Jones v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 19-788V

Filed: June 24, 2025

* * * * * * * * * * * * * * *

TAMI JONES, Trustee for the heirs of *

Charley Boon, Deceased, *

*

Petitioner, *

*

v. *

*

SECRETARY OF HEALTH *

AND HUMAN SERVICES, *

*

Respondent. *

* * * * * * * * * * * * * * *

Randall Knutson, Esq., Knutson & Casey Law Firm, Mankato, MN, for petitioner.

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

DECISION1

Roth, Special Master:

On May 29, 2019, Charley Boon (“petitioner”) filed a timely petition pursuant to the

National Vaccine Injury Compensation Program, 42 U.S.C. § 300aa-10 et seq.2 (“Vaccine Act” or

“the Program”). Petitioner alleged that he suffered from Guillain-Barré Syndrome (“GBS”) as the

result of an influenza (“flu”) vaccine he received on September 27, 2016. Petition, ECF No. 1. Mr.

Boon passed away on November 23, 2019. See Pet. Ex. 49.

Upon careful evaluation of all the evidence submitted, I find that petitioner has not

provided preponderant evidence that the flu vaccine Mr. Boon received on September 27, 2016

caused and/or contributed to the injury alleged.

1

Because this Decision contains a reasoned explanation for the action taken in this case, it must be made publicly

accessible and will be posted on the United States Court of Federal Claims’ website, and/or at

https://www.govinfo.gov/app/collection/uscourts/national/cofc, in accordance with the E-Government Act of 2002.

44 U.S.C. § 3501 note (2018) (Federal Management and Promotion of Electronic Government Services). This means

the Decision will be available to anyone with access to the internet. In accordance with Vaccine Rule 18(b), the

parties have 14 days to identify and move to redact medical or other information, the disclosure of which would

constitute an unwarranted invasion of privacy. Any changes will appear in the document posted on the website.

2

National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755. Hereinafter, for ease of citation,

all “§” references to the Vaccine Act will be to the pertinent subparagraph of 42 U.S.C. § 300aa (2012).

I. Procedural History

The petition was filed on May 29, 2019. ECF No. 1. On August 19, 2020, petitioner filed

a Motion to Substitute Patty Boon, the trustee for the heirs of Charley Boon, as petitioner following

Mr. Boon’s passing. ECF No. 27-28. After Mrs. Boon passed away in 2024, Tami Jones was

substituted as both the trustee and petitioner. ECF No. 67-68.

Between June 14, 2019, and October 1, 2020, petitioner filed medical records and

affidavits. Petitioner’s Exhibits (“Pet. Ex.”) 1-25, 51-54; ECF Nos. 7-9, 29. On June 14, 2019,

petitioner filed the expert report of Dr. James Dahlgren, along with medical literature. Pet. Ex. 26-

48, ECF Nos. 9, 15-17.

Respondent filed his Rule 4(c) Report on January 25, 2021, recommending against

compensation. ECF No. 32.

Petitioner then filed three supplemental reports with accompanying literature from Dr.

Dahlgren. Pet. Ex. 55-63, ECF Nos. 34-35; Pet. Ex. 64, ECF No. 40; Pet. Ex. 65-72, ECF No. 49.

Respondent filed expert reports and corresponding literature from Dr. Dara Jamieson and

Dr. You-Wen He. Resp. Ex A-B, ECF Nos. 36-38; Resp. Ex. C, ECF No. 46; Resp. Ex. D-E, ECF

No. 47.

A status conference was held on April 27, 2022, to discuss the issues in the case, including

but not limited to the shortcomings of Dr. Dahlgren’s reports and his failure to persuasively address

the three prongs of Althen, and the onset of petitioner’s symptoms more than three months after

vaccination. Petitioner was ordered to file a status report advising how she wanted to proceed. ECF

No. 50.

In lieu of a status report, petitioner filed a cursory pleading on July 7, 2022, titled “Motion

for a Ruling on the Record,” which simply asked the Court to decide the case on the record as it

stands. ECF No. 52. Petitioner was then ordered to provide a more detailed submission. A six-

page memorandum was filed on August 11, 2022. ECF Nos. 53-54.

Respondent filed a response on October 26, 2022, arguing that petitioner had failed to

provide preponderant evidence that petitioner’s September 27, 2016 flu vaccination caused his

alleged injuries. ECF No. 57. Petitioner did not file a reply.

I have determined that the parties have had a full and fair opportunity to present their cases

and that it is appropriate to resolve this issue without a hearing. See Vaccine Rule 8(d); Vaccine

Rule 3(b)(2); Kreizenbeck v. Sec’y of Health & Human Servs., 945 F.3d 1362, 1366 (Fed. Cir.

2020) (noting that “special masters must determine that the record is comprehensive and fully

developed before ruling on the record.”). Accordingly, this matter is now ripe for resolution.

2

II. Issues to Be Determined

The issues to be determined herein are whether petitioner suffered from GBS or CIDP,

whether a flu vaccine can cause GBS or CIDP, and whether either GBS or CIDP can have an onset

of symptoms in excess of three months, or at least 94 days, after receipt of a flu vaccine.

III. Factual Background3

A. Medical History Prior to the Influenza Vaccine

Petitioner affirmed and his medical records support a prior medical history that included

prostate cancer with prostatectomy, skin cancer, appendectomy, lumbar spine fracture at L5,

hypertension, hyperlipidemia, seizure disorder with epilepsy, and arteriosclerotic heart disease

with angioplasty. Petition at 1; Pet. Ex. 2; Pet. Ex. 5 at 96. In December 2014, he fell at work and

fractured his hip, requiring surgery. See Pet. Ex. 5 at 97-107. In June 2015, petitioner saw his

primary care physician (“PCP”) because his wife was concerned that he “waddles” and “shuffles

his feet when walking.” The PCP noted that he was “off balance.” Pet. Ex. 5 at 94. Petitioner saw

his PCP for follow-up in September 2015. He complained that he walked abnormally due to his

hip fracture and wanted to know if there was something he could take. Id. at 93. The PCP noted

extensive medical problems, and that petitioner waddled back and forth and shifted his weight

consistent with osteoarthritis from his hip fracture. Id. An examination was otherwise normal, and

petitioner was noted to be doing well, working in the hardware department of Home Depot and

walking five to six miles a day at work. Id.

On November 10, 2015, petitioner presented for a flu vaccine. His wife reported concerns

for Parkinson’s disease and dementia. Pet. Ex. 5 at 92. Petitioner received a flu vaccine without

event. The PCP noted that petitioner walked up and down the hall and did not shuffle his feet. His

wife was given reassurances regarding his mental status but was “not convinced.” Id.

In February 2016, petitioner’s wife called his PCP with continued concerns that he had

dementia that was worsening and requested a referral. Id. at 92.

B. Medical History Following the Flu Vaccine

Petitioner received a high dose flu vaccine at a CVS Pharmacy on September 27, 2016.

Pet. Ex. 3. He was 69 years old.

Petitioner affirmed that on October 24, 2016, he suffered from “severe flu symptoms” and

took over the counter medications including Dayquil Severe and Nyquil for three days. Pet. Ex. 2

at 1. Two months later “at the end of December 2016, I was suffering from numbness in my hands

and feet on both sides…” Pet. Ex. 2 at 2.

Petitioner presented to the emergency room (“ER”) on December 31, 2016, reporting

bilateral numbness in his hands and fingertips for several days that started around his knees and

went down to his ankles. His feet and toes were not involved. Pet. Ex. 5 at 41, 142. He reported

3

All references to “petitioner” throughout this section refer to Mr. Charley Boon.

3

shuffling his feet for the past two to three years and a fall a week ago. He learned forward when

he walked. His wife reported that he was “extremely anxious and nervous” and sometimes wakes

up at 2:00 am afraid that he will be late to work at Home Depot at 6:00 am. Id. at 41. He reported

an episode of double vision on Christmas day that lasted for 15 minutes. He also complained of

chills and sweats, but no fever or other symptoms. Id. He was admitted for testing, which was

negative, and he was discharged in stable condition with instructions to follow up with his PCP.

Id. at 44.4

On January 4, 2017, petitioner presented to the PCP for follow-up. His memory was “a

little bit off.” He fell that morning, was having trouble walking, and was using a front-wheeled

walker. Pet. Ex. 5 at 86. Petitioner had an extensive work-up in the hospital including an MRI of

the brain. He had ataxia.5 His underlying diseases were noted as epilepsy with seizure disorder,

arteriosclerotic heart disease with old MI status post angioplasty in 1997, prostate cancer, hip

fracture two years ago, and peripheral neuropathy. 6 Id.

Petitioner was admitted to the hospital on January 10, 2017, with a sudden onset of severe

weakness and numbness in both arms and both legs with increasing fatigue. Pet. Ex. 5 at 87; Pet.

Ex. 6 at 2. The differential diagnosis included polyneuropathy and GBS. Pet. Ex. 5 at 91. After

extensive testing, it was determined that his symptoms were the result of C5 quadriplegia, and he

underwent anterior discectomy and fusion at levels C3-C4 and C4-C5 on January 17, 2017.

Petitioner’s symptoms were “markedly improved” following surgery. Pet. Ex. 6 at 2, 17-19.

However, his condition deteriorated again the next day, but his numbness was not as bad as prior

to surgery. Id. at 2. He was discharged to a nursing home on January 22, 2017, with diagnoses of

C5 level quadriplegia with cervical myelomalacia, memory impairment, and anxiety. Id.

Petitioner was reexamined by a neurologist on February 7, 2017. Pet. Ex. 5 at 64. The

doctor noted that when he was seen on January 11, 2017, his history was consistent with cervical

myelopathy at C4-C5 with no findings of transverse myelitis (“TM”), neuromyelitis optica

(“NMO”), WNV poliomyelitis, or atypical extremely rapid motor neuron disease. Id. He had

surgery with improvement of his lower limb sensory symptoms, but he did not have significant

motor improvement. His wife reported that he had been walking abnormally “for over a year or

two, scuffing the toes of his feet.” Id. He was last able to stand and walk in December. He lays in

bed most of the day, working with a physical therapist at times. He has fluctuating confusion but

is normal at times. No imaging or labs had been done since he was in the hospital. Id. The

impression was quadriparesis in the setting of cervical myelopathy present for perhaps two weeks

prior to diagnosis, with an examination at that time notable for marked upper motor neuron pattern

quadriparesis C4/C5 level, and lower limb sensory disturbance. Id. at 65. He had no sensory

complaints following surgery, but still had quadriparesis. The time course, diagnostics, and clinical

examination remained consistent with cervical spine dysfunction. There was concern for possible

permanent spinal injury perhaps related to cord infarction due to the little improvement post-

4

A complete record from this hospitalization was filed as Petitioner’s Exhibit 6.

5

Ataxia refers to the “failure of muscular coordination; irregularity of muscular action.” Ataxia, DORLAND’S

ILLUSTRATED MEDICAL DICTIONARY 168 (33rd ed. 2019) [hereinafter DORLAND’S].

6

Peripheral neuropathy, also called polyneuropathy, is “neuropathy of several peripheral nerves simultaneously.”

Polyneuropathy, DORLAND’S 1468.

4

surgery and no significant progression. It was also noted that he “might be exhibiting signs of

autonomic dysfunction. Id.

Between January 22, 2017 and February 21, 2017, petitioner’s weakness in his upper and

lower extremities increased. Pet. Ex. 5 at 26, 30. He was readmitted to the hospital on February

21, 2017 for additional testing after he was discharged home against medical advice on February

14, 2017. Pet. Ex. 5 at 26, 30, 140; Pet. Ex. 6 at 294. It was noted that his strength was significantly

better after surgery, but he had not maintained that improvement and regressed some. His main

complaints before surgery were numbness in his arms and legs which was improved after surgery,

but his weakness had increased. Pet. Ex. 6 at 294. He developed neurogenic bladder dysfunction.

Pet. Ex. 5 at 26.

Extensive testing had not shed light on a diagnosis other than cervical spine stenosis

causing quadriplegia. Pet. Ex. 6 at 296. On re-evaluation by neurology, there were no

fasciculations, respiratory or bulbar symptoms. Id. at 300. Given his time course, prior diagnostics,

and plateau and stabilization of neurologic symptoms, there were no other plausible neurological

etiologies. The neurologist remained concerned for possible permanent spinal cord injury from

prolonged compression or spinal cord infarct, and postoperative seroma or other phlegmon7 needed

to be ruled out. Id. at 300-01. On examination, his upper quadriparesis had worsened a bit since he

was examined on February 7, 2017. However, there was no history or diagnostics suggestive of or

consistent with NMO, transverse myelitis, or any other neurological conditions. The neurologist

felt that empirical IVIG would be worthwhile for “very atypical multifocal motor neuropathy,

despite history and exam not necessarily consistent with this.” Id. at 301-02. He received three

days of IVIG without any change. Petitioner developed a pressure ulcer and was discharged to San

Diego Rehabilitation on February 24, 2017. Id. at 301-02, 320, 331, 426.

Petitioner remained at the rehabilitation facility until March 1, 2017. Pet. Ex. 6 at 426.

After neurological reevaluation, repeat IVIG was planned for two weeks later. Prednisone was

started, along with Bactrim for a UTI. Due to a change in insurance, his stay at the rehabilitation

facility was shortened and his PCP and neurologist changed. Petitioner was discharged home, but

it was strongly recommended that he be admitted to another facility for further rehabilitation. Id.

at 428, 434.

On March 1, 2017, the day of his discharge, petitioner was evaluated by a new PCP. Pet.

