Bost v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 22-01V

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CHRISTOPER BOST, * Chief Special Master Corcoran

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Petitioner, * Filed: March 18, 2026

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v. *

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SECRETARY OF HEALTH *

AND HUMAN SERVICES, *

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Respondent. *

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David J. Carney, Green & Schafle, LLC, Philadelphia, PA, for Petitioner.

Dima Atiya, U.S. Department of Justice, Washington, DC, for Respondent.

RULING ON ENTITLEMENT 1

On January 4, 2022, Christopher Bost filed a petition for compensation under the National

Childhood Vaccine Injury Act of 1986, as amended, 42 U.S.C. §§ 300aa-10 et seq. (“Vaccine

Act” or “Vaccine Program”). 2 Petitioner alleges that as a result of receiving a seasonal influenza

(“flu”) vaccine on September 18, 2020, he developed Chronic Inflammatory Demyelinating

Polyneuropathy (“CIDP”). See Petition at 1.

The matter was deemed appropriately resolved via ruling on the record, and both sides have

completed briefing of their positions. See Petitioner’s Motion, dated April 21, 2025 (ECF No. 42)

(“Br.”); Respondent’s Opposition, dated June 23, 2025 (ECF No. 43) (“Opp.”); Petitioner’s Reply,

dated July 21, 2025 (ECF No. 44) (“Reply”). Now the matter is ripe for resolution. For the reasons

set forth in more detail below, I hereby find that the Petitioner has preponderantly established that

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

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

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

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

its present form. Id.

2

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

100 Stat. 3758, codified as amended at 42 U.S.C. §§ 300aa-10 through 34 (2012). Individual section references

hereafter will be to § 300aa of the Vaccine Act (but will omit that statutory prefix).

the flu vaccine likely did cause his CIDP, and I therefore grant entitlement.

I. Petitioner’s Medical History

Vaccination and Initial Symptoms

Petitioner was 57 years old at the time he received the flu vaccine on September 18, 2020.

Ex. 1 at 4. He then reported a one-month history of left heel and toe pain/numbness. Id. at 5, 7.

There is no other record evidence of any initial, if limited, adverse vaccine reaction (such as

malaise or situs pain), at this time. However, Petitioner maintains in a witness statement that

approximately one week later (September 26, 2020), his legs felt tired, and that he began to

experience new toe numbness in his left foot. Ex. 2 at 2.

Approximately a month after vaccination (October 20, 2020), Mr. Bost saw Certified

Registered Nurse Practitioner (“CRNP”) Jessica Heffelfinger at St. Luke’s Health Center, and

reported weakening of both legs over the previous four weeks. Ex. 6 at 93. He specifically noted

that he had initially experienced numbness in his toes (reported on the day of vaccination, as noted

above) which had progressed, and he was now finding it difficult to climb hills or steps. Id. On

examination, Petitioner exhibited abnormal coordination and gait, with difficulty lifting his legs.

Ex. 6 at 93–94. CRNP Heffelfinger recommended an MRI of his spine and a blood test for Lyme

disease, and although the antibody panel was negative, the MRI showed a discrete hypodense foci

at L5, which was concerning for a neoplastic process and foraminal narrowing at L5-S1. Ex. 3 at

51; Ex. 6 at 85, 92.

Twenty days later, Petitioner went to neurosurgeon Evan S. Marlin, M.D., on November

10, 2020, and reported gait and balance issues related to the weakness in his legs and the numbness

in his feet. Ex. 4 at 5. He now specifically stated that he had noticed weakness and numbness in

his feet on September 26, 2020 (six days post-vaccination). Id. Exam revealed decreased deep

tendon reflexes in Petitioner’s knees and ankles, and a diminished sense of vibration in his left

lower leg. Id. at 6. Dr. Marlin referred Petitioner to neurology. Id. On November 18, 2020, Mr.

Bost underwent a CT of the abdomen and pelvis. Ex. 6 at 56. Its findings included “[c]ircumscribed

1.1 cm lesion . . . in the left kidney with borderline Hounsfield density and equivocal

enhancement,” gallstones, and a non-obstructing right renal calculus. Id. at 57.

On November 30, 2020—now more than two months post-vaccination—Petitioner had a

follow-up visit with CRNP Heffelfinger for treatment of bilateral leg weakness and numbness. Ex.

6 at 47–48. An electromyogram (“EMG”), MRI of the thoracic spine and brain, and laboratory

testing was ordered, and Petitioner was referred to neurology. Id. at 47. The MRI (performed on

December 9, 2020) revealed an abnormality consistent with gait and leg weakness, but no

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intracranial pathology. Ex. 3 at 7, 11, 17. It was interpreted as showing a mild thoracic degenerative

spondylosis with no significant canal stenosis and no abnormal cord signal. Id. at 8.

Thus, by the end of 2020 (more than three months post-vaccination), Petitioner had yet to

be diagnosed with CIDP, or any demyelinating polyneuropathy for that matter—although he

clearly was experiencing a number of neurologic symptoms in this post-vaccination timeframe,

with no etiology yet proposed for them.

Treatment in 2021 and CIDP Diagnosis

On January 18, 2021, Mr. Bost had a follow-up visit with CRNP Heffelfinger, and he now

reported numbness in his fingertips and along his feet bilaterally. Ex. 6 at 4–5. He underwent an

EMG a few days later, and its results were deemed abnormal, showing evidence of mixed motor

and sensory neuropathy with acute and chronic axonal changes. Ex. 9 at 20.

On January 25, 2021, Petitioner saw neurologist Aaron C. Lasker, M.D., who was informed

of Petitioner’s history of ascending bilateral lower extremity weakness and numbness. Ex. 9 at 15

Id. On examination, Mr. Bost was unable to stand up from a chair unassisted, and ambulated with

a walker. Id. at 16. Dr. Lasker also observed Petitioner’s weakness in the lower extremities, and

inability to move his feet, plus the presence of decreased knee reflexes, absent ankle reflexes, and

decreased sensation in the legs. Id. at 16–17. Based on the results of this examination, the EMG

study, and the MRI results, Dr. Lasker diagnosed Petitioner with CIDP and referred him to the

hospital for admission. Id. at 15.

Petitioner was subsequently admitted to St. Luke’s Hospital in Bethlehem, PA from

January 26 – February 12, 2021. Ex. 10 at 123, 2345. On initial examination, he displayed pedal

paresthesia, required a walker or cane to ambulate, had reduced strength in his arms and lower

legs, and had absent strength and deep tendon reflexes in his ankles and toes, plus evidence of

elevated protein in cerebrospinal fluid testing. Id. at 2344–45. Neurologist Shilpa R. Pradhan,

D.O., analyzed Petitioner’s EMG and nerve conduction studies (“NCS”) of his arms and legs and

found the findings to be “abnormal,” showing “evidence of subacute demyelination

polyneuropathy with conduction block, prolongation of distal latencies and temporal dispersion,”

all of which were considered to be consistent with CIDP. Id. at 2364. Dr. Pradhan and another St.

Luke’s neurologist also concurred that Petitioner’s lumbar spine MRI showed an “enhancement of

the nerve roots of the cauda equina consistent with an inflammatory process such as CIDP.” Id. at

159.

While hospitalized, Petitioner received a five-day course of intravenous immune globulin

(“IVIG”) which ended on February 1, 2021. Ex. 10 at 2150. Petitioner had thereafter been

scheduled to be discharged on February 4th, but at that time he displayed “increased numbness in

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[his] bilateral hands as well as clumsiness in [his] right hand which was new,” and instead was

held over as an in-patient in order to receive a five-day course of plasmapheresis treatments. Id.

These treatments resulted in some improvement, but failed to resolve petitioner’s leg weakness.

Id. Petitioner was ultimately discharged to inpatient rehabilitation on February 12, 2021, and he

remained there until March 16, 2021. Ex. 10 at 123, 135. He thereafter participated in outpatient

physical therapy (“PT”) and occupational therapy (“OT”) through July 6, 2021. Ex. 7 at 20, 77.

Petitioner subsequently saw Dr. Pradhan on four separate occasions between mid-March

and early November 2021. Ex. 8 at 1–17. At the March 2021 visit, Petitioner exhibited an inability

to stand or walk, but could transfer independently, and was experiencing stocking-glove pattern

numbness. Id. at 4. He was prescribed oral prednisone and IVIG every three weeks, and it was

recommended he continue PT and OT as an outpatient. Id. at 1–2.

By June, Petitioner was displaying improvement in his proximal muscles in his legs, and

could now stand for short periods, although he was also experiencing hand weakness. Ex. 8 at 6.

Petitioner could now stand for short periods of time. Id. In reaction (and since Petitioner did not

seem to be experiencing any side effects from the IVIG treatments), Dr. Pradhan increased his

IVIG dose. Id. The same combination of some improvement coupled with lingering weakness

sequelae was observed in September 2021 and into November. Id. at 11; Ex. 10 at 13. Additional

treatments with other medications were discussed (and the surgical implantation of a pain

medication access device occurred in November). Ex. 10 at 32.

In September 2021, Petitioner also sought medical care for decreased vision in his left eye.

Ex. 17 at 45. Although the vision issues were attributed to bilateral cataracts and papilledema, and

MRI of the brain and optical orbit was scheduled for October. Id. at 49–50. The MRIs yielded

normal results, and it was specifically noted that they showed “no CNS [central nervous system]

inflammation.” Id. at 43.

Records for subsequent treatment Petitioner received have been filed, but they do not aid

in resolution of causation, or shed light on the parties’ disputes, and are therefore not summarized

or discussed herein.

II. Experts

A. Petitioner’s Experts

1. Dr. Joseph Jeret – Dr. Jeret, a neurologist, prepared two reports on

Petitioner’s behalf. Report, dated Jan. 3, 2024, filed as Ex. 19 (ECF No. 23-1) (“First Jeret Rep.”);

Report, dated Aug. 15, 2024, filed as Ex. 147 (ECF No. 31-1) (“Second Jeret Rep.”).

