Court Opinion

ID: 4694869
Source: CourtListenerOpinion
Date Created: 2021-06-11 20:04:42.72328+00
Date Added: 2024-06-11T08:05:32.190982
License: Public Domain

In the United States Court of Federal Claims
                                 OFFICE OF SPECIAL MASTERS
                                          No. 15-1553V
                                      Filed: May 17, 2021
                                          PUBLISHED

    JONATHAN PATTON,                                               Special Master Horner

                         Petitioner,
    v.                                                             Decision Dismissing Petition;
                                                                   Influenza Vaccination; Brachial
    SECRETARY OF HEALTH AND                                        Neuritis; Radiculomyelitis
    HUMAN SERVICES,

                        Respondent.

Michael Andrew London, Douglas & London, P.C., New York, NY, for petitioner.
Claudia Barnes Gangi, U.S. Department of Justice, Washington, D.C., for respondent.

                                                DECISION1

       On December 21, 2015, petitioner Jonathan Patton2 filed a petition under the
National Childhood Vaccine Injury Act, 42 U.S.C. § 300aa-10-34 (2012),3 alleging that
he suffered brachial neuritis (“BN”), otherwise known as parsonage-turner syndrome
(“PTS”) or neuralgic amyotrophy (“NA”),4 as a result of his January 11, 2013 influenza

1
  Because this decision contains a reasoned explanation for the special master’s action in this case, it will
be posted on the United States Court of Federal Claims’ website in accordance with the E-Government
Act of 2002. See 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), petitioner has 14 days to identify and move to redact
medical or other information the disclosure of which would constitute an unwarranted invasion of privacy.
If the special master, upon review, agrees that the identified material fits within this definition, it will be
redacted from public access.
2
 In f act, when the petition was filed Mr. Patton was a minor and the action was brought by his mother on
his behalf . Petitioner was subsequently substituted as petitioner on February 18, 2016. (ECF No. 10.)
3
 All ref erences to “§ 300aa” below refer to the relevant section of the Vaccine Act at 42 U.S.C. § 300aa-
10-34.
4
 Throughout the record of this case, these three terms – i.e. BN, PTS, and NA – are variously used to
describe the same basic condition. Notwithstanding any nuances, the parties and experts have treated
the terms as interchangeable. For consistency this decision will use the term brachial neuritis except
where other of the terms are included in quotation; however, no distinction is intended.

                                                       1
vaccination. (ECF No. 1.) He later amended his claim to allege that he also
experienced radiculomyelitis as a result of the same vaccination.5 (ECF No. 34.)

        For the reasons set forth below, I find that petitioner is not entitled to an award of
compensation for his injury. Specifically, there is not preponderant evidence that
petitioner suffered radiculomyelitis. Although petitioner more likely than not suffered
brachial neuritis, petitioner has not established by preponderant evidence that his
brachial neuritis was caused by his vaccination.

    I.       Applicable Statutory Scheme

        Under the National Vaccine Injury Compensation Program, compensation
awards are made to individuals who have suffered injuries after receiving vaccines. In
general, to gain an award, a petitioner must make a number of factual demonstrations,
including showing that an individual received a vaccination covered by the statute;
received it in the United States; suffered a serious, long-standing injury; and has
received no previous award or settlement on account of the injury. Finally – and the key
question in most cases under the Program – the petitioner must also establish a causal
link between the vaccination and the injury. In some cases, the petitioner may simply
demonstrate the occurrence of what has been called a “Table Injury.” That is,
petitioners may show that they suffered an injury of the type enumerated in the “Vaccine
Injury Table,” corresponding to the vaccination in question, within an applicable time
period following the vaccination also specified in the Table. In such cases, the Table
Injury is presumed to have been caused by the vaccine. § 300aa-13(a)(1)(A); § 300 aa-
11(c)(1)(C)(i); § 300aa-14(a); § 300aa-13(a)(1)(B).

        In many cases, however, the vaccine recipient may have suffered an injury not
covered by the Vaccine Injury Table. In these “off-table” cases, an alternative means
exists to demonstrate entitlement to a Program award. The petitioner may demonstrate
entitlement by showing that the recipient’s injury was “caused-in-fact” by the vaccine
they received, a showing often referred to as “actual causation.” § 300aa-13(a)(1)(B); §
300aa-11(c)(1)(C)(ii). In off-table cases, the presumptions available under the Vaccine
Injury Table are inoperative, and the burden is on the petitioner to introduce evidence
demonstrating that the vaccination was responsible for the injury in question. Althen v.
Sec’y of Health & Human Servs., 418 F.3d 1274, 1278 (Fed. Cir. 2005); Hines v. Sec’y
of Health & Human Servs., 940 F.2d 1518, 1525 (Fed. Cir. 1991).

      To show actual causation, petitioner must satisfy the “preponderance of the
evidence” standard, the same standard ordinarily used in tort litigation. § 300aa-

5
 As with petitioner’s brachial neuritis, there is some variation in terminology in the record regarding this
additional condition. Ref erence is made most often throughout the record to “radiculomyelitis,” but
petitioner’s first expert referenced the same condition as “myelo-radiculitis.” In medical terminology,
“myel(o)” is “a combining form denoting relationship to marrow, to the spinal cord, or to myelin” and
radiculitis refers to “inflammation of the root of the spinal nerve.” (Dorland’s Illustrated Medical Dictionary,
p. 1202, 1547 (33rd ed. 2020).) Conversely, “radicular” generally refers to something that is “of or
pertaining to a root” and “myelitis” refers to inflammation of the spinal cord. Id. For consistency this
decision will reference “radiculomyelitis” except where the other term is used in quotation.

                                                       2
13(a)(1)(A); see also Althen, 418 F.3d at 1279; Hines, 940 F.2d at 1525. Under that
standard, the petitioner must show that it is “more probable than not” that the
vaccination caused the alleged injury. Althen, 418 F.3d at 1279. The petitioner need
not show that the vaccination was the sole cause of the injury or condition, but must
demonstrate that the vaccination was a “substantial factor” and a “but for” cause.
Shyface v. Sec’y of Health & Human Servs., 165 F.3d 1344, 1352 (Fed. Cir. 1999).
This standard has been interpreted to require “proof of a logical sequence of cause and
effect showing that the vaccination was the reason for the injury;” the logical sequence
must be supported by “reputable medical or scientific explanation, i.e., evidence in the
form of scientific studies or expert medical testimony.” Althen, 418 F.3d at 1278; Grant
v. Sec’y of Health & Human Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992). A petitioner
may not receive a Vaccine Program award based solely on his or her assertions; rather,
the petition must be supported by either medical records or by the opinion of a
competent physician. § 300aa-13(a)(1).

       In what has become the predominant framing of this burden of proof, the Althen
court described the “causation-in-fact” standard, as follows:

         Concisely stated, Althen’s burden is to show by preponderant evidence
         that the vaccination brought about her injury by providing: (1) a medical
         theory causally connecting the vaccination and the injury; (2) a logical
         sequence of cause and effect showing that the vaccination was the
         reason for the injury; and (3) a showing of proximate temporal
         relationship between vaccination and injury. If Althen satisfies this
         burden, she is “entitled to recover unless the [government] shows, also
         by a preponderance of the evidence, that the injury was in fact caused
         by factors unrelated to the vaccine.”

Althen, 418 F.3d at 1278 (citations omitted). The Althen court explained that petitioners
are not required to provide medical literature supporting their theory of causation so
long as they supply the medical opinion of an expert. Id. at 1279-80. The Althen court
also indicated that Program fact finders may rely upon “circumstantial evidence” to
determine causation, a standard it held to be consistent with the “system created by
Congress, in which close calls regarding causation are resolved in favor of injured
claimants.” Id. at 1280.

        In this case, petitioner alleges that he suffered brachial neuritis and
radiculomyelitis as a result of his influenza vaccination. Because neither of these
injuries are listed as a Table Injury relative to the flu vaccine, petitioner must satisfy the
above-described Althen test for establishing causation in fact. See 42 C.F.R. § 100.3(a).

   II.      Procedural History

        On December 21, 2015, petitioner’s mother filed a petition on his behalf seeking
compensation for the injury of brachial neuritis. (ECF No. 1.) Petitioner was later
substituted as petitioner once he reached the age of majority. (ECF Nos. 9, 10.) The
case was assigned to then Chief Special Master Nora Beth Dorsey on December 22,

                                              3
2015. (ECF No. 4.) Following an initial status conference on February 18, 2016,
petitioner submitted medical records and a Statement of Completion. (Exs. 1-8, ECF
Nos. 8, 12, 13.)

       On June 20, 2016, respondent filed his Rule 4(c) report identifying a number of
missing medical records and recommending against compensation. (ECF No. 15.)
Following respondent’s Rule 4(c) report, petitioner filed additional medical records and a
second Statement of Completion on September 2, 2016. (ECF Nos. 21, 23.)

        This case was reassigned to Special Master Laura D. Millman on December 5,
2016. (ECF No. 25.) After the case was reassigned, petitioner filed an expert report
from Dr. Thomas F. Morgan, who opined that petitioner had suffered radiculomyelitis.
(ECF No. 31, Ex. 12.) Shortly thereafter, on June 19, 2017, petitioner amended his
petition to allege that he suffered radiculomyelitis. (ECF No. 34.) Respondent filed a
responsive expert report from Dr. Vinay Chaudhry on November 7, 2017. (ECF No. 40,
Ex. A.) Dr. Chaudhry disagreed that petitioner had either brachial neuritis or
radiculomyelitis. The parties filed further supplemental reports by each expert before
this case was reassigned to me on June 6, 2019. (ECF No. 42; Ex. 17 (Morgan
supplemental report); ECF No. 44; Ex. G (Chaudhry supplemental report); ECF No. 47
(Notice of Reassignment).)

        On July 12, 2019, the parties confirmed that the case was ripe for an entitlement
hearing. (ECF No. 50.) On August 20, 2019, I scheduled a two-day entitlement hearing
for October 27, 2020. (ECF No. 54.) Petitioner subsequently advised, however, that
Dr. Morgan would no longer be participating as an expert in the vaccine program and
therefore would not be testifying at the entitlement hearing. Petitioner indicated in a
status report on May 11, 2020 that he wished to file a report by a different expert who
would testify in place of Dr. Morgan. (ECF No. 55.) Petitioner filed an expert report
from Dr. Salvatore Q. Napoli on August 25, 2020. (ECF No. 65, Ex. 21.) Dr. Napoli
opined that petitioner suffered both brachial neuritis and radiculomyelitis. Respondent
filed a responsive report from Dr. Chaudhry on September 14, 2020. (ECF No. 66-2,
Ex. H.)

       An entitlement hearing was held on October 27, 2020. 6 (See ECF No. 80,
Transcript of Proceedings (“Tr”), October 27, 2020). Drs. Napoli and Chaudhry testified.
Following the entitlement hearing, petitioner and respondent filed post-hearing briefs on
November 17, 2020 and December 10, 2020. (ECF Nos. 81, 82.) This case is now ripe
for resolution.

6
    Due to Covid-19, the hearing was held remotely via Webex video conference.

                                                    4
      III.    Factual History

        Apart from a history of nosebleeds, petitioner was a healthy 15-year old boy prior
to receiving a flu vaccine on January 11, 2013. (Ex. 2, p. 3.)7 There are no records of
any physical or mental trauma beyond an ankle laceration. (Id.) Petitioner received the
typical childhood vaccines during his infancy and never experienced any neurological
symptoms nor was he ever diagnosed with any neurological or autoimmune condition.
(Ex. 1, pp. 1-2; ECF No. 72, p. 1.) Petitioner’s pertinent medical history begins on
January 11, 2013, when he received the flu vaccine that serves as the basis for this
claim.

        On January 17, 2013, six days after receiving the flu vaccine, petitioner awoke
early in the morning with a nosebleed that was more severe than usual. (Ex. 2, p. 2.)
Petitioner was unable to move his arms, describing the feeling as “dead weight.” (Id.)
After alerting his mother of his condition, petitioner was brought and admitted to the All
Children’s Hospital (“ACH”) Emergency Department. (Id.) Petitioner’s arms were so
weak at this point that he was unable to dress himself or fasten his seatbelt on his own.
(Ex. 7, p. 59.) He also reported he had experienced an occipital headache, neck pain,
and bilateral shoulder pain since waking. (Id.)

        Petitioner was initially examined around 3:42 AM on January 17, 2013 at ACH
ED by Dr. Ricardo Jimenez. (Ex. 7, p. 58.) Dr. Jimenez’s neurological exam revealed
bilateral upper extremity weakness and left pronator drift. Petitioner was able to lift his
legs against resistance without difficulty. (Id. at 60.) Petitioner showed downgoing
Babinski on the right, and upgoing on the left. (Id.) Dr. Jimenez did not observe any
ankle clonus. (Id.) Petitioner’s deep tendon reflexes were intact, sensation was intact
to bilateral face in all nerve distributions, upper extremities, and lower extremities. (Id.)
Petitioner also presented with a severe headache, described as a “6-7/10.” (Id. at 59.)
Dr. Jimenez was concerned that petitioner was experiencing ischemia and ordered a
stat CT scan. (Id. at 60.)