Ex. 10 at 2. His medical history included partial quadriplegia and abnormal movement of his upper

limbs and with shuffling gait for the past two years. Id. His wife reported some mild memory

deficits. His history over the past two months was also detailed, noting that he was working 40

hours a week at Home Depot three months ago but was now in a wheelchair. Id. On physical

examination, he had weakness in all four extremities that was more pronounced in the proximal

muscles and on the right side of his body. His reflexes could not be elicited, and he had muscle

wasting. Id. at 3.

Petitioner presented to a new neurologist on March 16, 2017. Pet. Ex. 11 at 2. He was

unable to walk, had numbness and tingling in his hands and fingers, and had memory problems.

The onset of symptoms was reported as around December 28, 2016, when he developed tingling

7

Phlegmon is “acute subcutaneous inflammation, sometimes with abscess.” Phlegmon, DORLAND’S 1413.

5

in all limbs over two days while off work. He went to the ER on New Years Day, was admitted

for testing, and sent home on January 3, 2017. On January 6, 2017, he presented to his doctor and

was unable to stand. Throughout that weekend, he became immobile and was admitted to the

hospital. Id. He underwent extensive testing and spinal surgery, but it was unclear if the surgery

helped. He spent several weeks in rehabilitation. After additional testing was done, he was

admitted to the hospital again. Id. He had been shuffling his feet for two years before, and his wife

showed a video taken in April 2016 of him sitting, moving the fingers on both hands and

questioned if it was a clue to some neurological condition. He received three days of IVIG in

February and started feeling better and getting stronger. He was thinking more clearly now. Id.

The assessment at this visit was idiopathic peripheral neuropathy. Pet. Ex. 11 at 6. The neurologist

wrote that petitioner may have had an episode of GBS, but GBS patients do not need to be retreated

unless they show worsening, which typically happens before nadir and petitioner was “well beyond

that.” Id. It was unclear if he could participate in extensive physical rehabilitation. However, he

was admitted to rehabilitation from March 21, 2017 through April 15, 2017. He was discharged

home in stable condition with a diagnosis of GBS. Pet. Ex. 13 at 1-3.

Petitioner returned to his PCP on April 17, 2017, who noted that he was discharged from

acute in-patient rehabilitation due to lack of progression. He reported regaining some strength with

improvement to fine motor movement. His goal was to go back to work, but he was tired all the

time and did not want to participate in rehabilitation. Pet. Ex. 10 at 6.

Mrs. Boon contacted the neurologist in May 2017 to advise that petitioner was declining

and to request another round of IVIG. Pet. Ex. 11 at 7. The neurologist asked if petitioner had a

spinal tap done, which would have shown elevated protein on CSF consistent with GBS/CIDP. He

also noted that petitioner had no reflexes at his last visit, which could be compatible with

GBS/CIDP. Id. Mrs. Boon confirmed that petitioner had not had a spinal tap. Petitioner was

admitted to the hospital that day for five days of IVIG. Pet. Ex. 11 at 7; Pet. Ex. 14 at 1. He was

noted to have increasing weakness with difficulty swallowing upon admission. He improved with

five days of IVIG but was not strong enough to go home and was transferred to acute rehabilitation.

Pet. Ex. 14 at 1-2. The discharge diagnoses included acute exacerbation of underlying GBS,

neurogenic bladder, urinary tract infection, and recent left calf deep vein thrombosis. Id. at 1.

Petitioner presented to the PCP on June 5, 2017. He was able to stand from a seated position

with assistance and take a few steps with a walker. He could shower with a chair and was receiving

PT at home. He was able to feed himself. Pet. Ex. 10 at 14.

At a follow-up neurology appointment on June 9, 2017, petitioner reported he was able to

get in and out of the car more easily since the IVIG treatment. Pet. Ex. 11 at 9. His wife reported

he only does things if told to and he does not seem to be trying to improve. He fell the day before.

He received PT at home three times a week. He was supposed to have EMG/NCS testing while in

acute rehabilitation but that was never done. Id. On examination, the neurologist noted slow

mentation, but petitioner demonstrated “fairly good power” in his upper and lower extremities.

Reflexes were hard to elicit. He could stand with assistance and take a few steps with help. Id. at

10. He was to be monitored for recurrent or worsening weakness, which may require a five-day

course of IVIG. The neurologist noted “[i]f this happens then I would diagnose him with CIDP.”

Petitioner was taking blood thinners, so a lumbar puncture was never done. Id. at 11.

6

Petitioner relapsed and was diagnosed with CIDP on July 28, 2017. His neurologist ordered

IVIG every three weeks six months. Pet. Ex. 15 at 73. In the months that followed, his condition

declined, and PT was recommended. Pet. Ex. 11 at 15.

Petitioner returned to the neurologist on October 9, 2017. He fell a month prior when his

walker got caught and went to the ER. He was still receiving IVIG, was not sleeping well, and

lacked motivation to exercise on his own. His memory was better, but he would probably need

assistance throughout life. Pet. Ex. 11 at 17. His diagnosis was CIDP with ongoing IVIG needed.

Id. at 21.

There was a ten-month gap in the medical records. Petitioner was admitted to the hospital

again from August 4, 2018 until August 20, 2018 for congestive heart failure. He underwent

coronary artery bypass graft, mitral valve replacement, and left atrial appendage clipping and was

discharged without complication. Pet. Ex. 22 at 1-2, 24-25. He was hospitalized again from

September 12, 2018 until September 16, 2018 for tachycardia and hypotension. Pet. Ex. 52 at 2159.

On November 14, 2018, Petitioner’s IVIG was re-ordered for two days every three weeks

for six months. Pet. Ex. 53 at 227.

On April 2, 2019, petitioner was admitted to the hospital for a hip fracture following a fall.

Pet. Ex. 53 at 257. He underwent pinning of his right hip and was discharged home on April 5,

2019. Id.

Petitioner suffered a CIDP flare on August 22, 2019, and was admitted to the hospital for

five days of IVIG. He was discharged to acute rehabilitation on August 27, 2019. Pet. Ex. 53 at

747-48.

On November 15, 2019, petitioner’s condition worsened, and he was admitted to the

hospital unable to stand or lift his arms. He received five days of IVIG treatment without

improvement, and a feeding tube was placed. Pet. Ex. 54 at 216-17. His respiratory status

worsened, and he passed away on November 23, 2019. The cause of death was listed as acute

respiratory failure, CIDP, severe malnutrition, severe deconditioning, atrial fibrillation, neurogenic

bladder, and anemia. Pet. Ex. 49.

IV. Expert Opinions

A. Petitioner’s Expert, Dr. James Dahlgren8

Dr. Dahlgren provided four reports. Pet. Ex. 26; Pet. Ex. 55; Pet. Ex. 64; Pet. Ex. 65. He

initially opined that petitioner developed GBS as a result of the flu vaccine. Pet. Ex. 26 at 12.

Later, he opined that petitioner developed GBS and CIDP as a result of the flu vaccine and that

8

Dr. Dahlgren received his medical degree from University of California, San Francisco, and is board-certified in

internal medicine. Pet. Ex. 27. He completed residencies in internal medicine at both Boston Veteran’s Hospital in

Boston and Cedars-Sinai Medical Center in Los Angeles and a fellowship in infectious diseases at UCLA Medical

Center in Los Angeles. Dr. Dahlgren is currently in private practice in internal medicine and occupational and

environmental medicine, with a subspecialty in toxicology. Id.

7

both diseases share the same causal mechanism, with chronicity being the main difference. Pet.

Ex. 55 at 12-13.

1. Dr. Dahlgren’s First Report

In his first report, Dr. Dahlgren summarized petitioner’s medical history and his receipt of

the high dose Fluzone vaccine followed by the onset of numbness in his hands and feet three

months after the vaccine. Pet. Ex. 26. Dr. Dahlgren noted that there is no evidence that petitioner

had an acute infection, particularly any diarrheal infection, in the weeks prior to the onset of his

GBS. Based on the literature he reviewed, “[t]he mechanism of an acute infection is an immune

trigger for GBS, a similar mechanism that is triggered by a vaccination.” Pet. Ex. 26 at 2.

Therefore, the only plausible causative trigger in this case was the flu vaccine. Id.

Dr. Dahlgren asserted that GBS is a documented risk of flu vaccination, and “[t]he

mechanism for vaccine induced autoimmunity has been extensively studied and is accepted

science.” Pet. Ex. 26 at 3. A vaccine stimulates the immune system, causing an autoimmune

disease like GBS to occur due to loss of tolerance to normal antigens or antigen mimicry. In GBS,

the immune system attacks the nerve cells, causing injury to the myelin sheath covering the nerves.

GBS patients usually have sensory and motor dysfunction and can have autonomic neuropathy9 as

well. Petitioner had sensory and motor dysfunction, which is “the most common presentation.” Id.

Dr. Dahlgren addressed the Vaccine Table’s 3-to-42-day period for onset of GBS after flu

vaccine and petitioner’s onset of GBS three months after his vaccine, arguing that “[t]his 42-day

latency is arbitrary and fails to consider all the evidence. There are vaccine induced autoimmune

disease cases, which have their onset within 42 days, but not all.” Pet. Ex. 26 at 3 (emphasis in

original). He cited to literature which he argued showed onset in excess of 42 days: the two tables

in Prestel showed GBS up to 150 days post-H1N1 and seasonal flu vaccine, and that older

individuals are at higher risk of GBS following flu vaccine. Pet. Ex. 26 at 4-5; Pet. Ex. 40.10

Soriano showed onset of autoimmune disease 60 days or more following a flu vaccine, and Dr.

Dahlgren referenced a table contained therein discussing the onset of giant cell arteritis and

polymyalgia rheumatica within 90 days of a flu vaccine. Pet. Ex. 26 at 5-6; Pet. Ex. 45.11 Marks

& Halpin reported onset of symptoms up to ten weeks post vaccination, and Schonberger showed

GBS cases occurring at 16 weeks following flu vaccination. Pet. Ex. 26 at 6-7; Pet. Ex. 3912; Pet.

Ex. 43.13 Kaplan used eight weeks as the surveillance period to define the parameters of their study

of GBS after flu vaccine. Pet. Ex. 26 at 7; Pet. Ex. 37.14 Watad, a study of cases of autoimmune

9

Autonomic neuropathy is “any neuropathy of the autonomic nervous system, causing symptoms such as orthostatic

hypertension, disordered bowel, bladder, or sexual functions, or abnormal pupillary reflexes; it is a complication of

many diseases including Adie syndrome, chronic alcoholism, diabetes mellitus, dysautonomia, and Shy-Drager

syndrome.” Autonomic neuropathy, DORLAND’S 1251.

10

Jürgen Prestel et al., Risk of Guillain-Barré syndrome following pandemic influenza A (H1N1) 2009 vaccination in

Germany, 23 PHARMACOEPIDEMIOLOGY & DRUG SAFETY 1192 (2014), filed as “Pet. Ex. 40.”

11

A. Soriano et al., Giant cell arteritis and polymyalgia rheumatica after influenza vaccination: report of 10 cases

and review of the literature, 21 LUPUS 153 (2012), filed as “Pet. Ex. 45.”

12

James S. Marks & Thomas J. Halpin, Guillain-Barré Syndrome in Recipients of A/New Jersey Influenza Vaccine,

243 J. AM. MED. ASS’N 2490 (1980), filed as “Pet. Ex. 39.”

13

Lawrence B. Schonberger et al., Guillain-Barre Syndrome Following Vaccination in the National Influenza

Immunization Program, United States, 1976-1977, 110 AM. J. EPIDEMIOLOGY 105 (1979), filed as “Pet. Ex. 43.”

14

Jonathan Kaplan et al., Guillain-Barré Syndrome in the United States, 1979-1980 and 1980-1981, 248 J. AM. MED.

8

diseases triggered by an exposure to an immune triggering event, determined a latency period from

three days to five years. Pet. Ex. 26 at 8; Pet. Ex. 48.15 Tomljenovic described ten cases of systemic

lupus erythematosus (“SLE”) following hepatitis B vaccine, with onset of autoimmune symptoms

56.3 days after vaccination. Pet. Ex. 26 at 8; Pet. Ex. 37.16 Agmon-Levin showed onset of SLE in

mice nine weeks after receipt of the hepatitis B vaccine. Pet. Ex. 26 at 8; Pet. Ex. 28.17

Colafrancesco found a three-month latency period between H1N1 vaccination and the onset of

Sjogren’s syndrome, an autoimmune disease. Pet. Ex. 26 at 8-9; Pet. Ex. 31.18 Liu & Kaplowitz

discussed hypersensitivity reactions to drugs as a potential trigger for autoimmune hepatitis. Pet.

Ex. 26 at 9-10; Pet. Ex. 38.19

Dr. Dahlgren argued that Dodd was the basis for the 42-day limitation and was based on a

statistical study of cerebral spinal fluid changes, not clinical presentation. Dodd also cited

Farrington to support the 42-day latency explaining that “[t]he point of the Farrington study is to

provide a statistical model,” which is a probability tool that is “complex and not easily applied to

the complex interactions of vaccine triggers for autoimmune diseases like GBS.” Dodd did report

that there is a “much larger risk” of GBS following vaccination in subjects over 65, but many

studies “arbitrarily used a 6-week cut off to simplify the study process . . . They could have used

a longer cut-off and found additional cases.” Pet. Ex. 26 at 10-11; Pet. Ex. 3220; Pet. Ex. 33.21

Further, Sevjar discussed that the Brighton Collaboration GBS Working Group recommendation

does not preclude a vaccine-induced autoimmune reaction occurring after 42 days. Pet. Ex. 26 at

11; Pet. Ex. 44.22

Dr. Dahlgren concluded that petitioner developed GBS from a flu vaccine, and the peer

reviewed scientific literature “proves that the 42 day rule should not be applied as a hard and fast

deadline.” Pet. Ex. 26 at 12. The flu vaccine was a substantial contributing factor to the onset of

petitioner’s GBS. Id.

