# M. v. Secretary of Health and Human Services

> United States Court of Federal Claims · September 12, 2024

URL: https://www.frixlaw.com/law-library/cases/10734249

## Case

- **Court:** United States Court of Federal Claims
- **Decided:** September 12, 2024
- **Precedential status:** Unpublished
- **Opinion:** Opinion
- **Judges:** Nora Beth Dorsey
- **Cited by:** 0 later opinions in the Frix Law Library

## Citator (automated)

- No negative treatment found by the automated citator. That is not the same as a confirmation that the case is good law; read the citing cases.
- Full citator and citing cases: https://www.frixlaw.com/law-library/cases/10734249

## How later opinions describe it (automated extraction)

- noting that “clear, cogent, and consistent testimony can overcome such missing or contradictory medical records”
- noting that “close calls” are resolved in Petitioner’s favor
- noting that special masters are bound by both § 13(b)(1) and Vaccine Rule 8(b)(1) to consider only evidence that is 44 both “relevant” and “reliable”

## Opinion text

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
Originally Filed: July 18, 2024
Reissued for Public Availability: September 12, 2024

* * * * * * * * * * * * * * * * * * * * ** * * *
M.M., * PUBLISHED
*
Petitioner, * No. 18-583V
*
v. * Special Master Nora Beth Dorsey
*
SECRETARY OF HEALTH * Dismissal; Influenza (“Flu”) Vaccine;
AND HUMAN SERVICES, * Guillain-Barré Syndrome (“GBS”);
* Neuroinflammation; Asthma; Significant
Respondent. * Aggravation.
************************

M.M., pro se, Yonkers, NY, for Petitioner.
Nina Ren, U.S. Department of Justice, Washington, DC, for Respondent.

DECISION 1

On April 24, 2018, M.M. (“Petitioner”) filed a petition for compensation under the
National Vaccine Injury Compensation Program (“Vaccine Act” or “the Program”), 42 U.S.C. §
300aa-10 et seq. (2018), 2 alleging that she suffered an “exacerbation of asthma[] and an
unspecified neurological injury/complication” as a result of receiving an influenza (“flu”)
vaccination on September 19, 2015. Petition at Preamble (ECF No. 1). Respondent argued
against compensation, stating the case was “not appropriate for compensation under the terms of
the Vaccine Act.” Respondent’s Report (“Resp. Rept.”) at 1 (ECF No. 21).

After carefully analyzing and weighing the evidence presented in accordance with the
applicable legal standards, the undersigned finds Petitioner failed to provide preponderant
evidence that the flu vaccination caused her to develop a neurological condition or an
exacerbation of asthma. Thus, Petitioner has failed to satisfy her burden of proof under Althen v.
Secretary of Health & Human Services, 418 F.3d 1274, 1280 (Fed. Cir. 2005) and Loving v.

1
Pursuant to Vaccine Rule 18(b), this Decision was initially filed on July 18, 2024, and the
parties were afforded 14 days to propose redactions. The parties did not propose any redactions.
Accordingly, this Decision is reissued in its original form for posting on the Court’s website.
2
The National Vaccine Injury Compensation Program is set forth in Part 2 of the National
Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755, codified as amended,
42 U.S.C. §§ 300aa-10 to -34 (2018) (“Vaccine Act” or “the Act”). All citations in this Decision
to individual sections of the Vaccine Act are to 42 U.S.C.A. § 300aa.
Secretary of Health & Human Services, 86 Fed. Cl. 135, 142-44 (2009). Accordingly, the
petition must be dismissed.

I. ISSUES TO BE DECIDED

The parties stipulate Petitioner received a flu vaccine on September 19, 2015 when she
was 53 years old. Joint Submission, filed July 3, 2023, at 1 (ECF No. 126). The parties also
stipulate that at the time of vaccination, Petitioner “already had an approximately [20-year]
history of asthma, which included hospitalization in 2011 and an [emergency department
(“ED”)] visit in 2012.” Id. Thus, the parties do not dispute that Petitioner had pre-existing
asthma.

The parties dispute Petitioner’s neurological diagnosis, including whether she “developed
any definable neuroinflammatory autoimmune disease” or “suffered a neurological injury.” Joint
Submission at 1-2. Although the parties do not define “neuroinflammatory autoimmune disease”
or “neurological injury,” Petitioner’s primary care physician (“PCP”), Dr. Gary Rogg, referenced
Petitioner’s neurological condition as “neuropathic changes related to [Guillain-Barré Syndrome
(“GBS”)].” Petitioner’s Exhibit (“Pet. Ex.”) 2 at 102. And Petitioner’s expert immunologist, Dr.
Omid Akbari, referenced her injuries as “neuroinflammation[3] in the . . . nervous system” and
“neuropathic changes related to GBS.” Pet. Ex. 13 at 1, 10. Therefore, the undersigned will use
these definitions, “neuroinflammation” and “neuropathic changes related to GBS,” for the
purposes of analyzing Petitioner’s diagnosis.

Also, the parties dispute causation, particularly (1) whether Petitioner has preponderantly
established that the flu vaccine caused her neurological injury, and (2) whether Petitioner
preponderantly established that the flu vaccine significantly aggravated her preexisting asthma.
Joint Submission at 2. Lastly, if Petitioner did establish that the flu vaccination “caused a
neurological injury or significantly aggravated her preexisting asthma,” the parties dispute
whether there is “preponderant evidence that those conditions were due to an unrelated factor,
i.e., an intervening upper respiratory infection [(“URI”)].” Id. at 2.

II. MEDICAL TERMINOLOGY

GBS is an acute demyelinating polyneuropathy characterized by symmetrical limb
weakness and decreased or absent reflexes, and it reaches its peak severity at approximately four
weeks. Resp. Ex. B.1 at 1. 4 Sensory symptoms, like numbness and tingling, begin distally and
usually are symmetrical. Id. Diagnosis is based on the clinical course and diagnostic studies.

3
Neuroinflammation is “inflammation of a nerve or of the nervous system.”
Neuroinflammation, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.
com/dorland/definition?id=33741 (last visited July 3, 2024).
4
Bianca van den Berg et al., Guillain-Barré Syndrome: Pathogenesis, Diagnosis, Treatment and
Prognosis, 10 Nature Revs. Neurology 469 (2014).

2
Resp. Ex. B.2 at 1. 5 While GBS includes a “spectrum of neuropathic disorders that may differ in
the underlying pathogenesis and clinical manifestations,” there is consensus as to the clinical
course of the majority of patients although there is considerable variability. Id. at 2, 7. Most
patients have symmetrical limb weakness and decreased or absent deep tendon reflexes, a
monophasic disease course, and cerebrospinal fluid (“CSF”) with increased protein cell count.
Id. at 7-10. Additionally, electromyography (“EMG”)/nerve conduction study (“NCS”) findings
show demyelinating polyneuropathy. Id. GBS is “of unknown etiology, frequently seen after an
enteric or respiratory infection. An autoimmune mechanism following viral infection has been
postulated.” Guillain-Barré Syndrome, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=110689 (last visited June 27, 2024).

Asthma is defined as “recurrent attacks of paroxysmal [sudden and intense] dyspnea,[6]
with airway inflammation and wheezing due to spasmodic contraction of the bronchi.” Asthma,
Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=4552
(last visited July 3, 2024). Some cases of asthma are “allergic manifestations in sensitized
persons [described as allergic or atopic]; others are provoked by factors such as vigorous
exercise, irritant particles, psychologic stresses, and others.” Id.

III. BACKGROUND

A. Procedural History

Petitioner filed her petition on April 24, 2018. Petition. Petitioner filed an affidavit and
medical records throughout 2018. 7 Pet. Exs. 1-12. Respondent filed his Rule 4(c) report,
arguing against compensation, on February 4, 2019. Resp. Rept. at 1.

On June 27, 2019, Petitioner filed an expert report from Dr. Akbari. Pet. Ex. 13. On
November 4, 2019, Respondent filed an expert report from Dr. Arnold Levinson. Resp. Ex. B.

The undersigned held a Rule 5 conference on January 16, 2020. Order Staying Case
dated Jan. 17, 2020 (ECF No. 41). The undersigned briefly gave her preliminary findings then
stayed the proceedings for six months to allow Petitioner the opportunity to investigate a
diagnosis, including a complete workup and additional testing. Id. at 1-2. By December 2021,
Petitioner had still not undergone the necessary testing. Order dated May 4, 2021 (ECF No. 58);
Order dated Dec. 2, 2021 (ECF No. 75).

At a status conference on February 3, 2022, the undersigned emphasized Petitioner’s
need for further evidence and expert opinion from a medical doctor. Order dated Feb. 3, 2022

5
Christiaan Fokke et al., Diagnosis of Guillain Barré Syndrome and Validation of Brighton
Criteria, 137 Brain 33 (2014).
6
Dyspnea is “breathlessness or shortness of breath; difficult or labored respiration.” Dyspnea,
Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?
id=15277 (last visited July 3, 2024).
7
Petitioner continued to file medical records throughout the course of litigation.

3
(ECF No. 87). On April 22, 2022, Petitioner submitted an affidavit indicating she had
appointments scheduled but because she was exposed to Covid-19, they had been rescheduled
for a later date. Pet. Ex. 66 at 1. On May 12, 2022, Petitioner’s counsel moved to withdraw
because she could not secure another expert to support Petitioner’s claim “and d[id] not believe
[Petitioner] ha[d] reasonable basis to continue with this claim.” Motion to Withdraw, filed May
12, 2022, at 1 (ECF No. 100).

Thereafter, the undersigned granted Petitioner, who opted to proceed pro se, additional
time to submit supporting evidence. See Order dated July 19, 2022 (ECF No. 112); Order dated
Sept. 20, 2022 (ECF No. 114); Order dated Oct. 26, 2022 (ECF No. 116).

By May 2023, the undersigned noted Petitioner still had not submitted any new records
or medical opinion. Order dated May 5, 2023 (ECF No. 123). Accordingly, the undersigned
ordered the parties to propose a plan for resolving the case. Id. at 3-4.

The parties agreed to proceed with a ruling on the record. Joint Status Rept., filed June 5,
2023 (ECF No. 124). Petitioner filed a motion for a ruling on the record on September 5, 2023.
Pet. Motion for Ruling on the Record (“Pet. Mot.”), filed Sept. 5, 2023 (ECF No. 129).
Respondent filed his response on October 31, 2023. Resp. Response to Pet. Mot. (“Resp.
Response”), filed Oct. 31, 2023 (ECF No. 130). Petitioner did not file a reply.

This matter is now ripe for adjudication.

B. Factual History

1. Summary of Medical Records 8

a. Prior to Vaccination (2012 to 2015)

Prior to the vaccination at issue, medical records dating back to 2012 show that Petitioner
had multiple medical problems, including a history of “gastroesophageal reflux disease, mitral
valve prolapse, asthma, irritable bowel syndrome, kidney stones, melanoma resection, 25 and 10
years ago, Lyme disease treated in the past with [intravenous (“IV”)] antibiotics,
hypercholesterolemia,” and headaches and was diagnosed with “chronic paroxysmal hemicrania”
which was treated with Indocin. Pet. Ex. 3 at 5. She also had prior head trauma, and
computerized tomography (“CT”) scan of the brain in 2004 showed lipoma and nonspecific
findings “likely representing benign bony lesion[s].” Id. Petitioner also had a history of
ventricular tachycardia treated with Verapamil, atypical chest pain, and mitral valve prolapse.
Id. In addition to these conditions, Petitioner also had “intermittent pruritus” of the “left
shoulder blade area,” a “history of left rotator cuff injury,” and a history of “benign [] left breast
biopsies.” Id. She had significant eye conditions, including diminished vision in her right eye,

8
Due to Petitioner’s significant visual problems, she frequently saw her ophthalmologist.
Except for early visits, information about these visits are not included in these summaries, as
they do not appear to be relevant to the issues herein. Further, there are many visits to other
physicians and health care providers in the medical records that are not included for the sake of
brevity, however, the undersigned has reviewed all of the Petitioner’s medical records.

4
diagnosed as endophthalmitis, and she also had conjunctivitis, exudative senile macular
degeneration of the retina, bilateral dry eyes, and progressive degenerative myopia. Id. at 11, 13,
16-17, 19, 23. In September 2012, she had “[c]ellulits and abscess of [the] face.” Id. at 34. In
October 2012, Petitioner was diagnosed with pharyngitis and chronic rhinitis. Id. at 55, 58. She
had lumbar radiculitis in October, and two falls in November 2012, sustaining a coccyx fracture
and left knee and ankle injuries. Id. at 63-64, 69, 80-83. After these falls, she developed
bilateral numbness of the anterior thighs, pain in her left shoulder, and “pain and numbness
radiating to the left 4th and 5th fingers.” Id. at 90. On physical examination in December 2012,
Petitioner had slightly decreased sensation in the distribution of the left C7 nerve root and a
number of other abnormal findings. Id. X-rays revealed degenerative changes of cervical
intervertebral disc, rotator cuff sprain, and closed fracture of metacarpal bones. Id. at 92-94.
Magnetic resonance imaging (“MRI”) showed degenerative changes and medial meniscal tear of
the left knee. Id. at 104.

Regarding Petitioner’s history of asthma, her records show that in October 2012, she had
mild to moderate persistent asthma, for which she was prescribed Singular, Asmanex, Flonase
and ProAir HFA Aerosol inhaler. Pet. Ex. 3 at 41-42. She also took Proventil 9 when needed.
Id. In 2013, Petitioner had lost weight, resulting in significant improvement in her asthma. Id. at
156. Her medication was adjusted due to improvement in her condition and lack of insurance.
Id.

In a letter authored by her physician in 2013, 10 Petitioner was noted to also have a history
of cancer in 1987 and a history of Epstein-Barr virus. Pet. Ex. 3 at 107. She was noted to suffer
from asthma, irritable bowel syndrome, nephrolithiasis, kidney infections, thyroid nodule,
lipoma, and “multiple lesions in her brain which have caused debilitating headaches.” Id. She
had also suffered a “major bleed in her right eye” resulting in partial blindness. Id. In November
2013, Petitioner had a fall onto her right knee causing swelling and pain and was subsequently
diagnosed with a right knee meniscus tear, Baker’s cyst, degenerative arthritis, and
neuroforaminal stenosis of the right lumbar spine. Id. at 170, 176-77, 182. She also had
episodes of shingles in November and December 2013. Id. at 174.

