In the United States Court of Federal Claims
                                OFFICE OF SPECIAL MASTERS
                                            Filed: July 27, 2020

* * * * * * * * * * * * * *                *
ANNA CONTE,                                *      No. 17-403V
                                           *
               Petitioner,                 *      Special Master Sanders
                                           *
v.                                         *
                                           *
SECRETARY OF HEALTH                        *      Ruling on the Record; Insufficient Proof;
AND HUMAN SERVICES,                        *      Influenza (“flu”) Vaccine; Guillain-Barré
                                           *      syndrome (“GBS”)
               Respondent.                 *
* * * * * * * * * * * * * * *
Isaiah R. Kalinowski, Maglio Christopher and Toale, PA, Washington, DC, for Petitioner.
Darryl R. Wishard, United States Department of Justice, Washington, DC, for Respondent.

                                                DECISION 1

       On March 22, 2017, Anna Conte (“Petitioner”) filed a petition for compensation in the
National Vaccine Injury Compensation Program (“Vaccine Program” or “the 

, ECF No. 1. Petitioner alleges that the influenza (“flu”) vaccine she received on September 30,
2015, caused her to develop Guillain-Barré syndrome (“GBS”).

the record,
however, does not show an entitlement to an award in the Program.

    I.      Procedural History

       Petitioner filed her petition on March 22, 2017.

day, Petitioner filed
twelve exhibits consisting of medical records. See Pet’r’s Exs. 1–13, 3 ECF Nos. 5-2–5-10, 6-2–
6-6. Petitioner filed an additional medical records exhibit and a statement of completion on April
21, 2017. See Pet’r’s Ex. 14, ECF No. 11-2; ECF No. 12.

1
  This decision shall be posted on the United States Court of Federal Claims’ website, in accordance with
the E-Government Act of 2002, 44 U.S.C. § 3501 note (2012) (Federal Management and Promotion of
Electronic Government Services). This means the Decision will be available to anyone with access to
the Internet. In accordance with Vaccine Rule 18(b), a party has 14 days to identify and move to delete
medical or other information that satisfies the criteria in § 300aa-12(d)(4)(B). Further, consistent with the
rule requirement, a motion for redaction must include a proposed redacted decision. If, upon review, I
agree that the identified material fits within the requirements of that provision, such material will be deleted
from public access.
2
  The Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, 42 U.S.C. §§ 300aa-
10 to -34.
3
  Petitioner filed exhibit 7 in two parts. See Pet’r’s Exs. 7.1–7.2.
        On August 21, 2017, Respondent filed a status report in which he indicated that he had
“completed his preliminary review of the records and has not identified any additional records that
are missing at this time.” ECF No. 18. The next day, I ordered Respondent to file his Rule 4(c)
report by October 20, 2017. Non-PDF Order, docketed Aug. 22, 2017. Respondent filed a motion
for extension of time on October 22, 2017, ECF No. 19, which I granted, see Non-PDF Order,
docketed Oct. 23, 2017, and Respondent filed his Rule 4(c) report on November 2, 2017, Resp’t’s
Report, ECF No. 20. Respondent argued in his report that “Petitioner is not entitled to
compensation under the terms of the Vaccine Act[]” and requested that I dismiss the petition.

        I held a Rule 5 conference with the parties on November 15, 2017, see Min. Entry, docketed
Nov. 15, 2017, and ordered Petitioner to file an expert report by January 31, 2018, ECF No. 21.
Petitioner filed three affidavits on December 19, 2017. Pet’r’s Exs. 16–18, ECF Nos. 24-2–24-4.
On January 24, 2018, Petitioner filed an expert report authored by Zurab Nadareishvili, M.D.,
along with his curriculum vitae and sixteen pieces of supporting medical literature. Pet’r’s Exs.
19–36, ECF Nos. 25-2–25-3, 26-2–26-10, 27-2–27-8. The next day, I ordered Respondent to file
a responsive expert report by March 26, 2018. Non-PDF Order, docketed Jan. 25, 2018.

        Petitioner filed an additional exhibit consisting of medical records on March 13, 2018.
Pet’r’s Ex. 37, ECF No. 28-2. On March 23, 2018, Respondent filed a motion for extension of
time to submit a responsive expert report, ECF No. 29, which I granted, ECF No. 30. Respondent
subsequently filed an expert report authored by Vinay Chaudry, M.D., along with his curriculum
vitae and one piece of supporting medical literature on May 25, 2018. Resp’t’s Exs. A–C, ECF
Nos. 31-1–31-3. On May 30, 2018, I ordered Petitioner to file a responsive expert report by July
24, 2018. Non-PDF Order, docketed May 30, 2018. On July 23, 2018, Petitioner filed a responsive
supplemental expert report by Dr. Nadareishvili and one piece of supporting medical literature.
Pet’r’s Exs. 38–39, ECF Nos. 32-2–32-3.

        On September 19, 2018, I conducted a review of Petitioner’s medical records and both
parties’ expert reports filed to that point and issued an order containing a list of questions for each
expert to address by November 19, 2018. ECF No. 33. Petitioner filed Dr. Nadareishvili’s
responses to my questions, along with two pieces of medical literature, on November 16, 2018.
Pet’r’s Exs. 40–42, ECF Nos. 34-1–34-3.

        On the same day, Petitioner filed a motion to exclude the testimony of Respondent’s expert,
Dr. Chaudry, because “it does not meet the legal threshold of Daubert v. Merrell Dow
Pharmaceuticals, Inc., 

(1993), in that it does not apply scientific methodology, and
does not provide evidence to support its claim.” Pet’r’s Mot. to Exclude Testimony of Dr. Chaudry
at 2, ECF No. 35. On November 19, 2018, Respondent filed a motion for extension of time to
respond to my questions and a request that I stay Petitioner’s pending motion because “it would
be premature to decide [P]etitioner’s motion” while “Dr. Chaudhry is still in the process of
providing written testimony for the Court’s consideration[,]” ECF No. 36. I issued an order
granting Respondent’s motion on November 20, 2018, and ordered Respondent to file his expert’s
responses to my questions by January 18, 2019. ECF No. 37. In the same order, I also stayed
Petitioner’s motion to exclude Dr. Chaudry’s testimony.

        Petitioner filed an additional affidavit on December 22, 2018. Pet’r’s Ex. 43, ECF No. 38-
2. On February 28, 2019, Respondent filed an expert report containing Dr. Chaudry’s responses
to my questions and to Dr. Nadareishvili’s most recent expert report, along with seven pieces of
supporting medical literature. Resp’t’s Exs. D–K, ECF Nos. 39-1–39-8. Petitioner filed a status
report on March 12, 2019, in which she indicated that she did not believe that any “further expert
reports are necessary.” ECF No. 40.
        After conducting a review of both parties’ responses to my previous questions and the
accompanying medical literature, I issued an order on April 11, 2019, in which I directed additional
questions to the parties’ experts and ordered the parties to file their responses by May 13, 2019.
ECF No. 42. Petitioner filed Dr. Nadareishvili’s responses and three pieces of supporting medical
literature on April 22, 2019. Pet’r’s Exs. 44–47, ECF Nos. 43-1–43-4. After one extension of
time, Respondent filed Dr. Chaudry’s responses to my questions and three pieces of supporting
medical literature on May 20, 2019. See ECF Nos. 44–45; Resp’t’s Exs. L–O, ECF No. 46-1–46-
4. On June 24, 2019, Petitioner filed a status report in which she again indicated that she did not
believe that any “further expert reports are necessary.” ECF No. 47.

        I held a status conference with the parties on July 31, 2019, Min. Entry, docketed July 31,
2019, during which “[t]he parties discussed how the case should proceed and determined that it
should be decided on the record[,]” ECF No. 48. I ordered Petitioner to file any additional
evidence that she would like to be considered by August 30, 2019.

2019,
Petitioner filed one piece of medical literature. Pet’r’s Ex. 48, ECF No. 49-2.

          Neither party has filed any additional evidence. This matter is now ripe for consideration.

    II.      Factual Background

          A. Relevant Medical History

        On July 23, 2015, Petitioner presented to S. Brett Whitfield, M.D., an orthopedic surgeon,
for a consultation regarding “severe arthritis” and a “problem with her right finger.” Pet’r’s Ex. 9
at 12. Dr. Whitfield noted that Petitioner had “had injections” for her severe arthritis in the past
and had recently received an injection in one of her knees.

“very
well with the [recent] injection.”

her knee arthritis, Petitioner complained that,
a day prior, “[s]he was lifting something and felt some pain[]” in her right hand.

included “[m]allet finger,” 4 “osteopenia 5 . . . [of her] bilateral lower
extremities[,]” and “[s]evere patellofemoral arthritis[ in her] bilateral knees.”

Dr.


4
  A mallet finger is defined as “partial permanent flexion of the terminal phalanx of a finger caused by a
ball or other object striking the end or back of the finger, resulting in rupture of the attachment of the
extensor tendon.” Dorland’s Illustrated Medical Dictionary 701 (33rd ed. 2020) [hereinafter
“Dorland’s”].
5
  Osteopenia is defined as “1. any decrease in bone mass below the normal[; or] 2. reduced bone mass due
to decrease in the rate of osteogenesis to the extent that there is insufficient compensation for normal bone
lysis.” Dorland’s at 1329. Lysis is defined as “dissolution or destruction of an organ or structure, such as
the destruction of bone by loss of calcium . . . .”

Whitfield placed Petitioner’s injured finger in a “stack splint” and prescribed her Mobic 6 for her
knees, although he noted that she did not need any additional injections at that time.

2015, Petitioner presented to her primary care physician (“PCP”) with
chief complaints of “[b]ack pain, hypertension, and dyslipidemia.” 7 Pet’r’s Ex. 10 at 42. The
history of present illness (“HPI”) section of the note reflects that Petitioner had “a long history of
pain across [her] lower back[, which was a] little bit more frequent lately.”

blood pressure was elevated.

her Tylenol for her back pain
and ordered an x-ray of her lumbosacral spine.

Petitioner also received the flu vaccine
at issue at this visit.

Pet’r’s Ex. 1 at 1. Petitioner underwent a lumbosacral spine x-ray
on October 1, 2015, which revealed “known degenerative disc disease at L4-5 and L5-S1 with
anterior spondylolisthesis 8 of L4 relative to L5.” Pet’r’s Ex. 10 at 239. It also showed “[t]iny
calcification in the projection of the right upper quadrant which measures approximately [nine
millimeters]” and “[s]cattered arterial atherosclerotic plaque formation of aorta.”

her PCP on October 28, 2015, with complaints of “[n]umbness [in]
both hands, pain at the base of both thumbs[, and h]ypertension.”

Petitioner reported
that “[f]or the past [two] or [three] weeks[, she] has had numbness in both hands[, e]specially the
fingertips.”

she had to “wake[] up through the night and . . . shake her
hands to get the feeling back.”

“[a]bout [two] weeks ago[, she] had pain[at the]
base of the right thumb[,]” and “now [has] pain at the base of the left thumb.”

nerve conduction studies (“NCS”) of both of Petitioner’s hands and prescribed tramadol 9 for her
osteoarthritic pain.

Two days later, on October 30, 2015, Petitioner called her PCP and
reported that “she may have to go to the [emergency room] because of the pain in her hands” and
“that the med[ication] [the PCP had] prescribed doesn’t help” her pain.

        On November 2, 2015, Petitioner presented to Beckley Appalachian Regional Healthcare
(“BARH”) hospital with complaints of “back pain radiating down [her] right arm [for one] day.”
Pet’r’s Ex. 4 at 179–81. Petitioner reported that she also experienced “some nausea and chest
tightness[]” and that “Tylenol helps some with [the] pain.”

She explained “that she has
had back pain off and on for several years secondary to osteoarthritis 10 and degenerative joint

6
  Mobic is the “trademark for a preparation of meloxicam.” Dorland’s at 1154. Meloxicam is “a
nonsteroidal anti-inflammatory drug used in the treatment of osteoarthritis; administered orally.”

  Dyslipidemia is defined as “an abnormality in, or an abnormal amount of, lipids and lipoproteins in the
blood . . . .” Dorland’s at 572.
8
   Spondylolisthesis is “the forward displacement . . . of one vertebrae over another, usually of the fifth
lumbar over the body of the sacrum, or of the fourth lumbar over the fifth, usually due to a developmental
defect in the pars interarticularis.” Dorland’s at 1725. The sacrum is “the triangular bone just below the
lumbar vertebrae[.]”

  Tramadol hydrochloride is “an opioid analgesic used for the treatment of moderate to moderately severe
pain following surgical procedures and oral surgery; administered orally.” Dorland’s at 1920.
10
   Osteoarthritis is defined as “a non-inflammatory degenerative joint disease seen mainly in older persons,
characterized by degeneration of the articular cartilage, hypertrophy of bone at the margins, and changes in
the synovial membrane. It is accompanied by pain, usually after prolonged activity, and stiffness,
particularly in the morning or with inactivity.” Dorland’s at 1326. Osteoarthritis is also known as
degenerative joint disease.

disease.” 11

Petitioner’s blood pressure was elevated upon exam.

emergency room, Petitioner “went to the bathroom and had [a] syncopal episode 12 while there[,]”
after which Petitioner “denie[d] pain but” complained of “severe weakness.”

Petitioner
was admitted for further evaluation.

underwent computed tomography 13 (“CT”) scans of her chest,
abdomen, and pelvis, which were all unremarkable. See Pet’r’s Ex. 9 at 43–47. Doctors also ruled
out acute cardiopulmonary disease and acute coronary syndrome. Pet’r’s Ex. 4 at 98. Petitioner
also had a normal neurological exam.