ASS’N 698 (1982), filed as “Pet. Ex. 37.”

15

Abdulla Watad et al., The autoimmune/inflammatory syndrome induced by adjuvants (ASIA)/Shoenfeld’s syndrome:

descriptive analysis of 300 patients from the international ASIA syndrome registry, 37 CLINICAL RHEUMATOLOGY

483 (2018), filed as “Pet. Ex. 48.”

16

Lucija Tomljenovic et al., Vaccination in Autoimmune Animal Models, ISR. MED. ASS’N J. 657 (2014), filed as “Pet.

Ex. 37.”

17

Nancy Agmon-Levin et al., Immunization with hepatitis B vaccine accelerates SLE-like disease in a murine model,

54 J. AUTOIMMUNITY 21 (2014), filed as “Pet. Ex. 28.”

18

Serena Colafrancesco et al., Autoimmune/Inflammatory Syndrome Induced by Adjuvants and Sjogren’s Syndrome,

18 ISR. MED. ASS’N J. 150 (2016), filed as “Pet. Ex. 31.”

19

Zhang-Xu Liu & Neil Kaplowitz, Immune-mediated drug-induced liver disease, 6 CLINICAL LIVER DISEASE 755

(2002), filed as “Pet. Ex. 38.”

20

Caitlin N. Dodd et al., International collaboration to assess the risk of Guillain Barré Syndrome following Influenza

A (H1N1) 2009 monovalent vaccines, 31 VACCINE 4448 (2013), filed as “Pet. Ex. 32.”

21

C.P. Farrington, Relative Incidence Estimation From Case Series for Vaccine Safety Evaluation, 51 BIOMETRICS

228 (1995), filed as “Pet. Ex. 33.”

22

James J. Sejvar et al., Guillain-Barré syndrome and Fisher syndrome: Case definitions and guidelines for collection,

analysis, and presentation of immunization safety data, 29 VACCINE 599 (2011), filed as “Pet. Ex. 44.”

9

2. Dr. Dahlgren’s Second Report

In his second report, Dr. Dahlgren again argued that 42 days is not the limit for onset of

neurological symptoms of inflammatory demyelinating neuropathy following vaccine

administration. Dr. Dahlgren now referred to petitioner’s condition as CIDP.23 Pet. Ex. 55 at 1-2.

Dr. Dahlgren explained that while petitioner presented to his physician reporting new onset

of neurological complaints 12 weeks after vaccination, it is not clear from the records how long he

had been experiencing these symptoms when he went to the doctor. Pet. Ex. 55 at 1-2. Further, Dr.

Dahlgren noted that petitioner had a history of memory problems. He experienced flu-like

symptoms from October 24 to 27, 2015, which he did not report to his physician in December

2015. He only reported that he had weakness for “several” days. Id. Therefore, the date of onset

of his weakness should not be considered “as a definitive line disqualification to a conclusion that

the flu vaccine was the triggering event for what was eventually diagnosed as CIDP.” Pet. Ex. 55

at 2.

According to Dr. Dahlgren, GBS and CIDP have the same mechanism causing autoimmune

damage to myelin, and both are treated with IVIG. The “only difference between GBS and CIDP

is the duration of the illness.” Pet. Ex. 55 at 2. Both have a common etiology, which is the

formation of antibodies against myelin that occurs due to “a breakdown in self-recognition due to

a failure in the body’s immune system.” Id. at 2-3. Individual susceptibility predisposes to this

error in the immune system. Vaccines intentionally stimulate the immune system and “a rare

number of individuals experience an overactive, erroneous complication of an errant immune

reaction.” Id.

Dr. Dahlgren referenced petitioner’s medical records as containing diagnoses of both GBS

and CIDP, indicating that his treating physicians recognized the overlap of the two diseases. He

did not include citations to the medical records. Pet. Ex. 55 at 2, 3-5.

Dr. Dahlgren cited to several studies as supportive of his opinion that GBS and CIDP are

the same disease, with the only difference being duration. GBS is acute and self-limited, while

23

The petition was never amended to allege CIDP.

10

CIDP is ongoing and has an onset period longer than 42 days. Pet. Ex. 55 at 5-12; Pet. Ex. 5624;

Pet. Ex. 5825; Pet. Ex. 5926; Pet. Ex. 6027; Pet. Ex. 63.28

Dr. Dahlgren concluded that petitioner developed the “autoimmune neurological condition

of GBS and CIDP.” Pet. Ex. 55 at 13. IVIG helped, but he had a relapse of CIDP that did not

respond to therapy, and he died from complications of CIDP. His autoimmune neurological

conditions were the result of the flu vaccination. Id.

3. Dr. Dahlgren’s Third Report

In his third report, Dr. Dahlgren submitted that Dr. Jamieson failed to address the issues he

raised in his first two reports, and he therefore need not respond to her opinion that GBS is not

related to vaccines. Pet. Ex. 64 at 1.

Dr. Dahlgren quoted from Dr. Jamieson’s report, criticizing that she did not “provide a

single quote or citation about CIDP and the epidemiology showing a link of CIDP to vaccines,”

but rather simply suggested that GBS and CIDP are completely different diseases. Pet. Ex. 64 at

1-2. Thus, her opinion is contrary to the CDC and the vaccine injury table. Id.

Dr. Dahlgren further submitted that Dr. Jamieson failed to address the literature he relied

on, referring only to literature that suggested there was no link between autoimmune diseases,

GBS, and vaccines: “[h]er medical expertise is outdated and contrary to modern medicine theory.”

Pet. Ex. 64 at 2.

24

Stefan Blum & Pamela A. McCombe, Genetics of Guillain-Barré syndrome (GBS) and chronic inflammatory

demyelinating polyradiculopathy (CIDP): current knowledge and future directions, 19 J. PERIPHERAL NERVOUS SYS.

88 (2014), filed as “Pet. Ex. 56.” This article describes GBS as an inflammatory polyradiculoneuropathy with several

subgroups and variants, while CIDP is a chronic or relapsing motor and sensory neuropathy with inflammation and

demyelination of the peripheral nerves thought to be immune-mediated. Both are autoimmune diseases with genetic

susceptibility.

25

Hubertus Köller et al., Chronic Inflammatory Demyelinating Polyneuropathy, 352 N. ENG. J. MED. 1343 (2005),

filed as “Pet. Ex. 58.” This is a 2005 article discussing CIDP as characterized by symmetrical weakness in both

proximal and distal muscles that progressively increases for more than two months, setting it apart from GBS, which

is self-limited. CIDP can be relapsing or chronic and progressive. Id. at 1. The article discusses other demyelinating

inflammatory neuropathies and conditions that may be concurrent with CIDP, testing, and the pathogenesis and

treatments for CIDP. Id. at 2-3

26

Krista Kuitwaard et al., Recurrences, vaccinations and long-term symptoms in GBS and CIDP¸ 14 J. PERIPHERAL

NERVOUS SYS. 310 (2009), filed as “Pet. Ex. 59.” This article was based on questionnaires responded to by individuals

who received vaccinations and were already diagnosed with GBS or CIDP to determine if there was an increase in

symptoms following the vaccination. The study noted a host of flaws.

27

Krista Kuitwaard et al., Letter to the Editor: Individual patients who experienced both Guillain-Barré syndrome

and CIDP, 14 J. PERIPHERAL NERVOUS SYS. 66 (2009), filed as “Pet. Ex. 60.” A 2009 letter to the editor, this discussed

the cases of four patients who suffered from both GBS and CIDP, concluding that this extremely uncommon

occurrence in a single patient cannot be excluded and questioning whether the two diseases are part of a clinical and

pathophysiological continuum instead of fully separate diseases.

28

Paula Restrepo-Jiménez et al., The Immunotherapy of Guillain-Barré Syndrome, EXPERT OP. BIOLOGICAL THEORY

(2018), filed as “Pet. Ex. 63.” This manuscript on treatment for GBS included that GBS usually develops one to two

weeks after an infection, reaching peak after two to four weeks. CIDP was not discussed.

11

Dr. Dahlgren argued that the Vaccine Court already determined that GBS is compensable

and added it to the vaccine table as a table injury. Since the evidence supports GBS and CIDP as

related, CIDP like GBS is a complication of vaccine administration.29 Pet. Ex. 64 at 3.

Dr. Dahlgren opined, “[q]uite simply, vaccines increase the activity of the immune system,

and in some rare cases, an abnormal autoimmune system attacks and damages the myelin around

nerves.” Pet. Ex. 64 at 3. He added that Dr. Jamieson failed to counter “that medical theory”,

relying on “her own naked opinion, without any foundation, except quoting herself.” Id.

Based on his opinion that the Vaccine Court has accepted GBS as being caused by

vaccinations, it is Dr. Dahlgren’s opinion that the issues here are the 42-day cut off for onset and

whether CIDP is a similar autoimmune disease to GBS and caused by the same mechanisms. Pet.

Ex. 64 at 3. He submitted that Dr. Jamieson agreed IVIG is effective in treating both diseases,

which suggests that both GBS and CIDP arise from a common mechanism. Id. Dr. Dahlgren

concluded though inartfully stated, that “[w]hen a disease has a common mechanism and response

to treatment and occurring (sic) after a common over an aberrant over stimulation of the immune

system, they are related entities.” Id. at 4.

4. Dr. Dahlgren’s Fourth Report

In a fourth report, Dr. Dahlgren addressed Dr. He’s opinions. He concluded that, like Dr.

Jamieson, Dr. He provided nothing of substance beyond personal opinions that petitioner’s

illnesses were coincidence and unrelated to his vaccination. Pet. Ex. 65 at 1.

Dr. Dahlgren discussed the literature relied on by Dr. He, concluding that neither Dr.

Jamieson nor Dr. He refuted the content of his three prior reports. He added that although Dr. He

disagreed with his opinion that GBS and CIDP involve the same mechanism causing damage to

the myelin sheath from formation of antibodies, the literature Dr. He relied on supported “the

concept of autoimmunity including GBS and CIDP being caused by vaccines.” Pet. Ex. 65 at 1-6.

Dr. Dahlgren’s opinions remained the same because the respondent’s experts did not provide a

scientific argument that contradicted his provided evidence. Id. at 6.

B. Respondent’s Expert, Dr. Dara Jamieson30

Dr. Jamieson issued two reports. Resp. Ex. A; Resp. Ex. C.

1. Dr. Jamieson’s First Report

In her first report, Dr. Jamieson detailed petitioner’s medical history, including three days

of severe flu symptoms approximately one month after his receipt of the flu vaccine. Resp. Ex. A

29

The Court’s decisions about a vaccine and a particular condition or injury have no bearing on if or when a vaccine

is added to a Table or whether an injury is determined to be a Table injury. See § 300aa-14(c).

30

Dr. Jamieson is a board-certified neurologist. Resp. Ex. B. She received her medical degree from the University of

Pennsylvania and completed her residency in neurology at the University of Pennsylvania Hospital, as well as a

fellowship at the Cerebrovascular Research Center in the University of Pennsylvania School of Medicine’s

Department of Neurology. Id. She is currently a Clinical Associate Professor of Neurology at Weill Cornell Medicine.

Id.

12

at 2-10. She noted the onset of petitioner’s neurological symptoms as between 12 and 13 weeks

after his vaccination with worsening extended over more than the next two months. Id. at 11-12.

Petitioner had no “obvious motor or sensory deficits” when he was examined on December 31,

2016. Weakness was first noted on examination on January 11, 2017, and became more

pronounced thereafter. Id. at 12.

In Dr. Jamieson’s opinion, petitioner was misdiagnosed with cervical myelopathy and

underwent an unnecessary cervical decompression surgery. Resp. Ex. A at 12. He was then treated

with steroids for motor and sensory deficits which are beneficial in treating CIDP, but not GBS.

When the steroids were discontinued, his weakness worsened and IVIG was initiated, which

improved his extremity weakness. Petitioner suffered a remitting and relapsing course that is

indicative of CIDP and required regular IVIG treatments. Id. Unfortunately, other intervening and

unrelated medical conditions including dementia, atrial fibrillation, deep vein thrombosis,

congestive heart failure, severe coronary artery disease, severe mitral valve regurgitation, and

hypertension worsened his general health. Id.

Dr. Jamieson opined that petitioner’s illness course was the classic pattern of CIDP, with

relapsing and remitting symptoms over a three-year period. Resp. Ex. A at 12. Petitioner’s course

was distinguishable from GBS, which reaches nadir within four weeks of onset, while petitioner

experienced a slow initial neurological deterioration over more than two months. In her opinion,

petitioner never had GBS. Id. at 12-13.

Dr. Jamieson explained that the first symptoms of GBS are numbness, paresthesia,

weakness, pain in the limbs, or a combination of these. The main feature is the bilateral and

relatively symmetric weakness of the limbs that progresses over a period of 12 hours to 28 days

before a plateau is reached. Resp. Ex. A at 13; Resp. Ex. A, Tab 3.31 It is believed that the

demyelination of the peripheral nerves in GBS/AIDP is related to a preceding triggering event,

most commonly an infection but also surgery, trauma, vaccination, or bone marrow

transplantation, and the immune response to this event is directed toward the myelin or axon of

the peripheral nerve, resulting in demyelinating, axonal, or mixed forms of GBS. Resp. Ex. A at

13. GBS is often post-infectious with onset of rapidly progressive and monophasic illness shortly

after illness, with two thirds of patients reporting preceding respiratory or gastrointestinal

symptoms within four weeks of onset of weakness and usually ten to 14 days after infection. Id.

