Nieves v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 18-1602V

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*

ANDRES NIEVES, * Chief Special Master Corcoran

*

*

Petitioner, * Filed: April 17, 2023

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v. *

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SECRETARY OF HEALTH AND *

HUMAN SERVICES, *

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Respondent. *

*

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Michael A. Baseluos, Baseluos Law Firm, PLLC, San Antonio, TX, for Petitioner.

Ryan D. Pyles, U.S. Dep’t of Justice, Washington, DC, for Respondent.

DECISION 1

On October 17, 2018, Andres Nieves filed a petition seeking compensation under the

National Vaccine Injury Compensation Program (the “Vaccine Program”) 2 alleging that he

suffered Guillain-Barré syndrome (“GBS”) caused by his receipt of the influenza (“flu”) vaccine

on October 28, 2015. Petition (ECF No. 1) at 1. After Respondent’s Rule 4(c) Report, I determined

that the record could not support a Table flu-GBS claim, since Petitioner had been diagnosed with

chronic inflammatory demyelinating polyneuropathy (“CIDP”). See Order, dated January 11, 2021

(ECF No. 42). However, I observed that the Petitioner might be able to substantiate a causation-

1

As provided by 42 U.S.C. § 300aa-12(d)(4)(B), the parties may object to the Decision’s inclusion of certain kinds of

confidential information. Specifically, under Vaccine Rule 18(b), each party has fourteen days within which to request

redaction “of any information furnished by that party: (1) that is a trade secret or commercial or financial in substance

and is privileged or confidential; or (2) that includes medical files or similar files, the disclosure of which would

constitute a clearly unwarranted invasion of privacy.” Vaccine Rule 18(b). Otherwise, the whole Decision will be

available to the public in its present form. Id.

2

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

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

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

in-fact claim based on the CIDP diagnosis (although Respondent contested its accuracy)—and to

that end, the parties have submitted a number of expert reports and briefs.

Now, and for the reasons stated below, I hereby deny entitlement. The overall record

preponderantly supports the CIDP diagnosis. But the record and expert reports do not also support

the finding that the flu vaccine caused Petitioner’s injuries, or (and most importantly) that

Petitioner’s onset of neurologic symptoms occurred in a medically acceptable timeframe when

measured from the date of vaccination.

I. Factual Background and Medical History

Pre-Vaccination Medical History

Before Mr. Nieves ever received the flu vaccine that is the basis for his claim, he had

repeatedly visited healthcare professionals over many years, complaining of symptoms that to

some extent echo some of his post-vaccination maladies. Mr. Nieves has a past medical history

significant for sinusitis, fibromyalgia rheumatica with myositis, obesity, status post-lap band

surgery, anxiety, cervical spinal stenosis with related radiculopathy, muscle spasms, and right

carpal tunnel syndrome. Ex. 2 at 2–4; Ex. 3 at 3–121; Ex. 4 at 1–222; Ex. 7 at 1–22. He had been

prescribed neuropathic pain relief medication for some of his symptoms, but it provided little

relief. Ex. 2 at 29.

In 2013, Mr. Nieves saw a neurosurgeon with complaints of pain radiating to both

shoulders and arms with sensations of heaviness, weakness, numbness, and tingling. Ex. 2 at 29–

30. This was associated with some difficulty buttoning shirts, tying shoes, and accompanied by

frequent falling. Id. In addition, he reported limb weakness, pain (neck and back), and other

neurologic-like symptoms (arm and leg weakness, numbness, and difficulty walking) in late 2014.

Ex. 4 at 12–15. Cervical decompression surgery was planned. Id. at 15; see also id. at 114

(operative report for Dec. 10, 2014 surgery).

Even in the nine-plus months prior to vaccination, Petitioner continued to display some

symptoms echoing what he claims occurred post-vaccination. Thus, in February 2015, Petitioner

had a follow-up visit after his cervical spine surgery, and at that time it was recorded that he had

been prescribed medication for fibromyalgia, although the Petitioner at this time denied the

diagnosis, maintaining instead he merely experienced muscle spasms. Ex. 3 at 97–98.

October 2015 Vaccination and Subsequent Medical History

On October 28, 2015, Mr. Nieves (then 57 years old) received a seasonal flu vaccine in his

right arm. Ex. 1 at 10. That same day, he alleges, he began feeling “feverish and a little achy.”

Affidavit, dated November 16, 2020, filed as Ex. 19 (ECF No. 41-2) (“Nieves Aff.”) at 2. The next

2

day (October 29, 2015), 3 Mr. Nieves recalls “waking up with general malaise and flu like

symptoms with some aches and pains all over [] [his] body.” Id. He presented to his primary care

physician that day with complaints of a mild allergic response four hours after receiving the flu

shot, representing that it had resolved but that he was experiencing “generalized arthralgias without

arthritis.” Ex. 5 at 2. Petitioner otherwise reported “[f]eeling generally well,” however, and his

exam revealed no specific or acute neurologic issues this time. Id. He was advised to take ibuprofen

and a muscle spasm relaxant/sedative, with follow-up as needed. Id.

Mr. Nieves alleges that a bit more than three days after the vaccination (or by the late

evening of October 31st), he began “feeling strange,” and noticed that his “walking was a little

different.” Nieves Aff. at 2. He also recalls that he began losing some sensation in his hands and

feet. Id. He experienced more sensory issues and tingling/numbness in his hands and feet the next

day (November 1, 2015). Id. These symptoms are arguably initial manifestations of a neurologic

problem. (An entry in Mr. Nieves’s affidavit recounting his condition as of November 4, 2015,

also expresses his suspicion that the back pain he later began to feel was attributable to an altered

gait, which in turn began “when I started feeling paresthesia and loss of sensation in my feet dating

back to November 1.” Nieves Aff. at 3 (emphasis added).

On November 2, 2015, Mr. Nieves reported to the emergency room with complaints of

fatigue, leg pain, and lower back pain, informing treaters that his symptoms had existed for five

days (which, if correct, meant the vaccination date (October 28th) was their start). Ex. 3 at 89–90.

He also noted difficulty walking due to his symptoms. Id.at 91. (Petitioner’s affidavit also states

that as of this date he was having a hard time walking, and felt like he was losing sensation when

“grabbing and holding things.” Nieves Aff. at 2). A neurologic exam at this time did reveal

weakness in Petitioner’s extremities, but Petitioner was ultimately discharged. Id. at 92, 97.

The next day (November 3, 2015), Petitioner was seen by neurologist Dr. Anna Marieta

Moise. Ex. 3 at 83–87. He reported at this time “paresthesias in his distal extremities since he got

his flu shot one week ago.” Id. at 84 (emphasis added). One week would approximately place onset

on October 27–28th (or right around the day of vaccination). He also stated that he was having

difficulty walking/balance issues, plus a headache predating vaccination. Id. The record from this

visit includes the notation “fibromyalgia?” in its brief medical history recitation but no comment

on the term is provided. Id. Dr. Moise’s exam showed normal strength and reflexes, however, and

only “subjective decreased sensation,” plus a normal gait. Id. at 86.

Based on the exam and Petitioner’s presentation, Dr. Moise opined that his paresthesias

were most likely due to nutritional deficiencies connected to Petitioner’s lap-band surgery earlier

that year—but “not consistent with AIDP [the most common GBS variant] 4 given normal strength

3

Petitioner’s affidavit appears to shift from reporting dates in 2015 to 2016, within the same month. See Nieves Aff.

at 1. But the 2016 references are very likely merely a typographical error.

4

AIDP stands for “acute inflammatory demyelinating polyradiculoneuropathy.”

3

and normal reflexes.” Ex. 3 at 86. She proposed only that Petitioner receive vitamin/nutritional

supplements. Id. Another treater (Dr. Ethelyn Johnson) saw Petitioner on November 3, 2015, and

Petitioner informed her as well that he had experienced “multiple complaints since receiving flu

shot 1 week ago,” including walking issues, limb weakness, and paresthesias. Id. at 87. 5 This

treater’s impression expressed doubt as to the propriety of a GBS diagnosis, since Petitioner

displayed “good strength on exam, gait minimally impaired, reflexes +1 bilat.” Id. at 89.

On November 4, 2015, Mr. Nieves returned to the emergency room and was again seen by

Dr. Johnson. Ex. 3 at 76–78. He now reported worsening back pain, generalized weakness, and

ongoing difficulty walking, comparable to his complaints from the day before. Id. at 76. However,

the exam revealed normal results. Id. at 77. Petitioner was assessed with pain, given medications

for treatment, and referred to a pain clinic for additional follow-up. Id. Less than a week later

(November 9, 2015), Mr. Nieves again returned to the emergency room, reporting worsening low

back pain radiating up to his neck and shoulders and down to his lower extremities. Ex. 3 at 67.

However, he denied “weakness, numbness, or tingling in the lower extremity.” Id. at 67–68. He

was assessed with chronic back pain—and it was again proposed that his condition was not likely

reflective of a primary neurological problem, whether GBS or cord compression. Id.

On November 10, 2015, Mr. Nieves returned to his primary care physician, now

complaining of weakness, fatigue, and generalized muscle pain he claimed had manifested after

receipt of the flu vaccine. Ex. 5 at 1. He denied any ascending/progressive weakness at this time,

however. Id. An exam revealed normal strength and reflexes, and hence no neurologic issues,

although his gait was classified as “slow.” Petitioner was nevertheless referred to a hospital

emergency department for further evaluation and neurology care. Id. at 7.

Later that day, Mr. Nieves was admitted to Methodist Hospital in San Antonio, Texas,

where he remained an in-patient for ten days. Ex. 3 at 65; Ex. 9 at 16–18. His history (consistent

with what is reviewed above) noted fever and present myalgias “[s]ince the flu shot,” with

“progressive tingling, numbness,” falls, weakness, and fatigue. Id. at 16. At this point, “some

concern for Guillain-Barre” was expressed by a treater. Ex. 9 at 16, 17. A neurologic evaluation at

the hospital revealed some weakness and areflexia, plus ascending numbness. Id. at 16. In addition,

a lumbar puncture showed mildly elevated protein levels, and based on the foregoing Mr. Nieves

was diagnosed with GBS and treated with IVIG. 6 Id.

In the course of these treatments, Petitioner experienced some improvement, and he was

discharged 10 days later, on November 20, 2015, with a treatment plan to continue physical therapy

5

This record specifically observes that Petitioner’s history referenced fibromyalgia, but that Mr. Nieves disputed the

diagnosis. Ex. 3 at 87.

6

“Intravenous Immunoglobulin” is defined as “a therapy treatment for patients with antibody deficiencies. It is

prepared from a pool of immunoglobulins (antibodies) from the plasma of thousands of healthy donors.” Intravenous

Immunoglobulin, American College of Rheumatology, https://www.rheumatology.org/I-Am-A/Patient-

Caregiver/Treatments/Intravenous-Immunoglobulin-IVIG (last visited Apr. 17, 2023).

4

(“PT”) and occupational therapy (“OT”). Ex. 3 at 65. Diagnosis at discharge remained GBS. Ex.

6 at 107–117; 122–125; 150–154. Petitioner began PT that same late fall, but did not find it to

result in objective improvement, although his weakness subsided a bit. Ex. 3 at 48, 50; Ex. 6 at 35,

80.

Subsequent Symptoms and CIDP Diagnosis

Two months later, on January 8, 2016, Mr. Nieves was seen by neurologist Dr. Adetoun

Musa. Ex. 3 at 44–48. Mr. Nieves indicated he was experiencing worsening paresthesias, balance

issues, and that his weakness had not improved with PT/OT, or since his prior IVIG treatment in

November the prior year. Id. at 45. Dr. Musa’s exam revealed some weakness and sensory issues,

but normal reflexes, and he ultimately opined that Petitioner had the AIDP GBS variant—although

given the prolonged duration of symptoms, Dr. Musa also proposed CIDP as a potential counter-

explanation. Id. at 47. He noted the need for Petitioner to undergo an EMG. 7 Id. at 48.

The scheduled EMG testing occurred on February 8, 2016, and it revealed the presence of

generalized sensorimotor polyneuropathy, predominately demyelinating in type and mild in

degree. Ex. 3 at 43. These findings were deemed to be consistent with an acquired segmental

demyelinating polyneuropathy, like that seen in CIDP and related disorders. Id. On February 11,

2016, Mr. Nieves returned to Dr. Musa who agreed the EMG results were confirmatory of CIDP,

and proposed that Petitioner undergo another round of IVIG. Id. at 38–42.

Subsequent History and Questions About Diagnosis

Not long after the February consultation with Dr. Musa, Petitioner returned again to the

hospital emergency room on February 16, 2016, now complaining of weakness in all extremities

and back pain that “shoots down his lower extremities with pressure or movement.” Ex. 3 at 28.

His exam revealed largely normal reflexes, but weakness deemed secondary to pain, and he was

admitted with CIDP and received additional IVIG treatment. Mr. Nieves was thereafter discharged,

with a plan to continue outpatient treatment at the infusion clinic. Id. at 25–38; Ex. 11 at 1–17. In

March, Petitioner went back to Dr. Musa, and although he complained of generalized neuropathic

pain, his exam was again mostly normal. Dr. Musa repeated his prior impression of CIDP, and

proposed a treatment plan including recurring monthly IVIG infusions for six months plus a repeat

EMG/NCS at that time. Ex. 3 at 15–18; Ex. 8 at 76–80.

By mid-April 2016, Petitioner had completed an IVIG treatment, but found that its benefits

wore off after a few weeks, leaving him with painful muscle spasms and cramps involving his

7

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

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

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

transmitting, and recording the signals. Electromyography, Dorland’s Medical Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=15854&searchterm=electromyography (last visited Apr. 17,

2023).

5

neck, shoulders, and lower back. Ex. 8 at 59–62. In May, he started a second round of PT. Although

he struggled with increased pain during the sessions, his therapist proposed that his reaction might

reflect an “elevated pain response” to the activity itself. Id. at 47. Ultimately, the chronic muscle

spasms and cramps Petitioner experienced while active prevented his successful utilization of PT,

and he was eventually discharged due to lack of progress. Id. at 18–30; Ex. 11 at 69–98.

In September of that same year, Petitioner now reported to a different set of neurologic

treaters that despite six months of treatment, he did not deem the IVIG to be helpful. Ex. 11 at 67.

On September 20, 2016, petitioner underwent a second EMG, as planned by Dr. Musa in March.

But this study now showed no evidence of an acquired segmental demyelinating polyneuropathy,

inconsistent with what would be expected for a chronic and ongoing neuropathic condition like

CIDP. Ex. 11 at 63 (“NO evidence of an acquired segmental demyelinating polyneuropathy like

that can be seen in chronic inflammatory demyelinating polyradiculopathy (CIDP) and related

disorders”). In addition, the EMG revealed bilateral median neuropathy, or carpal tunnel

syndrome. Id. at 63–65. A third EMG performed in December 2016 was also inconsistent with

CIDP, while confirming the presence of a mild case of carpal tunnel syndrome. Ex. 11 at 63.

On December 21, 2016, petitioner saw neurologist Dr. Nidhi Kasatwar, complaining of

“continued cramps in his hands and legs and also his abdomen with fluttering of muscles.” Ex. 11

at 61. Examination showed fairly normal strength, however ( 4/5 on his right side, likely limited

due to pain, and 5/5 on the left), with normal sensation and reflexes, although Petitioner displayed

an abnormal gait and required a cane for ambulation. Id. at 62. Dr. Kasatwar took note of the recent

EMG that had been negative for CIDP (while supportive of a carpal tunnel diagnosis), and settled

on an impression focusing on Petitioner’s history of cervical radiculopathy, obesity, and

fibromyalgia, with continued cramps and muscle pain. It was now proposed that Petitioner cease

the IVIG infusions, and instead seek primary care treatment for chronic pain. Id.

Limited records have been offered detailing Petitioner’s subsequent course. For example,

after this case’s initiation, Petitioner visited yet another neurologist, Dr. Juan Bahamon, in August

2019, reporting to Dr. Bahamon that he had experienced CIDP (although the record from this visit

notes that Dr. Bahamon lacked “independent medical records” to corroborate what he was told

about Petitioner’s history). Ex. 14 at 1. Dr Bahamon expressed uncertainty as to whether “we are

dealing with an incomplete recovery of a monophasic [GBS],” but expressed doubt about CIDP

given an exam revealing the existence of deep tendon reflexes.” Id. at 7.