Petitioner was assessed with atypical chest
pain that doctors thought was “most likely secondary to uncontrolled hypertension.”

Doctors noted that they had brought Petitioner’s blood pressure “under control by adding
lisinopril 14 to her regimen, as well as [administering] IV hydralazine.” 15

reflects that Petitioner’s “chest discomfort did not return during her stay[]” in the hospital, and that
upon discharge, her blood pressure “was well controlled . . . .”

Doctors directed
Petitioner to follow-up with her PCP.

        On November 9, 2015, Petitioner walked in to her PCP’s office, stated that she was still
experiencing pain, and requested “an xray [sic.] to see whats [sic.] going on with her hands.”
Pet’r’s Ex. 10 at 38. Petitioner underwent an x-ray of her hands on the same day, which revealed
“[o]steoporosis 16 and osteoarthropathy.” 17

She returned to her PCP on November 16,
2015, with complaints of “pain in both hands[, e]specially at the base of the thumbs[, and s]ome
numbness and tingling in the tips of the fingers.”

Petitioner also complained of
“localized pain [in her] left lateral ribs” beginning two or three days prior.

her with carpal tunnel syndrome (“CTS”) 18 and prescribed “symptomatic treatment for

11
    Degenerative joint disease is also known as osteoarthritis. Dorland’s at 1326. For a definition of
osteoarthritis, see supra note 9.
12
   Syncope is defined as “a temporary suspension of consciousness due to generalized cerebral ischemia . .
. .” Dorland’s at 1788. Ischemia is defined as a “deficiency of blood in a part, usually due to functional
constriction or actual obstruction of a blood vessel.”

   A computed tomography scan is a “tomography in which the emergent x-ray beam is measured by a
scintillation counter; the electronic impulses are recorded digitally and then are processed by a computer
for reconstruction display.” Dorland’s at 1905. It is also known as a CT scan.

recording of internal body images at a predetermined plane by means of the tomograph . . . .”

“an apparatus for moving an x-ray source in one direction as the film is moved in the opposite
direction, thus showing in detail a predetermined plane of tissue while blurring or eliminating detail in other
planes.”

   Lisinopril is “the lysine derivative of the active form of enalapril; an angiotensin-converting enzyme
inhibitor used in the treatment of hypertension (alone or in combination with a thiazide diuretic), congestive
heart failure, and acute myocardial infarction; administered orally.” Dorland’s at 1052.
15
   Hydralazine is “a peripheral vasodilator used as an antihypertensive.” Dorland’s at 865. Vasodilator is
defined as “1. causing dilation of the blood vessels[; or] 2. a motor nerve or chemical compound that causes
dilation of the blood vessels.”

   Osteoporosis is defined as “reduction in bone mineral density, leading to fractures after minimal trauma.”
Dorland’s at 1329.
17
   Osteoarthropathy is defined as “any disease of the joints or bones.” Dorland’s at 1326.
18
   Carpal tunnel syndrome is defined as “an entrapment neuropathy characterized by pain and burning or
tingling paesthesias in the fingers and hand, sometimes extending to the elbow. Symptoms result from

                                                      5
[her] left rib pain.”

         The next day, Petitioner returned to BARH hospital with complaints of “upper back pain[
that] . . . prevents her from getting sleep . . . .” Pet’r’s Ex. 4 at 74–75. She described the pain as
“sharp in nature” and “rated [it eight-to-nine out of ten]” on the pain scale.

Her physical
exam was normal, and Petitioner did not have any motor or sensory deficits.

Doctors
diagnosed Petitioner with postural lower back pain and discharged her home.

2015, Petitioner returned to her PCP with complaints of “[b]ack pain,
left rib pain, [and] numbness [in] both [of her] hands.” Pet’r’s Ex. 10 at 34. Petitioner described
“pain in [the] mid[-]thoracic spine area and to the left[,]” as well as “pain in [her] left ribs[,
e]specially” in the “T7-T8 range.”

Petitioner’s prior x-rays and
noted “[s]ome osteoporosis and osteoarthritis[,]” and referred her for another NCS, an MRI of her
thoracic spine, and an x-ray of her left ribs.

Petitioner also received a Lortab 19
prescription to manage her pain.

to the emergency department at BARH hospital on November
24, 2015, for an “[i]njury to [her] upper back and thoracic spine.” Pet’r’s Ex. 4 at 55. She
complained of “upper back pain[ that was] sharp[ and] radiate[d] to [the] anterior chest wall . . . .”

She stated that the pain was “worse with sitting up or laying down.”

showed “no evidence [of an] acute cardiopulmonary process” or a “displaced left rib
fracture.” Pet’r’s Ex. 10 at 335, 337. Petitioner had a normal physical examination, including a
normal neurological examination with “no motor . . . [or] sensory deficit[s].” Pet’r’s Ex. 4 at 56–
57. Doctors again discharged Petitioner home with diagnoses of low back pain and chronic back
pain.

        Petitioner had an appointment with Thomas Kowalkowski, M.D., a urologist, on November
30, 2015, for a chief complaint of blood in her urine. Pet’r’s Ex. 5 at 39. Her active problems list
included “flaccid neuropathic bladder” 20 and “urinary retention.”

of the note
states that Petitioner presented for a “consultation regarding hematuria.” 21

that Petitioner had “[n]o change in urinary frequency and no incomplete emptying of [her]
bladder.”

He also noted that Petitioner did not have any “dysuria.” 22

+4 hemoglobulin in Petitioner’s urine.

Petitioner with a
“microscopic hematuria” and ordered renal and pelvic ultrasounds, which were unremarkable. Id.;
see also

compression of the median nerve in the carpal tunnel.” Dorland’s at 1794.
19
   Lortab is the “trademark for combination preparations of hydrocodone bitartrate and acetaminophen.”
Dorland’s at 1061. Hydrocodone bitartrate is “the bitartrate salt of hydrocodone, used as an analgesic and
antitussive; administered orally.”

   Neuropathic bladder refers to “any condition of dysfunction of the urinary bladder caused by a lesion of
the central or peripheral nervous system.” Dorland’s at 219. The central nervous system is “the part of the
nervous system consisting of the brain and spinal cord.”

The peripheral nervous system is “the
part of the nervous system consisting of nerves and ganglia outside the brain and spinal cord.”

   Hematuria is defined as “blood . . . in the urine . . . .” Dorland’s at 824.
22
   Dysuria is defined as “1. painful urination[; or] 2. any difficulty of urination.” Dorland’s at 579.

                                                     6
        On December 1, 2015, Petitioner presented to Dr. Whitfield for a consultation. Pet’r’s Ex.
9 at 5. Petitioner complained of “increased numbness and tingling in both hands . . . [that] began
about three weeks ago[] . . . in the fingertips and . . . has progressed toward the palm.”

the “[p]aresthesias affect[ed] her thumb, index finger[,] and middle finger more so than
the ulnar two digits.”

“[b]oth hands are equal, though the right hand began
before the left.”

that “she developed some paresthesias about the toes on
both of her feet[,]” but did not state when this began.

weakness in her upper
or lower extremities.”

Petitioner’s recent back pain and
hospitalizations, which resulted in a diagnosis of a “muscle strain.”

“[d]ecreased sensation about the palmar aspect of the thumb, index finger[,] and middle finger
bilaterally.”

He also noted that Petitioner had normal range of motion (“ROM”), reflexes,
and no motor deficits.

His assessment included “[b]ilateral [CTS] versus peripheral
neuropathy[]” and “[l]ower extremity neuropathy of unclear etiology.”

“severe osteoporosis” and “upper back pain [that he] suspect[ed resulted from a] compression
fracture given [Petitioner’s] osteoporosis.”

an MRI of Petitioner’s
lumbar spine, an EMG, and fit Petitioner with hand braces to attempt to control her CTS.

        Petitioner underwent an EMG study with Barry Vaught, M.D., on December 3, 2015.

Dr. Vaught described the results as “abnormal” and concluded that there was
“electrophysiologic evidence for severe bilateral median mononeuropathy at the wrists, consistent
with [CTS].”

He also wrote that there was “no evidence [of] ulnar neuropathy on either
side or cervical radiculopathy on the right.”

with this diagnosis
after reviewing these results with Petitioner at an appointment on December 9, 2015, and directed
Petitioner to follow-up with Dr. Whitfield. Pet’r’s Ex. 10 at 31–32.

        On December 22, 2015, Petitioner returned to Dr. Whitfield for a follow-up. Pet’r’s Ex. 9
at 2. Petitioner “complain[ed] of pain about the bilateral hands, . . . paresthesias about both of her
hands[,] and state[d] that she has decreased sensation and . . . feels like she is picking things up,
but she is not.”

of some pain about the thoracic spine that
radiates across the axilla region to her breast on the right side.”

revealed “[d]ecreased sensation about the palmar aspect of the thumb, index finger[,] and middle
finger bilaterally.”

Petitioner with severe bilateral CTS, lower
extremity neuropathy of unclear etiology, and severe osteoporosis that he “suspect[ed caused a]
compression fracture . . . .”

He planned on performing a “carpal tunnel release” 23 because
this procedure would “give the nerve the best chance of survival[, but noted that] it is possible that
permanent nerve damage has been done.”

Petitioner to physical therapy
(“PT”) for her back pain.

to the emergency department at BARH hospital on December 29,
2015, “with a chief complaint of [right] foot and shin pain[]” caused by a fall at church the previous

23
   Carpal tunnel, or canalis car´pi, is defined as “an osseofibrous tunnel for passage of the tendons of the
flexor muscles of the hand and digits, formed by the flexor retinaculum as it roofs over the concavity of the
carpus on the palmer surface . . . .” Dorland’s at 274. The carpus is “the joint between the forearm and
hand, made up of eight bones . . . .”

A release is defined as a “surgical incision or cutting of
soft tissue to bring about relaxation.”

It is not clear whether or when Petitioner underwent this
procedure.

                                                      7
day. Pet’r’s Ex. 4 at 43. Petitioner stated that she “bent over to pick up some plant leaves and
when [she] raised up[,] [she] lost [her] balance[]” and fell.

not reveal any
“obvious swelling, reddening, contusion, [or] deformity,” and a neurological exam was normal.

pain “an [eight] on a [one-to-ten] pain scale.”

with an ankle injury and was noted to be “unsteady and at risk for multiple falls.”

        On December 31, 2019, Petitioner reported to University of Virginia Hospital East. 24
Pet’r’s Ex. 11 at 2; Pet’r’s Ex. 6 at 463. Petitioner had an abnormal urinalysis, Pet’r’s Ex. 11 at
2–3, as well as an abnormal complete blood count panel, Pet’r’s Ex. 6 at 463. A lumbar spine
MRI revealed “[n]o evidence of [an] acute fracture or other acute abnormality.” Pet’r’s Ex. 11 at
20–21. Petitioner was diagnosed with bilateral lower extremity pain and weakness and was
discharged home with a prescription for oxycodone 25 and directions to follow-up with orthopedics.
Pet’r’s Ex. 6 at 463–64.

        Petitioner presented to the emergency department at BARH hospital in a wheelchair on
January 2, 2016, with complaints of “left side facial drooping and left extremity weakness”
beginning one day prior. Pet’r’s Ex. 4 at 33. Although Petitioner was “able to speak and answer
questions[,]” doctors noted that Petitioner had a “left-sided facial droop[,]” left lower extremity
weakness such that she was unable to “raise [her] left leg off [of the] bed[,]” and “[u]nequal hand
grips with [the] left hand weaker[]” than the right.

head CT, which was
negative for stroke, see Pet’r’s Ex. 10 at 483, and doctors diagnosed her with hemiplegia and
slurred speech and transferred her to St. Mary’s Hospital, Pet’r’s Ex. 4 at 35.

        Upon arrival at St. Mary’s hospital, Petitioner continued to have “[l]eft-sided facial
weakness[]” and “[d]ifficulty closing [her] right eye[,]” as well as moderate weakness in both legs
and feet. Pet’r’s Ex. 10 at 403. She related to her treating doctors “that she has had bilateral lower
extremity [sic.] and difficulty walking since [December 29, 2015].”

Doctors wrote that
Petitioner “has never had a finding of neurologic deficiency in either leg.”

“CTA of [her] head and neck[, which] showed no acute infarct[ion].” 26

Doctors also reviewed Petitioner’s previous lumbar spine MRI, which “did not show any
significant disk abnormalities causing central canal stenosis.”

that
Petitioner’s previous head CT did not reveal any “acute bleed.”

The assessment
included “[q]uestionable [transient ischemic attack (“TIA”)] 27 versus Bell’s palsy” and
“[d]ifficulty with ambulation secondary to pain.”

for a neurology
consultation.

n initial consultation with Ijaz Ahmad, M.D., a neurologist, on January 3,

24
   It is unclear what specific complaints compelled Petitioner to present to the emergency department on
this date. See Pet’r’s Ex. 11 at 2–22; see also Pet’r’s Ex. 6 at 463–70.
25
   Oxycodone is “an opioid agonist analgesic derived from morphine.” Dorland’s at 1337.
26
   Infarction is defined as “1. infarct[; or] 2. the formation of an infarct.” Dorland’s at 923. An infarct is
“an area of coagulation necrosis in a tissue due to local ischemia resulting from obstruction of circulation
to the area, most commonly by a thrombus or embolus.”

For a definition of ischemia, see supra
note 11.
27
   A transient ischemic attack is defined as “a brief attack (from a few minutes to an hour) of cerebral
dysfunction of vascular origin, with no persistent neurologic deficit . . . .” Dorland’s at 175.