Limb weakness, which may include sensory and/or cranial nerve symptoms, develops a week or

two after immune stimulation and progresses to clinical deficit within two to four weeks. IVIG or

plasma exchange (“PLEX”) are used as treatment for GBS/AIDP, and unlike CIDP, these

conditions do not respond to steroids. Most GBS patients make a full recovery, and reoccurrence

is exceedingly rare. Id. at 13-14.

Dr. Jamieson pointed out that CIDP is distinctively different from GBS. CIDP is an

immune-mediated peripheral neuropathy that generally presents with gradual worsening,

symmetrical numbness and tingling followed by hand, feet, upper arm, and thigh motor weakness.

Extremity pain and abnormal sensation can occur. There is also obvious motor deficit, less

prominent than the sensory loss, and decreased or absent reflexes. Resp. Ex. A at 14.

31

Nobuhiro Yuki & Hans-Peter Hartung, Guillain-Barré Syndrome, 366 N. ENG. J. MED. 2294 (2012), filed as “Resp.

Ex. A, Tab 3.”

13

Unlike the rapidly evolving GBS, CIDP develops slowly over more than eight weeks, and

the evolution of initial symptoms can take at least two months to reach clinical nadir from onset.

Resp. Ex. A at 14. Deficits involving respiratory muscles, autonomic function, and cranial nerve

are less prominent in CIDP. CIDP also generally does not have an immunological trigger, like a

prior infection in GBS. Id. at 15.

Dr. Jamieson agreed that GBS and CIDP have immune pathophysiology with similar

findings on EMG/NCV studies depending on the timing of the studies, but the specific antigenic

targets, immune effectors and responses to treatment are different. Resp. Ex. A at 15. The

pathogenesis of CIDP is poorly understood but appears to involve both humoral immunity32 and

cellular immunity33 given its chronic course, while the rapid course of GBS suggests only humoral

immunity is involved. These are “distinctly different diseases,” so that the pathophysiological and

epidemiological attributes of GBS and CIDP cannot be extrapolated to the other. Id. at 15-16.

Finally, CIDP is treating with IVIG with steroids and PLEX, while steroids are not used to

treat GBS. Both respond to IVIG and PLEX, though clinical improvement is permanent for GBS

but only transient for CIDP. Chronic steroid or steroid sparing medications are not used to treat

GBS because of the lack of response and other treatment options, but these are used to treat CIDP.

Resp. Ex. A at 16.

Dr. Jamieson summarized that arguments about an association between GBS and influenza

vaccine are not applicable to CIDP because they are different neurological diseases. Resp. Ex. A

at 16. Beyond the 1976 H1N1 vaccination program, “there has been no consistently proven

association” between flu vaccine and the development of GBS. Id. Dr. Jamieson detailed the many

studies regarding GBS and flu vaccine noting that only case reports contained instances of CIDP

following vaccination. Id. at 16-17. Further, the CDC found the evidence inadequate to accept or

reject a causal relationship between the flu vaccine and CIDP. Id. at 18-19.

Dr. Jamieson concluded that petitioner developed CIDP, not GBS, that developed three

months after the flu vaccine. GBS and CIDP are two distinct peripheral neuropathies, and

conflating their immunological similarities and vaccination associations is not supported by the

evidence. Resp. Ex. A at 20. There is no immunological or epidemiological evidence that a

temporally remote flu vaccine can trigger CIDP, a disease not identified as caused or triggered by

vaccinations. It would be more likely that his flu-like syndrome two months before was the trigger

or contributing factor, if there was one. Id. at 20-21.

2. Dr. Jamieson’s Second Report

Dr. Jamieson responded to Dr. Dahlgren in her second report. Resp. Ex. C. She noted that

the literature Dr. Dahlgren relied on distinguishes GBS and CIDP, as stated in her initial report.

32

Humoral immunity is immunity mediated by antibodies. Humoral immunity, DORLAND’S 906.

33

Cellular or cell-mediated immunity is “immunity mediated by T lymphocytes either through release of lymphokines

or through exertion of direct cytotoxicity, transmissible by transfer of lymphocytes but not serum; it includes type IV

hypersensitivity reactions and systemic responses to viral or microbial infections or to tumor cells.” Cell-mediated

immunity, DORLAND’S 906.

14

Resp. Ex. C at 1-2; Pet. Ex. 5634; Pet. Ex. 58.35 Further, she argued that Dr. Dahlgren’s opinion

that the fact that GBS and CIDP can both be treated with IVIG suggests a common mechanism is

like suggesting that asthma and MS have a common mechanism because both are treated with

steroids: “Treatment of two diseases with a commonly used immunotherapy does not imply an

overlapping pathophysiological mechanism.” Id. at 2. Many unrelated autoimmune diseases are

treated with the same therapies. Arguably, if the response to treatment defined pathophysiological

mechanism, then the difference in response to steroid between GBS and CIDP mitigates their

commonality. Id.

Dr. Jamieson wrote that Dr. Dahlgren “criticizes the use of epidemiological evidence to

refute an association between GBS and vaccination, yet he sends only references of a few case

reports of supposed CIDP after vaccination to support a linkage.” Not only were his references

unpersuasive of his opinion, but some were also referenced in her report in support of her opinions.

Resp. Ex. C at 2-3; Pet. Ex. 5736; Pet. Ex. 5937; Pet. Ex. 62.38

Dr. Jamieson agreed that the issues in the case are the onset far in excess of 42 days and

whether CIDP and GBS are similar autoimmune diseases caused by the same mechanism, and she

maintained that GBS and CIDP are distinct autoimmune disease that cannot be conflated. Further,

she stated that Dr. Dahlgren failed to provide any literature that supports a causative link between

an influenza vaccination and CIDP developing three months later, or that a distinct disease with a

supposed vaccine association within a certain timeframe can be replaced by a different disease

outside that timeframe. Resp. Ex. C at 3.

Dr. Jamieson reiterated that there is no support for an association between a flu vaccine

and onset of CIDP symptoms three months later, and that petitioner’s flu-like symptoms two

months prior to the onset were more likely the cause of his chronic neuropathy. Resp. Ex. C at 3.

C. Respondent’s Expert, Dr. You-Wen He39

Dr. He issued one report. Resp. Ex. D.

Dr. He detailed petitioner’s medical history, specifically his receipt of a high dose flu

vaccine on September 27, 2016, his severe flu-like symptoms one month later that were treated

with over-the-counter medications, and the development of symptoms of GBS and CIDP three

months after receipt of the flu vaccination. He further noted that petitioner had a family history of

34

Blum & McCombe, supra note 24.

35

Köller et al., supra note 25.

36

J.M. Brostoff et al., Post-influenza vaccine chronic inflammatory demyelinating polyneuropathy, 37 AGE & AGING

229 (2007), filed as “Pet. Ex. 57.”

37

Kuitwaard et al., supra note 26.

38

Gauthier Remiche et al., Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) associated to

hereditary neuropathy with liability to pressure palsies (HNPP) and revealed after influenza AH1N1 vaccination, 113

ACTA NEUROLOGICA BELGICA 519 (2013), filed as “Pet. Ex. 63.”

39

Dr. He received his medical degree in China from the Fourth Military Medical University and his Ph.D. in

microbiology and immunology from the University of Miami. Resp. Ex. E. He has been a professor of immunology

in the Duke University Medical Center Department of Immunology since 2000. Id.

15

autoimmune diseases including a sister with lupus and a grandmother with diabetes, thyroid

disease, arthritis, and lupus. Resp. Ex. D at 3; Pet. Ex 4 at 3.

Dr. He described GBS as an inflammatory polyneuropathy characterized by acute onset,

rapid progression, symmetrical weakness, and hyporeflexia or areflexia. Resp. Ex. D at 3. GBS is

post-infectious, with two thirds of patients reporting either respiratory or gastrointestinal tract

infection before onset. Id. at 4; Resp. Ex. D, Tab 140; Resp. Ex. D, Tab 3.41 GBS has been

associated with campylobacter jejuni, cytomegalovirus, Epstein-Barr virus, mycoplasma

pneumonia, haemophilus influenza, influenza A virus, enterovirus, hepatitis E, varicella zoster,

and Zika virus. Resp. Ex. D at 4; Resp. Ex. D, Tab 142; Resp. Ex. D, Tab 343; Resp. Ex. D, Tab

5.44 Although not firmly established, cross-reactive autoantibodies may play a role in the

immunopathogenesis of GBS, attacking peripheral nerves and causing demyelination and axonal

damage. Resp. Ex. D at 4; Resp. Ex. D, Tab 1.45

Dr. He described CIDP as an acquired, immune-mediated neuropathy affecting peripheral

nerves and nerve roots, characterized by a relapsing and remitting or progressive course that is

steroid responsive and has electrodiagnostic or pathologic features of demyelination. The cause

and specific immunologic triggers are unclear. Resp. Ex. D at 5; Resp. Ex. D, Tab 9.46 Evidence

beyond a temporal relationship between vaccination and the development of CIDP has not been

provided in any literature. Resp. Ex. D at 5; Resp. Ex. D, Tab 8.47

Dr. He opined that while it is generally accepted that H1N1 influenza vaccines have been

associated with an increased risk GBS, other seasonal influenza vaccines have not. Resp. Ex. D at

4-5. Dr. He then addressed Dr. Dahlgren’s opinions and the papers he relied upon. Resp. Ex. D at

6-8; Pet. Ex. 3048; Pet. Ex. 3449; Pet. Ex. 3550; Pet. Ex. 3651; Pet. Ex. 3952; Pet. Ex. 4153; Pet. Ex.

40

Bianca van den Berg et al., Guillain-Barré syndrome: pathogenesis, diagnosis, treatment and prognosis, 10 NAT’L

REV. NEUROLOGY 469 (2014), filed as “Resp. Ex. D, Tab 1.”

41

Peter D. Donofrio, Guillain-Barré Syndrome, 23 CONTINUUM 1295 (2017), filed as “Resp. Ex. D, Tab 3.”

42

van den Berg et al., supra note 40.

43

Donofrio, supra note 41.

44

Badrul Islam et al., Guillain-Barré syndrome following varicella-zoster virus infection, 37 EUR. J. CLINICAL

MICROBIOLOGY & INFECTIOUS DISEASES 511 (2018), filed as “Resp. Ex. D, Tab 5.”

45

van den Berg et al., supra note 40.

46

Richard A. Lewis & Suraj Ashok Muley, Chronic inflammatory demyelinating polyneuropathy: Etiology, clinical

features, and diagnosis, UPTODATE (Nov. 23, 2021, 1:57 PM), https://www.uptodate.com/contents/chronic-

inflammatory-demyelinating-polyneuropathy-etiology-clinical-features-and-diagnosis, filed as “Resp. Ex. D, Tab 9.”

47

INST. OF MED., ADVERSE EFFECTS OF VACCINES: EVIDENCE & CAUSALITY (Kathleen Stratton et al.

eds., 2012), filed as “Resp. Ex. D, Tab 8.”

48

L.H. Martín Arias et al., Guillain-Barré syndrome and influenza vaccines: A meta-analysis, 33 VACCINE 3773

(2015), filed as “Pet. Ex. 30.”

49

Penina Haber et al., Guillain-Barré Syndrome Following Influenza Vaccination, 292 J. AM. MED. ASS’N 2478

(2004), filed as “Pet. Ex. 34.”

50

Penina Haber et al., Post-licensure surveillance of quadrivalent inactivated influenza (IIV4) vaccine in the United

States, Vaccine Adverse Event Reporting System (VAERS), July 1,2013—May 31, 2015, 34 VACCINE 2507 (2016),

filed as “Pet. Ex. 35.”

51

Eugene S. Hurwitz et al., Guillain-Barré Syndrome and the 1978-1979 Influenza Vaccine, 304 N.E. J. MED. 1557

(1981), filed as “Pet. Ex. 36.”

52

Marks & Halpin, supra note 12.

53

Daniel A. Salmon et al., Association between Guillain-Barré syndrome and influenza A (H1N1) 2009 monovalent

inactivated vaccines in the USA: a meta-analysis, 381 LANCET 1461 (2013), filed as “Pet. Ex. 41.”

16

42.54 Dr. He summarized that two of the papers, Marks & Halpin and Salmon, reported the

increased risk of GBS following receipt of the pandemic swine flu vaccine. The other five studies

did not support a causal relationship between the seasonal flu vaccine and GBS, and there were no

reports filed of GBS caused by Fluzone, the vaccine petitioner received. Resp. Ex. D at 8.

Further, Dr. He asserted that Dr. Dahlgren ignored two important potential contributing

factors for petitioner’s alleged GBS and CIDP: the severe flu symptoms he reported as occurring

on October 24, 2016, and his family history of autoimmune disease making petitioner genetically

predisposed to develop autoimmune diseases such as GBS and CIDP. He added that it was

“extremely unlikely” that an immune response to a flu vaccine could result in onset of GBS and

CIDP three months later. Resp. Ex. D at 8.

Dr. He explained that latency period is defined as the “the time that passes between being

exposed to something that can cause disease (such as radiation or a virus) and having symptoms.”

Resp. Ex. D at 9. He argued that Dr. Dahlgren incorrectly used this term, and that calling a time

period for a disease to develop “latency” indicates an established causal relationship, which there

is not between the seasonal flu vaccine and GBS and CIDP. Id.