II. Expert Reports

A. Petitioner’s Experts

1. Marcel Kinsbourne, M.D.

Dr. Kinsbourne, a pediatric neurologist, submitted three written reports addressing both the

proper diagnosis for Mr. Nieves’s condition as well as the underlying causation dispute. See

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generally Report, dated Jan. 27, 2020, filed as Ex. 17 (ECF No. 23-2) (“Kinsbourne Rep.”); Report,

dated Nov. 14, 2020, filed as Ex. 20 (ECF No. 41-3) (“Second Kinsbourne Rep.”); Report, dated

Dec. 4, 2021, filed as Ex. 26 (ECF No. 55-1) (“Third Kinsbourne Rep.”).

Dr. Kinsbourne received his medical degree from Oxford University in England, along

with his Bachelor of Arts, and his Master of Arts. See Kinsbourne Rep. at 1. 8 He then received his

M.D. from the State of North Carolina. Id. Thereafter, Dr. Kinsbourne did several years of different

post-doctoral training in neurology, pediatrics, and chest diseases, and is a member of the

American Board of Pediatrics and Royal College of Physicians. Id. at 1–2. Dr. Kinsbourne was

previously a professor of psychology, professor of pediatrics, lecturer in neurology, adjunct

professor of linguistics and cognitive science, adjunct professor of occupational therapy, director

of the behavioral neurology department at the Eunice Kennedy Shriver Center, and other positions

related to neurologic and cognitive studies. Id. at 2–3. He also has held positions on several

editorial boards, professional societies, and administrative assignments. Id. at 4–6. Dr. Kinsbourne

has conducted research into pediatric disorders, developmental delays and factors, cerebral

deficiencies, learning disabilities, therapies, and epilepsy. Id. at 6–39. Importantly, however, Dr.

Kinsbourne has not treated patients, pediatric or otherwise, for almost thirty years. 9

First Report

Dr. Kinsbourne began with an overview of Mr. Nieves’s medical history. See generally

Kinsbourne Rep. at 2–5. Significantly, he observed in the record multiple instances in which

(despite initial concerns for GBS) treaters interpreted test results, coupled with Petitioner’s

persistent symptoms, to be consistent with CIDP. Id. at 5. Petitioner’s CIDP eventually “stalled,”

but left him with motor/sensory limits as well as chronic pain. Id.

Dr. Kinsbourne deemed the CIDP diagnosis consistent with the record evidence. In

particular, he emphasized that CIDP could exist even in the presence of active/normal reflexes,

noting that a number of articles revealed that to be common, and that Petitioner’s treaters had

deemed other testing consistent with some form of polyneuropathy despite an absence of areflexia.

Kinsbourne Rep. at 5. He also suggested that Petitioner’s relatively-quick onset and initial

symptoms (which misled treaters to deem GBS a possibility) might reflect an acute onset form of

CIDP). Id. at 6. Indeed, Dr. Kinsbourne embraced the view that CIDP is “closely similar” to GBS,

mainly distinguishable by the former’s chronic nature. Id. at 6–7; M. Dalakas, Pathophysiology of

Autoimmune Polyneuropathies, 42 Presse Med. e181, e182 (2013), filed as Ex. 17 Ref. 3 (ECF

No. 24-1) (“Dalakas”). Otherwise, CIDP and GBS share the same immunologic mechanisms and

8

Although Petitioner purported to file a separate CV for Dr. Kinsbourne (see Ex. 16 (ECF No. 23-1)), the document

so labeled was simply an extra copy of his expert report—and it does not appear Petitioner ever subsequently filed a

CV for Dr. Kinsbourne. But the first report begins with a paragraph labeled “qualifications,” and I therefore refer to

it for this information about his education and professional experience

9

See L.M. v. Sec’y of Health & Hum. Servs., No. 14-714V, 2019 WL 4072130 (Fed. Cl. Spec. Mstr. July 23, 2019)

(discussing Dr. Kinsbourne’s more recent practice experience).

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many clinical features—and the fact that less is known about triggering agents for CIDP could

simply be the product of the fact that “onset of CIDP is usually far in the past and easily forgotten,”

whereas GBS is acute and monophasic in course. Kinsbourne Rep. at 7.

Next, Dr. Kinsbourne attempted to grapple with a record that was (as Respondent’s experts

argue) in some ways inconsistent with CIDP, proposing that Petitioner had experienced a particular

CIDP variant, characterized by an acute onset but manifesting mostly “toward sensory deficit.”

Kinsbourne Rep. at 7. Mr. Nieves did not display weakness per se, but instead a hesitancy “to exert

and to maintain full muscular effort” given the pain he was experiencing—as evidence by his

inability to complete physical therapy. Id. Thus, Dr. Kinsbourne explained instances (such as at an

August 2019 neurologic visit) when Petitioner displayed “giveaway weakness” 10 as reflecting

Petitioner’s involuntary unwillingness to engage in painful exertions. Id; Ex. 14 at 1–7.

Dr. Kinsbourne cited several items of literature that he maintained recognized a “pure

sensory” CIDP variant. See, e.g., S. Oh et al., Chronic Sensory Demyelinating Neuropathy:

Chronic Inflammatory Demyelinating Polyneuropathy Presenting as a Pure Sensory Neuropathy,

55 J. Neurol., Neurosurg. and Psych. 677 (1992), filed as Ex. 17 Ref. 14 (ECF 26-4) (discussing

ten relevant patient cases). He also noted that pain was a common, “long-term residual symptom,”

in addition to CIDP’s other symptom features (although he mainly supported this contention with

reference to case series reports). See, e.g., S. Boukhris et al., Pain as the Presenting Symptom of

Chronic Inflammatory Demyelinating Polyradiculoneuropathy: A Study of 11 Cases, 10 J. Periph.

Nerv. Syst. 329 (2005), filed as Ex. 17 Ref. 1 (ECF No. 23-3); K. Kuitwaard et al., Recurrences,

Vaccinations and Long-Term Symptoms in GBS and CIDP, 14 J. Periph. Nwerv. Syst. 4, 310

(2009), filed as Ex. 17 Ref. 7 (ECF No. 25-2) (“Kuitwaard”) at 311. Mr. Nieves’s sequelae were

all consistent with CIDP’s features. Kinsbourne Rep. at 8.

Dr. Kinsbourne did not accept the possibility that Petitioner’s CIDP had eventually

remitted, or that his longer-term symptoms course undermined the diagnosis. He particularly

questioned the negative electrodiagnostic results from testing performed on Petitioner in the fall

of 2016, maintaining that such testing had a variable sensitivity, and that “CIDP may continue to

be active” even when this kind of testing did not reveal its presence. Kinsbourne Rep. at 8; Y.

Rajabally et al., Validity of Diagnostic Criteria for Chronic Inflammatory Demyelinating

Polyneuropathy: A Multicenter European Study, 80 J. Neurol., Neurosurg. and Psych. 1 (2009),

filed as Ex. 17 Ref. 16 (ECF No. 27-1) (“Rajabally”) at 1 (comparing different criteria, including

electromyographic testing, for levels of sensitivity in establishing CIPD diagnoses).

The flu vaccine Petitioner received was in Dr. Kinsbourne’s view likely causal of

Petitioner’s CIDP. He maintained that the immunologic mechanism relevant to GBS—molecular

mimicry between vaccine components and myelin surface gangliosides, resulting in an antibody-

10

“Giveaway” weakness has been defined as “a lack of effort, or an impression by the examiner that the effort was

poor.” Sanchez v. Sec'y of Health & Hum. Servs., No. 18-1012V, 2022 WL 1013264, at *7 n.15 (Fed. Cl. Spec. Mstr.

Mar. 11, 2022).

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driven cross-reaction against those gangliosides—applied also to CIDP. Kinsbourne Rep. at 8–10.

At most, any pathogenic difference between GBS and CIDP was attributable to a lymphocyte

receptor that was effective in “switching off an ongoing immune response by causing T cell

apoptosis.” Id. at 9; C. Comi, Fas-Mediated T-cell Apoptosis in Chronic Inflammatory

Demyelinating Polyneuropathy, 16 (Supp.) J. Periph. Nervs. Syst. 45 (2011), filed as Ex. 7 Ref. 2

(ECF No. 23-4). While some individuals would realize the “benefit” of this receptor (and thus

experience only GBS), others do not, with the attendant result of a chronic form of polyneuropathy,

CIDP. Thus, a “host variable, independent of the causation” of the illness explained why a person

would experience the more chronic form of polyneuropathy. Kinsbourne Rep. at 9.

Otherwise, Dr. Kinsbourne argued that while good epidemiologic evidence did not exist to

establish an association between a “rare disorder” like CIDP and the flu vaccine, case reports

established such a link. Kinsbourne Rep. at 9; J. Pritchard et al., Risk of Relapse of Guillain-Barré

Syndrome or Chronic Inflammatory Demyelinating Polyradiculoneuropathy Following

Immunisation, 73 J. Neurol., Neurosurg. and Psych. 348 (2002), filed as Ex. 17 Ref. 15 (ECF No.

26-5) (“Pritchard”) (questionnaire distributed by GBS patient support group in U.K. identified 65

of 179 CIDP patients who received vaccinations after their diagnosis, and two experienced relapse

after receipt of the flu vaccine). Another study that took into account VAERS 11 data also observed

instances of post-vaccination neuropathies. D. Vellozzi et al., Safety of Trivalent Inactivated

Influenza Vaccines in Adults: Background for Pandemic Influenza Vaccine Safety Monitoring, 27

Vaccine 2114 (2009), filed as Ex. 17 Ref. 23 (ECF No. 27-7) (“Vellozzi”). Vellozzi did not

specifically look for reported instances of CIDP, and it overall deemed the version of the flu

vaccine it analyzed to be safe, but it did observe enough reported instances of GBS post-

vaccination to warrant closer review. Vellozzi at 2118–19.

Dr. Kinsbourne also proposed that the onset timeframe was medically-acceptable.

Kinsbourne Rep. at 10. He allowed for the fact that Petitioner had reported an “apparently

transitory respiratory allergic reaction” within hours of vaccination, as well as leg and lower back

pain five days later. Id. at 2. In his reading of the record, however, Mr. Nieves had presented with

CIDP/GBS “prodromal manifestations” five days post-vaccination, with more specific neurologic

symptoms (toe numbness) the next day (possibly meaning the day after Mr. Nieves’s ER visit on

November 2, 2015). Id. at 6. Such timing was consistent with an acute onset-form of CIDP, and

was also consistent with the “temporal interval for neuroimmune polyneuropathies.” Id. at 6, 10.

Dr. Kinsbourne discounted Petitioner’s documented identification (on November 3, 2015) of

symptoms (a “one-week history of paresthesias in his distal extremities”), since that would place

11

The Vaccine Adverse Event Reporting System (“VAERS”) is a national passive-reporting warning system designed

to detect safety problems in U.S.-licensed vaccines. See About VAERS, VAERS, https://vaers hhs.gov/about html (last

visited Mar. 22, 2023). It is managed by both the CDC and the FDA. VAERS monitors and analyzes reports of vaccine

related injuries and side effects from both healthcare professionals and individuals. See generally Carda v. Sec’y of

Health & Hum. Servs., No. 14-191V, 2017 WL 6887368, at *6 (Fed. Cl. Spec. Mstr. Nov. 16, 2017).

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onset before vaccination—contrary to Petitioner’s contention (made, it should be emphasized, in

non-contemporaneous witness statements) that he was symptoms-free at that time.

Second Report

Dr. Kinsbourne’s second report was filed in reaction to Respondent’s arguments that onset

of Petitioner’s symptoms did not fit the timeframe for a Table flu-GBS claim. 12 He noted that the

medical community accepted the likelihood of post-vaccination malaise (soreness at the injection

situs; fever; and aches, among other things), and that such symptoms could manifest in reaction to

the speedy cytokine upregulation encouraged by vaccinations generally. Second Kinsbourne Rep.

at 1–2. The effects of this increase in cytokines, associated with the immune system’s innate

response to an external trigger (including vaccines), could be seen within hours to two days post-

vaccination. Id. at 2–3. Here, Mr. Nieves had reported some initial “allergic reaction” within hours

of receiving the flu vaccine, along with joint pain, and these non-neurologic symptoms were all

consistent with the expected vaccine reaction. Id. at 3. They thus were distinguishable from the

kind of neurologic symptoms reflective of CIDP.

Later records did reveal CIDP manifestations—just not as close-in-time to vaccination.

However, Dr. Kinsbourne was somewhat vague in specifying an onset date for these neurologic

symptoms. Thus, in distinguishing Petitioner’s immediate, vaccine-induced malaise, Dr.

Kinsbourne acknowledged that Petitioner’s CIDP onset could not have been the day of, or after,

vaccination, but instead “must have begun later.” Second Kinsbourne Rep. at 2. He also noted that

even at the time of Petitioner’s November 2, 2015 ER visit, CIDP “could not yet be reliably

diagnosed.” Id. (emphasis added). Indeed, he disputed Petitioner’s own reporting of symptoms

having begun close-in-time to vaccination (as reflected in the contemporary records). Id. at 4–5.

Instead, Dr. Kinsbourne emphasized Petitioner’s complaints about “progressive tingling,

numbness and frequent falls” as reflective of CIDP—but these were only reported November 9,

2015. Second Kinsbourne Rep. at 5. Ultimately, he embraced this timeframe (which might place

manifestation of neurologic symptoms as late as 10–12 days post-vaccination) as consistent with

“the 3-42 day risk period for the onset of GBS/acute onset CIDP”—even though this opinion was

not only inconsistent with Dr. Kinsbourne’s first report (See First Kinsbourne Rep. at 10 (“[t]he

onset of Mr. Nieves’s polyneuropathy followed the influenza vaccination after five days”)), but

also with the literal medical record (even allowing for the possibility that Petitioner mistook his

immediate malaise as associated with his later neurologic issues).

Third Report

The final written report submitted by Dr. Kinsbourne addressed the first expert report

offered by one of Respondent’s experts, Dr. Brian Callaghan. He began by revisiting his opinion

12

The special master to whom the case was originally assigned had observed the record evidence (also reviewed

above) suggesting an onset too close-in-time to vaccination to be consistent with the 3–42 day time interval required

for a Table flu-GBS claim. See generally Order, dated May 1, 2020 (ECF No. 30).

10

about Petitioner’s diagnosis, dismissing Dr. Callaghan’s argument out of hand that Mr. Nieves’s

documented, pre-existing comorbidities had anything to do with his CIDP. Third Kinsbourne Rep.

at 1. He emphasized the difficulty of diagnosing CIDP, casting the issue in a different light: in his

view, it was less misdiagnosed than underdiagnosed. Id; U. Chaudhary and Y. Rajabally,

Underdiagnosis and Diagnostic Delay in Chronic Inflammatory Demyelinating Polyneuropathy,

268 J. Neurol. 1366 (2021), filed as Ex. 26 Ref. 3 (ECF No. 59-3). Thus, the mere fact that not all

criteria for the condition were precisely met in Petitioner’s case did not mean there was “a more

fitting diagnosis.” Third Kinsbourne Rep. at 2. And the sudden appearance of Petitioner’s post-

vaccination neurologic symptoms only confirmed that he had experienced an “acute onset” form

of CIDP (although such individuals could go on to experience the kind of chronic symptoms more

characteristic of CIDP). Id. at 2, 5–7. 13 Dr. Kinsbourne also disagreed with Dr. Callaghan’s effort

to distinguish GBS and CIDP, arguing that despite their many distinctions (which he deemed

“mainly why they have been given different names”) it remained reasonable to view CIDP as

“chronic” GBS. Id.

Dr. Kinsbourne also attempted to bulwark his prior assertions that the flu vaccine could

cause CIDP. He made the general argument that epidemiologic evidence would be unable to detect

rare events like autoimmune-driven polyneuropathies, that such evidence was required to prevail

in Vaccine Program cases in any event, and that even the evidence cited for this point by Dr.