         After petitioner’s CT scan came back negative, Dr. Jimenez reported that
petitioner’s upper extremity weakness was more distal than proximal. (Ex. 7, p. 60.)
After his CT, petitioner’s Babinski was upgoing on the right, downgoing on the left, and
equivocal at times. (Id.) Petitioner’s pronator drift had resolved and his sensation
remained intact. (Id.) Petitioner was able to walk on his tiptoes and heels, but had
difficulty walking heel-toe. (Id.) He was able to stand on his right leg, but had difficulty
taking his left heel and going up and down on his right shin which was also apparent
when he was lying down. (Id.) Petitioner’s bloodwork showed a high concentration of
carboxyhemoglobin and methemoglobin.8 (Id. at 62, 66.)
7
    Exhibit 2 was not bates-stamped. This decision cites to the pagination generated by CM/ECF.
8
 Carboxyhemoglobin refers to hemoglobin bound to carbon dioxide instead of oxygen. (Dorland’s., p.
284.) Carboxyhemoglobinemia, the presence of carboxyhemoglobin in the blood, is associated with
carbon monoxide poisoning. (Id. at 284, 1459.) Methemoglobin is a pigment formed in blood due to
oxidation. It is normally present in small amounts, but excess methemoglobin – methemoglobinemia –
can be associated with injury or toxic agents and can cause cyanosis and headache as well as dizziness,

                                                     5
       Dr. Jimenez recorded differential diagnoses of central nervous system mass,
carbon monoxide poisoning, dehydration, electrolyte abnormality, unspecified
headache, migraine, tension headache, intracranial hemorrhage, meningitis, post-
concussion syndrome, shunt malfunction, and stroke. (Ex. 7, p. 60.) Dr. Jiminez was
particularly concerned that petitioner was suffering from ischemia. 9 (Id.) Dr. Jiminez
ordered brain and spinal MRIs which showed no abnormalities other than a small
central disc protrusion at the C5 and C6 level. (Id. at 63.)

        Petitioner was later examined by Dr. Leslie Carrol. (Ex. 7, p. 72.) During this
exam, petitioner was unable to bring his hands up to his face due to weakness, unable
to fully clench his fists or extend his fingers, and unable to shrug his shoulders. (Id. at
69.) Petitioner showed normal strength in his lower extremities, and abnormal
sensation to light touch on his neck, upper chest above the nipple line, and bilateral
upper extremities including all of his fingers. (Id.) Petitioner reported that a light touch
on his chest or left upper back would create a painful, hot sensation. (Id.) He
experienced normal sensation in his bilateral lower extremities. (Id.) He was initially
unable to sit up on his own due to pain in his upper back. (Id.) Dr. Carroll did not
examine petitioner’s gait because she was afraid that petitioner would fall due to his
weakness. (Id.)

        Dr. Carrol listed differential diagnoses of spinal cord compression, spinal cord
ischemia, acute demyelinating process, Guillain-Barre Syndrome (“GBS”), and carbon
monoxide toxicity. (Id. at 72.) It was noted that carbon monoxide toxicity was unlikely
due to petitioner’s normal mental state, metabolic acidosis, respiratory function, and
complexion. (Id.) GBS was believed to be unlikely because petitioner’s symptoms did
not ascend from his lower extremities. (Id.) Due to the puzzling presentation of
petitioner’s condition, a neurological consult was scheduled. (Id.)

         Petitioner was examined by neurosurgeon, Dr. Luis Rodriguez on January 17,
2013. (Ex. 7, p. 77.) Dr. Rodriguez noted that petitioner’s weakness had improved and
that it is unlikely his symptoms were related to the central disc bulge found on his MRI.
(Id. at 75-77.)

        Petitioner was evaluated by neurologist Dr. Steven Parrish Winesett on January
18, 2013 at 10:09 AM. (Id. at 73.) Dr. Winesett noted an unremarkable medical history
except for a flu shot several days prior. (Id. at 73-74.) Dr. Winesett explained that
petitioner did not report severe pain but did have mild shooting pains across his chest
the night before. (Id. at73.) Petitioner was able to shrug his shoulders at this time and
told Dr. Winesett that his condition had been improving since he was admitted. (Id.)
Petitioner’s motor exam showed significant increase in his strength since he had been
admitted the previous morning: up to 4/5 in his right deltoid but inability to raise it above
45 degrees, 4+/5 strength in both biceps, 4+/5 strength in his left deltoid, 4+/5 strength

f atigue, ataxia, dyspnea, tachycardia, nausea, vomiting, and drowsiness. It can lead to coma and
sometimes death. (Id. at 1130.)
9
    A condition related to loss of blood supply to the spinal cord. (Dorland’s, p. 949.)

                                                        6
in his hands, and good triceps strength. (Id. at 74.) Petitioner’s biceps, brachioradialis,
patella, and ankle reflexes were all symmetrical and normal. (Id.) Petitioner
experienced good, although somewhat slow, finger tapping, with a sensory level at his
upper chest. (Id.)

       Dr. Winesett’s impression was that petitioner was suffering from “possible
Parsonage Turner Syndrome with an autoimmune brachial plexitis.” (Id.) He also
reported, however, that “[o]ther autoimmune processes are also possible.” (Id. at 74.)
Dr. Winesett recommended an MRI of petitioner’s brachial plexus to ensure that there
were no mass lesions, an EMG and nerve conduction study in two weeks “when it
would be more useful,” and a spinal tap if petitioner’s condition deteriorated. (Id. at 74-
75.)

        Petitioner was seen by Drs. Ronald A. Ford and Jordan Larden on January 18
and 19, 2013. (Ex. 7, pp. 78, 81.) On January 18, Dr. Ford noted that petitioner had 4/5
distal strength in his bilateral upper extremities, 5/5 proximal strength in his bilateral
upper extremities, and 5/5 strength in his bilateral lower extremities. (Id. at 83.) Dr.
Ford noted that the top of his differential diagnosis was “brachial plexopathy secondary
to flu vaccination,” but also considered autoimmune etiologies with “ANA, CRP, ESR.”
(Id. at 83-84.) On January 19, Dr. Ford observed poor grip strength, but 4/5 distal
strength in petitioner’s bilateral upper extremities, 5/5 proximal strength in petitioner’s
bilateral upper extremities, and 5/5 strength in bilateral lower extremities. (Id. at 79.)
Dr. Ford believed that petitioner’s recent flu vaccine was the “most likely etiology” of his
bilateral upper extremity weakness and neuropathic pain. (Id. at 80.) Dr. Ford also
noted that he would consider IVIG or steroids if petitioner’s condition deteriorated. (Id.)

          Petitioner was examined by Dr. Winesett again on January 19 and 20, 2013.
(Ex. 7, pp. 84-85.) On January 19, Dr. Winesett noted that petitioner continued to
improve, could bring food to his mouth, and was able to scratch his nose. (Id. at 85.)
Dr. Winesett also noted that petitioner had good biceps strength and could raise his
arms over his head. (Id.) Petitioner’s grip strength had returned to normal, his deltoids
were still weak on the right side at approximately 4+/5 at this time, and stronger, but not
back to normal on the left. (Id.) Dr. Winesett noted that he intended to order a brachial
MRI, but that overall, he believed petitioner’s weakness was improving and did not see
the need for IVIG or plasmapheresis at the time. (Id.) The following day, January 20,
Dr. Winesett reported additional progress, noting that petitioner could lift his hands
above his head, had very strong grip, had much more rapid finger-tapping, but had “a
little bit” of pain in the back of his neck and shoulders. (Id. at 84.) Dr. Winesett believed
that petitioner’s condition was a result of “resolving [PTS].” (Id.)

        Prior to discharge from ACH, petitioner was evaluated by Occupational Therapist
Lisa J. Kezar, OTR/L. (Ex. 7, pp. 158-63.) Ms. Kezar found that petitioner presented
with a “significant decline” in bilateral upper extremity active range of motion (“AROM”).
(Id. at 160.) Ms. Kezar noted a right-shoulder-flexion of 1-10 degrees before
compensatory scapular elevation and abduction, decreased AROM of the pinky, and 0-
40 degrees left-shoulder flexion. (Id.) Ms. Kezar also noted that petitioner’s bilateral

                                              7
UE strength was “significantly compromised” with his shoulder movements being the
most significantly impacted. (Id. at 161.) Ms. Kezar did not test petitioner’s sensation,
and believed that he may have “some altered sensation due to brachial plexus
involvement” but believed that petitioner’s condition was “primarily motor based.” (Id.)

       Petitioner was discharged from ACH on January 20, 2013 with a diagnosis of
brachial neuritis and neuropathic pain. (Ex. 2, p. 9.) Petitioner was seen by his primary
care physician Dr. Lynne Ellis on January 21, 2013 who noted that petitioner had “a
reaction to our flu vaccine.” (Ex. 1, p. 2.)

        Petitioner attended physical therapy at the Therapy and Sports Center in Saint
Petersburg, Florida from January 22, 2013 to September 24, 2013. (Ex. 4, pp. 4-34.)
He was initially admitted with an injury described as a “result of the flu shot 1/11/13,”
with onset being noted as starting on January 17, 2013. (Id. at 4.) Records from the
Therapy and Sports Center show that petitioner’s strength and endurance consistently
improved shortly after he began physical therapy and remained at around 90 to 100%
for the remainder of his therapy. (See generally, Ex. 4.)

        After he was discharged from ACH, petitioner received several follow-up exams
from Dr. Winesett. (Ex. 3, pp. 1, 3, 5.) The first follow-up occurred on January 30, 2013.
(Id. at 5.) During that exam, petitioner received a nerve conduction study of his left arm
and leg, and an EMG of his left and right upper arms, the results of these studies were
normal besides a rare fasciculation on petitioner’s EMG. (Id. at 5-8.)

        Petitioner returned to Dr. Winesett on April 15, 2013. (Ex. 3, p. 1.) Dr. Winesett
noted that petitioner’s bilateral shoulder weakness had resolved after some months, and
that he was “back to normal except for his right leg has continued to be numb.” (Id.)
Petitioner’s motor exam showed normal tone, bulk, and strength in all four extremities.
(Id.) However, Dr. Winesett noted that petitioner’s sensory exam was “quite abnormal”
in that petitioner experienced a distinct change in sensation by about 50% at about one
centimeter from the midline in the front and back, and at the T4 nerve root distribution in
the front and back. (Id.) Dr. Winesett observed normal and symmetric reflexes in all
four extremities, downgoing Babinskis, normal gait, and normal coordination. (Id.) Dr.
Winesett also noted that a Magnetic Resonance Angiography (“MRA”) of petitioner’s
brain and cervical spine was normal. (Id. at 2.) On May 1, 2013, Dr. Winesett
performed a cervical and thoracic spinal MRI, the results of which were normal apart
from the subtle bulge at C5-C6 observed during petitioner’s initial MRI on January 18,
2013. (Id. at 3.)

      Petitioner later saw podiatrist Dr. Kopelman for an unrelated toe contusion where
he reported continued right leg numbness. (Ex. 5, p. 7.)

        The final record from Dr. Winesett documents a neurological follow up exam on
November 13, 2013. (Ex. 8, p. 17.) Dr. Winesett noted at this exam that petitioner’s
condition had largely resolved apart from some numbness in his mid-chest. (Id.)
Petitioner’s motor exam was normal, but did reveal a slight postural tremor that Dr.

                                             8
Winesett did not believe was related to petitioner’s brachial neuritis. (Id.) Dr. Winesett
concluded this exam with a diagnosis of slowly recovering brachial neuritis. (Id.)

     IV.    Experts

            a. Petitioner’s First Expert, Thomas F. Morgan, M.D – Initial Report

        Petitioner initially filed an expert report from neurologist Thomas F. Morgan,
M.D., to support his claim.10 (Ex. 12.) Dr. Morgan believed that petitioner’s symptoms
of hyperreflexia in the lower extremities, bilateral weakness of the upper extremities,
and burning paresthesia across the chest support an anatomic diagnosis of
radiculomyelitis. (Id. at 3.) Dr. Morgan explained that although petitioner’s normal EMG
and nerve conduction tests do not support a finding of pure brachial plexopathy, such a
diagnosis cannot be ruled out without a spinal fluid analysis, which petitioner never
received. (Id.) Consequently, Dr. Morgan was unable to diagnose or rule out a pure
brachial plexopathy based on petitioner’s existing medical records. (Id.) Instead, Dr.
Morgan believed that petitioner suffered radiculomyelitis triggered by an immune
response to his January 11, 2013 flu vaccination. (Id. at 3-4.) Dr. Morgan opined that
the lack of spinal fluid analysis does not impact this clinical diagnosis because the
symptoms with which petitioner presented to the ER are consistent with radiculomyelitis.
(Id. at 4.)

        Dr. Morgan further opined that petitioner’s immune antibody response from his flu
vaccine triggered a mechanism known as “molecular mimicry”, causing a cross reaction
“with the myelin of his dorsal and ventral nerve roots and a portion of the adjacent spinal
cord,” causing funicular spinal cord pain from C5 to T4.” (Id.) He concluded his report
by noting that the time of onset of petitioner’s post vaccinal reaction is consistent with
the time of onset for a molecular mimicry immune response following a vaccine and
therefore, the temporal relationship between the condition and the vaccine should not
be at issue. (Id.)

            b. Respondent’s Expert, Vinay Chaudhry, M.D. – Initial Report

        Respondent filed a report by neurologist Vinay Chaudhry, M.D. in response to
petitioner’s expert report by Dr. Morgan.11 (Ex. A.) Dr. Chaudhry did not agree that

10
  Dr. Morgan received his medical degree from Meharry Medical College in 1970. (Ex. 13, p. 1.) He is
board certified by the American Board of Independent Medical Examiners, the American Board of
Psychiatry and Neurology, and the Rhode Island Board of Medical Licensure and Discipline. (Id. at 3.)
As of the date of his curriculum vitae, Dr. Morgan is an assistant clinical professor at Brown University
where he also serves on the university healthcare team and as a neurology consultant. (Id. at 4.) Dr.
Morgan has authored numerous publications relating to neurology and neuropathology and has
conducted a variety of neurological studies. (Id. at 4-5.)
11
  Dr. Chaudhry received his medical degrees in 1980 f rom the All India Institute of Medical Sciences in
New Delhi, India. (Ex. B, p. 1.) He received his MBA in the Business of Medicine from Johns Hopkins
University in 2009. (Id.) Dr. Chaudhry is licensed in the state of Maryland and holds over a dozen
certif ications from organizations in the United States, United Kingdom, and India. (Id. at 28-29.) Dr.
Chaudhry was chief resident of neurology at the University of Alabama School of Medicine, and a clinical

                                                    9
petitioner’s clinical presentation and lab results support a diagnosis of either brachial
neuritis or radiculomyelitis.

