Rushing v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 19-397V

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JANE B. RUSHING, * Chief Special Master Corcoran

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Petitioner, * Filed: February 16, 2024

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v. *

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SECRETARY OF HEALTH *

AND HUMAN SERVICES, *

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Respondent. *

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Nancy R. Meyers, Turning Point Litigation, Greensboro, NC, for Petitioner.

Jennifer A. Shah, U.S. Department of Justice, Washington, DC, for Respondent.

RULING ON ENTITLEMENT 1

On March 14, 2019, Jane B. Rushing filed this action seeking compensation under the

National Vaccine Injury Compensation Program (the “Program”). 2 Petition (ECF No. 1).

Petitioner alleges the Table claim that an influenza (“flu”) vaccine she received on November 20,

2012, caused her to incur Guillain-Barré syndrome (“GBS”). Id.

Although it would seem a claim based on a vaccine received over six years before the

Petition’s filing might be untimely, Petitioner relies on the “lookback” provision of the Vaccine

Act, which allows a claim based upon an injury newly-added to the Table to be considered timely,

1

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

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

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

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

in its present form. Id.

2

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

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

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

if the claim has been initiated not later than two years after the effective date of the Table revision

(and provided the alleged injury itself occurred within eight years before the effective date). See

Section 16(b)).

Petitioner alleges that she meets the requirements of a flu vaccine-GBS Table claim, and

therefore the lookback “saves” the claim—the Table was amended to add such a claim in 2017,

and this Petition was filed within the two-year, post-amendment window. Respondent disagrees,

maintaining that Petitioner’s injury (a) has another explanation (the chemotherapy regime she had

undergone pre-vaccination), and (b) is otherwise not properly understood to be GBS. The parties

have offered expert reports, treater opinions, and briefs in support of their respective positions. See

Petitioner’s Brief, dated May 9, 2023 (ECF No. 57) (“Br.”); Respondent’s Opposition, dated July

19, 2023 (ECF No. 60) (“Opp.”); Petitioner’s Reply, dated Aug. 24, 2023 (ECF No. 61). Now, I

find that Petitioner has met the flu vaccine-GBS Table requirements—and therefore the lookback

does indeed “save” the claim.

I. Fact History

Pre-Vaccination Conditions

Ms. Rushing’s past medical history included a number of chronic conditions, including

hypertension, myocardial infarction, coronary artery disease, osteoporosis, and gastroesophageal

reflux disease. Ex. 4 at 9466. Certain treatment she had been receiving in the months prior to the

relevant vaccination has special relevance herein.

Specifically, on June 14, 2012, Petitioner had a right mastectomy after being diagnosed

with breast cancer. Ex. 4 at 9465. In the ensuing two months, she underwent four cycles of

chemotherapy. Id. Thereafter, from September 13 to December 7, 2012, she received weekly

secondary chemotherapy treatments of Taxol, 3 an antineoplastic agent used to treat breast and

other cancers. Id. In this timeframe, Petitioner received 960 mg/m2 cumulative dose of the drug.

See Ex. E at 2 (Dr. Callaghan’s supplemental expert report). As discussed in more detail below,

Respondent contends that Petitioner’s symptoms could be attributed to this chemotherapy regime,

although Petitioner does not agree.

The medical record also establishes that Petitioner may have been experiencing

neuropathic symptoms well before the subject vaccination (but after her chemotherapy regime had

been started). On October 12, 2012, more than one month before the vaccination, Ms. Rushing

saw her oncologist, Dr. Garry Schwartz, after her fourth weekly Taxol treatment. Ex. 13 at 24–25.

3

Taxol is defined as “a microtubule-stabilizing drug that is approved by the Food and Drug Administration for the

treatment of ovarian, breast, and lung cancer, as well as Kaposi’s sarcoma.” B. Weaver, How Taxol/Paclitaxel Kills

Cancer Cells, 25 Mol Biol Cell 2677 (2014), https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4161504/ (last visited

Feb. 16, 2024).

2

At this time, she complained of generalized fatigue, a seven-pound weight loss since her last visit,

and numbness that radiated from her armpit down to her right hand. Id. Dr. Schwartz could not

reproduce the numbness on exam, though he opined that it was mechanical in origin. Id. A month

later, on November 7, 2012, she saw Dr. Schwartz again and reported that the Taxol treatment was

causing other kinds of symptoms (weight loss or a feeling of coldness). Ex. 13 at 26. On exam,

she was hypotensive and displayed thickened extremities with non-pitting edema. Id.

Vaccination and Neuropathic Concerns

Petitioner was sixty-eight years old when she received the flu vaccine on November 20,

2012. Ex. 1 at 2. The record reveals no immediate vaccine reaction, but ten days later (November

30, 2012) she saw Nurse Tina Evans in Dr. Schwartz’s office and reported “continuing neuropathy

in her hands” that had “been ongoing for the past 2-3 [weekly] treatments.” Ex. 13 at 28. The

record indicates that Petitioner was deemed to have “stage III invasive lobular carcinoma of the

right breast,” and had “completed 4 cycles of dose dense Adriamycin/Cytoxan and has now

completed 10 weekly doses of Taxol. She is due for dose 11 today.” Id. However, on December 3,

2012, Petitioner called Dr. Schwartz’s office, noting that although she was that morning

experiencing some dizziness and weakness, she overall felt a little better. Id. at 37.

On December 7, 2012, Petitioner saw Dr. Schwartz for another appointment (she was

scheduled to complete her Taxol treatment at this time). Ex. 3 at 29. The record of this visit

includes Dr. Schwartz’s comment that Petitioner “overall look[ed] well, but the cumulative effects

of chemotherapy seem[ed] to be wearing her down somewhat.” Id. Petitioner reported mild nausea

and minor weight loss since her previous visit, but her main complaints at that time were myalgias

and arthralgias, particularly of the lower extremities, plus some neuropathic feeling in her hands

and cold sensitivity, adding that the symptoms “had escalated over the last 2 weeks,” requiring her

to medicate. Id.

On exam, Petitioner displayed thickened lower extremities with non-pitting edema, as well

as mild discomfort in the lumbar spine and a chemotherapy-induced rash on her arms. Ex. 3 at 29.

Dr. Schwartz ultimately characterized her symptoms as “very consistent with chemotherapy

effect.” Id. He predicted that things should “markedly improve once chemotherapy gets out of her

system over the next few weeks,” noting that she was scheduled to begin six weeks of radiation

therapy in January 2013, followed by adjuvant therapy with an oral chemotherapy medication. Id.

A week later, however, Ms. Rushing returned to Dr. Schwartz’s office on December 13,

2012, for an unscheduled sick visit. Ex. 3 at 25. She now complained of more persistent bone pain,

particularly in her legs and left hip (and extending to her left buttock), that she reported made sleep

difficult. Id. Her bloodwork was normal, as was a hip x-ray. Id. at 19–24. She also reported

constipation and a rash on her arms, plus concerns about loss of appetite. Id. Exam revealed mild

3

hypotension, and she was given one liter of IV saline solution, anti-nausea medication, and a

corticosteroid. Id. at 26.

On December 17, 2012, Petitioner’s husband called Dr. Schwartz’s office, communicating

his concerns about numbness and tingling she was experiencing in her hands, feet, and legs. Ex. 3

at 18. Petitioner was again advised that the chemotherapy side effects would “slowly resolve,” but

she decided to try a medication for relief of neuropathic pain. Id. Her husband called back two

days later, however, now reporting that Petitioner’s generalized weakness and nutritional status

had resulted in her falling down at home. Id. at 17. (The nurse who documented the call also

memorialized the fact that Petitioner had reported feeling well the previous day). Id.

On December 21, 2012, Petitioner returned to Dr. Schwartz for treatment associated with

“complications of Taxol therapy.” Ex. 3 at 13. Dr. Schwartz recorded his impression that she now

looked quite weak, and she informed him she had experienced several falls over the prior week

due to pain and instability. Id. She also reported increasing numbness in her feet and ankles,

making it difficult to button or zip her clothing, that she felt “freezing all the time,” especially in

her fingers and toes, and that she felt a brief electric-shock sensation whenever her arms were

touched. Id. She also could not walk independently and was using a walker. Id. On exam, she had

intact sensation in her lower extremities and preserved plantar flexion, but decreased dorsiflexion

in both lower extremities, as well as reduced hip flexor strength, particularly on the left side. Id. at

14. Her most recent lab work was normal. Id.

Based on the foregoing, Dr. Schwartz opined that Petitioner’s neuropathy had “taken a

rapid turn for the worse,” and he deemed it a grade three neuropathy of the upper extremities. Ex.

3 at 14. He continued to propose she receive medication for neuropathic pain, Gabapentin, even

though he noted it might contribute to her hypotension and instability. Id. He also prescribed a

five-day course of prednisone to address her left buttock pain (adding that a longer course might

be warranted if the cause of her symptoms was polymyalgia rheumatica), and decided she should

not at that time start radiation therapy—but otherwise did not note any view that her symptoms

reflected possible GBS. Id.

Several days later (December 26th), Petitioner was again in Dr. Schwartz’s office, and was

seen at this time by Nurse Evans. Ex. 3 at 7. She complained of left eye redness and swelling,

along with leg swelling that caused a tight feeling, particularly in her ankles. Id. She also described

a fall two days earlier while she was trying to navigate two stairs in her home, that she felt as

though her legs might give out, and continued to experience numbness and tingling along the solar

aspect of both feet (although it was at least “no worse than previous” if not better). Id. Exam

revealed the existence of possible conjunctivitis, and the leg swelling was proposed by Nurse

Evans to be a side effect of the steroidal medications Petitioner was receiving. Id. at 7, 8. But Nurse

Evans ordered additional bloodwork and helped schedule Petitioner for a visit with a neurologist

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in mid-January 2013. Id. (Before leaving this treatment visit, Petitioner fell while in the bathroom

and fractured her ankle, resulting in an emergency room visit. Ex. 4 at 9465, 9975–78. She later

that same month required an orthopedic procedure for ankle repair. Id. at 9446, 9469, 9881–83).

Treatment for Neurologic Issues in 2013

On January 2, 2013, Petitioner was readmitted to the hospital on the advice of Dr.

Schwartz’s office due to her ongoing and unresolved symptoms. Ex. 4 at 9465. It was observed

that she had become weaker after her ankle surgery, and that her husband’s own physical maladies

made it difficult for him to care for her. Id. at 9465–66. She was also deemed by Nurse Evans to

have developed some kind of neuropathy with weakness “during chemotherapy; significantly more

so after her last dose.” Id. at 9467. Petitioner informed treaters that although her pain levels had

improved, she felt tired and weak, and was still experiencing numbness and tingling in her hands

and feet. Id. at 9466. On exam, Petitioner again displayed pitting edema of the legs. Ex. 4 at 9467.

She also displayed good upper extremity grip strength, strong right leg strength, along with weak

left leg strength. Id. at 9511. But a whole-body bone scan ordered for her during her hospitalization

was negative for malignancy. Id. at 9784.