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Dr. Jeret received his undergraduate degree from SUNY Brooklyn College, New York in

1984, and his medical degree from SUNY Health Science Center at Brooklyn in 1988. Curriculum

Vitae, filed as Ex. 20 (ECF No. 23-2) (“Jeret CV”) at 1. Thereafter, he completed a one-year

general internal medicine preliminary year at Maimonides Medical Center, followed by a three-

year residency in Neurology and a one-year fellowship in Clinical Neurophysiology at SUNY

Downstate. Id. He is board certified in Neurology by the American Board of Psychiatry and

Neurology and is currently employed by Optum Health Care as an active neurologist and is on

staff at two community hospitals—Mount Sinai South Nassau Hospital and Mercy Medical Center.

Id.; Jeret Rep. at 1. Dr. Jeret has published numerous articles in areas related to neurology,

reflecting his broad general practice. Id. at 2–7; Jeret Rep. at 2.

First Report

Dr. Jeret’s initial report included a review of Petitioner’s medical history. First Jeret Rep. at

5–14. Based upon Petitioner’s clinical symptoms, course, and EMG/NCS testing, Dr. Jeret

concluded that Petitioner likely had CIDP. Id. at 14, 16. Dr. Jeret defined CIDP as falling within the

context of other, related peripheral neuropathies, like GBS. Id. at 3–4. He deemed CIDP the “chronic

counterpart” to GBS, highlighting the fact that both are immune-mediated, driven in part by

damaging inflammation, involve demyelination (damage to a nerve’s myelin sheath), and impact

more than one nerve (hence “polyneuropathy”). Id.

The diagnostic criteria for CIDP, Dr. Jeret maintained, has been heavily debated for years.

First Jeret Rep. at 4. The diagnostic criteria used by Dr. Jeret comes from the European Federation

of Neurological Societies/Peripheral Nerve Society (“EFNS/PNS”), which requires:

1. Clinical: CIDP should be considered in any patient with a progressive

polyradiculoneuropathy that progresses over more than 2 months.

2. Electrodiagnostic: at least one of the following:

i. Distal motor latency prolonged > 50% from ULN in 2 nerves

ii. Motor NCV reduced > 30% below LLN in 2 nerves

iii. F-wave prolonged > 30% ULN in 2 nerves (> 50% if motor

amplitude reduced <80% below LLN)

iv. Absent F-waves in 2 nerves (with other criteria)

v. Partial motor conduction block in 1-2 nerves (with other criteria)

vi. Abnormal temporal dispersion in 2 nerves

vii. Increased motor action potential duration

Joint Task Force of the EFNS and the PNS, EFNS/PNS Guideline on Management of Chronic

Inflammatory Demyelinating Polyradiculoneuropathy: Report of a Joint Task Force of the EFNS

and PNS, 12 J. Periph Nerv. Systm. 1–9 (2010), filed as Ex. 31 (ECF No. 23-13) (“EFNS/PNS

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Guideline”). Based on Petitioner’s medical history, Petitioner had satisfied these elements and was

correctly diagnosed with CIDP, Dr. Jeret opined. First Jeret Rep. at 14.

Vaccines generally, Dr. Jeret maintained, are associated with CIDP. First Jeret Rep. at 4; K.

Gorson & A. Ropper, Chronic Inflammatory Demyelinating Polyradiculoneuropathy (CIDP): A

Review of Clinical Symptoms and Treatment Approaches in Clinical Practice, 4 J. Clin Neuromusc.

Dis. 174, 177 (2003), filed as Ex. 29 (ECF No. 23-11) (“Gorson & Ropper”); P. McCombe et al.,

Chronic inflammatory demyelinating polyradiculoneuropathy: A clinical and electrophysiological

study of 92 cases, 110 Brain 1617–30, (1987), filed as Ex. 34 (ECF No. 23-16) (“McCombe”). And

Dr. Jeret deemed molecular mimicry (an autoimmune mechanism in which foreign antigens with

similarity to a self-structure/tissue result in the production of antibodies against the antigen that

mistakenly then attack self) an “immune error” that could trigger demyelinating neuropathies like

GBS or CIDP. First Jeret Rep. at 15–16. The flu vaccine in particular could cause CIDP. Id. at 16.

One study in particular found that 11% of CIDP patients had prior vaccinations, including the flu

vaccine. Id. ((citing K. Kuitwaard et al., Recurrences, Vaccination, and Long-Term Symptoms in

GBS and CIDP, 14 J. Periph. Nerv. Sys. 310, (2009), filed as Ex. 86 (ECF No. 25-11)

(“Kuitwaard”)).

Dr. Jeret also opined that Petitioner’s CIDP did not begin before his flu vaccine. First Jeret

Rep. at 14. Based on Petitioner’s medical records, any pre-vaccination toe numbness was likely an

outlier. Id. Multiple providers who reviewed Petitioner’s history also did not believe this was not

the beginning of Petitioner’s CIDP symptoms. Id. Further evidence of pre-vaccination toe

numbness being unrelated to Petitioner’s CIDP was evident from the treater who administered the

flu vaccine (since it was likely vaccination would not have been recommended otherwise). Id.

Second Report

Dr. Jeret used his second report to respond to Dr. Hawse’s and Dr. Bromberg’s reports and

the criticisms of his arguments. Second Jeret Rep. at 1. Dr. Jeret asserted that Dr. Hawse had failed

to appreciate how the flu vaccine-GBS association could be applied to CIDP as well. Id. The

Vaccine Table finds such a relationship between the flu vaccine and GBS, which is sufficient of

causation in and of itself for a Table claim. Id. Therefore, Dr. Hawse improperly minimized the

epidemiologic evidence that the flu vaccine is causally associated with GBS, and how it can be

used to show a causal relationship between the flu vaccine and CIDP. Id. Dr. Jeret also criticized

Dr. Hawse’s argument that the flu vaccine cannot both reduce the risk of GBS and also cause it.

Id. at 1–2. While vaccines do prevent disease, they can also cause injury in rare cases (as evidenced

by the petitioners who bring claims before the Program). Id.

Dr. Jeret agreed with Dr. Bromberg’s opinion that the Petitioner did not suffer from GBS,

and that some of Petitioner’s symptoms can be seen with CIDP. Second Jeret Rep. at 2. This

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included the fact that elevated CSF protein is not by itself diagnostic of CIDP; that papilledema is

not a diagnostic clue; and that enlarged lumbosacral nerve roots, while associated with CIDP, are

not definitive for diagnosis. Id. However, where the two disagreed was on the propriety of the

CIDP diagnosis. Dr. Bromberg did not believe Petitioner’s EMG/NCV results reflected CIDP. Id.

Dr. Bromberg went so far as to claim that Petitioner’s EMG results did not satisfy the EFNS/PNS

diagnostic criteria—which contradicted his previous statements—and that Petitioner’s exam was

performed incorrectly by his treating providers. Id. Dr. Jeret pointed out Dr. Bromberg’s

contradiction, and Dr. Bromberg’s concession that he has no evidence that the EMG test was

improperly performed. Id.

Dr. Jeret otherwise defended his CIDP diagnosis. Not only did Petitioner’s medical records

satisfy the EFNS/PNS criteria, but multiple treating providers had diagnosed Petitioner with CIDP.

Second Jeret Rep. at 3. Further, while Dr. Bromberg believed that these treating providers were

mistaken in their diagnosis, Dr. Jeret held that their medical opinion should not be dismissed

simply because formal research criteria were not fully met. Id. Dr. Jeret cited a 2023 study showing

that 73.2% of CIDP patients do not satisfy the newest EFNS/PNS criteria, thereby underscoring

the clinical legitimacy of Mr. Bost’s diagnosis. Id. (citing K. Gable, Chronic Immune-Mediated

Demyelinating Neuropathies, 29 Continuum 1357–77, (2023), filed as Ex. 149 (ECF No. 39-1)

(“Gable”)).

2. Dr. Noga Or-Geva – Dr. Or-Geva is a neuroimmunology research scientist

who prepared two written reports on behalf of Petitioner advocating that the flu vaccine could cause

a peripheral neuropathy like CIDP. Report, dated Jan. 3, 2024, filed as Ex. 21 (ECF No. 24-1) (“First

Or-Geva Rep.”); Report, dated Aug. 15, 2024, filed as Ex. 148 (ECF No. 31-2) (“Second Or-Geva

Rep.”).

Dr. Or-Geva received her bachelor’s degree from Tel Aviv University, and her master’s

degree and Ph.D. in Immunology and Regenerative Medicine at the Weizmann Institute of Science.

Curriculum Vitae, filed as Ex. 22 (ECF No. 24-2) at 1. She is currently a research scientist in

Neuroimmunology and Transplantation Medicine at Stanford University, where she conducts

research on post-infectious neuroimmune and psychiatric disease aimed at the discovery of novel

mechanisms and the identification of biomarkers to improve patient treatment. Id. She has also

published numerous articles in areas related to neuroimmunology. Id. at 2–3.

First Report

Dr. Or-Geva concluded that the Petitioner’s CIDP developed in large part by the flu vaccine.

See First Or-Geva Rep. at 38. Her first report centered around her review of the case and laying out

her causal theory. She began by including a summary of Petitioner’s medical history, an overview

of autoimmune disease processes, and how vaccines might arguably relate to them (through the

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functioning of the immune system). See generally id. While Dr. Or-Geva’s credentials and expertise

do not extend to diagnosing neurologic conditions, she accepted the CIDP diagnosis.