Moving to 2014, Petitioner had follow-up visits with her pulmonologist for her asthma in
April and December 2014. She was diagnosed with “mild intermittent asthma, clinically stable,”
and advised to continue her current regimen and her albuterol inhaler as needed. Pet. Ex. 3 at
216, 279. On July 9, 2014 and February 22, 2015, her pulmonologist, Dr. Scott M. Klares, wrote
letters advising that Petitioner had “significant asthma that require[d] the use of a nebulizer. As
a result of her nebulizer requirement, it [was] important that electrical service [] be maintained at

9
Proventil is trademark for albuterol which is a β-adrenergic agonist “administered by inhalation
as a bronchodilator for the treatment and prophylaxis of bronchospasm associated with
bronchitis, pulmonary emphysema, or other chronic obstructive airway disease, the treatment of
asthma-associated bronchospasm, and the prophylaxis of exercise-induced bronchospasm.”
Albuterol, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/
definition?id=1569 (last visited June 27, 2024); Proventil, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=41542 (last visited June 27, 2024).
10
An almost identical letter was written on July 22, 2015. Pet. Ex. 3 at 319.

5
her residence to aid in treatment of her underlying medical condition.” Id. at 236, 290. Thus,
Petitioner had significant asthma and continued to require her nebulizer for treatment.

In September 2014, Petitioner continued to complain of “squeezing precordial chest
discomfort with radiation down the arm” and was diagnosed with chest pain syndrome. Pet. Ex.
3 at 246. Her asthma was described as “under good control.” Id. Diagnostic cardiac
cauterization was recommended. Id. at 246-47. On November 12, 2014, Petitioner was
evaluated for back, hip, and knee pain. Id. at 272. She complained of “numbness that radiate[d]
down the right leg to her ankle, and occasionally she fe[lt] weakness with inability to lift up her
foot when she [was] running and walking.” Id. She also complained of pain when using stairs,
and right hip and groin pain. Id. Physical examination revealed deep tendon reflexes were “1 to
2+” in bilateral lower extremities with intact sensation. Id. Muscle testing was normal in all
four extremities. Id. She had tenderness of the “right lumbar paraspinal” muscles. Id. Flexion
and extension were limited. Id. Petitioner was diagnosed with “lumbar degenerative disk
disease and mild lumbar radiculopathy” 11 and “right hip strain and arthritis.” Id.

In June 2015, Petitioner complained of right thumb pain and bilateral knee pain. Pet. Ex.
3 at 304. MRI of the right knee revealed a tear of the medial meniscus, joint effusion, and
popliteal cyst. Id. at 296. The left knee had a tear of the medial meniscus and small joint
effusion. Id. at 297. Petitioner continued to seek treatment for her orthopedic problems
throughout 2015.

Vaccine history included receipt of flu vaccinations on January 9, 2008, November 13,
2008, September 8, 2011, and September 25, 2012, and a tetanus, diphtheria, acellular pertussis
(“Tdap”) vaccination on September 25, 2012. Pet. Ex. 3 at 35, 115. There is no evidence to
suggest that Petitioner suffered any adverse reactions to these vaccinations.

b. Vaccination and Six-Month Period After Vaccination
(September 19, 2015 through March 2016)

Petitioner received the flu vaccination at issue on September 19, 2015. Pet. Ex. 1 at 1.

Several weeks later, on October 12, 2015, Petitioner saw her ophthalmologist, Dr.
Howard Charles, with complaints of fluctuating bilateral blurred vision. Pet. Ex. 3 at 346.
Petitioner attributed the visual symptoms to “a cold and the medication she [was] currently
taking for the cold.” Id. She was taking Tylenol Sinus medication. Id.

The following day, October 13, 2015, Petitioner presented to the Jacobi Medical Center
(“JMC”) ED. Pet. Ex. 4 at 6, 15. Chief complaints were shortness of breath, chest tightness, and
a cough that produced yellow mucus for about six days. Id. at 6, 15, 20, 30, 33. Onset was
Thursday, October 8, 2015. Id. at 6. Petitioner had a cough and wheezing but was “able to
speak in full sentences.” Id. She reported “symptoms all started following the flu vaccination a

11
Lumbar radiculopathy is “any disease of lumbar nerve roots, such as from disk herniation or
compression by a tumor or bony spur, with lower back pain and often paresthesias.” Lumbar
Radiculopathy, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/
definition?id=101394 (last visited June 20, 2024).

6
few weeks ago, progressed into a[n] [URI,] and [over the counter] med[ications] were not
helping.” Id. at 20. She had gotten “[w]orse the past [four] days.” Id. Petitioner received three
rounds of breathing treatments and Prednisone. Id. at 14-16. A chest X-ray was normal. Id. at
23. The diagnosis was asthma and Petitioner was discharged with a prescription for prednisone,
40mg for five days. Id. at 20-23. In a follow-up call on October 16, with the ED care manager,
Petitioner stated she was able to see her PCP and was diagnosed with pneumonia. 12 Id. at 31.
There was no report of numbness or tingling in the extremities. See id.

Petitioner presented to pulmonologist Dr. Klares on October 14, 2015. Pet. Ex. 3 at 349.
Petitioner “was in her usual state of health until last week, she got a flu shot. She state[d]
afterwards, she began to have some increasing cough, congestion, . . . increasing sinus pressure,
[and] yellowish mucus.” Id. She reported she went to the ED where “they wanted to admit her,
but due to insurance reasons . . . she was discharged.” Id. Petitioner stated her breathing was
better, but she still had increased mucus, increasing sinus pressure, and sinus tenderness. Id.
She did not report any neurological symptoms. See id. On examination, she had a normal
temperature, moderate nasal mucosal edema, moderate sinus tenderness, and minimal cough and
wheezing with forced expiration. Id. Dr. Klares’ impression was asthma exacerbation which he
opined “appear[ed] [to be] related to the URI and acute sinusitis.” Id. He prescribed amoxicillin
and instructed her to continue the prednisone and albuterol. Id. He also resumed her Asmanex
inhaler and advised Petitioner to continue using her albuterol inhaler for the next two days and
use fluticasone nasal spray for her upper airway congestion. Id. Petitioner was not diagnosed
with pneumonia. See id. She did not report numbness or tingling of her extremities. See id.

On October 19, Petitioner called Dr. Klares’ office reporting that she “still ha[d]
wheezing.” Pet. Ex. 3 at 353. On October 20, Petitioner again called Dr. Klares and reported
she was still “not feeling much better.” Id. at 352. She also developed a fever up to 101.9℉ the
night before. Id. Dr. Klares wanted to evaluate her further that day, but Petitioner reported she
did not have transportation to get to his office. Id.

On October 22, Petitioner returned to the ED complaining of shortness of breath and a
cough. Pet. Ex. 4 at 43, 45. History indicated the “symptoms began while doing normal activity
[two] weeks prior following flu shot earlier this month and suspected URI.” Id. at 43. There
was also “change in the color of the sputum[,] initially clear now ‘yellowish’ exacerbated by
deep inspiration and exertion.” Id. Petitioner tried an inhaler, nebulizer, and oral steroids
without relief. Id. Since the start of October, Petitioner was using her rescue inhaler once per
day, as compared to previously using it once every two weeks. Id. It was noted that the
“[c]urrent symptoms [were] similar to a prior asthma exacerbation.” Id. She reported fevers,
chills, fatigue, congestion, and runny nose. Id. at 44. She denied numbness, paresethias, and
weakness. Id. Physical examination revealed bilateral upper lung wheezing and decreased air
movement. Id. at 45.

Notes indicated that Petitioner’s “complaints of [shortness of breath] cough, and
diminished activity with fevers[,] and chills could indicate URI/early pneumonia though no
crackles were heard on auscultation.” Pet. Ex. 4 at 45. The attending physician also noted that
depending on the pending bloodwork, infection could be a diagnosis. Id. at 45-46. Clinical

12
There is no record of Petitioner being diagnosed with pneumonia.

7
course was also suspicious of asthma exacerbation. Id. at 46. Chest X-ray was normal while a
bloodwork showed an elevated white blood cell count of 13 (normal range 3.5-11). Id. at 50-51,
53. On re-examination, Petitioner continued to have a dry cough. Id. at 46-48. During her visit
to the ED, she received three nebulizer treatments and was offered admission but declined. Id.

On October 28, 2015, Petitioner called Dr. Klares’ office reporting she had a flu vaccine
on October 9, 2015, 13 and was in the ED the next day. Pet. Ex. 3 at 354. She stated that she was
being treated for asthma, pneumonia, and bronchitis. Id.

On November 4, 2015, Petitioner saw Dr. Klares and complained that her symptoms had
gotten worse and she was unable to fill her prescription for Asmanex due to insurance issues.
Pet. Ex. 3 at 355. She had “dyspnea with exertion, but no marked wheezing” or mucus. Id. Her
general complaint was “overall weakness.” Id. She was scheduled to finish her amoxicillin that
day and taper her prednisone. Id. Notes also indicated it was recommended that she see a
neurologist for “concern about some tingling in her hands.” Id. On physical examination,
Petitioner did not have wheezing and had normal extremity strength. Id. The impression was
asthma exacerbation, although “[c]linically, it [was] markedly improved.” Id. Dr. Klares
questioned whether Petitioner’s “tingling feeling in the fingertips” was related to her prednisone.
Id. She was given a regimen for tapering her prednisone for another week and instructed to
begin using Asmanex and continue with her albuterol. Id. Dr. Klares referred her for a
neurology evaluation “[g]iven her concerns.” Id. She was given a note excusing her from work
from Sunday, October 27 to Tuesday, December 1, 2015. Id. at 360.

Petitioner was seen at the JMC asthma clinic on November 5 by Dr. Jared Liebelt and Dr.
Chang Shim. Pet. Ex. 4 at 83. Petitioner reported her history of intermittent asthma which had
been diagnosed in the 1990s with triggers including pollen, cold weather, exercise, and stress.
Id. She also had seven dogs in her home. Id. She “developed URI symptoms following [flu]
vaccine” with two subsequent ED visits for treatment. Id. She had just finished her most recent
course of prednisone and had recently started a new job where she had exposure to dust and
rodent droppings. Id. She still used her albuterol inhaler every four hours. Id. On examination,
Petitioner appeared anxious, had an occasional cough, and some lung wheezing, but she was able
to speak in full sentences and was not in distress. Id. at 84. Diagnosis was prolonged asthma
exacerbation “likely provoked by viral URI.” Id. A two-week course of prednisone was
prescribed. Id. There is no documentation of numbness and tingling of the extremities. See id.

On November 11, 2015, Petitioner saw her PCP, Dr. Rogg. Pet. Ex. 2 at 81. The reason
for the appointment was listed as “[g]ot flu shot, developed [URI], in and out of hospital.” Id.
Petitioner reported an “asthma attack” following the flu vaccine and being treated with
prednisone, inhalers, and amoxicillin for pneumonia. Id. She reported ongoing reflux cough
with weather changes. Id. “[T]ingling [bilateral] hands [and] feet since flu shot” was noted on
review of symptoms. Id. at 82. Petitioner also had shortness of breath and cough, but denied
wheezing, and general weakness. Id. at 81-82. Examination was normal except for occasional
rhonchi on lung examination. Id. at 81. Dr. Rogg’s assessment was mild persistent asthma

13
This date appears erroneous. Petitioner’s records show that she received the flu vaccination on
September 19, 2015.

8
without complication and dysesthesia. 14 Id. at 82. He prescribed additional inhalers (Symbicort
and Atrovent) as well as Singulair. 15 Id. Assessment included dysesthesia. Id.

Petitioner returned to the JMC asthma clinic for a follow-up on November 12, 2015. Pet.
Ex. 4 at 96. She reported generalized weakness, malaise, and exertional wheezing with shortness
of breath. Id. On examination, she had poor inspiratory effort but no wheezing. Id. at 97. Dr.
Liebelt noted that although Petitioner reported persistent symptoms, her peak flow 16 was normal.
Id. He stated that Petitioner had a prolonged viral illness but that her respiratory function
“appear[ed] to be back at baseline.” Id.

Approximately nine weeks after vaccination, on November 24, 2015, Petitioner saw
neurologist Dr. Leslie S. Saland. Pet. Ex. 3 at 366. Petitioner described that “she had a flu shot
in September and about [three] weeks afterwards[,] developed upper respiratory symptoms with
diagnosis of bronchial pneumonia and asthma exacerbation.” Id. She “recall[ed] around the
same time the infection and asthma exacerbation developed[,] she noticed difficulty swallowing
and also paresthesias in the fingers and also the toes bilaterally, more [in] the upper extremities.”
Id. She noted “some decreased dexterity in the hands with difficulty grasping and she ha[d]
dropped things recently, her balance [was] mildly off in her legs feel weak proximally.” Id. She
reported numbness and tingling “prominent when she [woke] up in the morning but then [would]
recur intermittently throughout the day, also the feet[,] predominantly in the toes[,] occur[ed]
similarly and this ha[d] become less frequent since going off steroids.” Id. Petitioner also
reported aching and pain in the upper and lower back that had improved. Id. She had been off
steroids for approximately two and one-half weeks. Id. Review of symptoms was positive for
extremity weakness and numbness, dyspnea, chest pain, back and joint pain, and negative for
fatigue, malaise, and cough. Id. at 367.

On physical examination, Petitioner had normal cranial nerve function, normal strength,
normal muscle tone, normal sensation, 1+ deep tendon reflexes “except 2-3+ at the knees,”

14
Dysesthesia is the “distortion of any sense, especially of that of touch . . . an unpleasant
abnormal sensation produced by normal stimuli.” Dysesthesia, Dorland’s Med. Dictionary
Online, https://www.dorlandsonline.com/dorland/definition?id=15186 (last visited June 20,
2024).
15
Singulair is trademark for montelukast sodium which is “a leukotriene receptor antagonist
used as an antiasthmatic agent.” Montelukast Sodium, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=32122 (last visited June 27, 2024);
Singulair, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/
definition?id=45902 (last visited June 27, 2024).
16
A peak flow meter is used for measuring “the flow of air in the early part of forced
exhalation.” Peak Flow Meter, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=89029 (last visited June 27, 2024).

9
positive Tinel signs 17 at both wrists and fibular heads, and normal coordination. Pet. Ex. 3 at
369. Gait was “[n]otable for kyphotic posture with a dropped head when ambulat[ing],”
“diminished arm swing,” and “difficulty walking tandemly although Romberg [was] negative.”
Id. Dr. Saland’s assessment was that Petitioner had “paresthesias in the hands and feet occurring
intermittently and less frequently since [three] weeks after the flu shot when she also developed a
severe exacerbation of her asthma in the setting of a pulmonary infection . . . . She also ha[d]
proximal weakness in the legs and had some difficulty swallowing that was intermittent and
ha[d] also improved.” Id. at 369-70. Dr. Saland opined that the etiology of Petitioner’s
neurological symptoms was “not clear.” Id. at 370. Dr. Saland also questioned whether
Petitioner’s symptoms could be related to her recent steroid use. Id. Dr. Saland noted there was
no sign of cranial nerve dysfunction. Id. The diagnoses were paresthesias, steroid-induced
myopathy, drug-induced myopathy, and dysphagia (problems swallowing). Id. at 371. Dr.
Saland ordered lab testing, MRIs of the brain and cervical spine, and an EMG/NCS. Id. at 370.
Lab testing results were normal including Lyme antibody, Lyme Western Blot, copper, folate,
Sjogren’s antibodies (SSA/SSB), rheumatoid factor, anti-nuclear antibodies (“ANA”), anti-CCP,
RPR, free T4, and TSH. Id. at 601-07. Her vitamin B12 level was a low-normal at 256 (normal
193-928) but methylmalonic acid 18 was normal. Id. at 604, 608.

