VICP Registry Case Source Bundle
Canonical URL: https://vicp-registry.org/case/USCOURTS-cofc-1_16-vv-00269
Package ID: USCOURTS-cofc-1_16-vv-00269
Petitioner: Duane Morgan
Filed: 2016-02-26
Decided: 2023-05-22
Vaccine: influenza
Vaccination date: 2014-10-22
Condition: brachial neuritis and adhesive capsulitis
Outcome: entitlement_granted_pending_damages
Award amount USD: 

AI-assisted case summary:
On February 26, 2016, Duane Morgan filed a petition for compensation under the National Vaccine Injury Compensation Program, alleging that an intradermal influenza vaccine administered on October 22, 2014, caused him to suffer from brachial neuritis and adhesive capsulitis. Mr. Morgan, who was 60 years old at the time of vaccination, reported experiencing pain, redness, and swelling at the injection site within days of the vaccination, which progressed to severe pain, weakness, and numbness in his left arm and hand. His treating physicians, including orthopedist Dr. Russell Huffman and neurologist Dr. Eric Zager, diagnosed him with brachial neuritis (also known as Parsonage-Turner Syndrome) and adhesive capsulitis, finding a causal relationship to the vaccine. Petitioner's experts, Dr. Huffman, Dr. Vera Byers (immunologist), and Dr. Maria Fangchun Chen (neurologist), presented medical theories explaining how the intradermal vaccine could trigger an inflammatory response leading to nerve damage and subsequent adhesive capsulitis. They argued that the intradermal administration, due to the skin's rich immune cell network, could induce a heightened inflammatory cascade, potentially leading to vasculitis and nerve damage. Respondent, represented by Ryan D. Pyles of the U.S. Department of Justice, argued that Mr. Morgan's condition was more likely caused by his long-standing diabetes, presenting expert opinions from neurologist Dr. Brian Callaghan and immunologist Dr. S. Mark Tompkins. Respondent's experts suggested that Mr. Morgan suffered from diabetic cervical radiculoplexopathy and that his adhesive capsulitis was also likely diabetes-related. They contended that the evidence for diabetes as the cause outweighed the evidence for vaccination. The Special Master, Thomas L. Gowen, reviewed the extensive medical records and expert reports. He found that Mr. Morgan's medical records and expert testimony established a logical sequence of cause and effect, a sound medical theory, and a proximate temporal relationship between the vaccine and his injury, satisfying the Althen criteria for off-Table injuries. The Special Master concluded that Mr. Morgan's symptoms and clinical course were more consistent with vaccine-induced brachial neuritis and adhesive capsulitis than with diabetic neuropathy. Therefore, the Special Master ruled that Duane Morgan was entitled to compensation, with a separate order to be issued for damages.

Theory of causation field:
Petitioner Duane Morgan, a 60-year-old male, received an intradermal influenza vaccine on October 22, 2014, and subsequently developed brachial neuritis and adhesive capsulitis. Petitioner's experts, Drs. Huffman, Byers, and Chen, proposed that the intradermal vaccine administration, due to the skin's dense network of antigen-presenting cells and unique microvascular/lymphatic structures, elicits a heightened innate immune response with rapid upregulation of pro-inflammatory cytokines (e.g., TNF-α, IL-1β). This inflammatory cascade can lead to vasculitis affecting the nerves of the brachial plexus, causing brachial neuritis. They further posited that the pain and inflammation associated with brachial neuritis could lead to secondary adhesive capsulitis. This theory was supported by medical literature on intradermal vaccination mechanisms and case reports of vaccine-associated brachial neuritis. Respondent's experts, Drs. Callaghan and Tompkins, argued that Mr. Morgan's condition was caused by underlying diabetes, specifically diabetic cervical radiculoplexopathy, and that the vaccine was not the cause. They contended that diabetic neuropathy is a more likely explanation and that the evidence for vaccination-induced brachial neuritis was insufficient. Special Master Gowen found that petitioner established by preponderant evidence: (1) a reputable medical theory that the intradermal flu vaccine can cause brachial neuritis via an inflammatory cascade and vasculitis; (2) a logical sequence of cause and effect, noting Mr. Morgan's symptom onset shortly after vaccination, his clinical presentation consistent with brachial neuritis rather than diabetic neuropathy, and the failure of alternative explanations to account for his condition; and (3) a proximate temporal relationship, with symptoms appearing within days of vaccination. The Special Master ruled in favor of entitlement, finding the vaccine to be the cause of Mr. Morgan's brachial neuritis and adhesive capsulitis. Attorneys for petitioner were Paul R. Brazil and Muller Brazil, LLP. Attorney for respondent was Ryan D. Pyles. The decision was issued by Special Master Thomas L. Gowen on May 22, 2023.

Public staged source text:

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DOCUMENT 1: USCOURTS-cofc-1_16-vv-00269-0
Date issued/filed: 2023-06-12
Pages: 39
Docket text: PUBLIC RULING (Originally filed: 05/22/2023) regarding 100 Ruling on Entitlement. Signed by Special Master Thomas L. Gowen. (hs) Service on parties made.
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Case 1:16-vv-00269-UNJ Document 102 Filed 06/12/23 Page 1 of 39
In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
Filed: May 22, 2023
* * * * * * * * * * * * * * * * * * *
DUANE MORGAN, * Published
*
* No. 16-269V
Petitioner, *
v. * Special Master Gowen
*
SECRETARY OF HEALTH * Ruling on Entitlement; Influenza
AND HUMAN SERVICES, * Vaccine; Brachial Neuritis.
*
Respondent. *
* * * * * * * * * * * * * * * * * * *
Paul R. Brazil, Muller Brazil, LLP, Dresher, PA, for petitioner.
Ryan D. Pyles, U.S. Dept. of Justice, Washington, D.C., for respondent.
RULING ON ENTITLEMENT1
On February 26, 2016, Duane Morgan (“petitioner”) filed a petition for compensation in
the National Vaccine Injury Compensation Program.2 Petition (ECF No. 1). Petitioner alleged
that as a result of receiving the influenza vaccine on October 22, 2014, he suffered from adhesive
capsulitis and brachial neuritis. Amended Petition (ECF No. 26). After a review of the record,
petitioner has established by preponderant evidence that he is entitled to compensation.
I. Procedural History
Petitioner filed his claim for compensation on February 26, 2016, alleging that the
intradermal flu vaccine caused him to suffer brachial neuritis in his left arm and shoulder.
1 Pursuant to the E-Government Act of 2002, see 44 U.S.C. § 3501 note (2018) (Federal Management and Promotion
of Electronic Government Services because this opinion contains a reasoned explanation for the action in this
case, I intend to post it on the website of the United States Court of Federal Claims. The Court’s website is at
http://www.uscfc.uscourts.gov/aggregator/sources/7. Before the opinion is posted on the Court’s website, each party
has 14 days to file a motion requesting redaction “of any information furnished by that party: (1) that is a trade
secret or commercial or financial in substance and is privileged or confidential; or (2) that includes medical
files or similar files, the disclosure of which would constitute a clearly unwarranted invasion of privacy.” Vaccine
Rule 18(b). An objecting party must provide the Court with a proposed redacted version of the opinion. Id. If
neither party files a motion for redaction within 14 days, the opinion will be posted on the Court’s website
without any changes. Id.
2 The National Vaccine Injury Compensation Program is set forth in Part 2 of the National Childhood Vaccine
Injury Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755, codified as amended, 42 U.S.C. §§ 300aa-10 to 34 (2012)
(hereinafter “Vaccine Act” or “the Act”). Hereinafter, individual section references will be to 42 U.S.C. § 300aa of
the Act.

Case 1:16-vv-00269-UNJ Document 102 Filed 06/12/23 Page 2 of 39
Amended Petition. The petition was accompanied by medical records to support his claim.
Petitioner’s Exhibits (“Pet. Exs.”) 1-7.
On July 27, 2016, respondent filed the Rule 4c report stating that this case was not
appropriate for compensation. Respondent’s (“Resp”) Report (“Rept.”) (ECF No. 16).
Respondent stated that the medical records demonstrate that petitioner received the flu vaccine
administered intradermally (not subcutaneously nor intramuscularly), and that petitioner is
alleging injuries “to structures deep within the shoulder joint,” which “the vaccine administration
method used here could not have impacted.” Id. at 9. Respondent also asserted that petitioner’s
report written by Dr. Russell Huffman “fails to even mention the method of vaccine
administration, much less address how an intradermal vaccine could cause the petitioner’s
injuries.” Id. at 9. Additionally, respondent questioned the onset of petitioner’s shoulder pain.
Id.
Petitioner filed an expert report from his treating orthopedist, Russell Huffman, MD,
MPH on December 19, 2016. Pet. Ex. 8 (ECF No. 24).3 Dr. Huffman, petitioner’s treating
orthopedic surgeon, opined that petitioner’s left shoulder symptoms and injury was caused by the
flu vaccination petitioner received on October 22, 2014. Pet. Ex. 8 at 1. Petitioner amended his
petition on January 4, 2017.
The case was reassigned to my docket on March 6, 2017 and a status conference was held
on March 30, 2017. During the status conference, I explained that petitioner’s alleged injuries
“suggested the likelihood of an inflammatory process,” and I recommended that petitioner obtain
an appropriate expert to discuss the causal mechanism. Scheduling Order (ECF No. 33).
Petitioner filed an expert report by Vera Byers, M.D.4 on June 28, 2017. Pet. Ex. 9 (ECF
No. 34). Respondent filed an expert report by Dr. Noel Rose on September 15, 2017. Resp. Ex.
3 Dr. G Russell Huffman is a practicing orthopaedic surgeon. Pet. Ex. 40 at 1. He received his undergraduate
degree from Davidson College in 1992 and his medical degree from Duke University School of Medicine in 1998.
Id. Following graduation, he had a surgical internship at the University of California San Francisco and completed
his residency in orthopaedic surgery in 2003. Id. Dr. Huffman is licensed to practice medicine in California and
Pennsylvania. Id. at 2. In 2005, he became and is still an attending orthopaedic surgeon at Penn Presbyterian
Medical Center and the University of Pennsylvania Hospital. Id. at 1. He is the director of the University of
Pennsylvania Shoulder and Elbow Fellowship program. Id. at 1. Dr. Huffman is an editorial member of multiple
orthopapedic focused journals, including the Journal of Shoulder and Elbow Surgery and the American Journal of
Sports Medicine. Id. at 3. He has been the led author or co-authored multiple research publications on varying
topics related to orthopadics. Id. at 12-16. Given Dr. Huffman’s credentials in the field of orthopadics, he is
accepted as an expert in the field of orthopadics.
4 Dr. Byers received Ph.D. in immunology in 1969 from the University of California and received her medical
degree in 1981 from the University of California at San Francisco. Pet. Ex. 39 at 1. Dr. Byers was in private
practice seeking patients with allergic and autoimmune diseases, along with cancer from 1984-1987. Id. at 3. She is
currently the president of Immunology, Inc., where she has designed and run clinical drug trials in autoimmune
diseases, HIV, atopic dermatitis, and certain types of cancers. Id. at 2. She has had multiple academic positions,
and is currently serving as an adjunct professor of Microbiology and Immunology at Texas Tech University. Id. at
4. Dr. Byers is a reviewer for Clinical Trial Grant Program at the National Cancer Institute. Id. at 5. Further, Dr.
Byers has authored or co-authored numerous medical articles in peer reviewed journals. Id. at 6-14. Dr. Byers has
testified before in Vaccine Program cases as an expert immunology, thus is accepted as an expert in immunology for
this matters as well.