CIDP, Dr. Or-Geva contended, is known as an acquired autoimmune condition affecting the

peripheral nervous system in approximately up to eight out of 100,000 individuals. First Or-Geva

Rep. at 22 (citing H. Koller et al., Chronic Inflammatory Demyelinating Polyneuropathy, 352 N

Engl J Med 1343 (2005), filed as Ex. 83 (ECF No. 25-8); J. Vallat et al., Chronic inflammatory

demyelinating polyradiculoneuropathy: diagnostic and therapeutic challenges for a treatable

condition, 9 Lancet Neurol. 402, (2010), filed as Ex. 132 (ECF No. 26-22) (“Vallat”)). Its exact

cause remains unidentified, but studies suggest that both cell-mediated and antibody-mediated

immune responses are likely contributors. Id. (citing Y. Rajabally et al., Antecedent Infections and

Vaccinations in Chronic Inflammatory Demyelinating Polyneuropathy: A European Collaborative

Study, 64 Muscle & Nerve 657–61, (2021), filed as Ex. 116 (ECF No. 26-6)). Unlike GBS, where

many cases are preceded by infections, only a small fraction of CIDP cases follow an infectious or

post-vaccination event. Id. at 13–16.

The pathogenesis of CIDP involves multiple steps that could be implicated by or involve an

immune response. T-helper cells (T cells that assist B cells in the production of antibodies) have

been found to be elevated in CIDP, while T-regulatory cells have generally been recorded in lower

numbers in CIDP patients. First Or-Geva Rep. at 10, 14 (citing L. Chi et al., Impairment of

Circulating CD4+ CD25+ Regulatory T Cells in Patients with Chronic Inflammatory

Demyelinating Polyradiculoneuropathy, 13 J. Peripheral Nervous System 54–63, (2008), filed as

Ex. 54 (ECF No. 24-12) (“Chi”)). This combination would reflect a skewing towards an

inflammatory autoimmune chronic response. Id. at 14. Dr. Or-Geva opined that flu vaccines are

known to provoke a comparable immune response—giving weight to the probability that the flu

vaccine can cause CIDP. Id. at 25–26.

In addition, Petitioner had displayed indicators of immune dysregulation, including elevated

cerebrospinal fluid protein, heightened inflammatory markers in the blood, and increased

autoantibodies. First Or-Geva Rep. at 23, 35–36. Dr. Or-Geva opined that this immune

dysregulation, in the absence of alternative triggers, pointed to an unresolved vaccine-induced

autoimmune response—likely instigated by molecular mimicry between vaccine components and

self structures. Id. at 35–36.

To support her opinion, Dr. Or-Geva conducted a homology analysis between the

components of the 2020–21 Flublok Quadrivalent influenza vaccine and human neural proteins

associated with CIDP. First Or-Geva Rep. at 30. Studies have shown that 50% amino acid similarity

between host and vaccine proteins is sufficient to instigate an immune response. Id. at 10 (citing R.

Root-Bernstein, Rethinking Molecular Mimicry in Rheumatic Heart Disease and Autoimmune

Myocarditis: Laminin, Collagen IV, CAR, and B1AR as Initial targets of Disease, 2 Frontiers in

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Pediatrics 1–17, (Aug. 2014), filed as Ex. 118 (ECF No. 26-9) (“Root-Bernstein”)). Dr. Or-Geva

conducted a BLAST 3 search between the Flublok vaccine and human proteins looking for results

that had greater than fifty percent homology in a ten amino acid chain. Id. at 31. The results of Dr.

Or-Geva’s BLAST analysis between the Flublok vaccine and human neural proteins found that

vaccine hemagglutinin proteins shared both sequence and structural similarity with human neural

proteins such as Contactin-1, Contactin-2, Neurofascin, and Myelin associated glycoprotein. Id. at

31–33. From these results, Dr. Or-Geva reasoned that the similarities between the vaccine and these

proteins provided a pathway for molecular mimicry to occur. Id. at 33.

Dr. Or-Geva’s conclusions were, she contended, mirrored in reliable scientific literature.

First Or-Geva Rep. at 36. Epidemiological data reveals that a small percentage of individuals

experience CIDP-like symptoms after receiving a flu vaccine. Id. Also, animal models (specifically,

Experimental Allergic Neuritis (“EAN”) and Spontaneous Autoimmune Peripheral Polyneuropathy

(“SAPP”)), have been instrumental in helping medical science understand CIDP, by providing

further information about the condition’s likely pathologic features. Id. (citing K. Hagen & S.

Ousman, The Immune Response and Aging in Chronic Inflammatory Demyelinating

Polyradiculoneuropathy, 18 J. Neuroinflammation 1, 12 (2018), filed as Ex. 75 (ECF No. 24-33)).

CIDP is likely a multifactorial autoimmune disease that involves innate immunity, T-cell responses,

and autoantibody attacks, and not solely mediated by autoantibodies (as once previously thought).

Id. Dr. Or-Geva acknowledged that the Flublok vaccine has not undergone direct testing in CIDP

animal models, but held that the parallels with GBS research and Petitioner’s presentation support

biologic possibility. Id.

Dr. Or-Geva also discussed some post-vaccination studies purportedly establishing a

connection between vaccination and the triggering of CIDP. First Or-Geva Rep. at 19. These studies

show that although CIDP is less frequently associated with preceding infections and/or vaccines

than GBS, it still can be seen to follow infection in a meaningful percentage of post-vaccination

instances. Id. (discussing P. Doneddu et al., Atypical CIDP: diagnostic criteria, progression and

treatment response. Data from the Italian CIDP Database, 90 J. Neurol. Neurosurg. Psychiatry

125–32, (2019), filed as Ex. 29 (ECF No. 23-9) (“Doneddu”) ((finding that an antecedent event,

such as vaccination, occurred within one to forty-two days before CIDP onset in 1.5% of the studied

cohort)).

Dr. Or-Geva ended her first report maintaining Petitioner’s CIDP onset likely began eight

days post-vaccination, consistent with an accelerated onset often seen in patients with acute-onset

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According to its own website, the “Basic Local Alignment Search Tool” (BLAST) “finds regions of local similarity

between sequences. The program compares nucleotide or protein sequences to sequence databases and calculates the

statistical significance of matches. BLAST can be used to infer functional and evolutionary relationships between

sequences as well as help identify members of gene families.” See https://blast.ncbi.nlm.nih.gov/Blast.cgi (last visited

Mar. 17, 2026). It is common in the Program for immunology experts to utilize BLAST searches when arguing about

whether a vaccine’s protein components mimic self-structures.

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CIDP. First Or-Geva Rep. at 37–38. Roughly 16% of CIDP patients experience symptoms onset

within eight weeks of a suspected trigger, with a more rapid onset in some instances (even if CIDP

usually begins in a more insidious manner, and over time). Id. This kind of onset is consistent with

the recognized general risk timeframe for many autoimmune injuries. See id. (citing Adverse Effects

of Vaccines: Evidence and Causality (K. Stratton et al., eds., 2012), filed as Ex. 44 (ECF No. 23-

24) (the “2012 IOM Report”) (reporting a heightened risk of autoimmune reactions within the first

six weeks after vaccination)).

Second Report

Dr. Or-Geva’s authored a second report affirming her causation theory and responding to

criticisms of Dr. Hawse. See generally Second Or-Geva Rep. The main criticism she had to

overcome was Dr. Hawse’s contention that there was insufficient evidence to support the causal

theory.

Dr. Hawse claimed that Dr. Or-Geva provided no evidence to suggest that the flu vaccine

induces bystander activation (a secondary and more non-specific immune cross-reactive response

occurring in the wake of a primary response), but she provided scientific articles that, she

contended, demonstrated the flu vaccine led to the expansion of both specific and nonspecific B

cells that support the presence of vaccine-induced bystander effects. Second Or-Geva Rep. at 3

(discussing F. Horns et al., Memory B Cell Activation, Broad Anti-influenza Antibodies, and

Bystander Activation Revealed by Single-Cell Transcriptomics, 30 Cell Reps. 905–13, (2020),

filed as Ex. 159 (ECF No. 39-11)). In addition, Dr. Or-Geva conceded Dr. Hawse’s argument that

there was no evidence linking T cell cross-reactivity to post-flu vaccination CIDP, but held that

this did not invalidate the causal hypothesis. Id. at 5. It is true that cross-reactivity is a common

feature of T cells that does not regularly lead to autoimmune disease. Id. But such an activation

could lead to an autoimmune response mediated by molecular mimicry or bystander activation, as

seen in molecular mimicry’s role in GBS. Id.

Dr. Or-Geva also defended her use of articles not directly relevant to both the flu vaccine

and CIDP. The lack of direct evidence of a causal link between the flu vaccine and CIDP does not

speak against the existence of the potential link. Rather, Dr. Or-Geva maintained, seeing case

report or passive surveillance evidence that vaccines trigger autoimmune diseases “underscore[s]

the potential for similar immunological mechanisms to occur with the flu vaccination.” Second

Or-Geva Rep. at 6. Dr. Or-Geva also used articles that discussed the flu vaccine and GBS and

applied their logic to the flu vaccine and CIDP because the two are related neuropathies that share

many of the same characteristics. Id. at 7–8. In addition, Dr. Or-Geva offered case reports and

studies that discussed known infectious causes of GBS, COVID-19, or multiple sclerosis. Id. at 6–

8. Dr. Or-Geva acknowledged that she was not suggesting that CIDP is associated with these, but

that such evidence helped exemplify that similar immunological mechanisms shown in various

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vaccines could also apply to the flu vaccine. See id. at 8, 10. And Dr. Or-Geva’s intent with using

articles that discussed other causes of CIDP (like melanoma-associated CIDP) was to illustrate

that molecular mimicry can come from different sources, like tumors or vaccines. Id.

In addition, Dr. Or-Geva addressed challenges to her use of sequence and structural

alignment tools to identify homology between the components of the flu vaccine and human

proteins. Second Or-Geva Rep. at 4–5, 12–13. She maintained that a sequence of five out of ten

peptides in an amino acid chain was sufficient to prove homology based on foundational studies.