Petitioner underwent a preoperative evaluation on November 30, 2015, for surgery on her
right thumb. Pet. Ex. 3 at 376. Petitioner did not report shortness of breath or any neurological
symptoms. See id. Assessment was “mild intermittent asthma without complication.” Id. at
381. There was no reference to acute symptoms related to asthma or numbness and tingling in
the extremities.

On December 4, 2015, Petitioner saw Dr. Rogg who noted that Petitioner was undergoing
a “neurological evaluation [] for [GBS]” by Dr. Saland following the flu vaccine. Pet. Ex. 2 at
78. Dr. Rogg noted her symptoms started on October 5, and that she had shortness of breath and
had “gone to the hospital.” Id. Petitioner complained of a low-grade fever and reported that her
asthma was still “bothersome.” Id. She also had an eyelid infection. Id. On examination, she
had coarse rhonchi. Id. Dr. Rogg diagnosed facial cellulitis, bronchitis, and mild persistent
asthma. Id. at 78-79. He prescribed prednisone for her asthma. Id. at 79. At this visit Petitioner
did not complain of numbness or tingling.

Petitioner returned to Dr. Rogg on December 14 because she “[could not] take a deep
breath, [and got] winded easily.” Pet. Ex. 2 at 75. She reported ongoing asthma symptoms since
receiving the flu vaccine as well as dysesthesias. Id. On examination, she had occasional lung
rhonchi. Id. Dr. Rogg added unspecified fatigue to his list of diagnoses and ordered extensive

17
Tinel sign refers to “a tingling sensation in the distal end of a limb when percussion is made
over the site of a divided nerve. It indicates a partial lesion or the beginning regeneration of the
nerve.” Tinel Sign, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/
dorland/definition?id=106510 (last visited June 27, 2024).
18
Methylmalonic acid is “a carboxylic acid occurring in excess in the blood and other body
fluids in methylmalonicacidemia.” Methylmalonic Acid, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=30997 (last visited June 27, 2024).

10
lab testing. Id. at 76. Testing showed a normal/negative CBC, sedimentation rate, C-reactive
protein, rheumatoid factor, and ANA. Id. at 84-88.

On December 18, 2015, Dr. Saland performed a NCS on Petitioner’s upper extremities
for her complaints of paresthesias, right more than the left, “that began [three] weeks after a flu
shot in September accompanied by a respiratory infection and asthma exacerbation.” Pet. Ex. 3
at 386. History noted Petitioner had “now improved off the [p]rednisone for several weeks but
with some residual paresthesias in right hand.” Id. The NCS showed a “mild right median
neuropathy at the wrist . . . consistent with carpal tunnel syndrome.” 19 Id. at 386-88. There was
no evidence of a large fiber peripheral neuropathy in the upper extremities. Id. Petitioner was
unable to stay for the EMG needle testing. Id. at 387-88.

Dr. Saland authored a letter dated December 24, 2015, stating Petitioner “experienced
various neurological symptoms approximately [three] weeks after receiving the [flu] vaccine at
work in September 2015. The possibility of an autoimmune response affecting her nervous
system [was] considered likely and she [was] currently undergoing a workup for additional
clarification.” Pet. Ex. 3 at 392.

Petitioner returned to Dr. Rogg on January 5, 2016, and reported she had a tentative
diagnosis of GBS. 20 Pet. Ex. 2 at 72. She had been on prednisone for about three days as her
asthma was bothersome due to the cold weather. Id. Review of symptoms, physical
examination, and diagnoses were consistent with those documented at her previous visits. Id. at
72-73. On January 13, Dr. Rogg wrote a letter stating Petitioner had developed symptoms after a
flu vaccine which had not resolved and that she was being evaluated by a neurologist for an
adverse reaction to the flu vaccine. Id. at 112. He stated that “it appear[ed] as though the
vaccine had considerable influence on these symptoms.” Id. Petitioner continued to see Dr.
Rogg at monthly intervals throughout 2016 with Dr. Rogg writing “to whom it may concern”
letters after several of these visits. See generally Pet Ex. 2.

On December 24, 2015 and January 13, 2016, Dr. Saland authored letters stating that
Petitioner “experienced various neurological symptoms approximately [three] weeks after a [flu]
vaccine at work” and the “possibility of an autoimmune response affecting her nervous system is
considered likely.” Pet. Ex. 3 at 392, 398. In the second letter, Dr. Saland stated “the [flu]
vaccine was likely a substantial factor in provoking the autoimmune reaction that occurred. She
currently [was] undergoing further workup for additional clarification.” Id. at 398.

At a cardiology appointment on January 15, 2016 for the purpose of obtaining clearance
for trigger finger surgery, Petitioner complained of her heart racing and symptoms of atypical
chest pain but she did not report any other problems. Pet. Ex. 3 at 399. In review of systems,

19
Carpal tunnel syndrome is “an entrapment neuropathy characterized by pain and burning or
tingling paresthesias in the fingers and hand, sometimes extending to the elbow. Symptoms
result from compression of the median nerve in the carpal tunnel.” Carpal Tunnel Syndrome,
Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/
definition?id=110370 (last visited June 20, 2024).
20
It is not clear what health care provider gave Petitioner the tentative diagnosis of GBS.

11
Petitioner gave a history of “a series” of asthma flares in September “after flu shot and the
question of [GBS], which improved.” Id. at 399-400. Currently, she was using her asthma
inhalers only as needed “which ha[d] been her baseline in recent years.” Id. at 400. She did not
report of numbness or tingling of her extremities. See id. The cardiologist recommended that
Petitioner have Holter monitor testing of her heart rhythm prior to undergoing elective thumb
surgery. Id. at 401. No concerns were documented regarding any pulmonary or neurological
conditions that would preclude surgery. 21

On January 28, 2016, Petitioner presented for an urgent care visit after a chair fell on her
toe. Pet. Ex. 3 at 406. Review of systems was negative for extremity weakness or numbness.
Id. She was instructed to ice and elevate her toe and take pain medication as needed. Id. at 408.
X-rays did not show any fracture. Id. at 411.

Petitioner saw Dr. Rogg on February 29, 2016 for follow-up of her breathing. Pet. Ex. 2
at 68. She reported that since her flu vaccine, she had been more reliant on her Proventil. Id.
She reported a Zoster outbreak, and that she was undergoing an evaluation for GBS post-flu
vaccination. Id. Assessment included dysesthesia. Id.

On March 2, 2016, Petitioner called Dr. Saland’s office to cancel the EMG that was
scheduled that week because she had shingles that were very painful. Pet. Ex. 3 at 420.

On March 7, 2016, Petitioner saw endocrinologist Dr. Jeffrey Powell for an unrelated
kidney issue. Pet. Ex. 3 at 421. As part of the history taken, Petitioner reported she got a flu
shot and two weeks later developed an URI. Id. She “could not breathe” and “her asthma
became severe.” Id. She also reported that “a few weeks after this flu shot, she developed pins-
and-needles in her legs.” Id. She was referred to a neurologist (Dr. Saland) and “diagnosed with
[GBS] from the flu shot. She [said] this [was] slowly getting better.” Id. at 421-22. On
examination, her lungs were clear and she had normal deep tendon reflexes bilaterally in her
upper extremities. Id. at 422.

Six months after the flu vaccination, on March 29, 2016, Petitioner returned to Dr. Saland
for neurological follow-up. Pet. Ex. 3 at 433. Petitioner had not followed through with the brain
and cervical spine MRIs and had “cancelled appointments to complete EMG as she ha[d] not
been able to go back to work for pulmonary reasons related to her asthma.” Id. Petitioner
reported “significant improvement” since her prior visit in November 2015, but “continue[d] to
describe milder burning and tingling in the arms mostly forearms[,] left greater than right[,] as
well as paresthesias in the fingers and toes mostly[,] the [third] and [fourth] fingers and also
middle toes.” Id. Neurologic examination was normal and reflexes were “intact and
symmetric.” Id. at 435. Dr. Saland noted that Petitioner’s earlier proximal leg weakness and
dysphagia had resolved, that her upper extremity NCS was notable only for mild carpal tunnel
syndrome. Id. at 436. Petitioner had not returned for a lower extremity NCS or needle EMG.
Id. In the assessment, Dr. Saland concluded that “the etiology of [Petitioner’s] symptoms
remain[ed] unclear and further work up [was] again suggested. Examination [was] essentially
normal.” Id. Petitioner was informed of a neurology clinic where she could be seen for free or
for lower cost based on financial ability to pay. Id.

21
Thumb surgery was scheduled for January 18, 2015. Pet. Ex. 3 at 389.

12
Also on March 29, 2016, Petitioner underwent a treadmill stress test for her symptom of
heart racing. Pet. Ex. 3 at 557. Compared with her prior stress test done in 2012, her “exercise
time had improved” and she was “overall stable/improved.” Id. There was no indication that
Petitioner had shortness of breath or asthma symptoms during the stress test. Id. Based on the
study, Petitioner was cleared for her hand surgery. Id.

c. April 2016 through September 2016 (Completion of One Year
Post-Vaccination)

On May 2, 2016, Petitioner saw neurologist Dr. Sami Khella. Pet. Ex. 5 at 2. She
repeated the history documented before, that Petitioner’s asthma had been well controlled for the
past two-and-one-half to three years but that on September 19, 2015, she received a flu shot and
two weeks later, developed “pins and needles in toes and hands and ankles” and had an asthmatic
attack. Id. Petitioner reported she saw her pulmonologist who prescribed medications for
bronchitis. Id. Her paresthesias increased and she developed leg weakness and trouble
swallowing. Id. Petitioner also reported that had decreased reflexes, muscle weakness, difficulty
with steps, and dropping things. Id. “She continued to progress for more than [eight] weeks but
ha[d] since stabilized and improved but ha[d] residual weakness.” Id. Neurologic examination
was normal. Id. at 3-5. She had normal strength, deep tendon reflexes, and sensation. Id. Dr.
Khella’s impression was that Petitioner had “sensory motor symptoms and severe asthma that
developed within [two to three] [weeks] of taking the trivalent flu vaccine.” Id. at 5. Dr. Khella
noted Petitioner had a normal neurological examination when she was seen by Dr. Saland on
November 25, 2015. Id. Dr. Khella concluded that Petitioner “continue[d] to have sensory
symptoms but ha[d] a normal neurological examination. It [was] possible that she had [GBS]”
but “[s]he [was] currently stable.” Id.

Dr. Rogg saw Petitioner on May 10, 2016 for “[l]eg heaviness.” Pet. Ex. 2 at 59. History
noted that since Petitioner had been on Pravastatin, 22 she was having “muscle aches, heaviness
especially [in her] lower legs.” Id. Assessment was “[m]yalgia.” Id. Due to the complaint of
myalgia, Dr. Rogg discontinued the Pravastatin. Id. Petitioner saw Dr. Rogg on May 16, 2016,
complaining of “[w]orsening body aches” and “nausea.” Id. at 56. She was assessed with
“[m]oderate persistent asthma with acute exacerbation” and “[v]iral syndrome.” Id. She had no
neurological complaints.

On May 31, 2016, Petitioner saw Dr. Julia Shih at the JMC Primary Care Clinic. Pet. Ex.
4 at 119. Petitioner reported she “developed GBS symptoms (? autoimmune phenomenon from
vaccine)” but those symptoms had since resolved. Id. She reported one asthma flare in the last
month requiring oral steroids and stated that she had been “obtaining steroid monthly for

22
Pravastatin is “an antihyperlipidemic agent . . . used to lower blood lipid levels in the treatment
of hypercholesterolemia and other forms of dyslipidemia and to reduce the risk of morbidity and
mortality associated with atherosclerosis and coronary heart disease.” Pravastatin Sodium,
Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=
40666 (last visited June 27, 2024).

13
asthma” since her reaction to the flu vaccine. 23 Id. at 120. Petitioner was referred to a
pulmonologist due to her requirement for monthly steroids for asthma flares and was prescribed
a steroid inhaler, albuterol inhaler, and Singulair. Id. at 121.

Petitioner returned to Dr. Rogg June 7 and June 14, 2016. Pet. Ex. 2 at 50, 53. On June
7, she complained of “pin, needles,” for two weeks. Id. at 53. Diagnosis was dysesthesia. Id.
She also had a URI and mild asthma. Id. On June 14, she complained of “weakness in arms and
legs.” Id. at 50. Over the weekend she had increased tingling and lost her balance and fell. Id.
Petitioner returned to see Dr. Rogg on July 8 and August 15, 2016. Id. at 44-47.

d. October 2016 through 2018

On October 6, 2016, Petitioner reported to Dr. Rogg that her chest felt tight and
congested and she continued to have dysesthesias in her hands and legs. Pet. Ex. 2 at 116. On
examination, she had bilateral rhonchi. Id. Dr. Rogg diagnosed an asthma exacerbation and
administered a systemic steroid injection. Id. He also diagnosed a vitamin B12 deficiency and
ordered labs for parietal cell antibodies and intrinsic factor blocking antibody. Id.

On October 17, 2016, Dr. Rogg wrote another letter stating that Petitioner continued to be
evaluated and treated for symptoms post-flu vaccine which included asthma and neuropathic
changes. Pet. Ex. 2 at 103. He stated that she had been recently diagnosed with an asthma
exacerbation and “found to have a significant vitamin B12 deficiency caused by an autoimmune
reaction to the flu vaccine exacerbating her neurological symptoms.” Id.

At an appointment with Dr. Rogg on October 27, it was noted that Petitioner’s breathing
had been fluctuating since the last visit. Pet. Ex. 2 at 41. It was also noted that the test for
parietal cell antibodies was positive. Id. Diagnoses were acute asthma exacerbation and vitamin
B12 deficiency. Id. at 41-42.

Petitioner returned to Dr. Rogg on December 9, 2016 for fluctuating asthma symptoms
and continued paresthesias. Pet. Ex. 2 at 32. Dr. Rogg noted that Petitioner was seen by another
provider in the office in November for cellulitis of the eye. Id. at 32, 34, 36. A pulmonary
functions test was ordered but could not be completed because of Petitioner’s coughing and
wheezing. Id. at 32. He diagnosed Petitioner with mild persistent asthma, B12 deficiency,
dysesthesia, and GBS. Id. at 32-33. On December 13, Dr. Rogg wrote a letter stating that
Petitioner’s flu vaccine caused an autoimmune response which resulted in asthma aggravation
and exacerbation, neuropathic changes related to GBS, acute vitamin B12 deficiency, cellulitis of
the face, and infection of the nasal mucosa. Id. at 102. Petitioner continued to see Dr. Rogg
every one to two months throughout 2017 and 2018. See generally Pet. Ex. 2.

