reports are
not formally compared against unvaccinated controls, such that reliable conclusions about
causation could be reached (even if VAERS generally serves a public purpose). Id. at 8, 9 (“it
generally cannot be determined if a vaccine caused an adverse event using VAERS data”).

It is not facially evident how Shimabukuro supports Petitioner on the issue of causation.
At most, it underscores the fact that case reports (comparable to VAERS datapoints describing a
single instance in which a particular adverse event was reported post-vaccination) have some
evidentiary value, but of a very low sort when applied to the issue of causation. This is already a
concept widely understood in the Vaccine Program. 14 Shimabukuro clearly indicates that VAERS
data does not establish causation—and thus whatever instances Petitioner could mine from that
data where a treater or individual reported experiencing PMR in the wake of receipt of a
pneumococcal vaccine would not make causation due to the vaccine more likely. Rather, VAERS
reports should lead to medical or scientific investigation into a potential causal link—a kind of
evidence lacking in this case.

IV. Procedural History

As noted above, this matter was initiated in September 2022. Respondent filed a status
report on April 12, 2023, indicating his intent to defend the matter, but acknowledging the lack of
filed medical records at that time. See Status Report, dated Apr. 12, 2023 (ECF No. 19). Petitioner
completed the filing of all pertinent medical records on August 15, 2023. Thereafter, the process
of obtaining expert reports began, with the final report from Dr. Efthimiou filed in September
2024. I issued a scheduling order on October 2, 2024, setting forth a briefing scheduling for a
ruling on the record.

14
It has been repeatedly observed in the Program that VAERS data is not particularly probative of causation unless
supplemented with other reliable evidence—since a VAERS report only establishes a temporal, post-vaccination
occurrence. See Vig v. Sec’y of Health & Hum. Servs., No. 01-198V, 2013 WL 6596683, at *17 (Fed. Cl. Spec. Mstr.
Nov. 14, 2013) (“VAERS is a stocked pond, containing only reports of adverse events after vaccinations but no data
about the number of vaccines administered or the occurrence of the same adverse event in individuals who have not
been vaccinated”).

22
I originally denied entitlement. However, Petitioner sought review of that determination,
and was successful. See Motion for Review, dated Nov. 5, 2025 (ECF No. 45). In the Remand
Order, the Court directs the following:

The Court is thus compelled to remand this action to the chief special
master, where he faces the classic APA choice: he can bolster his original
reason for denying entitlement or essentially “rehear” the case should he
decide to rest his decision on new reasons. In other words, if the chief
special master believes that his conclusions in the case regarding Althen
prong one are correct, he can simply issue a new decision that explains how
he reached those conclusions.

Remand Order at *9 (citations omitted).

V. Parties’ Arguments

Petitioner

Petitioner initially maintains that the evidentiary record preponderantly establishes that
PMR is his proper diagnosis. Br. at 1–2. As support, Petitioner emphasizes that following the
receipt of the vaccine he reported symptoms of chills, muscle aches, and joint aches, and that he
continued to report such clinical symptoms of PMR in the weeks after. Id. at 2, 3. In addition,
several of Petitioner’s treating physicians involved in his care “opined that [Petitioner]
diagnostically suffered from a clinical picture that included the diagnosis of PMR, even though his
clinical picture represents a refractory subtype of PMR illness.” Id. at 2 (referencing Ex. 5 at 93–
95; Ex. 2 at 53; Ex. 5 at 36). Moreover, Petitioner’s current treating rheumatologist opined in a
filed statement that he would “lean more towards a diagnosis of PMR” and that Petitioner’s
“largest areas of symptom involvement included his shoulders with some lower extremity and
hand involvement. Id. at 6 (citing Dr. Elmore Treater Letter, dated July 22, 2024 (ECF No. 35-3)
at 1, 2). And through highly relevant and recently published items of literature, Petitioner argues
that Dr. Efthimiou provided “reputable support for his opinion that PMR patients are known to
have a similar clinical set of medical facts as [Petitioner].” Br. at 8.