        Dr. Chaudhry noted that brachial neuritis is “typically heralded by the abrupt
onset of severe pain (≥ 7/10) located in the shoulder or upper arm region that lasts for
2-3 weeks.” (Ex. A, p. 3 (citing Jeroen van Eijk, Jan T. Groothuis & Nens van Alfen,
Neuralgic Amyotrophy: An Update on Diagnosis, Pathophysiology, and Treatment
Muscle Nerve, 53 M USCLE AND NERVE 337 (2016) (Ex. C)).) Dr. Chaudhry indicated that
petitioner awoke with weakness instead of severe pain and that petitioner’s treating
neurologist, Dr. Winesett, specifically noted that petitioner only experienced some
shooting pain but never any severe pain. (Ex. A, p. 3.) Dr. Chaudhry also explained
that although petitioner suffered headaches that were a 6 to 7 on the pain scale,
headaches are not a symptom of brachial neuritis. (Id.) Additionally, Dr. Chaudhry
explained that recovery from brachial neuritis takes at least several months and often 2-
3 years. (van Eijk, Groothuis, & van Alfen, supra, at Ex. C.) In petitioner’s case, he was
showing fluctuating improvement within hours and had almost fully recovered within
three months. (Id. at Ex. A, pp. 4-5, (citing Ex. 3, p. 4).)

        According to Dr. Chaudhry, in cases of brachial neuritis, prominent weakness
and wasting occurs in shoulder girdle muscles in the distribution of individual nerves.
(Id. at 3.) Most often, the long thoracic, suprascapular and anterior interosseous nerves
are involved. (Id.) Brachial neuritis patients often experience tingling of the superficial
radial and lateral antebrachial cutaneous nerves, and a numb path on the lateral upper
arm in the axillary nerve distribution. (Chee Keong Chan et al., Cervical Cord
Compression Presenting with Sciatica-like Leg Pain, 20 EUR. SPINE J. 217 (2011) (EX.
E).) Further, when bilateral involvement occurs with brachial neuritis, such involvement
is asymmetrical and follows a specific nerve distribution. (Ex. A, p. 4.) Petitioner
however, experienced abrupt, symmetrical and bilateral weakness of the upper
extremities and did not experience any sensory loss in any of the nerve distributions
associated with brachial neuritis. Petitioner also noted neck, chest, and leg symptoms
including varying pain, sensory loss, and weakness in these areas, which Dr. Chaudhry
explained are inconsistent with brachial neuritis. (Id.)

        Dr. Chaudhry also noted that injuries to the brachial plexus result in loss of
reflexes, weakness, and sensory loss. (Id. at 5.) Petitioner however, had normal
reflexes and sensation in his biceps, brachioradialis, patella, and ankle. (Id.)
Additionally, petitioner’s nerve conduction, EMG findings, and MRIs were all normal and
showed no change in petitioner’s brachial plexus which, according to Dr. Chaudhry,
“virtually excludes nerve injury.” (Id.) Dr. Chaudhry explained that petitioner’s clinical
manifestation, normal EMG, and normal brachial plexus MRI all rule out any injury to the
brachial plexus and therefore rule out a brachial neuritis diagnosis. (Id.) Dr. Chaudhry

and research f ellow focusing on neuromuscular diseases at Johns Hopkins University. (Id. at 2.) He has
taught neurology at Johns Hopkins since 1989 and has authored over 120 scholarly articles and textbook
chapters on neurological disorders. (Ex. A, p. 1.) Dr. Chaudhry evaluates over 2000 patients a year
mostly related to peripheral nerve disease. (Id.)

                                                  10
suggested that Dr. Morgan was mistaken when he noted that petitioner developed
painful bilateral upper extremity weakness from C5 to T4, because there is no evidence
that his initial presentation of weakness was associated with pain. (Id.)

        Dr. Chaudhry also disagreed with Dr. Morgan’s proposed diagnosis of
radiculomyelitis. Dr. Chaudhry explained that the first component of radiculomyelitis is
radiculopathy which he describes as a nerve root injury associated with abnormal nerve
conduction and EMG. (Ex. A, p. 6.) Radiculopathy is also accompanied by reduced or
absent reflexes, but Dr. Chaudhry noted that petitioner exhibited normal or increased
reflexes. (Id.) Further, Dr. Chaudhry noted EMG findings in brachial neuritis cases are
identical to those in radiculopathy cases. (Id.) Thus, Dr. Chaudhry believed that
petitioner’s normal EMG rules out radiculopathy in the same way it rules out brachial
neuritis. (Id.)

       According to Dr. Chaudhry, radiculomyelitis involves acute transverse myelitis
which is “invariably associated with paralysis in the legs, urinary urgency, incontinence,
pathological brisk reflexes, and spasticity in addition to a sensory level.” (Chitra
Krishnan & Benjamin Greenberg, Transverse Myelitis, UPTODATE (2017) (Ex. F).)
Because he found no evidence that petitioner had any incontinence, leg paralysis, or
abnormal reflexes, Dr. Chaudhry concluded that petitioner’s symptoms were
inconsistent with myelitis. (Ex. A, p. 6.)

       Dr. Chaudhry opined that Dr. Morgan’s diagnosis of radiculomyelitis is unreliable
because petitioner’s medical records lack any objective diagnostic studies supporting
such a diagnosis. (Id.) He indicated that not only are the clinical findings inconsistent
with radiculomyelitis, but petitioner’s normal medical imaging explicitly rules out
radiculopathy and myelitis. (Id.) Dr. Chaudhry concluded that petitioner suffered from
neither radiculopathy nor myelitis and thus did not suffer from radiculomyelitis. (Id.)

         Dr. Chaudhry conceded that petitioner did suffer some abnormal condition,
potentially as a result of his high carboxyhemoglobin and high methemoglobin levels.
(Id. at 7.) However, Dr. Chaudhry opined that petitioner’s symptoms, EMG, and MRI all
fail to support either a diagnosis of brachial neuritis or radiculomyelitis. (Id.)

          c. Dr. Morgan’s Supplemental Report

        In response to Dr. Chaudhry, Dr. Morgan agreed that petitioner’s clinical
manifestations, normal EMGs, and normal MRIs do not support a diagnosis of brachial
neuritis, which he had initially declined to rule out. (Ex. 17, p. 1.) Dr. Morgan disagreed
with Dr. Chaudhry however, regarding whether petitioner originally complained of upper
extremity pain. (Id.) Dr. Morgan cited records from ACH, which note that petitioner was
suffering from neck and shoulder pain in addition to upper extremity weakness. (Id.
(citing Ex. 7, p. 76.)) He suggested that Dr. Chaudhry confused radiculomyelitis with
classic transverse myelitis, and that petitioner’s neck and shoulder pain, while
inconsistent with transverse myelitis, are nonetheless consistent with radiculomyelitis.
(Ex. 17, p. 1.)

                                            11
        Dr. Morgan believed that although there is no evidence in the record clearly
supporting his preferred diagnosis, this is only because petitioner did not receive the
tests necessary to collect such evidence. (Id. at 1-2.) Dr. Morgan explained that the
pathology of radiculopathy can be evidenced by an abnormal EMG, but that neither
petitioner’s ascending sensory tracts in the spinal cord nor his motor nerve roots at C8
through T4 were tested by somatosensory evoked responses or EMG and nerve
conduction. (Id. at 2.) Because petitioner’s pain was referred up to the C5 level in the
spinal cord and did not involve the C5 nerve roots itself, Dr. Morgan believed that EMG
and nerve conductions for the brachial plexus or peripheral radiculopathy would not
have detected any abnormalities even if these tests were ordered. (Id.)

        Dr. Morgan suggested that, contrary to Dr. Chaudhry’s report, reduced or absent
reflexes would “not necessarily be reflected in a myeloradiculitis located from C5
through T4.” (Id.) He did concede Dr. Chaudhry’s point however, that petitioner did not
have a classic presentation for acute transverse myelitis. (Id.) Instead, Dr. Morgan
argued that petitioner had a “subacute post vaccinal myelo-radiculitis that was an
atypical presentation,” sparing the C5 nerve. (Id.) Dr. Morgan noted that the medical
literature shows that atypical cases often require repeated examinations to localize
abnormalities to the spinal cord. (Id. (citing Allan H. Ropper, Martin A. Samuels &
Joshua P. Klein, Adams and Victor’s Principles of Neurology (10th ed. 2014) (Ex. 18)).)
Dr. Morgan explained that petitioner did not receive repeat cervical or thoracic MRI
scans with gadolinium, nor somatosensory evoked response tests for the spinal cord
tracts, any of which, in his opinion, would have localized petitioner’s injury to the spinal
cord. (Ex. 17, p. 2.)

        Dr. Morgan believed that petitioner’s myelitis in effect simulated brachial neuritis,
which led to that diagnosis being made by the treating physicians. Although petitioner’s
normal EMG, normal MRI studies, and clinical presentation were against brachial
neuritis, the tests run on petitioner did not observe the spinal cord from C5 to T4, which
Dr. Morgan seemingly presumes would have confirmed petitioner’s myelitis. (Id.) Dr.
Morgan believed that petitioner’s condition is anatomically located in the spinal cord
consistent with a post vaccinal immune mediated neurologic syndrome, and not his
brachial plexus. (Ex. 17, p. 3.)

       Dr. Morgan disagreed with Dr. Chaudhry’s conclusion that petitioner’s symptoms
were unclear and of uncertain cause. According to Dr. Morgan, the first step of basic
diagnosis is to “localize patient’s complaints, symptoms and signs and to determine the
neuro-anatomic location of the problem.” (Id.) Dr. Morgan believed that the anatomic
location of petitioner’s symptoms was “the spinal cord myelitis that effected the exiting
nerve roots to account for his myelo radiculitis.” (Id.) According to Dr. Morgan, this
location would indicate a “subacute, post vaccinal myelo-radiculitis.” (Ex. 17, p. 3 (citing
Ex. 20).) Dr. Morgan suggested that further diagnostic testing such as a high field MRI,
somatosensory response testing, and spinal fluid analysis would have been helpful, but
that even without these studies, he believed that petitioner suffered from “a post
vaccinal myelo-radiculitis and not a diagnosis of uncertain cause.” (Ex. 17, p. 3.)

                                             12
            d. Dr. Chaudhry’s First Supplemental Report

        Dr. Chaudhry’s first supplemental report specifically responded to points raised
by Dr. Morgan’s supplemental report. First, Dr. Chaudhry noted the inconsistency
between Dr. Morgan’s first report, wherein he stated that petitioner presented with
clinical findings of myelitis and brachial neuritis, and Dr. Morgan’s supplemental report,
wherein he conceded that petitioner’s clinical presentation does not support a diagnosis
of brachial neuritis. (Ex. G, p. 1.) Dr. Chaudhry further stressed that none of
petitioner’s treating physicians entertained a radiculomyelitis diagnosis even though a
variety of other neurological conditions were considered. (Id.) Additionally, Dr.
Chaudhry reiterated that petitioner never had a spinal fluid evaluation, never had an
MRI which supported such a diagnosis, and was never treated for spinal cord
inflammation which is a common symptom of myelitis. (Id. at 1-2.)

        Dr. Chaudhry pointed out that Dr. Morgan’s conclusion that petitioner’s EMG was
normal because the C5 nerve was spared by his radiculomyelitis is incorrect. According
to Dr. Chaudhry, several symptoms indicate a C5 nerve root involvement including
weakness in petitioner’s biceps, deltoids, and hands. (Id. at 2.) Further, Dr. Morgan
suggested twice in his first report that petitioner’s C5 nerve root was involved, and again
in his supplemental report. (Id.) Dr. Chaudhry explained that Dr. Morgan incorrectly
noted that reduced or absent reflexes are not reflected in radiculomyelitis from C5 to T4.
(Id.) However, physicians routinely test reflexes of the biceps, brachioradialis, and
triceps when diagnosing radiculomyelitis. (Id.) Each of these muscles involve either the
C5, C6, or C7 nerve root, and therefore, reduced or absent reflexes from C5 to T4 can
indeed be reflected in radiculomyelitis. (Id.)

        Dr. Chaudhry concluded his report by noting that Dr. Morgan’s diagnosis of
myelitis is not supported by any of petitioner’s medical records, and in fact, can be
excluded by petitioner’s multiple normal MRIs. (Id. at 3.) Further, Dr. Chaudhry pointed
out that Dr. Morgan provided no references nor support from the record for his finding of
“atypical myeloradiculitis.” (Id.) First, the degree of myelitis that Dr. Morgan references
involves eight spinal cord levels and should have shown some abnormalities on
petitioner’s MRIs. (Id.) Additionally, a Somatosensory Evoked Potential study was
ordered on May 8, 2013, and while the results of this study are missing from the record,
Dr. Chaudhry noted that there were no notes referencing the test on a follow up by Dr.
Winesett. (Id.) Based on the above findings, Dr. Chaudhry indicated he is unable to
agree with Dr. Morgan’s diagnosis of atypical radiculomyelitis. (Ex. G, p. 3.)

            e. Petitioner’s Second Expert, Salvatore Napoli, M.D.