On May 16, 2017, Petitioner saw Dr. Eleanor Weinstein at the JMC Primary Care Clinic.
Pet. Ex. 11 at 5. History repeated the notes entered at the clinic on May 31, 2016. Id.; see Pet.
Ex. 4 at 119. Dr. Weinstein added that Petitioner had recently had issues with her asthma and
was on prednisone a few times. Pet. Ex. 11 at 6. Dr. Weinstein’s assessment was mild persistent

23
The medical records do not document that Petitioner had received oral steroids monthly for
asthma flairs.

14
asthma, noting a reported “bad reaction to flu vaccine,” and questioning a behavioral health
issue. Id. at 7. Lab testing showed a normal CBC, chemistry panel, and vitamin B12. Id. at 47-
48.

Petitioner followed-up with Dr. Rogg on June 7, 2017. Pet. Ex. 2 at 19. Diagnoses at
this visit included moderate asthma and neuropathy. Id. at 21. At an August 28 visit with Dr.
Rogg, Petitioner had continued asthma and paresthesias and reported a recent episode of
shingles. Id. at 16. On examination, her lungs were clear, and she had a resolving blistering rash
on the right abdominal wall. Id. at 17. On September 29, 2017, Petitioner reported “recurring
asthma symptoms,” as well as “recurrent heaviness in legs with tingling [and] fatigue.” Id. at 13.
Dr. Rogg noted “stable, [c]hronic inflammatory demyelinating polyneuropathy material was
published to portal,” suggesting that he provided such material to Petitioner. Id. at 14. On
October 10, Petitioner reported to Dr. Rogg that she had two episodes of shingles in September,
treated with Valtrex. Id. at 10. She also reported “ongoing congestion.” Id.

Dr. Weinstein saw Petitioner again in July, September, October, and November 2017,
and throughout 2018. See generally Pet. Ex. 11. At her October visit, Petitioner reported taking
prednisone for about five days every month due to asthma symptoms as well as regular use of
inhalers and Singulair. Id. at 12. Petitioner reported intermittent tingling in her feet which she
believed was “due to GBS from her flu vaccine in 2015.” Id.

On December 12, 2017, Petitioner complained to Dr. Rogg of ongoing fatigue, weakness,
paresthesias, and twitching of her face. Pet. Ex. 2 at 7. On examination, Petitioner had
occasional rhonchi and dysesthesias of her upper and lower extremities. Id. at 8. Dr. Rogg
authored another letter stating the flu vaccine caused an autoimmune response and chronic
immune dysregulation which caused Petitioner to have “continued volatile, overly vigorous
inflammatory episodes” resulting in “uncontrollable” asthma, neuropathic changes related to
GBS, acute B12 deficiency, cellulitis of the face, infections of the nasal mucosa, exacerbation of
shingles, arthritis, muscle weakness/fatigue, and increased susceptibility to infection. Id. at 96.

At a visit on March 23, 2018, Dr. Rogg noted that Petitioner had no insurance and was on
the waiting list to see a neurologist at JMC. Pet. Ex. 2 at 1. He stated that her symptoms were
likely related to a GBS variant but that she needed additional evaluation to include testing for
small fiber neuropathy. Id. He prescribed gabapentin. Id. On April 27, 2018, Dr. Rogg
increased the gabapentin dosage and discussed the need for a pulmonary evaluation. Pet. Ex. 8
at 2.

On June 8, 2018, Petitioner saw Dr. Weinstein reporting “a resurgence of what she
consider[ed] to be symptoms related to GBS” and more asthma symptoms requiring her to use
more prednisone. Pet. Ex. 11 at 25-26. Dr. Weinstein diagnosed persistent asthma and referred
her to a pulmonologist. Id. at 27. Dr. Weinstein noted that she had seen no documentation that
Petitioner had GBS and referred her to a neurologist for evaluation. Id. Much of the care she
received in June 2018, and later, was due to a fall Petitioner had on June 24, 2018, when she
injured her right knee. Id. at 38-60.

15
e. Neurology Evaluations in 2020 and 2021

In 2020, Petitioner presented, via telehealth, to neurologist Dr. Steven Krieger. Pet. Ex.
65 at 10; Pet. Ex. 67 at 7. History noted Petitioner had “no remote neuro symptoms.” Pet. Ex.
65 at 2, 10. History also indicated Petitioner developed “limb and [right] face paresthesias and
pain after flu shot and asthma exacerbation in Fall 2015.” Id. at 14; Pet. Ex. 67 at 11. Petitioner
stated that she had an “upper extremity EMG” that was “non-specific” but “considered for
GBS.” Pet. Ex. 65 at 10. Dr. Krieger suggested a possible clinically isolated syndrome as a
diagnosis, but noted he needed Petitioner’s prior records and additional MRIs for further
analysis. Id. at 14; Pet. Ex. 67 at 11. Dr. Krieger ordered MRIs “since symptoms began [in]
2015 and ha[d] not worsened.” Pet. Ex. 65 at 14.

On June 19, 2021, Petitioner had MRIs of her brain and cervical spine. Pet. Ex. 72 at 2-4.
She did not have any demyelinating lesions in the cervical spinal cord. Id. at 3. The brain MRI
showed a few nonspecific periventricular FLAIR hyperintense lesions. Id. at 4. Petitioner
followed up with Dr. Krieger on June 22. Pet. Ex. 69 at 2; Pet. Ex. 71 at 6. He indicated
Petitioner’s prior test results were unremarkable. Pet. Ex. 69 at 5. Dr. Krieger concluded that
Petitioner’s reported history, “coupled with the absence of long-tract findings on exam (albeit
limited in video visit context) with a non-diagnostic [b]rain and negative [cervical] spine MRI[s]
preclude[d] a diagnosis of [multiple sclerosis] at [that] time.” Id. at 6. Further, Dr. Krieger felt
that Petitioner’s brain MRI was inconsistent with acute disseminated encephalomyelitis (or
similar conditions although he noted relevant event (2015 flu vaccine) had occurred six years
earlier. Id. He referred Petitioner to another provider for an evaluation regarding whether she
possibly had small fiber neuropathy. 24 Id.

On September 16, 2021, Petitioner attended a video evaluation with neurologist Dr.
Vanessa Tiongson. Pet. Ex. 73 at 2. History notes indicated that seven days after a flu shot in
2015, Petitioner had upper respiratory symptoms, an asthma flair, and parsethesias in her hands
and feet which progressively worsened. Id. at 2-3. Dr. Tiongson’s impression was that
Petitioner’s paresthesia, “[i]f started after [the] flu shot, could have been GBS with residual
symptoms [versus a] [chronic inflammatory demyelinating polyradiculoneuropathy (“CIDP”) 25]-

24
It does not appear Petitioner pursued this referral.
25
CIDP is “a type of demyelinating polyneuropathy similar to [GBS] but progressing more
slowly or in a fluctuating pattern.” Chronic Inflammatory Polyradiculoneuropathy, Dorland’s
Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=99422 (last
visited June 27, 2024).

16
type picture.” Id. at 7. Dr. Tiongson also noted that Petitioner had a “vitamin B12 deficiency
with potentially insufficient treatment.” 26 Id. at 7.

No other relevant medical records were filed.

2. Letters from Dr. Gary Rogg

In addition to medical records reflecting office visits, Dr. Rogg’s records also contain
letters regarding Petitioner. There are several versions of the letters. The first set of letters are
dated December 4, 2015, January 13, 2015, February 29, 2016, March 16, 2016, March 31, 2016,
April 7, 2016, April 19, 2016, May 11, 2016, September 28, 2016, and October 17, 2016. Pet.
Ex. 3 at 103-14. In these letters Dr. Rogg stated that due to Petitioner’s medical status she was
unable to work. Some of these letters refer to symptoms that began after she received a flu
vaccine in September and state that she was undergoing an evaluation by neurology for an
adverse reaction. Several of the letters reference symptoms related to “uncontrolled asthma and
neuropathic changes.” Id. at 103-07, 109-10.

Letters dated December 13 and December 22, 2016 include a more extensive list of
problems attributed to the flu vaccine. Pet. Ex. 2 at 101-02. Dr. Rogg stated that the flu vaccine
Petitioner received in October of 2015, caused an “autoimmune response, which resulted in:
[a]ggravation and exacerbation of her previously controlled asthma of which is now
uncontrollable,” “[n]europathic changes related to [GBS],” “[a]cute vitamin B-12 deficiency,”
“[c]ellulitis of the face,” and “[i]nfections in the nasal mucosa.” Id. at 101. Dr. Rogg noted that
due to financial hardships, Petitioner had been unable to receive medical care for these problems,
and that she required follow-up care with specialists. He concluded that Petitioner was “released
to only perform part-time work at home, sedentary desk employment, not to exceed 30 hours per
week.” Id.

The next set of letters include an even longer list of problems attributed to the flu
vaccine. Pet. Ex. 2 at 93-100. These letters are dated January 26, 2017, June 7, 2017, September
29, 2017, October 10, 2017, December 12, 2017, December 19, 2017, February 6, 2018, and
March 23, 2018, in which Dr. Rogg again stated that Petitioner was under his care and treatment
for “evaluation of symptoms starting post flu vaccine.” Id. at 93-94, 96-100. Dr. Rogg stated
that the “flu vaccine . . . caused an autoimmune response and chronic immune dysregulation. As
a result, [Petitioner] suffer[ed] from continued volatile, overly vigorous, inflammatory episodes”
which in addition to the problems stated above, included “[e]xacerbation of [s]hingles,”
“[m]uscle weakness and fatigue,” “[i]ncrease susceptibility to infection,” and arthritis. Id. Dr.
Rogg noted that due to financial hardships, Petitioner had been unable to receive medical care for

26
Neurologic symptoms can develop from a vitamin B12 deficiency. Larry E. Johnson, Vitamin
B12 Deficiency, Merck Manual Online, https://www.merckmanuals.com/professional/
nutritional-disorders/vitamin-deficiency,-dependency,-and-toxicity/vitamin-b12-deficiency (last
visited July 3, 2024). “In early stages, decreased position and vibratory sensation in the
extremities is accompanied by mild to moderate weakness and hyporeflexia. In later stages,
spasticity, extensor plantar responses, greater loss of position and vibratory sensation in the
lower extremities, and ataxia emerge.” Id.

17
these problems, and that she required follow-up care with specialists. He concluded that
Petitioner was “temporarily, totally disabled and [] completely unable to work.” Id. at 93-100.

Additionally, Petitioner submitted further letters from Dr. Rogg as individual exhibits.
Pet. Exs. 8-10, 12. On April 27, August 9, 2018, and November 14, 2018, Dr. Rogg authored
letters stating he was Petitioner’s PCP, and that Petitioner was “still under treatment and
evaluation for symptoms starting post flu vaccine.” Pet. Ex. 8 at 1; Pet. Ex. 9 at 1; Pet. Ex. 12 at
1. He wrote that Petitioner received the flu vaccine in September/October 2015 27 and that the flu
vaccine “caused an autoimmune response and chronic immune dysregulation.” Pet. Ex. 8 at 1;
Pet. Ex. 9 at 1; Pet. Ex. 12 at 1. These letters contain the same information as the letters
summarized above. Again, Dr. Rogg noted that due to Petitioner’s “financial hardships and lack
of insurance coverage she [was] unable to receive appropriate care to address the above
symptoms,” but that she still required treatments and testing pending insurance coverage. Pet.
Ex. 8 at 1; Pet. Ex. 9 at 1; Pet. Ex. 12 at 1.

On August 15, 2018, Dr. Rogg authored a letter again stating that Petitioner was under
his care. Pet. Ex. 10 at 1. In this letter he opined “[t]he administration of the flu vaccine in
September 2015 [] caused in [Petitioner] an autoimmune response and chronic immune
dysregulation.” Id. He added that this “resulted in recurrent exacerbation of [s]hingles requiring
Valtrex.” Id. Her initial outbreak of shingles occurred on November 13, 2013. Id.

3. Petitioner’s Affidavit

Petitioner averred that prior to receiving the flu vaccine on September 19, 2015, her
health “was excellent with no physical restrictions.” Pet. Ex. 6 at ¶¶ 4-5. While she is an
“asthmatic,” she had been “symptom free” from 2011 to 2012 and “until the time [she] received
the [flu] vaccine administration [on] September 19, 2015.” Id. at ¶ 6. She had received the flu
vaccine in prior years without any known complications. Id. at ¶ 7.

By October 3, 2015, Petitioner began experiencing “mild upper respiratory symptoms
and ‘pins and needles’ in [her] hands/fingers and feet/toes.” Pet. Ex. 6 at ¶ 8. The symptoms
“became progressively worse and greatly intensified by October 8, 2015.” Id. at ¶ 9. By
October 13, 2015, Petitioner’s “attempts to self-medicate at home were unsuccessful” and she
presented to the ED “with a full-blown asthmatic attack, upper respiratory symptoms, and
intensifying ‘pins and needles.’” Id. at ¶ 10. In the ED, she received breathing treatments,
oxygen, and steroids. Id. at ¶ 11. It was recommended she be admitted to the hospital, however,
Petitioner declined because she did not have insurance. Id.

On October 14, 2015, Petitioner presented to her pulmonologist, Dr. Klares. Pet. Ex. 6 at
¶ 12. He revised her medications, put her on antibiotics, and referred her to Dr. Saland for her
neurological symptoms. Id. Petitioner returned to the ED on October 22, 2015 for a “full-blown
asthmatic attack/difficulty breathing.” Id. at ¶ 13. She again received breathing treatments,
oxygen, and steroids, and declined admission due to insurance. Id. Petitioner again followed up
with Dr. Klares on November 4, 2015. Id. at ¶ 14.

27
Petitioner received the flu vaccine at issue on September 19, 2015. Pet. Ex. 1 at 1.

18
Petitioner averred that “[d]espite her visits to the [ED], [her] symptoms were not
improving.” Pet. Ex. 6 at ¶ 15. Therefore, on November 5, 2015, Petitioner sought treatment at
the JMC Asthma Clinic where she received breathing treatments, oxygen, and steroids. Id.