Petitioner was subsequently discharged to a skilled nursing facility with the diagnosis of

failure to thrive, and she remained at the facility through the middle of January 2013. Ex. 4 at

9789; see generally Ex. 5. During this timeframe, on January 15, 2013 (now eight weeks post-

vaccination), Petitioner underwent a lumbar MRI and lumbar puncture at the direction of

neurologist David Schmidt, M.D. Ex. 6 at 111, 114. The MRI revealed the existence of lumbar

spondylosis causing mild to moderate stenosis at levels L2-3, L3-4, and L4-5. Id. at 111. The

lumbar puncture revealed an elevated cerebrospinal fluid (“CSF”) protein level of 94 (range 15-

45). Id. at 114. No specific diagnosis was recorded or treatment ordered in reaction to these

findings.

Within a week of discharge from the skilled nursing facility, Petitioner was readmitted to

the hospital after complaining of lower extremity weakness. Ex. 5 at 56; Ex. 6 at 7. She was

examined on admission by family physician Jonathan Shraga, M.D. Ex. 6 at 7. Dr. Shraga notes

in the relevant record from this visit that he had discussed Petitioner’s course with Dr. Schwartz,

who explained to Dr. Shraga that he had initially attributed her neuropathy to her chemotherapy,

but now felt that “[chemotherapy] not [] contributing at this time.” Id. (emphasis added). The

history section for this record also noted that Petitioner had received an influenza vaccination in

November. Id. Petitioner informed treaters at this time that she continued to experience ongoing

bilateral finger tingling, although her lower extremities were her primary concern. Ex. 6 at 7. On

exam, she displayed preserved upper extremity strength and intact sensation, but decreased

strength and intact sensation in her lower extremities, trace reflexes in the left knee, and absent

5

reflexes in the right knee. Id. at 9. Dr. Shraga’s concern was the possibility that Petitioner had an

inflammatory demyelinating polyneuropathy. Id.

Dr. Shraga ordered a neurology consult, and later that month (January 22, 2013), Petitioner

underwent an EMG 4/NCS 5 conducted by neuromuscular specialist, Dr. Francois Picot. Ex. 44 at

2–3. Dr. Picot interpreted the study results as consistent with an axonal polyradiculopathy. Id. at

3. He could not rule out a lumbosacral plexopathy or a diffuse lower extremity polyradiculopathy,

however. Id. at 3. The same day, Petitioner again saw Dr. Schwartz, who now deemed her

condition to be consistent with GBS—adding that she had received the flu vaccine in November.

Ex. 6 at 67. Ms. Rushing that same month received a five-day course of IVIG. 6 Id. at 69. But it did

not improve her leg symptoms or function. Id. at 38–39. On January 23, 2013, Petitioner underwent

a repeat lumbar puncture, which revealed an elevated CSF protein level of 79. Ex. 4 at 9301.

On January 28, 2013, Dr. Schwartz memorialized in a record the fact that he had discussed

Petitioner’s potential polyradiculopathy diagnosis with another treater that morning. Ex. 4 at 9281.

Dr. Schwartz noted a lack of response to IVIG, and that the other treater’s “informal opinion is the

current findings are not classic for GBS and more likely a GB-like syndrome that may be post-

viral.” Id. However, Dr. Schwartz also proposed that the likelihood Petitioner’s neuropathic

symptoms, and worsening course, were attributable to her prior Taxol treatment to be “extremely

rare esp[ecially] without upper extremity changes.” Id. Dr. Schwartz ultimately opined that “no

clear etiology w[ould] be found,” and questioned whether an underlying inflammatory process was

causing her radiculopathy. Id. at 9282.

During a visit with Dr. Picot on January 28th, Petitioner displayed absent reflexes, some

upper extremity weakness, limited leg strength, and reduced sensation in mid-thigh and left knee.

Ex. 6 at 10, 12. But, like Dr. Schwartz, Dr. Picot had trouble pinpointing the best diagnostic

explanation for Petitioner’s symptoms. Thus, although “[s]he has been diagnosed with the

possibility of having the axonal form of Guillain-Barre syndrome,” he could not “rule out the

possibility, in addition to a possible polyneuroradiculopathy, a possible lumbosacral

4

Electromyography is the process by which “an electrodiagnostic technique for recording the extracellular activity

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

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

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

https://www.dorlandsonline.com/dorland/definition?id=15854&searchterm=electromyography (last visited Feb. 16,

2024).

5

A nerve conduction study measures the amount and speed of conduction of an electrical impulse through a nerve to

determine nerve damage and destruction. Nerve Conduction Studies, Health Library, Johns Hopkins Medicine,

https://www.hopkinsmedicine.org/health/treatment-tests-and-therapies/nerve-conduction-studies (last visited Feb. 16,

2024).

6

Intravenous immunoglobulin (“IVIG”) is a blood product used to treat patients with antibody deficiencies, including

neurological disorders. Clinical Use of Intravenous Immunoglobulin, NCBI (2005)

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1809480/ (last visited on Feb.1 6, 2024).

6

polyradiculopathy,” or “the effects of chemotherapy,” especially given the overall mix of

presenting symptoms and test findings. Id. at 12. Dr. Picot also noted that a “paraneoplastic

process” attributable to her prior breast cancer might be explanatory. Id. And although “[f]lu shots

have been associated” with GBS, her symptoms would reflect an “atypical presentation” for a

vaccine-caused neuropathy given the attenuated timeframe between onset and vaccination. Id.

Dr. Schwartz had another office visit with Petitioner on January 30, 2013, just prior to her

hospitalization discharge. Ex. 4 at 9271. At this time, she displayed no upper extremity symptoms,

plus very slight improvement in the movement of her right leg, and Dr. Schwartz proposed

decreasing her neuropathic pain medication dose. Id. Upon discharge to an inpatient rehabilitation

facility, Petitioner’s differential diagnosis included axonal GBS versus polyneural radiculopathy

or lumbosacral polyradiculopathy. Ex. 6 at 5.

Petitioner remained in this rehab facility for approximately five weeks, or until March 8,

2013. Ex. 4 at 9438. In the course of the stay, urinary retention resulted in Petitioner being

diagnosed with neurogenic bladder requiring intermittent catheterization, but otherwise she

experienced increased mobility and functionality. Id. at 9438–39. She saw Dr. Schwartz again after

discharge, and he now expressed less confidence in the possibility that her symptoms were the by-

product of chemotherapy. Ex. 13 at 46. Dr. Schwartz noted that Petitioner’s “paraneoplastic panel”

was negative and that “[t]he best explanation at this time [for her polyradiculopathy] is possibly

connected with her influenza vaccine that was given in late November versus an idiopathic event.”

Id. at 47.

Thereafter, From May 22 through December 18, 2013, Ms. Rushing attended thirty-five

outpatient physical therapy (“PT”) sessions. Ex. 4 at 146–279. The course of therapy was helpful,

and by its conclusion she no longer needed a wheelchair and also displayed improved lower

extremity strength. On October 13, 2013, she followed up with Dr. Schwartz, and although she

still had neuropathy affecting her hands and feet, as well as lower extremity weakness, she was

ambulating well with a walker. Ex. 7 at 61.

Subsequent Treatment

Petitioner has filed records of her treatment and health history after January 2014, but they

mostly illuminate her subsequent progress rather than provide diagnostic explanations for her post-

vaccination condition. Thus, she showed some recovery in follow-up visits with Dr. Picot in

February 2014 (despite ongoing foot weakness and pain). Ex. 8 at 3, 5. She ceased neurologic

treatment by July 2015. Ex. 7 at 124. And although she was hospitalized in November 2017 (now

five years post-vaccination) after experiencing weakness, and a treater opined she might be

displaying deconditioning versus chronic inflammatory demyelinating polyneuropathy (“CIDP”),

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no confirmation of the CIDP diagnosis was obtained and she was discharged with the diagnosis

listed as “weakness likely 2/2 deconditioning, shingles.” Ex. 10 at 23, 24, 26.

II. Expert Reports & Treater Statements

A. Treater Statements

1. Dr. Francois J. Picot – Dr. Picot was one of Ms. Rushing’s neurologic

treaters, and he has offered in this case several witness statements in support of the claim. See

Statement, dated July 31, 2020, filed as Ex. 16 (ECF No. 26-1) (“First Picot Statement”);

Statement, dated Oct. 26, 2022, filed as Ex. 70 (ECF No. 50-1) (“Second Picot Statement”). None

of the statements are notarized, nor do they meet the requirements of a sworn declaration under

federal law. 28 U.S.C.A. § 1746.

Dr. Picot’s second statement sets forth his general medical credentials. He is a

neuromuscular specialist with Atrium Health Neurology in Huntersville, North Carolina. Second

Picot Statement at 1. He received his medical degree from Tulane University. Id. Thereafter, Dr.

Picot completed his residency at the University of Maryland, followed by a fellowship at the State

University of New York. Id. Dr. Picot’s practice involves treating patients with neurological

disorders, including GBS. Id.

As both statements represent (although the second in somewhat greater detail than the

first), Dr. Picot treated Petitioner in January 2013, seeing her again in February 2014. First Picot

Statement at 1; Second Picot Statement at 1. He deems her GBS to have been an “axonal form.”

Second Picot Statement at 1. In support, he references the EMG he performed, adding that its

results “would not be expected for neuropathy from Taxol treatment.” Id. He also represents she

first experienced neurologic symptoms associated with GBS in early December 2012. Id.

Dr. Picot opines that Petitioner’s November 2012 vaccination played some substantial role

in Petitioner’s GBS. However, his first statement sets forth this opinion in wholly conclusory form,

with no explanation for his reasoning. See First Picot Statement at 1. The second statement makes

clear, however, that his causation views are based on review of, and concurrence with, the treater

reports of Dr. Schwartz plus Dr. Steinman’s immunology opinion. Second Picot Statement at 1.

Dr. Picot’s second statement also opines that he deemed alternative causation explanations, like

effects of Taxol, unpersuasive, since Petitioner received only a low dose of it (with no greater

evidence that this dosage level had ever caused injury in a comparable patient), and because she

“had no use of either leg” as of her late-January 2013 hospitalization. Id. Otherwise, he opined that

her EMG results were inconsistent with a Taxol-related neuropathy. Id.

2. Dr. Garry Schwartz – Dr. Schwartz, Petitioner’s oncologist treater, offered

several statements and reports to support the claim. See Statement, dated July 27, 2020, filed as

Ex. 15 (ECF No. 24-1) (“First Schwartz Statement”); Statement, dated August 22, 2022, filed as

Ex. 43 (ECF No. 42-1); Statement, dated September 7, 2022, filed as Ex. 60 (ECF No. 48-1)

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(“Schwartz Rep.”). Like Dr. Picot’s contributions, none are sworn statements, but the third

submission contains annotations that make it more of an expert report (even if offered by one of

Petitioner’s actual treaters). Petitioner has not filed a CV for Dr. Schwartz.