Id. at 4 (citing Root-Bernstein). Sequence structure alignment tools, like BLAST searches and 3-

D models, are widely recognized and commonly used tools to perform sequence alignments. To

show this, Dr. Or-Geva provided numerous articles supporting their use to identify potential

molecular mimics. Id. at 12–13 (citing, e.g., Root-Bernstein).

Dr. Or-Geva also corrected Dr. Hawse’s assessment of some of her arguments. For

instance, Dr. Hawse had asserted that Dr. Or-Geva’s argument that the flu vaccine both reduces

instances of GBS by preventing the flu, but also contribute to autoimmune reactions and the

development of CIDP, is counter intuitive. Second Or-Geva Rep. at 1–2. In fact, both were

possible. Dr. Hawse also opined that an increase in T regulatory cells seen after influenza

vaccination would likely bulwark an immunity response. Id. In reaction, Dr. Or-Geva noted that

Dr. Hawse’s arguments did not account for the functional competence of regulatory T cells. Id.

Even with a greater amount of T regulatory cells after vaccination, if those cells were functionally

impaired, then they could fail to stop an autoimmune disease like CIDP. Id.

B. Respondent’s Witnesses

1. Dr. Mark Bromberg – Dr. Bromberg, a neurologist, prepared two written reports

on behalf of Respondent. Report, dated Apr. 18, 2024, filed as Ex. C (ECF No. 28-20) (“First

Bromberg Rep.”); Report, dated Oct. 28, 2024, filed as Ex. F (ECF No. 34-2) (“Second Bromberg

Rep.”).

Dr. Bromberg received his Ph.D. in Neurophysiology from the University of Vermont in

1973 and subsequently undertook a National Institute of Health Postdoctoral Fellowship at the

University of Washington’s Department of Physiology and Biophysics where he researched the

peripheral nervous system. Curriculum Vitae, dated Apr. 18, 2024, filed as Ex. D (ECF No. 28-

28) (“Bromberg CV”) at 1. Afterwards, he pursued and obtained his M.D. from the University of

Michigan, where he stayed to complete his residency in their Department of Neurology. Id. Dr.

Bromberg has a lifelong certification in neurology from the American Board of Psychiatry and

Neurology. First Bromberg Rep. at 1. Currently, Dr. Bromberg is an academic neurologist teaching

at the University of Utah’s Department of Neurology. where he performs clinical research focusing

on neuromuscular disorders. Bromberg CV at 1; First Bromberg Rep. at 1. Dr. Bromberg’s

11

research has led him to author over one hundred scientific articles, book and journal chapters, and

reviews relating to neurology. See Bromberg CV at 19–43.

First Report

Relying on his understanding of CIDP and neuropathies, Dr. Bromberg contended that the

CIDP diagnosis was not consistent with Petitioner’s medical record or treatment course. First

Bromberg Rep. at 9. He began with a full overview of Petitioner’s medical history. Id. at 2–8. Dr.

Bromberg noted, for example, that Petitioner was complaining about toe numbness before

receiving the vaccine. Id. at 9. This toe numbness progressed into bilateral leg weakness. Id. Dr.

Bromberg claimed that numbness preceding weakness is consistent with the course of peripheral

neuropathies. Id. Therefore, Petitioner’s symptoms likely began before vaccination. Id.

Dr. Bromberg then argued that Petitioner’s underlying nerve pathology did not fit with

CIDP. First Bromberg Rep. at 9. Dr. Bromberg provided his own description of CIDP based on

the 2010 EFNS/PNS diagnostic criteria. Id. (citing EFNS/PNS Guideline). Based on these criteria,

Dr. Bromberg opined that Petitioner did not meet the requirements for CIDP. Id. The Petitioner’s

medical records did not exhibit signs of absent tendon reflexes, his neuropathy only affected his

distal arm nerves late into its progression, and his overall progression had extended longer than

eight weeks. Id. at 9–10.

Looking at electrodiagnostic criteria of Petitioner’s nerves, Dr. Bromberg conceded that

Petitioner’s electrodiagnostic test results did satisfy EFNS/PNS criteria, but just barely. First

Bromberg Rep. at 10–12. Petitioner’s motor nerve conduction study fulfilled the EFN/PNS criteria

with a more than 30% reduction of proximal relative to the distal negative peak CMAP amplitude

for the right and left median and the right ulnar motor nerves. Id. at 10–11. However, Dr. Bromberg

noted inconsistencies in Petitioner’s nerve conduction study results that would make a CIDP

diagnosis improbable. Id. at 11. For example, Petitioner showed “uniform slowing,” which is not

internally consistent for CIDP. Id. Similarly, Dr. Bromberg expressed concern that Petitioner’s

nerve conduction studies were not properly conducted as there were only eight shocks to elicit F-

waves instead of the customary ten to twenty. Id.

Dr. Bromberg also expressed doubts about Petitioner’s CIDP diagnosis due to Petitioner’s

inadequate response to IVIG treatment. First Bromberg Rep. at 12. Dr. Bromberg maintained that

CIDP is expected to respond to treatments such as IVIG, prednisone, and plasmapheresis. Id.

However, the Petitioner did not respond to treatment for extended periods of time. Id. Therefore,

Dr. Bromberg opined that Petitioner did not have an immune-mediated or immune-treatment

responsive neuropathy—which would exclude a diagnosis of CIDP. Id. Because Petitioner did not

fulfill the EFNS/PNS diagnostic criteria for CIDP, Dr. Bromberg held that differential diagnoses

must be considered. Id. at 13–15.

12

Dr. Bromberg questioned as well Dr. Jeret’s failure to comment on Petitioner’s lack of

distal and proximal weakness and the preservation of Petitioner’s reflexes, plus some

inconsistencies with Petitioner’s electrodiagnostic criteria, and Petitioner’s lack of treatment

response. First Bromberg Rep. at 16–17. These omissions undermined Dr. Jeret’s diagnosis, in Dr.

Bromberg’s opinion. See id.

Second Report

Dr. Bromberg’s supplemental report reiterated his observations and beliefs about

Petitioner’s diagnosis. Second Bromberg Rep. at 1. CIDP, he noted, is an immune-mediated

neuropathy the diagnosis of which relies on testing, clinical presentation, and response to treatment

to diagnose. Id. The Petitioner’s clinical presentation and medical records, however, were

inconsistent with that diagnosis. Id. While Dr. Jeret noted that not all CIDP patients satisfy the

EFN/PNS diagnostic criteria, Dr. Bromberg maintained that the clinical, electrodiagnostic

features, and response to treatment for a chronic immune-mediated neuropathy were not met in

this case. Id. For example, Petitioner did not exhibit a progression of weakness; did not lose his

reflexes, contradictory to what Dr. Jeret claimed; and did not experience a clear response to

treatment for immune-mediated neuropathies. Id. Rather, Dr. Bromberg held that Petitioner’s

injury progression had features of an axonal neuropathy, and other diagnoses beyond CIDP should

be evaluated. Id.

2. Dr. William Hawse – An academic immunologist, Dr. Hawes offered two

written expert reports on Respondent’s behalf. Report, dated Apr. 18, 2024, filed as Ex. A (ECF

No. 28-1) (“First Hawes Rep.”); Report, dated Oct. 28, 2024, filed as Ex. E (ECF No. 34-1)

(“Second Hawes Rep.”).

Dr. Hawse is an Assistant Professor in the Department of Immunology at the University of

Pittsburgh School of Medicine. See Curriculum Vitae, dated Apr. 18, 2024, filed as Ex. B (ECF

No. 28-19) (“Hawse CV”) at 1. He earned his Ph.D. in Biophysical Chemistry at Johns Hopkins

and currently runs a laboratory studying CD4+ T-cell generation and immune tolerance to inform

therapeutic strategies for autoimmune diseases. Id.; First Hawse Rep. at 1. Dr. Hawse has

published multiple peer-reviewed articles on the subject. Hawse CV at 2–5. He is not, however, a

medical doctor or experimental clinician, and thus does not offer commentary on diagnosis. See

First Hawse Rep. at 2.

First Report

Dr. Hawse’s first expert report focused on analyzing and responding to Dr. Or-Geva’s

immunological theory. The main thrust of Dr. Hawse’s criticisms regarded his belief that there

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was a general lack of direct evidence linking vaccine-induced immune changes to CIDP’s

pathogenesis. See generally First Hawse Rep. While Dr. Or-Geva’s theory invoked several

immune-mediated mechanisms for autoimmune diseases—epitope spreading, bystander

activation, and molecular mimicry—there was a lack of reliable evidence that the flu vaccine can

cause CIDP, with evidence suggesting the opposite. Id. at 4. Scientific studies, for example, do not

observe significant bystander activation as occurring in individuals who have received a flu

vaccine. Id. (citing F. Wimmers et al., The Single-Cell Epigenomic and Transcriptional Landscape

of Immunity to Influenza Vaccination, 184 Cell 3915–35, (Jul. 22, 2021), filed as Ex. A Tab 9

(ECF No. 28-10); K. Murali-Krishna et al., Counting Antigen-Specific CD8 T cells: A Reevaluation

of Bystander Activation During Viral Infection, 8 Immunity 177–87, (Feb 1998), filed as Ex. A

Tab 3 (ECF No. 28-4); S. Ehl et al., Bystander Activation of Cytotoxic T cells: Studies on the

Mechanism and Evaluation of In Vivo Significance in a Transgenic Mouse Model, 185 J. Exp.

Med. 1241–51 (Apr. 7, 1997), filed as Ex. A Tab 4 (ECF No. 28-5)). In addition, the studies

provided did not support a direct causal link between the flu vaccine and CIDP. Id. at 13

(discussing Vallat at 402 (“[h]owever, by contrast with GBS, a single triggering antigen has not

yet been found, except in rare cases of CIDP associated with melanoma, in which tumor cells share

carbohydrate epitopes with Schwann cells”)).