Dr. He stated that the primary immune response to an antigen reaches peak level at ten to

17 days and a secondary response to the same antigen reaches peak level in two to seven days after

priming, then starts to decline immediately thereafter. Resp. Ex. D at 9. With flu vaccination,

antibody-secreting cells peak at seven to eight days then rapidly decline, with low numbers of

antibody-secreting cells detected at 11 days post-vaccination. In less than three weeks, antigen-

specific T cells undergo a contraction phase, forming a stable memory T cell pool. Resp. Ex. D at

9; Resp. Ex. D, Tab 1055; Resp. Ex. D, Tab 11.56 Summarily, an immune response to a foreign

antigen completes its process in about three weeks, and a six-week timeframe covers two cycles

of the immune response. Therefore, six weeks or 42 days is “undoubtedly more than enough time”

for a vaccine-induced immune response to occur. Resp. Ex. D at 9. The 1976 swine flu vaccination

campaign showed no increased risk of GBS beyond six weeks, consistent with this time frame.

Therefore, it is unlikely that the flu vaccine triggered the onset of petitioner’s alleged GBS and

subsequent CIDP symptoms three months later. Id; Resp. Ex. D, Tab 12.57

Dr. He addressed the literature relied on by Dr. Dahlgren in detail. Resp. Ex. D at 10. He

noted that Prestel58 investigated the Miller Fisher variant of GBS after the 2009 H1N1 pandemic

vaccination, not a seasonal flu vaccine, and these are very different because the seasonal flu

vaccine does not contain adjuvants. Further, the risk period was defined as five to 42 days after

vaccination while the control period was 43-150 days, and cases that occurred at days 43-150 were

54

Sukhminder K. Sandhu et al., Near real-time surveillance for Guillain-Barré syndrome after influenza vaccination

among the Medicare population, 2010/11 to 2013/14, 35 VACCINE 2986 (2017), filed as “Pet. Ex. 42.”

55

Rebecca J. Cox et al., An early humoral immune response in peripheral blood following parenteral inactivated

influenza vaccination, 12 VACCINE 993 (1994), filed as “Resp. Ex. D, Tab 10.”

56

Matthew A. Williams & Michael J. Bevan, Effector and Memory CTL Differentiation, 25 ANN. REV. IMMUNOLOGY

171 (2007), filed as “Resp. Ex. D, Tab 11.”

57

Thomas J. Safranek et al., Reassessment of the Association between Guillain-Barré Syndrome and Receipt of Swine

Influenza Vaccine in 1976-1977: Results of a Two-State Study, 133 AM. J. EPIDEMIOLOGY 940 (1991), filed as “Resp.

Ex. D, Tab 12.”

58

Prestel et al., supra note 10.

17

studied as vaccination-unrelated controls, with no increased risk of GBS following the swine flu

vaccine found beyond six weeks. Dr. He also noted that Dr. Dahlgren misinterpreted Table 4 of

Prestel, explaining that age was not a modifier and there was no difference between age groups in

terms of GBS risk following Pandemix vaccination. Id. at 10-11. Similarly, Kaplan59 suggested no

increased risk of GBS with flu vaccines, noting that the “trigger agent” present in the 1976 swine

flu vaccine was not present in subsequent flu vaccines. Id. at 12. Marks & Halpin60 discussed the

1976 swine flu pandemic having an increased risk of GBS within six weeks of swine flu

vaccination but no increased risk beyond 6 weeks, and Schonberger61 reported GBS after the 1976

swine flu vaccine with an increased risk concentrated primarily within the five-week period after

vaccination. Id. at 11-12.

Watad62 had no relevance to flu vaccine and GBS and studied the relationship between

ASIA and adjuvants, but petitioner’s flu vaccine did not have an adjuvant. Resp. Ex. D at 13.

Soriano63, Tomljenovic64, Agmon-Levin65, and Liu & Kaplowitz66 all studied vaccines other than

the flu vaccine and diseases other than GBS. Id. at 11, 13-15. According to Dr. He, Dr. Dahlgren

mischaracterized Colafranceso67, which did not study any disease latency as he alleged. Resp. Ex.

D at 14.

Dr. He detailed the differences between an immune response to a viral infection versus that

to a vaccination, concluding that the fact that petitioner experienced severe flu symptoms a month

after his vaccination suggests that the infection, not the vaccination, “is a much more likely trigger

of his alleged GBS and CIDP.” Resp. Ex. D at 15-16. Dr. He claimed that Dr. Dahlgren failed to

discuss this illness and misinterpreted the studies he relied on to argue that a three-month onset

following vaccination was reasonable. Id. at 19.

Dr. He then addressed Dr. Dahlgren’s supplemental report and opinions related to the flu

vaccine and CIDP. He noted that Köller68 summarized different aspects of CIDP but did not discuss

any information related to vaccination, and Restrepo-Jimenez69 discussed immunotherapy for

GBS, not vaccines. Resp. Ex. D at 19. According to Dr. He, updated literature indicates that in the

majority of patients, the specific immunologic triggers or causes of CIDP remain unclear, and no

specific predisposing risk factors for CIDP have been identified. Blum & McCombe70 did not

present any evidence to suggest any relationship between vaccination and CIDP. Resp. Ex. D at

20; Resp. Ex. D, Tab 9.71 Dr. He agreed that there need to be more studies comparing GBS and

CIDP in order to understand the pathogenesis of the two diseases. Resp. Ex. D at 20.

59

Kaplan et al., supra note 14.

60

Marks & Halpin, supra note 12.

61

Schonberger et al., supra note 13.

62

Watad et al., supra note 15.

63

Soriano et al., supra note 11.

64

Tomljenovic et al., supra note 16.

65

Agmon-Levin et al., supra note 17.

66

Liu & Kaplowitz et al., supra note 19.

67

Colafrancesco et al., supra note 18.

68

Köller et al., supra note 25.

69

Restrepo-Jiménez et al., supra note 28.

70

Blum & McCombe, supra note 24.

71

Lewis & Muley, supra note 46.

18

Dr. He submitted that the Kuitwaard72 study did not investigate vaccinations as a cause of

CIDP or GBS, but rather whether vaccinations led to recurrences of GBS or increased disability

in CIDP in patients who were already diagnosed with GBS or CIDP. The study found no recurrence

or increased symptoms in GBS and increased symptoms in a fraction of CIDP patients, with no

evidence to suggest a causal link. Resp. Ex. D at 21. Further, the study supported genetics as a

factor in autoimmune disease, which supports that petitioner’s family history of autoimmune

disease was a more important factor in his development of GBS and CIDP than the vaccine. Id.

Dr. He opined that the second Kuitwaard73 study did not support Dr. Dahlgren’s claim that

there is an overlap between GBS and CIDP. Resp. Ex. D at 21. One of the four patients that the

article focused on developed GBS following a flu vaccination at age 39 and developed CIDP at

age 68. He added that it was unclear which flu vaccine the patient received at age 39 and what his

history was in the 29 years between the onset of GBS and CIDP, and it was just a reporting of

temporal relation. Id. at 21-22. Dr. He stated that the IOM concluded that Brostoff74 and

Pritchard75 did not provide any mechanistic evidence beyond a temporal relationship and therefore

cannot be used as evidence to draw causal conclusions. Id. at 22.

Dr. He summarized that Dr. Dahlgren cited references showing results of disease

recurrences after flu vaccination and a case report of CIDP after H1N1 vaccination, but “did not

provide convincing evidence” to connect seasonal flu vaccines including Fluzone to GBS or CIDP

after three months. Resp. Ex. D at 23. He concluded that Dr. Dahlgren did not provide any reliable

evidence to support his theory that the Fluzone vaccine caused petitioner’s GBS and/or CIDP that

led to his death. Id. at 24.

V. Standards for Adjudication

A. Legal Standard Regarding Causation

The Vaccine Act provides two avenues for petitioners to receive compensation. First, a

petitioner may demonstrate a “Table” injury—i.e., an injury listed on the Vaccine Injury Table

that occurred within the provided time period. 42 U.S.C. § 300aa-11(c)(1)(C)(i). “In such a case,

causation is presumed.” Capizzano v. Sec’y of Health & Human Servs., 440 F.3d 1317, 1320 (Fed.

Cir. 2006); see § 13(a)(1)(B). Second, where the alleged injury is not listed on the Vaccine Injury

Table, a petitioner may demonstrate an “off-Table” injury, which requires that the petitioner

“prove by a preponderance of the evidence that the vaccine at issue caused the injury.” Capizzano,

440 F.3d at 1320; see § 11(c)(1)(C)(ii); see also Wright v. Sec’y of Health & Human Servs., 22

F.4th 999, 1006 (Fed. Cir. 2022) (defining the term “residual effects” in the Act, as “detrimental

conditions within the patient, such as lingering or recurring signs and symptoms” of the alleged

vaccine injury, which are compensable). A petitioner need not show that the vaccination was the

sole cause, or even the predominant cause, of the alleged injury; showing that the vaccination was

72

Kuitwaard et al., supra note 26.

73

Kuitwaard et al., supra note 27.

74

Brostoff et al., supra note 35.

75

J. Pritchard et al., Risk of relapse of Guillain-Barré syndrome or chronic inflammatory demyelinating

polyradiculoneuropathy following immunization, 73 J. NEUROLOGY, NEUROSURGERY, & PSYCHIATRY 348 (2002),

filed as “Pet. Ex. 61.”

19

a “substantial factor” and a “but for” cause of the injury is sufficient for recovery. Pafford v. Sec’y

of Health & Human Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006); Shyface v. Sec’y of Health &

Human Servs., 165 F.3d 1344, 1352 (Fed. Cir. 1999). Petitioners are not required “to eliminate

alternative causes as part of establishing [their] prima facie case.” Doe v. Sec’y of Health & Human

Servs., 601 F.3d 1349, 1357-58 (Fed. Cir. 2010); see Walther v. Sec’y of Health & Human Servs.,

485 F.3d 1146, 1152 (Fed. Cir. 2007) (holding that a “petitioner does not bear the burden of

eliminating alternative independent potential causes”). Once a petitioner has proven causation by

preponderant evidence, “the burden then shifts to the respondent to show by a preponderance of

the evidence that the injury is due to factors unrelated to the administration of the vaccine.”

Deribeaux ex rel. Deribeaux v. Sec’y of Health & Human Servs., 717 F.3d 1363, 1367 (Fed. Cir.

2013) (citing 42 U.S.C. § 300aa-13(a)(1)(B)).

To prove causation, a petitioner must satisfy the three-pronged test established in Althen v.

Sec’y of Health & Human Servs., 418 F.3d 1274 (Fed. Cir. 2005). Althen requires that a petitioner

show by preponderant evidence that a vaccination they received caused their injury “by providing:

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

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

a proximate temporal relationship between vaccination and injury.” Id. at 1278. Together, these

prongs must show “that the vaccine was ‘not only a but-for cause of the injury but also a substantial

factor in bringing about the injury.’” Stone v. Sec’y of Health & Human Servs., 676 F.3d 1373,

1379 (Fed. Cir. 2012) (quoting Shyface, 165 F.3d at 1352-53). Causation is determined on a case-

by-case basis, with “no hard and fast per se scientific or medical rules.” Knudsen v. Sec’y of Health

& Human Servs., 35 F.3d 543, 548 (Fed. Cir. 1994). Petitioners are not required to identify

“specific biological mechanisms” to establish causation, nor are they required to present

“epidemiologic studies, rechallenge, the presence of pathological markers or genetic disposition,

or general acceptance in the scientific or medical communities.” Capizzano, 440 F.3d at 1325

(quoting Althen, 418 F.3d at 1280). “[C]lose calls regarding causation are resolved in favor of

injured claimants.” Althen, 418 F.3d at 1280.

Each Althen prong requires a different showing. Under the first prong, a petitioner must

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

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

petitioner’s “theory of causation must be supported by a ‘reputable medical or scientific

explanation.’” Andreu, 569 F.3d at 1379 (quoting Althen, 418 F.3d at 1278). This theory need only

be “legally probable, not medically or scientifically certain.” Id. at 1380 (emphasis omitted)

(quoting Knudsen, 35 F.3d at 548). Nevertheless, “petitioners [must] proffer trustworthy testimony

from experts who can find support for their theories in medical literature.” LaLonde, 746 F.3d at

1341.

The second Althen prong requires proof of a “logical sequence of cause and effect.”

Capizzano, 440 F.3d at 1326 (quoting Althen, 418 F.3d at 1278). Even if the vaccination can cause

the injury, a petitioner must show “that it did so in [this] particular case.” Hodges v. Sec’y of Health

& Human Servs., 9 F.3d 958, 962 n.4 (Fed. Cir. 1993) (citation omitted). “A reputable medical or

scientific explanation must support this logical sequence of cause and effect,” Id. at 961 (citation

omitted), and “treating physicians are likely to be in the best position to determine whether a

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

20

Paluck v. Sec’y of Health & Human Servs., 786 F.3d 1373, 1385 (Fed. Cir. 2015) (quoting Andreu,

569 F.3d at 1375).

The third Althen prong requires that a petitioner establish a “proximate temporal

relationship” between the vaccination and the alleged injury. Althen, 418 F.3d at 1281. This

“requires preponderant proof that the onset of symptoms occurred within a timeframe for which,

given the medical understanding of the disorder’s etiology, it is medically acceptable to infer

causation-in-fact.” De Bazan v. Sec’y of Health & Human Servs., 539 F.3d 1347, 1352 (Fed. Cir.