       Following Dr. Morgan’s withdrawal as an expert in the case, petitioner filed a
report by neurologist Dr. Salvatore Napoli.12 (ECF No. 65; Ex. 21.) Dr. Napoli

12
   Dr. Napoli received his medical degree from Albany Medical College in 1999. (Ex. 22, p. 2.) He is
currently the president and owner of the Neurology Center of New England, specializing in MS care with
f ocuses on other neurological diseases. (Id. at 1.) He also holds staff positions at Beth Israel at Milton

                                                    13
reintroduced the brachial neuritis diagnosed by petitioner’s treating physicians as a
relevant condition, beginning his report by describing brachial neuritis as a condition
characterized by severe onset of regional pain, muscle weakness, and wasting. (Ex.
21, p. 4.) He explained that most patients experience these symptoms in a single
event, but approximately 12% of patients experience multiple bouts or recurrences
involving either the same limb or the contralateral limb. (Id. (citing Mark A Ferrante &
Francesc Graus, Neuralgic Amyotrophy, NEUROLOGY M EDLINK (2020) (Ex. 23) (herein
“Medlink”).) According to Dr. Napoli, these recurrent cases may also involve the same
nerves or have a different distribution of nerve involvement. (Ex. 21, p. 4.) Dr. Napoli
noted that in cases of bilateral symptoms like petitioner experienced, the involvement is
“sequential in the majority and simultaneous in the minority.” (Id. (citing Medlink supra at
Ex. 23.)) Dr. Napoli believed that the medical literature suggests both sides can be
involved at the same time and petitioner’s physicians seemed aware of this given their
diagnosis of brachial neuritis. (Ex. 21, p. 4.) Dr. Napoli further explained that available
evidence suggests that an autoimmune pathogenesis is likely related to a genetic
susceptibility that most commonly generates an axonal-loss lesion. (Id.) (citing Medlink
supra at Ex. 23.)

        According to Dr. Napoli, “it is a known fact” that brachial neuritis has a wide
variety of clinical presentations. (Ex. 21, p. 4.) However, the distinctive features include
a recognized trigger, regional pain, and regional muscle weakness. (Id.) Even when
this presentation is inconclusive, the disorder is typically recognized by the important
features of pain and muscle weakness which are almost always present. (Id.) In a
study of 281 brachial neuritis patients, only 8% presented without pain. (Id. (citing Mark
A. Ferrante & Asa J. Wilbourn, Lesion Distribution Among 281 Patients with Sporadic
Nerualgic Amyotrophy, 55 M USCLE & NERVE 858 (2017) (herein “Ferrante and Wilbourn”)
(Ex. 27).) Although reports found that a majority of patients presented with focal pain,
Dr. Napoli noted that a minority of patients can present with focal sensory loss like
petitioner. (Ex. 21, p. 4 (citing Ferrante & Wilbourn, supra, at Ex. 27, p. 2.)

        Dr. Napoli explained that the Ferrante study identified a trigger in 73% of brachial
neuritis patients. (Ex. 21, p. 4.) Dr. Napoli indicated that the study reported that 5% of
the cases were associated with a vaccination, and 24% of cases were associated with
an upper respiratory or nondescript flulike illness. (Id.) Dr. Napoli suggested that these
vaccine and viral associations support the assertion that brachial neuritis can have an
autoimmune etiology. (Id.) He also noted that the Medlink study found that the most
commonly affected nerves in brachial neuritis cases are the suprascapular nerve and
the long thoracic nerve, both of which are pure motor nerves. (Id.) According to Dr.
Napoli, petitioner’s distribution of weakness suggests that at least one, and potentially
both of these nerves were involved. (Id.)

Hospital and Steward Norwood Hospital. (Id.) Dr. Napoli was also an instructor in neurology at the
Brigham and Women’s Hospital MS Center at Harvard Medical School. (Id.) He holds a Massachusetts
f ull medical license and is certified by the American Board of Psychiatry and Neurology. (Id. at 2.) He
has published three papers on multiple sclerosis and neuromyelitis optica, and participated in 17 different
clinical trials and research projects focused a variety of neurological disorders. (Id. at 3-5.)

                                                    14
       Dr. Napoli also agreed, however, that petitioner also suffered radiculomeylitis,
defining the term as “inflammation that affects the spinal cord and nerve roots and can
cause pain, sensory disturbance and weakness, among other symptoms.” (Id. at 5.)
He indicated that a diagnosis of radiculomyelitis can sometimes, but not always, be
supported by diagnostic tests like MRIs. (Ex. 21, p. 5.) He also explained that “there
have been case reports showing MRI negative cases of myelopathy and clinical
transverse myelitis.” (Id.) The key to diagnosis, Dr. Napoli opined, is looking at how
the patient presents clinically instead of depending solely on negative diagnostic tests.
(Id.)

       Dr. Napoli opined that petitioner’s clinical presentation was consistent with both
brachial neuritis and radiculomyelitis. He explained that a radiculomyelitis diagnosis
would be supported by petitioner’s T4 sensory level with alternating upper motor neuron
signs that are seen in transverse myelitis (e.g. petitioner’s Babinski signs). (Id.) Dr.
Napoli admitted that petitioner did not present with classic transverse myelitis
symptoms, but that his symptoms, complaints, and physical exam support a finding of
radiculomyelitis. (Id.) According to Dr. Napoli, petitioner’s symptoms in his right arm
and right leg, sensory level involving the chest and nipple, hemisensory loss, and signs
of Babinski localized his lesion to the C5-T4 level are consistent with radiculomyelitis.
(Id.)

       Dr. Napoli believed that molecular mimicry explains how petitioner’s flu
vaccination caused his injury. He explained that molecular mimicry occurs where, after
vaccination or infection, a patient’s immune system will target not only the vaccine
antigens, but also host antigens present in the patient’s body which share any homology
with the vaccine antigens. (Ex. 21, p. 5 (citing Riita Lahesmaa et al., Molecular
Mimickry Between HLA B27 and Yersinia, Salmonella, Shigella and Klebsiella within the
Same Region of HLA α1-helix, 86 CLINICAL & EXPERIMENTAL IMMUNOLOGY 399 (1991)
(EX. 24)).) In these cases, the patient’s immune system will target itself in addition to
the vaccine antigens and create an immune response that may cause various
neurological disorders. (Ex. 21, p. 5.)

       Dr. Napoli noted that there have been many examples of flu vaccines triggering
peripheral and central nervous system disorders similar to brachial neuritis and
radiculomyelitis, with Guillain-Barre Syndrome (“GBS”) being the most prominent. (Id.)
A study conducted by Schonberger et al. in the 1970’s found 532 GBS patients had
received flu vaccines prior to the onset of their symptoms. (Lawrence Schonberger et
al., Guillain-Barre Syndrome Following Vaccination in The National Influenza
Immunization Program, United States, 1976-1977, AM. J. OF EPIDEMIOLOGY 105 (1979)
(Ex. 25).) In 1976, a statistically significant association was found between an
increased risk for GBS and the novel swine flu vaccine. (Ex. 21, p. 6.) A third study by
Haber et al. which found case reports of GBS following various types of vaccine
administrations, including influenza, rabies, oral polio, and hepatitis. (Penina Haber et
al., Vaccines and Guillain-Barre Syndrome, 32 DRUG SAFETY 309 (2009) (Ex. 26).)

                                            15
        In addition to reports of GBS, Dr. Napoli cited several case reports of acute
brachial neuritis reported after various vaccinations, including influenza. (Ex. 21, p. 6.)
In one case, a 66-year-old man presented with acute brachial neuritis with an onset
beginning approximately one week after receiving the flu vaccine. (Jimmy D. Miller et
al., Acute Brachial Plexus Neuritis: An Uncommon Cause of Shoulder Pain, 62 AM.
FAMILY PHYSICIAN 2067 (2000) (Ex. 28).) This same study noted that up to 15% of cases
had been reported to occur following vaccinations. (Id.) A second case reported a 46-
year-old woman whose symptoms began within days of receiving a flu vaccine. (Maliha
Farhana Shaikh, Tanya Jane Baqai & Hasan Tahir, Acute brachial neuritis following
influenza vaccination, BMJ CASE REP. (2012) (Ex. 29).) A third case reported a 65-year-
old man who experienced symptoms within six days of vaccination, and a final case
described a 61-year-old male who experienced symptoms within six weeks after
vaccination. (Otto Hansen, Akut brakial neuropati efter influenzavaccination, 167
UGESKRIFT FOR LAEGER 1297 (2005) (Ex. 30); D. H. Marks, Parsonage-Turner
Syndrome Associated With Influenza Vaccination: A Case Report With Discussion Of
Vaccination Neurologic Complications And Causation, 21 THE INTERNET J. OF
NEUROLOGY 1 (2019) (EX. 31).) Dr. Napoli cited these cases to conclude that there is a
reasonably possible link between vaccines and neurological disorders such as brachial
neuritis and radiculomyelitis. (Ex. 21, p. 6.)

         Dr. Napoli indicated that GBS cases have developed within a five-week period
following vaccination. (Schonberger et al., supra, at Ex. 25.) He suggested this GBS
timeline is consistent with the previously cited case reports of both brachial neuritis and
radiculomyelitis, which showed onsets ranging from several days to weeks following
vaccination. (Ex. 21, p. 6.) Because the onset of petitioner’s symptoms occurred within
six days of his vaccination, Dr. Napoli concluded that petitioner’s injury is consistent with
the appropriate timeline for post-vaccine neurologic injuries. (Id.) Based on the opinion
of Dr. Winesett as well as the timeframe for brachial neuritis onset following vaccination,
it is his opinion that petitioner’s flu vaccination caused his brachial neuritis. (Id. at 7.)
Dr. Napoli concluded that petitioner’s radiculomyelitis and brachial neuritis were both
caused by his January 11, 2013 flu vaccination. (Id.)

          f. Dr. Chaudhry’s Second Supplemental Report

        In his final report, Dr. Chaudhry addressed Dr. Napoli’s conclusion that petitioner
suffered from brachial neuritis. Dr. Chaudhry indicated that the onset of petitioner’s
symptoms are inconsistent with brachial neuritis, reiterating that brachial neuritis is
associated with the abrupt onset of severe pain in the shoulder or upper arm region
lasting for two to three weeks, followed by weakness in the distribution of the nerves of
the plexus. (Ex. H, p. 1.) Petitioner experienced weakness instead of severe pain and
began to recover within 24 hours. (Id.) Dr. Chaudhry further explained that brachial
neuritis is a dysfunction of one or two nerves of the brachial plexus which results in
weakness and atrophy of those muscles on a single side. (Id.) In petitioner’s case, the
entire brachial plexus was involved, and his symptoms occurred bilaterally. (Id.)
According to Dr. Chaudhry, brachial neuritis also involves axonal degeneration and
atrophy which recovers through a drawn-out regeneration process typically lasting six

                                             16
months to a year. (Id. at 2.) Petitioner however, showed significant signs of
improvement within 24 hours. (Id.) Further, Dr. Chaudhry noted that none of
petitioner’s EMG or MRI findings suggest any abnormalities which should be present in
a brachial neuritis patient. (Id.)

        Dr. Chaudhry accepted Dr. Napoli’s argument that a small percentage of brachial
neuritis cases involve bilateral involvement and present without pain, but noted that
“none of the clinical features, electrophysiological features, [or] imaging features [were]
indicative of brachial neuritis.” (Id.) He further indicated that Dr. Napoli failed to explain
petitioner’s rapid improvement, normal imaging, and fluctuating symptoms and thus, has
not presented any evidence that this was in fact an atypical case of brachial neuritis.
(Id.)

       Dr. Chaudhry noted that Dr. Napoli “does not provide a single reference” to the
term “radiculomyelitis” but defines it as “inflammation that affects the spinal cord and
nerve root.” (Id.) Consequently, Dr. Chaudhry’s discussion of Dr. Napoli’s
radiculomyelitis diagnosis focused on both radiculitis (inflammation of the C5 to T4
nerve roots) and myelitis (inflammation of the C5 to T4 spinal cord).

       Dr. Chaudhry does not believe that petitioner suffered radiculitis because there
were no EMG changes in the associated muscles and his MRIs were normal. (Id.)
There was also no sensory loss in petitioner’s arms, and petitioner’s reflexes were
normal. (Id.) Further, petitioner’s rapid improvement within 24 hours suggests that he
was not suffering from nerve root inflammation because, if that were the case, it would
certainly not improve so much within one day. (Id. at 3.) Finally, the only finding that
suggests a nerve root injury is petitioner’s numbness at T4 on the right side. (Id.)
However, Dr. Chaudhry noted that this symptom only appeared on an April 2013 follow
up exam and was no longer significant by November 2013. (Id.) Consequently, Dr.
Chaudhry concluded that nothing in petitioner’s medical records support a radiculitis
diagnosis. (Id.)

        Dr. Chaudhry further explained that spinal cord disorders such as myelitis are
characterized by motor, sensory, and autonomic abnormalities below the spinal cord
injury. (Ex. H, p. 3.) Dr. Chaudhry noted that a spinal cord injury from C5 to T4 should
cause bilateral lower extremity weakness, but that petitioner had normal lower extremity
strength. (Id.) Additionally, a C5 to T4 injury should cause bladder incontinence,
sensory loss up to the cervical spinal cord level, pathologically brisk reflexes, and
Babinski, but petitioner did not exhibit any of these symptoms at the time that he was
thought to have a lesion at the T4 sensory level. (Id.)

       Most importantly, Dr. Chaudhry opined that spinal cord inflammation
demonstrated by either a CSF pleocytosis elevated IgG index, or MRI evidence is a
required criterion for transverse myelitis diagnosis. (Id. at 4.) Although petitioner did
not have a spinal tap, two MRIs failed to show any spinal cord involvement. (Id.)
Further, petitioner had no sensory, motor, or autonomic dysfunction attributable to the
spinal cord either on admission or discharge. (Id.) Instead, he developed a transient

                                             17
sensory level three months after his discharge. (Id.) Dr. Chaudhry opined that
petitioner’s two normal MRIs specifically exclude a diagnosis of myelitis, and therefore,
Dr. Napoli’s radiculomyelitis diagnosis is incorrect. (Id.)