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Case 1:16-vv-00269-UNJ Document 102 Filed 06/12/23 Page 3 of 39
1 (ECF No. 37). I held another status conference on October 10, 2017, where I explained that
Dr. Byers had presented a persuasive medical theory of causation and recommended that the
parties engage in settlement discussions. Scheduling Order (ECF No. 42).
Respondent opted to continue to defend against petitioner’s claim. Therefore, petitioner
filed a supplemental responsive expert report by Dr. Byers. Pet. Ex. 10 (ECF No. 47). An
entitlement hearing had been set for April 21, 2020. Pre-hearing Order (ECF No. 56).
On January 31, 2020, respondent filed an expert report from Brian Callaghan, M.D.5,
with medical literature on which he relied. Resp. Ex. A (ECF No. 62). Petitioner filed an expert
report from Maria Fangchun Chen, M.D., PhD6, and the medical literature she relied upon. Pet.
Ex. 19 (ECF No. 65).
The entitlement hearing for April 21, 2020 was cancelled and I held a status conference
on March 30, 2020. Scheduling Order (ECF No. 70). During this status conference, I explained
Dr. Chen’s report provided additional support to petitioner’s theory of vaccine causation. Id. at
4. Additionally, I recommended that the parties seek to resolve the case through settlement
negotiations. Id. at 5.
On May 4, 2021, respondent filed an additional supplemental report from Mark
Tompkins, Ph.D7, and medical literature that was referenced by Dr. Tompkins and another report
5 Dr. Callaghan graduated from the University of Michigan with a Bachelor of Science degree in 1996. Resp. Ex. B
at 1. He graduated from the University of Pennsylvania Medical Center with a medical degree in 2004. Id. He
remained at the University of Pennsylvania Medical Center for an internship in preliminary medicine from 2004 –
2005 and a residency in neurology from 2005 – 2008. Id. Afterwards, Dr. Callaghan affiliated with the University
of Michigan Medical School, at first to accept a fellowship in neuromuscular medicine and to enroll in a master’s
degree in clinical research design and statistical analysis, which he completed in 2011. Id. In 2009, he was hired
onto the Michigan faculty, where he is currently an associate professor in neurology. Id. Dr. Callaghan stated that
he has primary interest in patients with neuropathy, such as brachial neuritis and cervical radiculplexus neuropathy.
Resp. Ex. A at 1. He also is the Director of the ALS Clinic at the VA Ann Arbor Health System. Resp. Ex. B at 2.
Dr. Callaghan has an extensive list of peer review publications that he authored or was a contributor. Id. Thus, Dr.
Callaghan is accepted as an expert in neurology.
6 Dr. Maria Fang-Chun Chen is a neurologist that currently teaches at the Perlman School of Medicine at the
University of Pennsylvania Medical School. Pet. Ex. 20, Tab A. Dr. Chen graduated from Louisiana State
University in 1999. She received her Ph.D. from the University of Pennsylvania in 2005 and her medical degree
from the same in 2007. Id. Dr. Chen explained that her Ph. D is in molecular virology. Pet. Ex. 19 at 1. She did
her residency in neurology at the Hospital of the University of Pennsylvania. Pet. Ex. 20, Tab A. Dr. Chen’s is
licensed to practice in Pennsylvania and she is a board certified neurologist. Id. at 2. She is currently an Assistant
Professor of Clinical Neurology at Penn Medicine. Id. In her report, she averred that she sees over 2000 patients in
her outpatient clinic at Penn Medicine. Pet. Ex. 19 at 1. Further, she currently has over 200 outpatients with
neuropathies in her care. Id. Dr. Chen stated that medical-legal consultation contributes 1-5% to her yearly salary.
Id. Dr. Chen is admitted an expert in neurology in this matter.
7 Dr. Tompkins graduated from the University of Illinois with a Bachelor of Science degree in 1990. Resp. Ex. D at
1. He graduated from Emory University with a Ph.D. in Immunology in 1997. Id. From 1997 to 2002, he held a
post-doctoral research position at Northwestern University Medical School. Id. at 1, 3. Dr. Tompkins stated that his
postdoctoral training has focused on the immunologic mechanisms of induction of autoimmune disease, specifically
interrogating antigen-and virus-induced models of experimental encephalomyelitis; models for the neurologic
autoimmune disease, multiple sclerosis. Resp. Ex. C at 1. He stated that he has been funded by the NIH and other
3

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from Dr. Callaghan. Resp. Exs. C and E. Petitioner filed a responsive supplemental report from
Dr. Chen on June 17, 2021. Pet. Ex. 25 (ECF No. 92).
On July 16, 2021, petitioner filed a motion for a ruling on the record. Pet. Mot. (ECF No.
93). Respondent filed a response on October 15, 2021, agreeing to have the case resolved on the
record Resp. Brief (ECF No. 96). On November 19, 2021, petitioner filed a reply to
respondent’s response. Pet. Reply (ECF No. 97).
This matter is now ripe for adjudication.
II. Evidence Filed
a. Medical Records
Petitioner, a 60-year-old man, presented to Dr. David Peet Jr. on October 22, 2014 for a
“re-evaluation of fibromyalgia, chronic stiffness, and severe pain.” Pet. Ex. 2 at 79. Under
“Review of Systems,” petitioner reported that he did not have any neck, joint, or muscle pain.
Id. His musculoskeletal examination was normal. Id. at 81. Petitioner was diagnosed with
diabetes mellitus without mention of complication and not uncontrolled and “other chronic
pain.” Id. at 82. He was administered the intradermal flu shot in his left arm.
On January 19, 2015, petitioner had a follow-up appointment with Dr. Peet for a follow-
up for his diabetes. Pet. Ex. 2 at 84. His musculoskeletal exam noted normal range of motion,
normal strength, and no tenderness. Id. at 86. This time, Dr. Peet diagnosed petitioner with
diabetes without complication and “myalgia and myositis, unspecified.” Id. at 87.
On March 2, 2015, petitioner had an appointment with Dr. Michael Barmach for pain in
his left shoulder to hand. Pet. Ex. 2 at 89. Under “Chief Complaint,” it noted, “[he] received flu
shot on 10/22/2014 from our practice. The flu shot was given in the left deltoid, about 3 days
after injection, there was some pain, redness, and swelling. Was seen again on 1/19/2015 with
Dr. Peet and showed him the lump that had lasted since injection.” Id. Petitioner reported that
he was having pain on the left side of his neck, and it was not relieved with heat. Id. He also
reported that the pain radiated down to his elbow, numbness in his left hand, and it hurt to move
his arm in all directions. Id. Petitioner also reported a raised rash around the area of the shot for
several weeks. Id. He described the pain as “knife-like.” Id. His physical exam was notable for
“palpable muscle spasms along the left trapezius and petitioner was only able to flex his left arm
approximately 80 degrees before it became too painful. Id. at 91. Further, his neurologic exam
showed that petitioner had weakness in his left arm, both proximally and distally, compared to
his right arm. Id. Dr. Barmach diagnosed petitioner with brachial neuritis or radiculitis. Id. Dr.
Barmach also wrote, “[Pt] believes symptoms started after flu shot, but I believe more
coincidental. I believe symptoms due to neck pathology and getting radicular pain.” Id. Dr.
federal agencies since 2007, for research focused on novel vaccines, adjuvants, and therapies, and mechanism of
vaccine-or therapeutic-associated protection and diseases. Id. Dr. Tompkins is currently a full professor at the
University of Georgia, College of Veterinary Medicine, where he spends 80% of his time doing research and 20%
teaching. Resp. Ex. D at 2. Additionally, Dr. Tompkins is the Assistant Department Head and Curriculum
Coordinator of the Department of Infectious Diseases, College of Veterinary Medicine at the University of Georgia.
Dr. Tompkins is accepted as an expert in the subject of immunology.
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Barmach prescribed a Medrol dose pack for symptom relief and referred petitioner to an
orthopedist for an evaluation. Id.
Petitioner had an appointment with orthopedist, Dr. Gracie on March 16, 2015. Pet. Ex.
3 at 5. Petitioner reported he had left shoulder pain for five months. Id. He stated that he
received the flu shot in October 2014 and “the pain seemed to start after that.” Id. Petitioner
again stated that the area where he received the injection was “raised and swollen for awhile.”
Id. Now, the pain radiates down to his elbow and at times petitioner was experiencing numbness
in his hands. Id. The six-day Medrol pack did not provide any symptom relief. Id. He next saw
Dr. Russell Huffman at Penn Orthopedics who performed an exam of petitioner’s left shoulder.
Petitioner had a positive impingement sign, tenderness over the deltoid area, and “restricted
internal rotation with the left thumb going only to the sacrum.” Id. Dr. Huffman stated that
there were no cervical radicular findings. Id. Dr. Huffman diagnosed petitioner with “left
rotator cuff tendinitis,” and that he was concerned about petitioner developing adhesive
capsulitis. Id. He ordered petitioner to physical therapy.
Petitioner presented to his first physical therapy appointment on March 23, 2015. Pet.
Ex. 3 at 11. It was noted that petitioner was referred to physical therapy “secondary to left
shoulder pain, stiffness, and swelling after getting a flu shot on 10/22/2014.” Id. Petitioner
reported that his pain was an 8 out of 10 at best and 9/10 at worst. Id. Petitioner demonstrated
decreased range of motion compared to his right shoulder in all planes of movement. Id. He
also had tenderness throughout his left subacromial area, especially over the biceps long head
and supraspinatus tendons. Id.
On April 7, 2015, petitioner underwent a left shoulder MRI at Einstein Medical Center.
Pet. Ex. 3 at 10. The MRI revealed partial-thickness tears of the supraspinatus, infraspinatus,
and subscapularis tendons; a subacromial subdeltoid bursitis; and mild scarring of the rotator
interval with thickening of the coracohumeral ligament, consistent with subacute or chronic
adhesive capsulitis. Id.
Petitioner had an appointment with Dr. Huffman on May 28, 2015. Pet. Ex. 6 at 29. Dr.
Huffman wrote that petitioner received “an influenza injection….by a nurse practitioner. This is
fairly standard, although it may have been a little high in the anterior deltoid.” Id. He continued,
writing that petitioner started “having pain and swelling, inflammation, and a sensation of heat,”
that night. Id. Petitioner’s physical exam revealed that he had “zero degrees of external rotation,
compared to 45 degrees on the contralateral side,” and “70 degrees of abduction compared to
90.” Id. Additionally, petitioner had limited glenohumeral abduction and his “arc of range of
motion on the left side,” was 30 degrees compared to 125 degrees on the right side. Id. Dr.
Huffman noted that petitioner had some fluid in the subacromial bursa, capsular thickening in the
axillary recess which was consistent with adhesive capsulitis, and some AC joint arthrosis. Id.
Dr. Huffman assessed petitioner with, “idiopathic adhesive capsulitis with onset temporally and
most likely causally related to the influenza injection.” Id. Dr. Huffman wrote that petitioner
was “heading off an inflammatory cascade,” and he administered a corticosteroid injection to the
petitioner. Id. at 30.