Petitioner next addresses the causation prongs set forth by the Federal Circuit in Althen v.
Sec'y of Health & Hum. Servs., 418 F.3d 1274, 1278 (Fed. Cir. 2005). First, Petitioner contends
that he has established a medically and scientifically reliable theory causally connecting
vaccination and the alleged injury. Br. at 21. Relying on clinical evidence and mechanistic data,
Dr. Efthimiou preponderantly explained how associations examined in the various cited clinical
studies support a causal link that is biologically credible. Id. at 22. Petitioner notes that Dr.
Efthimiou provided several items of literature demonstrating that more than one vaccine, including

23
pneumococcal, is associated with triggering an onset of PMR. Id. at 23. Specifically, Petitioner
finds significant that the “most studied and associated” vaccine deemed causally connected with
PMR is the flu vaccine—which, Petitioner emphasizes that he “factually received just four weeks
prior to [his] receipt of [the] Prevnar 13 vaccine.” 15 Id. Moreover, because of the identified innate
immune mechanism responses common to both the flu and pneumococcal vaccines, Dr. Efthimiou
has preponderantly established “how an innate immune response from the Prevnar 13 vaccination
can cause the dysregulation of immune cells already present in [an] individual.” Id. at 26. Thus,
Petitioner argues that, via multiple types of evidence, Dr. Efthimiou has provided a sound a reliable
medical theory.

To further bulwark his position, Dr. Efthimiou relies on clinical studies involving the
pneumococcal and flu vaccines to explain specific immune mechanisms that causally link the
Prevnar 13 vaccine and a subsequent onset of PMR symptoms. Specifically, Dr. Efthimiou argues
that studies demonstrate that the innate immune responses of both the flu and pneumococcal
vaccines share overlapping responses. Thus, he has provided “a specific immune response
‘mechanism common to both vaccines,’ [that] credibly explains how [Petitioner’s Prevnar 13
innate immune response relevant to the flu and Prevnar 13 clinical evidence also provides relevant
support for a biologically credible causal mechanistic link.” See generally Obermoser. Moreover,
Dr. Efthimiou relies on studies to support his assertion that Petitioner, at the time of his receipt of
the Prevnar 13 vaccine, was expected to have a peaked and circulating flu vaccine immune
response, and therefore, his innate immune response to the Prevnar 13 vaccine could have caused
the dysregulation of immune cells already present and predisposing Petitioner to experience and
adverse reaction. Br. at 26.

(Notably, in arguing that he has met the “can cause” Althen prong, Petitioner consistently
maintains that he is only subject to a plausibility evidentiary standard. See, e.g., Br. at 22 (asserting
that the Federal Circuit has “clarified the issue of the appropriate standard under Althen's prong
1” to be “biological plausibility”), 23. As noted below, however, this is wholly contrary to the
preponderance standard, as the Federal Circuit clarified in a decision issued after the filing of
Petitioner’s brief).

Petitioner next asserts that he has provided a logical sequence of cause and effect showing
that the pneumococcal vaccine is the reason for his PMR injury. Br. at 15. Based on the objective
medical records and the cited medical literature, Dr. Efthimiou preponderantly explained how
Petitioner’s clinical presentation of pain, the morning stiffness, the generalized aches and pains,
the weight loss, and symptoms of fatigue were all indicative, according to Dr. Efthimiou, that

15
In his opposition, Respondent “contends that [P]etitioner has not plead this in his petition, nor in the [Motion for
Ruling on Record], that the flu vaccine caused in any way his PMR.” Opp. at 32. Moreover, Respondent argues that
Petitioner has failed to demonstrate how the two vaccines working in conjunction could cause PMR. Id. at 33. I do,
however, address the viability of this theory (which even if glancingly referenced, was not particularly well-
substantiated) below.

24
Petitioner was more likely than not suffering from an inflammatory condition consistent with the
diagnosis of PMR. Id. at 16. Because Petitioner’s symptoms started “abruptly” within several days
post-vaccination, and there being no record evidence to suggest Petitioner suffered similar
symptoms prior to receipt of the vaccine, a logical sequence of cause and effect has been shown.
Id. at 17. Furthermore, Dr. Efthimiou found no other cause factors present in Petitioner’s medical
history, clinical presentation, or alleged by Respondent’s experts, that would provide a better
causal explanation for Petitioner’s development of PMR. Id.

