# Nieves v. Secretary of Health and Human Services

> United States Court of Federal Claims · May 22, 2023

URL: https://www.frixlaw.com/law-library/cases/9396514

## Case

- **Court:** United States Court of Federal Claims
- **Decided:** May 22, 2023
- **Precedential status:** Published
- **Opinion:** Opinion
- **Judges:** Brian H. Corcoran
- **Cited by:** 0 later opinions in the Frix Law Library

## Citator (automated)

- No negative treatment found by the automated citator. That is not the same as a confirmation that the case is good law; read the citing cases.
- Full citator and citing cases: https://www.frixlaw.com/law-library/cases/9396514

## How later opinions describe it (automated extraction)

- noting that Moberly “addresses the petitioner’s overall burden of proving causation-in-fact under the Vaccine Act” by a preponderance standard

## Opinion text

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 18-1602V

*************************
*
ANDRES NIEVES, * Chief Special Master Corcoran
*
*
Petitioner, * Filed: April 17, 2023
*
v. *
*
SECRETARY OF HEALTH AND *
HUMAN SERVICES, *
*
Respondent. *
*
*************************

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

6
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).

7
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).

8
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).

9
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 l

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Source: Frix Law Library, https://www.frixlaw.com/law-library/cases/9396514. Public record. Not legal advice.