Dr. Hawse also noted a contradiction in the logic behind Dr. Or-Geva’s T cell theory. First

Hawse Rep. at 3. Dr. Or-Geva had maintained that flu vaccines reduce the instances of GBS by

preventing influenza—but at the same time are thought to contribute to autoimmune reactions

capable of causing CIDP. Id. This occurs, in Dr. Or-Geva’s opinion, due to a vaccine-instigated

reduction in the number of T regulatory cells. Id. However, Dr. Hawse cited studies showing that

T regulatory cells increase after vaccination. Id. (citing S. Wang et al., The Regulatory T cells in

Anti-Influenza Antibody Response Post Influenza Vaccination, 8 Hum. Vaccine Immunotherapy

1243–49, (Sep. 2012), filed as Ex. A Tab 1 (ECF No. 28-2) (“Wang”) (finding T regulatory cells

increased significantly in patients after receiving the flu vaccine)). The increase in T regulatory

numbers post-vaccination, as reported by Wang, would suggest increased protection from the

influenza vaccination against CIDP, not the contrary. See id.

Dr. Or-Geva’s reliance on articles that discuss different vaccines and injuries was also

unpersuasive, Dr. Hawse contended. Multiple pieces of literature offered by Dr. Or-Geva involved

molecular mimicry in the development of GBS after a C. Jejuni infection, or in the context of

diseases like multiple sclerosis. First Hawse Rep. at 6 (citing First Or-Geva Rep. at 11). These

articles have no bearing on CIDP’s association with the flu vaccine. Id. at 6–7. Also, while CIDP

has been characterized as the chronic form of GBS, the two demyelinating conditions have distinct

pathologies, and the studies on GBS cannot be extrapolated to CIDP. Id. GBS has actually been

recorded to follow infections in higher numbers than CIDP. Id. at 12 (discussing Doneddu, which

suggests that antecedent events including infection or vaccination are unlikely to be causal for

CIDP); B. Kieseier et al., Immune-Mediated Neuropathies, 4 Nature Revs. Disease Primers 31,

14

(2018), filed as Ex. 81 (ECF No. 25-6) (finding no pathogens associated with CIDP that have been

verified)). In addition, there is strong epidemiologic data that the flu vaccine is not even properly

associated with GBS. Id. at 7 (citing R. Baxter et al., Lack of association of Guillain-Barre

syndrome with vaccinations, 57 Clin. Infect. Dis. 197–204, (Jul. 2013), filed as Ex. A Tab 8 (ECF

No. 28-9) (finding no association between vaccination and development of GBS).

Dr. Hawse also took issue with Dr. Or-Geva’s homology approach, which involved only

matching common peptide chains by 50%. First Hawse Rep. at 5, 19. But a sequence of 5 out of

10 peptides in an amino acid chain is not sufficient to prove homology, as one different peptide

can have significant and unpredictable immunological outcomes. Id. (citing L. Nicholson et al.,

An Altered Peptide Ligand Mediates Immune Deviation and Prevents Autoimmune

encephalomyelitis, 3 Immunity 397–405, (Oct. 1995), filed as Ex. A Tab 6 (ECF No. 28-7)). Dr.

Or-Geva held that current research indicates that limited similarities between foreign agents and

host components are sufficient for an autoimmune cross-reaction, but Dr. Hawse maintained there

was insufficient evidence supporting that conclusion. Id. at 6 (citing D. Mason, A Very High Level

of Cross Reactivity is an Essential Feature of the T-Cell Receptor, 19 Immunol. Today 395–404,

(Sep. 1998), filed as Ex. A Tab 7 (ECF No. 28-8)). If, Dr. Hawse opined, Dr. Or-Geva’s

contentions were true, then the estimated prevalence of CIDP would increase significantly. Id.

Dr. Hawse raised additional problems with reliance on molecular mimicry to explain an

autoimmune cross reaction. He noted, for example, that shape homology between two proteins is

not sufficient alone to predict if an antibody will cross react between two proteins. First Hawse

Rep. at 20. Further, there was no evidence offered in this case that any of the proposed epitopes

can elicit an autoreactive immune response, nor are there any animal models that demonstrate that

these epitopes can cause CIDP. Id. at 19 (citing First Or-Geva Rep. at 51–58). Conducting his own

review, Dr. Hawse was unable to identify a structural homologue between molecular mimic

sequences between hemagglutinin and Contactin-1 (a putative self-protein involved in the

pathogenesis of CIDP). Id. at 21–24.

Second Report

Dr. Hawse used his supplemental expert report responding to Dr. Jeret’s criticisms of the

argument that studies of other diseases and vaccines had limited application to the specific context

of this case. Second Hawes Rep. at 1–2. Dr. Hawse retorted that CIDP has fundamental differences

from GBS, as well as other neuropathic and/or demyelinating conditions. Id. at 2. Dr. Hawse

reiterated that there is no peer-reviewed epidemiological evidence that supports a causal

relationship between the flu vaccine and GBS anyway. Id. Without Drs. Jeret and Or-Geva

providing new evidence relevant to how the influenza vaccination could cause CIDP, Dr. Hawse

maintained, his conclusion that the flu vaccination more likely than not did not generate an

autoreactive response to injure Petitioner was likely accurate.

15

III. Procedural History

This matter was initiated in January 2022. After Respondent filed his Rule 4(c) Report a

year later opposing entitlement, the parties began the process of obtaining expert opinions in

support of their respective positions, with the final such report filed in August 2024. The parties

briefed the claim on the record in 2025, and the matter is now ripe for resolution.

IV. Parties’ Arguments

Petitioner

Petitioner contends that he suffered CIDP caused by his receipt of a flu vaccine on

September 18, 2020. Br. at 2. In his brief, Petitioner address his diagnosis plus all three prongs of

the test for causation set by the Federal Circuit in Althen v. Sec’y of Health & Hum. Servs., 418

F.3d 1274, 1278 (Fed. Cir. 2005).

First, Petitioner asserts that his medical records, clinical presentation, diagnostic testing,

treatment response, and expert opinions confirm that he suffers from CIDP. Br. at 56–61. He

maintains that his pre-diagnosis evaluations and response to treatment support his diagnosis. Those

records establish that he was experiencing hallmark symptoms of CIDP, which include fatigue,

peripheral numbness, and lower extremity weakness. Br. at 56–57. While his symptoms started as

numbness in the foot, they gradually progressed into fatigue, bilateral extremity weakness,

unsteady gait that worsened until reaching a nadir in January of 2021. Id. As Dr. Jereth opined,

Petitioner’s nadir occurring months after symptom onset was indicative of a slower onset

neuropathy like CIDP. Id. at 58. Diagnostic and EMG testing also revealed findings supportive of

the diagnosis. Id. at 57. And his symptoms persisted despite repeated IVIG treatments—all

indicative of CIDP. Id. at 57–58

Thus, Petitioner maintains he can satisfy the EFNS/PNS diagnostic criteria for CIDP

(something even Respondent’s expert grudgingly conceded). Br. at 59–60. At most, Dr. Bromberg

raised concerns that Petitioner’s inconsistent response to IVIG therapy and preserved reflexes

undermined the diagnosis. Id. at 60. But Dr. Bromberg admitted that a lack of therapeutic response

did not exclude CIDP either. Id. Also, Petitioner’s record revealed declining and absent reflexes.

Id. at 61 (citing Ex. 4 at 5–7; Ex. 10 at 2124, 2344–55). And literature offered in the case, like

Gable, demonstrated that more than 70% of confirmed CIDP patients fail to meet the totality of

revised EFNS/PNS diagnostic criteria. Id. at 60.

Second, Petitioner reviews each Althen prong, contending they were all satisfied. He began

with the first, “can cause” prong. Br. at 85–86. In many prior decisions, other special masters have

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found that the flu vaccine can cause CIDP (even if barely in some instances). Id. at 84–85 (citing

Davis v. Sec'y of Health & Hum. Servs., No. 14-978V, 2022 WL 1654743, at *55 (Fed. Cl. Spec.

Mstr. Apr. 27, 2022) (granting entitlement where Petitioner claimed the flu vaccine caused his

CIDP); Nieves v. Sec’y Health & Hum. Servs., No. 18-1602V, 2023 WL 3580148, at *46 (Fed. Cl.

Spec. Mstr. May 22, 2023) (finding the evidence weighed presented a close call, thus compelling

the special master to find Petitioner had preponderantly showed the flu vaccine can cause CIDP,

but finding against entitlement as Petitioner did not satisfy Althen prong two and three), mot. for

review den’d, 167 Fed. Cl. 422 (2023)).

Petitioner also notes that he offered reliable evidence associating CIDP with vaccination.

Br. at 86. Examples of GBS following vaccination have been well-documented through the

mechanism of molecular mimicry, and this theory can be extrapolated to other similar

neuropathies. Id. (citing J. Brostoff et al., Post-Influenza Vaccine Chronic Inflammatory

Demyelinating Polyneuropathy, 37 Age and Ageing 229–30, (2008), filed as Ex. 24 (ECF No. 23-

6); 2012 IOM Report). And CIDP has been shown to develop after other vaccines like smallpox,

polio, flu, and tetanus vaccinations. Id. (citing Kuitwaard at 313–14; McCombe at 1617; Gorson

& Ropper at 176).

Petitioner’s causation theory relies on molecular mimicry—where the flu vaccine is

positive to trigger an inflammatory response due to cross-reaction between antibodies generated

to components of the flu vaccine and human proteins that the vaccine components mimic. Br. at

88. Shortly after vaccination, innate immune cells (like macrophages and dendritic cells) detect

viral proteins and release cytokines to alert the immune system. Id. Within the next few days, the

immune system produces antibodies to defend against future flu exposure. Id. Next, the process of

molecular mimicry takes place, where the immune system produces antibodies that mistake host

proteins for vaccine components based on similar makeup resulting in a cross-reactive attack. Id.

at 90. Thereafter, a number of secondary, aberrant immune reactions (like bystander activation of

nonspecific immune cells) can contribute to the damaging autoimmune process. Id. at 91–93

(citing Chi at 60–61).