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Petitioner returned to Dr. Huffman on June 23, 2015 for “left shoulder pain.” Pet. Ex. 6
at 32. It was noted that petitioner received a cortisone injection three weeks ago and it was
“ineffective.” Id. Dr. Huffman wrote that petitioner “had an influenza vaccine given high in the
deltoid region about 8 to 9 months ago. He has had persistent pain and symptoms since that
time. He has reactive capsulitis consistent with adhesive capsulitis. He also has AC joint
arthrosis.” Id. at 38. Dr. Huffman wrote that petitioner was “tired of conservative treatment,”
and that the corticosteroid injection did not provide any symptoms relief. Id. Dr. Huffman wrote
that the plan was for petitioner have a debridement and possible capsular release on July 15,
2015. Id.
On July 15, 2015, petitioner underwent an arthroscopic surgery of his left shoulder. Pet.
Ex. 6 at 39. His pre-operative diagnosis was, “rotator cuff tear; acromioclavicular joint arthritis;
adhesive capsulitis; and rotator cuff impingement.” Id. He had a rotator cuff repair, distal
clavicle excision, capsular release, and subacromial decompression. Id.
On August 18, 2015, petitioner underwent an EMG/NCS. Pet. Ex. 23 at 12. Petitioner
was being evaluated for “pain and numbness in his left upper extremity.” Id. It was recorded
that petitioner had “pain that originates in the left anterior shoulder and radiates down the arm to
the forearm.” Id. Petitioner reported intermittent numbness in all of the fingers of the left hand.
Id. Dr. Shawn Bird, the Chief of the Neuromuscular Division at the University of Pennsylvania
Hospital, performed a physical exam which showed that petitioner had absent reflex in his left
biceps and demonstrated weakness in the triceps of the left arm. Id. The NCS found that
petitioner’s left median sensory responses were slowed across the wrist and the left median-to-
ulnar comparison studies across the wrist were abnormal. Id. Additionally, petitioner’s left
lateral antebrachial cutaneous sensory response was absent. Id. The EMG revealed evidence of
“severe chronic denervation in the left biceps muscle,” and there was evidence of “mild, chronic
denervation in the abductor pollicis brevis muscle.” Id. The impression of EMG/NCS was,
“severe, chronic left musculocutaneous neuropathy and mild-to-moderate, left median
neuropathy at the wrist (carpal tunnel syndrome). Id.
Petitioner returned to Dr. Huffman on September 1, 2015. Pet. Ex. 6 at 8. Dr. Huffman
explained “because of the neurogenic nature of [petitioner’s] pain, we ordered an EMG which
was done by Dr. Shawn Bird that shows that he has a musculocutaneous nerve subacute or
chronic injury, which is, according to Dr. Bird, six or more months old.” Id. Petitioner had
atrophy of the biceps noted in the physical exam. Id. Additionally, petitioner had dysesthesia
and some signs of complex regional pain in the left upper extremity, which Dr. Huffman opined
were “consistent with a nerve injury.” Id. Dr. Huffman recommended that petitioner see Dr.
Eric Zager, a Penn neurologist, “who specializes in brachial plexus nerve injuries and treatment.”
Id. Dr. Huffman also wrote, “The surgery I did about a month ago, and I do not think it has any
relation to the nerve issues which are contributing overall to his arm pain and shoulder
dysfunction.” Id.
On October 21, 2015, petitioner had an appointment with neurologist, Dr. Eric Zager.
Pet. Ex. 23 at 11. Under History of Present Illness, Dr. Zager wrote that petitioner had a flu shot
on October 22, 2015 and “within a day of getting the injection [petitioner] complained of left
shoulder pain and swelling. His pain was so severe with movement he ultimately had a frozen
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shoulder. He consulted with ortho and had arthroscopic left shoulder surgery with Dr. Huffman
in July 2015. He did not recover well and feels his pain is now even worse.” Id. Petitioner
reported left shoulder and upper arm pain, hypersensitivity, and limited range of motion in his
entire arm. Id. On physical exam Dr. Zager noted normal strength in the right upper extremity
but 4/5 in the left deltoid, triceps, biceps, wrist extensors, wrist flexors, hand grip and 3/5 on
finger extensors. He also observed mild scapular winging, reduced range of motion in the left
shoulder, normal cervical range of motion, atrophy of the left biceps and reduced sensation in the
left upper extremity. Ex 13 at 625 Dr. Zager reviewed petitioner’s EMG/NCS and MRIs and
diagnosed petitioner with a primary diagnosis of Parsonage-Turner Syndrome. Id. He also
diagnosed petitioner with mild carpal tunnel syndrome of the left wrist. Id.
Petitioner had a follow-up appointment on October 27, 2015, with Dr. Huffman. Pet. Ex.
18 at 51. Dr. Huffman wrote that petitioner has severe pain and muscle atrophy in the
musculocutaneous nerve distribution of his left upper extremity and “diffuse pain and
dysfunction consistent with Complex Regional Pain Syndrome.” Id. Petitioner had 10 degrees
of external rotation and abduction to 60 degrees of his left shoulder. Id. Additionally, Dr.
Huffman noted that petitioner had “profound atrophy in the biceps, periscapular musculature and
upper arm.” Id. Dr. Huffman referred petitioner to Dr. Larry Chou for pain management for the
neurogenic pain. Id.
Petitioner had an appointment with Dr. Huffman on December 15, 2015. Pet. Ex. 18 at
57. At this appointment, Dr. Huffman wrote, “[Petitioner] had an influenza vaccine in his left
deltoid last October. He developed adhesive capsulitis and neurogenic sequelae. He continues
to recover from that.” Id. Dr. Huffman encouraged petitioner see Dr. Chou for the neuropathic
pain. Id.
Petitioner saw Dr. Huffman again on March 8, 2016. Pet. Ex. 18 at 63. At this
appointment, Dr. Huffman observed that petitioner had discoloration in his left arm and hand
“with obvious temperature changes with coolness and pallor even with a palpable radial pulse.”
Id. Additionally, Dr. Huffman wrote, “it is clear that he has some autonomous nervous
dysregulation in the left upper extremity.” Id. He ordered a repeat EMG/NCS. Id.
On October 4, 2016, petitioner had an appointment with Dr. Russell Huffman. Pet. Ex.
18 at 73. Dr. Huffman wrote, “…this 62-year-old gentleman had an adverse reaction to an
influenza vaccination. He developed adhesive capsulitis, Parsonage-Turner Syndrome, and also
musculocutaneous nerve involvement injury. He ultimately went on to develop adhesive
capsulitis today and had a contracture release.” Id. Petitioner had a repeat EMG. Dr. Huffman
saw petitioner on October 25, 2016 and wrote, “I had him get a new EMG as I saw small bit of
biceps recovery. The EMG confirms that he has some reinnervation of the musculocutaneous
nerve, although there is no real conduction across the lateral antebrachial cutaneous nerve. Id. at
77.
Petitioner returned to Dr. Huffman on April 4, 2017. Pet. Ex. 18 at 82. Dr. Huffman
noted that petitioner had “most of his shoulder motion back, but his pain, numbness, tingling and
dysesthesias have not improved.” Id. The physical exam showed petitioner had “pain with
active forward elevation, active abduction, but has good passive external rotation and passive
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abduction.” Id. Dr. Huffman wrote, “I suspect that he will live with this permanently.” Id. at
83.
On August 8, 2017, petitioner saw Dr. Huffman for a follow-up appointment. Pet. Ex. 18
at 89. Dr. Huffman again reiterated that petitioner received an influenza vaccine and developed
“adhesive capsulitis as well as a brachial plexopathy and Parsonage Turner Syndrome.” Id. Dr.
Huffman observed that petitioner had “return of motion, but his [petitioner’s] pain and
neurologic deficits have persisted.” Id. Dr. Huffman stated that petitioner still had weakness in
the musculocutaneous nerve distribution and that petitioner’s “biceps is firing, it is certainly
asymmetric compared with the contralateral side.” Id.
On April 16, 2019, Dr. Huffman recommended that petitioner have a repeat MRI of his
left shoulder and a repeat EMG. Id. at 101-02. Petitioner had a repeat EMG/NCS on May 14,
2019. Pet. Ex. 22 at 6. When petitioner presented for his EMG study, the “History,” explained
that petitioner’s October 2016 study “demonstrated a musculocutaneous neuropathy on the left
with significant reinnervation of the left biceps muscle and mild left carpal tunnel syndrome.”
Id. Petitioner reported that he was having increased pain in his left arm with use and felt as if his
arm was “heavy” and “weaker.” Id. The NCS demonstrated that petitioner had absent sensory
response in the left lateral antebrachial cutaneous and the “left median motor responses were
notable for a prolonged distal latency.” Id. Additionally, the needle EMG showed evidence of
“mild, chronic denervation in the left biceps and APB muscles.” Id. The impression was,
“There was good re-innervation of the biceps muscle with only mild, chronic denervation. This
finding will always be present as the sequela of the prior musculocutaneous nerve injury.” Id.
b. Petitioner’s Expert Reports
1. Dr. Russell Huffman
On December 19, 2016, petitioner filed an expert report from his treating orthopedist, Dr.
Huffman. Pet. Ex. 8 (ECF No. 24). Dr. Huffman stated that it was his opinion that petitioner’s
“symptoms and injury are directly and causally related to the vaccination he received on
10/22/2014.” Id. at 1.
Dr. Huffman wrote that petitioner had “no prior history of left arm or shoulder
symptoms,” and on the “same day of his influenza vaccination, he experienced acute pain and
swelling in his left shoulder.” Id. at 3. He continued, stating, “In the aftermath of his initial
symptoms, [petitioner] developed a brachial plexus neuropathy (Parsonage Turner syndrome) in
the musculocutaneous nerve and adhesive capsulitis.” Id.
Dr. Huffman explained that Parsonage Turner Syndrome and adhesive capsulitis are
“independently associated with adverse vaccination reactions.” Pet. Ex. 8. Dr. Huffman stated
that, “adhesive capsulitis is independently associated with Parsonage Turner syndrome, which
itself requires a viral prodromal syndrome or an inflammatory nidus such as a vaccination.” Id.
In reviewing petitioner’s history, Dr. Huffman noted petitioner’s left shoulder pain was
documented as occurring shortly after the vaccination leading to limited range of motion in the
left arm and shoulder. But it was not until March of 2015 that the concern for adhesive capsulitis
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arose. By the time he was seen by Dr. Huffman, petitioner was suffering from both Parsonage
Turner syndrome and adhesive capsulitis. Id. at 2.
He opined, “[Petitioner’s diagnoses of neuropathy and adhesive capsulitis both fit the
epidemiologic criteria for causality: temporal association (…immediate onset after the
vaccination); consistency and plausibility (the literature is clear on the association of vaccination
associated brachial neuropathy including of the musculocutaneous nerve and adhesive capsulitis
independently and in association with one another); and specificity (there is no other explanation
for his development of Parsonage Turner syndrome). Id.
2. Dr. Vera Byers
Petitioner submitted two expert reports from immunologist, Dr. Vera Byers. Pet. Exs. 9
and 10. After reviewing petitioner’s medical history, Dr. Byers observed that petitioner first
underwent a capsular release and rotator cuff repair, which did not relieve petitioner’s pain. Pet.