       Dr. Chaudhry suggested that while Dr. Napoli discusses molecular mimicry as a
hypothesis, he failed to provide any reference showing that brachial neuritis and
radiculomyelitis have a molecular mimicry pathogenesis. (Id.) Dr. Chaudhry explained
that while Dr. Napoli is correct that the flu vaccine has been linked to increased cases of
GBS, these findings have no bearing on brachial neuritis or radiculomyelitis. (Id.) Dr.
Chaudhry stressed that the Institute of Medicine has reviewed all epidemiological and
mechanistic evidence of flu related transverse myelitis and brachial neuritis but only
found a temporal, not a causal association. (Id. at 4-5.)

          g. Entitlement Hearing

       As noted above, Drs. Napoli and Chaudhry also testified during the October 27,
2020 entitlement hearing. Each provided testimony consistent with their above-
discussed opinions. That testimony is not separately summarized, but is referenced
and included in the analysis below.

   V.     Diagnosis

        Given the complexity of petitioner’s clinical presentation, the parties raise as a
threshold issue the question of whether I must first consider petitioner’s correct
diagnosis before proceeding to a causation-in-fact analysis under Althen. (See ECF
Nos. 81, 82.) Citing prior Circuit decisions in Lombardi and Broekelschen, respondent
argues that “when the existence of the claimed injury is in question, a threshold issue
preceding the causation analysis under Althen v. [Sec’y of Health & Human Servs.], 418
F.3d 1274 (Fed. Cir. 2005), is whether petitioner has established that he suffers from
the very injury that he alleges was caused by the vaccine.” (ECF No. 82, p. 1) (citing
Lombardi v. Sec’y of Health & Human Servs., 656 F.3d 1343 (Fed. Cir. 2011);
Broekelschen v. Sec’y of Health & Human Servs., 618 F.3d 1339, 1346 (Fed. Cir.
2010)).) Petitioner, on the other hand, argues that Lombardi and Broekelschen are
inapplicable in this case because such precedent only applies when the respondent has
presented evidence to support an alternative diagnosis. (ECF No. 81, pp. 1-2.) Here,
respondent has not presented any such evidence and petitioner argues that I am
therefore not required to find that any specific diagnoses exist before moving on to the
Althen analysis.

        Petitioner is correct that Broekelschen itself involved a dispute between the
parties as to the petitioner’s correct diagnosis. 618 F.3d at 1345. It was in that context
that the Federal Circuit first explained that the analysis of the three Althen prongs is
conducted relative to the alleged injury and thus, “the question of causation turn[s] on
which injury [the petitioner] suffered.” Id. at 1346. The Court concluded that “identifying
the injury is a prerequisite to the [Althen] analysis” and that it was therefore “appropriate
for the special master to first find which of [petitioner’s] diagnoses was best supported

                                             18
by the evidence presented . . . before applying the Althen test . . . .” Id. However, in
Lombardi, the Federal Circuit further considered the reasoning of Broekelschen and
applied it to a case, similar to the instant case, in which it was the petitioner who came
forward with multiple diagnoses. Lombardi, 656 F.3d at 1352-53. The Court explained:

       Lombardi argues that by finding that she had failed to prove the existence
       of any of her injuries, and therefore declining to conduct an Althen analysis
       on any of her alleged injuries, the special master penalized her for alleging
       that she suffered from more than one injury. Lombardi misstates the special
       master's reasoning. The special master did not require Lombardi to narrow
       the number of alleged injuries to one. But the statute places the burden on
       the petitioner to make a showing of at least one defined and recognized
       injury. Here, the special master merely found that Lombardi had failed to
       meet her burden to show by a preponderance of the evidence that she
       suffered from any medically recognized “injury,” not merely a symptom or
       manifestation of an unknown injury.

Id. at 1353; see also Lasnetski v. Sec’y of Health & Human Servs., 696 Fed. Appx. 497
(Fed. Cir. 2017).

        Petitioner stresses the competing consideration that “special masters are not
‘diagnosing’ vaccine-related injuries,” but instead determining whether there is vaccine
causation by preponderant evidence based on a review of the record as a whole. (ECF
No. 81, pp. 1-2 (quoting Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 549
(Fed. Cir. 1994).) In that regard, petitioner intimates that I should conduct an Althen
analysis, and find in petitioner’s favor, because petitioner has suffered autoimmune or
immune-related neurological injuries broadly. Critically, however, petitioner has not
articulated any basis for considering causation-in-fact based on anything other than his
alleged diagnoses of brachial neuritis and/or radiculomyelitis.

         Petitioner explained his showing under Althen as follows: “(1) Johnathan suffered
from Parsonage-Turner Syndrome and radiculomyelitis beginning on January 17, 2013;
(2) a medical theory casually connecting the influenza vaccination and his two
neurological injuries exists; (3) a temporal association exists between the vaccine and
both neurological injuries . . .; and (4) a logical sequence of cause and effect exists.”
(ECF No. 77, p. 42; ECF No. 81, p. 4 (emphasis added).) Moreover, during the hearing,
petitioner’s testifying expert, Dr. Napoli, repeatedly explained that his opinion was that
petitioner’s condition was explained as concurrent brachial neuritis and radiculomyelitis.
(Tr. 12, 48.) (For his part, petitioner’s prior expert, Dr. Morgan, relied on the presence
of radiculomyelitis but not brachial neuritis.) I specifically asked Dr. Napoli if he would
still opine that petitioner’s injury was vaccine-caused in the absence of a diagnosis of
either brachial neuritis or radiculomyelitis. (Tr. 116-17.) He responded that he would,
but when asked to explain the basis for that opinion he indicated that:

       Looking at his clinical scenario, this was a healthy 15-year-old boy who
       received a vaccine and within one week of the vaccine, mounted an immune
       response that now created this constellation of symptoms consistent with

                                            19
       what I believe to be radiculomyelitis and the brachial neuritis, which he was
       struggling with for a period of time and, I believe, still struggles to this day.
       And I believe the trigger was the vaccine.

(Tr. 117 (emphasis added).) Thus, both petitioner’s own framing of his case and his
experts’ causal opinions are explicitly predicated on the presence of brachial neuritis
and/or radiculomyelitis. Indeed, by his own description Dr. Napoli confirmed in effect
that he cannot separate his ultimate causal opinion from his own conclusion that
petitioner’s clinical presentation is consistent with brachial neuritis and/or
radiculomyelitis. Moreover, brachial neuritis and radiculomyelitis are two very different
explanations for petitioner’s symptoms, the former being a peripheral axonal nerve
injury and the latter representing spinal cord inflammation and possible demyelination.
As Dr. Chaudhry expressed during the hearing, an anatomical diagnosis is a threshold
question to discussing etiology. (Tr. 184.) He suggested that to jump to etiology without
resolving anatomical diagnosis is to say “‘Oh, I know what's causing it,’ without even
telling me what -- I can't even prove what it is, it's just leap of faith.” (Id.)

        In sum, petitioner has not articulated a basis for finding causation in the absence
of either a brachial neuritis or radiculomyelitis diagnosis and the question whether
petitioner suffered from radiculomyelitis, brachial neuritis, or a combination of both,
would result in distinct analyses under the Althen test. For these reasons, it is
appropriate to first resolve whether there is preponderant evidence that one or both of
these two conditions is present in this case before assessing whether petitioner has met
his burden under the Althen test.

              a. Radiculomyelitis

        As explained above, petitioner’s initial expert, Dr. Morgan, opined that petitioner’s
condition is entirely explained by radiculomyelitis. His second expert, Dr. Napoli, opined
that petitioner’s condition is explained in part by radiculomyelitis, but also by brachial
neuritis. Dr. Chaudhry opined on behalf of respondent that petitioner’s condition is not
consistent with either condition. Whereas petitioner was diagnosed with brachial
neuritis by his treating physicians, the suspicion of radiculomyelitis was not explored by
those physicians and stems only from his experts’ opinions. However, those opinions
are not well supported by petitioner’s medical history.

       Significantly, despite multiple MRI studies, there is no objective evidence
supporting the proposed radiculomyelitis diagnosis. Petitioner underwent MRI studies
on January 17, 2013 (brain and cervical spine) and May 1, 2013 (cervical and thoracic
spine), neither of which revealed any abnormalities consistent with radiculomyelitis.
(Ex. 7, pp. 71, 246-47; Ex. 3, p. 3.) Dr. Napoli testified that petitioner’s initial cervical
MRI would not have detected a lesion at the level he describes and a thoracic MRI was
not performed until later. (Tr. 76, 82.) However, Dr. Chaudhry explained that the report
of symptoms above the nipple line implicates an area higher on the spinal cord than Dr.
Napoli indicated. (Tr. 149.) Dr. Chaudhry opined, contrary to both Dr. Napoli and Dr.
Morgan, that inflammation of the nerve roots should have been visible on petitioner’s

                                              20
first MRI with contrast enhancement from C5 through T1 if it were present. (Tr. 155.)
Dr. Chaudhry explained that MRI is very sensitive to detecting spinal cord inflammation.
(Tr. 217.) Moreover, although the thoracic MRI was later, it was also performed at a
time when Dr. Winesett was specifically screening for a potential spinal explanation for
petitioner’s presentation of active sensory symptoms. (Ex. 7, pp. 7-8.)

       Dr. Napoli also opined that a normal spinal MRI does not rule out the possibility
of a “small” lesion. (Tr. 53.) However, it would still remain the case that the MRI
evidence of any lesion is lacking and, especially in light of all of the additional points
below, neither Dr. Napoli nor Dr. Morgan is persuasive in suggesting that any spinal
lesion should be inferred based solely on clinical presentation. Dr. Chaudry also
explained that a normal MRI in the context of myelitis would be “very rare” and, if it was
suspected, spinal tap and EMG, would provide further opportunities for confirmation. 13
(Tr. 215-16, 219.) However, no such confirmation exists in this case. Additionally, in
response to Dr. Morgan’s opinion Dr. Chaudhry questioned the seeming contrast
between the extent of symptoms implicated by Dr. Morgan’s (and subsequently Dr.
Napoli’s) theory, which he described as symptoms stemming from eight spinal levels,
and the suggested ability of the proposed spinal lesion to nonetheless be small or mild
enough to evade MRI detection. (Ex. G, pp. 2-3.)

       In addition to the lack of any objective evidence upon imaging, Dr. Napoli was
also unable to identify significant evidence of spinal involvement based on petitioner’s
overall presentation. With regard to petitioner’s symptom presentation, Dr. Napoli
described the following clinical symptoms of radiculomyelitis: band-like sensation across
the chest,14 hyperreflexia including intermittent bilateral upgoing toes (i.e. Babinski

13
  Specifically, Dr. Chaudhry indicated that nerve root damage at C5 should also have been detected by
petitioner’s EMG test. (Tr. 176.) Dr. Chaudhry explained that EMG would not reveal etiology, but could
detect the nerve root damage constituting the radiculitis. (Tr. 215.) Dr. Chaudhry suggested that EMG
may be considered where radiculopathy is still suspected after a normal MRI. (Tr. 216.) Dr. Morgan
conceded that radiculopathy can be detected by EMG, but opined that “[petitioner’s] ascending sensory
tracts in the spinal cord and the C8 through T4 motor nerve roots were not tested by . . . his EMG and
nerve conduction. (Ex.17, pp. 1-2.) He opined that petitioner’s pain was referred up to the C5 level rather
than the C5 root itself being affected. (Id.) Dr. Chaudhry indicated, however, that if petitioner had
weakness in his biceps, deltoids, and hands that was due to a spinal cord lesion, then the C5 nerve would
have been involved. (Ex G, p. 2.) Notably, Dr. Morgan did initially opine that petitioner had myelitis
af f ecting the C5 level. (Ex. 12, p. 4.) It was only after Dr. Chaudhry first raised the fact of the EMG
results counseling against a radiculomyelitis diagnosis (Ex. A, p. 6) that Dr. Morgan sought to explain
petitioner’s symptom presentation as referred pain (Ex. 17, pp. 1-2). Dr. Morgan indicated that reduced
or absent reflexes cited by Dr. Chaudhry “would not necessarily” be reflected in radiculomyelitis at C5
through T4. (Ex. 17, pp. 1-2.) Nonetheless, especially given Dr. Morgan’s acknowledgement that
radiculopathy can be detected on EMG, Dr. Chaudhry is persuasive in discussing what would normally be
expected whereas Dr. Morgan appears to strain to harmonize the EMG results with his opinion.
14
  On cross-examination, Dr. Napoli confirmed that his opinion that petitioner experienced a band-like
sensation across the chest was based on a notation that petitioner was experiencing “neuropathic pain” at
the level of his chest and nipples. (Tr. 75.) However, “neuropathic pain” is not specific to either the
central or peripheral nerves. In his earlier report, Dr. Napoli had discussed neuropathic pain in the
context of petitioner’s brachial neuritis diagnosis from Dr. Winesett (Ex. 21, p. 4) and separately
discussed sensory changes at T4 as evidence of radiculomyelitis (Id. at 6).

                                                    21
sign), numbness of the distal limbs, and bladder symptoms. (Tr. 30.) To Dr. Napoli, the
combination of peripheral and central nervous system findings and the location of the
band-like sensation indicates that inflammation existed at the C5 to T4 area of the
spinal cord. (Tr. 31.) Dr. Napoli indicated that ankle clonus, which can be seen in
conjunction with the Babinski sign, is a physiologic indicator of a lesion in the central as
opposed to peripheral nervous system. (Tr. 32.) Bilateral ankle clonus raises a high
suspicion for a spinal cord lesion.15 (Tr. 33.)

        However, Dr. Chaudhry explained that there was no leg weakness upon
petitioner’s initial neurological exam and sensation was intact. (Tr. 142-43, 145.) Dr.
Chaudhry also cautioned that the Babinski sign is subjective. Moreover, he further
explained that “no individual sign stands on its own.” (Tr. 143.) In this case, petitioner’s
first neurological exam showed intact (as opposed to brisk) deep tendon reflexes and no
ankle clonus, findings that are not consistent with a positive Babinski test. (Id.)
Whereas Dr. Napoli opined that an equivocal Babinski sign is itself an abnormal finding,
Dr. Chaudhry reasonably concluded that in the context of this medical record
“equivocal” suggests that treating physicians were unsure whether an abnormal finding
was actually present. (Tr. 144-45.) This is especially persuasive in light of the fact that
petitioner’s medical records show inconsistent results from the Babinski test.16 (Ex. 7,
p. 60; Ex. 3, p. 1.)