Lastly, Petitioner briefly maintains that he has established a preponderant showing of a
proximate temporal relationship between vaccination and the alleged injury. Br. at 34. Dr.
Efthimiou provided items of medical literature—involving the flu vaccine and a subsequent
development of PMR—that adequately supports his assertion that such clinical symptoms can
occur within a day of vaccination via the innate immune response. Id. at 35. When considering the
totality of the evidence (i.e., Petitioner’s medical records and the medical and scientific literature),
Petitioner maintains that Dr. Efthimiou preponderantly established a medically acceptable
timeframe that involves the vaccine initiating a fast and non-specific immune response resulting
in the development of PMR. Br. at 35.

Respondent

Respondent maintains that Petitioner has the burden of showing a defined and recognized
injury by preponderant evidence—and thus must establish PMR was the likely diagnostic
explanation for his injury. Opp. at 23. But Petitioner’s initial presenting symptoms were not
considered the more “classical” onset of proximal shoulder and hip stiffness. Id. at 24. Instead, his
first symptomatic complaints included weight loss, fatigue, and night sweats, with any report of
shoulder pain not occurring until approximately one-month post-vaccination. Id. Similarly,
Petitioner’s inflammatory markers, specifically his ESR/CRP levels, were not consistently
associated with either his improvement and/or exacerbation of his alleged symptoms. Id. at 25.
Moreover, his multiple reports of crippling pain and his lack of a complete response to prednisone
treatment, is again, unusual with a diagnosis of PMR. Id. Accordingly, Respondent contends that
Petitioner has failed to prove, by a preponderance of the evidence, that he more than likely suffered
from PMR. Id.

Respondent further argues that Petitioner has failed to submit preponderant evidence
establishing a reliable and persuasive medical theory. Opp. at 27. Respondent first notes that
“existing case law overwhelmingly favors a finding that PMR is not caused by vaccines,” and that
the case adds nothing new to Dr. Efthimiou’s previously relied-upon theories of causation in
similarly situated vaccine injury claims. Id. at 2, 729; Munoz v. Sec’y of Health & Hum. Servs.,
No. 21-11369V, 2024 WL 4113486 (Fed. Cl. Spec. Mstr. Aug. 12, 2024), mot. for review den’d,
174 Fed. Cl. 276 (2024), Rule 36 Affirmance, 2026 WL 1326559 (Fed. Cir. May 13, 2026).

25
In addition, Dr. Efthimiou’s theory is relatively “unclear.” Opp. at 29. The cited medical
literature is not only “scant,” but even several items of literature regarding the flu vaccine and
PMR relied upon by Dr. Efthimiou explicitly recognize the absence of a demonstrated causal
association. Id. at 31 (referencing Liozon at 5). And while Dr. Efthimiou did present a study that
supported the contention that some overlap exists between the pneumococcal and flu vaccines (i.e.,
specific gene profiles), he failed to identify which of the overlapping genes, if any, is relevant in
how vaccines activate the immune response. Id. at 33 (citing Obermoser at 3).

Next, Respondent contends that Petitioner has failed to submit preponderant evidence of a
logical sequence of cause and effect, pursuant to Althen prong two, showing that the pneumococcal
vaccine likely “did cause” his injury. Opp. at 34. A majority of Petitioner’s alleged symptoms
either pre-dated the vaccine at issue, were not commonly recognized symptoms of PMR, or were
caused by other injuries altogether. Id. at 35. For example, his hip pain was consistently attributed
to his osteoarthritis by treating physicians and his initial reported symptoms included fatigue,
muscle weakness, and loss of stamina. Id. (citing Ex. 5 at 41; Ex. 6 at 2). Moreover, Respondent
argues that Petitioner reportedly developed symptoms of PMR approximately twenty-four hours
post-vaccination, and relying on Petitioner’s own cited medical literature, such a timeframe is far
too quick for such a disease onset. Opp. at 35.

Respondent concludes his argument by stating that Petitioner did not present any reliable
evidence, that is consistent with his proposed theory, and in range with a medically acceptable
timeframe to infer causation. Id. at 36.