Ex. 9 at 6. She also agreed with Dr. Huffman that petitioner had Parsonage Turner syndrome
and that it was more likely than not, caused by the October 22, 2014 flu vaccine. Id. Dr. Byers
stated that petitioner’s torn rotator cuff “could have been present before the vaccination and just
exacerbated by the inflammation.” Id. Dr. Byers stated that “a few days after the vaccination,
petitioner presented with a “lump’ at the injection site.” Id. She stated that “the “lump”
indicates induration or infiltration at the site of macrophages/dendritic cells and T cells. The
macrophages/dendritic cells would be producing proinflammatory cytokines which call in more
macrophages as well as the antigen specific memory T cells, which would have been present
secondary to his many prior flu shots.” Id. She further stated that “antibody producing B cells
would have been activated. The macrophages would begin producing cytokines such as TNF-α
within a few hours, and the T and B cells would be activated within a few days. I believe that
this was the cause of his adhesive capsulitis.” Id.
Dr. Byers explained that Parsonage Turner syndrome (“PTS”) or idiopathic brachial
plexopathy consists of a syndrome characterized by the abrupt onset of unilateral shoulder pain.
Id. at 3. Dr. Byers stated that Parsonage Tuner Syndrome “is usually an autoimmune reaction
triggered by a viral infection or the viral antigen in the immunization.” Pet. Ex. 9 at 3. She
explained that it can occur post-surgery and “it is assumed that [PTS] is either caused by the
positioning of the body such that the brachial plexus becomes traumatically stretched, or trauma
associated with needles of the anesthetist entering the shoulder bursa.” Id. She stated that
involvement of the musculocutaneous nerve, that was damaged in this case, is not common, but
reported in medical literature. Id. She cited to a case report by Besleaga et al., which described
musculocutaneous neuropathy cases. Pet. Ex. 9, Tab 1. The authors explained that the
musculocutaneous nerve arises from the lateral cord of the brachial plexus and contains fibers
from the C5, C6, and C7 spinal nerve roots….The musculocutaneous nerve passes through the
coracobrachialis muscle and descends between the biceps brachii and brachialis muscles which it
innervates. Id. The authors noted that “the musculocutaneous anterior interosseous, ulnar, and
median nerves” have also been occasionally involved in Parsonage Turner syndrome, which “is a
rare disorder of unknown etiology, usually presenting with pain and weakness of the shoulder
and upper extremity.” Id. at 3. The authors stated that, “The exact etiology of the disorder is not
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fully understood, but 25% of cases occur after a viral infection, and 15% occur after
immunization.” Id. at 4.
Then Dr. Byers explained that intradermal vaccines are “more potent than the usual
subcutaneous or intramuscular administration.” Pet. Ex. 9 at 4. She stated that the intradermal
administration for influenza vaccines is very important in generating immune responses for older
adults. Id. She cited to an article by Hung et al., which measured influenza antibodies titers in
elderly and chronically ill adults to determine whether the intradermal vaccine would have the
same immunogenicity compared to the intramuscular flu vaccines. Pet. Ex. 9, Tab 7.8 Dr. Byers
noted that the authors found that antibody titers were significantly higher in the low dose
intradermal patients than in the full dose intramuscular patients. Pet. Ex. 9 at 4. She stated that
these findings were consistent with the findings of the Tsang et al., article which tested the
immunogenicity and safety of the Fluzone intradermal and high-dose flu vaccines in older adults.
Id.; Pet. Ex. 9, Tab 13.9 The authors found that the individuals who were administered the
intradermal flu vaccine had “post-vaccination geometric mean titers induced by the ID vaccines
that were superior to those induced by standard-dose intramuscular vaccines.” Pet. Ex. 9, Tab 13
at 1. The authors explained, “Intradermal vaccines exploit the numerous antigen-presenting
dendritic cells, macrophages, and T cells present in the skin as well as its dense network of
lymphatic and blood vessels. These features enable strong innate and adaptive immune
responses to be generated following intradermal exposure to vaccine antigens.” Id. at 2.
Interestingly, the study found that injection site swelling, injection site pruritus, injection site
pain, and injection site induration was higher in patients who received the intradermal vaccine
compared to those who received an intramuscular vaccination. Id.
Dr. Byers explained the lump that petitioner experienced at the vaccine injection site was
caused by the “whole area being flooded with cytokines.” Pet. Ex. 9 at 4. She explained that the
dermis has a dense network of immune stimulatory antigen-presenting cells (dendritic
cells/macrophages) and “it is also rich in micro vascular systems that enable interaction between
the cells of the immune system and the network of the regional lymph node.” Id. Further, the
intradermal administration of antigen improves the recruitment of the dendritic cells, which pick
up the foreign antigen, such as the vaccine, and then mature to produce pro-inflammatory
cytokines, mainly IL-1β and TNF-α. These promote the migration of the dendritic cells to the
para-cortical area of the regional lymph nodes, which allows the dendritic cells to present the
vaccine peptides to CD8+ T cells and CD4+ lymphocytes. Id.
While Dr. Byers presented two mechanisms of injury from the intradermal flu vaccine.
Pet. Ex. 9 at 5. The first mechanism is the “antigen-antibody complexes hanging up in the
vessels serving the musculocutaneous nerve. These complexes fix complement, thereby serving
as an inflammatory nidus which damage the underlying nerves.” Id. The other theory she
proposed was that the intradermal vaccine triggered the dendritic cells in the dermis, which then
induces the “the secretion of pro-inflammatory cytokines such as TNF-α….causing tissue
8 Hung, IF et al., Dose sparing intradermal trivalent influenza (2010/2011) vaccination overcomes reduced
immunogenicity of the 2009 H1N1 strain, 45 Vaccine 6427-35 (2012). [Pet. Ex. 9 Tab 7].
9 Tsang, Peter, et al., Immunogencity and safety of Fluzone intradermal and high-dose influenza vaccines in older
adults ≥ 65 years of age: A randomized, controlled phase III trial, 32 Vaccine 2507-2517 (2014). [Pet. Ex. 9, Tab
13].
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damage, and inducing cytokines by astrocytes and micoglia within the nerve itself.” Pet. Ex. 9 at
5. She continued, stating, “These dendritic cells respond with hours of antigen presentation, with
secretion of the cytokines, which can rapidly flood the area with inflammatory cells.” Id. She
explained, “Because of the temporal relationship I believe this…explanation is the most logical.”
Id.
Dr. Byers wrote that the temporal association between the vaccination and onset of
petitioner’s was “very rapid…as immediate to a day.” Pet. Ex. 9 at 7. She stated that,
“Activation of dendritic cells and production of cytokines begins within hours of vaccination.”
Id.
In her second report, Dr. Byers responded to Dr. Rose, respondent’s expert’s opinion that
there is “no epidemiologic basis for assigning a cause-and-effect association between Fluzone
intradermal influenza vaccine and PTS.” Pet. Ex. 10; see also Resp. Ex. 1 at 9. Dr. Byers stated
acknowledged that there are “no epidemiologic studies associating” the flu vaccine with brachial
neuritis, however, she noted that PTS is a “rare disorder” in which epidemiologic study would be
“almost impossible.” Pet. Ex. 10 at 2. Dr. Byers noted that Dr. Rose referenced an article by
van Alfen, which reviewed the clinical and pathophysiological concepts of PTS, and stated the
“neurologic community agrees [that] this disease has an autoimmune etiology.” Pet. Ex. 10 at 2.
The van Alfen article explained that “greater than 50% of patients with [PTS] report an immune
event before an attack led to the hypothesis that attacks are immunologically
precipitated…..Associations with different types of immunological events (for example,
infection, vaccination, surgery, pregnancy, childbirth, and immunotherapy) have been
reported…Overall, [PTS] is thought to be of autoimmune origin….” Resp. Ex. 1, Tab 2.10 Dr.
Byers stated that treatment for PTS has focused on “blocking proinflammatory cytokines,” and
the treatment involves “relatively nonspecific anti-inflammatory agents, such as steroids.” Pet.
Ex. 10 at 1.
Dr. Byers stated that it was her opinion that cytokines, which were initiated as the
immune reaction to the vaccine, caused neurologic damage. Pet. Ex. 10 at 1-2. She stated that,
the fact that “the most common side effect of vaccinations are injection site reactions caused by
the local effect of pro-inflammatory cytokines,” demonstrates that a “cytokine storm” could
easily affect the local area of the vaccination and damage the nerves, thus causing PTS. Id. at 2.
She stated, “The temporal association along with the absence of confounding factors leads to my
opinion, to a reasonable degree of medical certainty that [petitioner’s] PTS was caused by…the
vaccination he received on October 22, 2014.” Id. at 2.
3. Dr. Maria Fangchun Chen’s opinion on vaccine causation
Petitioner submitted two reports from Dr. Maria Chen, responding to respondent’s
experts’ opinions. Pet. Ex. 19 & 25. In her first report, Dr. Chen explains that “PTS or neuralgic
amyotrophy is a rare condition of an injury to the brachial plexus. Its incidence is cited at
approximately 2-3 cases per 100,000, although this is likely an under-estimation with likely
cases being misdiagnosed as musculoskeletal disorders of the shoulder or cervical
10 Van Alfen, Nens Clinical and Pathophysiological Concepts of Neuralgic Amyotrophy, 7(6) Nature Reviews
Neurol. 315-322 (2011). [Resp. Ex. 1, Tab 1; Pet. Ex. 20, Tab D].
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radiculopathies.” Pet. Ex. 19 at 2. She stated that the causes of PTS are not fully known, but
“when a proximal trigger is identified, the most common trigger are either due to post-viral
syndrome or post-immunization.” Id. Dr. Chen opined that the intradermal flu vaccine
petitioner received caused his Parsonage Turner syndrome. Id. at 5.
Dr. Chen also cited to the Van Alfen article, which found that, “The initial nerve trunk
pain and signs of peripheral nervous system inflammation, which shows up as brachial plexus
hyperintensity on acute-phase T2 weighted MRI scans, are thought to be additional arguments
for an immune process.” Pet. Ex. 20, Tab D at 6. The article explained, “Peripheral sensory
nerve biopsy samples from patients with subacute neuralgic amyotrophy showed epineural
perivascular T-cell infiltrates and CD20+ B lymphocyte germinal centers around a dorsal
ganglion.” Id. Further, the article observed that the “T-lymphocyte subsets during the acute
phase of neuralgic amyotrophy reported a decrease of CD8+T suppressor cytotoxic
lymphocytes” were also seen in other “autoimmune PNS disorders such as Guillain-Barre
syndrome and recurrent Bell’s palsy.” Id.
Dr. Chen wrote that “the inflammatory nature of [PTS] has been recognized since
biopsies of nerves demonstrate inflammatory cells such as T cell infiltrate and macrophages,
present in the blood vessel walls supplying the injured nerve, which is a vasculitic process.” Id.
Dr. Chen referenced an article by Collins and Hadden, which examined various nonsystemic
vasculitic neuropathies, including brachial plexus-neuropathy. Pet. Ex. 20, Tab C.11 The article
explained that brachial plexus-neuropathy effects motor nerves, especially those derived from the
upper plexus, and that “almost all patients experience acute, severe, continuous pain,” that can
last a median of 20 days.” Id. at 6. Then patients develop weakness within 1-2 weeks following
the pain. Id. The article reviewed other literature that examined nerve biopsies from patients
with brachial plexus-neuropathy and opined, “On the basis of [the] histopathological evidence
and the clinical phenotype of acute, painful, axonal, multifocal sensorimotor neuropathy,
neuralgic amyotrophy might represent a self-limited variant of [non-systemic vasculitic
neuropathy].” Id.; Pet. Ex. 19 at 3.
Dr. Chen explained that “Vasculitic-based injuries can be sudden and immediate, within
hours of the insult, as the inflammatory mediators in a vasculitic immune response initially
involve chemokines, cytokines, complement, and immune cells of the innate immune system
(dendritic cells, macrophages, natural killer cells) that do not need a prior memory to respond.”