First Statement

Dr. Schwartz’s first statement contains his review of Petitioner’s medical history, based on

his direct experience treating her. He notes that she had initially been diagnosed with breast cancer

in the spring of 2012, and later received chemotherapy—including “12 doses of weekly Taxol” in

the fall of 2012, ending December 7, 2012. First Schwartz Rep. at 1. He notes that he saw Petitioner

in mid-October of that year, and although she made some complaints about fatigue and extremity

discomfort (and even reported armpit numbness that radiated to her hand), her issues predated

chemotherapy, and were not otherwise consistent with neuropathy. Id.

Petitioner next reported hand neuropathy from her Taxol treatments on November 30, 2012

(and thus after vaccination), and Dr. Schwartz (admitting that “[p]eripheral neuropathy is a well-

recognized and common side effect of Taxol”) characterized these complaints as Taxol-associated.

First Schwartz Statement at 1, 2. However, the lower extremity complaints she later lodged on

December 7 th were in his assessment new, and distinguishable from the more minor neuropathic

issues she had reported a week before. Id. at 2. In particular, the cold sensitivity she was

experiencing was far more characteristic of Taxol-associated side effects than the new issues.

Later that December, Petitioner began to report leg and feet numbness and tingling—

another new symptom different from the more minor hand neuropathy. First Schwartz Rep. at 2.

And then she and her husband started to report falls, which Dr. Schwartz did not at all view as

consistent with “resolving chemotherapy side effects.” Id. This, plus the worsening of other lower

extremity symptoms, led Dr. Schwartz to conclude that Petitioner’s presentation could not be

chemotherapy-associated. Id. at 2–3. And by January, when Petitioner was hospitalized, Dr.

Schwartz was comfortable sharing his view about the nature and cause of her symptoms with

treaters like Dr. Shraga. Id. at 3. He was thus ultimately comfortable with the conclusion (which

he noted when he next saw Petitioner in March 2013) that Petitioner’s symptoms overall were not

likely due to chemotherapy (even if the initial symptoms were). Id. at 4.

Second Statement

Dr. Schwartz’s second statement is considerably more succinct than the first, and merely

provides his reaction to the expert reports filed as of that date. See Second Schwartz Statement at

1. He agrees with Dr. Steinman’s causation report over what Respondent had offered. He also

reiterates the view that Petitioner’s presentation in December 2012 was “far more consistent with

vaccine-induced GBS,” even if “Taxol-induced neuropathy” is more commonly observed. Id. In

support, Dr. Schwartz noted that of the “many hundreds” of his patients who have received Taxol,

he had never had a patient with the “degree of neuropathy” displayed by Ms. Rushing. Id.

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Third Statement

Dr. Schwartz’s final statement reads more like a full expert report and is supplemented by

nine literature cites. Schwartz Rep. at 6. In it, he attempts to provide a more detailed explanation

for why the dosage of Taxol received by Petitioner could not have caused the degree of neuropathy

she experienced, despite the opinions of Respondent’s experts.

Dr. Schwartz emphasized that toxicity to chemotherapy was “dose dependent,” and noted

that Petitioner had received what he considered a “relatively low dose” of Taxol—80 mg/m2

weekly, for a one-hour period, for a total of twelve weeks—meaning she had received cumulatively

960 mg/m2. Third Schwartz Statement at 1. But this was a significantly lower dosage than what

the patient subjects had received in studies referenced by Drs. Callaghan and McClain. One such

study sought to compare the antitumor effectiveness of Taxol against a different chemotherapy

drug. S. Jones et al., Randomized Phase III Study of Docetaxel Compared with Paclitaxel in

Metastatic Breast Cancer, 23 J. Clin. Oncol. 5542 (2020), filed as Ex. C Tab 2 (ECF No. 34-3)

(“Jones”).

Jones (like other studies discussed herein) evaluated the known neuropathic impact of two

comparable chemotherapeutic agents: Taxol (the marketing name for paclitaxel), and docetaxel (a

differently-formulated, stronger agent). Jones at 5542–43. It attempted to do so, however, via a

more scientifically-precise, randomized trial, evaluating over 400 breast cancer patients in North

America who received the two evaluated therapies. Id. at 5544. 224 subjects received Taxol—and

the study participants therein received, as a median, four cycles of treatment up to a maximum of

35, with a mean dose per cycle of 173 mg/m2. Id. This meant, Dr. Schwartz maintained, that some

studied individuals received cumulative doses up to 6,125 mg/m2, with no patients receiving doses

in the more limited range Petitioner did. Third Schwartz Statement at 1. Otherwise, Jones observed

far more instances of neurosensory than neuromotor adverse events from Taxol (59 percent of the

209 subjects who experienced any adverse event versus 12.6 percent), and the percentage of severe

neuromotor events was even lower. Jones at 5548.

The same dosage disparity in causing severe motor neuropathies was observed in another,

earlier article evaluating comparative effectiveness of different chemotherapy treatments. R.

Freilich et al., Motor Neuropathy Due to Docetaxel and Paclitaxel, 47 Neurol. 115 (1996), filed

as Ex. A Tab 1 (ECF No. 29-2) (“Freilich”). Freilich endeavored (like Jones, but well before it) to

compare the neuropathic effects of Taxol against docetaxel. Only four of the 64 evaluated patients

received Taxol, and each of the four received no less than 250 mg/m2 at a time, for a cumulative

dose of up to 6,250 mg/m2. Freilich at 116. Although all four experienced weakness eventually

progressing to motor symptoms as the cumulative dosage increased, even the subject receiving the

highest dose maintained the ability to ambulate, and no subjects experienced decreases in strength

in the one to two-month period after cessation of the chemotherapy. Freilich at 117–18. This was

contrary to Ms. Rushing’s experience. Third Schwartz Statement at 1–2.

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Dr. Schwartz noted other distinctions between Petitioner’s experience and the subjects in

Respondent’s cited studies. Third Schwartz Statement at 2. For example, although Respondent’s

experts maintained that Freilich underscored the association between Taxol-associated severe

neuropathies and elevated protein levels observed in CNS testing, this was based on data for only

two subjects—only one of whom had in fact received Taxol (and at a significantly higher dose as

well). Freilich at 117. Otherwise, none of Respondent’s studies involved an individual who

experienced a stage 4 motor neuropathy after receipt of a Taxol dosage comparable to

Petitioner’s—and where symptoms worsened even after treatment concluded. Third Schwartz

Statement at 2.

A study discussed only by Dr. McClain was also, in Dr. Schwartz’s estimation, unhelpful

to Respondent. Third Schwartz Statement at 3; C. Scripture et al., Peripheral Neuropathy Induced

by Paclitaxel: Recent Insights and Future Perspectives, 4 Current Neuropharm. 165 (2006), filed

as Ex. C Tab 1 (ECF No. 34-2) (“Scripture”). Scripture, a review article, discusses the then-current

state of scientific and medical views about Taxol’s known neuropathic side-effects and thinking

about how to mitigate them. In particular, Scripture (a) confirms that a sensory neuropathy is the

most common side-effect, and (b) that this adverse effect is “dose- and infusion-duration related,

and most frequently occurs when the dose . . . exceeds 250 mg/m2 infused over [more than] 24

hours.” Scripture at 166, 167 (lower dosages per cycle associated with milder neuropathic

symptoms, which might not manifest until cumulative dosage exceeded 1,400 mg/m2). Thus, in

Dr. Schwartz’s reading, Scripture confirmed not only that Taxol was associated only with a more

limited, sensory-style neuropathy, but that dosage mattered—and that the evidence referenced in

Scripture for the latter point came from the Freilich article. Third Schwartz Statement at 3. Only

very high dosages not relevant to Petitioner’s experience—more than 250 mg/m2 in a cycle—could

a more severe, motor neuropathy occur. Id.

Other studies not mentioned by Respondent’s experts were, Dr. Schwartz maintained, fully

consistent with his opinion about the dosage-severity relationship. One study considered the effect

of Taxol chemotherapy treatments received by 105 breast cancer patients over a 12-week period.

H. Timmins et al., Weekly Paclitaxel-Induced Neurotoxicity in Breast Cancer: Outcomes and Dose

Response, 26 The Oncologist 336 (2021), filed as Ex. 65 (ECF No. 49-5) (“Timmins”). The

dosages utilized therein were comparable to what Petitioner had received (80 mg/m2 at a single

weekly administration), and the patients experienced only the kind of more mild, sensory

neuropathic symptoms Petitioner first experienced (even if Timmons does also emphasize the

degree to which chemotherapy-induced neuropathic symptoms generally do not vanish once

treatment ends, but in fact can linger months beyond). Timmins at 367, 368–69. Although

symptoms severity did increase as the cumulative dosage went up, “no patient was non-

ambulatory, paralyzed, or required hospitalization.” Third Schwartz Statement at 4.

Overall, many studies confirmed the association between dosage and degree of neuropathic

symptoms. See, e.g., M. Green et al., Weekly Paclitaxel Improves Pathologic Complete Remission

in Operable Breast Cancer When Compared With Paclitaxel Once Every Three Weeks, 23 J. Clin.

11

Oncol. 5983 (2022), filed as Ex. 66 (ECF No. 49-6), at 5990 (“[Taxol] administered at a lower

dose of 80 mg/m was very well tolerated, with a reduced risk of neutropenic fever and grade 3

neuropathy, compared with once-every-three weeks [Taxol]”). One review article, compiling the

results of 14 clinical trials, confirmed that severe, motor-oriented neuropathies were exceedingly

uncommon, even at doses higher than what Petitioner had received. Third Schwartz Statement at

4–5; E. Rivera and M. Cianfrocca, Overview of Neuropathy Associated with Taxanes for the

Treatment of Metastatic Breast Cancer, 75 Cancer Chemother. Pharmacol. 659 (2015), filed as

Ex. F Tab 1 (51-6) at 661 Table 1 (reviewing results of 11 studies), 662.

B. Petitioner’s Experts

1. Dr. Lawrence Steinman – Dr. Steinman, a neurologist, prepared two written

reports for the Petitioner. Report, dated August 16, 2022, filed as Ex. 42 (ECF No. 41-1) (“First

Steinman Rep.”); Report, dated February 13, 2023, filed as Ex. 71 (ECF No. 55-1) (“Steinman

Second Rep.”). Dr. Steinman opines that the flu vaccine likely caused Petitioner’s neuropathy,

which is best understood to be GBS, and that her symptoms began in a timeframe consistent with

the Table claim’s requirements.

As shown in his CV, Dr. Steinman received his undergraduate degree from Dartmouth

College, and his medical degree from Harvard Medical School. Curriculum Vitae, filed as Ex. 45

on Aug. 23, 2022 (ECF No. 44-1) (“Steinman CV”) at 1. He then completed residencies in

neurology and pediatrics at Stanford University. Id. He has worked as a professor of neurology

and pediatrics at Stanford for the past 41 years. Id.; Steinman First Rep. at 2. He is board certified

in neurology from the American Board of Psychiatry and Neurology. Steinman CV at 2. Dr.

Steinman has also published hundreds of peer-reviewed publications on neurology and

autoimmune disease. Id. at 5–49. He holds several patents related to the diagnosis and treatment

of autoimmune and demyelinating diseases. Id. at 2–3. He presently serves as the George A.