       Upon petitioner’s second neurological exam, Dr. Chaudhry stressed that
although petitioner continued to decline overall, his lower extremity strength and
reflexes were clearly normal and there was no evidence of any abnormal Babinski sign
or ankle clonus.17 (Tr. 149.) Dr. Chaudhry also explained that petitioner was noted to
have difficulty initiating urine on only one occasion, which can have many causes and is
different from the type of bladder incontinence that is typically associated with spinal
issues. (Tr. 180, 234-35.)

       Dr. Chaudhry also stressed that it was not until later (in April) that Dr. Winesett
specifically expressed any concern regarding a spinal condition and that concern was
due solely to sensory findings at the T4 spinal level. At that time, petitioner had normal
strength in his legs, normal Babinski sign, and a follow up MRI specifically to screen for
myelitis was normal. (Tr. 180-81 (citing Ex. 8, p. 22).) Overall Dr. Chaudhry suggested
that symptoms (such as imbalance, leg and chest pain or numbness, urinary retention),
are not illuminating for spinal cord issues when the signs (such as reflex and strength
15
  Spinal cord compression would also be in the differential diagnosis, but Dr. Napoli opined that it was
appropriately ruled out. (Tr. 33-34.) Dr. Chaudhry agreed. (Tr. 236.)
16
   Dr. Napoli initially indicated that an equivocal finding on Babinski testing still constitutes an abnormal
f inding (Tr. 88), but later acknowledged that the medical records reflect that the medical examiner was
seeing f luctuating findings (Tr. 89). This is consistent with Dr. Chaudhry’s explanation that the Babinski
test is a subjective observation and the records reflect uncertainty regarding the presence of the
abnormal finding.
17
  On a later exam, petitioner had “three beats” of ankle clonus observed, but again in the context of
normal lower extremity strength. Dr. Chaudhry opined that in that context he would only accept “sustained
clonus” as an abnormal finding. (Tr. 152.)

                                                      22
tests) are normal. (Tr. 235.) Combined with the lack of radiography, Dr. Chaudhry
persuasively indicated that there is “not a shred of evidence” of spinal inflammation.
(Tr. 182.)

        Also highly significant, none of petitioner’s treating physicians agreed with
petitioner’s proposed theory of radiculomyelitis. Dr. Napoli cited a diagnosis of
radiculitis included in petitioner’s physical therapy records. (Tr. 51 (citing Ex. 1, p. 2).)
On cross examination, however, he acknowledged that radiculomyelitis was never
diagnosed by petitioner’s treating physicians nor specifically ruled in or out. (Tr. 53-54,
87.) Dr. Napoli also indicated that a spinal tap could be relevant to diagnosis of
radiculomyelitis, but acknowledged it was not done in this case. Instead, he noted that
he believes it was contemplated. (Tr. 45-46.) However, ascribing any significance to
just the fact of that contemplation would be speculative, especially in light of petitioner’s
complex presentation and broad differential diagnoses.

        I have also considered Dr. Morgan’s earlier opinion, but this does not change the
analysis. Although, unlike Dr. Napoli, Dr. Morgan relies on radiculomyelitis to explain
the entirety of petitioner’s symptoms, Dr. Morgan likewise acknowledges the lack of any
objective clinical testing to support the suspicion of radiculomyelitis, relying, as Dr.
Napoli has, on the idea that petitioner’s own lesion was situated in a manner that
evaded detection. (Ex. 12, pp. 3-4.) He also necessarily relies on the same overall
clinical presentation. Moreover, he acknowledges that if petitioner did have
radiculomyelitis it would necessarily have been both atypical and subacute. (Ex. 17, p.
2.) In that regard, Dr. Chaudhry’s competing opinion remains persuasive for all the
reasons discussed above in rebutting the opinion that petitioner’s clinical history
evidences radiculomyelitis.

        Accordingly, based on the opinion of petitioner’s treating physicians, the medical
literature, and the opinions of the experts in this case, I do not find preponderant
evidence that petitioner suffered radiculomyelitis as proposed by petitioner’s experts.

              b. Brachial Neuritis

        Although petitioner likely did not suffer radiculomyelitis, this still leaves the
question of whether petitioner’s own treating physicians reasonably diagnosed brachial
neuritis, a diagnosis that was also endorsed by Dr. Napoli. Based on the opinion of
petitioner’s treating physicians, the expert opinions, and medical literature, petitioner
has established his diagnosis of brachial neuritis by preponderant evidence. With
regard to the alleged brachial neuritis diagnosis, the opinion of petitioner’s treating
physicians provides strong evidentiary support.

        In Capizzano v. Secretary of Health & Human Services, the Federal Circuit held
that the opinions of treating physicians, in particular, the diagnoses they make and the
course of treatment they recommend are “quite probative” of whether there was a
logical sequence of cause and effect between vaccine and injury. 440 F.3d 1317, 1326
(Fed. Cir. 2006). Thus, treating physician opinions have historically been given

                                              23
significant weight when determining causation, but are similarly, if not more helpful in
the context of diagnosis. See, e.g., D'Angiolini v. Sec'y of Health & Human Servs., No.
99-578V, 2014 WL 1678145, at *24 (Fed. Cl. Spec. Mstr. Mar. 27, 2014) (finding a
treating physician’s opinion regarding diagnosis “worth a great deal” and “almost
definitive evidence on that point” while placing less weight on that physician’s opinion
regarding etiology), mot. for rev. denied, 122 Fed. Cl. 86 (2015), aff'd, 645 F. Appx.
1002 (Mem.) (Fed. Cir. 2016).

         In this case, after much consideration and examination of petitioner’s condition,
Drs. Ford and Larden, as well as, most notably, neurologist Dr. Winesett, all concluded
that petitioner’s most likely diagnosis was brachial neuritis. (See Ex. 2, p. 9; Ex. 7, pp.
74, 83-84; Ex. 8, p. 17.) Although petitioner’s treating physicians did not entertain
brachial neuritis as a differential diagnosis upon his initial admission to ACH (Ex. 7, p.
60), respondent’s expert, Dr. Chaudhry, acknowledged both that brachial neuritis is a
rare condition and also a “diagnosis of exclusion.” (Tr. at 207.) Thus, it follows that
brachial neuritis appropriately received increased consideration only as the significant
list of other differential diagnoses were excluded. Although petitioner had a
complicated, and in some instances potentially confounding, clinical presentation that
does not seem to fit neatly into any single diagnosis, Dr. Chaudry was not persuasive in
suggesting that the treating physicians’ diagnosis should be displaced in favor of simply
deeming petitioner’s condition wholly enigmatic.

        Dr. Chaudhry acknowledged that clinically this is a difficult case. Although he felt
petitioner’s clinical course could be consistent with an ischemic etiology, he was unable
to opine in favor of any more compelling diagnoses. (Tr. at 254, 265-66, 278.)
Additionally, to the extent Dr. Chaudhry discussed specific findings he felt were
inconsistent with brachial neuritis, he also acknowledged that there is no consensus
standard for the diagnostic criteria for brachial neuritis. (Tr. at 269-270.) Moreover, the
literature filed in this case supports the view that brachial neuritis encompasses a
variety of presentations. (See Medlink, supra, at Ex. 23; Ferrante & Wilbourn, supra, at
Ex. 27; Van Eijk, Groothuis & Van Alfen, supra, at Ex. C.) Consequently, I am
concerned that in this context the exacting standard Dr. Chaudhry seems to apply
regarding what he considered to be the relevant diagnostic criteria would have the effect
of heightening petitioner’s burden of proof. Although Dr. Chaudhry explained that
certain aspects of petitioner’s presentation may be less typical – for example the initial
bilateral presentation and lack of muscle wasting – Dr. Napoli demonstrated that these
presentations are known in the context of confirmed cases of brachial neuritis. (See
Medlink, supra, at Ex. 23, pp. 1-7.)

        Dr. Napoli further supported petitioner’s brachial neuritis diagnosis based on
petitioner’s clinical presentation and the medical literature detailing the diagnosis of
brachial neuritis. Dr. Napoli explained that “even if [petitioner’s] presentation is
inconclusive, the disorder is typically recognized by two important features of pain and
muscle weakness” and that “the most commonly affected nerves are the suprascapular
nerve and the long thoracic nerve.” (Ex. 21, p. 4 (citing Ferrante & Wilbourn, supra, at
Ex. 27, p. 1; Medlink, supra, at Ex. 23).) Petitioner’s medical records show that he

                                            24
presented to ACH urgent care with acute upper extremity weakness and pain so severe
that he was treated with morphine. (Ex. 2, p. 10-11.) Dr. Napoli explains that
petitioner’s distribution of weakness in his upper extremities supports a finding that
either one or both of his suprascapular and long thoracic nerves were affected by his
condition, lending further support to the diagnosis of brachial neuritis. (Ex. 21, p. 4.) In
response to Dr. Chaudhry’s concern regarding the lack of any muscle wasting, Dr.
Napoli suggested that muscle wasting may not be expected if a patient has a good
recovery. (Tr. 17, 113-14.)

        Some of Dr. Chaudhry’s concern regarding the brachial neuritis diagnosis stems
from petitioner’s inconsistent symptom presentation in the course of his diagnosis and
treatment. Although Dr. Chaudhry posited some other conditions, such as ischemic
injury or migraine, that could cause a fluctuating presentation, he indicated that he does
not know if any other condition could explain the inconsistencies and would be “only
guessing.” (Tr. 168.) However, Dr. Chaudhry also suggested based on these
conflicting or confounding notations that some of the observations of petitioner’s clinical
course may be less reliable than others in assessing petitioner’s symptoms, raising the
question of whether it was petitioner’s symptoms, or merely the observations of
petitioner’s multiple treaters, that were differing. (Tr. at 163-170.) This further
underscores the difficulty of reinterpreting the first-hand observations of the treating
physicians’ in this case with any confidence. In that regard, Dr. Chaudhry suggested
that the neurological opinion should be trusted over conflicting observations. (Tr. 164,
169-70.) As noted above, petitioner’s neurologist, Dr. Winesett, opined that petitioner
suffered brachial neuritis. (Ex. 8, p. 17.)

         Additionally, Dr. Chaudhry’s own interpretation of the medical record is not
persuasive in all instances; most notably, in his reports he disputed that petitioner
initially presented to the emergency department with pain. (Ex. H, p. 1.) During the
hearing he indicated that petitioner’s initial lack of extremity pain accompanying his
upper extremity weakness was a significant atypicality that affected his impression. (Tr.
135.) However, the medical records specifically indicate that at the time he awoke with
an inability to move his arms, he was also observed by his parents to be “crying in pain.”
(Ex. 2, p. 2.) This notation is included in a description of petitioner’s waking with upper
extremity symptoms and includes no mention of headache. (Id.) A further notation that
does address the headache likewise also confirms that petitioner had bilateral shoulder
pain “since waking up.” (Ex. 7, p. 59.) Additionally, Dr. Winesett noted that petitioner
had had “shooting pains” across his chest during the night of onset and also that upon
exam he was tender to touch around the shoulders. (Ex. 2, p. 6.) Moreover, when he
was taken to the emergency department he was administered morphine. (Id. at 9, 11.)
During the hearing, respondent’s counsel asked whether petitioner may have instead
been administered morphine in the emergency department for his reported headache;
however, Dr. Napoli persuasively explained that petitioner had other pain complaints,
including his upper extremities, and that morphine would be unusual treatment for a
headache. (Tr. 73-74, 118.)

                                             25
        Dr. Chaudhry also relied heavily on petitioner’s negative EMG to exclude brachial
neuritis. However, notwithstanding Dr. Chaudhry’s own testimony that EMG is a near
universal means of confirming brachial neuritis (Tr. 207-08), the medical literature he
cited suggests that nerve conduction and EMG studies must be approached cautiously
in assessing brachial neuritis and that negative EMGs should not be used to exclude a
diagnosis. (See Van Eijk, Groothuis & Van Alfen, supra, at Ex. C, pp. 5, 7 (explaining
that “NA is a clinical diagnosis first and foremost; there is no ancillary ‘litmus’ test that
can confirm or refute the diagnosis with a sufficient degree of certainty” and that “[I]n
practice, there is a very real chance of obtaining a negative [EMG] result due to
sampling error.”).) Dr. Chaudhry himself likewise admitted that, while he considers it
unlikely, it is possible for brachial neuritis to present with a normal EMG. (Tr. at 207-
08.) For his part, Dr. Napoli did not believe the long thoracic nerve, which he felt was
implicated by petitioner’s presentation, was tested. (Tr. 114.)