Pet. Ex. 19 at 3. Citing to the Sanofi-Pasteur Fluzone package insert, Dr. Chen states that “the
intradermal vaccination is effective because the application of the antigen into the skin generates
this robust innate immune response via mechanisms that are not present in an intramuscular
application.” Id. at 3. Dr. Chen stated:
First, skin harbors higher levels of antigen presenting cells that are necessary primary
players in presenting the viral antigen to components of the memory immune response.
Second, vaccine antigen and other small components are drained from the skin by
“unique microvascular and lymphatic structures of the skin to draining lymph nodes
11 Collins, Michael P, & Hadden, Robert, The nonsystemic vasculitic neuropathies, 13 Nature Neurol. Review, 302-
317 (2017). [Pet. Ex. 20, Tab C].
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where even more antigen presenting cells (dendritic cells and macrophages) reside.
Thirdly, the local skin injury generates molecular signals that cause inflammatory
cascades via damage associate molecular signals that reside in the skin.
Id. at 3. Dr. Chen stated that “this inflammatory cascade results in a local inflammatory
response,” as marked by “higher levels of injection site reaction.” Id. Dr. Chen observed that
the package insert demonstrated that the Fluzone intradermal had higher reports of injection-site
erythema, induration, and swelling compared to the intramuscular vaccination. Id.; see also
Resp. Ex. C, Tab 8 at 10.12 Specifically, the package insert explained that 76.4% of intradermal
Fluzone recipients had injection-site erythema compared to 13.2% of intramuscular flu recipients
and 56.4% of intradermal Fluzone recipients complained of injection-site swelling compared to
8.4% of intramuscular flu recipients. Resp. Ex. C, Tab 8 at 10. According to Dr. Chen, the
increased rates of injection-site reactions for the intradermal vaccine compared to the
intramuscular flu vaccine demonstrates that the “heightened innate immune response is a local
immune response which contributes to the development of a local vasculitic process in the same
arm in which the vaccine was administered.” Pet. Ex. 19 at 3. Dr. Chen also observed that the
package insert listed “brachial neuritis” as a “Nervous System Disorder” that was reported as an
adverse event in the post-approval use of the Fluzone intradermal vaccine. Id.; see also Pet. Ex.
20, Tab M at 10.
Dr. Chen also addressed Dr. Callaghan’s opinion that petitioner’s “severe, uncontrolled
diabetes,” could have been the cause of petitioner’s shoulder issues, including the brachial
neuritis. Pet. Ex. 19 at 4; Resp. Ex. A at 3-4. Dr. Chen argued that the Massie et al. article does
not demonstrate diabetes as a causal mechanism for brachial neuritis, but instead it describes “the
characteristics of brachial neuritis when brachial neuritis occurs in patients who have diabetes.”
Pet. Ex. 19 at 4; citing Resp. Ex. A, Tab 1 & Pet. Ex. 26.13 She stated that the Massie article
“specifically selected patients who had diabetes in order to further examine diabetic patients with
Parsonage Turner.” Id. She stated, “…the Massie study does nothing to clarify the picture of
Parsonage Turner when it occurs in diabetic patients v. nondiabetic patients.” Id. at 4. She
wrote that the “The main unique points of the Massie study was to report on MRI brachial plexus
findings and autonomic studies that seem to be predominant in diabetes. Notably the classic
finding of “increase[d] nerve T2 signal” in the brachial plexus found in 45 of 47 patients was not
seen in [petitioner].” Id. Then Dr. Chen observed that the Massie study also confirmed that
brachial neuritis has a wide variety of causes, including vaccinations. Pet. Ex. 19 at 4. The
study stated:
We speculate that diabetes mellitus is one of perhaps several risk factors that predisposes
patients to altered immunity leading to an auto-immune attack on the nerve small blood
vessels…..The various positive inflammatory and rheumatological markers are also
consistent with an alteration in the immune system. The majority of patients (49/85)
12 Package Insert Highlights: Fluzone Intradermal Quadrivalent (Influenza Vaccine); Suspension for Intradermal
Injection (2017). [Resp. Ex. C, Tab 8; Pet. Ex. 20, Tab M].
13 Massie, R. et al., Diabetic cervical radiculoplexus neuropathy: a distinct syndrome expanding the spectrum of
diabetic radiculoplexus neuropathies, 135 Brain 3074-3088 (2012). [Resp. Ex. A, Tab 1; Pet. Ex. 26]
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reported a potential immune trigger (10 post-viral/systemic illness, three post-
vaccination, 26 post-surgical procedures, and nine after minor trauma or heavy exercise.
Resp. Ex. A, Tab 1 at 14; Pet. Ex. 26 at 14.
Dr. Chen acknowledged that petitioner had uncontrolled diabetes up to two years prior to
the flu vaccination, but that he had not developed any neurological complications of diabetes.
Pet. Ex. 19 at 5. She stated, “It was not until the application of the Fluzone…on 10/22/2014 that
[petitioner] developed left arm pain and weakness. The flu vaccine was the only preceding
factor, and the only immune-based trigger prior to the onset of [petitioner’s] symptoms which
has been identified as Parsonage-Turner.” Id.
Responding to Dr. Callaghan and Dr. Tompkins supplemental reports, which continued to
assert that the cause of petitioner’s left arm pain and weakness was his uncontrolled diabetes, she
stated that “the clinical presentation and attributes of [petitioner’s] neuropathy is not consistent
with a diabetic amyotrophy. Pet. Ex. 25 at 1. She observed that Dr. Callaghan “admits that the
presentation of diabetic radiculoplexus neuropathy is less common in the arm and more
commonly occurs in the legs.” Id. at 1; see Resp. Ex. E at 1 (opining that “petitioner suffered
from a diabetic cervical radiculoplexus neuropathy.”). Dr. Chen states, “The prominent
associated feature that is seen with diabetic radiculoplexus neuropathy in many publications,
including Dr. Callaghan’s own publication, is the presence of weight loss (typically 15-30 lbs)
coinciding with the development of neuropathy. Pet. Ex. 25 at 1. She observed that petitioner
did not experience “any weight loss as evidenced” by the medical records. Id. Dr. Chen also
argued that “there is also often involvement of other body regions as evidence of a systemic
disease such as diabetes to be causal of the neuropathy,” but that petitioner’s physical
examinations and EMG did not show any evidence of further neuropathy in other body parts. Id.
at 2. She again referenced the Massie article, which explained that with diabetic lumbosacral
radiculoplexus neuropathy (DLPRN) “onset was predominately unilateral with subsequent
spread to the contralateral side in many,” and that “Involvement of other regions of the
Peripheral Nervous System was common in DLRPN…Thirty patients experienced concomitant
contralateral cervical disease, while 16 had thoracic radiculopathy…” Resp. Ex. A, Tab 1 at 4;
Pet. Ex. 26 at 4. Dr. Chen wrote that “[petitioner’s] neuropathy is limited to his left arm which is
unlike a DLPRN,” and that “The clinical presentation of [petitioner’s] neuropathy does not have
common features expected from a diabetic radiculoplexus neuropathy. The mere presence of
diabetes is not sufficient to make this diagnosis.” Pet. Ex. 25 at 2.
Dr. Chen then addressed Dr. Tompkins’ opinion that petitioner’s brachial neuritis was
“more commonly attributed to diabetes than to immunological causes.” Pet. Ex. 25 at 2. She
observes that Dr. Tompkins cites to the van Alfen article, which “demonstrates that brachial
neuritis is more commonly seen after precipitating events that generate immune response than
with diabetes.” Id. She stated that the van Alfen article identifies 246 cases of brachial neuritis
and that 4.3% of cases reported vaccination as the antecedent event, but none of the cases of
brachial neuritis were “attributed to diabetes.” Id.; see also Resp. Ex. C, Tab 3.14 The van Alfen
14 van Alfen, N. & van Engelen, B., The clinical spectrum of neuralgic amyotrophy in 246 cases, 129 Brain 438-450
(2006). [Resp. Ex. C, Tab 3].
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article explained that 53.2% of patients reported an antecedent event before onset of pain. Resp.
Ex. C, Tab 3 at 6. Fifty patients reported an infection prior to the onset of the brachial neuritis
and five patients reported a vaccination as the antecedent event. Id. Dr. Chen observed that
petitioner did not have any infectious event prior to the onset of his symptoms. Pet. Ex. 25 at 2.
Finally, Dr. Chen observed that Dr. Tompkins’ assertion that the “intradermal vaccine
does not elicit a greater innate or adaptive immune responses than the intramuscular vaccine, and
therefore it cannot cause brachial neuritis,” is inconsistent with some of the medical literature he
cited that shows evidence “that the intradermal Fluzone vaccine provides systemic immune
responses that are equivalent to the intramuscular flu vaccine, which notably have been attributed
to post-vaccine neurological adverse events, including brachial neuritis.” Pet. Ex. 25 at 2. Dr.
Chen asserts that Dr. Tompkin’s opinion that “there is no evidence to demonstrate the role of
innate immune response in causation of brachial neuritis,” and his reliance on Suarez to support
his opinion is flawed. Id. She states that, “This use of Suarez is flawed as the timing of the
biopsies was well past the acute phase of the disease. Even if an innate immune response had
been present, it cannot be detected if one waits until the response has abated to sample the tissue
in the chronic phase.” Id. at 2. The Suarez et al. article that Drs. Tompkins and Chen
referenced, examined biopsies from four patients with brachial plexus neuropathy. Pet. Ex. 38.15
The authors of this article wrote, “Although there is some information about the natural history
and frequency of this disorder (brachial plexus neuropathy), little is known about its cause or
pathogenesis. The clinical course and the reported association with viral infection,
immunization, interferon and interleukin-2 (IL-2) theory, and serum sickness suggest an
inflammatory-immune mechanism.” Id. at 1. The authors found “conspicuous mononuclear
inflammatory infiltrates…surrounding epineural and endoneurial vessels.” Id. Dr. Tompkins
interpreted the findings of Suarez to mean that “the observed infiltrates were predominantly T
and B cells, suggesting an adaptive immune response contributed to neuronal disease, rather than
the innate response proposed by Dr. Chen.” Resp. Ex. C at 4. In response, Dr. Chen states, “To
show definitive evidence that an innate immune response is present in the affected nerve is
practically impossible as we neurologists do not sample nerves acutely without empiric treatment
first, given the consequences of nerve sampling will most likely result in a neurological deficit
that is permanent and likely avoidable.” Pet. Ex. 25 at 2.
Dr. Chen also agreed with Dr. Tompkins that the intradermal flu vaccine may elicit a
greater innate immune response compared to intramuscular vaccines because the “innate antigen
presenting cells (in the skin) are better activated and those cells and the vaccine antigen are more
efficiently delivered to lymph nodes, activating the adaptive response.” Pet. Ex. 25 at 6; see also
Resp. Ex. C at 6. Dr. Chen stated that, “Dr. Tompkins points out that more efficient antigen
presenting cells are delivered to the lymph nodes to activate the adaptive response that would
then occur in the lymph nodes. Notably, the draining lymph nodes of the arm are in the axilla of
the arm, which also houses nerves of the brachial plexus.” Pet. Ex. 25 at 3. In her opinion, “an
enhanced immune response from the lymph nodes in the axilla is what injured the nerves of the
brachial plexus that also reside in the axilla. The timing of the onset of symptoms (3 days from
the vaccine) together with the mechanism that Dr. Tompkins provides, [offers] support for the
intradermal Fluzone vaccine to be the cause of [petitioner’s] brachial neuritis.” Id.