Callaghan at least provided “weakly positive” evidence in favor of causation. Third Kinsbourne

Rep. at 3–5; P. Doneddu et al., Risk Factors for Chronic Inflammatory Demyelinating

Polyradiculoneuroapthy (CIDP): Antecedent Events, Lifestyle and Dietary Habits. Data from the

Italian CIDP Database, 27 Eur. J. Neurol. 1, 3 (2019), filed as Ex. 26 Ref. 6 (ECF No. 59-6)

(“Doneddu I”) (seven of 411 CIDP patients reported pre-onset receipt of flu vaccine). With respect

to what antibodies likely drive CIDP, Dr. Kinsbourne deemed any distinction having “no obvious

relevance to the issue of vaccine causation,” since Respondent had not shown that the kind of

antibody likely to drive CIDP was different. Third Kinsbourne Rep. at 8. He also cited literature

that he said revealed “a small minority of patients” with CIDP displayed anti-ganglioside

antibodies in any event. L. Querol and C. Lleixa, Novel Immunological and Therapeutic Insights

in Guillain-Barré Syndrome and CIDP, Neurotherapeutics (2021) https://doi.org/10.1007/s13311-

021-01117-3, filed as Ex. 26 Ref. 7 (ECF No. 59-7) (“Querol”), at 4 (noting that “anti-ganglioside

antibodies have been reported in some CIDP cohorts,” but deeming it a “weak association,” and

acknowledging that “other meaningful clinical-immunological correlations with anti-ganglioside

antibodies have not been established yet” for CIDP).

13

In the context of this discussion, Dr. Kinsbourne repeated his prior assertion that the main explanation for CIDP’s

chronicity was a host genetic deficiency—the inability to “inhibit the continuation of the inflammatory polyneuropathy

at nadir.” Third Kinsbourne Rep. at 7. But Dr. Kinsbourne not only referenced Dr. Akbari’s opinion here, but

personally lacks the immunologic qualifications to comment reliably on this topic in comparison to Dr. Akbari, and

therefore I do not deem this portion of his opinion worthy of substantial weight.

11

2. Joseph Jeret, M.D.

Dr. Jeret, a neurologist with expertise in EMG/NCS studies and clinical familiarity with

peripheral neuropathies like CIDP, offered an expert report in reaction to that provided by

Respondent’s first expert, Dr. Callaghan, plus a supplemental report. Report, dated December 12,

2021, filed as Ex. 23 (ECF No. 53-2) (“First Jeret Rep.”); Report, dated Feb. 9, 2022, filed as Ex.

27 (ECF No. 72-1) (“Second Jeret Rep.”). Dr. Jeret offered his own interpretation of Petitioner’s

medical records, and agreed with the CIDP diagnosis.

Dr. Jeret received his undergraduate degree from CUNY Brooklyn College in Brooklyn,

New York in 1984, and his medical degree from SUNY Health Science Center at Brooklyn in

1988. Curriculum Vitae, filed as Ex. 22 (ECF No. 53-1) (“Jeret CV”) at 1. He completed a one-

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

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

Downstate. Jeret CV at 1; First Rep. at 1. He is board certified in Neurology by the American

Board of Psychiatry and Neurology and is currently employed by the Icahn School of Medicine at

Mount Sinai Medical Center in New York as an active physician in the Department of Neurology.

Id. He is also on staff at two community hospitals—South Nassau Community Hospital and Mercy

Medical Center. Id. Dr. Jeret has published numerous articles in areas related to neurology,

reflecting his broad general neurology practice. Id.

First Report

The first part of Dr. Jeret’s report consisted of an explanation of CIDP, plus the role EMG

and NCS testing play in diagnosing it. First Jeret Rep. at 2–6. He repeated Dr. Kinsbourne’s general

contentions that CIDP could be understood as a “chronic counterpart” to GBS, despite the

differences between the two. Id. at 3. He also noted that, as a general matter, less than two thirds

of CIDP patients would otherwise meet electromyographic clinical criteria for CIDP (and hence

other data, like the results of a lumbar puncture, were needed to confirm the diagnosis in many

cases). Id; K. Gorson and A. Ropper, Chronic Inflammatory Demyelinating

Polyradiculoneuropathy (CIDP): A Review of Clinical Syndromes and Treatment Approaches in

Clinical Practice, 4 J. Clin. Neuromusc. Dis. 4:174 (2003), filed as Ex. 23 Ref. 11 (ECF No. 57-

1) (“Gorson & Ropper”), at 178. 14 And he discussed the specific EMG/NCS testing findings

necessary to confirm CIDP. Id. at 4. But because the technical CIDP criteria were in many cases

unmet, despite other indicia that CIDP explained a patient’s condition, several “atypical CIDP”

variants had been proposed. First Jeret Rep. at 4; P.E. Doneddu et al., Atypical CIDP: Diagnostic

14

Gorson & Ropper also identified vaccines as “an associated systemic medical disorder,” including them among a

list of medications (presumably which have been associated with CIDP). See Gorson & Ropper at 177 Table 2.

However, the article does not provide any context at all for this assertion, and Table 2 more generally discusses CIDP

as a “ ‘secondary symptomatic’” inflammatory demyelinating neuropath[y],” adding that “the precise relationship of

the underlying illness to the neuropathy varies from case to case.” Id. at 176

12

Criteria, Progression and Treatment Response. Date from the Italian CIDP Database, 90 J.

Neurol. Neurosurg. Psychiatry 125 (2019), filed as Ex. 25 Ref. 5 (ECF No. 60-5) (“Doneddu II”).

Next, Dr. Jeret engaged in a granular evaluation of Mr. Nieves’s medical history, including

diagnoses and treatments he had received well before vaccination. First Jeret Rep. at 7–18. He

acknowledged, for example, concerns for fibromyalgia expressed for Petitioner as early as 2012,

but maintained that this diagnosis had never been formally confirmed. Id. at 7–8. He further

observed EMG testing consistent with carpal tunnel syndrome from 2013, but emphasized that

evidence of polyneuropathy had not been identified at that time. Id. at 8–9. Petitioner had also been

treated for ongoing neck pain, but Dr. Jeret noted that relevant records seemed to focus on some

form of spondylosis 15 or cervical stenosis as the proposed cause, rather than a neurologic

explanation for Petitioner’s symptoms. Id. at 8–9. Treatment sought by Petitioner in late 2013 in

reaction to episodes of falling had revealed no loss of reflexes. Id. at 9.

At a neurologic evaluation toward the end of 2013, Dr. Jeret acknowledged, Petitioner had

reported a long history of leg numbness, progressively worsening in the immediate four to five

months and featuring loss of leg sensation. First Jeret Rep. at 9. He also at this time revealed absent

reflexes, but no other major neurologic symptoms. Id. The months thereafter, treatment seemed

focused on Petitioner’s cervical stenosis/neck pain. However, Petitioner obtained yet another

neurologic consultation in November 2014, at which time he again reported numbness and

weakness in his limbs. Id. at 10. Moreover, exam revealed diminished reflexes and sensation

(although treatment again seemed oriented toward his cervical spine issues). Id. But by the spring

of 2015, Petitioner reported improvement in his neck pain symptoms and had an otherwise normal

exam. Id. at 11. Dr. Jeret deemed this to be Petitioner’s “pre-vaccine baseline,” characterized by

an absence of neurologic complaints (despite a several-year history to that point complaining of a

large variety of such issues). Id.

By contrast, Dr. Jeret emphasized a number of post-vaccination neurologic symptoms

findings that were consistent with CIDP. First Jeret Rep. at 18. By November 3, 2015, Petitioner

was reporting limb weakness and worsening paresthesias (consistent with his informing

neurologists at this time that he had experienced “a one-week history of paresthesias” since his

vaccination). Id. at 11. At this time, he also displayed some reduced sensation in distal upper and

lower extremities, plus reduced reflexes in the arms and ankles. Id.; Ex. 3 at 83–87. The next day,

when he took himself to the ER, Petitioner now displayed a normal neurologic exam overall, but

Dr. Jeret questioned its thoroughness. Id. at 11–12.

15

“Cervical Spondylosis” is defined as “degenerative joint disease affecting the cervical vertebrae, intervertebral

disks, and surrounding ligaments and connective tissue, sometimes with pain or paresthesia radiating along the upper

limbs as a result of pressure on the nerve roots.” Cervical Spondylosis, Dorland’s Medical Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=107846&searchterm=cervical%20spondylosis (last visited

Apr. 17, 2023).

13

When Petitioner returned to the ER on November 9, 2015, he again demonstrated no

weakness, numbness, or tingling—but after his admission to the hospital the next day, he reported

a history (since the vaccine) of progressive tingling, numbness and weakness—and at this time

(after an exam revealed diminished strength in the distal lower extremities) GBS was raised as a

concern. First Jeret Rep. at 12. A neurologic consultation on November 11th (which included an

exam revealing areflexia, limb weakness, and lack of sensory levels) confirmed the need for a

lumbar puncture. That testing confirmed the presence of a neuropathy—whether GBS or acute

CIDP. Id. at 13.

Dr. Jeret provided some specific discussion of the various EMG/NCS testing performed on

Petitioner. The February 2016 electromyographic testing results, for example, 16 found several

indicia of CIDP, including “acquired segmental demyelination,” “conduction block,” and “absent

F-wave.” First Jeret Rep. at 13–14; Ex. 3 at 43–44. The second post-vaccination EMG/NCS

testing, performed in September 2016, by contrast, revealed normal F-waves and no conduction

block, but Dr. Jeret deemed this consistent with “successfully-treated CIDP.” First Jeret Rep. at

17. Dr. Jeret did not comment on the results of the third such study, other than to suggest it was

merely a prerequisite for establishing care with a new neurologist. Id. at 18.

Given such a record, Dr. Jeret deemed Petitioner’s CIDP diagnosis to have ample

credibility and accuracy. Numerous specific symptoms Petitioner reported reflected neurologic

issues, and were confirmed by the February 2016 EMG/NCS testing. First Jeret Rep. at 18.

Resolution of symptoms in the months to come (as reflected in the follow-up EMG/NCS testing)

was attributable to successful treatment. Id. And this diagnosis had been embraced by several of

Petitioner’s treating neurologists. Id. at 18–19, 23. By contrast, only Dr. Callaghan rejected the

CIDP diagnosis—but in Dr. Jeret’s totality review of the record, there was ample evidence to

support the CIDP diagnosis even if not all of the strictest criteria could be shown to be met. Id. at

22.

Dr. Jeret did not accept other explanations for Petitioner’s symptoms. For example, he took

issue with the idea that Petitioner’s symptoms reflected fibromyalgia, as found in a record from

March 2016, arguing that this diagnosis was not derived from a doctor’s speculation but simply

existed in records due to “something said by the patient and then repeatedly cloned” in subsequent

records. First Jeret Rep. at 15, 23–24. In fact, Dr. Jeret felt that records from this timeframe actually

cast doubt on fibromyalgia as an explanation, and (unlike CIDP) no contemporaneous treaters ever

proposed it as an alternative diagnosis. Id. at 23–24; Ex. 3 at 13. He also maintained that

fibromyalgia would feature diminished reflexes on the testing findings from Petitioner’s first 2016

16

Dr. Jeret’s report confusingly identifies this as the “second” study; the record establishes it was the first EMG/NCS

testing performed on Petitioner post-vaccination. First Jeret Rep. at 13. Petitioner had received an EMG study in

November 2014, pre-vaccination—but it only demonstrated cervical radiculopathy, consistent with his neck pain

complaints, rather than polyneuropathy consistent with CIDP. Id. at 10. The record thus does not contain EMG/NCS

evidence supporting a CIDP diagnosis any time before the vaccination—but it is the post-vaccination EMGs that are

most relevant to Petitioner’s claim.

14

EMG or cerebrospinal fluid tests, while radiculopathy would not feature the EMG testing

“improvements” observed in the second 2016 EMG. Id. at 19. And he denied IVIG had been

unsuccessful, noting improvement over time in Petitioner’s strength, reflexes, and sensation

throughout the course of his receipt of such treatments. Id. at 16.

Next, Dr. Jeret proposed that the flu vaccine had likely caused Petitioner’s CIDP. He

observed as a general matter that aberrant immune responses could produce autoimmune diseases,

mediated by antibodies (produced in reaction to a foreign pathogen—or vaccine antigen) that (in

this case) would mistakenly attack peripheral nerve myelin. First Jeret Rep. at 19; J. Brostroff et

al., Post-Influenza Vaccine Chronic Inflammatory Demyelinating Polyneuropathy, 37 Age and

Ageing 229 (2007), filed as Ex. 23 Ref. 5 (ECF No. 56-5) (case report involving single patient).

This process could specifically be set into motion if a vaccine’s peptides mimicked “the body’s

own peptides.” First Jeret Rep. at 19. Here, items of literature filed in the case demonstrated that

CIDP was associated with a number of reported antecedents, including the flu vaccine. P.

McCombe et al., Chronic Inflammatory Demyelinating Polyradiculoneuropathy: A Clinical and

Electrophysiological Study of 92 Cases, 110 Brain 1617 (1987), filed as Ex. 23 Ref. 18 (ECF No.

57-8) (one-third of patients in study reported antecedent infection; vaccines not discussed);

Kuitwaard at 312 (questionnaire directed at GBS/CIDP patients revealed that (out of 76 CIDP

patients who had responded to the survey) eight reported a pre-onset vaccination (most often the

flu vaccine), and five of 24 CIDP patients who received the flu vaccine post-vaccination reported

a symptoms worsening).

In addition, case reports not only elucidated instances of CIDP after receipt of the flu

vaccine, but suggested relapses or symptoms worsening was possible in the wake of vaccination.

P. Kelkar, Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) with Rapid Progression

after Influenza Vaccination: A Report of Three Cases, 8 J. Clin. Neuromusc. Dis. 20 (2006), filed

as Ex. 23 Ref. 23 (ECF No. 57-6); Pritchard at 348 (two of 46 CIDP patients responding to

questionnaire reported relapse after receipt of flu vaccine). And indirect evidence of a causal link

was supplied by the fact that the “GBS/CIDP Organization” recommended that individuals who

experienced one of those two related neuropathies after vaccination not receive a vaccine a second

time, since this “assumes that one may receive CIDP from a vaccine.” First Jeret Rep. at 20. 17

Otherwise, since a CIDP diagnosis was so much more difficult, more direct proof of causation was

extremely hard to generate or identify. First Jeret Rep. at 20.

17

The link provided to the webpage purportedly containing this view does not work. However, another link of the

“GBS/CIDP Foundation International” page states that “[f]or the rare person who developed GBS within four to six

weeks of receiving an immunization, the Foundation advises to avoid the same immunization in the future.” See

https://www.gbs-cidp.org/support/resources/flu-shots-and-vaccinations/ (last accessed Apr. 17, 2023). Thus, this

admonition is specific only to those individuals who first develop GBS after vaccination, and only indirectly applies

to this case (since Petitioner does not allege he previously experienced a flu vaccine-caused neuropathy).

15

With respect to onset, Dr. Jeret proposed that the record established Petitioner’s neurologic

symptoms began no sooner than approximately five days post-vaccination—consistent with an

accepted “several day latency” (although he seemed to rely on Dr. Kinsbourne for this timeframe).

First Jeret Rep. at 20. In so maintaining, Dr. Jeret differentiated Mr. Nieves’s immediate symptoms

from what came later. Mr. Nieves initially reported a “mild allergic reaction” and arthralgias the

day after vaccination, but no numbness, weakness, or areflexia. First Jeret Rep. at 11, 20–21. But

the history contained in Petitioner’s November 11, 2015 neurologic evaluation “suggests that the

symptoms began ‘several days’ after the flu shot.” Id. at 13. And Dr. Jeret emphasized Dr. Musa’s

“precise history” taken in March 2016 (five months post-vaccination), which described non-

neurologic/subjective symptoms one week post-vaccination, with weakness “a week after that”

plus areflexia (suggesting an onset of more than one week after vaccination). Id. at 15.

But Dr. Jeret struggled to differentiate contrary records suggesting an earlier onset. Thus,

he noted that the Petitioner’s own chronology (prepared after the claim’s filing) identifies a loss

of sensation in his hands and feet (something neurologic) the evening of October 31, 2015—a little

over three days post-vaccination. First Jeret Rep. at 21; see generally Nieves Aff. But the medical

record also indicates that Petitioner not only reported a number of neurologic-like symptoms on

November 3rd (six days post-vaccination), but claimed he had been experiencing them for a week,

or at least “since” the October 28th vaccination. Id. at 11. Dr. Jeret also admitted that although at

the time of Petitioner’s mid-November 2015 hospitalization, he reported the kind of malaise-like

post-vaccination symptoms that could be distinguished from neurologic complaints, he also

reported progression of the latter kinds of issues from the time of vaccination, and hence (even at

this point) “the onset of the neurological symptoms is not clearly delineated.” First Jeret Rep. at

12. 18

Second Report

Dr. Jeret prepared a succinct additional report less than two months after the filing of his

first. But while it purports to “address several issues that have been addressed by the other

physicians,” it appears to have been filed mostly in reaction to my ordering the parties to brief the

case for a ruling on the record—and thus recapitulates points Dr. Jeret already covered in his initial

report.