Zimmerman Professor of Neurological Sciences, Neurology, Genetics and Pediatrics at Stanford

University. Id. at 1.

First Report

Much of Dr. Steinman’s first report includes the kind of “boilerplate” statements about his

expertise that he offers in almost all Vaccine Program cases in which he is retained as an expert.

See, e.g., First Steinman Rep. at 1–3. He also provided a medical records summary, although it is

consistent with what is set forth above in this decision. Id. at 3–9. Thus, only a few pages of this

report are germane to the present dispute. Id. at 9–11.

The heart of Dr. Steinman’s opinion begins with his explanation of Taxol’s components

and how they function. Taxol, he stated, is an “antineoplastic agent” that can (as a side effect to its

intended chemotherapy purpose) also “promote[] the formation of abnormal bundles of

12

microtubules within the cytoplasm,” leading to neuropathy from the dysfunction of those

microtubules. First Steinman Rep. at 9; see also Scripture at 165. Thus, the drug’s intended impact

on microtubules could also cause nerve harm—a well-understood risk factor for the

chemotherapeutic agent.

In most cases, Taxol produces sensory peripheral neuropathies that are “dose- and infusion-

duration related.” First Steinman Rep. at 9. By contrast, motor neuropathies are far less common

in patients receiving Taxol, except in instances involving higher doses. Id. Dr. Steinman

emphasized that although some articles (Freilich, for example) observed instances of motor

neuropathies in Taxol-receiving patients, they commonly remained ambulatory—which was not

in this case true of the Petitioner. Id. In addition, such literature noted the association between

cessation of the Taxol treatments and symptoms improvement—again, something not observed in

Petitioner’s case (since more than a month separated the end of her treatment and the acute

symptoms leading her to seek medical intervention in late-January 2013). First Steinman Rep. at

9, 11; see also V. Chaudhry et al., Peripheral Neuropathy From Taxol and Cisplantin Combination

Chemotherapy: Clinical and Electrophysiological Studies, 35 Ann. Neurol. 304 (1994), filed as

Ex. 57 (ECF No. 44-13), at 306 (out of 21 studied patients receiving Taxol, three-quarters

experienced sensory neuropathies, beginning sooner after administration of larger doses; axonal

neuropathies occurred in some patients, but severity was correlated with cumulative dose

amounts).

Dr. Steinman concurred with the diagnosis in this case of axonal GBS, noting that the

medical records provided support for it—evidence of the elevated CSF protein levels, along with

observed instances by Dr. Picot of lower extremity weakness. First Steinman Rep. at 10. Her

overall experience with the monophasic progression of the disease was also consistent with the

diagnosis—plus her nadir within 28 days of the proposed December 7 th onset, since in late

December she experienced the fall leading to the breaking of her ankle, and worsening of weakness

that encouraged treaters to pursue a lumbar puncture and MRI. Id. The lack of symptoms

responsiveness to IVIG was not significant to Dr. Steinman, since (as Dr. Picot had proposed) it

had likely been administered too late in her treatment course (when measured from onset).

Dr. Steinman accepted onset as beginning around the time of Petitioner’s complaints of

lower extremity pain on December 7, 2012—within the 3–42 day timeframe for onset, based on

the November 20 th vaccination. First Steinman Rep. at 10. He admitted that around this time, she

had also been experiencing the more “recognized” kind of Taxol-associated sensory neuropathic

symptoms (her fingertip sensations in particular), but deemed them distinguishable from the GBS

symptoms more likely caused by vaccination. Id. In so opining, Dr. Steinman disagreed with Dr.

Callaghan’s view that onset occurred in early November 2012 (meaning, if correct, that a nadir

almost two months later was inconsistent with GBS’s usual course). Id. at 11. The record, he

13

maintained, showed only sensory-type symptoms in November, with no actual GBS-oriented

symptoms before early December. Id.

Dr. Steinman also reacted to other points raised in the initial reports of Respondent’s

experts. For example, he deemed them to give insufficient weight to the treater opinions of Drs.

Schwartz and Picot, who had seen Petitioner at the time of her initial presenting symptoms. First

Steinman Rep. at 11.

Second Report

Dr. Steinman’s second report reacted solely to assertions made in Dr. Callaghan’s second

report—and his acknowledged focus was the “narrow issue” of the GBS diagnosis and onset—

although he began by addressing the argument that Petitioner’s Taxol treatment explained her

injury. Second Steinman Rep. at 1. Thus, although Dr. Callaghan had contended that many

instances of Taxol-induced neuropathy had some motor neuropathy features, such as leg weakness,

Petitioner’s presentation was characterized by a more severe form of motor neuropathy, which was

far less common in cases attributable to the chemotherapy. Id. And the medical records revealed

Petitioner’s own “instability and pain” had been severe enough in late-December 2012 to cause

her to fall several times—while at the same time her other neuropathic symptoms broadened and

increased. Id. A subsequent fall required surgery, and then continued symptoms progression led to

diagnostic testing (an MRI and lumbar puncture) that seemed to confirm GBS. Id. at 2.

Thereafter, other treaters who saw Petitioner in late-January 2013 noted that the severity

of Petitioner’s symptoms was not consistent with a Taxol-caused form of neuropathy. Second

Steinman Rep. at 3–4. Eventually, after hospitalization and associated testing Petitioner was

diagnosed with an axonal form of GBS. While the roles of Taxol versus the flu vaccine did not, in

Dr. Steinman’s estimation, present an “either/or proposition,” since both could cause neuropathic

symptoms, the evidence in his view did support the vaccine as causal, given treater statements—

even if Taxol could result in neurologic symptoms as well. Id. at 4–5.

2. Dr. M. Eric Gershwin – Dr. Gershwin is an immunologist and

rheumatologist, and he prepared a single report for Petitioner. Report, dated March 25, 2021, filed

as Ex. 17 (ECF No. 31-1) (“Gershwin Rep.”). Dr. Gershwin proposed that the flu vaccine caused

Petitioner’s GBS, and in a medically acceptable timeframe as well.

Dr. Gershwin received his undergraduate degree from Syracuse University, his medical

degree from Stanford University, and his graduate degree from the Centre for Astrophysics and

Supercomputing. See Curriculum Vitae, filed Mar. 30, 2021 (ECF No. 21-25) (“Gershwin CV”)

at 1. He completed his internship and residency at Tufts New England Medical Center, and two

fellowships in rheumatology and allergy/immunology at the National Institutes of Health. Id. at 2.

He is currently employed as Director of the Allergy-Clinical Immunology Program and Professor

14

of Medicine at University of California at Davis (“UC Davis”). Id. at 1–2. Dr. Gershwin is licensed

to practice medicine in California and is board certified in allergy and immunology, rheumatology,

and internal medicine. Id. at 2. He also publishes extensively and is well researched in

epidemiological studies. Id.

Dr. Gershwin included his own review of Petitioner’s history before commencing with his

opinion. Gershwin Rep. at 1–2. (He also provided a summary of his qualifications. Id. at 3). He

deemed her history “long and complicated,” but demurred from offering his own take on her proper

diagnosis, focusing instead on the role the flu vaccine could have played from a causation

standpoint. Id. at 2. He also offered a lengthy explanation of GBS generally and its known

etiologies (although I do not deem this matter to be contested, other than to the extent it bears on

the Taxol-causation question). Id. at 4–11. 7 One immediate point Dr. Gershwin made, however,

was to distinguish Petitioner’s “Taxol-related neuropathy”—which he proposed had likely begun

pre-vaccination—from her “GBS-related neuropathic symptoms.” Gershwin Rep. at 2. Then, after

explaining how vaccines generally prompt an immune reaction, Dr. Gershwin opined that “GBS

is an environmentally induced autoimmune disease,” and that the onset of Petitioner’s GBS-like

symptoms arose in a medically acceptable timeframe measured from vaccination. Id. at 15.

C. Respondent’s Experts

1. Dr. Brian Callaghan – Dr. Callaghan, a neurologist and academic, prepared

two expert reports on Respondent’s behalf. Report, dated October 5, 2020, filed as Ex. A (ECF

No. 29-1) (“First Callaghan Rep.”); Report, dated December 30, 2022, filed as Ex. E (ECF No.

51-1) (“Second Callaghan Rep.”). Dr Callaghan opines that Petitioner experienced a sensory and

motor neuropathy attributable only to her Taxol treatment.

Dr. Callaghan received his undergraduate degree from the University of Michigan, his

medical degree from the University of Pennsylvania in 2004, and his master’s in science from the

University of Michigan in 2011. Curriculum Vitae, filed as Exhibit B (ECF No. 29-6) (“Callaghan

CV”) at 1. He is board certified in psychiatry and neurology, as well as electrodiagnostic medicine.

Id. Dr. Callaghan was appointed to be a clinical lecturer at the University of Michigan Health

System’s Department of Neurology in 2009 and has been an Associate Professor of Neurology

there since 2018. Id. He has published more than 100 articles and medical book chapters, most of

which focus on neuropathies, and his research interest lies in diagnostic evaluation and testing of

peripheral neuropathies. First Callaghan Rep. at 1; Callaghan CV at 2, 11–20. Dr. Callaghan

reports that he encounters and treats approximately five patients with GBS per year, and five

patients with chemotherapy-induced neuropathy per year. First Callaghan Rep. at 1.

7

These points are in fact almost superfluous in this case, especially since it involves a Table injury, where causation

is presumed.

15

First Report

Dr. Callaghan’s initial report was based on his review of Petitioner’s medical history, plus

his own desktop research (performed solely for this case) into “the association of vaccines and

paclitaxel (Taxol) with axonal neuropathy.” First Callaghan Rep. at 1, 2–3. He had also had the

benefit of having reviewed the contents of Drs. Picot and Schwartz’s first letter-statements. Id. at

3.

Regarding the medical record, Dr. Callaghan emphasized that Petitioner’s first symptoms

were limited to fingertip numbness (even though her symptoms progressed to more widespread

numbness and tingling plus lower extremity weakness). First Callaghan Rep. at 3. He also noted

that Dr. Schwartz himself had initially deemed her presentation to be consistent with a Taxol-

caused sensory neuropathy, and that other testing conducted during the January 2013

hospitalization (MRIs, a lumbar puncture) produced unrevealing results—plus IVIG had not

proven beneficial. Id. at 3–4. Because Dr. Callaghan had not received record evidence of EMG

testing results, he did not opine on what they showed specifically (although he acknowledged that

records indicated they were consistent with a polyradiculopathy). Id.

Petitioner’s pre-vaccination Taxol treatments were, in Dr. Callaghan’s estimation, “[b]y

far the most likely cause” for her sensory neuropathy. First Callaghan Rep. at 4. He noted that

certain literature established Taxol to be a “well-known cause of sensory neuropathy” in patients

receiving this form of chemotherapy. Id. Motor neuropathy could also be a side effect of Taxol,

and Dr. Callaghan noted that (in his view) the chance of a “severe grade” form of motor neuropathy

was higher in individuals (like Petitioner) who were already suffering from a higher grade of

sensory neuropathy. Id. He based this contention, however, on the findings from Jones, which were

not only specific solely to the set of 200-plus studied individuals, but found severe forms of any

neuropathy, motor or not, to be far less common than a milder form. See Jones at 5548, Table 5.