15 Suarez, G.A., et al., Immune brachial plexus neuropathy: Suggestive evidence for an inflammatory immune
pathogenesis, 46 Neurol. 559-561 (1996). [Pet. Ex. 38].
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Dr. Chen concluded her report stating that, “Dr. Callaghan does not provide sufficient
evidence that [petitioner’s] neuropathy stemmed from his diabetes and the clinical presentation is
not aligned with the alternative diagnosis presented by Dr. Callaghan.” Pet. Ex. 25 at 3. She
also stated that “Similarly, Dr. Tompkins’s proposals of alternative diagnosis are equally flawed.
Notably, Dr. Tompkins highlights an aspect of the intradermal flu vaccination that supports the
causation of the vaccination with [petitioner’s] brachial neuritis.” Id. It is her opinion that the
intradermal flu vaccine petitioner received on October 22, 2014 was the cause of his left arm
brachial neuritis. Id.
c. Respondent’s Experts Reports
1. Dr. Brian Callaghan’s opinion on vaccine causation
Respondent submitted three expert reports from neurologist, Dr. Brian Callaghan. Resp.
Exs. A, E, & F. After reviewing petitioner’s medical records and the reports written by Drs.
Byers, Huffman, and Chen he disagreed with their opinions that “the evidence supports
vaccination as the most likely cause of [petitioner’s] adhesive capsulitis and neuropathy.” Resp.
Ex. A at 3. He states, “The timing of symptoms in relation to the vaccine is inconsistently
reported with reports of pain pre-dating his vaccination.” Id. Additionally, Dr. Callaghan opined
that petitioner did not have brachial neuritis, but “adhesive capsulitis and cervical
radiculoplexopathy” which was caused by petitioner’s underlying diabetes. Resp. Ex. E at 3;
Resp. Ex. F at 1-2.
Dr. Callaghan argued that left shoulder pain petitioner experienced was more likely
caused by “severe uncontrolled diabetes.” Resp. Ex. A at 3. It was his opinion that petitioner
had “diabetic cervical radiculoplexus neuropathy given the longstanding and uncontrolled
diabetes.” Resp. Ex. E at 1. He stated that, “Diabetic cervical radiculoplexus neuropathy is very
similar to brachial neuritis, but the trigger is secondary to diabetes.” Id. He stated, “In both
conditions, patients have severe shoulder pain followed by weakness followed by recovery. In
both conditions, a mononeuropathy such as musculocutaneous mononeuropathy can develop.”
Id. Dr. Callaghan wrote, “The evidence for diabetes being linked to this condition far outweighs
the evidence for vaccinations being linked to brachial neuritis.” Id. In his second report, he
stated that the clinical conditions of diabetic lumbosacral radiculplexus neuropathy and diabetic
cervical radiculoplexus neuropathy “share similar symptoms, signs, and underlying pathology,
including microvasculitis on nerve biopsy.” Resp. Ex. E at 1. Dr. Callaghan wrote, “…diabetic
lumbosacral radiculoplexus neuropathy, which is almost identical to diabetic cervical
radiculoplexus neuropathy, except that it affects the nerve plexus in the leg instead of the arm, is
well established as being caused by diabetes.” Id. at 1. He referenced an article by Dyck et al,
which described diabetic and non-diabetic lumbosacral radiculoplexus neuropathy (“DLRPN”)
pathophysiology and treatment. Resp. Ex. E, Tab 2.16 The article explained that DLRPN is
“well recognized, unlike the non-diabetic lumbosacral radiculoplexus neuropathy (“LSRPN”)”
and that “both disorders are a lumbosacral plexus neuropathy associated with weight loss, often
16 Dyck, James B. and Windebank, Anthony J., Diabetic and Nondiabetic lumbosacral radiculoplexus neuropathies:
New Insights Into Pathophysiology and Treatment, 25 Muscle and Nerve 477-491 (2002). [Resp. Ex. E, Tab 2].
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beginning focally or asymmetrically in the thigh or leg, but usually progressing to involve the
initially unaffected segment and the contralateral side.” Id. at 1. Dr. Callaghan argued that the
Dyck article demonstrates that diabetic lumbosacral radiculplexus neuropathy is much more
common than the “version that occurs in those without diabetes.” Resp. Ex. E at 1. However,
the authors of Dyck explain that the limited knowledge of non-diabetic lumbosacral
radiculplexus is “limited because of the small number of patients, lack of prolonged follow-up,
lack of sensory or autonomic test evaluations, and the relatively recent recognition of LSRPN as
a separate condition.” Resp. Ex. E, Tab 1 at 3.
In his third report, Dr. Callaghan asserted that Dr. Chen’s opinion that petitioner did not
have diabetic cervical radiculoplexopathy contradicted the Massie et al. article, which described
85 cases of diabetic cervical radiculoplexopathy. Resp. Ex. F at 1. Dr. Callaghan argued that
some of the characteristics of patients with diabetic cervical radiculoplexopathy described in the
Massie article was consistent with the petitioner’s presentation. Id. at 1. Specifically, Dr.
Callaghan stated that 65% of cases studied occurred without weight loss and 48% of patients
with diabetic cervical radiculoplexopathy had only one side affected, which would be similar to
the petitioner’s presentation. Id.; see also Pet. Ex. 26 at 8.
Finally, Dr. Callaghan opined that petitioner’s “longstanding diabetes” was also the cause
of his adhesive capsulitis. Resp. Ex. E at 2; Resp. Ex. F at 1. He stated that “the petitioner’s
concomitant adhesive capsulitis is also likely caused by diabetes, providing further evidence to
support diabetes as the underlying cause of both conditions.” Id. It was Dr. Callaghan’s opinion
that the timing of petitioner’s adhesive capsulitis “at the same time as the brachial neuritis lends
further evidence that diabetes is the likely cause.” He stated, “The most common condition that
causes adhesive capsulitis is diabetes.” Id. Dr. Callaghan asserted that the Zreik et al. article
“revealed that patients with diabetes are 5 times more likely to develop this condition compared
to those without diabetes. Resp. Ex. A, Tab 2.17 The Zreik article reviewed literature that
studied the prevalence of adhesive capsulitis in diabetes. Id. The authors found “an overall mean
prevalence of [adhesive capsulitis] in diabetes mellitus of 13.4%” and that “diabetic patients are
5 time more likely to develop adhesive capsulitis compared to non-diabetic controls.” Id. at 3.
Dr. Callaghan concluded that the intradermal flu vaccine petitioner received was not the
cause of his brachial neuritis, but it was petitioner’s diabetes. Resp. Ex. E at 3; Resp. Ex. F at 2.
He stated, “the most likely cause of both [adhesive capsulitis and cervical radiculoplexopathy] is
diabetes, especially considering the long duration and lack of control of petitioner’s diabetes.”
Id.
2. Dr. S. Mark Tompkins opinion on vaccine causation
Dr. S. Mark Tompkins, a Ph.D. immunologist, wrote two reports for respondent. Resp.
Ex. C, G. Summarizing the conclusion of both reports, Dr. Tompkins’ opinion is that
petitioner’s “pre-existing conditions” which are “associated with neuropathy remain the most
medically reliable explanations for the onset of petitioner’s neuropathy.” Resp. Ex. C at 7; Resp.
17 Zreik, N., Adhesive capsulitis of the shoulder and diabetes: a meta-analysis of prevalence, 6 Muscles, Ligaments
and Tendons J., 26-34 (2016). [Resp. Ex. A, Tab 2].
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Ex. G at 3. He stated that Drs. Beyers and Chen opinions that the intradermal flu vaccine can
cause brachial neuritis are not supported by the medical literature. Resp. Ex. C at 7.
In his first report, Dr. Tompkins acknowledged that post-marketing reporting for the
intradermal vaccine includes reports of brachial neuritis, but states that “post-marketing reporting
does not infer causality.” Resp. Ex. C at 7. He argued that because brachial neuritis is listed as
an adverse event in other injectable vaccines’ post-marketing data, “brachial neuritis is not
specifically associated with intradermal vaccinations as Dr. Chen suggests.” Id. He asserted that
the medical literature that Drs. Byers and Chen reference, specifically the Feinberg and van
Alfen articles, do not propose a specific mechanism of how brachial neuritis can be caused by
vaccination. Id. at 3.
In his two reports, Dr. Tompkins conceded that brachial neuritis can be an immune-
mediated disease. Resp. Ex. C at 3; Resp. Ex. G at 2. He stated that the Van Eijk et al. article
provides, “[BP] can be categorized as an organ-specific immune-mediated disorder. The
immune hypothesis is supported by the fact that half of affected patients report antecedent events
that trigger the immune system, mostly infections, but also surgery, childbirth, and physical or
mental strain.” Id.; Resp. Ex. C, Tab 1.18 Attempting to distinguish his opinion from Drs. Byers
and Chen, he asserted that brachial neuritis is caused by “an adaptive immune response.” Resp.
Ex. C at 4. Referencing the 2011 van Alfen article, Dr. Tompkins argued that the biopsies of
brachial neuritis patients “demonstrated T cell and other lymphocytic infiltrates in sensory
nerves.” Resp. Ex. C at 4. Specifically, van Alfen states, “Peripheral sensory nerve biopsy
samples from patients with subacute neuralgic amyotrophy showed epineural perivascular T-cell
infiltrates and CD20+ B-lymphocyte germinal centers around the dorsal ganglion.” Pet. Ex. 20,
Tab D at 6. Further, the article states that, “Other studies have found increased levels of
complement C5b-C9 and decreased levels of complement C3 without signs of immune
complexes in patients with acute neuralgic amyotrophy.” Id. van Alfen continues, stating, “A
study that characterized patients’ T-lymphocyte subsets during the acute phase of neuralgic
amyotrophy reported a decrease of CD8+T-suppressor lymphocytes-a profile also seen in
autoimmune PNS disorders, such as Guillain-Barré syndrome and recurrent Bell palsy.” Id.
Dr. Tompkins stated that “the window between preceding event and onset of disease
ranges from hours to weeks,” and “[w]hile the rapid onset of symptoms might suggest an innate
immune response, the infectious immune response that are argued to be triggers of brachial
neuritis may not be primary immune responses.” Resp. Ex. C at 4. He stated that the Suarez
article found the “presence of a “reactive germinal center with B lymphocytes,” in one brachial
neuritis sample, demonstrating the presence of memory immune cells and tissues in brachial
plexus biopsies.” Id. However, the Suarez article referenced by Dr. Tompkins, actually
reviewed samples of four patients with brachial plexus neuropathy, and all four biopsies
revealed, “Conspicuous mononuclear inflammatory infiltrates…surrounding epineurial and
endoneurial vessels.” Pet. Ex. 38. Additionally, the authors found that only one of the four
patients had a “reactive germinal center with small cleaved and large noncleaved CD20-positive
B lymphocytes” but all four patients’ infiltrates were composed of T-lymphocytes. Id. at 1. The
authors wrote, “The main observation from this series of patients with BPN was the presence of
18 Van Eijk, Jeroen, et al., Neuralgic Amyotrophy: An Update on Diagnosis, Pathophysiology, and Treatment, 53
Muscle & Nerve 337-350 (2016). [Resp. Ex. C, Tab 1].
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prominent collections of inflammatory cells (especially T lymphocytes) within the brachial
plexus.” Id.