For example, Dr. Jeret repeated his contention that Petitioner likely experienced “acute”

CIDP, noting that his medical history reflected CIDP in all regards except for its abrupt onset

18

Dr. Jeret more generally offered the comment that medical records (especially those that are created via electronic

entry into a computer file) often “clone,” or repeat verbatim, prior entries about patient histories without comment or

consideration, that doctors will truncate a series of symptoms into a streamlined temporal reference for ease, and

otherwise that “sloppy medical documentation” is common. First Jeret Rep. at 21. Of course, from the perspective of

fact finding in this case, this simply means that the inconsistent and vague record presented on this topic needs to be

closely scrutinized, differentiating between evidence deserving of weight from proof less trustworthy—and these

comments do not undermine the reasonability of giving immediately-contemporaneous proof more weight than

summaries or after-the-fact statements made after the claim’s filing.

16

(which made it resemble GBS). Second Jeret Rep. at 1. He then questioned the application of one

item of literature touted by Dr. Callaghan to this case, maintaining that it lacked statistical

significance and epidemiologic reliability (in the absence of a comparison control group), and that

it relied on inexact data about the studied patients’ symptoms onset. Id. at 1–2; Doneddu I at 2

(deeming it unlikely that antecedent events, including vaccination, could be risk factors for CIDP,

based on questionnaire). He maintained that case report-derived “anecdotal reports” of post-

vaccination CIDP were “the highest level of evidence that currently exists,” and therefore “[s]trict

Daubert principles cannot be applied” in evaluating causation (a questionable opinion for a non-

legal medical expert in a Vaccine Program case to advance). Id. at 2.

Dr. Jeret also maintained that no diagnosis other than CIDP was possible given Petitioner’s

medical history. The combination of symptoms experienced by Petitioner and that reflected

CIDP—“areflexia, elevated CSF protein, and the multiple EMG findings” from the February 2016

testing could not be explained by fibromyalgia or radiculopathy. Second Jeret Rep. at 2. And

numerous qualified treaters embraced the CIDP diagnosis (not to mention Drs. Jeret and

Kinsbourne). Id. at 3.

Third Report

Dr. Jeret’s concluding report was also succinct, and endeavored to rebut points made both

by Respondent’s neurologic expert, Dr. Callaghan, and immunologic expert, Dr. Mark Tompkins.

Dr. Jeret’s comments on the latter’s opinion were mainly limited to the observation that Dr.

Tompkins’s lack of clinical expertise cast doubt on his assertion that the “GBS/CDIP

Organization” warning about the danger of vaccination after vaccine-induced illness, especially

since the article Dr. Tompkins relied upon involved a much smaller group of opining neurologists.

Third Jeret Report at 1.

The remainder of this report addressed comments by Dr. Callaghan. First, Dr. Jeret

disclaimed Dr. Callaghan’s interpretation of the course of EMG testing as inconsistent with CIDP,

noting that (a) Respondent’s own literature established that IVIG treatment was not always

successful, but (b) in fact the record showed Petitioner had improved, as reflected by “the objective

EMG” results, and (c) the IVIG treatment would have been abandoned had treaters “truly doubted”

the CIDP diagnosis. Third Jeret Rep. at 1. Otherwise, the first post-vaccination EMG confirmed

the presence of sufficient criteria for CIDP to support the diagnosis, although Dr. Jeret admitted

that the results had never been made available in this case 19—forcing all experts to rely on

descriptions of such testing in the medical records. Id. at 1–2. Dr. Jeret reemphasized the different

clinical factors from the record that were consistent with a CIDP diagnosis (and in particular the

proof of absent reflexes and the CSF testing results). Id.

19

Petitioner attempted to obtain some of the EMG results and file them into the record of this case, but could not do

so. See Ex. 21 (ECF No. 48-1).

17

Second, Dr. Jeret rejected Dr. Callaghan’s emphasis on Petitioner’s allegedly-incompatible

“multitude of symptoms,” deeming them “unrelated” to his CIDP. Third Jeret Rep. at 2. That

diagnosis had not been rejected, he maintained, and it was corroborated by the fact that IVIG

treatment was never discontinued (since this suggested it was deemed to be beneficial). Id. In a

similar vein, Dr. Jeret did not accept fibromyalgia as an alternative diagnosis, proposing that the

criteria for it had not been met, that it appeared to have been cloned in computerized medical

records based on incorrect reporting by Mr. Nieves, and that it did not exclude a CIDP diagnosis

regardless. Id. And no contemporaneous treater had considered “anything other than nerve

demyelination” as explanatory for Petitioner’s condition. Id.

Dr. Jeret also sought to rebut Dr. Callaghan’s attacks on vaccine causation. He noted that

even literature offered by Dr. Callaghan (and discussed below) allowed for a post-vaccination risk

of CIDP. Third Jeret Rep. at 2–3. What limited epidemiologic evidence existed on the subject did

not categorically reject the possibility of causation. In addition, Dr. Jeret again argued that the

CIDP/GBS similarities outweighed their differences, and since molecular mimicry was “an

accepted theory cited repeatedly in multiple peer-reviewed publications,” there was no reason not

to embrace it in this context as well (as supported by literature filed by Dr. Jeret). Id. at 3; see also

First Jeret Rep. at 19 (citations omitted).

3. Omid Akbari, PhD.

Petitioner filed two reports from Dr. Omid Akbari, Ph.D. See generally Expert Report,

dated December 17, 2021, filed as Ex. 25 (ECF No. 54-2) (“First Akbari Rep.”); Report, dated

August 1, 2022, filed as Ex. 29 (ECF No. 88-2) (“Second Akbari Rep.”). Dr. Akbari opined that

Mr. Nieves’s CIDP was likely caused by the flu vaccine.

Dr. Akbari is a professor of allergy and immunology at Keck School of Medicine at the

University of Southern California. Akbari First Rep. at 1–3; Omid Akbari CV, filed as Ex. 24 (ECF

No. 54-1) (“Akbari CV”). He received his bachelor and master’s degrees from University College

London. Akbari CV at 1. He then received a Ph.D. in cellular and molecular immunology from the

National Institute for Medical Research in London before completing a postdoctoral fellowship at

Stanford University. Id. He has and continues to serve on the editorial board of several journals,

and he has numerous publications in the area of immunology and allergy research. Id. at 4–5, 9–

13. He has particular experience on the subjects of “immune tolerance and how immune cells

induce autoimmune and allergic diseases.” First Akbari Rep. at 2. Dr. Akbari is not a medical

doctor, however, and therefore he does not diagnose or treat patients with neurological diseases in

a clinical setting.

First Report

The initial part of Dr. Akbari’s first report contained an overview of Petitioner’s medical

history, and it was consistent with the observations of Petitioner’s two neurologic experts. First

Akbari Rep. at 3–6. He then discussed CIDP’s features, emphasizing (consistent with Drs.

18

Kinsbourne and Jeret) how difficult it was to identify consistent elements of it, as well as the fact

that CIDP often presented acutely. Id. at 6. He otherwise classified CIDP (like some

subgroup/variants of it) as a “chronic inflammatory neuropathy,” with a “distinct

pathophysiology” involving the “breakdown of myelin” attributable to T cells and macrophages.

Id. at 6–7. And he agreed with Dr. Kinsbourne that host susceptibility was likely a major (and most

significant) factor in whether a person was likely to incur an autoimmune disease like CIDP—and

in turn (since these diseases were themselves rare) why vaccine-induced instances of disease rarely

occurred (since most individuals were not susceptible). Id. at 21–22.

However, Dr. Akbari disputed Dr. Callaghan’s contention that CIDP was distinguishable

from GBS in a larger sense, emphasizing that “many features of immune cells and GBS and CIDP

are indeed comparable.” First Akbari Rep. at 8–9. He also denied that the fact that fewer

“diagnostic biomarkers” (meaning antibodies), if any, were associated with CIDP in comparison

to GBS was a meaningful basis for distinguishing the two, proposing that all autoimmune

peripheral neuropathies were mostly T cell and macrophage-mediated (and that in any event GBS-

associated antibodies were not even present in approximately half of GBS patients). Id. at 10. In a

similar vein, Dr. Akbari maintained that because “the target antigens for CIDP patients remain

elusive,” it was very difficult to even identify the antibodies that were likely central to it, as recent

studies acknowledged. Id; Querol at 4. Overall, however, GBS and CIDP had more in common

than not—although Dr. Akbari allowed (somewhat consistent with arguments made by Dr.

Kinsbourne) that “alteration of the suppressive function” of certain regulatory immune cells likely

contributed to a host propensity for autoimmune disease generally, and more specifically why

CIDP would become chronic in nature, rather than be monophasic as in the case of GBS. First

Akbari Rep. at 12–13, 15–16.

Next, Dr. Akbari proposed a mechanism for how the flu vaccine could lead to CIDP. He

began by noting that environmental stimuli (for example, infections) could trigger an autoimmune

process, allowing for the possibility that vaccines could as well. First Akbari Rep. at 22. He also

observed how frequently neuropathies followed vaccination. Id. at 13; D. Karussis and P. Petrou,

The Spectrum of Post-Vaccination Inflammatory CNS Demyelinating Syndromes, 13 Autoimmun

Rev. 3:215 (2014), filed as Ex. 25 Ref. 36 (ECF No. 64-6) (“Karussis”) (primarily if not

exclusively discussing central nervous system neuropathic illnesses, like transverse myelitis).

Other studies had suggested that flu vaccine peptide components derived from the wild virus could

stimulate “autoreactive T cells” to attack nerve gangliosides, and Dr. Akbari referenced evidence

for amino acid sequence homology between such components (in particular, hemagglutinin) and

the target (although he offered studies involving multiple sclerosis (“MS”)—a central nervous

system even more distinguishable from CIDP than CIDP is from GBS—to support this

contention). First Akbari Rep. at 13–14; S. Markovic-Plese et al., High Level of Cross-reactivity

in Influenza Virus Hemagglutinin-specific CD4+ T-cell Response: Implications for the Initiation

of Autoimmune Response in Multiple Sclerosis, 169 J Neuroimmunol. (1-2):31 (2005) filed as Ex.

19

25 Ref. 37 (ECF No. 64-7) (“Markovic-Plese”) (T helper cells 20 generated in lab in reaction to

influenza peptides taken from a patient suffering from multiple sclerosis (“MS”) revealed high

level of potential cross-reactivity, based on homology of amino acid sequences, with viral and

human peptide sequences, including some myelin-related peptides). Any cross-reactive

autoimmune process would be attributable to molecular mimicry, and Dr. Akbari noted that

“structural homology” was likely as important as sequential to causing a cross-reaction between a

foreign antigen and mimicked self-structure. First Akbari Rep. at 14–15. In fact, auto-reactive T

cells already possessed by a person could be involved as well. Id. at 15.

Dr. Akbari’s causal theory also touched briefly on the concept that vaccination could

stimulate some existing regulatory T cells that normally protect against autoimmunity, thereby

opening the door to disease. First Akbari Rep. at 16–17. However, Dr. Akbari offered little to

support this contention. Rather, he cited Kuitwaard, which only showed some symptoms increase

in vaccinated individuals already diagnosed with CIDP (and moreover based solely on their

individually-reported circumstances, rather than verified and independent evidence of vaccine

association). Kuitwaard at 312. And he referenced literature noting that in elderly populations, a

breakdown in the effectiveness of some T-regulator immune cells lead to a decreased

responsiveness to the flu vaccination—an observation that said nothing about whether the vaccine

was likely to cause an autoimmune disease by interference with these protective cells. First Akbari

Rep. at 17; I. Herrero-Fernandez et al., Effect of Homeostatic T-cell Proliferation in the Vaccine

Responsiveness Against Influenza in Elderly People, 16 Immunity & Ageing 14:1, 8 (2019), filed

as Ex. 25 Ref. 46 (ECF No. 65-6) (“Herrero-Fernandez”).

Thereafter, Dr. Akbari described the more typical conception of a causal mechanism

involving vaccines and injuries like CIDP: that they could stimulate the production of antibodies

resulting in an autoimmune cross-reactive damage to myelin. He noted the extent to which reliable

science had identified antibodies against myelin gangliosides in patients with peripheral

neuropathies, and that the ganglioside targets were the locus for the start of the myelin destruction.

First Akbari Rep. at 17; G. Zhang et al., Erythropoietin Enhances Nerve Repair in Anti-

Ganglioside Antibody-Mediated Models of Immune Neuropathy. 6 PLoS One10:e27067 (2011),

filed as Ex. 25 Ref. 48 (ECF No. 65-8) at 9. Vaccines had been observed to be so associated in

triggering such an autoimmune process as well (albeit in studies not specific to CIDP). First Akbari

Rep. at 18; N. Agmon-Levin et al., Transverse Myelitis and Vaccines: A Multi-Analysis, 18 Lupus

1198 (2009), filed as Ex. 25 Ref. 53 (ECF No. 66) (“Agmon-Levin”) (37 cases of post-vaccination

transverse myelitis (“TM”), obtained from 40-year literature search). 21

20

“Th Cells: T helper cells” are defined as “T cells [that] trigger reactions in other immune system cells . . . [t]hey are

activated in the lymph nodes by dendritic cells, which causes them to proliferate. After proliferation, they mature into

effector T cells.” See Snyder v. Sec’y of Health & Hum. Servs., No. 01-162V, 2009 WL 332044 (Fed. Cl. Spec. Mstr.

Feb. 12, 2009).

21

Agmon-Levin is often cited by Vaccine Program claimants as evidence of CNS-oriented autoimmune demyelinating

diseases after vaccination, but has been criticized. Its limited findings had to be dredged from a lengthy reporting

20

Dr. Callaghan had proposed (as discussed below) that antecedent infection was far less

implicated in CIDP than in GBS, but Dr. Akbari argued that items of literature previously offered

by Dr. Kinsbourne, such as Rajabally, did identify a meaningful number (10 percent) of infectious

associations for the studied 268 CIDP patients. First Akbari Rep. at 18; Rajabally at 657–58. This,

plus the fact that other vaccines had been shown associated with demyelination, bulwarked the

conclusion that the flu vaccine could be as well. Karussis at 215, 221. More generally, however,

Dr. Akbari questioned whether studies of any kind could accurately determine whether “an adverse

event would be directly linked to a vaccine,” given the impracticability of identifying trustworthy

biomarkers specifically, or the more general difficulty in both identifying rare adverse events

(which he suggested passive surveillance like VAERS could track) and linking those events to

specific biological mechanisms capable of explaining them. First Akbari Rep. at 23–24. It was

simply too difficult, scientifically-speaking, to conduct reliable studies that could analyze such

rare instances and draw conclusions from the testing with any degree of reliability. Id. at 24–26. 22

Respondent was, in Dr. Akbari’s view, demanding certainty. Id. at 26–27.

Regarding onset and timing, Dr. Akbari proposed that Mr. Nieves’s symptoms began

within five to six days of vaccination, relying to some extent on the reports his co-experts had

provided and their review of the medical history. First Akbari Rep. at 27–29. He deemed this

consistent with “what is described in the literature,” although he primarily relied on studies

involving GBS. Id. at 27; L. Polakowsi et al., Chart-Confirmed Guillain-Barré Syndrome After

2009 H1N1 Influenza Vaccination Among the Medicare Population, 2009-2010. 178 Am. J.

Epidemiol. 6:962 (2013), filed as Ex. 25 Ref. 75 (ECF No. 68-5), at 968–69 (post-vaccination risk

highest 8–21 days post-vaccination, although risk up to six weeks/42 days was still “slightly

increased” from a standpoint of statistical significance).