GBS caused by the flu vaccine, by contrast, was less likely. As a general matter, flu

vaccine-caused GBS was an unlikely occurrence. First Callaghan Rep. at 4. Since axonal

neuropathies constituted less than a fifth of all GBS cases in North America, that form was even

less common. S. Kuwabara & N. Yuki, Axonal Guillain-Barré Syndrome: Concepts and

Controversies, 12 Lancet Neurol. 1180 (2013), filed as Ex. A Tab 4 (ECF No. 29-5) (“Kuwabara”)

at 1181. Given the higher association between Taxol and neuropathies (in comparison to the rarity

of vaccine-caused GBS), it seemed most likely to Dr. Callaghan that Petitioner’s Taxol treatments

were the cause of her injury.

Dr. Callaghan in fact did not find persuasive the conclusion that Petitioner had experienced

GBS in the first place. He noted that although patients with axonal GBS usually display preserved

reflexes, Ms. Rushing had absent reflexes, a feature of more common forms of GBS. First

16

Callaghan Rep. at 3; Kuwabara at 1182. In addition, the timeframe from Petitioner’s neurologic

symptoms onset in early November 2012 and her nadir (which he deemed to have occurred during

her January 2013 hospitalization) was more than two months—inconsistent with GBS (which

should see nadir between 12 hours and 28 days of onset). 8

Finally, Dr. Callaghan disputed Dr. Schwartz’s suggestion that Petitioner had experienced

both a Taxol-induced sensory neuropathy plus axonal GBS. First Callaghan Rep. at 3. In support,

he argued that the EMG evidence of axonal “changes” was as consistent with GBS and with a

Taxol-associated neuropathy (although as noted he had not reviewed the EMG results directly).

Id. The elevated protein levels in CSF testing were also not indicative of GBS, since they “only

indicate[] that the injury occurred at the nerve root level,” and that otherwise such elevated levels

were a “known finding” for Taxol neuropathies. See, e.g., Freilich at 117 (elevated protein was the

sole abnormality seen in the two patients whose CSF was tested—although Freilich does not

otherwise comment on the association between this GBS indicator and Taxol). And he again

emphasized how (in his view) robust the evidence was supporting a Taxol-neuropathy association.

First Callaghan Rep. at 3.

Second Report

The second expert report submitted by Dr. Callaghan responded to the additional witness

statements provided by Drs. Picot and Schwartz, plus Dr. Steinman’s initial report. He first

attempted to rebut Dr. Steinman’s arguments that Taxol-caused neuropathies would not typically

present as motor neuropathies. See generally Second Callaghan Rep. at 1–2. Dr. Callaghan allowed

that more severe forms of motor neuropathies caused by Taxol were uncommon, but stressed that

some kind of motor neuropathy was still possible—and where observed, often involved leg

weakness as a “prominent symptom.” Id. at 1; H. Mo et al., Association of Taxane Type with

Patient-Reported Chemotherapy-Induced Peripheral Neuropathy Among Patients with Breast

Cancer, 5 JAMA Network Open 11:e2239788 (2022), filed as Ex. E Tab 1 (ECF No. 51-2)

(Chinese prospective cohort study of approximately 1200 subjects, 41.7 percent of whom received

Taxol; approximately 47 percent reported motor symptoms). He also noted that Petitioner had been

deemed to suffer from a “grade three” motor neuropathy, consistent with Petitioner’s presentation

(and the grade designation did not require her to be non-ambulatory, as Dr. Steinman argued).

Second Callaghan Rep. at 1.

8

In support of this argument, Dr. Callaghan asserted that this onset to nadir timeframe is “required” by the Table. First

Callaghan Rep. at 3. This contention is misleading. The Table only requires initial onset to occur in a defined

timeframe. 42 C.F.R. § 100.3(a)(XIV)(D). However, the qualifications and aids to interpretation for GBS do indicate

that the disease will usually have a nadir timeframe from onset consistent with Dr. Callaghan’s argument—and

therefore it is more than fair to assess, under the facts of this case, if nadir occurred as would be expected—and if not,

why.

17

Other factors also made Taxol more likely the cause of Petitioner’s total presentation, in

Dr. Callaghan’s view. Contrary to Dr. Steinman’s emphasis on Petitioner’s ongoing neurologic

issues even in the absence of the Taxol treatment (suggesting no association), Dr. Callaghan

pointed out that Petitioner had improved once the Taxol treatment fully ended (and without the

usual lingering GBS sequelae)—albeit the improvement was witnessed long after, in the fall of

2013. Second Callaghan Rep. at 1 (citing Ex. 7 at 3). He also maintained that Dr. Steinman

incorrectly contended that cessation of Taxol should result in immediate symptoms improvement,

since “[c]hemotherapy-induced neuropathy is well-known to persist in some patients.” Second

Callaghan Rep. at 2; G. Cavaletti et al., Chemotherapy-Induced Neuropathy, 13 Current Treatment

Options in Neurology 180, filed as Ex. E Tab 2 (ECF No. 51-3) (“Cavaletti”). Cavaletti is a review

article, and it does confirm the possibility of progression or worsening of symptoms even after

chemotherapy treatments cease (Cavaletti at 188), but (and although it does link motor symptoms

with Taxol) does not provide harder data useful in assessing when this is more or less likely to

occur.

Dr. Callaghan took issue with Dr. Steinman’s arguments about other factors relevant to the

proper characterization of Petitioner’s injury. Relying on the conclusion that Petitioner’s initial,

pre-vaccination symptoms were both neurologic and not simply reflective of a distinguishable case

of limited, Taxol-related symptoms, Dr. Callaghan maintained that her onset occurred during the

first week of November 2012—meaning nadir (reached after her January 2013 hospitalization)

took far too long for her condition to be deemed GBS. Second Callaghan Rep. at 2. In addition, he

again pointed out that IVIG has not assisted her, further making a Taxol-associated neuropathy

more likely. Id. Ultimately, Dr. Callaghan opined that Dr. Steinman was simply ignoring obvious

record proof that Taxol was to blame for Petitioner’s condition. Second Callaghan Rep. at 2.

Next, Dr. Callaghan responded to some of Dr. Schwartz’s points about the Taxol-

neuropathy association. Second Callaghan Rep. at 2–3. Although Dr. Schwartz had stressed that

his own personal treatment experience had never involved a person with as severe a neuropathy as

Ms. Rushing, Dr. Callaghan deemed the situation unsurprising, since the overall number of patients

who would face similar debilitating symptoms was low. This did not mean, however, that it was

unheard-of, and he referenced literature in support. Id. at 2; Jones at 5548.

Dr. Callaghan also disagreed with Dr. Schwartz’s argument that Taxol dosage levels made

a severe neuropathic response less likely. He noted that Freilich had observed neuropathies at doses

of 200 mg/m2, and becomes “dose limiting” (meaning treaters more often than not opt to reduce

dosage in light of observable worsening of neuropathic symptoms in response to Taxol) at 250

mg/m2—far less than the 960 mg/m2 cumulative dose Petitioner had received, and thus more than

enough to result in a more severe neuropathy. Freilich at 116. In Jones, moreover, “the median

number of Taxol cycles” for the 200-plus evaluated patients was four, with 173 mg/m2 per cycle—

meaning such individuals also received lower cumulative doses than Petitioner, even though some

18

developed severe motor neuropathies as well. Second Callaghan Rep. at 3. Jones itself does not,

however, correlate the severity of adverse outcomes to dosage specifically. Jones at 5548, Table

5.

Finally, Dr. Callaghan provided his reaction to Dr. Picot’s second statement. Dr. Picot had

asserted that he had “ruled out” a Taxol-caused neuropathy based on his examination of Petitioner,

but Dr. Callaghan questioned whether any “examination feature” from the filed record supported

that conclusion. Second Callaghan Rep. at 3. He again maintained that EMG findings could

support a Taxol-induced neuropathy as much as GBS axonal neuropathy, and therefore they could

not be reasonably relied upon to distinguish the cause. Id.

2. Dr. Kenneth McClain – Dr. McClain is a pediatric oncologist, and he

provided two written reports. Report, dated June 10, 2021, filed as Ex. C (ECF No. 34-1) (“First

McClain Rep.”); Report, dated December 22, 2022, filed as Ex. F (ECF No. 51-5) (“Second

McClain Rep.”). Dr. McClain concluded that Petitioner’s Taxol treatments best explained her

neuropathic symptoms.

Dr. McClain attended the dual M.D./Ph.D. program at the University of Chicago School

of Medicine from 1963 to 1973. Curriculum Vitae, filed as Ex. D (ECF No. 34-7) (“McClain CV”)

at 1. Thereafter, he completed a pediatric residency at The Johns Hopkins Hospital in 1976,

postdoctoral training at the National Institutes of Health in 1979, and a Hematology/Oncology

Fellowship at the Department of Pediatrics, University of Minnesota in 1981. Id. Dr. McClain is

currently a Professor of Pediatrics in the Department of Pediatrics at Baylor College of Medicine.

Id. at 3. He is board certified by the American Board of Pediatrics in General Pediatrics and

Hematology-Oncology. Id. at 5. Dr. McClain has published approximately 200 articles, many

regarding non-Hodgkin’s and Hodgkin’s lymphoma. Id. at 13–32. Dr. McClain reports that he has

over 40 years of experience treating children with a variety of chemotherapy drugs that can cause

neuropath, and that for the past 25 years, he as also treated and cared for adult patients with

histiocytic diseases. First McClain Rep. at 1.

First Report

Dr. McClain’s first report included a short summary of Petitioner’s disease course timeline,

before getting to the meat of his opinion. First McClain Rep. at 1–3. He stressed from that history

the fact that Petitioner’s initial symptoms had begun as early as mid-November 2012 and were

“consistent with grade 3-4 Taxol toxicity,” given their sensory character. Id. at 3. But the literature

on Taxol-induced neuropathies was also consistent with it causing more serious kinds of

neuropathy—and thus “there is clear precedent for ascribing the [P]etitioner’s motor neuropathy

to Taxol.” First McClain Rep. at 3.

19

The likelihood that a flu vaccine, by contrast, had been causal of Petitioner’s GBS was low,

in Dr. McClain’s opinion. Given that literature established that flu vaccine-associated GBS was

already rare—and that the axonal variant was one of the “least frequent” versions, the probability

that the flu vaccine in this case had caused her GBS was especially unlikely. In comparison, studies

like Jones revealed that a larger percentage of breast cancer patients receiving Taxol treatments

experienced “neuromotor deficits.” Jones at 5548, Table 5.