By November 1, 2015, Petitioner had been granted insurance from her employer. Pet.
Ex. 6 at ¶ 16. On November 11, Petitioner saw her PCP Dr. Rogg for her “increased and
intensifying symptoms” including difficulty breathing, walking, and swallowing; “[s]hortness of
breath;” “[u]ncontrolled asthma with exacerbations;” “[i]ntensifying pins-and-needles in upper
extremities;” “[m]uscle weakness in legs that spread upwards;” “[f]acial twitching;” “[r]apid
heartbeat;” and fatigue. Id. He did blood tests and adjusted her medications. Id. at ¶ 17. The
following day, Petitioner went to the JMC Asthma Clinic where they adjusted her asthma
medications. Id. at ¶ 18.

Petitioner saw neurologist Dr. Saland on November 24, 2015. Pet. Ex. 6 at ¶ 19. Dr.
Saland “did an extensive exam[ination] and ran blood tests due to the neurological symptoms
[Petitioner] had been experiencing.” Id. She was waiting on approval for additional testing and
imaging. Id.

Petitioner returned to Dr. Rogg on December 14, 2015 for cellulitis of her left eye and
face. Pet. Ex. 6 at ¶ 21. On December 18, Petitioner went back to Dr. Saland for an upper
extremity EMG. Id. at ¶ 22. At this time, Petitioner was still experiencing “[p]roblems with
asthma and oxygen exchange,” “[s]hortness of breath,” “[d]ifficulty breathing,” “[c]ongestion in
lungs,” and “[n]eurological symptoms.” Id.

On or about February 2, 2016, Petitioner suffered an outbreak of shingles and Dr. Rogg
prescribed Valtrex. Pet. Ex. 6 at ¶ 24. On February 9, Petitioner saw Dr. Rogg again and at that
time he was waiting approval for pulmonary rehabilitation. Id. at ¶ 25. On or about March 2,
2016, Petitioner suffered another outbreak and exacerbation of shingles. Id. at ¶ 26. She was
again prescribed Valtrex. Id.

On March 29, 2016, Petitioner had a follow-up appointment with Dr. Saland. Pet. Ex. 6
at ¶ 27. Dr. Saland “performed another extensive exam[ination] (due to [Petitioner’s] continued
neurologic symptoms) and ordered an EMG, MRI, and [s]wallowing [t]est.” Id. Petitioner
reported that unfortunately, her “insurance ended on April 1, 2016, so [she] was unable to have
these tests performed.” Id.

Petitioner followed up with Dr. Rogg on April 19, 2016. Pet. Ex. 6 at ¶ 29. At that time,
Dr. Rogg was “still trying to stabilize [Petitioner’s] asthma with different medication regimes.”
Id. Dr. Rogg also still wanted Petitioner to go for pulmonary rehabilitation, but due to
Petitioner’s “lack of insurance and financial hardship, [she] was not able to go” and she was also
“unable to afford some of [her] prescriptions.” Id.

On May 10, 2016, Petitioner presented to Dr. Rogg for an “unscheduled appointment” to
“address symptoms related to a potential medication adverse reaction.” Pet. Ex. 6 at ¶ 31. Dr.
Rogg determined it “might have been caused by the Pravastatin.” Id. Petitioner was still not
feeling better by May 16 when she had another “unscheduled appointment” with Dr. Rogg. Id.
at ¶ 32.

19
On May 31, 2016, Petitioner presented to Jacobi Medical. Pet. Ex. 6 at ¶ 33. “Due to
lack of insurance and financial hardship, Jacobi Medical recommended their medical clinic for
‘reduced-cost’ medical treatment and medication.” Id.

At an appointment with Dr. Rogg on June 7, 2016, Dr. Rogg prescribed Petitioner branch
chain amino acids as a supplement. Pet. Ex. 6 at ¶ 34. On June 14, Petitioner still was not
feeling well so Dr. Rogg ordered a series of blood tests which came back normal. Id. at ¶ 35.

At a follow-up appointment with Dr. Rogg on August 15, Petitioner had “ongoing
feelings of tingling in the extremities and issues with walking post-vaccine.” Pet. Ex. 6 at ¶ 37.
She also had complaints of left abdominal pain. Id. On August 30, Petitioner had an abdominal
ultrasound. Id. at ¶ 38. Petitioner reported “persistent, ongoing muscle aches and tingling—
primarily in the lower extremities.” Id. The results of the abdominal ultrasound were “attributed
to [Petitioner’s] persistent cough from [her] asthma.” Id.

On October 6, 2016, Petitioner had a follow-up with Dr. Rogg, who was “still trying to
stabilize [Petitioner’s] asthma and persistent cough”. Pet. Ex. 6 at ¶ 39. Petitioner reported that
her “chest felt tighter, more constricted[,] and congested.” Id. Dr. Rogg administered a Medrol
injection. Id. Bloods tests showed a vitamin B12 deficiency and Dr. Rogg recommended
weekly B12 injections and oral supplements. Id. At this visit, Petitioner again recalled having
“persistent, ongoing tingling in [her] extremities and muscle aches.” Id. On October 14,
Petitioner returned to Dr. Rogg for “exacerbation of [her] asthma and issues of fatigability and
tingling in [her] extremities.” Id. at ¶ 40.

At a follow-up with Dr. Rogg on December 9, 2016, Petitioner reported that due to
“fatigability and muscle weakness of [her] lower extremities, [she] fell on [her] right side (earlier
in the week).” Pet. Ex. 6 at ¶ 43. An X-ray of Petitioner’s ribs was normal. Id.

By February 2017, Dr. Rogg was “still trying to stabilize [Petitioner’s] asthma and
persistent cough with different medication regimes. . . . In addition, he still want[ed] [Petitioner]
to go for pulmonary consult and rehabilitation, but due to [her] lack of insurance and financial
hardship, [she was] not able to go to rehabilitation and [was] unable [to] fill some of the
prescriptions.” Pet. Ex. 6 at ¶¶ 44-45. Petitioner was still having “continued issues of chronic
fatigue and tingling in extremities (dropping objects).” Id.

On May 16, 2017, Petitioner had an appointment with Dr. Weinstein for follow-up for
her “symptoms related to [her] flu vaccine injury.” Pet. Ex. 6 at ¶ 47. “Due to the loss of
Charity Care, [Petitioner] was temporarily unable to be treated by Dr. Rogg.” Id. She continued
to have follow-up visits with Dr. Weinstein, Dr. Charles, and Dr. Rogg. Id. at ¶ 48. In January
2018, Petitioner injured her toe from a fall “due to [her] fatigue and pins and needles in [her]
lower extremities.” Id. at ¶ 49. In March 2018, Dr. Rogg prescribed Petitioner gabapentin for
her “persistent neurologic symptoms.” Id. at ¶ 50.

As of the date Petitioner executed this affidavit, April 27, 2018, Petitioner “continue[d] to
suffer with asthma symptoms, which are far worse than they were before [she] received the [flu]
vaccine on September 19, 2015.” Pet. Ex. 6 at ¶ 51. She averred “[t]his can be verified by

20
seeing that [she] was not taking steroids and other medications for the asthma until after the
receipt of the vaccine. In addition, [she had] tingling in [her] hands and feet, bilaterally.” Id.
Petitioner wrote that she “truly believes that the injuries [she was] suffering [] are related to the
[flu] vaccine she received on September 19, 2015.” Id. at ¶ 52.

4. Independent Medical Evaluation by Dr. Michael M. Conway 28

On October 8, 2016, Dr. Michael Conway reviewed Petitioner’s medical records from
October 2015 to June 2016 and summarized her case from the pulmonary perspective. Pet. Ex. 7
at 5. He did not address the neurological issues. Id. Dr. Conway’s impression was that while
Petitioner had an asthma exacerbation starting in October 2015, “the flu shot did not cause her
asthma exacerbation.” Id. at 6-7. He stated that “[m]ultiple well-performed large studies
reveal[ed] no increased incidence of asthma following flu vaccination.” Id. at 7. He opined
“[a]ny impairment that flows from poorly controlled asthma is not related to the flu shot” and
“[n]one of the treatment [Petitioner] ha[d] required [was] connected to her flu shot.” Id.

On November 1, 2016, Dr. Conway performed an independent medical evaluation
(“IME”) on Petitioner to evaluate “the relationship[,] if any[,] between an apparent exacerbation
of her underlying asthma and the flu shot she received in September 2015.” Pet. Ex. 7 at 1. He
did not review any additional records from the ones previously reviewed on October 8, 2016. Id.
Petitioner’s history, beginning in the mid 1980’s, eventually required regular medications
including Advair, Singulair, and intermittent prednisone. Id. From 2013 to 2015, Petitioner only
required the use of a rescue inhaler as needed. Id. In September 2015, she had a flu shot. Id. at
2. Dr. Conway noted Petitioner received one every year without difficulty in the past. Id.
“Approximately two weeks later she noted symptoms of a[] [URI] along with numbness and
tingling in her hands and feet. The URI symptoms were followed within [one to two] weeks by
an asthma exacerbation prompting an [ED] visit where she was treated” with multiple rounds of
albuterol nebulization, steroids and oxygen. Id. She was discharged with a prednisone taper and
a rescue inhaler as needed. Id. The following day, Petitioner went to her pulmonologist who
prescribed her an antibiotic and restarted her on Advair, Atrovent, and montelukast. Id. No
pulmonary function test was performed. Id. Petitioner had returned to the ED two more times
and had been on medication on and off since then. Id. “Her asthma remain[ed] poorly
controlled since November 2015.” Id. “For much of the last year she has not had regular
insurance covering medications, so at times she cannot afford to buy and use regular controller
medications.” Id.

Petitioner’s symptoms at the time of the IME were dyspnea, wheezing, and coughing.
Pet. Ex. 7 at 2. Specifically, she noted dyspnea after walking two blocks as well as at night. Id.
She was not able to exercise and felt she could not work regularly because of her persistent
asthma symptoms. Id. “Her neurologic symptoms ha[d] largely cleared.” Id. Review of
symptoms also noted “intermittent palpitations, fatigue, weakness, leg heaviness, paresthesias,
reflux esophagitis[,] and transient difficulty swallowing.” Id. at 3. Her physical examination
was unremarkable, and Dr. Conway noted her chest X-ray from 2015 was clear. Id. He

28
Dr. Conway opined that Petitioner could return to full time regular work without restrictions.
He found “there is no reason her asthma precludes regular work as a pharmacist.” Pet. Ex. 7 at
4.

21
conducted a pulmonary function test and noted Petitioner had difficulty with the test because she
“could not control her cough” and “was worse after [albuterol].” Id.

Dr. Conway opined his major finding had not changed from his October 8, 2016 review.
Pet. Ex. 7 at 2. He specifically opined “[t]he URI and asthma exacerbation that began [two] plus
weeks after the routine flu shot in September 2015 [were] clearly and definitely not secondary to
the flu shot.” Id. His opinion was based on “strong epidemiologic studies that have found no
association between [flu] vaccination and exacerbations of asthma, as well as on the clinical
course of her symptoms.” Id. “She noted the URI symptoms at least two weeks after the flu shot
and these symptoms were followed by an asthma exacerbation like she has noted in the past.”
Id. Dr. Conway stated it was unclear why Petitioner “had such difficulty with her asthma from
the 1980’s through 2013 and yet noted apparently spontaneous clearing from 2013 until 2015.”
Id. His diagnosis was moderate persistent asthma. Id.

C. Expert Reports

1. Petitioner’s Expert, Dr. Omid Akbari, Ph.D. 29

a. Background and Qualifications

Dr. Akbari is currently a Professor of Allergy and Immunology and Professor of
Medicine at Keck School of Medicine, University of Southern California. Pet. Ex. 13 at 2. He
received his Ph.D. in cellular and molecular immunology at the National Institute for Medical
Research in London, United Kingdom. Pet. Ex. 14 at 1. Thereafter he completed a postdoctoral
fellowship at Stanford University. Id. Dr. Akbari’s research is “focused on the role of immune
tolerance and how immune cells induce autoimmune and allergic diseases.” Pet. Ex. 13 at 2.
Additionally, in his laboratory, there are research studies “relevant to the issue of understanding
the medical theories involved in regard to how immunization may result in appropriate or
dysregulated immune responses causing unwanted inflammation and adverse effects.” Id. He
serves as an editor and reviewer on numerous journals and has authored or co-authored
numerous publications. Id.; Pet. Ex. 14 at 4-5, 8-13. Dr. Akbari is not a medical doctor and is
not qualified to diagnose or treat medical, pulmonary, and/or neurological conditions. See Pet.
Ex. 14.

b. Diagnosis Opinion

Although Dr. Akbari is not a medical doctor, he opined Petitioner suffered from
“neuroinflammation in the lungs and nervous system.” Pet. Ex. 13 at 1. He stated that she had
“overly inflammatory episodes which resulted in asthma exacerbation and neuropathic changes
related to [GBS].” Pet. Ex. 13 at 10. He based his opinions on the medical records and
“conclusions by clinical team.” Id. at 10.

29
Dr. Akbari provided one expert report. Pet. Ex. 13.

22
c. Causation Opinion

Dr. Akbari opined that the flu vaccination caused Petitioner “to develop inflammation in
the lungs and nervous system,” and that “stimulation of the immune system . . . followed by the
production of antibodies in response to the vaccines, [i]s a plausible medical theory causally
linking the [flu] vaccination with the development of symptoms in [Petitioner] including asthma
exacerbation and neuropathic symptoms.” Pet. Ex. 13 at 1, 16.

i. Althen Prong One

1. Neurological Condition

For how the flu vaccine can cause “neuroinflammation” and “neuropathic changes related
to [GBS],” Dr. Akbari relied on the theory of molecular mimicry. Pet. Ex. 13 at 4, 10. He
defined molecular mimicry as “the mechanism by which an immune stimulated response by
infection or other method, i.e. vaccination, can trigger cross-reactive antibodies or T cells that
cause the symptoms of autoimmune disease.” Id. at 4-5.

Then Dr. Akbari opined that from an “immunological and pathological perspective,
considerable overlap exists between central and peripheral myelitis including multiple sclerosis,
[GBS], acute disseminated encephalomyelitis.” Pet. Ex. 13 at 11. He stated these conditions are
“characterized by inflammatory infiltration of both T cells and macrophages into the nervous
system, as well as areas of demyelination.” Id. He used the terms neuroinflammation and
demyelinating disease 30 interchangeably. Id. at 11-12. Dr. Akbari opined that autoimmunity in
multiple sclerosis 31 and neuromyelitis 32 is “most likely mediated by antibodies directed against
myelin antigens, along with autoreactive T cells and macrophages that invade the myelin sheath,
axonal membranes, and/or the nodes of Ranvier.” Id. at 14. Additionally, he noted there is
“strong evidence for an antigen driven, T-cell mediated attack against peripheral nerve tissue
components in the pathogenesis of neuromyelitis and demyelinating diseases.” Id. at 15 (citing
Pet. Ex. 63). 33

30
A demyelinating disease is “any condition characterized by destruction of the myelin sheaths
of nerves.” Demyelinating Disease, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=70251 (last visited July 3, 2024).
31
Multiple sclerosis is “a disease in which there are foci of demyelination throughout the white
matter of the central nervous system, sometimes extending into the gray matter; symptoms
usually include weakness, incoordination, paresthesias, speech disturbances, and visual
complaints.” Multiple Sclerosis, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=105130 (last visited July 3, 2024).
32
Neuromyelitis is “inflammation of nervous and medullary substance; myelitis attended with
neuritis.” Neuromyelitis, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/
dorland/definition?id=33789 (last visited July 3, 2024).
33
Tanuja Chitnis, The Role of CD4 T Cells in the Pathogenesis of Multiple Sclerosis, 79 Int’l
Rev. Neurobiology 43 (2007).