        Moreover, Dr. Chaudhry’s opinion regarding petitioner’s EMG is in itself internally
inconsistent in its assessment of petitioner’s clinical care. During the entitlement hearing
I noted that petitioner’s EMG report from Dr. Winesett does not detail how the procedure
was conducted, nor the specific basis for Dr. Winesett’s interpretation of the exam as
negative for brachial neuritis. (Tr. at 271-72.) Dr. Chaudhry explained that, despite the
risks of sampling error, because Dr. Winesett was noted to have performed the EMG
specifically to evaluate petitioner for possible brachial neuritis, Dr. Winesett’s clinical
judgment would have led him to conduct the test properly to detect brachial neuritis.
(Tr. at 273-77.) However, Dr. Chaudhry also explained that interpreting EMG results is
subjective. (Tr. 272.) Moreover, Dr. Chaudhry disagrees with Dr. Winesett’s overall
clinical judgment that petitioner suffered brachial neuritis, a judgment which Dr.
Winesett maintained even after interpreting the EMG as negative. (Tr. at 156-57; see
also Ex. 8, p. 17.) Thus, it is difficult to fully credit Dr. Chaudhry’s opinion on this issue
because he simultaneously seeks to defer to Dr. Winesett’s judgment in the manner of
conducting petitioner’s EMG (a point the literature suggests may be potentially
problematic (Van Eijk, Groothuis & Van Alfen, supra, at Ex. C, p. 718)), while at the
same time dismissing Dr. Winesett’s subsequent clinical judgment as to the significance
of the negative finding he himself had generated. On this record Dr. Chaudhry has no
basis for parsing Dr. Winesett’s clinical judgment in administering the EMG test from his
clinical judgment in discounting the significance of the results, especially because, as
explained above, Dr. Chaudhry’s own reliance materials caution against relying on EMG
as a diagnostic touchstone.19

18
  Dr. Chaudhry’s reliance materials specifically caution that “[i]n contrast to NCS, needle EMG is
sensitive for detecting signs of denervation or reinnervation, but only when clinically affected muscles are
examined. There are about 50 different muscles in the upper extremity, so only a limited number can be
examined during a needle study. Many of the muscles involved in NA do not belong to the routine set of
muscles that practitioners most commonly explore during their EMG evaluation, thus sample error is very
common.” (Van Eijk, Groothuis & Van Alfen, supra, at Ex. C, p. 7.)
19
  The experts also had competing opinions regarding the best timing for administering an EMG in the
hopes of detecting brachial neuritis. (Tr. 43, 52 (Napoli), Tr. 172 (Chaudhry).)

                                                    26
        Finally, I note that respondent has stressed that petitioner’s initial expert, Dr.
Morgan, agreed that brachial neuritis is not an appropriate diagnosis for petitioner.
(ECF No. 74, p. 9.) And, indeed, Dr. Morgan did indicate that “I do agree with Dr.
Chaudhry that tests for brachial plexopathy including the normal EMG, normal imaging
studies and clinical presentation were against brachial plexitis and Parsonage Turner
Syndrome.” (Ex. 17, p. 2.) Importantly, however, Dr. Morgan’s opinion was premised on
his alternative explanation that petitioner’s clinical presentation could otherwise be
explained by radiculomyelitis. (Id. at 1-2.) Although Dr. Morgan located petitioner’s
injury in the spinal cord (Ex. 17, p. 3), he did initially opine that petitioner presented with
clinical findings of brachial plexopathy. (Ex. 12, p. 4). Moreover, even in his
supplemental report Dr. Morgan continued to explicitly disagree with Dr. Chaudhry’s
assessment of petitioner’s initial complaints of upper extremity pain and weakness. (Ex.
7, p. 1.) He opined that the myelitis he proposed “simulated bilateral brachial
plexopathy.” (Id. at 2.) He further indicated that “I respectfully disagree with Dr.
Chaudhry’s conclusions of Mr. Patton’s bilateral upper extremity and neck weakness,
left leg weakness, variable sensory features [as] not clear and of uncertain cause.” (Ex.
7, p. 3.) Accordingly, while Dr. Morgan’s opinion further demonstrates the difficulty in
reaching a definitive diagnosis in this case, it does not serve as significant ratification of
Dr. Chaudhry’s competing assessment regarding brachial neuritis.

       Based on the opinion of petitioner’s treating physicians, the medical literature,
and the opinions of the experts in this case, I find that petitioner has presented
preponderant evidence that he suffered from brachial neuritis. Notably, however, this
diagnosis does not capture the entirety of petitioner’s clinical presentation as it does not
seem to explain his lower extremity symptoms. Nonetheless, petitioner has not
provided preponderant evidence otherwise placing those symptoms within the context
of any defined and recognized injury.

   VI.     Analysis of Petitioner’s Claim Under Althen

       As explained above, petitioner’s burden is to demonstrate by preponderant
evidence, each of the three Althen prongs used to determine actual causation (i.e. an
acceptable medical theory, a logical sequence of cause and effect, and a proximate
temporal relationship). Althen, 418 F.3d at 1278. Because I have concluded that there
is preponderant evidence that petitioner suffered brachial neuritis but not
radiculomyelitis, this analysis will be focused on whether petitioner has demonstrated
his brachial neuritis to be vaccine-caused.

           a. Althen Prong One

        Under Althen prong one, a petitioner must provide a “sound and reliable” medical
theory demonstrating that the vaccine received can cause the type of injury alleged.
Boatmon v. Sec’y of Health & Human Servs., 941 F.3d 1351, 1359 (Fed. Cir. 2019).
Petitioner’s theory need only be “legally probable, not medically or scientifically certain.”
Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 549 (Fed. Cir. 1994).
However, the Federal Circuit has clarified that “simply identifying a ‘plausible’ theory of

                                              27
causation is insufficient for a petitioner to meet her burden of proof.” LaLonde v. Sec’y
of Health & Human Servs., 746 F.3d 1334, 1339 (Fed. Cir. 2014) (citing Moberly, 592
F.3d at 1322). Instead, petitioner “must provide a reputable medical or scientific
explanation that pertains specifically to [their] case.” Moberly, 592 F.3d at 1322. In
prior cases, this prong has been described as requiring petitioner to show that the
alleged vaccine can cause the alleged injury, while prong two requires petitioner to
show that the alleged vaccine did cause the alleged injury. See, e.g., Doe 11 v. Sec’y
of Health & Human Servs., 83 Fed. Cl. 157, 172–73 (2008), aff’d 601 F.3d 1349 (Fed.
Cir. 2010); Nussman v. Sec’y of Health & Human Servs., 83 Fed. Cl. 111, 117 (2008);
Banks v. Sec’y of Health & Human Servs., 2007 WL 2296047, at *24 (Fed. Cl. Spec.
Mstr. July 20, 2007); Zeller v. Sec’y of Health & Human Servs., 2008 WL 3845155, at
*25 (Fed. Cl. Spec. Mstr. July 30, 2008). Thus, to meet prong one of Althen, petitioner
must show by preponderant evidence that the flu vaccine is capable of causing brachial
neuritis.

        Tetanus containing vaccines are presumed to be capable of causing brachial
neuritis in this program. See 42 C.F.R. § 100. However, as explained above,
petitioner’s burden in this case is to show that the specific vaccine he received – the
influenza vaccine – can also cause brachial neuritis. In that regard, Dr. Napoli has
acknowledged that he has provided no evidence -- no study apart from anecdotal case
reports (Exs. 28-31)20 – directly indicating that the flu vaccine can cause brachial
neuritis. (Tr. 93, 97.) Instead, Dr. Napoli relies on the notion that brachial neuritis is
theorized to be an autoimmune condition associated with multiple triggers, both known
and unknown, including infections. (Tr. 16.) Thus, Dr. Napoli opined that the flu
vaccine can cause brachial neuritis via molecular mimicry. 21 (ECF No. 77, pp. 35-39;
Tr. 38-39.)

        However, special masters have repeatedly held in varying contexts that it is
insufficient for petitioners to merely invoke molecular mimicry without more. See, e.g.,
W.C. v. Sec’y Health & Human Servs., 704 F.3d 1352, 1361 (Fed. Cir. 2016) (finding
that the “special master reasonably considered the lack of evidence connecting the
cross-reactivity observed by Wucherpfenning to the facts of petitioner’s case to weigh
‘against finding that Dr. Tornatore’s opinion is perusaisve.’”); Issac v. Sec’y of Health &
Human Servs., No. 08-601V, 2012 WL 3609993, at *3-5, *21-22 (Fed. Cl. Spec. Mstr.
July 30, 2012), mot. for rev. denied, 108 Fed. Cl. 743 (2013), aff’d 540 Fed. Appx. 999
(Mem.) (Fed. Cir. 2013); Tullio v. Sec’y of Health & Human Servs., No. 15-51V, 2019

20
  “[C]ase reports ‘do not purport to establish causation definitively, and this deficiency does indeed
reduce their evidentiary value’…. [but] ‘the fact that case reports can by their nature only present indicia
of causation does not deprive them of all evidentiary weight.’” See Paluck v. Sec'y of Health & Human
Servs., 104 Fed. Cl. 457, 475 (2012) (quoting Campbell v. Sec'y of Health & Human Servs., 97 Fed. Cl.
650, 668 (2011), aff’d 786 F.3d 1373 (Fed. Cir. 2015)).
21
  Although Dr. Napoli explained that certain vaccines are believed to contain a protein that can mimic
nerve myelin, he stressed that it is very difficult to prove the presence of cross-reactivity and further that
molecular mimicry is not the only possible explanation for autoimmunity. (Tr. 58-59.) Critically, however,
Dr. Napoli did not actually describe any of the other causal theories to which he alluded.

                                                     28
WL 7580149, at *12-14 (Fed. Cl. Spec. Mstr. Dec. 19, 2019), mot. for rev. denied, 149
Fed. Cl. 448 (2020). Moreover, petitioners have previously tried and failed to
specifically connect brachial neuritis to the flu vaccine. E.g., Grow v. Sec’y of Health &
Human Servs., No. 16-13V, 2020 WL 7366332, at *24 (Fed. Cl. Spec. Mstr. Nov. 24,
2020) (finding that prong one was not met because “Dr. Gershwin only generally
describes how inflammation may factor into autoimmune responses [and] does not
explain how an inflammatory process is initiated by the flu vaccine specifically or how
such a response leads to [brachial neuritis].”).

        In this case, Dr. Napoli failed to provide any adequate explanation indicating how
the flu vaccine can induce brachial neuritis via molecular mimicry. Instead, Dr. Napoli
opined that evidence linking the flu vaccine to GBS is also broadly applicable in the
context of brachial neuritis. (Ex. 21, pp. 5-6.) To substantiate his theory, Dr. Napoli
sought to rely on evidence relating the flu vaccine to the Acute Inflammatory
Demyelinating Polyneuropathy (“AIDP”) form of GBS, which involves an autoimmune
process believed to involve a cross-reaction affecting myelin tissue, resulting in
demyelinating nerve damage. (Haber et al., supra, at Ex. 26, p. 3.) Given the
relationship between flu vaccines and GBS, Dr. Napoli characterized it as “not out of the
realm of possibility to think that the flu vaccine could cause other peripheral nerve
disorders.” (Tr. 94.) And, to be sure, the literature filed in this case does suggest that
the fact that brachial neuritis shares some triggers in common with inflammatory
demyelinating polyradiculopathies contributes to the general theory that brachial neuritis
has an immune basis. (E.g. Medlink, supra, at Ex. 23, p. 16.)

        Dr. Chaudhry persuasively explained, however, that cases of brachial neuritis
overwhelmingly result in axonal damage and not demyelination of the type seen in the
AIDP form of GBS. (Tr. at 131-33, 279-80; see also Van Eijk, Groothuis & Van Alfen,
supra, at Ex. C, p. 7.) Dr. Chaudhry analogized nerves to electrical wires, with myelin
forming an insulating sheath that surrounds the axons which make up the body of the
nerve. (Tr. 131-32.) Although Dr. Napoli cited literature identifying rare occurrences
(less than 1% of cases) of a brachial neuritis-like presentation consisting of
demyelinating injury 22 , that same literature emphasizes that brachial neuritis is generally
considered to result in axonal degeneration. (Medlink, supra, at Ex. 23, p. 2. (“available
evidence suggests that an autoimmune pathogenesis, likely related to a genetic
susceptibility most commonly generates an axon loss lesion (focal or multifocal) that
involves predominantly motor axons”).)

        Significantly then, Van Eijk et al., filed by respondent, discusses the autoimmune
basis for brachial neuritis as being evidenced specifically by studies of nerve biopsies
finding that the nerve axons represented the target of the autoimmune attack in brachial
neuritis. (Van Eijk, Groothuis & Van Alfen, supra, at Ex C, p. 5.) Both experts agreed
that axonal damage represents a more severe form of nerve injury as compared to

22
  To the extent that both the testifying experts and cited literature demonstrate that brachial neuritis lacks
def initive consensus criteria, it is difficult to conclude whether this rare occurrence of demyelinating
injuries ref erenced by Ferrante and Graus actually represent instances of brachial neuritis or simply a
dif ferent condition that closely resembles brachial neuritis. That issue is not discussed by this article.

                                                     29
demyelination (Tr. 84-85 (Napoli), 132 (Chaudhry)); however, Dr. Chaudhry also
explained that the two types of injury represent different pathogeneses, with myelin
sheath having susceptibility to different antigens. (Tr. 133.) Accordingly, Dr. Napoli’s
use of evidence linking AIDP to the flu vaccine, which is largely epidemiological rather
than mechanistic, is unpersuasive without more. These conditions result in distinct
forms of nerve damage and Dr. Napoli has provided no evidence suggesting that a
vaccine causing one type of nerve damage via molecular mimicry should be assumed
capable of causing the other.

        Dr. Napoli does suggest that Acute Motor Axonal Neuropathy (AMAN), a form of
GBS affecting the axons, has been hypothesized to result from molecular mimicry in the
case of C. Jejuni infections. However, he has not presented any evidence, apart from
his ipse dixit, showing any connection between AMAN and the flu vaccine. 23 Accord
Isaac v. Sec’y of Health & Human Servs., No. 08-601V, 2012 WL 3609993, at *22 (Fed.
Cl. Spec. Mstr. July 30, 2012) (noting that “[e]vidence that C. jenjuni causes GBS by
molecular mimicry does not constitute preponderant evidence that molecular mimicry is
a possible explanation for vaccine causation.”) Thus, the flu vaccine has not been
identified as a trigger for autoimmune axonal loss in either GBS or brachial neuritis.
Conversely, Dr. Chaudhry also stressed that C. Jejuni has not been shown to result in
brachial neuritis, further limiting the relevance of petitioner’s reference to AMAN and its
potential parallel to brachial neuritis. (Tr.186.)