Dr. Akbari particularly pointed to one study in which the majority of peripheral neuropathy

cases identified from a South Korean patient sample occurred within a week/seven days of

vaccination (comparable to Petitioner’s experience). Y. Park et al., Clinical Features of Post-

Vaccination Guillain-Barré Syndrome (GBS) in Korea, 32 J. Korean Med. Sci. 7:1154 (2017),

filed as Exhibit 25 Ref. 78 (ECF No. 68) (“Park”). Park considered post-vaccination GBS cases

submitted for compensation to the Korean Advisory Committee on Vaccination Injury

Compensation between 2002 and 2014 as part of the National Immunization Program in South

Korea. Park at 1154–55. In fact, of the 48 flu-GBS cases approved for compensation in South

Korea during that period, more than half (25) involved onset of neurological symptoms within two

period, suggesting not just that the injury is rare but that it is preponderantly unlikely. See, e.g., Pearson v. Sec'y of

Health & Hum. Servs., No. 16-9V, 2019 WL 3852633, at *14 (Fed. Cl Spec. Mstr. July 31, 2019) (giving limited

weight to Agmon-Levin in a case alleging that flu vaccine caused TM, since Agmon-Levin referenced only two post-

flu vaccine TM cases, despite the number of years of data considered).

22

It was for this reason that the IOM had (as previously referenced by Dr. Kinsbourne) been unable to confirm or

deny a vaccination link with CIDP. First Akbari Rep. at 26.

21

days of vaccination. Id. at 1155–56 and Fig. 1. Park does not, however, discuss whether that

timeframe was medically acceptable (or any other for that matter), nor does it set forth what criteria

applied in awarding injury compensation in these Korean cases. Park at 1155. Dr. Akbari deemed

reliance on GBS-specific studies reasonable, given the overlap between GBS and CIDP, and the

attendant difficulty in separating one from the other. First Akbari Rep. at 27.

Dr. Akbari’s first report also included several pages devoted to a discussion of CD4+ T

cells, or “T helper cells”—a kind of T cell understood not to directly attack foreign pathogens, but

instead to either assist with the production of antibodies by B cells or to induce inflammation

generally in the context of an infection. First Akbari Rep. at 11–13;9–21. He noted that one version

of a T helper cell (the Th17 cell) was observed in increased levels for patients with peripheral

neuropathies like CIDP, and thus likely was a factor in encouraging autoimmune disease. Id. at 11,

19–20, 21; S. Li et al., IL-17 and IL-22 in Cerebrospinal Fluid and Plasma are Elevated in

Guillain-Barré Syndrome, 2012 Mediators Inflamm. Article ID 260473 (2012), filed as Ex. 25

Ref. 57 (ECF No. 66-7) at 4 (proposing that certain cytokines associated with GBS and CIDP

likely had an association with the Th17 helper cells, especially since “GBS is classically regarded”

as being mediated in part by T helper cells).

Dr. Akbari further posited that both a wild flu infection and vaccination could

promote/upregulate this class of T cell. First Akbari Rep. at 12; Y. Lin et al., Th17 Cytokines and

Vaccine-Induced Immunity, 32 Semin. Immmunopathol. 79 (2010), filed as Ex. 25 Ref. 29 (ECF

No. 62-9) (“Lin”) at 86 (review article observing importance of Th17 T helper cells in immune

response to pathogens, and examining ways vaccines might aid their function, such as through

development of “cytokine coadjuvants”). Lin, however, does not find that vaccines cause

pathogenic increases in this class of T helper cells; instead (and at most), it discusses vaccines in

which upregulation of a specific cytokine (IL-17) is a goal of vaccination—in particular for

vaccines seeking protection against various bacteria. Lin at 80–82. And Lin considered only a

DNA version of the flu vaccine (distinguishable from the inactivated version at issue in this case)

as upregulating cytokines. Id. at 82 (Table 1) and 84.

Dr. Akbari linked this discussion to studies looking at the effects of including adjuvants in

a vaccine, like alum, and the role certain immune response pathways (the “inflammasome”) 23 play

in increasing an inflammatory milieux when stimulated by adjuvants. Akbari First Rep. at 19–20.

However, the flu vaccine (at least as administered in the U.S., and the version at issue herein) does

not contain an adjuvant—and Dr. Akbari’s discussion of this topic did not clarify why he deemed

23

I have previously discussed at length the role the inflammasome (a protein complex thought to provoke

inflammation as part of the innate/initial immune response) is theorized to play in the human immune system response.

See generally Olson v. Sec'y of Health & Hum. Servs., No. 13-439V, 2017 WL 3624085 (Fed. Cl. July 14, 2017)

(dismissal of case alleging HPV vaccine caused rheumatoid arthritis) , mot. for review den’d, 135 Fed. Cl. 670 (2017),

aff'd, 758 F. App'x 919 (Fed. Cir. 2018).

22

science positing a role for adjuvants to interfere with the immune process had anything to do with

this case.

Second Report

Dr. Akbari’s final report (at thirty pages plus references) exceeded the length of his first

report (raising the reasonable question of what he left out the first time). 24

Dr. Akbari added considerable detail to defending his contention that CIDP could be

triggered after the flu vaccine via the mechanism of molecular mimicry. After offering a caveat

that his theory could not be proven with certainty given the incomplete nature of the relevant

science on the topic, he reiterated his arguments that peptide sequences in the wild flu virus could

be recognized, due to mimicry, by T cells, disputing Dr. Tompkins’s claim that the T cells had not

been shown to be specific to the flu peptides, and stressing the reliability of these findings and

their utility in providing a means of establishing cross-reactivity potential in the context of

differing viral infections. Second Akbari Rep. at 10–11. He also defended literature involving the

animal model for central nervous system demyelinating diseases, “experimental autoimmune

encephalomyelitis,” or “EAE” 25 as a reasonable means for testing immunologic function in the

presence of demyelinating disease, noting that Dr. Tompkins had himself utilized it. Id. at 11–13.

In addition, Dr. Akbari offered some more recent literature addressing molecular mimicry

as a pathologic mechanism relevant to GBS. Second Akbari Rep. at 17–18; J. Laman et al.,

Guillain-Barré Syndrome: Expanding the Concept of Molecular Mimicry, 43 Trends in Immunol.

4:296 (2022), filed as Ex. 29 Ref. 21 (ECF No. 90-1) (“Laman”). Laman is a review article/opinion

piece embracing GBS as “the best-supported example of true molecular mimicry at the B cell

level,” and that a better understanding of the immunologic/pathogenic processes that drive it could

result it innovations in diagnostic techniques and treatment therapies “for other antibody-driven

neurological diseases.” Laman at 296. Dr. Akbari thus invoked Laman as evidence that “molecular

mimicry and structure mimicry do exist and are capable of causing . . . peripheral demyelination.”

Second Akbari Rep. at 18. However, the reliability of that contention is less in dispute herein than

whether molecular mimicry explains CIDP after vaccination—a subject Laman does not address.

In fact, Laman acknowledges that “the targets of neuropathogenic antibodies (or T cells) in patients

24

The parties (primarily due to the conduct of Petitioner and his counsel) also wasted time in the spring of 2022 with

needless motions practice about the propriety of additional expert filings, and the scope of what they would be

permitted to do. Recognizing that Petitioner should have the opportunity to rebut Dr. Tompkins’s report, I allowed the

filing of a final responsive report from Dr. Akbari. Order, dated May 23, 2022 (ECF No. 81) at 2. But I indicated (in

the hopes that the responsive report would be succinct, and not lard the record with even more secondary literature)

that the only additional articles filed should be recently-published items from 2022, that could not have been offered

before. Id. Incredibly (and part and parcel with the unnecessarily lengthy second report), Dr. Akbari identified, and

filed, nearly 20 such publications—though few (if any) reflect new discoveries about CIDP or its purported association

with the flu vaccine.

25

EAE is an animal model study allowing researchers to explore immune function in the context of an MS-like central

nervous system autoimmune disease. See Harrington v. Sec’y of Health & Hum. Servs., No. 14-43V, 2018 WL

4401976 (Fed. Cl. Spec. Mstr. Aug. 14, 2018).

23

not harboring antiganglioside antibodies” remain unknown, even for patients presenting with

demyelination (such as most CIDP patients). Laman at 305.

Another recent article revealed that “broadly reactive influenza antibodies” (some of which

could be produced in response to vaccination) “increases autoreactive antibodies . . . and induces

demyelinating diseases.” Second Akbari Rep. at 19–20; L. Labombarde et al., Induction of Broadly

Reactive Influenza Antibodies Increases Susceptibility to Autoimmunity, 38 Cell Rep. 10:1 (2022),

filed as Ex. 29 Ref. 24 (ECF No. 90-4) (“Labombarde”). Labombarde looked at this question both

via autoimmune disease experimental models like EAE (injecting the mice subjects directly with

lab-created autoreactive influenza antibodies) and by a comparison of levels of similar antibodies

in humans who had been infected by different wild virus flu strains from different seasons.

Labombarde at 4–12. Its authors did find that “the induction of autoreactive antibodies in

conjunction with broadly reactive antibodies, exacerbated autoimmunity.” Id. at 12. However,

Labombarde also forthrightly noted that this exacerbation only occurred “in the presence of

inflammation or underlying defects in tolerance,” so that “an increase in broadly reactive influenza

antibodies alone is not sufficient to induce autoimmune disease.” Id. at 13 (emphasis added).

In other words (and contrary to Dr. Akbari’s assertion), in the absence of an existing

inflammatory setting or demonstrated immune tolerance inhibition, external triggers that might

activate autoreactive immune cells were not also likely to encourage disease (or at least have not

been shown to have that capacity). Nor did Labombarde say anything about the role current

versions of the flu vaccine might play in encouraging the development of these antibodies; on the

contrary, its authors spoke on vaccination only in the context of the goal of generating a “universal

influenza vaccine” that does not yet exist. Labombarde at 13. While its authors proposed that such

a new vaccine formulation could help “generate durable, broadly reactive influenza antibodies,”

there was a danger that upregulation of these antibodies could in certain circumstances make

autoimmune disease more likely (albeit under the conditions mentioned above). Labombarde does

not conclude or propose that an inactivated form of the flu vaccine promotes disease in this manner.

Dr. Akbari also defended the amount of amino acid homology necessary for mimicry to

spark a cross-reaction, against Dr. Tompkins’s arguments. Second Akbari Rep. at 18–19.

Structural homology, he maintained, was as critical to causing a cross-reaction as sequential

similarity, and therefore rendered the latter less significant to whether an autoimmune process due

to mimicry was likely to occur. Id. at 19. But he stressed that his theory was not limited to the

concept that vaccine-induced autoimmune disease occurred as a result of molecular mimicry, but

that he also relied on “regulation of immune homeostasis”—and in particular for this case, the

failure of such regulatory processes (thereby permitting the chronic demyelination characteristic

of CIDP). Second Akbari Rep. at 13, 21. Properly-functioning immune regulation in the majority

of cases prevents cross-reactivity from causing autoimmune disease. Id. at 13–14, 20–21. But

literature offered by other experts, like Pritchard, established that patients with both GBS and

CIDP displayed decreased levels of these regulatory immune cells, and that their diminishment

likely was “a main factor resulting in a person’s predisposition to develop autoimmune disease

24

during activation of the immune system such as by receipt of a vaccine.” Id. at 15. Dr. Akbari also

offered a number of more recently-published articles about the significance of regulatory immune

cells in an environment of neuro-inflammatory diseases (although none advance the contention

that any vaccination would cause the dysregulation of such cells sufficient to trigger a peripheral

neuropathy like CIDP). Id. at 23–27 (citations omitted). 26

But Dr. Akbari admitted he could not provide “the exact mechanisms responsible for the

reduction” in regulatory cells. Second Akbari Rep. at 15. Indeed, he largely reiterated his prior

assertions that patients with demyelinating diseases often displayed high levels of T helper cells

and certain pro-inflammatory cytokines in their blood, leading to the conclusion that both played

a role in disease pathogenesis. Id. at 21–22. But he did not show that the flu vaccine pathogenically

increased these amounts, seeming instead to assume that those susceptible to disease due to

immune dysregulation specific to their host genetic variability would in turn suffer merely from

the increases in such immune cells attributable generally to vaccination. And he denied that the

flu vaccine could not cause such increases, taking issue with literature offered by Dr. Tompkins

for those points. Id. at 22–23. But in doing so, Dr. Akbari could only reference recent studies

specific to the COVID-19 vaccine (which mechanistically induces immune protection in a manner

wholly distinguishable from how the flu vaccine functions), arguing that they revealed an

association with demyelinating disease, and that the inflammatory response to vaccination was

(consistent with his theory herein) associated with the functioning of immune pathways as well as

immune system dysregulation. Id. at 27–29.

Dr. Akbari also offered a number of additional points in an effort to rebut narrower aspects

of the arguments of Respondent’s experts, but which are not central to this case’s resolution. For

example, the first five pages of his final report were devoted to casting doubt on the weight to be

given to two “low impact” 27 articles cited by Respondent’s immunologic expert, Dr. Tompkins, as

undermining a flu-CIDP association. Second Akbari Rep. at 1–5; See, e.g., S. Greene et al., Near

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

Datalink Project, 171 Am. J. Epid. 2:177 (2009), filed as Ex. D Tab 9 (ECF No. 84-9) (“Greene”)

(case-control study relying on data from patients enrolled in eight large medical care organizations,

comparing risk of adverse events (including peripheral neuropathies) for millions of flu vaccine

doses administered in three seasons between 2005 and 2008 revealed no statistically significant

26

These articles merely bulwark Dr. Akbari’s general points about the role immune regulation plays in autoimmune

disease, and therefore I do not include extensive discussion of them herein. To illustrate their less-than-ringing support

for his theory, however, I note that one such article discussed the capacity of a certain formulation of the flu vaccine

not at issue in this case to enhance vaccine immunogenicity via the T helper cell response. Second Akbari Rep. at 27;

L. Moise et al., Novel h7N9 Influenza Immunogen Design Enhances Mobilization of Seasonal Influenza T Cell Memory

in H3N2 Pre-Immune Mice, Human Vacc. & Iummunother., https://doi.org/10.1080/21645515.2022.2082191 (2022),

filed as Ex. 29, Ref. 37 (ECF No. 90-17) (“Moise”). Dr. Akbari noted only that Moise suggested that “suitable

conditions” could trigger dysregulated immune responses—and he proposed flu vaccine administration might

constitute such conditions—but Moise’s focus was on improving the efficacy of a totally different kind of flu vaccine.

27

Dr. Akbari defined this to mean the overall credibility or quality of a particular publication. Second Akbari Rep. at

2 n.2.

25

relationship). Dr. Akbari maintained that articles like Greene were biased given their

pharmaceutical industry funding, reflected design bias in the studies’ methodologies (which

resulted in larger vaccine coverage rates for the subject pools than would be seen in an unbiased,

general population study), and thus produced unreliable results that under-detected likely adverse

vaccine events. Second Akbari Rep. at 2–5. At bottom, Dr. Akbari maintained that it was

“unethical and possibly illegal” for Respondent’s experts to rely on any studies attributable to the

manufacturers of the vaccine “that caused injury in Mr. Nieves.” Id. at 6.

In addition, Dr. Akbari defended his discussion of immune pathway/inflammasome

stimulation by the flu vaccine as contributing to injury, despite Dr. Tompkins’s accurate

observation that the vaccine itself is not adjuvanted (and thus discussions of the impact of

adjuvants in stimulating that pathway were irrelevant in the context of this case). Second Akbari

Rep. at 6–9. In reaction, Dr. Akbari maintained that viral infections could themselves stimulate

these pathways, and that he never intended to refer only to adjuvants as having this potentiality.

Id. at 6–8. This stimulation would lead to the production of pro-inflammatory cytokines that could

in turn contribute to demyelinating disease, but more likely induce the class of T helper cells he

had previously identified as pathogenic. Id. at 8–9. But it is far from clear that Dr. Akbari’s

argument on this point does anything more than describe either how the immune system generally

reacts to a vaccine, or how the T helper cells he deems important to his theory arguably function

in CIDP—this aspect of his theory did not establish that the vaccine would likely trigger a

pathologic process, even if immune pathway responses bear generally on how the body responds

to vaccines and infections.