Second Report

The next written report offered by Dr. McClain repeated some of his prior review of the

record, although in so doing he emphasized points from the record in which treaters had squarely

attributed Petitioner’s symptoms to her Taxol treatments. Second McClain Rep. at 2. He also

observed that the two treaters offering opinions in this case (Drs. Schwartz and Picot) had noted

the extent to which Petitioner’s exam findings, symptoms, and testing results were not reflective

of “classic GBS,” but instead something atypical (even if they also discounted the Taxol therapy

as causal). Id. And other treaters (including Dr. Schwartz himself) had not firmly embraced the flu

vaccine as causal. Id. at 2–3.

Dr. McClain then took aim at the contention of the experts acting on Petitioner’s behalf,

all of whom maintained Taxol was not the cause of her overall neuropathic presentation. Even if

it were true, for example, that most Taxol patients would only experience sensory-style symptoms,

there are always patients who are outliers from the usual extent of drug side effects,” and thus

(since in rare cases more severe neuropathies had been associated with Taxol), the same could be

the case here. Second McClain Rep. at 3. Petitioner’s own circumstances (in particular, her weight

loss) likely increased her vulnerability to a severe side-effect. Id.

Also significant to Dr. McClain was the nature of Taxol. Like Dr. Steinman, he observed

that its effectiveness in treating cancer (and specifically the killing of breast cancer cells) was a

function of its impact on the cellular microtubule system—which had the secondary capacity to

damage nerve cells. Second McClain Rep. at 3. Aware of this side-effect, medical researchers had

investigated genetic polymorphisms that might explain why some individuals would experience

Taxol-associate neuropathic symptoms., identifying one genetic variant in particular as so

associated. S. Park et al., Paclitaxel-Induced Neuropathy: Potential Association of MAPT and

GSK3B Genotypes, 14 BMC Cancer 993 (2014), filed as Ex. F Tab 2 (ECF No. 51-7) (“Park”) at

996 (study of 21 Taxol-treated patients (most of whom had breast cancer) determined (based on

prevalence of specific genetic testing results) that “patient-specific factors such as genetic

polymorphisms may be important in identification of at-risk patients”). In Dr. McClain’s view, the

risk could be multiplied by other genetic factors as well—thereby increasing “overall neurotoxicity

risk.” Second McClain Rep. at 3 (quoting Park at 995). In this case, however, there is no identified

20

genetic testing results that might make more concrete the findings of Park to Ms. Rushing’s

experience.

Another study had identified even more gene variants that, if present, were likely to

compound the risk of a Taxol-induced neuropathy. G. Boora et al., Testing of Candidate Single

Nucleotide Variants Associated with Paclitaxel Neuropathy in the Trial NCCTG N08C1

(Alliance), 5 Cancer Medicine 4:631 (2016), filed as Ex. F Tab 4 (ECF No. 51-9) (genetic testing

aimed at identifying certain genetic variants more commonly associated with Taxol-induced

neuropathy). Petitioner’s reaction was likely attributable to some genetic-derived susceptibility—

although Dr. McClain did not identify whether Petitioner did likely possess this susceptibility

(beyond noting her clinical experience), or that axonal neuropathies post-Taxol only occurred

under such circumstances.

III. Procedural History

After the case’s initiation in March 2019, this matter was originally assigned to SPU, since

it appeared to assert a flu-GBS Table claim (and thus potentially could be resolved quickly if the

claim met the Table elements). Petitioner filed medical records supporting the claim, and then

Respondent’s Rule 4(c) Report was filed on May 22, 2020 (ECF No. 22). In the midst of the filing

of the expert reports and treater statements discussed above, I had set the matter for an entitlement

hearing, based on the nature of the dispute regarding the chemotherapy treatment as an alternative

cause. See Prehearing Order, dated August 16, 2022 (ECF No. 40). However, the parties later

informed me of their preference for the claim to be resolved on the papers, and I accordingly set a

schedule for briefing their positions. Order, dated September 6, 2022 (ECF No. 47). After some

schedule modifications, briefing was completed, and the matter has been ripe for decision since

August 2023.

IV. Parties’ Arguments

Petitioner argues that she has met her prima facie burden of demonstrating a Table

Injury 9—she received a flu vaccine, experienced GBS, and her onset fell within three to 42 days

of vaccination. Br. at 21. The only remaining issue was whether Respondent had met his burden

of establishing a factor unrelated to the flu vaccine—something Petitioner denied had occurred.

Id.

Petitioner maintains that her case “is unique in that her treating oncologist and

neuromuscular specialist both authored a total of five reports supporting her claim and clarifying

that, based on their first-hand knowledge of her condition and their in-person physical exams of

9

Petitioner also maintains he could meet all three Althen prongs for a non-Table case. Opp. at 23–24, 26.

21

her, they ruled out Taxol neuropathy as a cause of her symptoms.” Id.; Exs. 15, 16, 43, 60, 70.

Moreover, none of Petitioner’s treating physicians attributed her lower extremity paralysis to her

Taxol therapy during her hospitalization. Mot. at 21–22. Petitioner further notes that the

neurotoxicity of Taxol is dose-dependent, and that Respondent’s experts were unable to offer a

study where a patient developed a grade four motor neuropathy from a dose as low as hers. Id. at

24.

Respondent argues that Petitioner’s neuropathic symptoms were attributable to the Taxol

chemotherapy regime she had unquestionably undergone pre-vaccination. Respondent notes that

Taxol “can, and likely did,” cause Petitioner’s neurologic symptoms—further noting that “Taxol

is a well-known cause of sensory neuropathy occurring in as many as 49-67% of patients.” Opp.

at 18; First Callaghan Rep. at 4 (citing Freilich at 115). Moreover, Respondent maintains that “the

risk of developing GBS after an influenza vaccination is less than one in three million.” Opp. at

18; First Callaghan Rep. at 4. Thus, the likelihood of developing the form of GBS experienced by

Peitioner—axonal GBS—is even lower as “axonal GBS only accounts of 3-17% of all cases in

North America. First Callaghan Rep. at 4; Kuwabara at 1181. Respondent contends that the

medical records do not support a diagnosis of axonal GBS, but instead “the evidence supporting

Taxol neuropathy is clear with [Petitioner’s] clinical history, examination, and timing of symptoms

starting during treatment.” Opp. at 19.

V. Applicable Legal Standards

A. Petitioner’s Overall Burden in Vaccine Program Cases

To receive compensation in the Vaccine Program, a petitioner must prove either: (1) that

he suffered a “Table Injury”—i.e., an injury falling within the Vaccine Injury Table—

corresponding to one of the vaccinations in question within a statutorily prescribed period of time

or, in the alternative, (2) that his illnesses were actually caused by a vaccine (a “Non-Table

Injury”). See Sections 13(a)(1)(A), 11(c)(1), and 14(a), as amended by 42 C.F.R. § 100.3; §

11(c)(1)(C)(ii)(I); see also Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1321 (Fed.

Cir. 2010); Capizzano v. Sec’y of Health & Hum. Servs., 440 F.3d 1317, 1320 (Fed. Cir. 2006).10

In this case, Petitioner asserts the Table claim of GBS caused by the flu vaccine.

For both Table and Non-Table claims, Vaccine Program petitioners bear a “preponderance

of the evidence” burden of proof. Section 13(1)(a). That is, a petitioner must offer evidence that

leads the “trier of fact to believe that the existence of a fact is more probable than its nonexistence

before [he] may find in favor of the party who has the burden to persuade the judge of the fact’s

10

Decisions of special masters (some of which I reference in this ruling) constitute persuasive but not binding

authority. Hanlon v. Sec’y of Health & Hum. Servs., 40 Fed. Cl. 625, 630 (1998). By contrast, Federal Circuit rulings

concerning legal issues are binding on special masters. Guillory v. Sec’y of Health & Hum. Servs., 59 Fed. Cl. 121,

124 (2003), aff’d 104 F. Appx. 712 (Fed. Cir. 2004); see also Spooner v. Sec’y of Health & Hum. Servs., No. 13-159V,

2014 WL 504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014).

22

existence.” Moberly, 592 F.3d at 1322 n.2; see also Snowbank Enter. v. United States, 6 Cl. Ct.

476, 486 (1984) (mere conjecture or speculation is insufficient under a preponderance standard).

Proof of medical certainty is not required. Bunting v. Sec’y of Health & Hum. Servs., 931 F.2d

867, 873 (Fed. Cir. 1991). In particular, a petitioner must demonstrate that the vaccine was “not

only [the] but-for cause of the injury but also a substantial factor in bringing about the injury.”

Moberly, 592 F.3d at 1321 (quoting Shyface v. Sec’y of Health & Hum. Servs., 165 F.3d 1344,

1352–53 (Fed. Cir. 1999)); Pafford v. Sec’y of Health & Hum. Servs., 451 F.3d 1352, 1355 (Fed.

Cir. 2006). A petitioner may not receive a Vaccine Program award based solely on his assertions;

rather, the petition must be supported by either medical records or by the opinion of a competent

physician. Section 13(a)(1).

B. Legal Standards Governing Factual Determinations

The process for making determinations in Vaccine Program cases regarding factual issues

begins with consideration of the medical records. Section 11(c)(2). The special master is required

to consider “all [ ] relevant medical and scientific evidence contained in the record,” including

“any diagnosis, conclusion, medical judgment, or autopsy or coroner's report which is contained

in the record regarding the nature, causation, and aggravation of the petitioner's illness, disability,

injury, condition, or death,” as well as the “results of any diagnostic or evaluative test which are

contained in the record and the summaries and conclusions.” Section 13(b)(1)(A). The special

master is then required to weigh the evidence presented, including contemporaneous medical

records and testimony. See Burns v. Sec'y of Health & Hum. Servs., 3 F.3d 415, 417 (Fed. Cir.

1993) (determining that it is within the special master's discretion to determine whether to afford

greater weight to contemporaneous medical records than to other evidence, such as oral testimony

surrounding the events in question that was given at a later date, provided that such determination

is evidenced by a rational determination).

As noted by the Federal Circuit, “[m]edical records, in general, warrant consideration as

trustworthy evidence.” Cucuras, 993 F.2d at 1528; Doe/70 v. Sec'y of Health & Hum. Servs., 95

Fed. Cl. 598, 608 (2010) (“[g]iven the inconsistencies between petitioner's testimony and his

contemporaneous medical records, the special master's decision to rely on petitioner's medical

records was rational and consistent with applicable law”), aff'd, Rickett v. Sec'y of Health & Hum.

Servs., 468 F. App’x 952 (Fed. Cir. 2011) (non-precedential opinion). A series of linked

propositions explains why such records deserve some weight: (i) sick people visit medical

professionals; (ii) sick people attempt to honestly report their health problems to those

professionals; and (iii) medical professionals record what they are told or observe when examining

their patients in as accurate a manner as possible, so that they are aware of enough relevant facts

to make appropriate treatment decisions. Sanchez v. Sec'y of Health & Hum. Servs., No. 11–685V,

2013 WL 1880825, at *2 (Fed. Cl. Spec. Mstr. Apr. 10, 2013); Cucuras v. Sec'y of Health & Hum.

Servs., 26 Cl. Ct. 537, 543 (1992), aff'd, 993 F.2d at 1525 (Fed. Cir. 1993) (“[i]t strains reason to

23

conclude that petitioners would fail to accurately report the onset of their daughter's symptoms”).