                                                      8
2016. Pet’r’s Ex. 6 at 328. He wrote that Petitioner’s left-sided facial droop had “resolved.”

examination reveal[ed] normal strength, [but Petitioner] had proximal
weakness in the lower extremities at plus [four]” and was “areflexic in the lower extremities.”

He also wrote that Petitioner’s “[v]ibration [sensation was] moderate[ly] decreased[,]” and
that she “was unable to stand by herself.”

was [w]eakness in the
lower extremities with paresthesia[,]” although he also noted that “[o]ne has to consider acute
inflammatory polyradiculopathy.”

“[a]t this point[, he was] uncertain how
[acute inflammatory polyradiculopathy] is associated with weakness of the lower extremities . . .
.”

if indeed this is an acute inflammatory adenopathy[, then] facial
weakness is not unusual accompanying.”

tests, a NCS, and an EMG study.

day, Petitioner underwent an EMG study, which revealed “marked
asymmetrical prolongation of the distal latencies, particularly of the left median[ and] right ulnar
nerve.”

It also showed “reduced recruitment pattern in all of the muscles tested[,]
which was more pronounced in the proximal muscles of the lower extremities[,]” as well as
“evidence of loss of motor units and evidence of denervation pattern in the lumbar paraspinal
muscles.”

that “[t]hese findings are indicative of asymmetrical
predominantly demyelinating neuropathy[,] which seems to be acute.”

five-day
IVIG treatment, which Petitioner completed on January 9, 2016. See Pet’r’s Ex. 6 at 27–28.

        Petitioner “improved slightly” after the IVIG treatments, although “[s]he initially seemed
to get worse and was a max assist.” Pet’r’s Ex. 10 at 318. However, by January 13, 2016, Petitioner
was a “moderate assist and believe[d] that her legs [were] moving better.”

Petitioner received both PT and occupational therapy (“OT”) daily, see Pet’r’s Ex.
6 at 408–10, but “continued to have a lot of pain difficulties[,]” Pet’r’s Ex. 10 at 318. She also
experienced “significant urinary retention” issues, which doctors treated with a Foley catheter, and
autonomic dysfunction, which doctors believed was “probably related to her neurologic
condition.”

Petitioner was discharged on January 13, 2016, with diagnoses including
“[a]cute [GBS] per Dr. Ahmad[,]” “ambulatory dysfunction[,]” and “chronic back pain – disk
disease on MRI.”

She was transferred to HealthSouth for inpatient rehabilitation.

inpatient PT until February 1, 2016. See Pet’r’s Ex. 7 at 191.
During her stay, Petitioner developed pneumonia, which resolved prior to her discharge. See

Upon discharge, Petitioner’s functional status required “[s]upervision [with] eating and
grooming[, moderate] assistance with bathing[, t]otal assist[ance] with lower extremity dressing[,
and moderate] assist[ance] with toilet transfers.”

to experience urinary
retention issues and remained on a Foley catheter.

2016, Petitioner was readmitted to BARH hospital for a “catheter problem.”
Pet’r’s Ex. 4 at 8. Emergency medical services reported that Petitioner was “having severe lower
abdominal pain due to a possible blocked Foley catheter.”

was normal with no motor or sensory deficits.

Petitioner’s primary
diagnoses were “[u]rinary tract obstruction[,]” “[l]ower urinary tract symptoms[,]” and “[l]ower
urinary tract infectious disease.”

She was prescribed antibiotics and discharged home.

                                                 9
        Petitioner presented to Dr. Kowalkowski for a consultation on February 5, 2016. Pet’r’s
Ex. 5 at 31. Dr. Kowalkowski wrote that Petitioner “was gradually getting strength back in her
lower extremities but is unable to walk on her own yet.”
 Id. at 33. 
He also advised Petitioner to
“start [PT] for lower extremity strengthening[,]” as “[t]he quicker she is able to walk the better her
bladder function is going to be.”
 Id. Dr. Kowalkowski kept 
Petitioner’s Foley catheter in place
and wrote an order for home health care to change it once a month.
 Id.

        Petitioner attended her 
first outpatient PT session on February 16, 2016, at Athletic &
Physical Therapy Services. Pet’r’s Ex. 3 at 1. The physical therapist wrote that there was
“difficulty [with diagnosing GBS] and [Petitioner] was seen by several doctors before finally
having the [diagnosis].”
 Id. Petitioner had “good 
sitting balance but very poor standing balance
and [was a] max assist [on] transfers.”
 Id. She “also need[ed] 
assist[ance] with rolling on [a] table
and [moving from] supine to sitting.”
 Id. Petitioner had full 
ROM in her hips, knees, and ankles,
but had decreased strength in each.
 Id. She was assessed 
as having “[very] weak mid[-]trunk and
hips [but] better with quads and ankles[,]” as well as “severe atrophy of hips and quads.”
 Id. at 2.
The plan was for Petitioner to “be seen in [the] clinic [two-to-three] days a week for [four-to-six]
weeks . . . .”
 Id. Petitioner attended approximately 
eighteen PT sessions through April 6, 2016.
See
 id. at 3–20. 
At her last session, Petitioner showed improved strength and was “able to lower
[herself] from [an] elevated position but [was] not [able] to raise for [sic.] flexed position . . . .”
See
 id. at 20.
        On April 13, 2016, Petitioner underwent a repeat EMG study. Pet’r’s Ex. 10 at 347. The
results revealed “moderate prolongation of distal motor latencies in the upper extremities[ and] . .
. mild-to-moderate prolongation of distal motor latencies on the peroneal nerve.”
 Id. The test also
showed “decreased recruitment pattern, particularly in the lower extremities[,]” and “some
denervation potential in the right vastus medialis and lumbar paraspinal muscles.”
 Id. The
interpretation was 
“further slowing of the conduction velocities as compared to the previous exam
on January 2, 2016. Minimal denervation potentials were seen in the right quadriceps and lumbar
paraspinal muscles.”
 Id.

        Petitioner had a 
follow-up visit with Dr. Ahmad on May 17, 2016. Pet’r’s Ex. 12 at 2.
Petitioner complained of dizziness occurring “since [she was] discharged from [the] hospital.”
 Id.
She described it 
as “intermittent” and occurring “often.”
 Id. Petitioner also noted 
general
weakness that had improved with PT.
 Id. Petitioner complained of 
“episodes when [her] vision
[became] ‘weak’ and she [had] to blink her eyes to focus.”
 Id. On examination, Dr. 
Ahmad noted
“only minimal weakness along the proximal muscles in the lower extremities. Deep tendon
reflexes [(“DTRs”)] are 1+. Plantar responses are flexors. Sensory examination is unremarkable.”

Id. Dr. Ahmad also 
wrote that Petitioner’s dizziness “seems to be [of] peripheral etiology.”
 Id. at
3. 
He advised Petitioner to see an ear, nose, and throat doctor and directed her to follow-up with
him in two-to-three months.
 Id. at 2–3.
       On June 29, 2016, Petitioner was readmitted to BARH hospital for “dizziness” that began
“approximately [three] weeks ago[,]” but had been “intensifying since . . .[six] days prior to
presentation.” Pet’r’s Ex. 13 at 11. Petitioner reported that she had recently been diagnosed with



                                                  10
“benign paroxysmal positional vertigo.” 28
 Id. Petitioner also reported 
“intermittent chest pain
episodes for the past week at rest[]” with “palpitations [that] can last for several minutes in
duration.”
 Id. She described “get[ting] 
dizzy whenever she ben[t] forward to brush her teeth, and
[when she] sits back up and [into a] standing position[, she] becomes very lightheaded.”
 Id. The
doctor also 
wrote that Petitioner should “[a]void flu vaccination as flu vaccination exacerbated
[GBS].”
 Id. at 14. 
Petitioner was admitted for further evaluation.
 Id. at 12. 
She was discharged
on July 1, 2016, with diagnoses including “[d]izziness, vertigo, multifactorial related to allergic
rhinitis[,]” and “[a]typical chest pain in the absence of myocardial infarction, most likely
musculoskeletal in origin.”
 Id. at 26.
        B. Affidavits

            1. Petitioner’s Affidavit

        Petitioner filed her affidavit on December 19, 2017. Pet’r’s Ex. 16. Petitioner explained
that approximately four weeks after receiving the flu vaccination at issue, she “noticed the
emergence of adverse symptoms,” including “malaise that left [her] run-down and tired[]” and “a
tingling sensation in [her] fingers and toes[,]” which “transitioned into general muscle weakness.”

Id. at 1. 
She stated that the “weakness progressed, especially in [her] legs, and resulted in a fall
while at church in late October . . . .”
 Id. After this fall, 
Petitioner wrote that she “fell again a few
days later while at home.”
 Id. She presented to 
her PCP “to figure out and address the[se]
disturbing symptoms[,]” but was discharged without a diagnosis.
 Id.

        Petitioner wrote that 
she presented to the emergency room in “the early days of November
2015[,]” because her “symptoms continued to worsen[] and the pain in [her] hands grew . . .
intolerable . . . .”
 Id. at 2. 
At the emergency room, Petitioner stated that her “blood pressure was
noted to be very high,” a finding that she feels could have been because she “was in a great deal
of pain and discomfort” at that time.
 Id. Petitioner stated that 
“[a]ll the testing they performed on
[her] was unable to reveal a cause for [her] symptoms, so [she] was again discharged home.”
 Id.

        After another couple 
of weeks, Petitioner wrote that she “was back in the emergency
department” because her “symptoms grew even worse.”
 Id. She again noted 
that testing could
not reveal a cause of her symptoms, and after a couple of days, she was discharged home.
 Id.
Petitioner stated that 
“[t]his pattern continued a couple of more times and [she] sought help at the
University of Virginia Hospital on [December 31, 2015] . . . .”
 Id. She explained that 
“[b]y the
time [she] arrived there, [she] could no longer walk at all due to the pain and weakness in [her]
legs.”
 Id.

         On January 2, 
2016, Petitioner stated that she returned to BARH hospital because her “pain
. . . had progressed to the point of being unbearable,” and she was suffering from “weakness in
[her] arms and legs, and a drooping mouth.”
 Id. Petitioner explained that 
she was transferred to
St. Mary’s Hospital “once the emergency doctors agreed that [her] symptoms seemed to have a
neuropathic aspect.”
 Id. Petitioner noted that 
“a lumbar puncture . . . led Dr. Ahmed to determine

28
   Petitioner reported that she had been diagnosed with this condition by a “Dr. Payne.” Pet’r’s Ex. 13 at
11. However, it is unclear when this diagnosis was made or where this diagnosis is located in Petitioner’s
filed medical records.

                                                   11
that [she] had been suffering from [GBS],” and she was “started on treatments and . . . stayed at
St. Mary’s for two weeks.”
 Id.

        After her discharge 
from St. Mary’s Hospital, Petitioner wrote that she was transferred to
inpatient rehabilitation at HealthSouth, which “last[ed fifteen] hours a day and extend[ed] through
the end of February 2016.”
 Id. at 3. 
Despite noting that she “made very little progress” during her
inpatient stay, Petitioner stated that she “had to leave the hospital . . . to return home.”
 Id. Upon
discharge, Petitioner 
wrote that she “was an emotional wreck[]” because she left rehab “with deep
fear and depression with the realization that [she] might never walk again, that [she] would need
[twenty-four]-hour care, and that [she] would remain unable to hear the world around [her].” 29
 Id.

       Petitioner explained that
, “[t]hroughout the period from early December [2015] through
early March [2016], the pain was so unbearable that Oxycontin was insufficient to give [her]
comfort.”
 Id. In addition, she 
noted that “[t]he urinary catheter brought on an infection for which
[she] needed antibiotics, but which became recurrent and even more painful over time.”
 Id.
During this period, 
Petitioner wrote that she “was crying daily and really struggling with
depression.”
 Id. Also, during this 
time period, Petitioner stated that she “was thoroughly disabled
and living at home, [so her] daughter Maria and [her] oldest son Frank were [her] primary
caregivers and . . . did everything for [her] . . . .”
 Id.

        In late March 
of 2016, Petitioner stated that her “condition finally started to improve
somewhat . . ., but certainly did not resolve.”
 Id. She wrote that 
the “[urinary tract infections
(“UTIs”)] would not go away, and [she] developed an[] allergic response to the antibiotics [she]
was prescribed to treat it.”
 Id. In addition, she 
stated that the “urologist conditioned [the] removal
of the extremely uncomfortable catheter upon [her] being able to walk . . . .”
 Id. Petitioner wrote
that 
she only “had to return to the hospital . . . to receive intravenous antibiotics.”
 Id.

        Petitioner stated that 
she “regained the ability to stand in late April 2016.”
 Id. at 4. 
She
also noted that her “pain was becoming manageable if not tolerable” at this time as well.
 Id.
Petitioner stated that 
she “began to relearn how to walk” and had the catheter removed in early
May 2016.
 Id. However, she wrote 
that “[i]t was late August [2016] before [she] was able to walk
unassisted, albeit quite slowly.”
 Id. She concluded her 
affidavit by noting that “[t]he entire affair
has been a constant traumatic experience[].”
 

. 
Affidavit of Maria Fly

        Petitioner also submitted an affidavit from her daughter, Maria Fly, on December 19, 2017.
Pet’r’s Ex. 17. Ms. Fly stated that “[a]bout one week after [Petitioner was] administered a flu
vaccination . . ., [Petitioner] began to complain that she felt funny[ and that] she did not feel right.”

Id. at 1. 
Ms. Fly noted that she and her siblings “at first dismissed [Petitioner’s] complaints[]”
because Petitioner “could not pinpoint the exact nature of what she was feeling . . . .”
 Id. Ms. Fly
further 
noted that she and her siblings “had always understood that the flu shot can cause flu-like
symptoms . . . .”
 Id. However, Ms. Fly 
explained that “[o]ver the weeks that followed, . . .
[Petitioner] began expressing more specific complaints of pain in her back, her hands, and her feet,
29
  Petitioner also stated that “the staff at the rehab hospital lost [her] hearing aids and they were never
found.” Pet’r’s Ex. 16 at 3.