Then Dr. Tompkins argued that the intradermal flu vaccine does not elicit an increased
cytokine response, as Drs. Byers and Chen asserted in their reports. Resp. Ex. C at 5. Dr.
Tompkins agreed with Dr. Byers that the intradermal vaccines “may elicit inflammatory
cytokines, such as TNF-α and IL-1β, or IL-6,” but argued that her statement is based on
“established basic literature for intradermal vaccination and epidermal immunity, but there is
limited evidence for this during intradermal influenza vaccination in humans.” Id. He asserted
Tozuka et al., which is a study of early immune responses following the intradermal flu
vaccination in mice, demonstrates that the “improved immunogenicity of intradermal vaccination
may be the result of improved antigen delivery to the draining lymph node.” Id. at 5. Dr.
Tompkins wrote that, “The extensive distribution of lymphatic vessels in skin, compared to
muscle, enabled efficient delivery of antigen to draining lymph nodes.” Dr. Tompkins also
stated that the del Pilar Martin et al. article found increases of TNF-α and IL-1β, which are
inflammatory cytokines, six and 12 hours after mice were vaccinated with microneedle patches.
Id. at 5; see also Resp. Ex. C, Tab 6.19 The del Pilar Martin study examined cytokine expression
in the skin of mice after microneedle vaccination to better understand how intradermal
vaccinations confer protective immunity. Resp. Ex. C, Tab 6 at 1. The authors found
“significant increases in the levels of cytokines IL-1β, macrophage inflammatory protein 1 alpha
(MIP-α), tumor necrosis factor alpha (TNF-α), and monocyte chemoattractant protein 1 (MCP-
1),” after microneedle insertion alone, but increased further when using a microneedle coated
with the influenza vaccine. Id. at 2. The authors wrote, “The increase of these cytokine
expression levels has been demonstrated to contributed to the regulation of epidermal
Langerhans cell migration and the subsequent accumulation of dendritic cells in the draining
lymph nodes, in addition to the role in neutrophil and monocyte recruitment.” Id. Further, the
authors stated, “The skin cytokine profile analysis shows that skin immunization induces a local
innate immune response and a release of chemokines in the skin suggestive of the activation and
recruitment of immune cells to the site of vaccination.” Id. Dr. Tompkins acknowledges that
this study shows that some proinflammatory cytokines were increased at intradermal injection
sites, but argued that the study does not compare innate immune responses to intramuscular flu
vaccines, “so we cannot conclude that the cytokine levels elicited by microneedle patch
vaccination were greater than the standard influenza vaccination method.” Resp. Ex. C at 5.
To further his argument that the intradermal flu vaccine does not “elicit a cytokine storm
that might be involved in causing brachial neuritis or other neuroinflammatory events,” Dr.
Tompkins compares the immunogenicity of the intradermal flu vaccine to the flu vaccine
delivered intramuscularly. Resp. Ex. C at 5-6. He asserted that the Beran et al. study “directly
compared the safety and immunogenicity of 9µg intradermal flu vaccine to 15 µg intramuscular
flu vaccine and concluded the intradermal vaccine “showed comparable immunogenic and safety
profiles to intramuscular vaccination.”” Id. at 6; see also Resp. Ex. C, Tab 10.20 The Beran
19 del Pilar Martin, Maria, et al., Local response to Microneedle-Based Influenza Immunization in the Skin, 3 mBio
doi:10.1128/mBio.00012-12 (2012). [Resp. Ex. C, Tab 6].
20 Beran, Jiri, et al., Intradermal influenza vaccination of healthy adults using a microinjection system: a 3-year
randomised controlled safety and immunogenicity trial, 7 BMC doi:10.1186/1741-7015-7-13 (2009). [Resp. Ex. C,
Tab 10].
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study was a randomized controlled study where patients received the flu vaccine either by
intradermal injection or intramuscular injection. Resp. Ex. C, Tab 10 at 1. The authors did find
the immunogenicity between the intradermal and intramuscular flu vaccines to be comparable, as
Dr. Tompkins asserted. Id. at 7. More relevant to this case, however, is that the study also found
increased local injection site reactions were more frequently reported with patients who received
the intradermal vaccination. Id. at 13. The authors found that erythema was the most common
local reaction with the intradermal vaccine, “typically appearing within 3 days of vaccination.”
Id. at 7. Thirty seven percent of patients who received the intradermal vaccination reported pain
at the injection site, slightly below the 39% of patients who received the intramuscular
vaccination. Id. at 12. Further, the study found that induration at the injection site was higher in
those who received the intradermal vaccination compared to patients who received the
intramuscular vaccine. Id. The authors stated that the “increase in local reactions is linked to the
underlying inflammatory or immunological response in the skin, which is more visible with ID
than IM vaccination.” Id. at 13. Dr. Tompkins argued that the local immune reactions are
“atypical compared to intramuscular vaccination.” Resp. Ex. C at 6.
In his supplemental report, he again averred that the flu vaccine delivered intradermally
and intramuscularly “elicit similar inflammatory responses,” and that a local inflammatory
response triggered by the intradermal flu vaccine could not result in brachial neuritis. Resp. Ex.
G at 3. He acknowledged that the cytokine response from the intradermal flu vaccine is elevated,
but argued that this elevation in cytokines, along with dendritic cells would migrate to the
draining lymph nodes to activate antigen specific adaptive immune cells, “does not suggest a
localized response in the lymph node could trigger brachial neuropathy.” Id. Dr. Tompkins
refers to the Institute of Medicine (“IOM”) Report on Adverse Reactions to Vaccines to support
his opinion that the flu vaccine cannot result in an increased cytokine activation, as proposed by
Dr. Chen. Id. The relevant part from the IOM which Dr. Tompkins quoted provides, “In review
of the relevant literature related to the vaccine and adverse event combinations considered by the
committee, no evidence that directly or indirectly supports the over secretion of cytokines as an
operative mechanism was found.” Resp. Ex. G, Tab T at 105.21 Dr. Tompkins wrote, “In other
words, there is no evidence that cytokine cascades cause adverse events.” Resp. Ex. G at 3.
However, Dr. Tompkins fails to mention that the IOM also wrote:
Although the committee is not aware of reports of full-blown cytokine storm following
administration of any of the vaccines reviewed, more subtle imbalances of
proinflammatory and anti-inflammatory cytokines may occur following immunization
against rubella, human papillomavirus, or hepatitis B. Moreover, it is possible that the
unique immunogenetic makeup of an individual might predispose that individual to an
exaggerated cytokine imbalance following immune stimulation such as microbial
infection or vaccine administration.
Resp. Ex. G, Tab 1 at 105.
Finally, Dr. Tompkins agreed with Dr. Callaghan’s opinion that petitioner most likely
experienced neuropathy because of his underlying diabetes. Resp. Ex. G at 1; Resp. Ex. C at 6.
He stated, “…as Dr. Callaghan notes, rates of neuropathy are increased in persons with diabetes
21 Institute of Medicine, Adverse Effects of Vaccines: Evidence and Causality (2012). [Resp. Ex. G, Tab 1].
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mellitus and [petitioner’s] records note a diagnosis of diabetes mellitus and increased
hemoglobin A1c and glucose since at least November 2011.” Id. at 6. He also stated that the
Iqbal (cite) article found that the “incidence of neuropathy to be up to ten times higher in
diabetics compared to controls in two cohort studies.” Id. at 7. Then, somewhat paradoxically,
Dr. Tompkins opined that petitioner’s shoulder pathology of a partial rotator cuff tear and rotator
cuff tendinitis could result in “increased levels of proinflammatory cytokines, including IL-1β,
IL-6, and TNF-α” which could be the trigger for immune mediated brachial neuritis. Id. Dr.
Tompkins also contended that another possible cause of petitioner’s brachial neuritis is herpes
recrudescence. Id. He cited to an article which provides a case report of one individual with
“relapsing-remitting facial and brachial plexus neuritis caused by HSV-1.” Id. Dr. Tompkins
based his opinion that it could be possible that petitioner had an HSV-1 recurrence by
petitioner’s prescription for Valtrex, but acknowledged that “herpes recrudescence is not noted in
petitioner’s medical records.” Id. Dr. Tompkins states that “repeated HSV recrudescence events
could have provided the neuronal inflammation triggering petitioner’s brachial neuropathy.” Id.
Dr. Tompkins does appear to drop this argument in his supplemental expert report.
Dr. Tompkins concluded both reports stating that, “The pre-existing conditions associated
with neuropathy remain the most medically reliable explanation for the onset of petitioner’s
neuropathy.” Resp. Ex. C at 7; Resp. Ex. G at 3. He stated that, “Each of these triggers are
associated with brachial neuropathy, and have proposed mechanisms involving eliciting pro-
inflammatory cytokine responses to damage the neuron, or directly causing neuronal damage
through virus infection and bystander immune damage.” Resp. Ex. C at 7.
III. Legal Standard
The Vaccine Act was established to compensate vaccine-related injuries and deaths.
Section 10(a). “Congress designed the Vaccine Program to supplement the state law civil tort
system as a simple, fair and expeditious means for compensating vaccine-related injured persons.
The Program was established to award ‘vaccine-injured persons quickly, easily, and with certainty
and generosity.’” Rooks v. Sec’y of Health & Human Servs., 35 Fed. Cl. 1, 7 (1996) (quoting H.R.
No. 908 at 3, reprinted in 1986 U.S.C.C.A.N. at 6287, 6344).
A petitioner bears the burden of establishing his or her entitlement to compensation from
the Vaccine Program. The burden of proof is by a preponderance of the evidence. Section
13(a)(1).
A. Nature of Injury
The Federal Circuit established the test for actual causation of an off-Table injury in
Althen, 418 F.3d at 1278. In that case: “There was no dispute as to whether the petitioner,
Margaret Althen, actually suffered from a central nervous system demyelinating disorder.
Therefore, the Federal Circuit was not presented with a case in which the diagnosis itself was
questioned, but one in which causation of the injury by the vaccine was the issue in dispute.”
Doe v. Sec’y of Health & Hum. Servs., 94 Fed. Cl. 597, 611 (2010) (citing Althen, 418 F.3d at
1282), aff’d, Lombardi v. Sec’y of Health & Hum. Servs., 656 F.3d 1343 (Fed. Cir. 2011).
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Special masters are generally not tasked with diagnosing injuries. In Lombardi, the
Federal Circuit explained: “The function of a special master is not to ‘diagnose’ vaccine-related
injuries, but instead to determine ‘based on the record evidence as a whole and the totality of the
case, whether it has been shown by a preponderance of the evidence that a vaccine caused the
petitioner’s injury.’” Lombardi, 656 F.3d at 1343, citing Andreu v. Sec’y of Health & Hum.
Servs., 569 F.3d 1367, 1382 (Fed. Cir. 2009).
However, the Federal Circuit has determined that in certain instances, “if there is a
dispute as to the nature of a petitioner’s injury, the special master may opine on the nature of the
petitioner’s injury.” Contreras v. Sec’y of Health & Hum. Servs., 844 F.3d 1363, 1368 (Fed. Cir.
2017), citing Hibbard v. Sec’y of Health & Hum. Servs., 698 F.3d 1355 (Fed. Cir. 2012); see also
Locane v. Sec’y of Health & Hum. Servs., 686 F.3d 1375 (Fed. Cir. 2012); Broekelschen v. Sec’y
of Health & Hum. Servs., 618 F.3d 1339 (Fed. Cir. 2010)).