V. Applicable Law

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, 592 F.3d at 1321; Capizzano v. Sec’y of Health & Hum. Servs.,
440 F.3d 1317, 1320 (Fed. Cir. 2006). 16 There is no Table claim for PMR as an injury associated
with any covered vaccine, so Petitioner can only advance a causation-in-fact claim.

16
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. Appx. 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).

26
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, 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, 418 F.3d at 1278: “(1) a medical theory causally connecting the vaccination and
the injury; (2) a logical sequence of cause and effect showing that the vaccination was the reason
for the injury; and (3) a showing of proximate temporal relationship between vaccination and
injury.”

Each of the Althen prongs 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, 569 F.3d at 1378–79 (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.

27
In discussing the evidentiary standard applicable to the first Althen prong, the Federal
Circuit has (contrary to Petitioner’s assertions) consistently rejected the contention that it can be
satisfied merely by establishing the proposed causal theory’s scientific or medical plausibility. See
Cerrone v. Sec’y of Health & Hum. Servs., 146 F.4th 1113, 1121 (Fed. Cir. 2025) (arguing for a
plausibility standard of proof for prong one “understates the burden [a petitioner] bears under the
first factor in the Althen formulation”); Kalajdzic v. Sec’y of Health & Hum. Servs., No. 2023-
1321, 2024 WL 3064398, at *2 (Fed. Cir. June 20, 2024) (arguments “for a less than preponderance
standard” deemed “plainly inconsistent with our precedent” (citing Moberly, 592 F.3d at 1322));
Boatmon v. Sec’y of Health & Hum. Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019); 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”), aff’d, 2024 WL 2873301 (Fed. Cir.
June 7, 2024) (unpublished). 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).

Plausibility and preponderance are not synonyms. And claimants do not succeed in their
prong one evidentiary burden by offering enough items of reliable evidence to find that
“plausibility was preponderantly established.” Rather – and as recognized by the Federal Circuit
in Cerrone – characterizing a claimant’s goal as demonstrating merely a plausible causation theory
inherently amounts to lowering their burden of proof (since something that is plausible is not
necessarily more likely than not). Cerrone, 146 F.4th at 1121 (“[b]ut the petitioner must provide
the basis for a finding of causation by a preponderance of the evidence . . . As such, we have
repeatedly stated that ‘simply identifying a ‘plausible’ theory of causation is insufficient for a
petitioner to meet her burden of proof.’ LaLonde v. Sec'y of Health & Hum. Servs., 746 F.3d 1334,
1339 (Fed. Cir. 2014)”). It is not “more likely than not” that vaccine X can cause injury Y even if
the theory for how that would occur has some baseline plausibility, supported by some
individually-reliable items of evidence.

The second Althen prong requires proof of a logical sequence of cause and effect, usually
supported by facts derived from a petitioner’s medical records. Althen, 418 F.3d at 1278; Andreu,
569 F.3d at 1375–77; Capizzano, 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).

28
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).

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.

29
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
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

30
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:

(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

31
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”).

D. Disposition of Case Without Hearing

I am resolving Petitioner’s claim on the filed record, as per the parties’ request. The
Vaccine Act and Rules not only contemplate but encourage special masters to decide petitions on
the papers where (in the exercise of their discretion) they conclude that doing so will properly and
fairly resolve the case. Section 12(d)(2)(D); Vaccine Rule 8(d). The decision to rule on the record
in lieu of hearing has been affirmed on appeal. Kreizenbeck v. Sec’y of Health & Hum. Servs., 945
F.3d 1362, 1366 (Fed. Cir. 2020); see also Hooker v. Sec’y of Health & Hum. Servs., No. 02-472V,
2016 WL 3456435, at *21 n.19 (Fed. Cl. Spec. Mstr. May 19, 2016) (citing numerous cases where
special masters decided case on the papers in lieu of hearing and that decision was upheld). I am
not required to hold a hearing in every matter, no matter the preferences of the parties. Hovey v.