                                                   12
which became progressively worse.”
 Id. Ms. Fly recounted 
the “prolonged process of bringing
[Petitioner] to the doctors for diagnosis and treatment, only to be sent away without answers.”
 Id.
She noted that 
“[s]oon [Petitioner’s] pain was joined by numbness and tingling in her hands and
feet that was so uncomfortable that she could not rest.”
 Id. Ms. Fly wrote 
that this pain “was also
putting stress on [Petitioner’s] body, elevating her blood pressure to dangerous levels . . . .”
 Id.
Ms. Fly also 
noted that Petitioner’s “pain at night was horrific[] and stole her sleep from her.”
 Id.
at 2. 
Ms. Fly wrote that she has “videos of [Petitioner] rolling and thrashing in an attempt to relieve
her pain and try to sleep.”
 Id. Ms. Fly also 
explained that “[t]here were many instances where
[Petitioner] would not sleep for more than [thirty] minutes all night, and only catch a [fifteen]
minute nap during the day . . . .”
 Id.

         On December 27, 
2015, Ms. Fly stated that Petitioner “fell while attending church[,]” and
in light of her previous symptoms, Ms. Fly and her brother “decided to take [Petitioner] to the
University of Virginia hospital a few days later.”
 Id. However, Ms. Fly 
stated that the doctors
“had the same ineffectual response to [Petitioner’s] extreme condition, except to guess about
arthritis in [Petitioner’s] back.”
 Id. Ms. Fly recounted 
that Petitioner was discharged home “with
highly elevated blood pressure and no relief from her pain and sensory discomfort.”
 Id.

        Ms. Fly continued 
that on January 2, 2016, she and her brother “took breakfast to
[Petitioner’s] house” where Ms. Fly “first noticed a severe droop affecting the entire right side of
[Petitioner’s] face.”
 Id. Ms. Fly also 
noted that Petitioner “had very little control over the opening
and closing of her eyelid, and her mouth drooped so much[ that] she was drooling noticeably.”
 Id.
In addition, Ms. 
Fly recounted that Petitioner “could not walk at all.”
 Id. Because of Petitioner’s
condition, Ms. Fly and her brother “rushed [Petitioner] to [the] local emergency room . . . .”
 Id.
After doctors transferred 
Petitioner to St. Mary’s Hospital, Ms. Fly noted that Petitioner was
diagnosed with GBS and “began an eleven-day stay at the hospital.”
 Id. During this time, 
Ms. Fly
stated that Petitioner “could not walk and . . . was heavily medicated in an effort to ease her pain
and lower her dangerously elevated blood pressure.”
 Id. Ms. Fly stated 
that she remained in the
hospital with Petitioner “around the clock” for a majority of Petitioner’s time at St. Mary’s
Hospital.
 Id. at 3.
        After Petitioner’s inpatient rehabilitation, Ms. Fly stated that Petitioner’s “body had
become so weak that she could not walk or stand, and her bladder was not working properly,
requiring that she wear a continuous catheter.”
 Id. Ms. Fly recounted 
that Petitioner’s weakness
was so profound that Ms. Fly or her brother “had to pick [Petitioner] up to move her from one
place to another.”
 Id. Ms. Fly noted 
that Petitioner’s “sensory problems in her hands[]” made it
so that she “could barely grasp anything and could not hold onto anything . . . .”
 Id. Therefore,
Ms. Fly 
“got [Petitioner] a children’s ‘fat-handle’ spoon and fork set so she could try and feed
herself.”
 Id. Ms. Fly explained 
that, “from February into March of 2016,” she “was the one
primarily responsible for [Petitioner’s] personal care and for cooking [Petitioner’s] meals” because
Petitioner “was reduced to an invalid.”
 Id.

        Ms. Fly also 
stated that, once Petitioner was home from inpatient rehabilitation, “a home-
health therapist came to her house at first, but soon determined that [Petitioner] needed to attend
outpatient [PT] so she could use the exercise machines to strengthen her atrophied muscles, which
she began to do about three weeks after returning home.”
 Id. These PT sessions 
“were an hour or

                                                  13
more long, and typically convened three times a week.”
 Id. at 3.
        Ms. Fly also discussed Petitioner’s catheter and UTIs, which Ms. Fly described as “a source
of pain for [Petitioner] and stress for all of [Petitioner’s family].”
 Id. at 4. 
Ms. Fly explained that
“[w]henever [she] took [Petitioner] outside, [Ms. Fly] had to change [Petitioner’s] catheter bag to
a travel-sized bag.”
 Id. Ms. Fly also 
noted that Petitioner eventually required intravenous
antibiotics to treat her recurrent UTIs, which required hospitalization.
 Id. Even after the 
catheter
was removed, Ms. Fly stated that Petitioner “had to retrain her bladder[]” and “began wearing
adult diapers and still does today.”
 Id.

              3. 
Affidavit of Frank Conte

        Petitioner submitted a third affidavit, from her son, Frank Conte, on December 19, 2017.
Pet’r’s Ex. 18. Mr. Conte stated that he “noticed several days following [Petitioner’s flu]
vaccination . . . that she was just not herself.”
 Id. at 1. 
Specifically, he wrote that Petitioner “began
to complain of pain in her hands, back, and feet[,]” which “was soon disturbing her sleep.”
 Id.
Mr. Conte recounted 
that Petitioner “would pace through the house looking for a place to lie down
and get comfortable despite her discomfort and pain.”
 Id.

        Mr. Conte noted 
that he and his sister “brought [Petitioner] to doctors and the hospital on
several occasions, but they could not discover the cause of her problems,” all “while her pain
became unbearable for her . . . .”
 Id. In addition to 
her pain, Mr. Conte stated that Petitioner
experienced “weakness and instability, and . . . she fell a couple of times . . . .”
 Id. Mr. Conte
noted 
that, once Petitioner “developed the facial palsy[,] . . . she was seen by a neurologist” and
diagnosed with GBS.
 Id. at 2. 
However, Mr. Conte explained that by the time of diagnosis,
Petitioner “could not walk, and she could hardly use her hands at all. She was in constant, extreme
pain.”
 Id. Mr. Conte further 
noted that, “[a]fter eleven days at St. Mary’s Hospital and seventeen
days at HealthSouth [inpatient rehabilitation, Petitioner] was discharged home, but . . . [still] could
not walk or stand, and could barely hold utensils to eat.”
 Id.

        While Petitioner was 
recovering at her home, Mr. Conte stated that he “had to do
everything she needed done, whether to lift her onto the toilet, help her with other hygiene, to
administer her medications, and to help her dress.”
 Id. In addition, Mr. 
Conte explained that he
“carried [Petitioner] into and out of the car for all of her many medical appointments in the months
after hospital discharge.”
 Id. Mr. Conte also 
stated that he “became responsible to do all grocery
shopping, cleaning, laundry and related chores[]” for Petitioner during this time period.
 Id. He
concluded by 
explaining that, while Petitioner “did slowly improve and regain some strength[,]”
he nonetheless “still bear[s] most of the responsibilities around the house.”
 Id. at 3.
    III.      Experts

           A. Expert Qualifications

              1. Petitioner’s Expert, Zurab Nadareishvili, M.D., Ph.D.

           Dr. Nadareishvili received his medical and doctoral degrees from the Tbilisi State Medical

                                                   14
Institute in Tbilisi, Republic of Georgia in 1984 and 1991, respectively. Pet’r’s Ex. 20 at 1. He is
board certified in neurology and vascular neurology and is licensed to practice medicine in
Maryland and the District of Columbia.
 Id. at 2. 
He currently serves as the Medical Director of
the National Institute of Health (“NIH”) Stroke Program and the Chair of the Subsection of
Neurology, Department of Medicine at Suburban Hospital, which is part of Johns Hopkins
Medicine in Bethesda, Maryland.
 Id. at 1. 
He also serves as a faculty member in the Vascular
Neurology Clinical Fellowship program at the National Institute of Neurological Disorders and
Strokes within the NIH in Bethesda, Maryland, and as an Associate Clinical Professor of
Neurology at the George Washington University School of Medicine and Health in Washington,
D.C.
 Id. His curriculum vitae 
lists twenty-eight peer-reviewed articles of which he is a listed
author, as well as one book chapter and forty-one abstracts. See
 id. at 10–17. 
Dr. Nadareishvili
submitted three expert reports in this case. See Pet’r’s Exs. 19, 38, 44.

           2. Respondent’s Expert, Vinay Chaudry, M.D.

         Dr. Chaudry received his Bachelor of Medicine and Bachelor of Surgery from the All India
Institute of Medical Sciences in New Delhi, India, in 1980. Resp’t’s Ex. B at 2. He currently
serves as a Professor of Neurology at Johns Hopkins University School of Medicine and as the
Director of the EMG Laboratory at Johns Hopkins Hospital. Resp’t’s Ex. A at 1. He holds board
certifications in neurology, neuromuscular diseases, electrodiagnostic medicine—specifically in
NCSs and EMGs—and clinical neurophysiology. Id.; see also Resp’t’s Ex. B at 36. He wrote in
his first expert report that he has “an active clinical practice” where he “evaluate[s] 2,000 patients
a year[,] mostly related to peripheral nerve disease.” Resp’t’s Ex. A at 1. His curriculum vitae
lists over one hundred and fifty peer-reviewed articles, book chapters, and other publications of
which he is a listed author. See Resp’t’s Ex. B at 3–14. Dr. Chaudry submitted three expert reports
in this case. See Resp’t’s Exs. A, D, L.

       B. Expert Reports

           1. Dr. Nadareishvili’s Expert Reports

        In his first expert report, Dr. Nadareishvili described GBS as “a life-threatening, acute,
monophasic, autoimmune, peripheral neuropathy.” Pet’r’s Ex. 19 at 8. He noted that, “in its
classic form[, GBS] presents as a clinical syndrome of progressive, ascending numbness,
weakness, and (potentially) paralysis, affecting the lower extremity primarily, but often affecting
the upper extremity and, in severe cases, affecting the sensory and motor nerves of the torso.”
 Id.
Dr. Nadareishvili wrote 
that, “[w]ithin North America, [GBS] is typically understood to result
from [a]cute [i]nflammatory [d]emyelinating [p]olyneuropathy . . . (“AIDP”), in which an
immune-mediated process causes damage to the myelin sheathing of the peripheral nerves at or
near their root junctions . . ., and can result in damage to the nerve axons themselves.”
 Id. He also
noted 
that, “[w]hile the hallmark of the syndrome is that it is monophasic, the recovery curve . . .
is variable, leaving some with more complete recoveries and others with very significant residual
deficits.”
 Id.




                                                 15
         Along with his first expert report, Dr. Nadareishvili submitted a paper by Willison et al.,
in which the authors provide a more detailed discussion of GBS. See Pet’r’s Ex. 33. 30,31 They
state that “[GBS] is usually preceded by infection or other immune stimulation that induces an
aberrant autoimmune response targeting peripheral nerves and their spinal roots.”
 Id. at 1. 
In the
AIDP form of GBS, the “immune injury specifically takes place at the myelin sheath and related
Schwann-cell components . . . .”
 Id. at 3. 
Clinically, the authors note that “rapidly progressive
bilateral weakness is the key presenting symptom in most patients.”
 Id. at 5. 
This weakness is
“classically described as ascending, and usually starts in the distal lower extremities, but can start
more proximally in the legs or arms.”
 Id. They note that 
patients may also initially experience
“sensory signs, ataxia, and features of autonomic dysfunction.”
 Id. The authors also 
wrote that
“[m]uscle pain or radicular pain, often but not always in the spinal region, is another frequent
initial sign, which can complicate the diagnosis because pain can proceed weakness in about a
third of patients.”
 Id. They explain that 
“[m]ost patients . . . reach the nadir [of weakness] within
[two] weeks[,]” although “[p]rogression can last up to [six] weeks after onset (subacute [GBS]) in
some rare cases.”
 Id. In terms of 
patient outcomes, the authors state that “[t]he severity and
duration of the disease is highly diverse in patients and can range from mild weakness . . . to
patients becoming quadriplegic and ventilator dependent . . . .”
 Id. They also note
, however, that
“all patients start improving [eventually], although recovery could follow a protracted course and
result in severe, permanent disability.”
 Id.

         The authors of 
the Willison et al. paper also provide a panel in which they list the diagnostic
criteria for GBS.
 Id. The authors list 
“[p]rogressive weakness in [the] legs and arms (sometimes
initially only in the legs)” and “[a]reflexia (or decreased tendon reflexes in weak limbs)” as the
two “[f]eatures needed for diagnosis of [GBS] in clinical practice[.]”
 Id. They also note 
that NCSs
“[c]an be helpful in clinical practice, but are generally not required to diagnose [GBS].”
 Id.

       Dr. Nadareishvili then 
wrote that the “[s]tructural similarities between microbial and self-
peptides can result in the activation of autoreactive T cells[, which] has been referred to as
‘molecular mimicry.’” Pet’r’s Ex. 19 at 8–9. He explained that “[i]n a classical molecular mimicry
scenario, antibodies cross-react directly with viral and cellular proteins . . . .”
 Id. at 9. 
He further
explained that “[t]he causative process for this inflammatory destruction of the myelin on the
peripheral nerves is most commonly described as being initiated by cross-reactivity of certain
immune cells, from an initial immunologic response to an immune challenge . . ., and transferring
to inadvertent immune reaction against self cells.”
 Id. at 8. 
He listed “a virus, a bacterium, or a
vaccine” as examples of an immune challenge that could trigger this inflammatory process.
 Id.