Dr. Akbari pointed as well to several recent publications specific to an entirely different

issue: whether the Epstein-Barr virus (“EBV”) is associated with MS. Second Akbari Rep. at 15–

16 (citations omitted). He maintained these new articles demonstrated that T cells (albeit not the

helper cells discussed in his theory) that recognized the EBV could also recognize influenza A

virus, and likely “may respond to several flu antigens” as well. Second Akbari Rep. at 16. As a

result, evidence about EBV’s association with MS (a form of demyelinating disease) via molecular

mimicry was relevant to this case, and pointed toward a means of understanding “the

pathophysiological roots for the induction of GBS/CIDP after exposure” to the flu vaccine. Id. Dr.

Akbari did not, however, reference a comparable study specific to the injury at issue in this case;

indeed, the mere existence of the EBV studies somewhat undermines the contention that

epidemiology of this level of reliability could not be performed for other demyelinating injuries.

Finally, Dr. Akbari again emphasized the extent to which a wild flu infection or flu vaccine

had been shown in reliable studies to correlate with an increase in the T helper cells and associated

cytokines that were connected to GBS. Second Akbari Rep. at 22–24 (references omitted). He

specifically noted a more recent study demonstrating an increase of the Il-17 cytokine after

vaccination. Id. at 23; R. Bernard-Valnet et al., Influenza Vaccination Induces Autoimmunity

Against Orexinergic Neurons in a Mouse Model for Narcolepsy, 145 Brain 2018 (2022), filed as

Ex. 29 Ref. 13 (ECF No. 90-13) (“Bernard-Valnet”). But not only does Bernard-Valnet involve a

26

completely distinguishable, nondemyelinating injury (narcolepsy) that occurs in the brain (not the

peripheral nervous system), but its observations were specific to the Pandemrix flu vaccine—a

version that is adjuvanted, that is not administered in the United States, and that was not received

by Petitioner. Bernard-Valnet at 2021. 28

B. Respondent’s Experts

1. Brian Callaghan, M.D., M.S.

Dr. Callaghan, a neurology professor with specific expertise in peripheral neuropathies like

GBS and CIDP, offered two written expert reports on behalf of Respondent. Report, dated July 24,

2021, filed as Ex. A (ECF No. 50-1) (“First Callaghan Rep.”); Report, dated April 17, 2022, filed

as Ex. C (ECF No. 74-1) (“Second Callaghan Rep.”). He disputed the accuracy of Petitioner’s

CIDP diagnosis, and secondarily denied that the flu vaccine could cause it.

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

medical degree from the University of Pennsylvania in 2004, and his Master’s in Science from the

University of Michigan in 2011. Curriculum Vitae, filed as Exhibit B (ECF No. 50-2) (“Callaghan

CV”) at 1. He is board certified in psychiatry/neurology as well as electrodiagnostic medicine.

Callaghan CV at 1. Dr. Callaghan was appointed to be a clinical lecturer at the University of

Michigan Health System's Department of Neurology in 2009 and has been an Associate Professor

of Neurology there since 2018. Id. He has published more than 100 articles and medical book

chapters, most of which focus on neuropathies, and his research interest lies in diagnostic

evaluation and testing of peripheral neuropathies. First Callaghan Rep. at 1; Callaghan CV at 2,

11–20. Dr. Callaghan reports to treat approximately 30 patients with CIDP per year. First

Callaghan Rep. at 1.

First Report

Like Dr. Kinsbourne before him, Dr. Callaghan engaged in a lengthy review of the medical

record. See generally First Callaghan Rep. at 1–3. But he noted numerous aspects of that history

that he deemed inconsistent with a CIDP diagnosis. First, he pointed to evidence that Mr. Nieves

had experienced pre-vaccination symptoms congruent with his post-vaccination condition. Id. at

3–4 (noting pre-vaccination history of radiculopathy, chronic pain, and numbness/tingling; seen

for “numb legs and falls” in December 2013, reporting symptoms for many years, and displaying

absent reflexes; seen in November 2014 for radiating neck pain plus numbness and weakness).

28

I have in prior cases discussed at great length the distinctions between Pandemrix and the attenuated/inactivated

version of the flu vaccine administered in the U.S.—including the fact that there are wild viral antigens common to

both does not mean that studies specific to Pandemrix bear on other vaccine versions. See, e.g., D'Tiole v. Sec'y of

Health & Hum. Servs., No. 15-085V, 2016 WL 7664475, at *20–21 (Fed. Cl. Spec. Mstr. Nov. 28, 2016), mot. for

review den’d, 132 Fed. Cl. 421 (2017), aff'd, 726 F. App'x 809 (Fed. Cir. 2018).

27

Second, Dr. Callaghan emphasized the changing findings over time in Petitioner’s

EMG/NCS testing results. The first post-vaccination EMG (from February 2016—and thus

performed approximately three months after onset) “revealed a generalized polyneuropathy with

predominantly demyelinating features” that Dr. Callaghan agreed was consistent with the CIDP

diagnosis. First Callaghan Rep. at 2. The next such testing did not occur until seven months later,

in September 2016—but Petitioner now showed “no evidence of demyelination or CIDP.” Id. at

3, citing Ex. 11 at 64. A third EMG/NCS testing round produced comparable negative results.

Second Callaghan Rep. at 3.

Finally, Dr. Callaghan took note of Petitioner’s overall symptoms progression. When

Petitioner first sought emergency care in November 2015, reported pain levels were high, he was

ataxic, displayed absent reflexes, and complained of ascending weakness and tingling in his limbs.

First Callaghan Rep. at 2. IVIG was started, but proved over time ineffective—and substitute

treatments for neuropathic symptoms, like oral steroids, did no better. Id. By February 2016,

Petitioner was not displaying much weakness as opposed to pain, and other symptoms (specific to

the cervical or lumbar spine) continued to present that could not be deemed associated with CIDP.

Id. In the spring of 2016, IVIG’s only half-ameliorative nature was again observed, and while

Petitioner did display some symptoms comparable to what he had in the past, he also displayed

giveaway weakness. Id. at 3.

By the early fall of 2016, however (now nearly one year since the vaccination at issue), it

seemed more evident to treaters that IVIG was not helping ameliorate Petitioner’s symptoms. First

Callaghan Rep. at 3. In addition, he now displayed normal strength, reflexes, and sensation. Id. By

the end of the year, IVIG was discontinued, and Petitioner’s symptoms were more oriented to

lower back pain radiating into his legs plus cramps and spasms, with neurology treaters

recommending treatment for “symptoms related to fibromyalgia.” Id. As of a neurologic visit in

August 2019, it appeared treaters had begun to lean against CIDP as a diagnosis. Id., citing Ex. 14

at 1.

From the foregoing, Dr. Callaghan opined that Petitioner’s CIDP diagnosis was more likely

than not inapt. First Callaghan Rep. at 4–5. Mr. Nieves had experienced a host of pre-vaccination

symptoms that seemed consistent with what he displayed after vaccination. Id. at 4. The kinds of

treatments commonly employed for CIDP (or GBS for that matter), like IVIG and steroids, did not

prove effective. Id. at 4–5. EMG tests were only confirmatory for a neuropathy at the outset of his

illness, with follow-up testing not revealing the existence of a chronic demyelinating condition. In

addition, Petitioner’s exams revealed other “atypical features” like giveaway weakness, “spasms

that appeared more voluntary or functional,” unreasonable sensitivity to touch, and sensory issues

at the thoracic spinal cord level inconsistent with CIDP, not to mention many other distinguishable

symptoms. Id. at 4–5.

In Dr. Callaghan’s view, these factors (plus the record history of neurologists coming to

doubt the diagnosis) all undermined the CIDP diagnosis. First Callaghan Rep. at 5. In so opining,

28

he noted that even if Dr. Kinsbourne had offered literature descriptions of “atypical presentations

of CIDP,” he had not adequately defended the possibility that so many “atypical presentations

occurring together” in the instance of Petitioner’s medical history could still meet the diagnostic

criteria. Id. In fact, CIDP was frequently misdiagnosed. J. Allen and R. Lewis, CIDP Diagnostic

Pitfalls and Perception of Treatment Benefit, 85 Neurol. 498 (2015), filed as Ex. A Tab 3 (ECF

No. 51-3) (diagnostic criteria often not met, patients frequently reported improvement from

immunotherapy regardless of accuracy of diagnosis, and electrophysiologic evidence often

reviewed with liberal eye favoring diagnosis).

In addition to the foregoing, Dr. Callaghan offered an opinion on causation (although, and

as with Dr. Kinsbourne, it somewhat exceeded his otherwise-demonstrated neurologic expertise).

He noted that Dr. Kinsbourne relied heavily for this aspect of his opinion on “case reports and

series”—a kind of evidence Dr. Callaghan deemed to provide little value on the question of

causation, especially because case reports mostly only demonstrated a temporal relationship with

the vaccination and alleged injury. First Callaghan Rep. at 5. The survey studies Dr. Kinsbourne

offered only showed low percentages of post-vaccination CIDP (and in small sample groups as

well), and were of limited significance otherwise, as their authors admitted. Id. at 5–6.

By contrast, Dr. Callaghan pointed to what he deemed “the best study investigating

antecedent events,” Doneddu I, which he noted did not support a causal association. First

Callaghan Rep. at 6; Doneddu I at 3, 6 (only seven out of 411 CIDP patients (1.5 percent) in survey

reported receipt of vaccine (all flu vaccine) before onset, suggesting a causal relationship was

unlikely). Another review article discussing CIDP generally noted that although its pathogenesis

was thought to feature a synergistic interaction between the initial/innate “humoral” immune

response and the subsequent “cell-mediated” response, little was known about triggers, with “no

infectious agent” linked consistently to the disease’s start. E. Mathey et al., Chronic Inflammatory

Demyelinating Polyradiculopathy, 0 J. Neurol. Neurosurg. Psych. 1 (2015), filed as Ex. A Tab 1

(ECF No. 51-1) (“Mathey”), at 3.

The purported mechanistic and pathologic congruence between CIDP and GBS was also,

in Dr. Callaghan’s view, far less certain than Dr. Kinsbourne argued. He noted, for example, that

literature suggested CIDP actually occurred less often after antecedent infection or trauma (in

comparison to GBS), thus diminishing the likelihood that it occurred via molecular mimicry (as

was more generally understood to occur with GBS). First Callaghan Rep. at 6; E. Ubogu,

Inflammatory Neuropathies: Pathology, Molecular Markers and Targets for Specific Therapeutic

Intervention, 130 Acra Neuropathol. 4:445, filed as Ex. A Tab 5 (ECF No. 51-5) (“Ubogu”) at 15.

Ubogu also noted that “[a]ntibodies against peripheral nerve myelin proteins or node of Ranvier

components are too infrequently detected in the sera of CIDP patients to be considered pathogenic

or molecular markers of disease,” and the same was true for “[a]ntibodies against complex

gangliosides.” Id. at 15. The two conditions also likely had distinguishable pathogenic courses,

since “compromised immune tolerance” or immune regulatory dysfunction was relevant to CIDP’s

chronicity. Id. Indeed, Dr. Kinsbourne’s observations about the host variances in T cell apoptosis

29

that likely contributed to CIDP underscored their distinction. And literature identifying antibodies

against myelin surface gangliosides as driving GBS did not similarly propose that CIDP was

mediated in this fashion. First Callaghan Rep. at 6. 29

Dr. Callaghan also commented on questions raised within the medical records about

Petitioner’s onset. Although Petitioner’s history seemed to differentiate the initial symptoms

Petitioner reported close-in-time to vaccination from his later neurologic symptoms, Dr. Callaghan

did take note that at the time of Petitioner’s November 3rd ER visit, he specifically reported a week

of paresthesias—and obtained at that time a neurology consultation as well—suggesting that

neurologic symptoms had occurred far closer in time to vaccination than Dr. Kinsbourne allowed.

First Callaghan Rep. at 1. Yet Dr. Callaghan also stressed the degree to which Petitioner’s pre-

existing comorbidities explained his post-vaccination symptoms. Id. at 4–5. As a result (and in

keeping with his view overall that Petitioner was improperly diagnosed with CIDP), Dr. Callaghan

did not directly opine on when Petitioner’s arguably-neurologic symptoms likely first manifested.

Second Report

Dr. Callaghan’s second report reacted to the supplemental reports filed by Petitioner’s two

neurologic experts (Drs. Jeret and Kinsbourne). Beginning with the former, he noted that he had

been unable to review the precise EMG/NCS findings from Petitioner’s February 2016 testing,

making it difficult for him to comment specifically on whether contemporaneous interpretations

of them were accurate, or what they otherwise revealed. But even to the extent the first post-

vaccination electromyographic testing confirmed the CIDP diagnosis, the other studies did not—

and Petitioner’s experts had failed to persuasively explain why this was the case, even though

Petitioner’s recovery remained incomplete at these later times. Second Callaghan Rep. at 1.

Dr. Callaghan also commented on assertions about the Petitioner’s “atypical” form of

CIDP—noting that even if some patients did not meet all clinical criteria, “the vast majority do,”

and thus those criteria had value in weighing if Petitioner’s presentation was actually consistent

with CIDP. Second Callaghan Rep. at 1. Here, the combination of Petitioner’s consistently atypical

presentation, plus his many “incompatible” symptoms (which in general predated vaccination or

were not specific to CIDP), all added up, in Dr. Callaghan’s estimation, to an individual who had

not likely been properly diagnosed with CIDP. Id. at 1–2. As further support for this opinion, Dr.

Callaghan reiterated his prior observations that Mr. Nieves had not responded favorably to

polyneuropathy-specific treatments like IVIG, that the EMG/NCS testing performed after

February 2016 was inconsistent with the diagnosis, and that the record revealed treater doubt about

the accuracy of CIDP later in the course of Petitioner’s illness. Id. at 2. He rejected Dr. Jeret’s

29

I also note that both sides discussed whether a section of the Institute of Medicine’s Report on vaccine causation of

CIDP after the flu vaccine supported, or contradicted, causation. See First Kinsbourne Rep. at 9; First Callaghan Rep.

at 6; K. Stratton et al., Adverse Effects of Vaccine: Evidence and Causality, Institute of Medicine, National Academies

(2012), filed as Ex. 23 Ref. 28 (ECF No. 58-8) (the “IOM Report”). In this case, however, I find the IOM Report to

be too equivocal in its conclusions specific to this case to meaningfully “move the needle” on the causation question—

in either direction.

30

proposal that the subsequent negative EMG testing results reflected the success of IVIG treatment,

observing that the tests occurred “because [Petitioner] was not doing well with persistent

symptoms.” Id. at 3 (emphasis added).

In addition, Dr. Callaghan stressed his prior assertion that CIDP was not the same as GBS,

even if the two could appear similar at the outset and thus be difficult initially to distinguish, since

both ultimately had “different pathophysiologies.” Second Callaghan Rep. at 2. He again noted

that literature observed that CIDP was far less associated with antecedent infection, and that the

anti-ganglioside target believed integral to GBS’s autoimmune course had no analogue in the

context of CIDP. Id. at 2–3. And he took issue with Dr. Kinsbourne’s conception of CIDP and

GBS as being triggered in the same way (and thus “indistinguishable at onset”), but then diverging

mainly because of host genetic variability, emphasizing his own view that they were ultimately

not “the same disease.” Id. at 3.

Dr. Callaghan identified his own contemporaneous literature that he maintained did not

support a CIDP-vaccine association. Second Callaghan Rep. at 2; H. Köller et al., Chronic

Inflammatory Demyelinating Polyradiculopathy, 352 N. Engl. J. Med. 1343 (2005), filed as Ex. C

Tab 1 (ECF No. 74-2) (“Köller”); J-M. Vallat et al., Chronic Inflammatory Demyelinating

Polyradiculopathy: Diagnostic and Therapeutic Challenges for a Treatable Condition, 9 Lancet

Neurol. 402 (2010), filed as Ex. C Tab 2 (ECF No, 74-3) (“Vallat”). Neither article makes such an

affirmative representation, however, although both cast doubt on aspects of Petitioner’s theory

concurrent with Dr. Callaghan’ arguments. See, e.g., Köller at 1348 (noting that little is known

about “antigen specificity” driving CIDP). Vallat does not discuss vaccine causality either, but

mentions that “by contrast with GBS, a single triggering antigen has not yet been found” for CIDP.