2008). Typically, “a petitioner’s failure to satisfy the proximate temporal relationship prong is due

to the fact that onset was too late after the administration of a vaccine for the vaccine to be the

cause.” Id. However, “cases in which onset is too soon” also fail this prong; “in either case, the

temporal relationship is not such that it is medically acceptable to conclude that the vaccination

and the injury are causally linked.” Id.; see also Locane v. Sec’y of Health & Human Servs., 685

F.3d 1375, 1381 (Fed. Cir. 2012) (“[If] the illness was present before the vaccine was administered,

logically, the vaccine could not have caused the illness.”).

B. Legal Standard Regarding Fact Finding

The process for making factual determinations in Vaccine Program cases begins with

analyzing the medical records, which are required to be filed with the petition. § 11(c)(2). Medical

records created contemporaneously with the events they describe are presumed to be accurate and

“complete” such that they present all relevant information on a patient’s health problems. Cucuras

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

contemporaneous reports, “accuracy has an extra premium” given that the “proper treatment

hang[s] in the balance.” Id. Contemporaneous medical records that are clear, consistent, and

complete warrant substantial weight “as trustworthy evidence.” Id. Indeed, “where later testimony

conflicts with earlier contemporaneous documents, courts generally give the contemporaneous

documentation more weight.” Campbell ex rel. Campbell v. Sec’y of Health & Human Servs., 69

Fed. Cl. 775, 779 (2006); see United States v. U.S. Gypsum Co., 333 U.S. 364, 396 (1948). But

petitioners can support their claim with oral testimony if it is credible and consistent with the

medical records. See, e.g., Stevenson ex rel. Stevenson v. Sec’y of Health & Human Servs., No. 90-

2127V, 1994 WL 808592, at *7 (Fed. Cl. Spec. Mstr. June 27, 1994) (crediting the testimony of a

fact witness whose “memory was sound” and “recollections were consistent with the other factual

evidence”). In short, “the record as a whole” must be considered. § 13(a).

C. Evaluating Expert Testimony

Establishing a sound and reliable medical theory connecting the vaccine to the injury often

requires a petitioner to present expert testimony in support of his or her claim. Lampe v. Sec’y of

Health & Human Servs., 219 F.3d 1357, 1361 (Fed. Cir. 2000). The Supreme Court’s opinion in

Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579 (1993), requires that courts

determine the reliability of an expert opinion before it may be considered as evidence. “In short,

the requirement that an expert’s testimony pertain to ‘scientific knowledge’ establishes a standard

of evidentiary reliability.” Id. at 590 (citation omitted). Thus, for Vaccine Act claims, a “special

master is entitled to require some indicia of reliability to support the assertion of the expert

witness.” Moberly ex rel. Moberly v. Sec’y of Health & Human Servs., 592 F.3d 1315, 1324 (Fed.

21

Cir. 2010). The Daubert factors are used in the weighing of the reliability of scientific evidence

proffered. Davis v. Sec’y of Health & Human Servs., 94 Fed. Cl. 53, 66-67 (2010) (“uniquely in

this Circuit, the Daubert factors have been employed also as an acceptable evidentiary-gauging

tool with respect to persuasiveness of expert testimony already admitted”). Where both sides offer

expert testimony, a special master’s decision may be “based on the credibility of the experts and

the relative persuasiveness of their competing theories.” Broekelschen, 618 F.3d at 1347 (citing

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

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

great an analytical gap between the data and the opinion proffered.” Snyder ex rel. Snyder v. Sec’y

of Health & Human Servs., 88 Fed. Cl. 706, 743 (2009) (quoting Gen. Elec. Co. v. Joiner, 522

U.S. 136, 146 (1997)).

D. Consideration of Medical Literature

Finally, although this decision discusses some but not all the literature in detail, the

undersigned reviewed and considered all of the medical records and literature submitted in this

matter. See Moriarty ex rel. Moriarty v. Sec’y of Health & Human Servs., 844 F.3d 1322, 1328

(Fed. Cir. 2016) (“We generally presume that a special master considered the relevant record

evidence even though [s]he does not explicitly reference such evidence in h[er] decision.”);

Simanski v. Sec’y of Health & Human Servs., 115 Fed. Cl. 407, 436 (2014) (“[A] Special Master

is ‘not required to discuss every piece of evidence or testimony in her decision.’” (citation

omitted)), aff’d, 601 F. App’x 982 (Fed. Cir. 2015).

VI. Discussion

A. Petitioner’s Diagnosis

As a threshold matter, petitioner must first establish that he actually suffered the injury

alleged in the petition. See Broekelschen v. Sec’y of Health and Human Servs., 618 F.3d 1339,

1346 (Fed. Cir. 2010). As the Federal Circuit precedent establishes, in certain cases it is appropriate

to determine the nature of the petitioner’s injury before engaging in the Althen analysis. Id. Thus,

where “the existence and nature of the injury itself is in dispute, it is the special master’s duty to

first determine which injury is best supported” by the evidence. Lombardi v. Sec’y of Health and

Human Servs., 656 F.3d 1343, 1352 (Fed. Cir. 2011) (affirming a special master’s decision to

dismiss a petition when the petitioner could not establish that she had any of the three diagnoses

alleged) (citing Broekelschen, 618 F.3d at 1345) (emphasis added).

1. Overview of GBS and CIDP

Guillain-Barre Syndrome (“GBS”) is an acute autoimmune disorder of the peripheral

nerves characterized primarily by muscle weakness and loss of reflexes. Pet. Ex. 30 at 1.76 GBS is

often associated with a preceding gastrointestinal or upper respiratory tract infection, including

influenza, generally 10-14 days prior to onset. About 70% of patients report preceding illness,

though it is often benign and may be minimized or forgotten by the patient. Id.; Resp. Ex. A, Tab

76

Martín Arias et al., supra note 48.

22

4 at 1.77 The exact causes of GBS are unknown, but it is thought to be triggered by antigenic

stimulation resulting in demyelination and damage to the peripheral nerves. Pet. Ex. 30 at 1.78 GBS

has several subgroups that are described by corresponding diagnostic criteria and can be divided

on pathological grounds into acute inflammatory demyelinating polyradiculoneuropathy (“AIDP”)

and acute motor axonal neuropathy (“AMAN”). There are also variants of GBS such as Miller

Fisher Syndrome Pet. Ex. 56 at 1.79 GBS evolves over days, often beginning with numbness and

weakness in the lower limbs. The weakness can be rapid, resulting in quadriplegia within days.

Approximately 50% of GBS patients experience maximum weakness by two weeks, 80% by three

weeks, and 90% by four weeks. Progression beyond four weeks is unusual and raises concern for

other illnesses, particularly CIDP. Resp. Ex. A, Tab 4 at 2.80 Essentially all patients will have

areflexia or at least hyporeflexia at some point during the illness. About 50% will develop facial

weakness or other cranial nerve issues, and 30% develop respiratory failure and require intubation

and ventilation. Id. The Brighton Collaboration Diagnostic Criteria for GBS includes: bilateral and

flaccid weakness of limbs; decreased or absent deep tendon reflexes in the weak limbs;

monophasic illness and interval between onset and nadir of weakness between 12 hours and 28

days and subsequent clinical plateau; electrophysiologic findings consistent with GBS;

albuminocytologic dissociation – elevation of the CSF protein level above laboratory normal value

and CSF total white blood cell count less than 50 cells/ 2µL; and absence of an identified

alternative diagnosis for weakness. Id. at 6. Features that cast doubt or eliminate GBS as the

diagnosis include marked persistent asymmetry of weakness, bowel or bladder dysfunction at

onset, the presence of greater than 50 cells/ 2µL in CSF, sharp sensory level, severe pulmonary

dysfunction with little or no limb weakness at onset, fever at onset, and/or slow progression of

weakness more than four weeks. Id. at 7.

Chronic inflammatory demyelinating polyneuropathy (“CIDP”) is a chronic or

relapsing motor and sensory neuropathy, with inflammation and demyelination of the peripheral

nerve. Pet. Ex. 56 at 1.81 It is characterized by symmetrical weakness in both proximal and distal

muscles that progressively increases for more than two months, setting it apart from GBS, which

is self-limited. Pet. Ex. 58 at 1.82 CIDP is associated with impaired sensation, absent or diminished

tendon reflexes, an elevated cerebrospinal fluid protein level, demyelinating nerve conduction

studies, and signs of demyelination in nerve biopsy specimens. The course can be relapsing or

chronic and progressive. Id. CIDP responds well to corticosteroid treatment, distinguishing it from

other forms of acquired demyelinating polyneuropathies. Id. at 1-2. The cause of CIDP is

unknown, although abnormalities in both cellular and humoral immunity have been shown. Pet.

Ex. 70 at 1.83

Both GBS and CIDP are considered immune-mediated polyneuropathies associated with a

variable clinical courses and outcomes. There have been reports of rare patients affected by both

GBS and CIDP, suggesting that GBS and CIDP may constitute a continuum or that there are

77

Donofrio, supra note 41.

78

Martín Arias et al., supra note 48.

79

Blum & McCombe, supra note 24.

80

Donofrio, supra note 41.

81

Blum & McCombe, supra note 24.

82

Köller et al., supra note 25.

83

Richard A. Lewis, Chronic inflammatory demyelinating polyneuropathy, 30 CURRENT OPINION NEUROLOGY 1

(2017), filed as “Pet. Ex. 70.”

23

common host factors that influence susceptibility to these disorders. Pet. Ex. 60 at 1.84 While GBS

and CIDP have some similarities, there are also clear differences:

Antiganglioside antibodies are frequently detected in GBS, but are generally absent

in CIDP. Preceding infections are less frequently reported in CIDP, but infections

during the course of CIDP may clearly worsen symptoms . . . most CIDP patients

improve after steroids, whereas GBS patients do not. On the other hand, most GBS

and CIDP patients improve after IVIg or plasma exchange.

Pet Ex. 60 at 2.85 Most patients fit the diagnostic criteria of either GBS or CIDP, and though

extremely uncommon, a patient may have separate episodes of GBS and CIDP and must be

diagnosed and treated accordingly. Id.; see also Pet. Ex. 56.86

2. Determination of Diagnosis

The petition filed in this matter alleges and Dr. Dahlgren initially opined that petitioner

suffered from GBS as a result of a September 27, 2016 flu vaccination. See Petition, ECF No. 1;

Pet. Ex. 26. In his three subsequent reports, Dr. Dahlgren opined that petitioner suffered from both

GBS and CIDP, with the only difference between the two diseases being chronicity. Pet. Ex. 55;

Pet. Ex. 64; Pet. Ex. 65. It bears repeating that petitioner alleged that he suffered GBS as a result

of his Fluzone vaccination and never amended his petition to include CIDP, even though Dr.

Dahlgren ultimately opined that petitioner suffered both GBS and CIDP. Drs. Jamieson and He

disagreed, maintaining that GBS and CIDP are two distinct diseases, and one cannot be substituted

for the other. Resp. Ex. A; Resp. Ex. C; Resp. Ex. D. Dr. Jamieson opined that petitioner suffered

from CIDP. Resp. Ex. A; Resp. Ex. C.

Petitioner’s treating neurologist ultimately diagnosed him with CIDP due to the relapsing

and remitting nature of his condition and his response to IVIG and steroids. Pet. Ex. 11 at 11, 15,

21; Pet. Ex. 15 at 73; Pet. Ex. 53 at 747, 756. Petitioner died on November 23, 2019, and his cause

of death was listed as respiratory failure, CIDP, malnutrition, severe deconditioning, atrial

fibrillation, neurogenic bladder, and anemia. Pet. Ex. 49.

Treating doctors’ views about the appropriate diagnosis are often persuasive because the

doctors have direct experience with the patient they are diagnosing. See McCulloch v. Sec’y of

Health & Human Servs., No. 09-293V, 2015 WL 3640610, at *20 (Fed. Cl. Spec. Mstr. May 22,

2015). Based on the history of petitioner’s condition, the onset and progression of symptoms from

the end of December 2016 through February 2017, his response to steroids and later to IVIG, the

relapsing and remitting nature of his symptoms, and the opinion of his treating neurologist,

petitioner fit the criteria for a diagnosis of CIDP, not GBS which is a monophasic disease with

rapid onset that reaches nadir than resolves.

84

Kuitwaard et al., supra note 27.

85

Id.

86

Abnormalities of T cells, antibodies, and gene expression have been reported in the peripheral blood of subjects

with GBS and CIDP. Although the two have similar pathological features, the course of the diseases differ: “it would

seem very likely that subjects with GBS would differ from subjects with CIDP in their ability to regulate immune

attack on peripheral nerve, with GBS being an acute self-limited disease and CIDP an ongoing disease.” Blum &

McCombe, supra note 24 at 1, 10.

24

B. Althen Prongs

1. Petitioner Failed to Show an Appropriate Temporal Relationship Between

His Receipt of an Influenza Vaccine and His Development of CIDP.

The Vaccine Injury Table lists GBS as an injury resulting from the administration of the

flu vaccine when the first symptom or manifestation of onset appears within between three and

forty-two days, and specifically “not less than 3 days and not more than 42 days.” See 42 C.F.R. §

100.3(a)(XIV)(D). Petitioner reported onset of symptoms over three months, or at the earliest 94

days, after his receipt of the September 27, 2016 flu vaccine. Therefore, an important issue in this

case is onset, and whether three months or more after flu vaccination is a medically acceptable

timeframe for the onset of CIDP following a flu vaccine. Althen Prong III requires petitioner to

both “establish the time frame for which it is medically acceptable to infer causation,” and show

that the onset of his injury occurred during that causation period. Shapiro v. Sec’y of Health &

Human Servs., 105 Fed. Cl. 353, 360 (2012), aff’d, 503 F. App’x 952 (Fed. Cir. 2013).