Dr. Or-Geva’s reports, Petitioner maintained, establish that molecular mimicry is well-

supported in scientific literature, and that short peptide matches between vaccine components and

host proteins are sufficient for the cross-reaction due to mimicry to occur. Br. at 90 (citing Root-

Bernstein). And, Dr. Or-Geva’s BLAST results established the existence of amino acid chains in

the Flublok vaccine that share over 50% homology in human host proteins. Id. at 90–91. Such

homology would be sufficient for an autoimmune process leading to CIDP to occur. Id. at 94–96.

Dr. Or-Geva further emphasized the individuals who experience this adverse reaction might also

be predisposed to underlying sensitivities influenced by genetic and environmental factors. Id.

Next, Petitioner argues that he has preponderantly showed that the flu vaccine at issue

17

likely did cause his injury. The relevant inquiry on whether a vaccine did cause injury, Petitioner

maintained, is based upon record evidence of a clinical course consistent with the mechanism and

time frame within which the injury can occur following vaccination. Br. at 99 (citing Introini v.

Sec'y of Health & Hum. Servs., No. 20-176V, 2022 WL 16915818 (Fed. Cl. Spec. Mstr. Oct. 19,

2022)). Petitioner’s proposed medical theory is consistent with the development of autoimmune

disorders, he argues, based on his experts, medical records, and current scientific understanding of

autoimmune disorders. Relevant medical records show that Petitioner started experiencing

symptoms eight days after vaccination that progressed into numbness in his toes and calves

alongside progressive weakness—symptoms indicative of an autoimmune response by day sixteen

Id. at 101–03. His condition continued to worsen over the subsequent months following an

ascending pattern consistent with immune-mediated neuropathies. Id. During this time,

Petitioner’s physicians ruled out differential diagnoses of infection, malignancy, or metabolic

disorders—leaving a diagnosis of CIDP. Id. at 103.

Finally, Petitioner contends that he has preponderantly shown that the timing of his onset

was medically appropriate, measured from the time of his vaccination. See Br. at 103–11. The

record establishes that Petitioner’s onset occurred eight days after vaccination. See id. at 104.

While there is evidence of pre-vaccination toe numbness, Petitioner argues that this symptom (and

the heel pain, fatigue, and skin tags he also complained of at his September 18, 2020, visit) were

minor, localized, non-specific, and isolated from a neurologic dysfunction. Id. at 105 (citing Ex. 1

at 5, 8, 10). Petitioner’s first symptoms of true neurologic dysfunction appeared September 26,

2020, when he experienced fatigue in his legs and a new numbness in the toes of his left foot that

progressed into fatigue and new numbness in his toes, and bilateral leg weakness. Id. Petitioner

thereafter continued to relay to his medical providers that his neurologic symptoms began after a

walk on September 26, 2020, and both Drs. Or-Geva and Jeret concur that this was the most likely

onset date based on Petitioner’s medical history. Id. at 107–08.

Petitioner acknowledges that autoimmune diseases involve a complex interplay between

the innate and adaptive immune system that takes time to develop. Br. at. 107. And, while an eight-

day onset is generally considered short for immune-mediated injuries, Petitioner’s experts

confirmed it could be medically appropriate. Id. at 107–11. Dr. Or-Geva noted that 16% of patients

with CIDP develop symptoms within eight weeks if they are experiencing a form of acute CIDP.

Id. at 107–08 (citing First Or-Geva Rep. at 37). The timeframe at issue in this matter was consistent

with that longer period. See id. at 107–11.

Petitioner also filed a reply, which largely reiterated these prior points.

Respondent

Respondent disputes both the Petitioner’s alleged CIDP diagnosis and his success in

18

satisfying his burden under Althen. Opp. at 1–2.

Establishing a claimant’s injury can be a prerequisite to analyzing causation-in-fact.

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

Respondent deems the CIDP diagnosis to lack preponderant support based on Dr. Bromberg’s

findings. Opp. at 9, 15. Dr. Bromberg stressed that fulfillment of diagnostic criteria for CIDP is

set forth by the EFNS/PNS, as CIDP is commonly misdiagnosed. Id. And those criteria are not

met. Id. at 15–16. For example, one diagnostic requirement is “absent reflexes or reduced reflexes

in all limbs.” Id. at 15 (citing First Bromberg Rep. at 9). But Petitioner maintained his arm and

knee reflexes. Id. (citing First Bromberg Rep. at 9).

Petitioner’s neurologic and limb muscle evaluation results were also inconsistent with

CIDP. Opp. at 16–17. Petitioner’s motor nerve EMG results returned findings that only marginally

met the EFNS/PNS criteria, and were missing some features that would be normal to observe in

CIDP patients. Id. at 16 (citing First Bromberg Rep. at 10–11). Petitioner’s sensory nerve test

results, while consistent for CIDP, returned abnormalities present in large fiber neuropathies

generally and are not specific to CIDP. Id. at 17 (citing First Bromberg Rep. at 12). Petitioner’s

reaction to treatment was also inconsistent with CIDP. Opp. at 17. As Dr. Bromberg noted in his

report, patients with CIDP usually respond positively to either IVIG, prednisone, and/or

plasmapheresis treatment. Id. (citing First Bromberg Rep. at 12). But Petitioner did not respond to

any of these treatments over an extended period of time. Id. Lack of positive response indicates to

Dr. Bromberg and Respondent that the Petitioner did not likely have an immune-mediated or

immune-treatment responsive neuropathy. Id.

Respondent next attacked Petitioner’s causation-in-fact claim, arguing that Petitioner has

failed to submit preponderant evidence that would satisfy the Althen prong requirements. First, he

contended that Petitioner has not set forth a reliable medical theory establishing causation between

the flu vaccine and CIDP. Opp. at 18. There is no reliable, scientific evidence demonstrating that

the influenza vaccine, or any of its components, can cause CIDP via molecular mimicry. Id. at 19.

Dr. Jeret simply relies on the mere mention of molecular mimicry to support his theory. Id. And

the studies he cites either do not relate to both the flu vaccine and CIDP, or do not conclude that

there is a causal link between the two. Id. at 19–20. For example, McCombe retroactively looked

at CIDP patients and the six-weeks preceding their neuropathy onset. Of the patients reviewed,

only four patients received a preceding smallpox, tetanus, or polio vaccine before developing

CIDP. See generally McCombe. Gorson & Ropper did not conclude there is any causal connection

between vaccination and CIDP. Gorson & Ropper at 176. The authors of Kuitwaard evaluated

post-vaccine symptoms in patients who were diagnosed with GBS or CIDP before revieing the

subject vaccines, which does not speak to vaccine causation. Kuitwaard at 310. And Petitioner’s

experts conceded there is a lack of epidemiologic proof of causation between vaccines and CIDP,

likely driven by the disorder’s rarity. Opp. at 19 (citing Br. at 86).

19

In addition, Respondent noted that Dr. Or-Geva simply relies on the mere mention of some

other possible mechanisms, like epitope spreading and bystander activation, to support a causation

theory driven by one of those mechanisms, but without additional evidence tying the mechanism

to the specific injury and/or vaccine at issue. Opp. at 20. And the evidence she provided relating

to molecular mimicry itself was flawed. As Dr. Hawse noted, Dr. Or-Geva’s theory regarding

immune regulatory cells and the initiation of the adaptive immune response is counterintuitive, as

the influenza vaccination has been seen to increase the number of T-reg cells, which would protect

against autoimmune reactions. Id. at 21 (discussing First Hawse Rep. at 3; Wang at 1243). Dr. Or-

Geva’s reliance on demonstrations of sequential homology is also misplaced, since a partial amino

acid chain match “is unreliable to invoke homology,” given the impact of just one non-homologous

amino acid in a sequence. Id. at 21–22. And studies cited by Dr. Or-Geva either do not relate to

both the flu vaccine and CIDP, or discuss antecedent events—like infection—and CIDP not found

in the present case. See id. at 24 (discussing Vallat at 402 (finding that antibody triggering antigens

have only been found in rare cases of CIDP associated with melanoma)).

Respondent further argued that Petitioner has failed to establish that the flu vaccine likely

“did cause” his injury, or that there was a medically appropriate timeframe between onset and

vaccination. Opp. at 25–27. As Dr. Hawse explained, there was no reliable molecular mimic

between the flu vaccine and a human protein, and there is no reliable evidence that any proposed

mimics between the two can cause CIDP. Id. at 26 (citing First Hawse Rep. at 25). In addition,

while Petitioners claims his symptoms started eight days after vaccination, the record shows that

he was complaining of toe and heel numbness on the day of vaccination. Id. (citing Ex. 1 at 4).

This not only serves to undermine Petitioner’s argument that the vaccine “did cause” his injury,

but also the argument that there is a medically appropriate timeframe between Petitioner’s vaccine

and his injury. See id. at 26, 28

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 ex rel. Moberly v. Sec'y of Health & Hum. Servs., 592 F.3d

20

1315, 1321 (Fed. Cir. 2010); Capizzano v. Sec’y of Health & Hum. Servs., 440 F.3d 1317, 1320

(Fed. Cir. 2006). 4 There is no Table claim for CIDP caused by the flu vaccine.

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 even a generally accepted

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

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

4

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).

21

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 v.

Sec'y of Health & Hum. Servs, 121 Fed. Cl. 230, 245 (2015), vacated and remanded, 844 F.3d

1363 (Fed. Cir. 2017).

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

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

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

Servs., 146 F.4th 1113, 1121 (Fed. Cir. 2025) (the argument that Althen prong one requires only a

showing of plausibility “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).

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).

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,

22

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.