32
Sec’y of Health & Hum. Servs., 38 Fed. Cl. 397, 402–03 (1997) (determining that special master
acted within his discretion in denying evidentiary hearing); Burns, 3 F.3d at 417; Murphy v. Sec’y
of Health & Hum. Servs., No. 90-882V, 1991 WL 71500, at *2 (Fed. Cl. Spec. Mstr. Apr. 19,
1991).

ANALYSIS

I. Program Treatment of PMR as Vaccine Injury

As agreed to by the parties and reflected in their respective filed items of literature, PMR
is an inflammatory condition that causes joint and muscle pain and stiffness, mainly in the
shoulders and hips. Its symptoms may begin quickly or come on over several days to weeks, and
are frequently worse in the mornings. It exclusively affects individuals over the age of 50, with
its prevalence increasing with age. Salvarani & Muratore at 2; Camellino at 2. PMR is fairly
common in the impacted cohort of elderly individuals, second only to RA. Camellino at 1. It is
related to another inflammatory condition, GCA, which can cause headaches, vision troubles,
jaw pain and scalp tenderness, and can be jointly experienced with PMR. Id; Salvarani &
Muratore at 2.

As noted above, Petitioner has offered some items of literature suggesting a potential
vaccine trigger of PMR (primarily if not exclusively the flu or Tdap vaccines). But almost all
review articles discussing PMR that were filed in this case tend to express uncertainty as to not
only PMR’s pathogenesis, but its likely triggers. See, e.g., Camellino at 2 (“[a]t present, we do
not have a clear understanding of the aetiology and pathogenesis of PMR”); Salvarani &
Muratore at 2 (“[t]he cause of [PMR] is unknown”). At best, PMR is thought to be associated
with a particular “human leukocyte antigen” (cell surface proteins that help the immune system
with identification) 17 or gene mutation. Salvarani & Muratore at 2. While it has been speculated
that PMR may have an infectious trigger, based on “a cyclical pattern in incidence and seasonal
variation,” studies have yielded “inconclusive” results. Id. at 3; see also Camellino at 2.

Given the above, it is not surprising that PMR has not generally been deemed in the
Vaccine Program to be a likely vaccine-caused injury. Numerous, well-reasoned decisions reject
any association between PMR and covered vaccines. See generally Jett-Crawford v. Sec'y of
Health & Hum. Servs., No. 21-2157V, 2026 WL 1079719 (Fed. Cl. Spec. Mstr. Mar. 23, 2026)
(SM Dorsey) (flu vaccine not found to be causal of PMR); Eberline v. Sec’y of Health & Hum.

17
“Human Leukocyte Antigens” are defined as “histocompatibility antigens governed by genes of the HLA complex
(the human major histocompatibility complex), a region on the short arm of chromosome 6 containing several genetic
loci, each having multiple alleles…” Human Leukocyte Antigens, Dorland’s Medical Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=56923&searchterm=human+leukocyte+antigens (last visited
June 8, 2026).

33
Servs., No. 23-655V, 2025 WL 3852456 (Fed. Cl. Spec. Mstr. Dec. 1, 2025) (pneumococcal
vaccine not shown to cause PMR), mot. for review den’d, ___ Fed. Cl. ___ (slip op., Fed. Cl.
May 29, 2026); Munoz, 2024 WL 4113486; Sciortino v. Sec’y of Health & Hum. Servs., No. 22-
99V, 2024 WL 4579389 (Fed. Cl. Spec. Mstr. July 24, 2024) (flu vaccine not causal of PMR);
Thompson v. Sec’y of Health & Hum. Servs., No. 18-1217V, 2023 WL 9053982 (Fed. Cl. Spec.
Mstr. Dec. 5, 2023) (SM Oler) (pneumococcal vaccine not found causal of claimant’s PMR);
Van Dycke v. Sec’y of Health & Hum. Servs., No. 18-106V, 2023 WL 4310701 (Fed. Cl. Spec.
Mstr. June 7, 2023) (SM Dorsey) (Tdap vaccine not found causal of claimant’s PMR); Giesbrecht
v. Sec’y of Health & Hum. Servs., No. 16-1338V, 2023 WL 2721578 (Fed. Cl. Spec. Mstr. March
30, 2023) (SM Moran) (flu vaccine not found causal of claimant’s PMR); Kelly v. Sec’y of Health
& Hum. Servs., No. 17-1475V, 2022 WL 1781957 (Fed. Cl. Spec. Mstr. Oct. 12, 2022) (SM
Horner) (flu vaccine not found causal of claimant’s PMR); Suliman v. Sec’y of Health & Hum.
Servs., No. 13-993V, 2018 WL 6803697 (Fed. Cl. Spec. Mstr. Nov. 27, 2023) (SM Roth) (Tdap
vaccine not found causal of claimant’s PMR); C.P. v. Sec'y of Health & Hum. Servs., No. 14-
917V, 2019 WL 5483621 (Fed. Cl. Aug. 21, 2019) (SM Roth) (flu vaccine not causal of PMR). 18
While the special masters are not in agreement as to causation for a large number of adverse
events, this is one topic in which they are in uniformity.