23
Dr. Akbari digressed from explaining the theory here to a general discussion of the
immune system and development of autoimmune diseases. Pet. Ex. 13 at 6-8. He stated
immunization with a vaccine causes a local inflammatory reaction mediated by cells of the innate
immune system. Id. at 6. Thereafter, there is a recruitment of other immune cells by secreting
cytokines and activation of the adaptive immune system. Id. Regulatory T cells, which help
maintain tolerance to self-antigens and abrogate autoimmune disease, “actively suppress the
immune system by the cytokines they secrete and direct cellular interactions with the cells that
cause autoimmune disease.” Id. at 7. Dr. Akbari stated regulatory T cells “can suppress other
immune cells such as B cells, T cells, and dendritic cells to prevent autoimmune disease.” Id.
Therefore, he posited that alteration of the suppressive function of regulatory T cells is
associated with autoimmune diseases including GBS and neuroinflammatory disorders. Id.

Dr. Akbari cited clinical studies which allegedly showed the number of regulatory T cells
were significantly decreased in patients with neuroinflammation, specifically optic neuritis. Pet.
Ex. 13 at 7 (citing Pet. Ex. 29; 34 Pet. Ex. 30). 35 He opined the decreased number of regulatory T
cells “most likely is a main factor resulting in a person’s predisposition to develop neuro-
inflammatory disease during activation of the immune system such as by receipt of a vaccine.”
Id. at 8.

In contrast, he opined that an increased number of Th17 cells are seen with
neuroinflammatory diseases. Pet. Ex. 13 at 8 (citing Pet. Ex. 19 at 1; 36 Pet. Ex. 33 at 1). 37 Dr.
Akbari explained that Th17 cells secrete interleukin-17 (“IL-17”), a molecule known to induce
inflammation, and are involved in the pathogenesis of autoimmune diseases. Id. (citing Pet. Ex.
32 at 1). 38 He opined this is particularly true in patients with GBS, thus suggesting it is an
important factor in the pathogenesis of neuroinflammation and GBS. Id. (citing Pet. Ex. 33 at 1;
Pet. Ex. 35 at 1). 39

34
Hengri Cong et al., Change of Th17 Lymphocytes and Treg/Th17 in Typical and Atypical
Optic Neuritis, 11 PLoS ONE e0146270 (2016).
35
Guochun Chen et al., mTOR Regulates Neuroprotective Effect of Immunized CD4+Foxp3+T
Cells in Optic Nerve Ischemia, 6 Sci. Reps. 37805 (2016).
36
Marinos C. Dalakas, Future Perspectives in Target-Specific Immunotherapies of Myasthenia
Gravis, 8 Therapeutic Advances Neurological Disorders 316 (2015).
37
Shujuan Li et al., Circulating Th17, Th22, and Th1 Cells are Elevated in the Guillain-Barré
Syndrome and Downregulated by IVIg Treatments, 2014 Mediators Inflammation 740947.
38
José Francisco Zambrano-Zaragoza et al., Th17 Cells in Autoimmune and Infectious Diseases,
2014 Int’l J. Inflammation 651503.
39
F. Jadidi-Niaragh & A. Mirshafiey, Th17 Cell, the New Player of Neuroinflammatory Process
in Multiple Sclerosis, 74 Scandinavian J. Immunology 1 (2011).

24
He then again digressed and opined “[w]hen homeostasis is disrupted and the immune
system responds in favor of activation, . . . the host becomes susceptible to autoimmunity.” Pet.
Ex. 13 at 8. He added the disrupted balance leaves individuals “susceptible to an adverse
autoimmune reaction upon stimulation of the immune system” from either an infection or
immunization. Id.

As to the specific mechanism of disruption by vaccination here, Dr. Akbari returned to
his theory of molecular mimicry, “a mechanism in which the host and the microbe share an
immunologic epitope by either sequence or conformational homology.” Pet. Ex. 13 at 5 (citing
Pet. Ex. 17). 40 He opined that while it was “originally believed that similarity of a significant
portion of the protein peptide sequence between putative pathogens and self peptides” was
required to implicate molecular mimicry, Dr. Akbari believed “conversion of only a few crucial
residues can allow for cross-reactivity of immune cells.” Id. (citing Pet. Ex. 18). 41 According to
Dr. Akbari, “proteins of dissimilar sequence may have a common structure which elicits an
autoimmune response.” Id. “In spite of dissimilar sequence homology between self and foreign
peptide, weak electrostatic interactions between foreign peptide and the MHC can also mimic
self peptide to elicit an autoimmune response within the host.” Id. at 6. He concluded molecular
mimicry can occur “between two recognized peptides that have similar antigenic surfaces in the
absence of primary sequence homology.” Id.

Dr. Akbari proposed that flu viruses A and B are components contained in the flu
vaccine. Pet. Ex. 13 at 10. These components trigger an “immune response to myelin proteins
and complex sugar” associated with gangliosides. Id. “The immune response elicited to
gangliosides mainly targets the sugars on the vaccine, which are also a component of the myelin
sheath.” Id.

He cited two studies to show that cross-reactive T cells in response to flu vaccination
have been shown to cause demyelinating disease. Pet. Ex. 13 at 10-11. Markovic-Plese et al. 42
proposed cross-reactivity of a CD4+ T-cell clone specific for the immunodominant flu virus
hemagglutinin peptide (sequence RYVKQSTLKL) derived from a patient with neuromyelitis
and demyelinating disease. Id. (citing Pet. Ex. 41 at 1). Wucherpfennig et al. 43 tested peptides
containing protein sequences that share a similar structure with myelin basic protein to see if
they stimulated the production of T-cells. Pet. Ex. 43 at 1. The results showed that the flu A

40
Robert S. Fujinami et al., Molecular Mimicry, Bystander Activation, or Viral Persistence:
Infections and Autoimmune Disease, 19 Clinical Microbiology Revs. 80 (2006).
41
Adam P. Kohm et al., Mimicking the Way to Autoimmunity: An Evolving Theory of
Sequence and Structural Homology, 11 Trends Microbiology 101 (2003).
42
Silva Markovic-Plese et al., High Level of Cross-Reactivity in Influenza Virus Hemagglutinin-
Specific CD4+ T-Cell Response: Implications for the Initiation of Autoimmune Response in
Multiple Sclerosis, 169 J. Neuroimmunology 31 (2005).
43
Kai W. Wucherpfennig et al., Recognition of the Immunodominant Myelin Basic Protein
Peptide by Autoantibodies and HLA-DR2-Restricted T Cell Clones from Multiple Sclerosis
Patients, 100 J. Clinical Invest. 1114 (1997).

25
peptide sequence (among others) stimulated T-cells. Id. From these studies, Dr. Akbari
concluded the flu vaccine at issue “contains a protein that cross-reacts with myelin based
antigens in humans who had demyelinating disease.” Pet. Ex. 13 at 11.

Additionally, Dr. Akbari proposed another peptide to the major protein in the myelin
sheath known as myelin basic protein in the flu A vaccines. Pet. Ex. 13 at 11. He opined the
amino acid sequence of the hemagglutinin, FYKNLI, has “high homology” with the myelin basic
protein, FFKNIV, with the only variations being one aromatic amino acid “F” for “Y” and two
aliphatic amino acids, leucine and isoleucine. Id. He stated this is “another undeniable example
of a molecular mimicry with [flu] A strains appeared in vaccine that [Petitioner] received.” Id.

Relying on medical literature, Dr. Akbari opined this sequence is significant due to the
high homology of the amino acid sequence of hemagglutinin to myelin basic protein. Pet. Ex. 13
at 11. Gautam et al. 44 found that homology at just five amino acids with a self peptide can
induce clinical signs experimental autoimmune encephalomyelitis (“EAE”). Pet. Ex. 44 at 1; see
also Pet. Ex. 43. He opined this “clearly indicate[s] that a viral peptide with homology of [five]
amino acids with a self-peptide is sufficient to induce clinical signs of neuromyelitis and
demyelinating disease in animal models.” Pet. Ex. 13 at 11 (citing Pet. Exs. 43-44).

For further support of vaccine causation, Dr. Akbari cited medical literature documenting
post-vaccination inflammatory diseases. Pet. Ex. 13 at 10. Karussis and Petrou conducted a
PubMed search from 1979 to 2013 and found 71 cases of a temporal association between an
inflammatory central nervous system demyelinating disease and the administration of a vaccine.
Pet. Ex. 40 at 1. Of these 71 cases, 21 were associated with the flu vaccine. Id. at 1, 4-5 tbl.2.
The symptoms of the demyelinating syndromes and signs of neuroinflammation including GBS
often appeared a few days following vaccination with a mean of 14.2 days. Pet. Ex. 13 at 10
(citing Pet. Ex. 40 at 2).

2. Asthma Exacerbation

For how the flu vaccine can cause asthma exacerbation, Dr. Akbari relied on an auto-
reactive T cell mechanism. Pet. Ex. 13 at 1, 12-14. Dr. Akbari opined that vaccination caused
an exacerbation in Petitioner’s asthma by inducing lung inflammation. Id.

Then Dr. Akbari opined that “neuroimmune interaction has long been discussed in the
pathogenesis of allergic airway diseases, such as allergic asthma. Mediators released during
inflammation can alter the function of both sensory and parasympathetic neurons innervating the
airways.” Pet. Ex. 13 at 12. He did not explain how this opinion about neurons related to
asthma exacerbation.

44
Anand M. Gautam et al., A Viral Peptide with Limited Homology to a Self Peptide Can Induce
Clinical Signs of Experimental Autoimmune Encephalomyelitis, 161 J. Immunology 60 (1998).

26
Additionally, Dr. Akbari cited literature purportedly showing lung inflammation induced
by flu vaccination. Pet. Ex. 13 at 12. Hibino and Kondo 45 described two cases of interstitial
pneumonia secondary to the 2014-2015 seasonal flu vaccine which contained the A(H1N1)
antigen. Pet. Ex. 46 at 1. The patients had no history of allergy, inhalation exposure, smoking,
or family history of pulmonary diseases. Id. at 3-4. Serological tests were negative for
autoimmune markers. Id. at 4. However, the patients met the diagnostic criteria for drug-
induced interstitial lung disease. 46 Id. “Based on these findings, interstitial pneumonia
associated with the [flu] vaccine was diagnosed after excluding other causes of secondary
interstitial pneumonia, such as infectious and connective tissue disease. The pathophysiology of
drug-induced interstitial pneumonia, although not obvious, is believed to be cytotoxic or
immune-mediated lung injury.” Id. The authors did not reach a conclusion as to a causal
association, if any, between the flu vaccine and interstitial pneumonia. Id. at 4-5. And there was
no discussion of asthma exacerbation.

Watanabe et al. 47 described a patient who developed a fever one week after receiving a
flu vaccine. Pet. Ex. 47 at 1. Her chest X-ray revealed “patchy airspace infiltrates in both
lungs.” Id. She had no prior history of pulmonary disease and her chest X-ray the month prior
was normal. Id. The temporal relationship between vaccination and clinical symptoms
suggested a causative role. Id. The authors also reviewed six cases of flu vaccine-induced
interstitial lung disease. Id. at 2-3. Four of the cases had pre-existing lung diseases. Id. The
authors hypothesized that pre-existing lung diseases, flu vaccination, and genetic background
may be risk factors for interstitial lung disease but noted further studies were needed to evaluate
the association of vaccine-related interstitial lung disease. Id. at 3. There was no reference to
exacerbation of asthma.

Bhurayanontachi 48 described a patient who developed multiple organ failure, including
acute respiratory distress, five days after an H1N1 vaccination. Pet. Ex. 49 at 1. All vasculitic
screening was negative. Id. The diagnosis of the patient remained unclear; however, the authors
noted “vasculitis or an autoimmune disease [was] unlikely, and a severe adverse event following
the H1N1 vaccination could not be completely excluded.” Id. There was no mention of asthma
exacerbation.

45
Makoto Hibino & Tetsuri Kondo, Interstitial Pneumonia Associated with the Influenza
Vaccine: A Report of Two Cases, 56 Internal Med. 197 (2017).
46
Interstitial lung disease is “a heterogeneous group of noninfectious, nonmalignant disorders of
the lower respiratory tract, affecting primarily the alveolar wall structures but also often
involving the small airways and blood vessels of the lung parenchyma; slowly progressive loss
of alveolar-capillary units may lead to respiratory insufficiency and death.” Interstitial Lung
Disease, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?
id=70466 (last visited July 3, 2024).
47
Satoshi Watanabe et al., Influenza Vaccine-Induced Interstitial Lung Disease, 41 Eur.
Respiratory J. 474 (2013).
48
Rungsun Bhurayanontachi, Possible Life-Threatening Adverse Reaction to Monovalent H1N1
Vaccine, 14 Critical Care 422 (2010).

27
Umeda et al. 49 described a case of acute exacerbation of idiopathic pulmonary fibrosis 50
after a flu A H1N1 vaccination. Pet. Ex. 50 at 1. Two days after vaccination, the patient was
admitted to the hospital for aggravation of dyspnea and fever. Id. The patient was already
diagnosed with idiopathic pulmonary fibrosis and was a former smoker. Id. Prior to the
vaccination, chest X-ray did not show any worsening of his pre-existing respiratory condition.
Id. After his vaccination and hospital admission, chest X-ray showed “diffuse bilateral ground-
glass opacities superimposed on preceding reticular opacities.” Id. After examination (crackles
were audible in the bilateral lung bases) and lab testing, a diagnosis of exacerbation of idiopathic
pulmonary fibrosis was confirmed. Id. at 1-2. After extensive treatment, including steroids, his
symptoms improved but long-term oxygen therapy was required. Id. at 2. The authors
concluded the flu vaccine was “the most likely cause” of the acute exacerbation. Id. at 4. First,
they reasoned the patient received a seasonal flu vaccine one month prior to receiving the
pandemic (flu A H1N1) vaccination and a “second exposure to the same antigen might elicit a
response within a shorter period.” Id. Second, no other cause of deterioration was found. Id.
They noted flu vaccination was reported to induce inflammatory cytokines and implicated
bystander activation. Id. However, the authors also noted that while the patient had no
worsening of his respiratory symptoms prior to the flu A H1N1 vaccine, he did have a low-grade
fever prior and cautioned administering vaccines based on patients’ conditions. Id. There was
no mention of asthma or asthma exacerbation.