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

23

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

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

24

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

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 &

25

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, 618 F.3d at 1347 (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. Consideration of Medical Literature

Both parties filed numerous items of medical and scientific literature in this case, but not

all such items factor into the outcome of this decision. While I have reviewed all the medical

literature submitted in this case, I discuss only those articles that are most relevant to my

determination and/or are central to Petitioner’s case—just as I have not exhaustively discussed

every individual medical record filed. Moriarty v. Sec’y of Health & Hum. Servs., No. 2015–5072,

2016 WL 1358616, at *5 (Fed. Cir. Apr. 6, 2016) (“[w]e generally presume that a special master

considered the relevant record evidence even though he does not explicitly reference such evidence

in his decision”) (citation omitted); see also Paterek v. Sec’y of Health & Hum. Servs., 527 F.

App’x 875, 884 (Fed. Cir. 2013) (“[f]inding certain information not relevant does not lead to—and

likely undermines—the conclusion that it was not considered”).

26

ANALYSIS

I. Overview of CIDP and its Treatment in Prior Program Cases

CIDP is an immune-mediated demyelinating neuropathy that affects both large and small

fiber peripheral nerves, resulting in symptoms of numbness, tingling, weakness, imbalance, loss

of coordination and pain. See Gorson & Roper 174–75. CIDP shares some characteristics of

GBS—but it is not simply a chronic form of GBS, for there are key differences in clinical

presentation that distinguish the two, and they cannot be assumed to have the same pathogenic

mechanisms either. In particular, CIDP progresses over a longer period of time than GBS, which

features acute weakness within one to two weeks after onset. See Vallat at 404. In addition, little

is known about CIDP’s most likely causes, triggers, or pathogenesis, in comparison to GBS (where

a variety of specific infectious triggers have been identified, as well as the situs of cross-reactive

autoimmune attack). Id. at 402–03. Thus, although many Program decisions seem to have assumed

that what is known about GBS applies fully to CIDP given their similarities, this is not a well-

founded assumption.

Prior decisions have associated different vaccines with CIDP (more often than not the flu

vaccine), and petitioners have settled many such cases on favorable terms. 5 See Jastisan v. Sec’y

of Health & Hum. Servs., No. 13-937V, 2016 WL 4761950 (Fed. Cl. Spec. Mstr. Aug. 10, 2016).

I have myself acknowledged these outcomes in my own prior decisions, and the fact that such

determinations should be given some consideration as persuasive guidance. See, e.g., Mason v.

Sec'y of Health & Hum. Servs., No. 17-1383V, 2022 WL 600415, at *21 (Fed. Cl. Spec. Mstr. Feb.

4, 2022); Houston v. Sec'y of Health & Hum. Servs., No. 18-420V, 2021 WL 4259012, at *16 (Fed.

Cl. Aug. 19, 2021); Strong v. Sec’y of Health & Hum. Servs., No. 15-1108V, 2018 WL 1125666

(Fed. Cl. Spec. Mstr. Jan. 12, 2018).

I have thus been able to find that when the flu vaccine is at issue—as here—the reasoning

applicable to the flu vaccine-GBS association (which is far better substantiated than any other

covered vaccine) can be extended to CIDP, even though CIDP is not simply “chronic GBS.” See

Nieves, 2023 WL 3580148, at *45; Mason, 2022 WL 600415, at *27; Strong, 2018 WL 1125666,

at *19. I have been far less willing to engage in this kind of reasoning where other vaccines are

5

Of course, prior decisions from different cases do not control the outcome herein (and this goes double for cases that

are settled, and hence resolved without a reasoned determination). Boatmon, 941 F.3d at 1358–59; Hanlon, 40 Fed.

Cl. at 630. But special masters are empowered to draw upon their experience in resolving Vaccine Act claims. Doe v.

Sec’y of Health & Hum. Servs., 76 Fed. Cl. 328, 338–39 (2007) (“[o]ne reason that proceedings are more expeditious

in the hands of special masters is that the special masters have the expertise and experience to know the type of

information that is most probative of a claim”) (emphasis added). They would therefore be remiss in ignoring prior

cases presenting similar theories or factual circumstances, along with the reasoning employed in reaching such

decisions.

27

involved 6—but the Program’s interest in consistent outcomes (coupled with the treatment of the

flu vaccine as associated not just with GBS, but other acute CNS demyelinating diseases like optic

neuritis and transverse myelitis) had encouraged me to reach this conclusion—even though there

are good, scientifically-reliable reasons to question this association. While my prior decisions do

not mandate the outcome herein, they provide helpful guidance.

II. Petitioner Likely Experienced CIDP

A special master’s function is not to diagnose vaccine-related injuries, but to determine

whether it has been shown “based on the record evidence as a whole and the totality of the case . .

. ” that a given diagnosis possesses preponderant evidentiary support (the same standard applicable

to any element of a claimant’s Althen burden of proof). Andreu, 569 F.3d at 1382 (quoting

Knudsen, 35 F.3d at 549). In many cases. determination of whether an alleged injury has been

preponderantly established bears on a case’s resolution. Broekelschen, 618 F.3d at 1349.

Here, and despite reasoned objections by Respondent’s neurologic expert Dr. Bromberg,

the medical record preponderates in favor of the CIDP diagnosis. As literature filed in this case

establishes, there exist accepted and medically-reliable criteria for diagnosing this disorder. See

EFNS/PNS Guideline. Dr. Jeret persuasively referenced numerous aspects of the medical record

that supported Petitioner’s CIDP diagnosis. Petitioner’s clinical progression took between three to

four months to reach its nadir, which is inconsistent with the typically rapid progression of GBS—

and thus the first requirement of the EFNS/PNS CIDP diagnostic criterion was met. The second

was also met, as Petitioner’s test results showed prolonged distal motor latency by over 50%,

slowed nerve conduction velocity by more than 30%, and abnormal temporal dispersion in two

nerves. Ex. 5 at 16. In addition, Petitioner’s treaters accepted the CIDP diagnosis, even when

Petitioner’s condition did not improve during IVIG treatments (and in any event, the record is

more inconclusive as to the effects of IVIG treatment overall than in establishing its failure).

Dr. Bromberg raised fair points undermining a CIDP diagnosis, like Petitioner’s preserved

reflexes. However, Dr. Bromberg did concede that Petitioner’s test results fell within the

EFNS/PNS diagnostic guidelines, and there are more factors favoring the diagnosis in this case

than suggesting its error. Petitioner has offered enough evidence for me to deem it more likely than

not that he did experience CIDP.

6

I have repeatedly found that CIDP has not been preponderantly shown to be caused by other vaccines, like Tdap—

and in so doing, have rejected attempts to apply in blanket fashion evidence specific to the flu vaccine-GBS context.

See generally DeVaughn v. Sec'y of Health & Hum. Servs., No. 22-832V, 2025 WL 758128, at *18–21 (Fed. Cl. Spec.

Mstr. Feb. 10, 2025) (Td vaccine not shown to likely cause CIDP); Howard v. Sec'y of Health & Hum. Servs., No. 16-

1592V, 2022 WL 4869354, at *23 (Fed. Cl. Spec. Mstr. Aug. 31, 2022) (“for purposes of Program determinations, it

is improper to think of GBS and CIDP as ‘two sides of the same coin,’ despite their overlap…Petitioners cannot just

‘borrow’ what is known about GBS and vaccination generally as a template for proving causation in the context of a

CIDP injury”), mot. for review den’d, 2023 WL 4117370, (Fed. Cl. May 18, 2023), aff’d, 2024 WL 2873301 (Fed.

Cir. June 7, 2024).

28

III. Petitioner’s CIDP Did Not Likely Predate Vaccination

Respondent also contends that Petitioner’s CIDP likely predated vaccination, based upon

evidence of his complaints of toe numbness the very day he received the flu vaccine at issue. Opp.

at 15. It is of course the case that (except in the context of claims that a vaccine significantly

aggravated a preexisting illness) vaccine causation cannot be shown for a condition or injury that

began before vaccination. Shalala v. Whitecotton, 514 U.S. 268, 274, 115 S. Ct. 1477, 1480, 131

L. Ed. 2d 374 (1995) (quoting § 11(c)(1)(C)(i)). Thus, this matter presents the fact question of

whether Petitioner’s neurologic injury already existed on the day he was vaccinated.

In the Vaccine Program, onset of an alleged vaccine injury is marked by the “first symptom

or manifestation of onset.” See Section 16(a)(2). As the Federal Circuit stated in Markovich v.

Sec'y of Health & Hum. Servs., 477 F.3d 1353, 1357 (Fed. Cir. 2007), there is a difference between

a “symptom” and “manifestation of onset”—but because of the Act’s use of the disjunctive “or,”

either can constitute the start of a disease process (even though a symptom could be nonspecific,

or hard to link to what was later viewed as a full disease). Markovich, 477 F.3d at 1357–59. By

contrast, the date of diagnosis (which may in turn result from the accumulation of clinical and

testing evidence over time) does not mark onset. Carson v. Sec'y of Health & Hum. Servs., 727

F.3d 1365, 1369 (Fed. Cir. 2013). Onset may therefore have occurred even before the ill individual

understands a presenting symptom to be concerning. See Markovich, 477 F.3d at 1357 (“[a]

symptom may be indicative of a variety of conditions or ailments, and it may be difficult for lay

persons to appreciate the medical significance of a symptom with regard to a particular injury”)

(emphasis added).

Here, Petitioner unquestionably reported heel and toe pain/numbness for a month prior to

the date he was vaccinated—and this report was made the day of vaccination. Ex. 1 at 5. But the

record otherwise supports onset beginning after vaccination—something Petitioner consistently

reported in his subsequent medical encounters. Ex. 4 at 5; Ex. 5 at 16; Ex. 6 at 93–94. Moreover,

the complaints Petitioner made at the time of vaccination had a non-specific character to them.