        Respondent has also stressed that the Institute of Medicine (“IOM”) 24 examined
the relevant medical literature and found no epidemiology evaluating the risk of brachial

23
   All f orms of GBS, including AMAN, enjoy a causal presumption under the vaccine injury table when
f ollowing influenza vaccination. Importantly, however, petitioner does not allege any form of GBS.
Theref ore, the causal presumption is inoperable in this case. Moreover, GBS was added to the vaccine
injury table on the basis of studies showing a causal association between the 1976 swine flu vaccine and
demyelinating GBS. National Vaccine Injury Compensation Program: Revisions to the Vaccine Injury
Table, 82 Fed. Reg. 6294-01 (Jan. 19, 2017) (to be codified at 42 C.F.R. 100). The government
explained that seasonal flu vaccines “include multiple antigens that change from year-to-year, and
enhanced surveillance . . . may not occur with each virus strain change.” Id. Further, “[i]n light of this
inf ormation . . . the ACCV recommended that the Secretary add GBS consistent with one of its Guiding
Principles: That where there is credible evidence to both support and reject a change to the Table, the
change should, whenever possible, be made to the benefit of petitioners.” Id. Thus, especially in light of
such policy considerations, the fact that axonal forms of GBS enjoy a causal presumption does not in
itself suggest meaningful evidence that the flu vaccine can cause axonal nerve damage, especially in the
context of a different condition. Literature filed by petitioner explains that, although there are hypotheses
f or the etiology of GBS that could potentially apply to both demyelinating and axonal damage, separate
explanations have also been advanced that would be unique to AMAN and the etiology remains
unresolved. (Haber et al., supra, Ex. 26, p. 5.)
24
  The Institute of Medicine is the medical arm of the National Academy of Sciences. The National
Academy of Sciences (“NAS”) was created by Congress in 1863 to be an advisor to the federal
government on scientific and technical matters (see An Act to Incorporate the National Academy of
Sciences, ch. 111, 12 Stat. 806 (1863)), and the Institute of Medicine is an offshoot of the NAS
established in 1970 to provide advice concerning medical issues. When it enacted the Vaccine Act in
1986, Congress directed that the IOM conduct studies concerning potential causal relationships between
vaccines and illnesses. See § 300aa–1 note.

                                                     30
neuritis following the flu vaccine. (Adverse Effects of Vaccine: Evidence & Causation,
INSTITUTE OF M EDICINE (Ex. K, p. 3).) Additionally, the IOM examined two studies
constituting mechanistic evidence regarding the etiology of brachial neuritis, but found
that neither provided evidence linking the mechanisms to the flu vaccine. (Id.) IOM
reports are routinely relied upon by special masters as trustworthy evidence. See, e.g.
Crutchfield v. Sec’y Health & Human Servs., 125 Fed. Cl. 251 (2014) (noting that “it was
appropriate for the special master to consider the medical literature presented, including
the IOM report” and that “the court often has relied on the findings of the Institute of
Medicine.”)25 Importantly, however, special masters are not bound by the IOM’s
conclusions and it has been observed that the IOM employs a standard f or finding
causation that is higher than what is required by petitioner’s burden of proof. E.g.
Raymo v. Sec’y of Health & Human Servs., No. 11-654V, 2014 WL 1092274, at *21,
n.39 (Fed. Cl. Spec. Mstr. Feb. 24, 2014). In this case, the IOM’s conclusion is
informative but not dispositive, serving on this record to underscore Dr. Napoli’s failure
to come forward with any significant evidence implicating the flu vaccine in the disease
process(es) at work in the development of brachial neuritis specifically or autoimmune
axonal damage generally.

      In light of the above, I find that petitioner has failed to present preponderant
evidence showing that the influenza vaccine can cause brachial neuritis.

            b. Althen Prong Two

        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 1375-77; Capizzano, 440 F.3d at 1326; Grant v.
Sec’y of Health & Human Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992). However,
medical records and/or statements of a treating physician do not per se bind the special

25
  See also, Isaac v. Sec’y Health & Human Servs., 108 Fed. Cl. 743, 755 (2013), aff'd, 540 Fed. Appx.
999 (Mem.) (Fed. Cir. 2013) (affirming the special master's reliance on findings of the IOM); Porter v.
Sec’y Health & Human Servs., 663 F.3d 1242, 1252 (Fed.Cir.2011) (noting the special master's comment
that “IOM reports are f avored, although not dispositive, in the Vaccine Act Program,” then affirming the
special master's decision); Cedillo v. Sec’y Health & Human Servs., No. 98–916V, 2010 WL 331968, at
*94 (Fed. Cl. Spec .Mstr. Feb. 12, 2009), mot. for rev. denied, 89 Fed. Cl. 158 (2009) (af firming special
master's reliance on conclusions of IOM), aff'd, 617 F.3d 1328 (Fed.Cir.2010); Rodriguez v. Sec’y Health
& Human Servs., 67 Fed. Cl. 409, 410 (2005) (relying on IOM report regarding vaccine causation of an
injury); Althen v. Sec’y Health & Human Servs., No. 00–170V, 2003 WL 21439669, at *11, n.28 (Fed. Cl.
Spec. Mstr. June 3, 2003) (“Due to the IOM's statutory charge, the scope of its review, and the cross-
section of experts making up the committee reviewing the adverse events associated with vaccines, the
court considers their determinations authoritative and subject to great deference.”), rev'd on other
grounds, 58 Fed. Cl. 270, 272–74 (2003) (citing IOM reports frequently in support of various scientific
propositions), aff'd, 418 F.3d 1274 (Fed. Cir. 2005); Terran v. Sec’y Health & Human Servs., 41 Fed. Cl.
330, 337 (1998) (af f irming special master's reliance on conclusions of IOM), aff'd, 195 F.3d 1302 (Fed.
Cir.1999), cert. denied, 531 U.S. 812 (2000); Cucuras v. Sec’y Health & Human Servs., 993 F.2d 1525,
1529 (Fed. Cir. 1993) (noting that the special master had placed “a great deal of weight” on an IOM report
in reaching a decision, then affirming the special master's decision); Stroud v. Sec’y Health & Human
Servs., 113 F.3d 1258 (Fed. Cir. 1997) (unpublished)(special master may rely upon an IOM report that
neither party filed as evidence); Ultimo v. Sec’y Health & Human Servs., 28 Fed. Cl. 148, 152 (1993)
(proper for a special master to rely on IOM report).

                                                   31
master to adopt their conclusions, even if they must be considered and carefully
evaluated. See Section 13(b)(1) (providing that “[a]ny such diagnosis, conclusion,
judgment test result, report, or summary shall not be binding on the special master or
court.”); Snyder v. Sec’y of Health & Human Servs., 88 Fed. Cl. 706, 746 n.67 (2009)
(“there is nothing . . . that mandates that the testimony of a treating physician is
sacrosanct—that it must be accepted in its entirety and cannot be rebutted.”). As
described in the preceding section, this prong is at times distinguished from the first by
requiring the petitioner to show that the vaccine petitioner received did in-fact cause
their injury, instead of merely showing that it can cause their injury.

        The parties agree that brachial neuritis can occur within days of an antecedent
trigger. (Medlink, supra, at Ex. 23, pp. 2-7; Van Eijk, Groothuis & Van Alfen, supra, Ex.
C, pp. 1-2.) Here, petitioner presented with symptoms of brachial neuritis within days of
his flu vaccination. This timing of onset fits squarely within the accepted timeline for
brachial neuritis to develop following an antecedent event. Standing alone, however, a
temporal association is not sufficient to satisfy Althen prong two. Veryzer v. Sec’y of
Health & Human Servs., 100 Fed. Cl. 344, 356 (2011) (explaining that a “temporal
relationship alone will not demonstrate the requisite causal link and that petitioner must
posit a medical theory causally connecting the vaccine and injury.”).

        Petitioner’s initial presentation seemed to confuse his treating physicians at ACH
who initially listed 13 differential diagnoses including central nervous system mass,
carbon monoxide poisoning, dehydration, electrolyte abnormality, unspecified
headache, migraine, tension headache, intracranial hemorrhage, meningitis, post-
concussion syndrome, shunt malfunction, and stroke. (Ex. 7, p. 60.) However, as
petitioner was further examined, his treating physicians and physical therapists settled
on a diagnosis of possible or probable brachial neuritis (referenced as Parsonage-
Turner Syndrome) that they related to his flu vaccination. (Ex. 7, pp. 17, 47, 53, 85.)
Importantly, however, petitioner’s medical records show no evidence of any diagnostic
labs such as lumbar puncture which may have helped support a causal, and not merely
temporal, link between the vaccine and his injury.

        Thus, although petitioner’s treating physicians did ultimately settle on the
diagnosis of brachial neuritis, their further opinion that the condition was caused by
petitioner’s flu vaccination relies exclusively on the temporal relationship and the lack of
any known alternative triggers. This conclusion carries little weight in light of my finding
that petitioner has not satisfied Althen prong one relative to brachial neuritis. See e.g.
Grow, 2020 WL 7366332 at * 27 (“Therefore, the treating physicians’ notation
temporally associating the flu vaccine with PTS are entitled to little weight in Petitioner’s
case, because the association is based solely on a temporal relationship reported by
Petitioner.”); D'Angiolini v. Sec'y of Health & Human Servs., No. 99-578V, 2014 WL
1678145 (Fed. Cl. Spec. Mstr. Mar. 27, 2014) (noting that “there is a difference between
a doctor’s opinion regarding diagnosis and a doctor’s opinion regarding etiology and
quoting Tamraz v. Lincoln Electric Co, 620 F. 3d 664, 674 (6th Cir. 2010) for the
proposition that physicians “may testify to both [diagnosis and etiology] but the reliability

                                             32
of one does not guarantee the reliability of the other”), mot. for rev. denied, 122 Fed. Cl.
86 (2015), aff'd, 645 F. Appx 1002 (Mem.) (Fed. Cir. 2016).

        Although Dr. Napoli suspected petitioner’s brachial neuritis symptoms were
caused by demyelination based on the speed of his recovery, he acknowledged that
there is no evidence on this record distinguishing whether petitioner’s symptoms were
caused by demyelination or axonal damage. (Tr. 107.) Dr. Napoli’s opinion that
radiculomyelitis and brachial neuritis may together provide an explanation for
petitioner’s symptoms is also based on the assumption that the two conditions petitioner
purportedly suffered both represented demyelinating conditions. (Tr. 107.) However,
this point is refuted by Dr. Chaudhry and has not otherwise been substantiated by any
of petitioner’s submissions. Dr. Chaudry persuasively opined that cases of brachial
neuritis overwhelmingly result in axonal damage and not demyelination. (Tr. at 131-33,
279-80; see also Van Eijk, Groothuis & Van Alfen, supra, at Ex. C, p. 7.) And, in any
event, Dr. Napoli’s and Dr. Morgan’s suspicion of radiculomyelitis was not considered
by any of petitioner’s treating physicians and, for the reasons discussed in Section V.a.,
above, is not supported by preponderant evidence. Petitioner has failed to show by
preponderant evidence a logical sequence of cause and effect whereby the flu vaccine
would have induced an autoimmune reaction that caused his axonal-loss lesion
resulting in brachial neuritis.

        Additionally, petitioner’s own presentation is inconsistent with the presentation of
AIDP, which formed the basis for petitioner’s presentation linking the flu vaccine to
peripheral demyelinating injury. AIDP patients present with symptoms of ascending
weakness and sensory loss from the lower extremities to the upper extremities in the
early stages (Krishnan & Greenberg, supra, at Ex. F, p. 21), while brachial neuritis
patients present with new-onset pain in the shoulder or upper arm developing into
paresis typically involving the long thoracic, suprascapular, and anterior interosseous
nerves. (Van Eijk, Groothuis & Van Alfen, supra, at Ex. C, p. 1.) Here, petitioner
presented with symptoms diagnosed as brachial neuritis and not symptoms of AIDP.
Although petitioner had some lower extremity symptoms, it was his upper extremity
symptoms that presented most prominently upon onset. None of the experts, or the
treating physicians ultimately, opined that petitioner suffered AIDP.

        Although petitioner’s condition does remain somewhat enigmatic, he has not
articulated any basis for concluding that his flu vaccine could be responsible for a logical
sequence of cause and effect leading to his constellation of symptoms. Accordingly, I
find that petitioner has not met his burden under Althen prong two.

          c. Althen Prong Three

        The third Althen prong requires establishing a “proximate temporal relationship”
between the vaccination and the injury alleged. Althen, 418 F.3d at 1281. This
standard has been defined as requiring a “medically-acceptable temporal relationship.”
Id. Here the parties agree that onset of petitioner’s symptoms occurred within six days
of his vaccination and therefore falls within the “medically appropriate timeframe for the

                                             33
onset of an immunological injury.” (See ECF No. 74, p. 18; see also ECF No. 77 pp.
39-41.) Consequently, I find that petitioner has carried his burden under Althen prong
three. However, petitioner’s failure to meet prongs one and two means that petitioner
cannot be compensated. Hibbard v. Sec’y of Health & Human Servs., 698 F.3d 1355,
1364-65 (Fed. Cir. 2012) (holding the special master did not err in resolving the case
pursuant to prong two when respondent conceded that petitioner met prong three).

     VII.   Conclusion

        For all the reasons discussed above, I find that petitioner has failed to carry his
burden of showing by preponderant evidence that his flu vaccination was the actual
cause of his injury. Specifically, I find that petitioner has failed to demonstrate that he
suffered any identifiable injury or condition other than the brachial neuritis diagnosed by
his treating physicians. I further find that he has failed both to present a medical theory
causally connecting the flu vaccine to brachial neuritis and to present preponderant
evidence establishing a logical sequence of cause and effect showing that the flu
vaccine did cause his condition. Therefore, this case is dismissed.26

IT IS SO ORDERED.
                                                           s/Daniel T. Horner
                                                           Daniel T. Horner
                                                           Special Master

26
  In the absence of a timely-filed motion for review of this Decision, the Clerk of the Court shall enter
judgment accordingly.

                                                     34