C.P., one of the earliest of these decisions, provides some insight into why claims
involving PMR as a purported vaccine-associated adverse event regularly fail. The petitioner
referenced some of the same items of literature filed in this matter to suggest the flu vaccine
could be associated with PMR. See, e.g., C.P., 2019 WL 5483621, at *23 (discussing Soriano).
He proposed an immune reaction to the vaccine could spark PMR in a susceptible population (in
particular the elderly), and that molecular mimicry could be the pathogenic basis for the
development of a rheumatic condition. Id. at *22–25. But Special Master Roth stressed that no
known autoantibodies associated with PMR had been identified (eliminating the relevance of
arguments relying on molecular mimicry, and no filed literature supported the conclusion that
PM R was likely after receipt of a flu vaccine. Id. at *26–27. At bottom, PMR was a disease of
“unknown cause” that could not be preponderantly associated with the flu vaccine. Id. at *28.

My determination in the Munoz case also illustrates some of the deficiencies with the
causation theories often offered in these matters, even though it involved a different vaccine.
There, a claimant alleged receipt of a Tdap vaccine led to PMR, manifesting a few days after.
Munoz, 2024 WL 4113486, at *1. The PMR diagnosis was not disputed. Id. at *12. Dr. Efthimiou
was the Munoz petitioner’s expert, and he testified at trial (comparable to the theory proposed
here) that (a) PMR was a combination of autoimmune and autoinflammatory in mechanism, (b)
it was likely propagated in part by T helper cells and antibodies, (c) it could have an

18
Many of these cases, like the present, involve references to GCA as well, as an alternative injury or one overlapping
with PMR.

34
environmental trigger, (d) vaccines could spark it—first by proinflammatory immune cells
generated in the innate phase, then by adaptive responses to the vaccine at issue, and (e) that case
reports underscored the Tdap-PMR association. Id. at *2–5. Dr. Efthimiou further referenced
some items of literature filed in this case, like Soriano and Falsetti, and he made no evidentiary
showing of a specific autoantibody he deemed would drive pathogenesis in reaction to
vaccination. Id. at *5. 19

I denied entitlement, determining that Dr. Efthimiou’s theory was comparable to other
failed theories I had heard in other cases, or had been offered in prior negative PMR decisions.
Munoz, 2024 WL 4113486, at *13–14. I noted the theory was generic in its invocation of the
expected immune response to vaccination as becoming pathogenic but lacking specificity to the
relevant vaccine, and that it failed to identify things like a likely autoantibody driving the disease
process, or how the vaccine might result in its creation. Id. Denial of entitlement was upheld on
review by the Court of Federal Claims. Munoz v. Sec'y of Health & Hum. Servs., 174 Fed. Cl.
276 (2024). Petitioner thereafter pursued an appeal of the matter with the Federal Circuit—but it
resulted in a Rule 36 affirmance. Munoz v. Sec'y of Health & Hum. Servs., No. 2025-1409, 2026
WL 1326559 (Fed. Cir. May 13, 2026) (Fed. Cir. R. Rule 36 Judgment of Affirmance Without
Opinion). 20 Thus, the reasoning I employed in rejecting causation in that matter has been tested
on appeal, without success—and notably, although Munoz involved a different vaccine, Dr.
Efthimiou’s theory herein relies upon Tdap heavily as analogous to the pneumococcal vaccine,
given the conjugate included in the latter.