         However, Dr. Nadareishvili 
also wrote that “[m]olecular mimicry is but one of several
potential mechanisms by which an auto-immune [sic.] reaction to a foreign antigen can ultimately
result in nerve demyelination.”
 Id. at 9. 
He explained that “there is also a well-established model
of T-cell activation to cross-reaction against myelin basic protein[,]” which could “damage nearby
cells, leading to collaterally damaging effects to cell structures, both by release of cytokines and
by macrophage activation.”
 Id. He also discussed 
the “fertile field model,” whereby “activation
of an immune response by an immunogen with sequence homology to self proteins may prime
autoreactive T-cells in the host, but might lack the momentum to initiate an adverse auto-immune
30
     Hugh J. Willison et al., Guillain-Barré Syndrome, 388 LANCET 717 (2016).
31
     Respondent also filed this article in support of Dr. Chaudry’s second expert report. See Resp’t’s Ex. G.

                                                      16
[sic.] reaction independently.”
 Id. He continued, “[h]owever, 
a later immune stimulation or
coincidental immune stimulation event by a vaccine or other immunogen, even one without cross-
reactive antigens or sequence similarity, could initiate an autoimmune reaction in a susceptible
host that could lead to inflammatory demyelination.”
 Id. He also briefly 
discussed bystander
activation, noting that “[c]omponents of the vaccine could facilitate aberrant immune responses
against self-antigens by binding to specific stimulating receptors to hyperactivate immune cells to
overcome self-tolerance . . . .”
 Id. at 11–12.
        In his first expert report, Dr. Nadareishvili opined that GBS can be caused by vaccination
via molecular mimicry.
 Id. at 9. 
He argued that “[i]t is well established that vaccines interact with
[the] innate and adaptive immune system[s] to boost reactivation of memory B cells generated
during primary vaccination.”
 Id. at 11. 
He explained that this interaction “is characterized by the
rapid increase of higher titers of antibodies that will have a higher affinity for the target antigen(s)
than those antibodies generated during primary vaccination to establish or boost vaccine specific
immunity.”
 Id. He then articulated 
how a vaccine could spur molecular mimicry: “the inactivated
vaccines are taken up by antigen processing cells, which then breakdown the component proteins
into small peptides prior to presentation to B and T lymphocytes.”
 Id.

        Dr. Nadareishvili argued 
that “[a]ll objective, diagnostic evidence in [Petitioner’s] medical
record supports . . . the diagnosis of AIDP-GBS over and above any other potential diagnosis.”
 Id.
at 13. 
He noted that any “competing diagnoses . . . were abandoned by most of [Petitioner’s]
treating physicians once objective evidence confirmed” this diagnosis in January 2016.
 Id. In
addition, he 
wrote that Petitioner’s course was “monophasic, without any fluctuating pattern that
would suggest chronic inflammatory demyelinating polyneuropathy [(“CIDP”)].”
 Id. at 13–14.
        Dr. Nadareishvili disagreed with Respondent’s contention that Petitioner’s first
manifestation of symptoms occurred in late December 2016.
 Id. at 14; 
see also Resp’t’s Report at
11. He instead noted that “lower extremity neuropathy . . . was present at least as early as
[Petitioner’s] first visit to the orthopedist, Dr. Whitfield, on December 1, 2015.” Pet’r’s Ex. 19 at
14 (citing Pet’r’s Ex. 9 at 5).

        In addition, Dr. Nadareishvili disagreed with Respondent’s argument that Petitioner’s
“symptoms and complaints within the three to forty-two[-]day period post-vaccination were
clearly attributed by her doctors to CTS and her pre[-]existing hypertension and chronic back
pain.” See
 id. at 14–15 
(quoting Resp’t’s Report at 12). Dr. Nadareishvili described CTS as
“typically a chronic condition associated with repetitive use that progresses over time, and it is
usually asymmetric in presentation, dependent on which hand is used more in the manner that
aggravates the nerve.”
 Id. at 15. 
He wrote that CTS does not “typically involve[] . . . the ulnar
nerve.”
 Id. He also wrote 
that, in severe cases of CTS, there is an “expect[ation] of a limitation
in wrist mobility due to inflammation of the connective tissues . . . .”
 Id.

         Dr. Nadareishvili argued 
that Petitioner did not fit the “clinical presentation” of CTS.
 Id.
He began this 
discussion by noting that Petitioner “suffered a rather abrupt onset of sharp pain that
was bilateral, and nearly symmetric in distribution between her hands.”
 Id. Because Petitioner is
retired, Dr. Nadareishvili found it “difficult to imagine that [Petitioner] would be performing some
new movement that would cause such an acute flare up of nerve pain . . . .”
 Id. He also wrote 
that

                                                  17
“there was no evidence that [Petitioner’s] wrist mobility was affected[,]” and the wrist splints
prescribed by Dr. Whitfield, “a typical and effective treatment for [CTS,] had no effect in
alleviating [Petitioner’s] symptoms . . . .”
 Id. In addition, Dr. 
Nadareishvili noted that Petitioner’s
EMG results “showed involvement of both the median and ulnar nerves of the hand[,]” a finding
which Dr. Nadareishvili believed was “glossed over in service to confirming the CTS diagnosis
for which [Petitioner] was referred.”
 Id. at 15–16. 
He continued, “[t]he testing is clear that
[Petitioner’s] neuropathy was severe, which would be quite unexpected with a chronic condition
like [CTS].”
 Id. at 16. 
Dr. Nadareishvili noted that Dr. Ahmad, Petitioner’s neurologist who made
the GBS diagnosis, “did not support [a] diagnosis of [CTS,]” noting that “[e]ven in follow-up
appointments . . ., [Dr. Ahmad] never mentioned” a CTS diagnosis.
 Id.

        Rather, Dr. Nadareishvili 
believed that, “taken together, [Petitioner’s] symptoms show a
progressive course of immune-mediated neuropathy.”
 Id. at 19. 
He discussed four symptoms that
he described as diagnostic of GBS. First, he noted that the “first reference to . . . pain and
paresthesias in [Petitioner’s] lower extremities was in Dr. Whitfield’s notes following
[Petitioner’s] December 1, 2015 initial visit . . . .”
 Id. at 16. 
He opined that “[t]his finding would
be characteristic of [GBS] . . . .”
 Id. at 16–17. 
Second, Dr. Nadareishvili noted that Petitioner’s
“lower extremity weakness, . . . reduced grip strength, and . . . facial drooping are all clearly
manifestations of [GBS] . . . .”
 Id. at 19.
        Third, Dr. Nadareishvili discussed “the torsional pain, which [Petitioner] consistently
reported, even if [doctors] inconsistently described and diagnosed.”
 Id. at 17. 
He noted that
Petitioner first complained of this pain on November 2, 2015, when she “reported . . . chest pain
that radiated to [her] back[ that] was severe enough to wake her from sleep.”
 Id. Doctors “sent
[Petitioner] 
home with recommendations for treatment of hypertension.”
 Id. Dr. Nadareishvili
then 
briefly reviewed the numerous visits Petitioner had for torsional pain over the course of the
next month, including a visit with Dr. Whitfield on December 1, 2015, during which Dr. Whitfield
“presume[d] a compression fracture must be the cause.”
 Id. at 17–18. 
Dr. Nadareishvili argued
that Petitioner’s complaints “do not conform to an orthopedic, spinal, or cardiac explanation, and,
indeed, no objective evidence exists in the record to support these as the source of [Petitioner’s]
pain.”
 Id. at 18. 
Instead, Dr. Nadareishvili believed that they are “much more consistent with
widespread, polyneuropathic pain, as the pain would be more locally limited if it arose from a
spinal injury or cardiac condition.”
 Id. He noted that 
“there are case reports and general
acceptance of thoracic, abdominal, and back pain as acceptable (albeit atypical) presenting
symptoms for [GBS].”
 Id. He continued, “[t]he 
pain in and around the back in particular
represents the ongoing radiculopathic process of AIDP, which typically presents with distal
symptomatology even when the neuropathy is more proximal to the spinal cord.”
 Id. He also cited
to medical articles accompanying his first report to support the proposition that there are “GBS
cases which presented first with pain in the torso[,] more typically in the lower back, but also in
the abdomen and upper back.”
 Id.

        Dr. Nadareishvili submitted 
a case report by Wong et al., where the authors “report a [GBS]
case in which abdominal pain was the patient’s initial symptom and her main complaint.” Pet’r’s
Ex. 34 at 1. 32 The authors noted that the patient, a nineteen-year-old woman, presented with “a
32
     P.S. Wong et al., Abdominal Pain as a Presenting Symptom of the Guillain-Barré Syndrome, 5 ARCHIVES
OF EMERGENCY MED.         242 (1988).

                                                    18
[three]-week history of stabbing pains in the right side of her abdomen.”
 Id. The patient described
the pain as “last[ing] for minutes or several hours, occur[ring] once every [two] days[,] and
sometimes woke her up from sleep.”
 Id. The patient also 
related that “[t]he pains were relieved
by moving about.”
 Id. Three days before 
the patient presented to the hospital, “she noticed similar
shooting pains in both legs and some weakness when walking upstairs,” and “[o]n the day of
admission, she fell to the floor when she tried to get out of bed.”
 Id. When she arrived 
at the
hospital, she stated that “her legs felt weak and painful but the abdominal pain was the symptom
which she emphasized (in spite of her weakness).”
 Id. at 2. 
On exam, the patient had “absent
[tendon reflexes] in the legs but with reinforcement there was a patchy preservation in the arms[,]”
and “the patient was not able to walk unaided.”
 Id. The patient was 
ultimately diagnosed with
GBS after an EMG study.
 Id. The only conclusion 
the authors make in the case report is that “[i]t
is . . . important to diagnose [GBS] early[,]” and they expressed a desire to “draw attention to
abdominal pain being a presenting symptom[]” of GBS.
 Id. at 3.
         Fourth, Dr. Nadareishvili “believe[s] that [Petitioner] was experiencing autonomic
dysfunction as a part of her onset of [GBS].”
 Id. at 18. 
He noted that Petitioner “did not have a
history of autonomic dysfunction prior to her vaccination . . . .”
 Id. However, Petitioner developed
“uncontrolled hypertension that resulted in syncopal episodes” as well as “urinary retention” post
vaccination.
 Id. at 18–19. 
Dr. Nadareishvili argued that “[a]utonomic dysregulation and
dysfunction can certainly signal the onset of [GBS].”
 Id. at 19. 
Along with his first expert report,
Dr. Nadareishvili submitted a case report by Ferraro-herrera et al., which documents a sixty-one-
year-old male GBS patient whose presenting symptom was hypertension. Pet’r’s Ex. 36 at 1. The
patient had “a history of mild hypertension” and “was admitted to the coronary care unit because
of three episodes of chest pain while at rest and bifrontal headache.”
 Id. He “also reported 
poorly
controlled blood pressure . . . for a few days prior to admission.”
 Id. The patient had 
a normal
initial evaluation with a normal neurological examination.
 Id. However, on “the 
second day after
admission, the patient began to develop progressive gait ataxia followed by the onset of bilateral
proximal lower extremity weakness, areflexia, and numbness on the palms and soles of his feet.”

Id. He was diagnosed 
with GBS based on a cerebral spinal fluid (“CSF”) study.
 Id. The authors
state 
that “[h]ypertension occurs in [sixty percent] to [seventy percent] of patients with GBS.”
 Id.
at 2. 
They also note that “[c]ardiovascular dysautonomy is often present in patients with extensive
motor involvement, and may be present both during the late progressive phase of the disease and
during the plateau phase.”
 Id. The authors do 
not draw any conclusions, however, regarding
hypertension as a presenting symptom of GBS, noting only that “[p]atients with new
cardiovascular symptomology should be followed for any subsequent changes in their neurological
examination that are suggestive of GBS.”
 Id.

        Dr. Nadareishvili conceded 
that Petitioner’s “progression of symptoms falls outside the
normative standards accepted by the [Vaccine Injury] Table criteria” for GBS. Pet’r’s Ex. 19 at
19. However, he nonetheless had “no trouble describing [Petitioner’s] syndrome as [AIDP]
presenting clinically as [GBS].”
 Id. He wrote that 
his “analysis is affected somewhat by the level
of care [Petitioner] was given[,]” arguing that if Petitioner’s “symptoms had been recognized as
immune-mediated polyneuropathy prior to January 2016,” then Petitioner would have received
IVIG treatment and her course would have begun to reverse, and therefore timing “would not even
be an issue to dispute . . . .”
 Id. at 20.



                                                19
        With his second expert report, Dr. Nadareishvili submitted a paper by Oh et al., in which
the authors discuss “subacute inflammatory demyelinating polyneuropathy (“SIDP”) and . . .
present the diagnostic criteria for this disease.” Pet’r’s Ex. 39 at 1. 33 The authors coined this term
for patients that fell outside of either the GBS or CIDP timing criteria; i.e. “cases [that] had
progression of peripheral neuropathy over a [four]-to-[eight] week period . . . .”
 Id. at 4. 
The
authors recommended that the following four criteria be used when making a “definite” SIDP
diagnosis:

          The diagnosis of “definite SIDP” was made when all four of the following
          mandatory criteria were met: 1) progressive motor and/or sensory dysfunction
          consistent with neuropathy in more than one limb with time to nadir between [four]
          and [eight] weeks, 2) electrophysiologic evidence of demyelination in at least two
          nerves, 3) no known etiology of neuropathy other than associated diseases, and 4)
          no relapse on adequate follow-up.