Accordingly, if the medical records are clear, consistent, and complete, then they should

be afforded substantial weight. Lowrie v. Sec'y of Health & Hum. Servs., No. 03–1585V, 2005 WL

6117475, at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed, contemporaneous medical records

are often found to be deserving of greater evidentiary weight than oral testimony—especially

where such testimony conflicts with the record evidence. Cucuras, 993 F.2d at 1528; see also

Murphy v. Sec'y of Health & Hum. Servs., 23 Cl. Ct. 726, 733 (1991), aff'd per curiam, 968 F.2d

1226 (Fed. Cir. 1992), cert. den'd, Murphy v. Sullivan, 506 U.S. 974 (1992) (citing United States

v. United States Gypsum Co., 333 U.S. 364, 396 (1947) (“[i]t has generally been held that oral

testimony which is in conflict with contemporaneous documents is entitled to little evidentiary

weight.”)).

However, the Federal Circuit has also noted that there is no formal “presumption” that

records are accurate or superior on their face to other forms of evidence. Kirby v. Sec’y of Health

& Hum. Servs., 997 F.3d 1378, 1383 (Fed. Cir. 2021). There are certainly situations in which

compelling oral or written testimony (provided in the form of an affidavit or declaration) may be

more persuasive than written records, such as where records are deemed to be incomplete or

inaccurate. Campbell v. Sec'y of Health & Hum. Servs., 69 Fed. Cl. 775, 779 (2006) (“like any

norm based upon common sense and experience, this rule should not be treated as an absolute and

must yield where the factual predicates for its application are weak or lacking”); Lowrie, 2005 WL

6117475, at *19 (“[w]ritten records which are, themselves, inconsistent, should be accorded less

deference than those which are internally consistent”) (quoting Murphy, 23 Cl. Ct. at 733)).

Ultimately, a determination regarding a witness's credibility is needed when determining the

weight that such testimony should be afforded. Andreu, 569 F.3d at 1379; Bradley v. Sec'y of

Health & Hum. Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).

When witness testimony is offered to overcome the presumption of accuracy afforded to

contemporaneous medical records, such testimony must be “consistent, clear, cogent, and

compelling.” Sanchez, 2013 WL 1880825, at *3 (citing Blutstein v. Sec'y of Health & Hum. Servs.,

No. 90–2808V, 1998 WL 408611, at *5 (Fed. Cl. Spec. Mstr. June 30, 1998)). In determining the

accuracy and completeness of medical records, the Court of Federal Claims has listed four possible

explanations for inconsistencies between contemporaneously created medical records and later

testimony: (1) a person's failure to recount to the medical professional everything that happened

during the relevant time period; (2) the medical professional's failure to document everything

reported to her or him; (3) a person's faulty recollection of the events when presenting testimony;

or (4) a person's purposeful recounting of symptoms that did not exist. La Londe v. Sec'y of Health

& Hum. Servs., 110 Fed. Cl. 184, 203–04 (2013), aff'd, 746 F.3d 1334 (Fed. Cir. 2014). In making

a determination regarding whether to afford greater weight to contemporaneous medical records

or other evidence, such as testimony at hearing, there must be evidence that this decision was the

24

result of a rational determination. Burns, 3 F.3d at 417.

C. Analysis of Expert Testimony

Establishing a sound and reliable medical theory often requires a petitioner to present

expert testimony in support of his claim. Lampe v. Sec’y of Health & Hum. Servs., 219 F.3d 1357,

1361 (Fed. Cir. 2000). Vaccine Program expert testimony is usually evaluated according to the

factors for analyzing scientific reliability set forth in Daubert v. Merrell Dow Pharm., Inc., 509

U.S. 579, 594–96 (1993). See Cedillo v. Sec’y of Health & Hum. Servs., 617 F.3d 1328, 1339 (Fed.

Cir. 2010) (citing Terran v. Sec’y of Health & Hum. Servs., 195 F.3d 1302, 1316 (Fed. Cir. 1999).

Under Daubert, the factors for analyzing the reliability of testimony are:

(1) whether a theory or technique can be (and has been) tested; (2) whether the

theory or technique has been subjected to peer review and publication; (3) whether

there is a known or potential rate of error and whether there are standards for

controlling the error; and (4) whether the theory or technique enjoys general

acceptance within a relevant scientific community.

Terran, 195 F.3d at 1316 n.2 (citing Daubert, 509 U.S. at 592–95).

In the Vaccine Program the Daubert factors play a slightly different role than they do when

applied in other federal judicial settings, like the district courts. Typically, Daubert factors are

employed by judges (in the performance of their evidentiary gatekeeper roles) to exclude evidence

that is unreliable or could confuse a jury. By contrast, in Vaccine Program cases these factors are

used in the weighing of the reliability of scientific evidence proffered. Davis v. Sec'y of Health &

Hum. Servs., 94 Fed. Cl. 53, 66–67 (2010) (“uniquely in this Circuit, the Daubert factors have

been employed also as an acceptable evidentiary-gauging tool with respect to persuasiveness of

expert testimony already admitted”). The flexible use of the Daubert factors to evaluate the

persuasiveness and reliability of expert testimony has routinely been upheld. See, e.g., Snyder, 88

Fed. Cl. at 742–45. In this matter (as in numerous other Vaccine Program cases), Daubert has not

been employed at the threshold, to determine what evidence should be admitted, but instead to

determine whether expert testimony offered is reliable and/or persuasive.

Respondent frequently offers one or more experts in order to rebut a petitioner’s case.

Where both sides offer expert testimony, a special master's decision may be “based on the

credibility of the experts and the relative persuasiveness of their competing theories.”

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

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

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

great an analytical gap between the data and the opinion proffered.” Snyder, 88 Fed. Cl. at 743

25

(quoting Gen. Elec. Co. v. Joiner, 522 U.S. 146 (1997)); see also Isaac v. Sec'y of Health & Hum.

Servs., No. 08–601V, 2012 WL 3609993, at *17 (Fed. Cl. Spec. Mstr. July 30, 2012), mot. for

review den'd, 108 Fed. Cl. 743 (2013), aff'd, 540 F. App’x. 999 (Fed. Cir. 2013) (citing Cedillo,

617 F.3d at 1339). Weighing the relative persuasiveness of competing expert testimony, based on

a particular expert's credibility, is part of the overall reliability analysis to which special masters

must subject expert testimony in Vaccine Program cases. Moberly, 592 F.3d at 1325–26

(“[a]ssessments as to the reliability of expert testimony often turn on credibility determinations”);

see also Porter v. Sec'y of Health & Hum. Servs., 663 F.3d 1242, 1250 (Fed. Cir. 2011) (“this court

has unambiguously explained that special masters are expected to consider the credibility of expert

witnesses in evaluating petitions for compensation under the Vaccine Act”).

D. Consideration of Medical Literature

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

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

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

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

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

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

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

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

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

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

E. Standards for Ruling on the Record

I am resolving Petitioner’s claim on the filed record, based on the parties’ decision to forego

the hearing I had originally scheduled. The Vaccine Act and Rules not only contemplate but

encourage special masters to decide petitions on the papers where (in the exercise of their

discretion) they conclude that doing so will properly and fairly resolve the case. Section

12(d)(2)(D); Vaccine Rule 8(d). The decision to rule on the record in lieu of hearing has been

affirmed on appeal. Kreizenbeck v. Sec’y of Health & Hum. Servs., 945 F.3d 1362, 1366 (Fed. Cir.

2020); see also Hooker v. Sec’y of Health & Hum. Servs., No. 02-472V, 2016 WL 3456435, at *21

n.19 (Fed. Cl. Spec. Mstr. May 19, 2016) (citing numerous cases where special masters decided

case on the papers in lieu of hearing and that decision was upheld). I am simply not required to

hold a hearing in every matter, no matter the preferences of the parties. Hovey v. Sec’y of Health

& Hum. Servs., 38 Fed. Cl. 397, 402–03 (1997) (determining that special master acted within his

discretion in denying evidentiary hearing); Burns, 3 F.3d at 417; Murphy v. Sec’y of Health &

Hum. Servs., No. 90-882V, 1991 WL 71500, at *2 (Fed. Cl. Spec. Mstr. Apr. 19, 1991).

26

ANALYSIS

I. Petitioner Has Met Her Prima Facie Burden of Proof for a Table Flu

Vaccine-GBS Claim

GBS is listed as a Table injury for the flu vaccine, and thus a claimant seeking to meet its

requirements need not establish vaccine causation. Instead, Petitioner herein must show (a) receipt

of a covered form of the flu vaccine, (b) that she did in fact experience GBS, as defined in the

Table’s “qualifications and aids to interpretation,” and (c) that her symptoms onset (whether or not

GBS could then be diagnosed, or was) occurred between three and 42 days after vaccination. 42

C.F.R. § 100.3. There is no dispute that Petitioner received a version of the flu vaccine covered by

the Program, but some disagreement as to whether (a) Petitioner actually experienced GBS, (b) its

onset occurred in the timeframe set for the claim, and/or (c) Petitioner’s neuropathy was “drug-

induced”—caused by her undisputed Taxol treatments. Although these matters were reasonably

disputed, and resolution of some of the items present close calls, I determine that the balance of

evidence favors Petitioner.

First, the medical record supports Petitioner’s favored diagnosis of an axonal form of GBS.

The Table itself recognizes that some GBS variants are cognizable claims, and this includes the

axonal form, often referred to with the acronym “AMAN” (or “acute motor axonal neuropathy”).11

Swaiss v. Sec’y of Health & Hum. Servs., No. 15-286V, 2019 WL 6520791 (Fed. Cl. Spec. Mstr.

Nov. 4, 2019). Thus, the fact that Petitioner’s form of GBS is less common does not render the

diagnosis suspect, assuming it has record support. As it stands, Petitioner’s favored diagnosis does

have such support. Ex. 6 at 5, 12, 67. And Petitioner has also offered the opinion of a

contemporaneous treater who actually saw Petitioner, Dr. Picot (though I give far more weight to

his second statement than his first, conclusory comment). First Picot Statement at 1; Second Picot

Statement at 1. Dr. Callaghan’s alternative reading of the record is reasonable, and he does observe

findings not fully consistent with the proposed GBS diagnosis. But although there are cases where

the record is sufficiently ambiguous to cause me to look to the opinions of after-the-fact experts

for guidance or interpretation, giving them greater weight, here the record itself is enough to

support Petitioner’s contention on diagnosis.

Second, I find that it is not preponderantly likely that Petitioner’s Taxol treatments were

causal of her GBS—even though the record does establish she had the kind of common neuropathic

symptoms associated with Taxol while, and not long after, she was receiving it as chemotherapy.

It is undisputed that Taxol can cause some kinds of neuropathy—more often than not a mild,

limited sensory form, but also potentially a motor/axonal form. But Petitioner’s expert group

persuasively established that the relatively low dosage levels Petitioner received are not usually

11

By contrast, a different variant—chronic immune demyelinating polyneuropathy, or “CIDP”—is a defined

exclusionary diagnosis that, if present, means a Table flu-GBS claim cannot be substantiated. Section 14(b).