Another on-point determination is Thompson, which also involved the pneumococcal
vaccine (although there was no dispute as to the accuracy of the PMR diagnosis in that case).
Thompson, 2023 WL 9053982, at *2. The petitioner’s causal theory was that the vaccine
promoted (as part of the innate immune response) upregulation of cytokines, leading to immune
dysregulation followed by an autoimmune condition. Id. at *13. The special master found,
however, that theory as proposed over-relied on aberrant cytokine upregulation (an oft-rejected
concept) and literature involving different vaccines. Id. at *14–16. She also emphasized how
many times other special masters had rejected theories of vaccine causation of PMR. Id. at *16
(citing five prior decisions, including Suliman, Kelly, Giesbrecht, and Van Dyke). And Thompson
also features some of the same literature offered in this case, like Soriano or Falsetti. Id. at *1, 6.
In addition, my dismissal of the claim in Eberline alleging that the pneumococcal claim can cause
PMR was recently affirmed by the Court. Eberline, ___ Fed. Cl. ___ (slip op., Fed. Cl. May 29,

19
Other recent decisions dismissing claims that covered vaccines can cause PMR also involve the same items of
literature filed in this case. See, e.g., Jett-Crawford, 2026 WL 1079719, at *10-13 (discussing Hysa, Soriano, Liozon,
and Falsetti).
20
While a Rule 36 affirmance is not precedential in a meaningful sense, the Munoz appeal did offer that particular
petitioner the chance to raise arguments about my reasoning, or lack thereof, in dismissing the claim—and those
arguments were deemed to warrant almost no serious consideration by the Circuit. And it bears emphasis that the same
attorney who represents this Petitioner also represented the Munoz petitioner.

35
2026). Eberline, as here, involved not only current Petitioner’s counsel, but also expert assistance
from Dr. Efthimiou, who offered an opinion very similar to what is offered in this case, and cited
literature like Camellino, Soriano, Hysa, and Obermoser. Eberline, 2025 WL 3852456, at *4–6.

Although I can and do in this case rely more on my own direct experience in resolving
PMR claims like Munoz or Eberline, the decisions of other special masters relevant to PMR also
provide persuasive, useful guidance for resolving this matter.

II. Petitioner Has Not Carried His Althen Prong One Burden of Proof

As is well understood in the Program, the failure to establish even one of the three Althen
prongs in the context of a causation-in-fact claim is sufficient basis for a claim’s dismissal.
Dobrydnev v. Sec’y of Health & Hum. Servs., 566 Fed. Appx. 976, 980 (Fed. Cir. 2014). Because I
find that the first prong has not been preponderantly established, no discussion of Petitioner’s
success with respect to the other prongs is necessary. (I assume for purposes of argument Petitioner
did likely experience PMR, despite Respondent’s well-reasoned objections to the diagnosis).

A. Petitioner Has Not Linked the Pneumococcal Vaccine to PMR

It is of course axiomatic that claimants can prove causation with a mix of direct and
circumstantial evidence, if not all circumstantial evidence. Nevertheless, it is common in Program
cases for claimants to identify whatever direct evidence they can muster. One kind of semi-direct
evidence is proof of the fact that a vaccine’s wild infectious analog is itself associated with the
asserted injury. See, e.g., Peterson v. Sec’y of Health & Hum. Servs., No. 22-322V, 2025 WL
3269458, at *29 (Fed. Cl. Spec. Mstr. Oct. 30, 2025) (stating that “[i]n many vaccine injury cases,
a claimant can point to the fact that a vaccine’s wild viral or bacterial analog is itself associated
with the alleged injury”). For example, in cases involving neuropathic injuries (such as transverse
myelitis), claimants will often point out that a variety of wild infections are associated with spinal
cord neuroinflammation (opening the door a bit to the conclusion that a comparable vaccine could
have the same impact).