Id. Dr. Nadareishvili did 
not assert in any of his expert reports that Petitioner suffered from SIDP.

        Dr. Nadareishvili also argued that “the record is clear of infectious causes that would
explain [Petitioner’s] injury to the exclusion of the vaccination.” Pet’r’s Ex. 19 at 20. He opined
that the vaccination “stands in isolation as the only immune stimulus that would explain an
immune-mediated neuropathic process[,]” and that it “was the only antigenic insult for which there
is evidence in the medical record throughout September, October, November, or December of
2015.”
 Id. While he concedes 
that there was a “suspicion of a urinary tract infection,” Dr.
Nadareishvili wrote that “there was no clinical symptoms associated to corroborate an infection,
and no objective evidence from ultrasound to support it either.”
 Id. He also noted 
that Petitioner
“denied fever, gastrointestinal symptoms, or symptoms of respiratory infection[]” at every
appointment during the relevant time period.
 Id. Therefore, he argued 
that the “vaccination[]
stands alone as the only potential causal factor for” Petitioner’s GBS.

              2. Dr. Chaudry’s Expert Reports

        Dr. Chaudry wrote that he “agree[s] with Dr. Nadareishvili that [Petitioner] likely suffered
from GBS, but [he] disagrees with [Dr. Nadareishvili] that the onset of GBS was within [forty-
two] days from the date of vaccination or that [Petitioner’s] GBS was caused by the [flu]
vaccination.” Resp’t’s Ex. A at 8. He argued that the onset of Petitioner’s GBS was “a day or a
few days before [January 1, 2016].”
 Id. at 12. 
He continued, “[t]his would be approximately three
months after the [flu] vaccination, which is not an appropriate temporal relationship for
[establishing] a causal connection.”
 Id. Rather, Dr. Chaudry 
“agree[s] with [Petitioner’s] treating
physicians that her intervening symptoms were related to [CTS], severe bilateral knee arthritis,
and long standing back issues.”
 Id.

       In his first 
expert report, Dr. Chaudry disagreed with many of Dr. Nadareishvili’s
contentions regarding the timeline of Petitioner’s symptom development. As an initial matter, Dr.
Chaudry argued that Petitioner was symptomatic prior to receiving the flu vaccination on
September 30, 2015.
 Id. at 8. 
He cited to a visit Petitioner had with Dr. Whitfield on July 23,
33
     S.J. Oh et al., Subacute Inflammatory Demyelinating Polyneuropathy, 61 NEUROLOGY 1507 (2003).

                                                  20
2015, where she reported “difficulty going up and down stairs as well as difficulty rising from a
seated position[,]” as evidence that Petitioner was symptomatic prior to vaccination.
 Id. (citing
Pet’r’s Ex. 
9 at 12). Dr. Chaudry also noted that Dr. Whitfield “documented severe patellofemoral
arthritis of [Petitioner’s] bilateral knees[,] which were being treated with injections[]” prior to
vaccination.
 Id. In addition, Dr. 
Chaudry wrote that, on the day of vaccination, Petitioner “not
only endorsed a long history of low back pain . . . but also noted that this ‘was a little bit more
frequent lately.’”
 Id. (quoting Pet’r’s Ex. 
10 at 42).

         Dr. Chaudry argued that Petitioner suffered from CTS after receiving the flu vaccination
on September 30, 2015. He submitted an article by Ibrahim et al., which defined CTS as “a
compressive neuropathy,” or “a mononeuropathy or radiculopathy caused by mechanical
distortion produced by a compressive force.” Resp’t’s Ex. C at 1. 34 The authors explained that
the “[p]rimary features of CTS include pain in the hand, unpleasant tingling, pain or numbness in
the distal distribution of the median nerve (thumb, index, middle finger[,] and the radial side of
the ring finger), and a reduction of the grip strength and function of the affected hand.”
 Id. at 2.
They also noted that CTS “[s]ymptoms tend to be worse at night,” and that many CTS patients
“describe a phenomenon termed the ‘flick sign’, in which shaking or flicking their wrists relieves
symptoms.”
 Id. In terms of 
treatment, the authors noted that options fall into two categories:
“conservative and surgical.”
 Id. at 6. 
They listed “oral and transvenous steroids, corticosteroids,
. . . carpal bone mobilisation [sic.] and the use of hand splints[]” as conservative options, and
explained that patients using these options tend “to experience[] significant short term benefits,”
although “their efficacy in the long term remains unclear.”
 Id.

        The authors of 
this study also discussed how CTS is diagnosed.
 Id. at 4–6. 
They wrote
that a NCS “is considered to be the gold standard in the diagnosis of CTS[] because it is an
objective test that provides information on the physiological health of the median nerve across the
carpal tunnel.”
 Id. at 5. 
They explained that, during a NCS, a technician “compar[es] the latency
and amplitude of a median nerve segment across the carpal tunnel to another nerve segment that
does not go through the carpal tunnel, such as the radial or ulnar nerve.”
 Id. Then, the nerve 
is
stimulated by a transcutaneous pulse of electricity, which induces an action potential in the
nerve[,]” and “[a] recording electrode . . . detects the wave of depolarization as it passes by the
surface electrode.”
 Id. They noted that 
this type of NCS “is the most sensitive and accurate
technique, with a sensitivity 35 of [eighty]–[ninety-two percent] and specificity 36 of [eighty]–
[ninety-nine percent].”
 Id. The authors also 
discussed Phalen’s and Tinsel’s tests, which they
described as “[t]he two provocative tests most commonly used in the clinical setting . . . .”
 Id. at
4. 
They explained that, in a Phalen’s test, “the patient is asked to flex their wrist and keep it in
that position for [sixty] seconds. A positive response is if it leads to pain or paresthesia in the
distribution of the median nerve.”
 Id. They noted that 
the Phalen’s test has sensitivity “in the

34
   I. Ibrahin et al., Carpal Tunnel Syndrome: A Review of the Recent Literature, 6 (Supp. 1: M8) OPEN
ORTHOPEDICS J. 69 (2012).
35
   Sensitivity refers to “the conditional probability that a person having will be correctly identified by a
clinical test, i.e., the number of true-positive results divided by the total number with the disease . . . .”
Dorland’s at 1664.
36
   Specificity refers to “the conditional probability that a person not having a disease will be correctly
identified by a clinical test, i.e., the number of true-negative results divided by the total number of those
without the disease . . . .” Dorland’s at 1714.

                                                     21
range of [sixty-seven percent–eighty-three percent],” and a specificity that “ranges between [forty
percent–ninety-eight percent].”
 Id. The authors further 
explained that a Tinsel’s test “is performed
by tapping over the volar surface of the wrist. A positive response [occurs when] this causes
paresthesia in the fingers innervated by the median nerve: the thumb, index, middle finger and the
radial side of the ring finger.”
 Id. They noted that 
the Tinsel’s test “has a sensitivity in the range
of [forty-eight percent–seventy-three percent],” and a specificity in the range of “[thirty percent–
ninety-four percent].”
 Id.

        Dr. Chaudry also 
submitted an article by R. Shiri in which the author conducted a “systemic
review and meta-analysis . . . to assess whether [rheumatoid arthritis (“RA”)] and osteoarthritis . .
. increase the risk of CTS.” Resp’t’s Ex. O at 2. 37 The author concluded that the “systemic review
and meta-analysis found an increased risk of CTS in individuals who suffer from RA or
[osteoarthritis].”
 Id. at 7. 
The author also noted that “it seems that arthritis does predict the
development of CTS.”
 Id.

        In his first 
expert report, Dr. Chaudry argued that Petitioner’s complaints of “numbness in
both hands[,] especially the fingertips, and waking up through the night having to shake her hands
to get the feeling back[]” made on October 28, 2015, “are indeed classic symptoms of [CTS].”
Resp’t’s Ex. A at 8. He wrote that “[p]ins and needles, tingling, and numbness in distal distribution
of the median nerve (thumb, middle[,] and part of [the] ring finger)[,]” as well as “symptoms being
worse at night and getting better with shaking are highly typical for CTS.”
 Id. He noted that 
Dr.
Whitfield documented that Petitioner had positive Phalen’s and Tinsel’s tests at a December 1,
2015 appointment.
 Id. (citing Pet’r’s Ex. 
9 at 6). He also discussed wrist splints, which were
unsuccessful in relieving Petitioner’s symptoms.
 Id. at 12. 
He explained that “wrist splints don’t
always relieve symptoms of [CTS].”
 Id. He also noted 
that Petitioner “did at some point undergo
release of [her CTS] . . ., which may be one reason why her symptoms improved.” Id.; see also
Pet’r’s Ex. 6 at 328. Dr. Chaudry also drew a connection between Petitioner’s arthritis and her
CTS, noting that her “arthritis symptoms had become more prominent with severe knee pain, rib
pain, [and] back pain, which may be one explanation why her CTS became more symptomatic in
October 2015.” Resp’t’s Ex. L at 3.

        Dr. Chaudry also took issue with Dr. Nadareishvili’s interpretation of Petitioner’s nerve
conduction/EMG test conducted on December 3, 2015, concluding that Dr. Nadareishvili
“reinterprets [the test results] . . . incorrectly.” Resp’t’s Ex. A at 10 (citing Pet’r’s Ex. 9 at 37).
Dr. Chaudry provided a detailed interpretation of this test. See Resp’t’s Ex. D at 5–7. He wrote
that Petitioner’s “bilateral ulnar sensory amplitudes are normal . . . whereas [Petitioner’s] median
sensory amplitude is absent on the right side and reduced on the left.”
 Id. at 7. 
These findings
“corresponded with numbness and sensory abnormalities only in the median nerve distribution,
[with her] ulnar [nerve] being normal.”
 Id. Dr. Chaudry disagreed 
with Dr. Nadareishvili’s
interpretation of “minimal reduction (only [one percent]) of amplitudes of right ulnar . . . and left
ulnar [nerve] amplitude[s,]” as well as an “[eighty percent] reduction of median amplitudes[,]” as
being abnormal.
 Id. Rather, Dr. Chaudry 
agreed with Dr. Vaught’s interpretation that these
findings were normal, “given the normal sensory response, normal latency, normal conduction
velocity, normal needle EMG of the [first dorsal interosseous] muscle[,] and . . . [Petitioner’s] age
37
   R. Shiri, Arthritis as a Risk Factor for Carpal Tunnel Syndrome: A Meta-Analysis, 45:5 SCANDINAVIAN
J. OF RHEUMATOLOGY 339 (2016).

                                                  22
and history of arthritis in the hands.”
 Id. He argued that 
“[t]he exclusive involvement of bilateral
median nerves, with sparing of adjacent ulnar nerves[,] virtually excludes polyneuropathy.”
 Id.
He noted that 
two other physicians, Dr. Oar and Dr. Whitfield, both “agreed with the diagnosis of
severe [CTS].”
 Id. Dr. Chaudry opined 
that “GBS cannot be an explanation [for Petitioner’s hand
symptoms] because of the selective nerve involvement, normal clinical and EMG examination of
the rest of the peripheral nervous system, and presentation of weakness over two months after the
onset of [Petitioner’s] paresthesias.” Resp’t’s Ex. L at 3. Therefore, Dr. Chaudry argued that
Petitioner was indeed suffering from CTS after vaccination. Resp’t’s Ex. A at 10.

        While Dr. Chaudry agreed that Petitioner eventually did develop GBS, he argued that the
onset of her condition did not occur until much later than under Dr. Nadareishvili’s theory. He
submitted an article by Vriesendorp in which the author discusses “[t]he clinical features . . . of
GBS in adults . . . .” Resp’t’s Ex. H at 2. 38 The author wrote that “GBS is thought to result from
an immune response to a preceding infection that cross-reacts with peripheral nerve components
because of molecular mimicry[,]” and that “[a] small percentage of patients develop GBS after
another triggering event such as immunization . . . .”
 Id. The author noted 
that “cardinal clinical
features of . . . GBS are progressive, fairly symmetric muscle weakness accompanied by absent or
depressed [DTRs].”
 Id. The author also 
wrote that “GBS is associated with” other clinical
features, such as “weakness usually start[ing] in the legs, but it begins in the arms or facial muscles
in about [ten] percent of patients[;] . . . [f]acial nerve palsies occur in more than [fifty] percent [of
patients; and p]ain due to nerve root inflammation, typically located in the back and extremities,
can be a presenting feature and is reported during the acute phase by two-thirds of patients with
all forms of GBS.”
 Id. at 2–3. 
The author stated that “GBS usually progress over a period of about
two weeks[ and b]y four weeks after initial symptoms, [over ninety] percent of GBS patients have
reached the nadir of the disease.”
 Id. at 3. 
If the progression of the disease is eight weeks or
longer, the author wrote that that disease course “is consistent with [CIDP].”
 Id.

        Dr. Chaudry did 
not believe that Petitioner’s development of symptoms post vaccination
through the end of 2015 were manifestations of GBS. Resp’t’s Ex. A at 9–11. He began this
discussion by reviewing Petitioner’s emergency room visit on November 2, 2015, for back and
chest pain.
 Id. at 9. 
He noted that the records from this visit reflect a “normal” neurological
examination.
 Id. He also wrote 
that doctors noted “[c]hest discomfort for several days and several
years of back pain secondary to osteoarthritis and degenerative joint disease . . . .”
 Id. He also
noted 
that Petitioner had a near-syncopal episode during this visit, after which “she noted severe
weakness.”
 Id. However, Dr. Chaudry 
argued that “[i]t is not uncommon for patients to feel weak
all over after having a near-syncopal episode.”
 Id. After another normal 
neurological evaluation,
Petitioner was discharged home.
 Id. Therefore, Dr. Chaudry 
argued that this weakness was not a
sign of GBS because “[p]atients with GBS don’t have transient weakness like” what Petitioner
experienced.
 Id.