Audrit et al. 51 described inflammatory lung disease, including asthma, but the article
relates to the nervous system of airways and how it is affected by inflammatory lung disease.
Pet. Ex. 51 at 1. The authors do not discuss how vaccines in general, or the flu vaccine
specifically, can exacerbate asthma.

ii. Althen Prongs Two and Three

Dr. Akbari opined, “to a high degree of certainty, and by a preponderance of scientific
evidence,” that “had it not been for the flu vaccination, [Petitioner] would not have developed
symptoms such as neuropathy and asthma exacerbation.” Pet. Ex. 13 at 15. Based on his review
of the record, Dr. Akbari stated, “the presence of symptoms is essentially based on the temporal
relationship between the administration of the flu vaccine and the development of asthma
exacerbation and neuropathic changes in [Petitioner].” Id. at 16. “To a high degree of medical
certainty, had it not been for the flu vaccination, [Petitioner] would not have developed [asthma
exacerbation and neuropathic changes].” Id.

49
Yukihiro Umeda et al., Acute Exacerbation of Idiopathic Pulmonary Fibrosis After Pandemic
Influenza A (H1N1) Vaccination, 49 Internal Med. 2333 (2010).
50
Idiopathic pulmonary fibrosis is “chronic inflammation and progressive fibrosis of the
pulmonary alveolar walls, with steadily progressive dyspnea, resulting finally in death from
oxygen lack or right heart failure.” Idiopathic Pulmonary Fibrosis, Dorland’s Med. Dictionary
Online, https://www.dorlandsonline.com/dorland/definition?id=75788 (last visited July 3, 2024).
51
Katrin Julia Audrit et al., The Nervous System of Airway and Its Remodeling in Inflammatory
Lung Disease, 367 Cell Tissue Rsch. 571 (2017).

28
2. Respondent’s Expert, Dr. Arnold I. Levinson, M.D. 52

a. Background and Qualifications

Dr. Levinson is board certified in internal medicine and allergy and clinical immunology.
Resp. Ex. B at 1; Resp. Ex. C at 2. He received his M.D. from the University of Maryland.
Resp. Ex. C at 1. He completed fellowships at the Johns Hopkins Hospital and the University of
Pennsylvania School of Medicine, and post-doctoral fellowships in immunology at the
University of Pennsylvania School of Medicine and the University of California, San Francisco
Medical Center. Id. Dr. Levinson is currently an Emeritus Professor of Medicine and Neurology
at the Perelman School of Medicine at the University of Pennsylvania. Resp. Ex. B at 1. During
his 37-year tenure at University of Pennsylvania, Dr. Levinson “conducted a clinical practice in
which [he] evaluated and treated patients with a broad range of immune‐mediated diseases
including autoimmune, hypersensitivity, and immunodeficiency disorders.” Id. Dr. Levinson
has authored or co-authored numerous publications. Resp. Ex. C at 10-21.

b. Diagnosis Opinion

Dr. Levinson agreed Petitioner had an exacerbation of her asthma. Resp. Ex. B at 11-12.
However, he disagreed it was caused by her flu vaccination. Id. Instead, he opined her
worsening was caused by a URI. Id.

Dr. Levinson disagreed that Petitioner suffered from neuroinflammation or GBS. Resp.
Ex. B at 6. He did not believe Petitioner suffered from any autoimmune demyelinating disorder
or definable neuroinflammatory disorder. Id. at 12.

Regarding GBS, Dr. Levinson explained it is a “syndrome that encompasses many
variants that most commonly present as an acute immune-mediated polyneuropathy following an
infectious illness.” Resp. Ex. B at 6 (citing Resp. Ex. B.1 at 1). The most common variants are
acute inflammatory demyelinating polyneuropathy (“AIDP”) and acute motor axonal neuropathy
(“AMAN”). Id. (citing Resp. Ex. B.1 at 1). A characteristic diagnostic finding in GBS is
albuminocytologic dissociation 53 on CSF analysis. Id. at 7. Additionally, EMG/NCS studies can
show evidence of an acute demyelinating polyneuropathy or evidence of an axonal neuropathy.
Id.

“All GBS variants are considered to be autoimmune, i.e., caused by an immune-mediated
reaction against peripheral nerve constituents.” Resp. Ex. B at 7. “In particular, peripheral nerve
injury is considered to be mediated by complement-dependent IgG antibodies and T cells
targeted to unknown antigenic epitopes on peripheral nerve Schwann cells and myelin in the

52
Dr. Levinson provided one expert report. Resp. Ex. B.
53
Albuminocytologic dissociation is the “increase of protein with normal cell count in the spinal
fluid.” Albuminocytologic Dissociation, Dorland’s Med. Dictionary Online,
https://www.dorlandsonline.com/dorland/definition?id=71273 (last visited July 3, 2024).

29
AIDP form of GBS and primarily peripheral nerve glycolipid antigens in the other variants.” Id.
Dr. Levinson opined the most common event linked to GBS is an antecedent infection. Id.

Dr. Levinson took issue with Dr. Akbari’s use of the term neuroinflammation to
characterize Petitioner’s neurological symptoms. Resp. Ex. B at 7. While he believed it is
appropriate to use this “non-specific term” in some instances, such as in relation to multiple
sclerosis, acute disseminated encephalomyelitis, and GBS, “where inflammatory demyelination
is operative,” he explained “there is no basis for applying this term to what ailed [] [P]etitioner
neurologically.” Id. This is because Petitioner’s medical records do not provide evidence that
“her neurological symptoms were/are caused by an underlying neuroinflammatory process.” Id.
And he pointed out that GBS was never diagnosed by Petitioner’s neurologists. Id. at 7-8.

In evaluating Petitioner’s neurology records, Dr. Levinson noted that Dr. Saland
“considered the possibility” that Petitioner’s paresthesias may have been the result of “an
autoimmune process possibly caused by the vaccination. However, no
discussion/characterization of the speculated autoimmune process was offered and GBS, per se,
was not diagnosed.” Resp. Ex. B at 8. Similarly, Dr. Khella assessed the “possibility” that
Petitioner had GBS. Id. Dr. Levinson opined that the “possibility [was] extremely remote.” Id.
He opined that Petitioner’s clinical complaints, neurological examination, and nerve conduction
testing results were “highly inconsistent” with GBS. Id. Moreover, Dr. Levinson observed that
Petitioner’s “most vexing symptom” was paresthesias in her hands and toes which had improved
by the time of her visit with Dr. Saland. Id.

Further, there was no progression of Petitioner’s neurologic symptoms which is usually
common in GBS. Resp. Ex. B at 8. And Dr. Levinson opined there were no signs of a
peripheral neuropathy on neurological examination other than right median nerve entrapment,
which was diagnosed as carpal tunnel syndrome. Id. The nerve conduction study, done at the
time she was symptomatic, did not show evidence of an inflammatory/demyelinating
neuropathy. Id. According to Dr. Levinson the study also ruled out a large fiber peripheral
polyneuropathy. Id.

To support his opinions about diagnosis, Dr. Levinson cited a study by Fokke et al. that
evaluated the diagnostic characteristics of 494 patient with GBS and affirmed the diagnostic
criteria for GBS developed by the National Institute of Neurological Disorders and Stroke
(“NINDS”) and the Brighton Collaboration. 54 Resp. Ex. B.2 6 tbl.5. Only 1% of the patients
presented with normal strength, only 2% presented with normal tendon reflexes in the legs, zero
patients had normal reflexes at the nadir of their illness, 15% had normal CSF cell count, and
only 1% had a normal nerve conduction study. Id. In contrast, physical examinations of
Petitioner revealed normal strength, normal reflexes, normal cell count, and normal NCS; thus,
using these diagnostic findings, Petitioner’s diagnostic studies were not consistent with GBS. Id.

54
The Brighton Collaboration is “a community aiming to promote and improve vaccine safety.
[They] enhance the science of vaccine research by providing standardized, validated, and
objective methods for monitoring vaccine safety and benefit-risk profiles.” Brighton
Collaboration, https://brightoncollaboration.org/ (last visited July 3, 2024).

30
Dr. Levinson concluded “the preponderance of medical evidence strongly militates
against the diagnosis of GBS as defined by inclusionary criteria established by the Brighton
Collaborative Group guideline[s].” 55 Resp. Ex. B at 8 (citing Resp. Ex. B.2). He further opined
there is no evidence she suffered an autoimmune response, immune dysregulation, or any
autoimmune demyelinating disorder. Id. at 8-9.

c. Causation Opinion

i. Neurological Condition

Dr. Levinson opined that while Dr. Akbari’s proposed theory of molecular mimicry is
widely accepted by immunologists, it is not relevant here because Petitioner did not suffer from a
definable neuroinflammatory autoimmune disease. Resp. Ex. B at 8-9. Accordingly, he opined
the literature is not relevant. Id.

Dr. Akbari relied on Markovic-Plese et al. and Wucherpfennig et al. to opine that the flu
vaccine Petitioner received “contains a protein that cross-reacts with myelin based antigens in
humans who had demyelinating disease.” Pet. Ex. 13 at 11. Dr. Levinson opined this conclusion
drawn from publications is conflated and misleading. Resp. Ex. B at 9. “Whether or not [the
flu] vaccine contains a protein that cross-reacts with human-based myelin expressed proteins, the
theoretical possibility that said cross-reactivity might cause demyelination in some humans is
immaterial in this case.” Id. He reasoned this is because it is “highly unlikely” Petitioner
suffered an autoimmune demyelinating disorder. Id.

ii. Asthma Exacerbation

Dr. Levinson agreed Petitioner had an exacerbation of her asthma but he disagreed that it
was caused by the vaccine. Resp. Ex. B at 11. Instead, based on “the well-defined role of viral
[URIs] in asthma exacerbations and the lack of reliable data that speak to a role for the flu
vaccine in such exacerbations,” Dr. Levinson opined that “the [URI] experienced by []
[P]etitioner [two to three] weeks post vaccination was the overwhelming cause of that
exacerbation.” Id. at 12.

Dr. Levinson questioned Dr. Akbari’s discussion surrounding autoreactive T cells and
asthma because Dr. Levinson opined that asthma—allergic or non-allergic—is not an
autoimmune disease. Resp. Ex. B at 10. Rather, “[t]he T cells that do promote allergic asthma
react to exogenous allergens not self-antigens.” Id. Thus, Dr. Levinson opined that Dr. Akbari’s
causation theory “is totally incongruent with the pathophysiologic basis of asthma” and that there
is “no basis to consider that autoimmune reactions contribute to acute exacerbations or chronic
persistence of asthma symptomatology.” Id. at 10, 12.

55
In support, Dr. Levinson noted Petitioner had intact deep tendon reflexes, normal motor and
sensory examinations, normal NCS, and “no physical signs of an underlying peripheral
neuropathy on neurological examination other than . . . carpal tunnel syndrome.” Resp. Ex. B at
8.

31
While Dr. Akbari referred to publications on the worsening of idiopathic pulmonary lung
disease following H1N1 vaccinations to support his position, Dr. Levinson opined “the
clinicopathologic characteristics of [those] disorders are quite different from those of asthma.”
Resp. Ex. B at 9. Dr. Levinson stated there is no literature reporting an asthma exacerbation
following an inactivated flu vaccine or a plausible biological mechanism for such alleged
outcome. Id. Moreover, Dr. Levinson added that “[n]o reliable data” were provided to support
Petitioner’s claim that the vaccination caused the asthma to pursue a chronic course, and “no
plausible biologic mechanism was offered to explain the worsened disease pattern.” Id. at 10.

Rather, Dr. Levinson cited a 2011 Institute of Medicine (“IOM”) 56 report rejecting a
causal relationship between the inactivated flu vaccine and asthma exacerbation. Resp. Ex. B at
9-10 (citing Resp. Ex. A). The IOM report addressed whether the inactivated flu vaccine caused
asthma exacerbation and determined there was no association with “a high degree of confidence
in the epidemiologic evidence based on nine studies with validity and precision to assess an
association between inactivated influenza vaccine and asthma exacerbation or reactive airway
disease episodes in children and adults.” Resp. Ex. A at 350.

1. Alternate Cause

Dr. Levinson believed Dr. Akbari “ignored the ‘elephant in the room,’ i.e., the [URI] that
preceded the exacerbation of [Petitioner’s] asthma.” Resp. Ex. B at 11. He stated that many of
Petitioner’s healthcare providers noted the occurrence of the “likely virus-induced” URI in
documenting the chain of events following Petitioner’s September 19, 2015 flu vaccination. Id.

Dr. Levinson cited medical literature for support that URIs are common precipitants of
asthma. Resp. Ex. B at 11. Busse et al. 57 wrote “[r]espiratory viral infections can also have a
significant influence on those patients with established asthma, where viral respiratory infections
are found in association with asthma exacerbations in nearly 80% of these episodes.” Resp. Ex.
B.3 at 2. Further, the “association between viral respiratory infections and asthma exacerbations
is seen in both children and adults.” Id.

According to Dr. Levinson, the reasoning for this is because both viral infections and
allergic inflammations can damage the airway epithelium and allergic inflammation can impede
anti-viral defense mechanisms. Resp. Ex. B at 11.

Therefore, Dr. Levinson agreed with Dr. Conway that the URI, not the vaccination, was
the cause of Petitioner’s asthma exacerbation. Resp. Ex. B at 11. Dr. Levinson opined “to a
degree of medical certainty” that Petitioner’s URI two to three weeks after the flu vaccination
“was the overwhelming cause” of Petitioner’s asthma exacerbation. Id. at 12.

56
Inst. of Med., Influenza Vaccine, in Adverse Effects of Vaccines: Evidence and Causality 293,
309 (Kathleen Stratton et al. eds., 2012).
57
William W. Busse et al., The Role of Viral Respiratory Infections in Asthma and Asthma
Exacerbations, 376 Lancet 826 (2010).

32
IV. DISCUSSION

A. Standards for Adjudication

The Vaccine Act was established to compensate vaccine-related injuries and deaths. §
10(a). “Congress designed the Vaccine Program to supplement the state law civil tort system as
a simple, fair and expeditious means for compensating vaccine-related injured persons. The
Program was established to award ‘vaccine-injured persons quickly, easily, and with certainty
and generosity.’” Rooks v. Sec’y of Health & Hum. Servs., 35 Fed. Cl. 1, 7 (1996) (quoting
H.R. Rep. No. 908 at 3, reprinted in 1986 U.S.C.C.A.N. at 6287, 6344).