Vallat at 402. 30

In addition, Dr. Callaghan criticized the extent to which Petitioner’s experts mostly looked

to case reports—“valuable tools in flagging areas for future study,” he agreed, but inadequate

otherwise to establish causation. Second Callaghan Rep. at 3. Dr. Callaghan also defended his

invocation of Doneddu I as unsupportive of causation, deeming it “The best study on the subject”

despite limitations, and reiterating that it revealed a very low-positive association with vaccination

and CIDP in comparison to other antecedent occurrences. Doneddu I at 3. Petitioner’s experts

ultimately admitted that they could do no better than point to case reports—underscoring, in Dr.

Callaghan’s opinion, the lack of vaccine association (since no more reliable scientific studies had

yet been produced).

30

Köller, however, does acknowledge the possibility that in rare circumstances molecular mimicry between

gangliosides and antigenic mimics could explain CIDP’s pathogenesis, although its authors limited that to the context

where the CIDP patient was shown to have been infected with the Campylobacter jejuni bacteria known already to

trigger some forms of GBS via this process. Köller at 1351. It is undisputed that the flu vaccine does not contain any

aspects of C. jejuni.

31

2. S. Mark Tompkins, PhD.

Dr. Tompkins acted as Respondent’s primary expert on immunologic issues raised in this

case, and prepared a single written report. Report, dated June 1, 2022, filed as Ex. D (ECF No. 83-

1) (“Tompkins Rep.”). He maintained the flu vaccine had not been reliably shown to be causal of

CIDP.

Dr. Tompkins received his B.S. in Microbiology at the University of Illinois in 1990, and

his Ph.D. in Immunology and Molecular Pathogenesis at Emory University in 1997. Curriculum

Vitae, filed as Ex. E (ECF No. 83-2) (“Tompkins CV”) at 1. Dr. Tompkins then completed post-

doctoral training in Immunology at Northwestern University in Chicago and later in

Virology/Immunology at CBER/FDA in Bethesda, Maryland. Id.; Tompkins First Rep. at 1. He

has held several academic positions since 2005. Tompkins CV at 2. Currently, Dr. Tompkins is a

Professor of Infectious Diseases in the Center for Vaccines and Immunology at the College of

Veterinary Medicine, University of Georgia, where he teaches graduate students immunology and

virology, as well as train pre- and post-doctoral fellows in his laboratory. Id.; Tompkins First Rep.

at 1. In addition, Dr. Tompkins has co-authored approximately more than 100 peer-reviewed

papers and book chapters in the fields of immunology and virology. Id.

Like the other experts in this case, Dr. Tompkins included in his report an evaluation of

Petitioner’s medical history before turning to his actual opinion. Tompkins Rep. at 1–2. Given his

admitted lack of clinical or neurologic-specific expertise, Dr. Tompkins did not offer an opinion

on diagnosis, but instead focused almost wholly on causation. Id. at 2. Overall, he disputed that a

theory relying on molecular mimicry could explain how the flu vaccine would cause CIDP, as

embraced by Drs. Kinsbourne and Jeret, or that a combination of mechanisms amounting to a

“dysregulated immune response” (increases in pro-inflammatory T-helper cells plus imbalances

in the protections usually provided by regulating immune cells), as proposed by Dr. Akbari, would

produce the same pathogenic result. Id. at 3.

First, Dr. Tompkins denied that Petitioner’s experts had offered any general reliable

evidence connecting the inactivated/unadjuvanted version of the flu vaccine (the one at issue in

this case) 31 and CIDP. Tompkins Rep. at 3–5. One article relied upon for such an association was

subject to reporting bias (since it employed patient reports of post-vaccination CIDP for proof

rather than independent evidence (see generally Kuitwaard), while another involved merely two

patients out of 46 as experiencing even arguably-associated flu vaccine-induced relapses. See, e.g.,

Pritchard at 348.

31

Dr. Tompkins also included in his report a section discussing Dr. Akbari’s argument about vaccine immune pathway

stimulation attributable to vaccine adjuvants, noting (as I have already observed) that the flu vaccine contains no

adjuvant. Tompkins Rep. at 8.

32

Case reports were also in Dr. Tompkins’s estimation weak proof of causation, since they

only established temporal associations. Tompkins Rep. at 3–4. An article like Agmon-Levin

(which did not even focus on CIDP) required a 40-year review of literature—and even then could

identify only 37 instances of temporal associations between autoimmune injuries and vaccination,

underscoring the unlikely nature of a causal connection. Id. at 4; Agmon-Levin at 1199, 1202. And

Dr. Tompkins deemed the recommendation of the “GBS/CIDP Organization” not to obtain a

vaccine after incurring (purportedly) vaccine-caused disease to be not only lacking in scientific

substantiation, but contradicted by other recent publications revealing a consensus among

neurologists that vaccination was not likely to be harmful. See, e.g., B. Roy et al., Influenza

Vaccination in Autoimmune Neuromuscular Diseases: A Survey of Current Practices and

Perceptions, 63 Muscle & Nerve 918 (2021), filed as Ex. D Tab 2 (ECF No. 84-2) “(Roy”). Roy

(relying on questionnaires, as with Kuitwaard) found that 60 to 66.7 percent of surveyed neurology

practitioner specialists treating CIDP and other peripheral neuropathies recommended the flu

vaccine to any patient without regard for the possibility of an adverse impact. Roy at 920. By

contrast, broader evaluations of more than four million flu vaccine doses for adverse events,

including CIDP, found no increased risk. See generally Greene.

Second, Dr. Tompkins questioned the reliability of Dr. Akbari’s view that the flu vaccine

could somehow cause autoreactive T cells to spark an autoimmune attack resulting in CIDP.

Tompkins Rep. at 4–6. He noted that to support this contention, Dr. Akbari invoked in vitro studies

involving MS to show homology between wild flu peptides and T helper cells, and that the process

of demonstrating the homologies was the result of an experimentally-driven “artificial selection

process,” rather than reflecting what was likely to happen in vivo, and/or in response to the vaccine

itself. Id. at 4; see generally Markovic-Plese. It could not be assumed any cross-reactivity was

disease-causing due to myelin destruction, even if homology could be demonstrated. Tompkins

Rep. at 6. Moreover, the specificity of these T cells to the flu peptide was uncertain, since the

studies showed they responded to many other different viruses. Tompkins Rep. at 4; Markovic-

Plese at 35 Table 2. The “diversity in influenza hemagglutinin sequences” of amino acids meant

that consistent homology with vaccine components could often not be demonstrated, despite the

experimental results of studies like Markovic-Plese. Tompkins Rep. at 5,6. 32

32

Dr. Tompkins also leveled a common criticism about literature offered by petitioners involving EAE. As he

observed, EAE utilizes a particularly strong kind of adjuvant to elicit disease far in excess of what a normal vaccine

would contain (and of course the flu vaccine has no adjuvant as already observed). Tompkins Rep. at 6. But this means

that not only does the EAE model directly create “extreme inflammatory responses,” but also permits the animal

immune system to encounter far greater numbers of antigenic peptide sequences, greatly increasing the likelihood of

a mimic and/or cross reaction. Id.

I do not deem EAE studies per se underserving of weight simply because they involve a model that exaggerates

circumstances for purposes of research. EAE is, after all, designed specifically to permit scientists to model an

inflammatory autoimmune context in order to test various hypotheses, and the findings it can derive have significance

even if obtained in an intentionally-experimental context. However, Dr. Tompkins’s criticisms illuminate why their

findings are not wholly comparable to what would be experienced after vaccination.

33

Dr. Tompkins also observed that as a general matter, sequential homology was common in

nature, but alone could not establish a likelihood for cross-reactivity leading to disease. Tompkins

Rep. at 6. In fact, because it was not all that challenging for researchers to demonstrate the

potentiality for molecular mimicry as a foundational mechanism for cross-reactivity, the real

question was why autoimmunity did not regularly occur—and produce disease. Tompkins Rep. at

6; C. Benoist and D. Mathis, Autoimmunity Provoked by Infection: How Good is the Case for T

Cell Epitope Mimicry? 2 Nat. Immunol. 9:797 (2001), filed as Ex. D Tab 4 (ECF No. 84-4)

(“Benoist”). Benoist, a review article discussing two commonly-cited examples 33 of mimicry as

the driver of autoimmune diseases, aimed to highlight the inherent contradiction between the

putative occurrence of disease proceeding via this mechanism and the fact that the autoreactive T

cells that would drive the disease process “remain innocuous unless somehow activated.” Benoist

at 797. After discussing the case for mimicry as pathogenically-determinative in both instances,

and giving due regard to the evidence favoring the contention, Benoist nevertheless concluded that

“the case is not yet convincing enough to espouse,” and that the ease with which mimics could be

identified only complicated the process of weighing if in fact mimicry was to blame. Id. at 800.

Third, Dr. Tompkins disputed the strength of Dr. Akbari’s argument that the flu vaccine

could cause the upregulation of purportedly-pathogenic T helper cells, and/or create an

inflammatory setting (due to cytokine increases) conducive for autoimmune disease. Tompkins

Rep. at 7. Authority offered to support the latter point came from a study involving a wild flu virus

infection—a context distinguishable from vaccination, since the infectious process would be far

more widespread in the human body, and thereby implicate far more of an innate response (during

which time cytokines would be greatly increased). J. Bermejo-Martin et al., Th1 and Th17

Hypercytokinemia as Early Host Response Signature in Severe Pandemic Influenza, 13 Critical

Care 6:1 (2009), filed as Ex. 25 Ref. 28 (ECF No. 62-8) (“Bermejo-Martin”). Bermejo-Martin

looked at levels of cytokines in the blood sera of 35 patients suffering from mild as well as severe

H1N1 wild-virus-infected patients, finding that the severely-ill patients displayed cytokines

associated with TH17 helper cells “commonly linked to the pathogenesis of

autoimmune/inflammatory diseases,” although its authors could not identify the “exact role” these

T helper cells played—including whether they were “detrimental or beneficial.” Bermejo-Martin

at 2. Thus, Bermejo-Martin arguably undercuts the conclusion that the T helper cells highlighted

by Dr. Akbari are necessarily pathogenic (while not supportive of the contention that vaccination

stimulates them in the first place).

Dr. Tompkins detected no support from other items of literature offered by Dr. Akbari for

the concept that the flu vaccine could trigger a response from pathogenic T helper cells. Lin, for

example, only discussed such a potentiality in the context of an “experimental DNA vaccine” that

in turn caused upregulation of cytokines specific to a kind of T helper cell (and in turn suggested

33

One involved Lyme arthritis (in which the inflammatory process continues even after eradication/elimination of the

underlying Lyme tick-borne bacterium), and the other a herpes virus-caused corneal inflammation. Benoist at 798–

800.

34

that these T cells could be beneficial in future iterations of the flu vaccine). Lin at 80–82. A more

recent study actually revealed that a different version of the flu vaccine intended to possess greater

immunogenicity only increased some cytokine levels but not others, and that “the proportion of

specific cytokine-secreting cells [the T helper cells] did not change post-vaccination.” Tompkins

Rep. at 7; D. Skribinski et al., Induction of Human T-cell and Cytokine Responses Following

Vaccination with a Novel Influenza Vaccine, 8 Sci. Rep. 18007:1 (2018), filed as Ex. D Tab 5

(ECF No. 84-5) (“Skribinski”), at 2. The current inactivated version of the vaccine, by contrast

(and the one at issue in this case) was deemed by Skribinski to be “poor at eliciting [T helper cell]

responses.” Id.

Fourth, Dr. Tompkins maintained that the flu vaccine did not likely result in

“dysregulation” of certain immune cells, like T effector cells, thought to contribute to autoimmune

processes when their moderating function is inhibited. Tompkins Rep. at 7–8. He noted that Dr.

Akbari relied in part for this contention on evidence that CIDP symptoms had in certain articles

been reported to recur after vaccination—but the literature invoked, like Kuitwaard, involved self-

reporting of symptoms but with no meaningfully-increased evidence of risk. Kuitwaard at 311–

13. Dr. Akbari had also offered an item of literature, Herrero-Fernandez, involving an elderly

cohort’s inhibited immune response as evidencing dysfunction by the regulating immune cells, but

the authors had actually observed “no statistically significant differences between vaccine

responders and non-responders” post-vaccination. Tompkins Rep. at 7; Herrero-Fernandez at 2.

And regardless, this latter point did not support the conclusion that the flu vaccine could cause

immune regulatory cell dysfunction sufficient to result in CIDP—only that “Treg cells have a role

in maintaining peripheral tolerance and can influence induction and recall of adaptive immune

responses.” Tompkins Rep. at 7–8.

Dr. Tompkins concluded by considering the question of Petitioner’s post-vaccination onset

timeframe from the standpoint of how long an immunologic process would take to unfold.

Tompkins Rep. at 8. The Petitioner, he noted, had in witness statements identified an onset no later

than the evening of October 31st, or a little more than three days post-vaccination. See Ex 19 at 2.

But (and referencing the IOM Report), Dr. Tompkins maintained that antibody response to

vaccination would occur no sooner than 7-10 days post-vaccination, and perhaps within three to

five days if the response was hastened due to recall from a prior exposure. IOM Report at 58. Even

if the shorter timeframe was applicable, Dr. Tompkins deemed three days too fast for a pathogenic

T helper cell-driven reaction sufficient to “elicit clinical signs” (which here were what led

Petitioner to seek medical treatment). Tompkins Rep. at 8. Even under a study creating

experimental “optimal conditions used to elicit autoimmune disease” (the aforementioned EAE

model) and involving the “passive transfer” of pathogenic T helper cells in an animal model, ten

days passed before disease was elicited. Id.; I. Stromnes & J. Goverman, Passive Induction of

Experimental Allergic Encephalomyelitis, 1 Nat. Protocols 4:1952, filed as Ex. D Tab 8 (ECF No.

84-8) (“Stromnes & Goverman”) at 1958. Such a timeframe did not match Petitioner’s

35

circumstances—and since the flu vaccine he received did not contain an adjuvant, it was likely a

disease process would take even longer to manifest in symptoms. Tompkins Rep. at 8.

III. Procedural History

As noted above, this case was initiated in October 2018, and it was originally assigned to

a different special master. After Respondent indicated his intent to contest entitlement, Petitioner

filed Dr. Kinsbourne’s first report. The parties were subsequently ordered to brief the disputed

issue of onset, since it was relevant to whether a viable flu vaccine-GBS claim had been presented.

See Order, May 1, 2020 (ECF No. 30). While such filings were pending, this case was reassigned

to me. See Docket Entry, July 20, 2020 (ECF No. 32).

Once that matter was briefed, I determined that no Table claim was tenable because of the

CIDP diagnosis, and ordered such a claim dismissed in January 2021. ECF No. 42. However, I

also observed that a causation-in-fact claim alleging that the flu vaccine had caused CIDP

remained, and to that end the parties filed additional expert support and literature. They later

briefed their respective positions, based on my determination that a ruling on the record was an

appropriate means for deciding the case. Scheduling Order, dated December 28, 2021 (ECF No.

63). Both sides have filed their briefs, and the matter is ripe for resolution. Petitioner’s

Memorandum, dated April 1, 2022 (ECF No. 73) (“Mot.”); Respondent’s Memorandum, dated

June 6, 2022 (ECF No. 85) (“Opp.”); Petitioner’s Reply, dated August 31, 2022 (ECF No. 92)

(“Reply”).

IV. Parties’ Arguments

A. Petitioner

1. Initial Memorandum — Petitioner’s brief addresses both the disputed

diagnosis and the causation prongs set forth under Althen v. Sec'y of Health & Hum. Servs., 418

F.3d 1274 (Fed. Cir. 2005). In support of his contention that he was properly diagnosed with CIDP,

he notes that both of his neurologic experts concur with the diagnosis, and that his initial

presentation and February 2016 EMG/NCS results are all consistent with the conclusion that he

experienced an acute form of CIDP, presenting much like GBS at first glance. Mot. at 1–3. Its

acute onset did not preclude it from being considered CIDP, especially in light of Petitioner’s

subsequent course. Id. at 2. And Petitioner’s contemporaneous treaters all agreed on the diagnosis

as well. Id. at 2.

Regarding the first Althen prong, Petitioner breaks down his causation theory into the

following components: (1) the immune cells in CIDP and GBS are comparable or have similar

functions in driving the respective diseases; (2) certain T helper cells secret cytokines involved in

demyelination, and those cytokines are increased by the flu vaccine; (3) immune pathway

complexes a/k/a the “inflammasome” are also involved (although Petitioner again spoke of its

36

stimulation by adjuvants not included in the relevant version of the flu vaccine); 34 and (4)

autoreactive T cells get stimulated due to sequential and structural homology between a protein

component of the vaccine and myelin antigens. Mot. at 5–7. He also maintained that CIDP’s

chronic features was attributable to a secondary failure of immune regulatory cells independent of

the initial autoimmune process. Id. at 7–8.