27

associated with severe neuropathies. Petitioner’s efforts to undermine the contention that Taxol

explained her symptoms gained significant help from Dr. Schwartz—an oncologist with direct

experience treating Petitioner, unlike Dr. McClain. Dr. Schwartz in fact represented that, in his

experience, he had never seen one of his patients develop such a severe post-chemotherapy

neuropathy—an assertion I give greater weight than Respondent’s objection that it remained

“possible” Taxol could also in rare cases result in a worsened form of neuropathy. I would require

more evidence than such reasoned speculation to find it preponderantly the case.

Many filed items of literature confirm Petitioner’s assertions about the association between

Taxol dosage and degree of likely neuropathy. Jones at 5548; Freilich at 117–18; Scripture at 166,

167. By contrast, no literature goes so far to identify GBS itself as a Taxol-associated injury, or

that in most cases a severe form is likely at the dosage levels Petitioner experienced. And in many

regards, the record itself is more consistent with Petitioner having experienced two forms of

neuropathy rather than one continuous and progressive condition. Ex. 6 at 9. Her worsening also

occurred well after the Taxol treatments had ended—something else rendering the facts

inconsistent with those studies, although I acknowledge Respondent’s point that Taxol-caused

neuropathies can progress even once treatment ends.

No doubt it has been established on this record that Taxol can be associated with more

severe symptoms as well, approaching even what Petitioner experienced. But Petitioner’s experts

persuasively explained why that was not likely under the facts of this case, offering credible

literature in support. At bottom, the dosage level Petitioner received was not likely high enough to

put her into the category of subjects from the studies discussed in Scripture.

Respondent’s experts’ arguments to the contrary—that it is possible Taxol could cause

GBS-like symptoms, and that this was statistically more likely than the flu vaccine—have some

facial appeal. It was certainly reasonable for Respondent to take note of the Taxol chemotherapy

regime, and question its causal role. It is undisputed Petitioner received it and experienced some

symptoms attributable to it—something even Dr. Schwartz felt had occurred (although he later felt

her degree of worsening was inconsistent with that as the cause). Taxol is definitely associated

with neuropathic symptoms. Indeed, some of the literature offered in this case reflects efforts by

medical science to evaluate how, or when, to administer Taxol, given its understood side-effects.

See, e.g., Timmins at 367, 68–69. I also deem relevant and worthy of consideration the articles

filed that suggest Taxol-induced neuropathies may have a genetic-susceptibility component that

explains why all Taxol-receiving patients do not go on to develop neuropathies—although there

was no evidence in this case that Petitioner was tested genetically or possessed the putatively-

associated variants (and their causal role was unquestionably not shown, in any event, to exceed

the role Taxol would play).

28

Ultimately, Respondent to no small extent seemed to rely on the argument that Taxol can

possibly and in rare circumstances cause severe neuropathies, while emphasizing a generally low

statistical likelihood that the flu vaccine can cause GBS. Of course, the second argument flies in

the face of the claim’s Table nature (and could only be overcome by showing of “factor

unrelated”—which Respondent did not successfully achieve).12 But otherwise, these are the kind

of arguments I often reject when a petitioner puts them forward in favor of causation. The mere

possibility, no matter how well reasoned, of something happening is not the same as a

determination it is “more likely than not.” In this case, the record persuasively establishes that

Taxol can likely cause some neuropathic symptoms, including motor-related—and that

Petitioner’s initial sensory symptoms were likely due to her chemotherapy regime. But the

argument that vaccine injuries are more rare than Taxol neuropathies does not undermine the

conclusion that in this case the Taxol was not the likely cause of Petitioner’s symptoms—any more

than the argument oft-advanced by Program claimants that the rarity of vaccine injuries mean their

burden of proof must be adjusted downward. Thus, although this record establishes some initial,

transient sensory neuropathic symptoms due to Taxol, it does not also establish that the second

“round” of symptoms flowed from the first.

Finally, the record preponderates in favor of the determination that Petitioner’s onset of

GBS-specific symptoms (which the record shows can be distinguished from her Taxol-associated

sensory neuropathic symptoms) occurred within the onset timeframe set by the Table—although

this issue presents the closest fact dispute between the parties. I decide it in Petitioner’s favor—

but just barely.

There is some ambiguity in the record about when Petitioner’s symptomatic issues

transitioned, from milder sensory issues to the more severe motor concerns she later expressed.

12

On the basis of this same record and relevant evidence, I could not find that Respondent carried his “factor unrelated”

burden (based on my initial determination that Petitioner met her prima facie burden of proof). Stone v. Sec’y of Health

& Hum. Servs., 95 Fed. Cl. 233, 237 (2010). One important aspect of that burden is the obligation placed on

Respondent to rule out vaccine causation—something A Petitioner need not do when establishing her prima facie

case. de Bazan v. Sec’y of Health & Hum. Servs., 539 F.3d 1351, 1354 (Fed. Cir. 2008).

In essence, although it is clearly established that Taxol can sometimes cause severe neuropathic symptoms affecting

motor nerves, I do not find the flu vaccine’s role can on this record be completely eliminated as substantial—especially

since Petitioner’s experts persuasively demonstrated that the dosage levels at issue never became high enough to likely

be so damaging. Thus, even if this were a case (and it could well be) that the interaction between Taxol and the impact

of the flu vaccine caused Petitioner’s later GBS, that finding would not eliminate the vaccine as causal in some

substantial part—and hence Respondent’s somewhat more difficult burden on the issue of “factor unrelated” was not

met. Id. There are cases where this showing can be met. See, e.g., White v. Sec’y of Health & Hum. Servs., No. 20-

1319V, 2023 WL 4204568, at *17 (Fed. Cl. Spec. Mstr. June 2, 2023), mot. for review den’d, 168 Fed. Cl. 660 (2023),

appeal docketed No. 2024-1372 (Fed. Cir. Jan. 23, 2024) (infection Petitioner possessed was far more likely to cause

GBS than the flu vaccine). Here, Taxol has been shown by Petitioner not to be commonly associated with the axonal

form of GBS—and to be uncommonly causal of axonal neuropathies more generally. I thus do not give much weight

to Respondent’s expert’s efforts to elucidate the comparative statistical commonality of flu vaccine-caused GBS

versus Taxol neuropathies.

29

But the record does establish that her complaints became qualitatively different in the second half

of December, toward the end of the month, when the numbness and tingling in her legs, feet, and

hands persisted, causing Petitioner to suffer multiple falls due to continued weakness. Ex. 13 at

34–39. Thereafter, it took treaters some time to coalesce around a GBS diagnosis—but this

consensus is not the same as when symptoms first manifested, which is of course the Program’s

only concern when attempting to determine whether onset occurred in a Table-designated

timeframe. Nieves v. Sec’y of Health & Hum. Servs., No. 18-1602V, 2023 WL 3580148, at *40

(Fed. Cl. Spec. Mstr. May 22, 2023), mot. for review den’d, 167 Fed. Cl. 422 (2023). Here, the

Table provides for up to 42 days for onset—and thus any onset by the last week of December

would fall into that timeframe. Dr. Callaghan’s nadir arguments do not undermine this

conclusion—for measuring from this onset (rather than when Petitioner first experienced the

distinguishable, Taxol-associated symptoms), it can be concluded that Petitioner’s condition

progressed downward over the ensuing four weeks, causing her to “hit bottom” by “1/25/13.” Ex.

A at 4; 42 C.F.R. § 100.3(c)(15)(ii)(C).

While these points find sufficient record and expert support for me to be comfortable to

conclude as I do, there is no doubt that overall this record is flush with factual ambiguities. Taxol’s

association with neuropathy as a side-effect is fully-established. Taxol treatments can also, less

commonly, result in more severe motor neuropathies. And those symptoms do not vanish simply

when treatment ends, as Petitioner struggled to establish. It was reasonable to suspect Petitioner’s

initial symptoms were the start of what she later experienced—indeed, treaters who saw her in

December 2012 and even closely thereafter thought this to be the case, at least initially (even if

they rationally altered their views later on, after added treatment experience with her). And not

only did Petitioner experience an uncommon form of GBS, but the diagnosis itself is not fully

confirmed by the record.

But the coin of the realm in the Vaccine Program, evidentiarily-speaking, is

preponderance, not certainty—and close cases can tip in a petitioner’s favor even when other

credible evidence suggests an alternative conclusion. In fact, case law encourages special masters

to decide such evenly-disputed matters for claimants. Strong v. Sec’y of Health & Hum. Servs.,

No. 15-1108V, 2018 WL 1125666, at *20 (Fed. Cl. Spec. Mstr. Jan. 12, 2018). Just as there are

many cases where I find a petitioner has not crossed the preponderant “line,” even though some

reliable evidence might favor his claim, the opposite can be the case as well—and is so here.

II. The Claim is Timely Under the Act’s Lookback provision

In many prior determinations, I have ruled that only “new” Table-version claims involving

a vaccine previously added to the Vaccine Program are “saved” by the Act’s lookback provision.

Randolph v. Sec’y of Health & Hum. Servs., No. 18-1231V, 2020 WL 542735, at *9 (Fed. Cl.

30

Spec. Mstr. Jan. 2, 2020). 13 Here, Petitioner’s claim is facially untimely, and thus can only go

forward if the lookback’s operations protect it. I find they do. As noted, the claim alleges a

successful Table claim of GBS after the flu vaccine. The matter was filed within two years of

amendment, and eight years from date of injury (since less than seven years passed from

Petitioner’s likely onset in mid to late-December 2012 and the filing of the claim in March 2019).

Thus, because I have found the Petition advances a meritorious Table claim, it is saved by the

lookback provision.

CONCLUSION

Based on the entire record in this case, I find that Petitioner has provided preponderant

evidence satisfying all requirements for a Table-GBS claim. Petitioner is thus entitled to

compensation. An order establishing a schedule for resolution of damages shall follow.

IT IS SO ORDERED.

/s/ Brian H. Corcoran

Brian H. Corcoran

Chief Special Master

13

Other special masters have taken a more expansive view of the lookback provision, and found it also saves certain

causation claims, reasoning (in a “rising tide lifting all boats” manner) that the mere existence of a new Table claim

makes comparable, but non-Table, causation claims more likely to succeed as well. See e.g., Simpson v. Sec’y of

Health & Hum. Servs., No. 17-944V, 2019 WL 11815360 (Fed. Cl. Spec. Mstr. Aug. 7, 2019) (46 to 47-day onset of

GBS after flu vaccine too long to constitute Table claim, but non-Table claim deemed timely filed based on lookback

provision). I of course am not bound by the decisions of other special masters, but I deem this reasoning unpersuasive.

It blurs the recognized distinction between Table claims (where the Government concedes causation if certain facts

are established) and causation claims. It also ignores the fact that there is a difference between “table” amendments

that allow new vaccines to be the basis of a claim, versus amendments adding a designated new injury. The ability to

claim a flu vaccine-related injury greatly predated the Table amendment adding the flu vaccine-GBS claim.

31