       Rather, Dr. Chaudry 
argued that onset of Petitioner’s GBS did not occur until shortly before
January 2, 2016, because she “did not lose her ability to ambulate until shortly before she

38
   Francine J. Vriesendorp, Guillain-Barré Syndrome in Adults: Clinical Features and Diagnosis,
UPTODATE, retrieved from www.uptodate.com/contents/guillain-barre-syndrome-in-adults-clinical-
features-and-diagnosis/
print.

                                                   23
presented” on that date.
 Id. at 11. 
He noted that at each of the ER visits Petitioner had on
November 2, 17, and 24, 2015, Petitioner “walked in” and “was documented to have normal
examination with normal cranial nerves . . . and no motor or sensory deficit.”
 Id. (citing Pet’r’s
Ex. 
4 at 44, 98). In addition, he wrote that Petitioner “was seen on [December 1, 2015,] and did
not report any weakness in her upper or lower extremities.”
 Id. (citing Petitioner’s Ex. 
9 at 5). He
also noted that a “detailed examination” conducted during a visit on December 22, 2015, “showed
normal strength in hip flexion, hip extension, quadriceps, hamstrings, dorsiflexion, and plantar
flexion and all reflexes . . . [were] 2+.”
 Id. While there was 
“noted decreased sensation in median
nerve distribution[,]” there was “no weakness . . . in [Petitioner’s] median, ulnar, and radial
muscles . . . .”
 Id. On December 29, 
2015, Petitioner “had no cranial nerve deficit and had no
motor or sensory deficit[,]” and she was subsequently “discharged home.”
 Id. Then, on January
2, 2016, records reflect that Petitioner suffered “acute onset of left[-]sided Bell’s [P]alsy at 3 PM
[the day prior, as well as] left[-]sided weakness, which was sufficient to warrant consideration of
stroke as a possible diagnosis.”
 Id. Dr. Chaudry opined 
that Petitioner’s onset date was
somewhere in this window.

        Dr. Chaudry also reviewed Petitioner’s urinary retention issues in his first expert report.

Id. He disagreed with 
Dr. Nadareishvili’s characterization of this symptom “as being from
autonomic dysfunction . . . .”
 Id. Rather, Dr. Chaudry 
argued that “it is better explained by
[Petitioner’s] narcotic use given that she had severe constipation as well.”
 Id. (citing Pet’r’s Ex. 
7
at 29).

         In addition, Dr. Chaudry also discussed “whether the ‘paresthesias about the toes on both
of [Petitioner’s] feet on December 1, 2015, could be evidence of early onset GBS . . . .” Resp’t’s
Ex. D at 1. Dr. Chaudry described paresthesias as “abnormal sensations experienced in the absence
of specific stimuli . . . usually described as a burning, tingling, or numbness.”
 Id. He noted that
this symptom is “thought to represent abnormal impulses . . . arising from sensory pathways
starting from peripheral nerves to the sensory cortex.”
 Id. (citing Resp’t’s Ex. 
E at 1). 39 When
paresthesias occurs because of a peripheral neuropathy, Dr. Chaudry explained that it “should be
associated with abnormalities on sensory examination, either reduced pinprick sensation, reduced
temperature sensation, reduced vibration sensation, or reduced joint and position[al] sense[,]” as
well as with “abnormalities on [DTR] testing[,] especially around the ankles.”
 Id. In terms of
GBS, Dr. Chaudry wrote that “[p]aresthesias can be part of [the] . . . syndrome[,]” but usually “are
persistent, progressive, and occur in the setting of rapidly progressive weakness and areflexia[,]”
which “peaks between [two] to [four] weeks” after onset.
 Id. Dr. Chaudry noted 
that a GBS
diagnosis “requires rapidly progressive weakness in the legs and arms and absent reflexes . . . .”

Id. at 2.
       In terms of Petitioner’s paresthesias, Dr. Chaudry argued that Petitioner’s “one episode of
paresthesias in the toes on [December 1, 2015,] was not associated with weakness . . . .”
 Id. In
addition, he 
noted that Petitioner also had a normal examination, including reflexes, on this date.

Id. Dr. Chaudry opined 
that, aside from a normal examination and reflexes, “the time frame of
evolution of symptoms is inconsistent with [a] GBS diagnosis[]” because “there was no symptom

39
  Paresthesia Information Page, National Institute of Neurological Disorders and Stroke (Dec. 29, 2018),
retrieved from www.ninds.nih.gov/Disorders/All-Disorders/Paresthesia-Information-Page.

                                                  24
of weakness in the two-month period” between vaccination and the end of December 2015.
 Id.
He noted that 
Petitioner’s “weakness was first noted towards the end of December 2015[,] and
peaked in early January 2016[,]” which would mean that Petitioner suffered “[t]wo[-]to[-three]
months of paresthesias followed by acute onset of weakness . . . .”
 Id. In Dr. Chaudry’s 
opinion,
this timeline “is not consistent with a diagnosis of GBS[,] which requires peak of illness to be less
than [four] weeks . . . .”
 Id. Dr. Chaudry also 
listed the following alternative causes for Petitioner’s
paresthesias: “entrapment neuropathy, lumbosacral radiculopathy, B12 deficiency (high
methylmalonic acid . . .), glucose intolerance . . ., anxiety/stress related phenomenon, or central
nervous system involvement.”
 Id. (citing Pet’r’s Ex. 
6 at 368; Pet’r’s Ex. 10 at 17). Therefore,
Dr. Chaudry concluded that the paresthesias noted in Petitioner’s December 1, 2015 office visit
was not evidence of early onset GBS.
 Id.

        Dr. Chaudry concluded 
his last expert report by writing that, “in [his] professional opinion,
[Petitioner] had typical symptoms, signs, and electrophysiology of [CTS] that had symptom onset
[on] or about [October 10, 2015]. This CTS had no causal relationship to the flu vaccine.
[Petitioner] developed typical symptoms, signs, and electrophysiology of GBS on or about
[December 29, 2015]. This GBS occurring over two months after the flu vaccine was not caused
by the flu vaccine.” Resp’t’s Ex. L at 4.

   IV.     Applicable Legal Standards

         To receive compensation under the Vaccine Act, Petitioner must demonstrate either that:
(1) she suffered a “Table injury” by receiving a covered vaccine and subsequently developing a
listed injury within the time frame prescribed by the Vaccine Injury Table set forth at 42 U.S.C. §
300aa-14, as amended by 42 C.F.R. § 100.3; or (2) that she suffered an “off-Table injury,” one not
listed on the Table as a result of her receipt of a covered vaccine. See 42 U.S.C. §§ 300aa-
11(c)(1)(C); Moberly v. Sec’y of Health & Human Servs., 
592 F.3d 1315
, 1321 (Fed. Cir. 2010);
Capizzano v. Sec’y of Health & Human Servs., 
440 F.3d 1317
, 1319–20 (Fed. Cir. 2006).
Petitioner concedes that she cannot meet the Table criteria for flu vaccine-caused GBS. See Pet’r’s
Ex. 19 at 12–13. Thus, she must prove that her GBS was caused-in-fact by the flu vaccine.

        To establish causation-in-fact, Petitioner must demonstrate by a preponderance of the
evidence that the vaccine was the cause of the injury. 42 U.S.C. § 300aa-13(a)(1)(A). Petitioner
is required to prove that the vaccine was “not only a but-for cause of the injury but also a substantial
factor in bringing about the injury.” 
Moberly, 592 F.3d at 1321
–22 (quoting Shyface v. Sec’y of
Health & Human Servs., 
165 F.3d 1344
, 1352–53 (Fed. Cir. 1999)).

        In the seminal case of Althen v. Secretary of the Department of Health and Human Services,
the Federal Circuit set forth a three-pronged test used to determine whether a petitioner has
established a causal link between a vaccine and the claimed injury. See 
418 F.3d 1274
, 1278–79
(Fed. Cir. 2005). The Althen test requires the petitioner to set forth: “(1) a medical theory causally
connecting the vaccination and the injury; (2) a logical sequence of cause and effect showing that
the vaccination was the reason for the injury; and (3) a showing of a proximate temporal
relationship between vaccination and injury.”
 Id. at 1278. 
To establish entitlement to
compensation under the Program, Petitioner is required to establish each of the three prongs of
Althen by a preponderance of the evidence. See
 id.

                                                  25
        Under the first Althen prong, Petitioner must offer a scientific or medical theory that
answers in the affirmative the question “can the vaccine[] at issue cause the type of injury alleged?”
See Pafford v. Sec’y of Health & Human Servs., No. 01-0165V, 
2004 WL 1717359
, at *4 (Fed.
Cl. Spec. Mstr. July 16, 2004), aff’d, 
64 Fed. Cl. 19 
(2005), aff’d, 
451 F.3d 1352 
(Fed. Cir. 2006).
To satisfy this prong, a petitioner’s theory must be based on a “sound and reliable medical or
scientific explanation.” Knudsen v. Sec’y of Health & Human Servs., 
35 F.3d 543
, 548 (Fed. Cir.
1994). Such a theory must only be “legally probable, not medically or scientifically certain.”
 Id.
at 548–49. 
However, as the Federal Circuit has made clear, “simply identifying a ‘plausible’
theory of causation is insufficient for a petitioner to meet her burden of proof.” LaLonde v. Sec’y
of Health and Human Servs., 
746 F.3d 1334
, 1339 (Fed. Cir. 2014) (citing 
Moberly, 592 F.3d at
1322
). Rather, “the statutory standard of preponderance of the evidence requires a petitioner to
demonstrate that the vaccine more likely than not caused the condition alleged.”
 Id.

        A petitioner is 
not required to present medical literature or epidemiological studies to meet
her burden. Grant v. Sec’y of Health and Human Servs., 
956 F.2d 1144
, 1149 (Fed. Cir. 1992);
Andreu v. Sec’y Health & Human Servs., 
569 F.3d 1367
, 1380 (Fed. Cir. 2009). However, to the
extent medical literature and epidemiological studies are provided, the special master will consider
them when deciding whether the petitioner has met her burden of proof. Special masters, despite
their expertise, are not empowered by statute to conclusively resolve what are essentially thorny
scientific and medical questions, and thus scientific evidence offered to establish Althen prong one
is viewed “not through the lens of the laboratorian, but instead from the vantage point of the
Vaccine Act’s preponderant evidence standard.” 
Andreu, 569 F.3d at 1380
. This does not negate
or reduce a petitioner’s ultimate burden to establish her overall entitlement to damages by
preponderant evidence. W.C. v. Sec’y of Health & Human Servs., 
704 F.3d 1352
, 1356 (Fed. Cir.
2013) (citations omitted).

        Under Althen’s second prong, petitioners must demonstrate that the vaccine actually did
cause the alleged injury in a particular case. See 
Althen, 418 F.3d at 1279
; Pafford, 
2004 WL
1717359
, at *4. The second Althen prong requires proof of a logical sequence of cause and effect,
usually supported by facts derived from a petitioner’s medical records. 
Althen, 418 F.3d at 1278
;
Andreu, 569 F.3d at 1380
; 
Capizzano, 440 F.3d at 1326
; 
Grant, 956 F.2d at 1148
. A petitioner
does not meet this obligation by showing only a temporal association between the vaccination and
the injury; instead, the petitioner “must explain how and why the injury occurred.” Pafford, 
2004
WL 1717359
, at *4 (emphasis in original).

        In Program cases, contemporaneous medical records and the opinions of treating
physicians are favored. 
Capizzano, 440 F.3d at 1326 
(citing Althen, 418F.3d at 1280). This is
because “treating physicians are likely to be in the best position to determine whether ‘a logical
sequence of cause and effect show[s] that the vaccination was the reason for the injury.’”
 Id. In
addition, “[m]edical 
records, in general, warrant consideration as trustworthy evidence. The
records contain information supplied to or by health professionals to facilitate diagnosis and
treatment of medical conditions. With proper treatment hanging in the balance, accuracy has an
extra premium. These records are also generally contemporaneous to the medical events.”
Cucuras v. Sec’y of Health and Human Servs., 
993 F.2d 1525
, 1528 (Fed. Cir. 1993). While a
special master must consider these opinions and records, they are not “binding on the special

                                                 26
master or court.” 42 U.S.C. § 300aa-13(b)(1). Rather, when “evaluating the weight to be afforded
to any such . . . [evidence], the special master . . . shall consider the entire record . . . .”
 Id.

        Under the third 
prong of Althen, a petitioner must show that the timing of the injury fits
with the causal theory. See 
Althen, 418 F.3d at 1278
. For example, if the petitioner’s theory
involves a process that takes several days to develop after vaccination, an injury that occurred
within a day of vaccination would not be temporally consistent with that theory. Conversely, if
the theory is one that anticipates a rapid development of a reaction post vaccination, the
development of the alleged injury weeks or months post vaccination would not be consistent with
that theory. Causation-in-fact cannot be inferred from temporal proximity alone. See 
Grant, 956
F.2d at 1148
; Thibaudeau v. Sec’y of Health & Human Servs., 
24 Cl. Ct. 400
, 403–04 (1991); see
also Hasler v. United States, 
718 F.2d 202
, 205 (6th Cir. 1983) (“Without more, [a] proximate
temporal relationship will not support a finding of causation.”).