Here, that has not been demonstrated, with no evidence suggesting that a wild
pneumococcal bacterial infection prompts or leads to PMR. (At best, other bacterial infections
have in the past been speculated to be associated. See, e.g., Camellino at 2). While this is certainly
not a requirement to prove entitlement, 21 its absence underscores the challenge Petitioner faces in
linking this vaccine with PMR (especially since no real environmental trigger of any kind is
understood to likely cause PMR).

21
I emphasize that I am not requiring this evidence from Petitioner as something he must offer in establishing
causation. I am instead noting its absence in this case.

36
In addition, Petitioner could offer little in the way of evidence associating the
pneumococcal vaccine itself with PMR. Even though PMR is considered to be a fairly common
rheumatic condition in the elderly population, evidence connecting it to this vaccine is lacking.
The only item of literature that appears to discuss the pneumococcal vaccine at all is Obermoser,
but it does not address potential adverse events that might be connected to it. And the case series
offered by Petitioner involve the flu or Tdap vaccines. See generally Soriano; Falsetti; Liozon. In
effect, Petitioner seeks to analogize causation in the context of the pneumococcal vaccine to other
vaccines (which themselves have not been preponderantly shown to be associated with PMR).

B. Not Enough is Known About PMR’s Pathogenesis to Find Vaccine Causation

Review literature specific to PMR underscores the extent to which little is known about
PMR’s pathogenesis or environmental triggers. See, e.g., Camellino at 2; Salvarani & Muratore at
2. In such a context, any number of speculative theories could be advanced (relying on the fact that
PMR may involve some immune dysregulation, or feature some immune cell involvement in the
processes leading to its clinical manifestation) as to how any vaccine might plausibly fit into its
pathogenesis. But absent more specific evidence about even general issues like PMR’s likely
instigating factors, it is speculative to propose the receipt of a vaccine is likely to trigger PMR.
Petitioner does not adequately or persuasively explain why vaccine causation is supported in the
context of a not-well-understood disease process.

C. Dr. Efthimiou’s Theory is Short on Specifics Involving the Pneumococcal Vaccine

Consistent with the generalized quality of Dr. Efthimiou’s opinion, he has not endeavored
to offer the kind of specific evidence that Program claimants often provide to link the
pneumococcal vaccine with PMR. Thus, no evidence has been offered that PMR is mediated by
antibodies produced in response to an environmental trigger; what those antibodies would be; and
how the pneumococcal vaccine would be associated with their production. This is not a case where
the claimant is making an effort to show that the mechanism of vaccine-induced molecular mimicry
could lead to a cross-reaction between antibodies generated in response to the vaccine and self
tissues that mimic vaccine components, resulting in an autoimmune attack.

D. Dr. Efthimiou’s Theory Conflates Expected Vaccine Impact on the Immune
System with Capacity to Cause Aberrant Results

One notable deficiency in Dr. Efthimiou’s theory is the extent to which he proposes that
the expected impact of vaccination—the fact that vaccines provoke cytokine production increases
during the initial, innate, immune phase, for example—would increase the likelihood of an aberrant
reaction. He relied generally on the idea that the impact of vaccination generally would be enough

37
to spark potential breaks in immune tolerance and/or an environment of immune dysregulation, in
which autoreactive T cells could cause harm.

This broad argument, however, seeks to convert the intended effect of vaccination, and/or
a vaccine’s understood capacity to provoke some immune response, into something potentially
pathogenic, but without sufficient probative evidence to connect all the dots. Palattao v. Sec'y of
Health & Hum. Servs., No. 13-591V, 2019 WL 989380, at *36 (Fed. Cl. Spec. Mstr. Feb. 4, 2019)
(“claimants cannot transmute scientific evidence exploring how vaccines normally function in the
immune system into a reliable and persuasive causation theory that any vaccine can be pathogenic
without a more specific showing that applies to the circumstances at hand”). As noted above in my
review of Dr. Efthimiou’s theory, the evidence he offered in support, and then Dr. Jameson’s
response, the causation theory in this case largely relies on the expected innate response to
vaccination to become harmful, with little specifics offered to substantiate that possibility beyond
bare plausibility

[Text truncated at 120,000 characters. The full text is on the page linked above.]

---

Source: Frix Law Library, https://www.frixlaw.com/law-library/cases/11386151. Public record. Not legal advice.