Dr. Dahlgren acknowledged that onset was more than three months following petitioner’s

receipt of the subject flu vaccine, but he argued that petitioner had memory problems, the 42 days

used in vaccine cases is an arbitrary number, and the literature he presented supports onset beyond

42 days following flu vaccine. See Pet. Ex. 26.

a. Onset of Petitioner’s Neurological Problems

Dr. Dahlgren suggested that even though petitioner presented to his physician 12 weeks

after vaccination, it is unclear when his symptoms started because of his memory problems and

because he reported that his symptoms started “several” days before his presentation but failed to

report that he suffered from flu-like symptoms from October 24 to 27, 2015. Pet. Ex. 55 at 1-2.

Dr. Dahlgren submitted that the foregoing was indictive of his memory problems, and the date of

onset of his weakness should therefore “not be considered as a definitive line disqualification to a

conclusion that the flu vaccine was the triggering event” for CIDP. Id. at 2.

However, petitioner’s wife regularly accompanied him to his medical visits and

supplemented his history as evidenced in the medical records. See Pet. Ex. 5 at 41, 64; Pet. Ex. 10

at 2; Pet. Ex. 11 at 2. She was present when petitioner presented to the ER reporting onset of

numbness “several days” prior, and when he reported onset of tingling in all limbs around

December 28, 2016, over the two days he was off from work. Pet. Ex. 5 at 41; Pet. Ex. 11 at 2.

She showed the doctor a video of petitioner moving his fingers while sitting still from April 2016

and questioned whether it was a clue to some neurological condition. Pet. Ex. 11 at 2. She did not

correct the onset of symptoms he reported. Therefore, an onset around December 28, 2016 is

consistent with the evidence.

b. Expected Interval Between Vaccination and Onset

Dr. Dahlgren defined “latency” as the duration of time between the vaccination and the

onset of symptoms and argued that the “42 day latency is arbitrary and fails to consider all the

evidence. Some vaccine induced autoimmune disease cases have their onset within 42 days, but

25

not all.” Pet. Ex. 26 at 3 (emphasis in original). Citing to medical literature that he submitted

supported onset occurring later than 42 days, Dr. Dahlgren concluded that the literature supports

his opinion that the 42-day period for onset “should not be applied as a hard and fast deadline.” Id.

at 4-12.; Pet. Ex. 55; Pet. Ex.

Dr. He described onset of symptoms three months after vaccination as “a long timeframe

that is extremely unlikely caused by any immune responses stimulated by his influenza vaccine.”

Resp. Ex. D at 8. Dr. He pointed out that Dr. Dahlgren misused the term “latency” throughout his

reports, because the term indicates an established causal relationship, “which is certainly not the

case” for the seasonal flu vaccine and GBS or CIDP. Id. at 9.

Dr. He explained that the six-week or 42-day temporal relationship between vaccination

and GBS in the Table is “very much consistent with the nature of an immune response to

vaccination or infection.” Resp. Ex. D at 9. In the case of a flu vaccination, antibody-secreting

cells peak at seven to eight days after vaccination then rapidly decline, with low numbers of

antibody-secreting cells detected 11 days post-vaccination. In less than three weeks, antigen-

specific T cells undergo a contraction phase, forming a stable memory T cell pool. Thus, an

immune response to a foreign antigen completes its process in about three weeks, and the six-week

timeframe covers two cycles of immune responses, which is “undoubtedly more than enough time”

for a vaccination-induced immune response to occur, if GBS was in fact caused by flu vaccine. Id.

Dr. He noted that the increased risk of GBS after the 1976 swine flu vaccination campaign was

within six weeks following vaccination, with no increased risk of GBS found beyond six weeks.

Id.; Resp. Ex. D, Tab 12.87

Dr. He then addressed the literature relied on by Dr. Dahlgren, noting that Dr. Dahlgren

“mischaracterized, misinterpreted, or made wrong claims based on his cited references.” Resp. Ex.

D at 19. Dr. He opined that much of the literature Dr. Dahlgren filed was not related to GBS, flu

vaccine, or both. Resp. Ex. D at 11-14; Pet. Ex. 4588; Pet. Ex. 4889; Pet. Ex. 3790; Pet. Ex. 2891;

Pet. Ex. 3892; Pet. Ex. 31.93 Further, none of the literature provided supports that onset could occur

more than three months after vaccination as alleged by Dr. Dahlgren. Resp. Ex. D at 16-19. In fact,

Dr. He explained that several of the studies filed by Dr. Dahlgren actually support the 42-day onset

interval. Id. at 17; Pet. Ex. 4394; Pet. Ex. 32.95 According to Dr. He, the onset of autoimmune

disease within three to 42 days is not only based on evidence from many studies but is also strongly

supported by the natural cycles of immune responses to foreign antigens. Resp. Ex. D at 9, 17. He

submitted that Sejvar concluded that six weeks “following any identified antecedent event would

represent a reasonable period of surveillance, beyond which biological plausibility of an

association with an identifiable antigenic stimulus (e.g., infectious illness, vaccination) declines.”

87

Safranek et al., supra note 57.

88

Soriano et al., supra note 11.

89

Watad et al., supra note 15.

90

Tomljenovic et al., supra note 16.

91

Agmon-Levin et al., supra note 17.

92

Liu & Kaplowitz, supra note 19.

93

Colafrancesco et al., supra note 18.

94

Schonberger at al., supra note 13.

95

Dodd et al., supra note 20.

26

Id. at 18; Pet. Ex. 44.96 Finally, Dr. He noted that latency was not discussed in any of the literature

relied on by Dr. Dahlgren. Resp. Ex. D at 17.

Dr. Jamieson did not address the onset issue in detail other than to say that there is no

immunological or epidemiological support for a flu vaccine triggering CIDP three months later.

She aptly stated that relying on literature discussing other diseases and other vaccines cannot be

substituted for a distinct disease and a flu vaccine. Resp. Ex. A at 20-21; Resp. Ex. C at 3.

Dr. Dahlgren is neither a neurologist nor immunologist. His opinions therefore carry less

weight than those of Dr. Jamieson and Dr. He. Further, the literature he relied on is unpersuasive

for a number of reasons: he conflated latency and onset, suggesting that the cited literature

discussed causation when they discussed temporal relationship; he relied on studies involving the

swine flu vaccine and GBS, not seasonal influenza vaccine; he conflated the progressive nature of

CIDP, which evolves over a period of two months before reaching nadir, with onset being in excess

of two months; and he relied on literature related to other vaccines and other autoimmune diseases,

which cannot be substituted for flu vaccine and GBS or CIDP. Finally, not one of the articles cited

by Dr. Dahlgren supported onset in excess of eight weeks. Petitioner’s onset was 94 days, or more

than three months after flu vaccination.

Regardless of whether I determined that petitioner suffered from GBS or CIDP, an onset

of 94 days or over three months after flu vaccination is wholly unsupported by the medical

literature. Past Program decisions have accepted eight weeks as the outer limit for the onset of a

non-Table claim of GBS following flu vaccine. See, e.g., Williams v. Sec'y of Health & Human

Servs., No. 19-1177V, 2021 WL 815921, at *5 (Fed. Cl. Spec. Mstr. Jan. 19, 2021) (finding over

100 days is not a reasonable timeframe for onset of a flu vaccine/GBS injury); Chinea v. Sec'y of

Health & Human Servs., No. 15-095V, 2019 WL 1873322, at *33 (Fed. Cl. Spec. Mstr. Mar. 15,

2019), review denied, 144 Fed. Cl. 378 (2019) (finding that the onset of the petitioner's GBS

occurred eleven to twelve weeks after her vaccination, which was beyond the six- to eight-week

medically appropriate timeframe for the occurrence of vaccine-induced GBS); Barone v. Sec'y of

Health & Human Servs., No. 11-707V, 2014 WL 6834557, at *13 (Fed. Cl. Spec. Mstr. Nov. 12,

2014) (finding eight weeks (56 days) is the longest reasonable timeframe for a flu vaccine/GBS

injury).

Petitioner has not presented any evidence to support the onset of GBS or CIDP 94 days or

over three months after a flu vaccine and has therefore failed to sustain his burden under Prong III.

2. Petitioner Has Not Articulated a Sound and Reliable Medical Theory

Causally Connecting Influenza Vaccine to GBS or CIDP.

Petitioner’s failure to prove Prong III is dispositive. However, the remaining Althen Prongs

will be addressed briefly, nonetheless.

The first Althen prong requires petitioner provide a “reputable medical theory”

demonstrating that the vaccines received can cause the type of injury alleged. Pafford, 451 F.3d at

1355-56 (citation omitted). To satisfy this prong, petitioner’s “theory of causation must be

96

Sejvar et al., supra note 22.

27

supported by a ‘reputable medical or scientific explanation.’” Andreu, 569 F.3d at 1379 (quoting

Althen, 418 F.3d at 1278). This theory need only be “legally probable, not medically or

scientifically certain.” Id. at 1380 (emphasis omitted) (quoting Knudsen, 35 F.3d at 548). This

standard was clarified by the Federal Circuit. See Boatmon v. Sec’y of Health & Human Servs.,

941 F.3d at 1351, 1359-60 (Fed. Cir. 2019) (stating that the correct standard for Althen prong one

is “reputable,” and “sound and reliable” not a “lower reasonable standard” (internal quotations

omitted)). Nevertheless, “petitioners [must] proffer trustworthy testimony from experts who can

find support for their theories in medical literature.” LaLonde, 746 F.3d at 1341.

To that end, the experts disagree regarding whether GBS and CIDP are the same disease

that only differ in chronicity or duration, and Drs. Jamieson and He argue that no studies support

the seasonal flu vaccine as a cause of GBS and/or CIDP.

a. Dr. Dahlgren’s Opinion

Dr. Dahlgren opined that petitioner developed the “autoimmune neurological condition of

GBS and CIDP” as a result of the flu vaccine he received on September 27, 2016. Pet. Ex. 55 at

13. According to Dr. Dahlgren, other than chronicity, GBS and CIDP are the same disease and

have the “same mechanism” or “common etiology” that causes autoimmune damage to myelin

through the formation of antibodies against myelin “due to the breakdown in self-recognition due

to a failure in the body’s immune system.” Id. at 2-3, 5-7; Pet. Ex. 26 at 3. A vaccine purposely

stimulates the immune system, and “a rare number of individuals experience an overactive,

erroneous complication of an errant immune reaction” based on predisposition due to individual

susceptibility. Pet. Ex. 55 at 3. For both GBS and CIDP, the “treatment is the same, IVIG.” Id. Dr.

Dahlgren articulated his “medical theory” as “[q]uite simply, vaccines increase the activity of the

immune system, and in some rare cases, an abnormal autoimmune system attacks and damages the

myelin around nerves.” Pet. Ex. 64 at 3. He added that in the medical records, petitioner’s treating

doctors referred to petitioner having both GBS and CIDP. Pet. Ex. 55 at 2-5.

Dr. Dahlgren addressed Dr. Jamieson’s opinion, noting that she agreed GBS and CIDP

share common pathology and treatment but have different presentations and prognoses. Pet. Ex.

64 at 4. He asserted that suggesting that a difference in clinical course makes them fundamentally

different diseases “is not correct science. When a disease has a common mechanism and response

to treatment and occurring (sic) after a common over aberrant over stimulation of the immune

system, they are related entities.” Id. Dr. Dahlgren added, “the epidemiology has many reasons to

fail to support a finding of causation because epidemiology alone cannot prove causation, only

additional underlying science can prove causation . . . Epidemiology only addresses association

and it takes other pieces of the picture to reach a conclusion about causation.” Id. at 4-5. Dr.

Dahlgren argued that Dr. Jamieson cited only to negative epidemiological studies to refute a

relationship between GBS and vaccines, but “[i]n the case of GBS and CIDP the mechanisms and

treatment responses are well worked out for GBS and CIDP and clinch the issue of causation. The

mechanism of the immune system attacking the myelin in both GBS and CIDP due to an altered

immune system is not addressed by Dr. Jamieson.” Id. at 5. He noted that Dr. Jamieson agreed that

IVIG is effective in both diseases, which suggests a common mechanism. Id. at 3.

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Dr. Dahlgren also noted that several of the articles Dr. He submitted “explain why in a few

cases there can be an autoimmune disease such as GBS and CIDP due to a rare defect in the

immune system of a few people who receive a vaccination. Pet. Ex. 65 at 4. He added that the

Segal & Shoenfeld97 article discusses molecular mimicry as a mechanism for autoimmunity from

vaccines. He opined that molecular mimicry is a well-studied mechanism to explain how GBS and

CIDP occur and that they have similar self-antigens to the myelin protective coating of the nerves.

Id. This is the only time throughout his four reports that Dr. Dahlgren referenced a mechanism by

which the flu vaccine could cause GBS and/or CIDP, but he provided no further explanation.

Dr. Dahlgren concluded that the Vaccine Court has already determined that GBS is a

compensable injury and since the evidence supports GBS and CIDP being related, CIDP, like GBS,

is a complication of vaccine administration and a compensable injury. Pet. Ex. 64 at 3-5.

b. Drs. Jamieson and He’s Opinions

Drs. Jamieson and He disagree with Dr. Dahlgren’s assertion that GBS and CIDP are the

same disease. The two diseases do not have the same pathophysiology and are not treated the same

way, so one therefore cannot be substituted for the other. Drs. Jamieson and He further disagree

that there is any support for the seasonal flu vaccine causing GBS or CIDP, noting that the literature

referring to vaccine-related GBS is specific to the 1976 and 2009 H1N1 vaccines, not seasonal flu

vaccines. Resp. Ex. A; Resp. Ex. C; Resp. Ex. D.