   V.      Analysis

           A. Althen Prong One

        Petitioner has met her burden with respect to Althen prong one. Dr. Nadareishvili presented
a detailed, well-reasoned theory based on molecular mimicry whereby the flu vaccine can cause
GBS. This occurs when immune system activation caused by the flu vaccine causes a cross-
reaction between antibodies to the flu and the peripheral nerves. This cross-reaction results in the
antibodies attacking the otherwise healthy cells of the peripheral nerves, resulting in GBS. He
provided a detailed discussion of the disease in his expert reports and supported his theory with
citations to medical literature, of which multiple were either submitted or cited to by Respondent.
This theory is well-established and well-settled in the Vaccine Program. See, e.g., Barone v. Sec’y
of Health and Human Servs., No. 11-707V, 
2014 WL 6834557 
(Fed. Cl. Spec. Mstr. Nov. 12,
2014); Stitt v. Sec’y of Health and Human Servs., No. 09-653V, 
2013 WL 3356791 
(Fed. Cl. Spec.
Mstr. May 31, 2013); Stewart v. Sec’y of Health and Human Servs., No. 06-777V, 
2011 WL
3241585 
(Fed. Cl. Spec. Mstr. July 8, 2011). Respondent did not, either through Dr. Chaudry’s
expert reports or other filings, present a counter-argument or attempt to discredit Petitioner’s
general causation theory in any way. Therefore, I find that Petitioner has presented preponderant
evidence that the flu vaccine can generally cause GBS.

           B. Symptom Onset and Diagnosis

        Subsequent to establishing general causation, Petitioner must also establish that her general
causation theory is applicable to her symptom onset and diagnoses. Petitioner argues that the first
manifestation of her GBS was the hand pain and paresthesias she first mentioned approximately
one-month post vaccination. Respondent, however, contends that Petitioner’s GBS did not begin
until at least December 29, 2015—approximately twelve weeks post vaccination—when she
developed weakness in her lower extremities. Respondent further contends that Petitioner’s
symptoms during the preceding time period were caused by other diagnoses. Therefore, before



                                                 27
determining whether Petitioner has met her burden with respect to Althen prong two, I must make
a factual determination as to exactly what conditions Petitioner suffered from and when.

        While Petitioner argues that her hand pain and paresthesia were not symptoms of CTS, the
evidence demonstrates that these symptoms were, more likely than not, manifestations of this
condition. The Ibrahim et al. article submitted by Respondent demonstrated that Petitioner’s
symptoms mirrored the primary features of CTS. Petitioner developed pain and numbness in her
hands, especially along the median nerve, which were worse at night and relieved by shaking her
hands. These symptoms closely track the description of CTS provided by the Ibrahim et al. study.
Additionally, Respondent submitted the Shiri article, which drew a connection between arthritis
and CTS. Resp’t’s Ex. O at 2. Petitioner had severe arthritis for which she received multiple
injections during 2014 and 2015. This makes a CTS diagnosis more likely.

         Petitioner also met the diagnostic criteria for a CTS diagnosis. She had positive Phalen’s
and Tinsel’s signs at an appointment with Dr. Whitfield on December 1, 2015, which the Ibrahim
et al. paper described as the “two provocative tests most commonly used in the clinical setting” to
diagnose CTS. Resp’t’s Ex. C at 4. Dr. Vaught also interpreted Petitioner’s EMG/NCS study as
being indicative of CTS, because he saw median nerve involvement but no ulnar nerve
involvement. In contrast, Petitioner’s EMG/NCS study conducted on January 4, 2016, revealed
both median and ulnar nerve involvement, a marked shift from Petitioner’s first EMG/NCS study
conducted in December of 2015. A finding of ulnar nerve involvement is not indicative of a CTS
diagnosis. In addition to Dr. Vaught, two other treaters diagnosed Petitioner with CTS, namely
Dr. Whitfield and Petitioner’s PCP. Therefore, based on Petitioner’s description of her hand
symptoms, the diagnostic evidence, and treaters’ diagnoses, I find it more likely than not that
Petitioner suffered from CTS in the weeks immediately following her vaccination and prior to her
development of symptoms associated with GBS.

        Petitioner complained of abdominal and back pain between her vaccination and GBS
diagnosis, and she argues these symptoms were manifestations of her GBS. However, Petitioner
complained of back pain on the day of vaccination and noted that it was occurring more frequently
at that time. See Pet’r’s Ex. 10 at 42. The timing of this complaint indicates a pre-existing
condition. In addition, Petitioner’s medical records demonstrate that her treaters diagnosed her
abdominal and back pain as either resulting from uncontrolled hypertension or her longstanding
osteoarthritis. Petitioner submitted a case report by Wong et al. to support her argument that these
symptoms were manifestations of her GBS. The mission of the authors was to “draw attention to
abdominal pain as being a presenting symptom[]” of GBS. Pet’r’s Ex. 34 at 3. The case report
did not discuss statistics regarding how many GBS patients first present with abdominal symptoms
nor how many patients develop abdominal pain during their disease course. See
 id. at 1–3. 
In fact,
the authors were unable to say if the case study patient suffered pain due to demyelination or
gastrointestinal dysfunction.
 Id. at 2. 
Therefore, this case report is not enough to establish by a
preponderance of the evidence that Petitioner’s symptoms of abdominal and back pain were
manifestations of her GBS.




                                                28
        Lastly, Petitioner argues that she suffered from autonomic dysfunction, namely
uncontrolled hypertension and urinary retention, during her GBS course. Similar to her back pain,
one of Petitioner’s chief complaints on the day she received the vaccination at issue was
hypertension. Pet’r’s Ex. 10 at 42. In that visit note, her PCP noted high blood pressure and a
history of hypertension since the year 2005.
 Id. Therefore, this condition 
preexisted the
vaccination. In addition, Petitioner only provided a single case report discussing hypertension as
a presenting symptom of GBS. See Pet’r’s Ex. 36. However, Petitioner did not explain how her
GBS course is analogous to the case report. Specifically, the patient’s symptoms in the case report
developed over a period of days, with profound lower extremity weakness developing two days
after presentation to the hospital with hypertension and headaches. Petitioner’s symptoms
developed over a period of months and she provided no context for how the case report is
applicable to the facts of her case. As for the symptom of urinary retention, Petitioner did not
complain of urinary retention until after she was hospitalized in January of 2016. At her urology
appointment on November 30, 2015, Petitioner explicitly denied any bladder retention issues. See
Pet’r’s Ex. 5 at 39–40. Petitioner is correct that this visit note lists “flaccid neuropathic bladder”
as an active problem; however, Dr. Kowalkowski did not assess Petitioner with this condition nor
provide any further context for this notation. Therefore, I find that Petitioner’s alleged autonomic
dysfunction occurring before she was hospitalized in January of 2016 were not manifestations of
her GBS.

        Based on the foregoing, I find that Petitioner suffered from CTS, back and abdominal pain
as a result of osteoarthritis, and urinary issues post vaccination that were not related to her GBS
course. With these findings in mind, I will now analyze the evidence as it relates to Althen prong
two.

           C. Althen Prong Two

        After analyzing the evidence submitted by both parties, I find that Petitioner did not
establish by a preponderance of the evidence that her symptoms met the criteria for a GBS
diagnosis until January 3, 2016. Dr. Nadareishvili argued in his expert reports that Petitioner
suffered from AIDP-GBS. Pet’r’s Ex. 19 at 13. Both parties submitted the Willison et al. article,
which explained that the two symptoms necessary for a GBS diagnosis in clinical practice are
“progressive weakness in the legs and arms” and “areflexia.” Pet’r’s Ex. 33 at 5; Resp’t’s Ex. G
at 5. Based on the medical records, Petitioner did not develop lower extremity weakness until at
least December 29, 2015, when she presented to the emergency room after a fall at church. See
Pet’r’s Ex. 4 at 43. Petitioner was not assessed with lower extremity weakness, however, until
December 31, 2015, when she was released from University of Virginia Hospital, Pet’r’s Ex. 6 at
463-64, or until January 2, 2016, when she presented to the emergency room with left extremity
weakness such that she could not raise her left leg off the hospital bed without support. See Pet’r’s
Ex. 4 at 33. Her treaters did not note areflexia until January 3, 2016, after Petitioner was transferred
to St. Mary’s Hospital. See Pet’r’s Ex. 6 at 329. Therefore, based on Petitioner’s own medical
literature, Petitioner could not have been clinically diagnosed with GBS until at least January 3,
2016.



                                                  29
         Petitioner attempts to use her office visits with Dr. Whitfield on December 1 and 22, 2015,
as evidence that her GBS began earlier than it was diagnosed. Petitioner’s complaints at those
visits belie that contention. At her December 1, 2015 office visit, Petitioner did complain of some
paresthesias about her toes. See Pet’r’s Ex. 9 at 5. However, Petitioner explicitly denied “any
weakness in her upper or lower extremities[]” at this visit.
 Id. Dr. Whitfield did 
not make any
notation in the objective portion of the record that Petitioner had any weakness or areflexia. See

id. Aside from his 
assessment of “[l]ower extremity neuropathy of unclear etiology[,]” Dr.
Whitefield did not provide any other information about this symptom. See
 id. at 5–9. 
At her
December 22, 2015 office visit, Petitioner did not make any complaints related to her lower
extremities. See
 id. at 2. 
Indeed, Dr. Whitfield did not note any findings of weakness or areflexia
in the objective portion of the office visit record. See
 id. at 2–4. 
In light of Petitioner’s complaints
at this visit and Dr. Whitfield’s notes, it seems that Dr. Whitfield, inadvertently or otherwise, may
have copied over his assessment of lower extremity neuropathy from Petitioner’s previous visit.
There are no notations anywhere else in the record related to Petitioner’s lower extremities. See

id. at 4. 
Accordingly, I find it more likely than not that Petitioner’s GBS did not manifest until
December 29, 2015 at the earliest.

        In addition to suffering from the conditions described in section V.B. above, Petitioner
failed to present persuasive evidence that GBS manifests in a way that is consistent with her
symptom development. She argues that the presenting symptom of her GBS was her hand pain
and paresthesia; however, this is inconsistent with how a typical GBS case develops based on
Petitioner’s own filed medical literature. Petitioner’s medical literature demonstrated that, in a
typical GBS case, the presenting symptom is progressive, ascending bilateral weakness, which
usually begins in the distal lower extremities. Respondent also filed medical literature to this
effect. Further, Dr. Nadareishvili argued that Petitioner’s GBS was a typical AIDP-GBS case.
Based on the filed literature and expert reports, Petitioner’s symptoms developed in what is an
atypical fashion. Dr. Nadareishvili did not present an argument as to why Petitioner’s symptoms
would develop in such a manner if she suffered from what he described as a typical case. While
Dr. Nadareishvili opined that Petitioner’s treaters did not diagnose her GBS until January 2016
because they erred in their treatment, see Pet’r’s Ex. 19 at 20 (Dr. Nadareishvili noting that his
“analysis [of Petitioner’s case] is affected somewhat by the level of care she was given.”), this
argument is unpersuasive. Dr. Nadareishvili did not support this argument with any citations to
medical literature or other supporting documentation.

        Petitioner finally attempts to argue that an absence of identified infectious causes in the
medical records supports the flu vaccine as the cause of her GBS. However, relying on a temporal
relationship and the absence of other known causes is not enough. See Pafford, 
2014 WL 1717359
,
at *9 (noting that the “Court has always held that vaccines are not the cause of every event that
occurs soon after their administration.”). Petitioner has not offered any persuasive scientific
evidence that GBS can manifest in the way in which she alleged her symptoms developed.
Accordingly, I find that Petitioner has failed to meet her burden under Althen prong two.




                                                  30
            D. Althen Prong Three

        As stated, based on the evidence submitted, I find it more likely than not that Petitioner’s
GBS manifested on approximately December 29, 2015. Accordingly, this is the onset date I will
use to analyze Petitioner’s claim under Althen prong three.

        Both parties submitted numerous articles discussing GBS and the timeline for symptom
development. The Willison et al. article, which both parties submitted, states that the progressive
course of GBS should last days to four weeks. Pet’r’s Ex. 33 at 5; Resp’t’s Ex. G at 5. The authors
of that study noted that “[m]ost patients . . . reach the nadir [of weakness] within [two] weeks[,]”
although it could “last up to [six] weeks after onset . . . in some rare cases.”
 Id. This timeline is
consistent throughout the literature. Petitioner began to develop symptoms normally associated as
presenting symptoms in GBS approximately three months post vaccination. She provided no
evidence that this is an appropriate temporal relationship in vaccine-induced GBS.

       While Petitioner argues the appropriate window is longer, the evidence submitted does not
support her position. Petitioner did submit evidence that SIDP could develop in an extended
timeframe; however, Dr. Nadareishvili explicitly argued that Petitioner developed AIDP-GBS, not
SIDP. Therefore, per Petitioner’s own expert, this article is inapplicable to Petitioner’s case. No
other piece of medical literature submitted by either party supports a twelve-week symptom
development of GBS. In addition, while not binding on my analysis, no other decision in the
Vaccine Program has found that GBS onset occurring twelve-weeks post flu vaccination is
appropriate for entitlement to compensation. See Barone, 
2014 WL 6834557
, at *13 (stating that
eight weeks is the longest reasonable timeframe for a flu vaccine-induced GBS and citing cases).
Therefore, I find that she has not met her burden under Althen prong three.

     VI.    Conclusion

       For the foregoing reasons, Petitioner’s claim is hereby DISMISSED for insufficient proof. The
Clerk of Court is directed to enter judgment accordingly. 40

             IT IS SO ORDERED.

                                              s/Herbrina D. Sanders
                                              Herbrina D. Sanders
                                              Special Master




40
  Pursuant to Vaccine Rule 11(a), entry of judgment is expedited by the parties’ joint filing of a notice
renouncing the right to seek review.

                                                   31