Petitioner’s burden of proof is by a preponderance of the evidence. § 13(a)(1). The
preponderance standard requires a petitioner to demonstrate that it is more likely than not that the
vaccine at issue caused the injury. Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315,
1322 n.2 (Fed. Cir. 2010). Proof of medical certainty is not required. Bunting v. Sec’y of Health
& Hum. Servs., 931 F.2d 867, 873 (Fed. Cir. 1991). Petitioner need not make a specific type of
evidentiary showing, i.e., “epidemiologic studies, rechallenge, the presence of pathological
markers or genetic predisposition, or general acceptance in the scientific or medical communities
to establish a logical sequence of cause and effect.” Capizzano v. Sec’y of Health & Hum.
Servs., 440 F.3d 1317, 1325 (Fed. Cir. 2006). Instead, Petitioner may satisfy her burden by
presenting circumstantial evidence and reliable medical opinions. Id. at 1325-26.

In particular, a petitioner must prove that the vaccine was “not only [the] but-for cause of
the injury but also a substantial factor in bringing about the injury.” Moberly, 592 F.3d at 1321
(quoting Shyface v. Sec’y of Health & Hum. Servs., 165 F.3d 1344, 1352-53 (Fed. Cir. 1999));
see also Pafford v. Sec’y of Health & Hum. Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006). The
received vaccine, however, need not be the predominant cause of the injury. Shyface, 165 F.3d
at 1351. A petitioner who satisfies this burden is entitled to compensation unless Respondent
can prove, by a preponderance of the evidence, that the vaccinee’s injury is “due to factors
unrelated to the administration of the vaccine.” § 13(a)(1)(B). However, if a petitioner fails to
establish a prima facie case, the burden does not shift. Bradley v. Sec’y of Health & Hum.
Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).

“Regardless of whether the burden ever shifts to the [R]espondent, the special master
may consider the evidence presented by the [R]espondent in determining whether the [P]etitioner
has established a prima facie case.” Flores v. Sec’y of Health & Hum. Servs., 115 Fed. Cl. 157,
162-63 (2014); see also Stone v. Sec’y of Health & Hum. Servs., 676 F.3d 1373, 1379 (Fed. Cir.
2012) (“[E]vidence of other possible sources of injury can be relevant not only to the ‘factors
unrelated’ defense, but also to whether prima facie showing has been made that the vaccine was
a substantial factor in causing the injury in question.”); de Bazan v. Sec’y of Health & Hum.
Servs., 539 F.3d 1347, 1353 (Fed. Cir. 2008) (“The government, like any defendant, is permitted
to offer evidence to demonstrate the inadequacy of the [P]etitioner’s evidence on a requisite
element of the [P]etitioner’s case-in-chief.”); Pafford, 451 F.3d at 1358-59 (“[T]he presence of
multiple potential causative agents makes it difficult to attribute ‘but for’ causation to the
vaccination. . . . [T]he Special Master properly introduced the presence of the other unrelated
contemporaneous events as just as likely to have been the triggering event as the vaccinations.”).

33
B. Factual Issues

Petitioner must prove, by a preponderance of the evidence, the factual circumstances
surrounding her claim. § 13(a)(1)(A). To resolve factual issues, the special master must weigh
the evidence presented, which may include contemporaneous medical records and testimony.
See Burns v. Sec’y of Health & Hum. Servs., 3 F.3d 415, 417 (Fed. Cir. 1993) (explaining that a
special master must decide what weight to give evidence including oral testimony and
contemporaneous medical records).

Medical records, specifically contemporaneous medical records, are presumed to be
accurate and generally “warrant consideration as trustworthy evidence.” Cucuras v. Sec’y of
Health & Hum. Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993). But see Kirby v. Sec’y of Health
& Hum. Servs., 997 F.3d 1378, 1382 (Fed. Cir. 2021) (rejecting the presumption that “medical
records are accurate and complete as to all the patient’s physical conditions”); Shapiro v. Sec’y
of Health & Hum. Servs., 101 Fed. Cl. 532, 538 (2011) (“[T]he absence of a reference to a
condition or circumstance is much less significant than a reference which negates the existence
of the condition or circumstance.” (quoting Murphy v. Sec’y of Health & Hum. Servs., 23 Cl. Ct.
726, 733 (1991), aff’d per curiam, 968 F.2d 1226 (Fed. Cir. 1992))), recons. den’d after remand,
105 Fed. Cl. 353 (2012), aff’d mem., 503 F. App’x 952 (Fed. Cir. 2013). The weight afforded to
contemporaneous records is due to the fact that they “contain information supplied to or by
health professionals to facilitate diagnosis and treatment of medical conditions. With proper
treatment hanging in the balance, accuracy has an extra premium.” Id. To overcome the
presumptive accuracy of medical records, a petitioner may present testimony which is
“consistent, clear, cogent, and compelling.” Sanchez v. Sec’y of Health & Hum. Servs., No. 11-
685V, 2013 WL 1880825, at *3 (Fed. Cl. Spec. Mstr. Apr. 10, 2013) (citing Blutstein v. Sec’y of
Health & Hum. Servs., No. 90-2808V, 1998 WL 408611, at *5 (Fed. Cl. Spec. Mstr. June 30,
1998)), mot. for rev. denied, 142 Fed. Cl. 247 (2019), vacated on other grounds & remanded, 809
F. App’x 843 (Fed Cir. 2020).

There are situations in which compelling testimony may be more persuasive than written
records, such as where records are deemed to be incomplete or inaccurate. Campbell v. Sec’y of
Health & Hum. Servs., 69 Fed. Cl. 775, 779 (2006) (“[L]ike any norm based upon common
sense and experience, this rule should not be treated as an absolute and must yield where the
factual predicates for its application are weak or lacking.”); Lowrie v. Sec’y of Health & Hum.
Servs., No. 03-1585V, 2005 WL 6117475, at *19 (Fed. Cl. Spec. Mstr. Dec. 12, 2005)
(“[W]ritten records which are, themselves, inconsistent, should be accorded less deference than
those which are internally consistent.” (quoting Murphy, 23 Cl. Ct. at 733)). Ultimately, a
determination regarding a witness’s credibility is needed when determining the weight that such
testimony should be afforded. Andreu v. Sec’y of Health & Hum. Servs., 569 F.3d 1367, 1379
(Fed. Cir. 2009); Bradley, 991 F.2d at 1575.

Despite the weight afforded medical records, special masters are not bound rigidly by
those records in determining onset of a petitioner’s symptoms. Valenzuela v. Sec’y of Health &
Hum. Servs., No. 90-1002V, 1991 WL 182241, at *3 (Fed. Cl. Spec. Mstr. Aug. 30, 1991); see
also Eng v. Sec’y of Health & Hum. Servs., No. 90-1754V, 1994 WL 67704, at *3 (Fed. Cl.
Spec. Mstr. Feb. 18, 1994) (Section 13(b)(2) “must be construed so as to give effect also to §
13(b)(1) which directs the special master or court to consider the medical records (reports,

34
diagnosis, conclusions, medical judgment, test reports, etc.), but does not require the special
master or court to be bound by them”).

C. Causation

To receive compensation through the Program, Petitioner must prove either (1) that she
suffered a “Table Injury”—i.e., an injury listed on the Vaccine Injury Table—corresponding to a
vaccine that she received, or (2) that she suffered an injury that was actually caused by a
vaccination. See §§ 11(c)(1), 13(a)(1)(A); Capizzano, 440 F.3d at 1319-20. Petitioner 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.” Moberly, 592 F.3d at 1321 (quoting Shyface, 165 F.3d at 1352-53).

Because Petitioner does not allege she suffered a Table Injury, she must prove a vaccine
she received actually caused her injury. To do so, Petitioner must establish, by preponderant
evidence: “(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.” Althen, 418 F.3d
at 1278.

The causation theory must relate to the injury alleged. Petitioner must provide a sound
and reliable medical or scientific explanation that pertains specifically to this case, although the
explanation need only be “legally probable, not medically or scientifically certain.” Knudsen v.
Sec’y of Health & Hum. Servs., 35 F.3d 543, 548-49 (Fed. Cir. 1994). Petitioner cannot
establish entitlement to compensation based solely on her assertions; rather, a vaccine claim must
be supported either by medical records or by the opinion of a medical doctor. § 13(a)(1). In
determining whether Petitioner is entitled to compensation, the special master shall consider all
material in the record, including “any . . . conclusion, [or] medical judgment . . . which is
contained in the record regarding . . . causation.” § 13(b)(1)(A). The special master must weigh
the submitted evidence and the testimony of the parties’ proffered experts and rule in Petitioner’s
favor when the evidence weighs in her favor. See Moberly, 592 F.3d at 1325-26 (“Finders of
fact are entitled—indeed, expected—to make determinations as to the reliability of the evidence
presented to them and, if appropriate, as to the credibility of the persons presenting that
evidence.”); Althen, 418 F.3d at 1280 (noting that “close calls” are resolved in Petitioner’s
favor).

Testimony that merely expresses the possibility—not the probability—is insufficient, by
itself, to substantiate a claim that such an injury occurred. See Waterman v. Sec’y of Health &
Hum. Servs., 123 Fed. Cl. 564, 573-74 (2015) (denying Petitioner’s motion for review and
noting that a possible causal link was not sufficient to meet the preponderance standard). The
Federal Circuit has made clear that the mere possibility of a link between a vaccination and a
petitioner’s injury is not sufficient to satisfy the preponderance standard. Moberly, 592 F.3d at
1322 (emphasizing that “proof of a ‘plausible’ or ‘possible’ causal link between the vaccine and
the injury” does not equate to proof of causation by a preponderance of the evidence); Boatmon
v. Sec’y of Health & Hum. Servs., 941 F.3d 1351, 1359-60 (Fed. Cir. 2019). While certainty is
by no means required, a possible mechanism does not rise to the level of preponderance.
Moberly, 592 F.3d at 1322; see also de Bazan, 539 F.3d at 1351.

35
D. Significant Aggravation

The elements of an off-Table significant aggravation case are set forth in Loving. See
Loving, 86 Fed. Cl. at 142-44; see also W.C. v. Sec’y of Health & Hum. Servs., 704 F.3d 1352,
1357 (Fed. Cir. 2013) (holding that “the Loving case provides the correct framework for
evaluating off-table significant aggravation claims”). The Loving court combined the Althen
test, which defines off-Table causation cases, with a test from Whitecotton. Whitecotton v.
Sec’y of Health & Hum. Servs., 17 F.3d 374 (Fed. Cir. 1994), rev’d sub nom., Shalala v.
Whitecotton, 514 U.S. 268 (1995) (concerning on-Table significant aggravation cases). The
resultant test has six components:

(1) the person’s condition prior to administration of the vaccine, (2) the person’s
current condition (or the condition following the vaccination if that is also
pertinent), (3) whether the person’s current condition constitutes a ‘significant
aggravation’ of the person’s condition prior to vaccination, (4) a medical theory
causally connecting such a significant worsened condition to the vaccination, (5) a
logical sequence of cause and effect showing that the vaccination was the reason
for the significant aggravation, and (6) a showing of a proximate temporal
relationship between the vaccination and the significant aggravation.

Loving, 86 Fed. Cl. at 144.

The statute defines “significant aggravation” as “any change for the worse in a pre-
existing condition which results in markedly greater disability, pain, or illness accompanied by
substantial deterioration in health.” § 33(4).

V. DIAGNOSIS ANALYSIS

As Federal Circuit precedent establishes, in certain cases it is appropriate to determine the
nature of an injury before engaging in the Althen analysis. Broekelschen v. Sec’y of Health &
Hum. Servs., 618 F.3d 1339, 1346 (Fed. Cir. 2010). Since “each prong of the Althen test is
decided relative to the injury[,]” determining facts relating to the claimed injury can be
significant. Id. Here, the parties dispute Petitioner’s neurological diagnosis, including whether
she “developed any definable neuroinflammatory diseases” or “suffered a neurological injury.”
Thus, it is appropriate to resolve this issue first.

Prior to her flu vaccination on September 19, 2015, records from 2012 show that
Petitioner had lumbar radiculitis, falls, a coccyx fracture, and knee and ankle injuries. After
these falls, Petitioner developed bilateral numbness of her thighs, and pain and numbness of her
left fourth and fifth fingers. She had decreased sensation in the distribution of the left C7 nerve
root. X-rays showed degenerative changes of her intervertebral discs. Records from 2014 show
that Petitioner had back, hip, and knee pain, and complained of radiating numbness down her
right leg to her ankle, and weakness with an inability to lift her foot when running and walking.
She was diagnosed with lumbar degenerative disk disease and mild lumbar radiculopathy.

Petitioner received the flu vaccine at issue on September 19, 2015. On October 13, she
presented to the ED for shortness of breath, chest tightness, cough, and wheezing. She reported

36
having a URI. The diagnosis was asthma. The records do not document any neurological
symptoms or concerns. The next day, Petitioner saw Dr. Klares, her pulmonologist, for her
asthma exacerbation. Dr. Klares did not document any neurology symptoms or concerns.
Petitioner returned to the ED on October 22 with shortness of breath and cough. At the visit,
Petitioner denied numbness, paresthesias, or weakness.

The first reference to any neurological symptoms was November 4, 2015, when
Petitioner returned to see her pulmonologist. Dr. Klares noted that Petitioner was concerned
about some tingling in her fingertips. Dr. Klares questioned whether the tingling symptom was
related to her steroid use, but due to Petitioner’s concerns, he referred her to a neurologist. The
records do not state the onset of Petitioner’s tingling in her fingers. However, when Petitioner
saw Dr. Rogg the following week, on November 11, 2015, she related her tingling back to the
receipt of the flu shot. She reported that she had bilateral tingling of her hands and feet “since
flu shot.” Pet. Ex. 2 at 82. At that visit, Dr. Rogg’s assessment included dysesthesia.

Petitioner saw neurologist Dr. Saland on November 24, 2015 and reported paresthesias in
her fingers and toes, some decreased dexterity, that her balance was mildly off, and her legs felt
weak. She also complained of some intermittent difficulty swallowing that had improved. Dr.
Saland also noted that Petitioner’s symptoms were becoming less frequent since she had
discontinued her steroids. Moreover, Petitioner’s neurological evaluation was normal. She had
normal strength, normal muscle tone, normal sensation, and she did not have areflexia or the loss
of her deep tendon reflexes. Dr. Saland questioned whether Petitioner’s symptoms could be due
to recent steroid use. Diagnoses included paresthesias, steroid-induced myopathy, drug-induced
myopathy, and dysphagia. Dr. Saland concluded that the cause of Petitioner’s neurological
symptoms was not clear. Therefore, as of November 24, 2015, Petitioner’s neurological
symptoms were “paresthesias.” Dr.. Saland did not reach

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Source: Frix Law Library, https://www.frixlaw.com/law-library/cases/10734249. Public record. Not legal advice.