Petitioner added that he was not in this case arguing for a cytokine-driven pathogenic

process. Mot. at 20. In addition (and in an effort to address points I have made in prior cases), 35 he

stressed that he was not simply maintaining that the science applicable to the flu-GBS relationship

applied (although he nevertheless maintained that the fact that this case involves the flu vaccine

means “there will be a stronger case for the concept that the influenza vaccination is capable in

general of causing demyelinating neuropathies”). Mot. at 4.

The “can cause” prong, Petitioner maintained, was also satisfied. Treaters not only

confirmed the CIDP diagnosis but ruled out other explanations (although Petitioner identified no

record instances in which vaccine causation was proposed or considered). Mot. at 24–25. He also

noted that experts like Dr. Jeret had rebutted the possibility of a fibromyalgia diagnosis, observing

that it seemed to be mentioned/repeated in the record mainly as an artifact of computer records-

keeping. Id. at 25. Otherwise, Petitioner reiterated support for the diagnosis discussed previously

in the brief.

The timeframe of Petitioner’s onset was, he maintained, medically acceptable in

relationship to his vaccination date. Mot. at 3–4, 25–27. He noted that Dr. Kinsbourne proposed a

five-day onset (or November 2, 2015), relying on his outline of Petitioner’s initial course, and

differentiating Mr. Nieves’s malaise-like symptoms (which were not deemed related) from what

came later. Id. at 25–26. At the same time, however (and reflecting the confusion on the issue that

the two neurologic/diagnostic reports submitted by Petitioner reveal), Petitioner contended that the

first “objective manifestation of polyneuropathy” did not occur until November 10, 2015—twelve

days post-vaccination, but still “a reasonable time interval” (and adding that five or twelve days

was medically acceptable under his theory). Id. at 26. He also maintained that because his own

“oral history” (which places onset either before or very close in time to vaccination) was

inconsistent with the records, the latter deserve more weight in this case. Id. at 26–27.

Petitioner also endeavored to address some of the cases likely relevant to this one, plus a

number of items of literature filed by both sides. See generally Mot. at 2–5, 8–24. I do not

34

See, e.g., Mot. at 6–7 (“there is a domino effect from aluminum adjuvants to inflammasome and cytokines in the IL

family which enhance the amplification of Th17 cells . . . and upset the ratio of Treg / Teffector cells leading to CIDP”)

(emphasis added). Indeed, Petitioner’s initial memorandum goes on to note all of the literature supporting the effect

of the non-included aluminum adjuvant. Id. at 17–20.

35

Houston v. Sec’y of Health & Hum. Servs., No. 18-420V, 2021 WL 4259012, at *16–17 (Fed. Cl. Spec. Mstr. 2021).

37

summarize the arguments based on these references, however, since they often amount simply to

reiterating what an item of literature said.

2. Reply — Petitioner offered a “reply” that was inexplicably longer than his

initial brief (and far longer than a reply should ever be). See generally Reply. He stressed again

that the CIDP diagnosis had preponderant support, noting the credentials of his experts to interpret

EMG findings, that the primary diagnostic criteria for CIDP were met, and that ample medical

record support established “hard findings” in support of the diagnosis. Reply at 1–6.

Petitioner also addressed (again) the Althen prongs and his success in meeting them. See

generally Reply at 16–33. In defending against the assertion that Petitioner had not shown that the

flu vaccine could cause T helper cells to release certain cytokines implicated in CIDP, he

complained that Dr. Akbari had (by my order) been limited to 2022 literature (begging the question

of why Dr. Akbari’s first report—which was under no such limitation—did not address this critical

causation issue in that 30-plus page report—which was then under no such filing constraint). 36 Id.

at 18. But he maintained that items like Lin, or articles on a different version of the vaccine

(involving a strain common to the trivalent vaccine, but which is adjuvanted), confirmed the

vaccine’s stimulatory capacity. Id. at 19–20.

Petitioner further clarified that his theory is not that the flu vaccine “dysregulates” the

immune regulatory system, but instead that it impacts the “balance” of these cells (a distinction

without a difference to no small extent). Id. at 21. He again referenced Bernard-Valnet, although

(as his extensive discussion reveals) the article involved not only a different condition

(narcolepsy), but an H1N1-specific version of the vaccine different from that at issue in this case.

Id. at 22–23. He again reviewed the purported impact of the flu vaccine on the immune pathways,

arguing that “still holds true” despite the fact that the vaccine lacks an adjuvant, repeating his

complaint about the unfairness of literature limits (and ignoring the fact that perhaps Petitioner

should have known the relevant vaccine lacked an adjuvant before Dr. Akbari advanced arguments

depending on the adjuvant effect). Id. at 23–26. And he maintained that the vaccine could via

molecular mimicry stimulate autoreactive T cells, even going so far as to repeat a chart contained

in Dr. Akbari’s supplemental report to show the process. Id. at 28. He further cited the recent

studies on the EBV association with MS as indirect proof of how autoreactive T cells could be

stimulated. Id. at 29–30.

36

Petitioner grossly misconstrues the context in which “limitations” on his use of literature were placed. As the docket

indicates, I became concerned in 2022 that the filings in this case were starting to exceed reasonable amounts; indeed,

Dr. Akbari alone offered 78 individual items of literature in support of his first report. I therefore warned Petitioner

that any “supplemental” report from Dr. Akbari needed to avoided adding even more articles “to the pile” for the sake

of a large record, but be concise and specific to anything Dr. Tompkins prepared. See Order, dated May 23, 2022 (ECF

No. 81). Instead, Dr. Akbari coupled his excessively long responsive report with 20 “recent” items of literature—few,

if any, of which are all that specific to the vaccine’s propensity to injure.

38

Regarding timeframe, Petitioner urges that more weight be given to medical record

evidence (and in particular to the views of treaters as to when “objective” proof of neurologic

symptoms were apparent to them) than to Petitioner’s affidavit and contemporaneous statements

about his symptoms (although he does not explain why in this case the latter are untrustworthy).

Reply at 6–7. Here, “true evidence of peripheral neuropathy” is not found before November 10,

2015 (based on the conclusions at that time of examining neurologists), and this accordingly

represents the correct onset. Id. at 7.

Other points previously asserted in Petitioner’s initial brief were given a more expansive

discussion or amplified. For example, Petitioner argued that epidemiologic evidence simply was

insufficiently powered to detect the rare event of a vaccine injury—and evidence Respondent

offered was either unreliable (Doneddu I) or outweighed by Petitioner’s evidence (Rajbally,

Kuitwaard, and the case report evidence cited). Reply at 8–9. He re-emphasized his claim that even

if GBS and CIDP were in some respects distinguishable, they could have the same etiologic trigger.

Id. at 10–13. In so arguing, he strained to highlight the similarities between the two, and (like many

other claimants before) seemed to view CIDP’s chronicity as not a meaningful distinction. Id. at

14 (“[o]utside of the time course, GBS and CIDP are similar”), 15–16. He deemed Respondent

responsible for proving GBS and CIDP cannot have the same trigger (as opposed to his burden to

prove the vaccine was the trigger). Id. at 16.

B. Respondent

Respondent contests both the propriety of the CIDP diagnosis as well as Petitioner’s

success in satisfying the Althen prongs. Regarding the former issue, Respondent underscored Dr.

Callaghan’s opinion that Petitioner likely “never had CIDP,” given that (1) IVIG did not appear

overall to have been effective, (2) the diagnosis found less support over time (and particularly by

late 2016); (3) EMG testing after the first (admittedly confirmatory) results in February 2016 did

not support the diagnosis; and (4) Petitioner’s overall complex presentation and history of

comorbidities went beyond the concept of “atypical” CIDP. Opp. at 16–17

Petitioner’s causation theory was also inadequately substantiated, Respondent argued.

Despite Petitioner’s protestations to the contrary, his theory was heavily based on molecular

mimicry as the pathogenic mechanism—but it had not been linked with enough specificity to the

circumstances of this case. Opp. at 17–18. Thus, it was speculative to assume the flu vaccine’s

propensity to increase cytokines (at least during the innate immune response) was pathogenic, and

not otherwise shown to make a cross-attack due to mimicry more likely. Id. at 18–19. Indeed, the

presence of specific cytokines or T helper cells in the context of CIDP did not mean they were

initially causal of the disease due to vaccination. Id. at 19. And arguments about stimulation of the

immune pathways were dependent on the presence of adjuvants that are not found in the flu

vaccine. Id. at 19.

39

Respondent, however, had offered reasonable and reliable epidemiologic studies

undercutting any association between the flu vaccine and CIDP. Opp. at 19–20, discussing

Doneddu, Ubogu, and Mathey. And case report evidence filed by Petitioner was unworthy of

significant weight, as recognized in prior Program decisions. Id. at 20.

The second Althen prong was also unmet in Respondent’s estimation. Because CIDP has

no known “prodrome ‘triggers’” it was speculative to deem the vaccination preceding it in this

case causal. Opp. at 21. The record contained no instances of treaters associating the vaccine with

Petitioner’s CIDP. Id. at 22. And the onset timeframe was not medically acceptable. Even if

Petitioner’s immediate malaise-like post-vaccination reaction was unrelated, Petitioner began

displaying arguably-neurologic symptoms close-in-time nevertheless, as he contemporaneously

reported to treaters. Id. at 22–23. And his own affidavit identified onset as late on October 31st—

three days post-vaccination. Id. at 23. Dr. Tompkins had deemed such a timeframe far too soon for

an immune response reliant on the adaptive, secondary generation of antibodies and immune cells

to occur. Id.

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 v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1321 (Fed.

Cir. 2010); Capizzano v. Sec’y of Health & Hum. Servs., 440 F.3d 1317, 1320 (Fed. Cir. 2006). 37

In this case, Petitioner was unable to advance a Table claim because of his CIDP diagnosis (as I

observed in dismissing that version of the claim). See ECF No. 42.

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

37

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).

40

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

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

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

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

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

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

physician. Section 13(a)(1).

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

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

Circuit in Althen, 418 F.3d at 1278: “(1) a medical theory causally connecting the vaccination and

the injury; (2) a logical sequence of cause and effect showing that the vaccination was the reason

for the injury; and (3) a showing of proximate temporal relationship between vaccination and

injury.”

Each of the Althen prongs requires a different showing. Under Althen prong one, petitioners

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

in original)).

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

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

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

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

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

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

41

Moberly, 592 F.3d at 1322)); see also Howard v. Sec'y of Health & Hum. Servs., No. 16-1592V,

slip op. (Fed. Cl. Feb. 27, 2023) (“[t]he standard has been preponderance for nearly four decades”).

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,

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 denied, 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

42

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. denied 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. denied (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) (it is

within the special master’s discretion to determine whether to afford greater weight to

contemporaneous medical records than to other evidence, such as oral testimony surrounding the

events in question that was given at a later date, provided that such determination is evidenced by

a rational determination).

Medical records that are created contemporaneously with the events they describe are

presumed to be accurate and “complete” (i.e., presenting all relevant information on a patient’s

health problems). 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 sub nom. Rickett v. Sec’y of Health

& Hum. Servs., 468 F. Appx. 952 (Fed. Cir. 2011) (non-precedential opinion). This presumption

is based on the linked propositions that (i) sick people visit medical professionals; (ii) sick people

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”).

43

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

be afforded substantial weight. Lowrie, 2005 WL 6117475, at *20. Indeed, contemporaneous

medical records are generally 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, 23 Cl. Ct. at 733 (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.”)).

There are, however, situations in which compelling oral testimony may be more persuasive

than written records, such as where records are deemed to be incomplete or inaccurate. Campbell

v. Sec’y of Health & Hum. Servs., 69 Fed. Cl. 775, 779 (2006) (“like any norm based upon common

sense and experience, this rule should not be treated as an absolute and must yield where the factual

predicates for its application are weak or lacking”); Lowrie, 2005 WL 6117475, at *19 (“’[w]ritten

records which are, themselves, inconsistent, should be accorded less deference than those which

are internally consistent’”) (quoting Murphy, 23 Cl. Ct. at 733)). Ultimately, a determination

regarding a witness’s credibility is needed when determining the weight that such testimony should

be afforded. Andreu, 569 F.3d at 1379; Bradley v. Sec’y of Health & Hum. Servs., 991 F.2d 1570,

1575 (Fed. Cir. 1993).

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

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

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

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

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

explanations for inconsistencies between contemporaneously created medical records and later

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

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

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

or (4) a person’s purposeful recounting of symptoms that did not exist. Lalonde 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

44

factors for analyzing scientific reliability set forth in Daubert v. Merrell Dow Pharmaceuticals,

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)). “The Daubert 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).

The Daubert factors play a slightly different role in Vaccine Program cases than they do

when applied in other federal judicial fora (such as the district courts). Daubert factors are usually

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

that is unreliable and/or could confuse a jury. In Vaccine Program cases, by contrast, these factors

are used in the weighing of the reliability of scientific evidence proffered. Davis v. Sec’y of Health

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

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

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

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

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

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

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

Respondent frequently offers one or more experts of his own in order to rebut a petitioner’s

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

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

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

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

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

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

(quoting Gen. Elec. Co. v. Joiner, 522 U.S. 136, 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 rev. denied, 108 Fed. Cl. 743 (2013), aff’d, 540 F. Appx. 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”).

45

Expert opinions based on unsupported facts may be given relatively little weight. See

Dobrydnev v. Sec’y of Health & Hum. Servs., 556 F. Appx. 976, 992–93 (Fed. Cir. 2014) (“[a]

doctor’s conclusion is only as good as the facts upon which it is based”) (citing Brooke Group Ltd.

v. Brown & Williamson Tobacco Corp., 509 U.S. 209, 242 (1993) (“[w]hen an expert assumes

facts that are not supported by a preponderance of the evidence, a finder of fact may properly reject

the expert’s opinion”)). Expert opinions that fail to address or are at odds with contemporaneous

medical records may therefore be less persuasive than those which correspond to such records. See

Gerami v. Sec’y of Health & Hum. Servs., No. 12-442V, 2013 WL 5998109, at *4 (Fed. Cl. Spec.

Mstr. Oct. 11, 2013), aff’d, 127 Fed. Cl. 299 (2014).

D. Consideration of Medical Literature

Both parties filed medical and scientific literature in this case, but not every filed item

factors 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., 844 F.3d 1322, 1328 (Fed. Cir. 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. Appx. 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”).

E. Determining Matter on Record Rather Than at Hearing

I have opted to decide this case based on written submissions and evidentiary filings,

including the numerous expert reports that have been submitted, despite Petitioner’s preference

for a hearing. The Vaccine Act and Rules not only contemplate but encourage special masters to

decide petitions (or components of a claim) on the papers rather than via evidentiary hearing,

where (in the exercise of their discretion) they conclude that the former means of adjudication

will properly and fairly resolve the case. Section 12(d)(2)(D); Vaccine Rule 8(d). The Federal

Circuit has recently affirmed this practice. Kreizenbeck v. Sec’y of Health & Hum. Servs., 945

F.3d 1362, 1365–66 (Fed. Cir. 2020). It simply is not the case that every Vaccine Act claim need

be resolved by hearing—even where the petitioner explicitly so requests.

46

ANALYSIS

I. An Overview of Relevant Medical Terms and Prior Decisions

A. GBS vs. CIDP

As noted above, CIDP has been defined as a progressive, immune-mediated peripheral

neuropathy that occurs due to an autoimmune attack. Dalakas at e182; Mathey at 1. It results in

weakness, numbness, paresthesia, and sensory ataxia that presents as relapsing-remitting, stepwise

progressive, or gradually progressive, and more often than not involves motor and sensory nerve

dysfunction. Ubogu at 11; Mathey at 1. These symptoms tend to be symmetrical and involve lower

and upper limbs, although variants can involve different phenotypic presentations. Dalakas at

e182; Mathey at 1 (clinical presentations of variants depend on differing “immunogenetic

variations”).

There is no doubt that GBS and CIDP overlap, and that the latter has ofte

This text is long and has been trimmed here. Open the source document for the complete record.