And Petitioner was not experiencing generalized neurological issues, such as dizziness, weakness,

headaches, or paresthesia at the same time that would corroborate a pre-existing neuropathy. See

Ex. 1 at 8. Such symptoms are in fact more suggestive of the start of CIDP. See Gorson & Ropper

at 175. In addition, Petitioner maintains he experienced new toe numbness and leg fatigue on

September 26, 2020—several days post-vaccination. Ex. 2 at 2. Petitioner maintained that it was

within weeks of this new symptom that he started to decline and experienced additional numbness,

bilateral leg weakness, and increasing fatigue, ultimately prompting medical attention. Id.

I conclude from all of the above that it is more likely Petitioner’s CIDP actually began in

the post-vaccination timeframe (although this still leaves the question whether onset began in a

medically-acceptable timeframe).

29

III. Petitioner Has Carried His Althen Burden of Proof

A. Prong Three

A temporal association alone between a vaccination and subsequent disease “does not

suffice to show a causal link” between the two. Grant, 956 F.2d at 1148. Rather, the third Althen

prong requires petitioners to establish a “proximate temporal relationship.” Althen, 418 F.3d at

1281 (emphasis added). To do so, the claimant 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, 539 F.3d at 1352. The

explanation for what is a “medically acceptable timeframe” must align with the theory of how the

relevant vaccine can cause an injury. Id.

In this case, the majority of Petitioner’s treating providers, including neurologists,

neurosurgeons, and physiatrists, placed his neurological symptoms as beginning within one to two

weeks after vaccination—not before. See Ex. 10 at 136–148, 322, 522, 2124. Notably, Petitioner’s

neurologist noted that his symptoms (bilateral leg weakness) began after his vaccination. Ex. 5 at

11. Also, Petitioner’s neurosurgeon documented the symptom onset date as September 26, 2020,

which matches representations contained in Petitioner’s affidavit. See Ex. 4 at 5; Exhibit 2 at 2.

Petitioner’s expert has provided evidence that an eight-day onset is medically appropriate. Dr. Or-

Geva in particular referenced the 2012 IOM Report, which underscores that an autoimmune

process can begin as late as six weeks after the trigger. See First Or-Geva Rep. at 37 (citing 2012

IOM Report).

There is prior vaccine caselaw supporting the medical acceptability of such onsets for

vaccine-induced CIDP. See, e.g., Kelley v. Sec'y of Health & Hum. Servs., 68 Fed. Cl. 84, 102

(Fed. Cl. 2005) (CIDP onset approximately two weeks after vaccination); Daily v. Sec'y of Health

& Hum. Servs., No. 07-173V, 2011 WL 2174535 (Fed. Cl. Spec. Mstr. May 11, 2011) (finding

that onset of CIDP within a few weeks of vaccination was a medically acceptable timeframe). I

similarly have noted this kind of timeframe to be reasonable (albeit in cases involving different

vaccines—and where prong one was not met). Houston, 2021 WL 4259012, at *20 (onset within

one to three weeks) I have only rejected vaccine-CIDP timeframes that were substantially longer.

See, e.g., Patel v. Sec'y of Health & Hum. Servs., No. 16-848V, 2020 WL 2954950, at *18–21

(Fed. Cl. Spec. Mstr. May 1, 2020) (seven months for vaccine-caused CIDP too long); Strong,

2018 WL 1125666, at *21 (Four months between flu vaccine and onset of CIDP was too long).

Thus, the third Althen prong has been satisfied.

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B. Prong One

Petitioner’s Althen prong one theory, and the evidence offered in its support, is not

particularly robust. For starters, the theory frequently relies on the flu vaccine-GBS association,

and evidence supporting it—even though CIDP is not only distinguishable but far more lightly

studied. Some literature specific to CIDP was offered in this case, but hardly in bulk quantity—

and the lack of availability of such proof does not excuse a claimant from meeting his preponderant

burden.

Another more prominent weakness is Petitioner’s reliance on molecular mimicry to “save

the day” in establishing a causation theory—a practice I have criticized in numerous prior

decisions. See, e.g., McKown v. Sec'y of Health & Hum. Servs., No. 15-1451V, 2019 WL 4072113,

at *50 (Fed. Cl. Spec. Mstr. July 15, 2019) (“[b]ut merely chanting the magic words ‘molecular

mimicry’ in a Vaccine Act case does not render a causation theory scientifically reliable, absent

additional evidence specifically tying the mechanism to the injury and/or vaccine in question”)

(emphasis in original), mot. for review denied, 76 Fed. Cl. 452 (2007). It is simply unlikely, from

a general standpoint (meaning not substantiated by studies or other secondary proof), that any

given covered vaccine can cause any given autoimmune disease by cross-reactivity due to

experimentally-demonstrated homology between some vaccine components and some putative

antigenic self-target. And the lazy invocation of molecular mimicry in every case involving an

autoimmune injury gains less and less persuasive thrust as time wears on.

At the same time, however, and as noted above, I have generally followed prior Program

case law and decisions finding that for purposes of the flu vaccine, it is reasonable to some degree

to accept the conclusions from prior decisions that the science applicable to the flu vaccine-GBS

association bears on CIDP as well. My embrace of that logic (which I have not extended to other

kinds of demyelinating neuropathies—or other vaccines) 7 helps ensure a degree of Program

consistency in how it treats comparable claims that are often litigated in these matters. I thus

similarly find in this case that overall prong one causation is met, despite my reasoned sense that

the theory may be a bit threadbare. 8

I note, however, that a stronger showing by Respondent in a future case could raise grounds

for re-evaluation of the assumed flu vaccine-CIDP association. In this case, much of Dr. Hawse’s

argument amounts to either a denial that Petitioner can support his theory with epidemiologic

7

Thus, special masters have very explicitly not found this kind of “cookie cutter” application of molecular mimicry

theory, based on what is known about the flu vaccine and GBS, should be applied to multiple sclerosis, even though

it too is a neuroinflammatory polyneuropathy with some features of demyelination. Townsend v. Sec'y of Health &

Hum. Servs., 170 Fed. Cl. Spec. Mstr. 130, 143–44 (2024), aff'd, No. 2024-1740, 2026 WL 570042 (Fed. Cir. Mar. 2,

2026).

8

While special masters deciding cases 15 to 20 years ago may have deemed the mechanistic capabilities of molecular

mimicry to spark an autoimmune disease to be limitless, the “march of science” has not corroborated that view.

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evidence (something no claimants are ever required to do), or that aspects of Petitioner’s theory

lack enough reliable support. More direct evidence relating to CIDP would breathe new life into

such arguments, and might occasion reconsideration of the wisdom of my going along with prior

Program assumptions that the flu vaccine likely can cause CIDP. But in this case, the tenor and

nature of Respondent’s arguments, while logical and reasonable, do not tip the scales away from

Petitioner.

C. Prong Two

There is no strong evidence in favor or against a finding that the vaccine “did cause”

Petitioner’s CIDP, but the record on this question slightly preponderates in favor of Petitioner.

A threshold question presented by the “did cause” analysis is whether Petitioner’s

neurologic symptoms began before or after his vaccine. Both parties have addressed the fact that

the Petitioner did complain of toe and heel numbness the day of his vaccination, and assert different

onset dates depending on their views as to the significance of this evidence. However, as explained

above, multiple treating providers considered this an outlier since Petitioner was not experiencing

any other neurological symptoms at the time. See Ex. 1 at 8; see also Ex. 10 at 136–148, 322, 522,

2124. Also, Petitioner’s post-vaccination foot pain continued to worsen over the course of months

and develop into more serious neurologic symptoms. While the first report of toe numbness it is

suspicious, the record evidence more likely that not weighs in favor of a post-vaccination onset

(consistent with the discussion above).

Another challenge to finding in favor of Petitioner on this prong is the short timeframe

between vaccination and Petitioner’s onset. Petitioner’s onset likely occurred within eight days of

vaccination—a fairly swift period for the adaptive response to vaccination to begin, and then

subsequently to result in clinical neurologic symptoms. CIDP onset would more commonly begin

at least a few weeks after vaccination (perhaps consistent with its indolent/insidious course). See,

e.g., Kelley, 68 Fed. Cl. at 102 (CIDP onset approximately two weeks after vaccination); Daily,

2011 WL 2174535 (finding that onset of CIDP within a few weeks of vaccination was a medically

acceptable timeframe). However, Petitioner’s experts were able to provide reliable evidence that,

while rare, patients with an acutely-presenting form of CIDP may actually see a faster post-trigger

onset. See 2012 IOM Report. And this case does not involve the kind of lengthy timeframe I have

deemed facially unreasonable. Patel, 2020 WL 2954950 at *18–21; Strong, 2018 WL 1125666, at

*21. All things being equal, an onset closer in time to vaccination has more heft to it than one that

occurs long after—and thus I cannot in this case highlight a long quiescent period as suggesting

no vaccine reaction was likely.

Other record evidence is inconclusive as to whether the flu vaccine was the likely cause of

Petitioner’s injury. Treater support for a vaccine association in this case is largely lacking, or was

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deemed a question they could not answer pro or con. See, e.g., Ex. 174 at 71, 77. Petitioner’s

treating providers did continue to mention that he had received a vaccine one to two weeks before

his symptom onset, but no treating provider opined his CIDP was likely attributable to the flu

vaccine.

Overall, however, Respondent’s challenges to Petitioner satisfying this prong are not

illuminating or all that persuasive. Respondent mainly relies on onset beginning before

vaccination—a finding I do not reach. While the evidence in this case of a “logical sequence of

cause and effect” is not all that compelling, I can conclude based on this record that it slightly

preponderates in Petitioner’s favor.

CONCLUSION

Petitioner has prevailed in establishing entitlement to a damages award. An order

establishing the parties’ initial obligations with respect to determining damages will follow.

IT IS SO ORDERED.

/s/ Brian H. Corcoran

Brian H. Corcoran

Chief Special Master

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