Dr. Jamieson distinguished the two diseases, explaining that CIDP develops slowly over

approximately eight weeks, with the initial symptoms taking at least two months to reach nadir.

Resp. Ex. A at 12-13. While CIDP may be relapsing and remitting, GBS has a rapid onset, reaches

nadir within four weeks of onset, and is monophasic though it may have some residual symptoms.

Id. The clinical presentations are also different. GBS presents with numbness, paresthesia, and

limb pain, and the main feature is bilateral and relatively symmetric weakness of the limbs that

progresses over 12 hours to 28 days before reaching nadir. Id. at 13. Most GBS patients have a full

recovery over weeks or months with physical and occupational therapy, and recurrence is

exceedingly rare. Id. at 14. CIDP patients present with gradually worsening symmetrical numbness

and tingling with motor weakness in the hands, feet, upper arms, and thighs, sometimes with

extremity pain and abnormal sensation. There are obvious motor deficits, less prominent sensory

loss, and decreased or absent reflexes. Id. at 14. The immunologic triggers of GBS and CIDP are

also different, with CIDP less frequently associated with a preceding event or disease than GBS.

Id. at 15. Finally, CIDP has not been associated with any vaccine. Id. at 18-20.

Dr. Jamieson agreed that IVIG is used to treat both GBS and CIDP but explained that

“[t]reatment of two diseases with a commonly used immunotherapy does not imply an overlapping

pathophysiological mechanism,” and IVIG is used as treatment for numerous unrelated

autoimmune diseases. Resp. Ex. C at 2. She argued that, if response to treatment defined

pathophysiological mechanism, then the fact that CIDP responds to steroids while GBS does not

mitigates any commonality between the two. Id.

97

Yahel Segal & Yehuda Shoenfeld, Vaccine-induced autoimmunity: the role of molecular mimicry and immune

crossreaction, 14 CELLULAR & MOLECULAR IMMUNOLOGY 1 (2018), filed as “Pet. Ex. 71.”

29

Dr. He also described GBS as an inflammatory polyneuropathy characterized by acute

onset, rapid progression, symmetrical weakness, and hyporeflexia or areflexia. Resp. Ex. D at 3.

He noted GBS is post-infectious, with two thirds of patients reporting either respiratory or

gastrointestinal tract infection before onset. Id. at 4. Although not firmly established, cross-reactive

autoantibodies may play a role in the immunopathogenesis of GBS, attacking peripheral nerves

and causing demyelination and axonal damage. Id.

Dr. He described CIDP as an acquired, immune-mediated neuropathy affecting the

peripheral nerves and nerve, roots characterized by a relapsing and remitting or a progressive

course, glucocorticoid responsiveness, and electrodiagnostic or pathologic features of

demyelination. Resp. Ex. D at 5. The cause and specific immunologic triggers are largely unclear,

and no evidence between vaccination and development of CIDP beyond temporal relationship has

been provided in any report. Id.

Dr. He argued that although it is generally accepted that H1N1 pandemic influenza

vaccines were associated with GBS, the same is not true for seasonal influenza vaccines. Resp.

Ex. D at 4-5. He addressed Dr. Dahlgren’s opinions and the seven papers he relied upon,

summarizing that none of them provided evidence of a causal link between seasonal influenza

vaccines and GBS. Specifically, he noted that while two of the papers reported an increased risk

of GBS in populations that received pandemic swine flu influenza vaccines, the other five showed

that there was no statistically significant excess risk of GBS after seasonal flu vaccination, and no

causal relationship between the two. Resp. Ex. D at 6-8; Pet. Ex. 3098; Pet. Ex. 3499; Pet. Ex. 35100;

Pet. Ex. 36101; Pet. Ex. 39; Pet. Ex. 41102; Pet. Ex. 42.103 Importantly, there is no report of GBS

caused by the Fluzone vaccine. Resp. Ex. D at 8.

Prior cases in the Program have addressed whether GBS and CIDP are distinct diseases or

a continuum of the same disease, referring to the two as “related” peripheral neuropathies with a

number of overlapping symptoms that “may” share a common pathogenesis. See Strong v. Sec’y

of Health & Human Servs., No. 15-1108V, 2018 WL 1125666 (Fed. Cl. Spec. Mstr. Jan. 12, 2018)

(referencing the “large and persuasive” body of evidence reliably connecting flu vaccine and GBS

and noting the common symptoms and pathogenesis of CIDP and GBS); Daily v. Sec’y of Health

& Human Servs., 2011 WL 2174535 (Fed. Cl. Spec. Mstr. May 11, 2011) (finding that a theory of

CIDP caused by molecular mimicry is plausible based on the premises that flu vaccination can

cause GBS, molecular mimicry can cause GBS, and there is a biological basis for similarity

between GBS and CIDP). The agreement in these cases, however, is that petitioner can satisfy

Althen Prong I by relying on the theory of molecular mimicry.

In this case, Dr. Dahlgren’s opinions are rooted in the fact that GBS following flu vaccine

is a Table injury. However, CIDP is not. For GBS to be considered a Table injury, onset must be

within 3 to 42 days of receipt of the flu vaccine. Here, petitioner’s onset was at least three months

98

Martín Arias et al., supra note 48.

99

Haber et al., supra note 49.

100

Haber et al., supra note 50.

101

Hurwitz et al., supra note 51.

102

Marks & Halpin, supra note 12.

103

Salmon et al., supra note 53.

30

after vaccination, and further, he was diagnosed with CIDP. Therefore, this case is an off-Table

claim by both timing and injury and requires a sound and reliable theory to sustain petitioner’s

burden under Althen Prong I.

Although petitioner is not required to provide proof of a specific biological mechanism,

simply referencing an article that mentions molecular mimicry as a potential mechanism for

vaccine-related GBS, and by extension CIDP, without more is insufficient to satisfy petitioner’s

burden. See Knudsen ex rel. Knudsen v. Sec’y of Health & Human Servs., 35 F. 3d 543, 549 (Fed.

Cir. 1994). Molecular mimicry is accepted in the Program as a biological mechanism, but there

must be some evidence that persuasively shows that a portion of a vaccine resembles a portion of

human tissue which contributes to causing the disease, and that the immune system will respond

to the relevant amino acid sequence.104 See Tullio v. Sec’y of Health and Human Servs., No. 15-

51V, 2019 WL 7580149 at *12-14 (Fed. Cl. Spec. Mstr. Dec. 19, 2019), mot. for rev. denied, 149

Fed. Cl. 448 (2020); See, e.g., Stricker v. Sec’y of Health & Human Servs., 170 Fed. Cl. 701, 720-

21 (2024); Duncan v. Sec’y of Health & Human Servs., 153 Fed. Cl. 642, 661 (2021) (finding the

special master did not err in rejecting a bare assertion of molecular mimicry and noting “there is

an important difference between the general theory of molecular mimicry and the more specific

theory that the vaccine . . . [at issue] is capable of triggering an autoimmune response that

culminates in the [petitioner's injury]”); Caredio v. Sec’y of Health & Human Servs., No. 17-79V,

2021 WL 6058835, at *11 (Fed. Cl. Spec. Mstr. Dec. 3, 2021) (indicating that a special master did

not err in requiring more than homology and citing Tullio); Yalacki v. Sec’y of Health & Human

Servs., 146 Fed. Cl. 80, 91-92 (2019) (ruling that the special master did not err in looking for

reliable evidence to support molecular mimicry as a theory); but see Patton v. Sec’y of Health &

Human Servs., 157 Fed. Cl. 159, 169 (2021) (finding that a special master erred in requiring

petitioner submit a study to establish medical theory causally connecting flu vaccine to brachial

neuritis).

Dr. Dahlgren is neither a neurologist nor an immunologist. His opinions speak to

generalities but fail to explain what in the Fluzone vaccine was similar to or shared homology with

host antigens to cause CIDP. In Dr. Dahlgren’s own words, his “medical theory” was “[q]uite

simply, vaccines increase the activity of the immune system, and in some rare cases, an abnormal

autoimmune system attacks and damages the myelin around the nerves.” Pet. Ex. 64 at 3. While

this may be true, CIDP has no known cause, and Dr. Dalhgren simply referenced the term

molecular mimicry in his fourth report, arguing that flu vaccine can cause GBS and CIDP due to

the similarity of the two diseases, but failed to connect the flu vaccine to either GBS or CIDP.

Nothing in Dr. Dahlgren’s reports nor the literature cited explains or references what antigens or

structures in the Fluzone vaccine share homology with possible host antigens and how those

antigens react to provide a causal connection between GBS or CIDP and seasonal flu vaccine over

three months after vaccination. See Dennington v. Sec’y of Health and Human Servs., 167 Fed. Cl.

640 (2023) appeal withdrawn, No. 2024-1214 (Fed. Cir. Mar. 25, 2024) (criticizing the lack of

specificity in petitioner’s expert report, suggesting that one could take the expert’s causation theory

and substitute any table vaccine and any autoimmune disorder with no change to the discussion –

“That is how general his molecular mimicry theory is—it does not matter which vaccine and which

autoimmune disorder are plugged in. But Althen prong one requires more.”).

104

The term generally used to describe this concept in molecular mimicry is homology, or “structural similarity due

to descent from a common form.” Homology, DORLAND’S 858.

31

It is well-established that the mere mention of molecular mimicry is insufficient to satisfy

Prong I. Accordingly, petitioner has failed to sustain his burden under Althen Prong I.

3. Petitioner Failed to Demonstrate a Logical Sequence of Cause and Effect.

The second Althen prong requires proof of a “logical sequence of cause and effect.”

Capizzano, 440 F.3d at 1326 (quoting Althen, 418 F.3d at 1278). In other words, even if the

vaccinations can cause the injury, petitioner must show “that it did so in [this] particular case.”

Hodges v. Sec’y of Health & Human Servs., 9 F.3d 958, 962 n.4 (Fed. Cir. 1993) (citation omitted).

“A reputable medical or scientific explanation must support this logical sequence of cause and

effect,” id. at 961 (citation omitted), and “treating physicians are likely to be in the best position

to determine whether a logical sequence of cause and effect show[s] that the vaccination was the

reason for the injury,” Paluck, 786 F.3d at 1385 (quoting Andreu, 569 F.3d at 1375). Petitioner is

not, however, required “to eliminate alternative causes as part of establishing [their] prima facie

case.” Doe v. Sec’y of Health & Human Servs., 601 F.3d 1349, 1357-58 (Fed. Cir. 2010); see

Walther v. Sec’y of Health & Human Servs., 485 F.3d 1146, 1152 (Fed. Cir. 2007) (holding that a

“petitioner does not bear the burden of eliminating alternative independent potential causes”).

Dr. Dahlgren provided little by way of a medical theory beyond stating, “vaccines increase

the activity of the immune system, and in some rare cases, an abnormal autoimmune system attacks

and damages the myelin around the nerves,” which was insufficient to satisfy Althen Prong I. Pet.

Ex. 64 at 3. He argued that petitioner had GBS and CIDP because his physicians included both in

the record and opined that the only difference between the two diseases is chronicity. Pet. Ex. 55

at 12-13. Dr. Jamieson disagreed, opining petitioner was inappropriately diagnosed with cervical

myelopathy and underwent an unnecessary cervical decompression, and he never had GBS, even

when he was initially symptomatic. Rather, he had CIDP with a relapsing and remitting course

over a three-year period. Resp. Ex. A at 12-13.

Petitioner was ultimately diagnosed with CIDP, and he experienced relapsing and remitting

symptoms from onset in December 2016 until his death in November 2019. He also suffered from

a host of other medical conditions that required intervention during that period. See Pet. Ex. 22 at

1, 24-25; Pet. Ex. 52 at 2159; Pet. Ex. 53 at 257-58, 747, 756; Pet. Ex. 54 at 216-17. When

petitioner passed away, his cause of death was respiratory failure and CIDP, along with several

other comorbidities. Pet. Ex. 49.

As discussed in detail above, petitioner failed to establish that the Fluzone vaccine he

received caused his CIDP over three months after vaccination. It is therefore axiomatic that he

would fail to prove a logical sequence of cause and effect between his Fluzone vaccination on

September 27, 2016 and his onset of symptoms around December 28, 2016. The preponderant

evidence supports that petitioner suffered from CIDP based on his clinical presentation, his

responsiveness to steroids and IVIG, and the timing of his onset and the subsequent relapsing and

remitting progression of his condition over the next three years until his death. Because petitioner

failed to provide a reliable theory for how the Fluzone vaccine could cause CIDP more than three

months after vaccination, he likewise failed to provide preponderant evidence of a logical

connection between the flu vaccine he received on September 27, 2016, and the onset of CIDP

more than three months later.

32

Accordingly, petitioner has failed to sustain his burden under Prong II.

VII. Conclusion

Upon careful evaluation of all the evidence submitted in this matter—the medical records,

petitioner’s affidavit, and the experts’ opinions and medical literature—I find that petitioner has

failed to show he is entitled to compensation under the Vaccine Act. The matter is hereby

dismissed, and the Clerk shall enter judgment accordingly.105

IT IS SO ORDERED.

s/ Mindy Michaels Roth

Mindy Michaels Roth

Special Master

105

Pursuant to Vaccine Rule 11(a), entry of judgment can be expedited by each party filing a notice renouncing the

right to seek review.

33