In Hibbard, the Federal Circuit reasoned: “If a special master can determine that a
petitioner did not suffer the injury that she claims was caused by the vaccine, there is no reason
why the special master should be required to undertake and answer the separate (and frequently
more difficult) question whether there is a medical theory, supported by ‘reputable medical or
scientific explanation,’ by which a vaccine can cause the kind of injury that the petitioner claims
to have suffered.” 698 F.3d at 1365.
While the special master is not required to reach a specific diagnosis, the special master
may appropriately evaluate at least the nature of petitioner’s injury and whether that aligns with
petitioner’s theory. For example, in Broekelschen, the petitioner posited “transverse myelitis
[which] is an inflammatory event caused by an immune response,” while the respondent posited
“anterior spinal artery syndrome, [which] is a vascular event caused by a blockage.” 618 F.3d at
1346. The Federal Circuit observed: “Nearly all of the evidence on causation was dependent on
the diagnosis” and because the injury itself [was] in dispute, the proposed injuries differ[ed]
significantly in their pathology, and the question of causation turn[ed] on which injury [the
petitioner] suffered.” Id. Accordingly, the Federal Circuit held “it was appropriate… for the
special master to first determine which injury was best supported by the evidence presented in
the record before applying the Althen test so that the special master could subsequently
determine causation relative to the injury.” Id.
In contrast, in Contreras, the Court of Federal Claims held that the special master erred
by diagnosing the petitioner’s illness – as TM and not Guillain-Barré syndrome (“GBS”) –
before evaluating the Althen prongs. 107 Fed. Cl. 280, 292-93. The Court reasoned that the case
contained “ample evidence that TM and GBS are similar diseases with similar pathologies” and
the parties’ “unified position [was] that an exact diagnosis of [the petitioner’s illness] was not
required to rule on causation.” Id. at 293. The Court of Federal Claims articulated that “the
general rule is that the special master should not conduct a differential diagnosis, at the outset of
the causation analysis, to choose one diagnosis over another, or over a combination of
diagnoses.” Id., aff’d 844 F.3d 1363; see also Andreu, 569 F.3d 1367, 1378 (holding that the
special master need not determine whether an initial seizure was febrile or afebrile for purposes
of assessing vaccine causation).
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Relevant to this inquiry, the Vaccine Act provides that a special master must consider the
record as a whole including any medical diagnosis contained therein. Section 300aa-13(b)(1).
However, no diagnosis in the medical records is “binding on the special master.” Id. Rather, “[i]n
evaluating the weight to be afforded to any such diagnosis… the special master… shall consider
the entire record and the course of the injury, disability, illness, or condition until the date of the
judgment of the special master.” Id. The special master shall also consider any expert opinions
and additional medical scientific evidence in the record. Id.
B. Causation
A petitioner may prevail by proving either that (1) the vaccinee suffered an injury listed
on the Vaccine Injury Table with onset beginning within a corresponding time period following
receipt of a corresponding vaccine (a “Table Injury”), for which causation is presumed or that (2)
the vaccinee suffered an injury that was actually caused by a vaccine. Under either method,
however, the petitioner must also show that the vaccinee “suffered the residual effects or
complications of the illness, disability, injury, or condition for more than six months after the
administration of the vaccine.” Section 11(c)(1)(D)(i).
In the present case, petitioner does not and cannot allege a Table injury. Thus, he bears
the burden of establishing actual causation. To do so, he must “show by preponderant evidence
that the vaccination brought about the injury by providing 1) a medical theory connecting the
vaccination and 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.” Althen v. Sec’y of Health & Human Servs., 418 F. 3d 1274, 1278 (Fed.
Cir. 2005). There must be preponderant evidence for each Althen prong. Caves v. Sec’y of
Health & Human Servs., 100 Fed. Cl. 119, 132 (2011), aff. per curiam, 463 Fed. Appx. 932 (Fed.
Cir. 2012).
Under Althen prong one, the causation theory must relate to the injury alleged. Thus, a
petitioner must provide a “reputable” medical or scientific explanation that the vaccine received
can cause the type of injury alleged. Pafford, 451 F.3d at 1355-56. The theory must be based on
a “sound and reliable medical or scientific explanation.” Knudsen, 35 F.3d at 548. It must only
be “legally probable, not medically or scientifically certain.” Id. at 549. However, the theory
still must be based on a “sound and reliable medical or scientific explanation.” Id. at 548. The
Federal Circuit explained in Althen that “while [that petitioner’s claim] involves the possible link
between [tetanus toxoid] vaccination and central nervous system injury, a sequence hitherto
unproven in medicine, the purpose of the Vaccine Act’s preponderance standard is to allow the
finding of causation in a field bereft of complete and direct proof of how vaccines affect the
human body.” Althen, 418 F.3d at 1280 (emphasis added).
Under Althen prong two, petitioner must prove “a logical sequence of cause and effect
showing that the vaccination was the reason for [her] injury.” Althen, 418 F.3d at 1278. This
prong is sometimes referred to as the “did it cause” test; i.e. in this particular case, did the
vaccine(s) cause the alleged injury. Broekelschen, 618 F. 3d at 1345 (“Because causation is
relative to the injury, a petitioner must provide a reputable medical or scientific explanation that
pertains specifically to the petitioner’s case”). Temporal association alone is not evidence of
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causation. See Grant v. Sec’y of Health & Human Servs., 9556 F.2d 1144, 1148 (Fed. Cir.
1992). This sequence of cause and effect is usually supported by facts derived from petitioner’s
medical records. Althen, 418 F.3d at 1278; Andreu, 569 F.3d at 1375-77; Capizzano, 440 F.3d at
1326; Grant, 956 F.2d at 1148.
Althen prong three requires establishing a “proximate temporal relationship” between the
vaccination and the injury alleged. Althen at 1281. That term has equated to the phrase
“medically-acceptable temporal relationship.” Id. A petitioner must offer “preponderant proof
that the onset of symptoms occurred within a timeframe which, given the medical understanding
of the disorder’s etiology, it is medically acceptable to infer causation.” de Bazan v. Sec’y of
Health & Human Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for what is
medically acceptable timeframe must align with the theory of how the relevant vaccine can cause
an injury (Althen prong one). Id. at 1352.
The preponderance of the evidence standard requires the petitioner to demonstrate that it
is “more likely than not” that the vaccine caused the injury. Moberly v. Sec’y of Health &
Human Servs., 592 F.3d 1315, 1322 n.2 (Fed. Cir. 2010). Proof of medical certainty is not
required. Bunting v. Sec’y of Health & Human Servs., 931 F.2d 867, 873 (Fed. Cir. 1991). A
petitioner must demonstrate that the vaccine was “not only [a] but for cause of the injury but also
a substantial factor in bringing about the injury.” Moberly, 592 F.3d at 1321 (quoting Shyface v.
Sec’y of Health & Human Servs., 135 F.3d 1344, 1352-53 (Fed. Cir. 1999); Pafford v. Sec’y of
Health and Human Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006). Causation is determined on a
case-by-case basis, with “no hard and fast per se scientific or medical rules.” Knudsen v. Sec’y
of Health & Human Servs., 35 F.3d 543, 548 (Fed. Cir. 1994). A fact-finder may rely upon
“circumstantial evidence” which is consistent with the “system created by Congress, in which
close calls regarding causation are resolved in favor of injured claimants.” Althen, 418 F. 3d at
1280.
The petitioner often presents expert testimony in support of his or her claim. Lampe v.
Sec’y of Health & Human Servs., 219 F.3d 1357, 1361 (Fed. Cir. 2000). Expert testimony in the
Vaccine Program is usually evaluated according to the factors set forth in Daubert v. Merrell
Dow Pharm., Inc., 509 U.S. 579, 594-96 (1993); see also Cedillo, 617 F.3d at 1339 (citing
Terran v. Sec’y of Health & Human Servs., 195 F.3d 1302, 1316 (Fed. Cir. 1999). A special
master may use the Daubert framework to evaluate the reliability of expert testimony, but expert
testimony need not meet each Daubert factor to be reliable. Boatmon v. Sec’y of Health &
Human Servs., 941 F.3d 1351 (Fed. Cir. 2019). The Daubert factors are “meant to be helpful,
not definitive,” and all factors “‘do not…necessarily apply even in every instance in which the
reliability of scientific testimony is challenged.’” Boatmon, 941 F. 3d at 1359 (citing Kumho
Tire Co. v. Carmichael, 526 U.S. 137, 151, 119 S. Ct. 1167, 143 L.Ed.2d 238 (1999). Thus, for
Vaccine Act claims, a “special master is entitled to require some indicia of reliability to support
the assertion of the expert witness.” Moberly at 1324. Where both sides offer expert testimony,
a special master’s decision may be “based on the credibility of the experts and the relative
persuasiveness of their competing theories.” Broekelschen v. Sec’y of Health & Human Servs.,
219 F.3d 1339, 1347 (Fed. Cir. 2010) (citing Lampe, 219 F.3d 1357 at 1362).
If the petitioner makes a prima facie case supporting vaccine causation-in-fact, the
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burden shifts to respondent to show by a preponderance of the evidence that the injury is instead
due to factors unrelated to the administration of the vaccine. Deribeaux v. Sec’y of Health &
Human Servs., 717 F.3d 1363, 1367 (Fed. Cir. 2013) (citing Section 13(a)(1)(B)). Respondent
has the burden of demonstrating that: “[A] factor unrelated to the vaccination is the more likely
or principal cause of injury alleged. Such a showing establishes that the factor unrelated, not the
vaccination, was ‘principally responsible’ for the injury. If the evidence or alternative cause is
seen in equipoise, then the government has failed in its burden of persuasion and compensation
must be awarded.” Knudsen, 35 F.3d at 551.
IV. Entitlement
A. Nature of petitioner’s condition
Here, the parties do not dispute that petitioner was suffering from some type of vasculitic
neuropathy of the left upper extremity. See Pet. Ex. 19 at 3; Resp. Ex. E at 1. On August 15,
2015, an EMG/NCS revealed “severe, chronic left musculocutaneous neuropathy.” Pet. Ex. 23
at 12. The Nerve Conduction Study found “the left lateral antebrachial cutaneous sensory
response was absent,” and the EMG found evidence of “severe chronic denervation in the left
biceps muscle.” Id. Petitioner’s treating physician, Dr. Huffman, who also provided an expert
opinion in this matter, diagnosed petitioner with “Parsonage-Turner syndrome.” Id. at 10.
The parties dispute whether petitioner has brachial neuritis or diabetic cervical
neuropathy. See Pet. Ex. 19, 25; Resp. Ex. A, E & F. Petitioner contends that he has brachial
neuritis that began three days post-vaccination and was correctly diagnosed by Dr. Huffman with
adhesive capsulitis occurring subsequently and secondary to the painful brachial neuritis.
Respondent argued that the correct diagnosis for petitioner is diabetic cervical
radiculoplexopathy, due to petitioner’s long-standing diabetes. Resp. Brief at 20; Resp. Ex. E at
1.
1. Neurologic amyotrophy
Neurologic amyotrophy, which is referred to as Parsonage-Turner syndrome or brachial
neuritis, is a “markedly underdiagnosed” disorder. Pet. Ex. 32 at 1; Resp. Ex. C, Tab 3; Pet. Ex.
20, Tab D at 1. According to two articles written by Nens van Alfen, which both parties
referenced, neurologic amyotrophy “is a distinct and painful peripheral neuropathy that causes
episodes of multifocal paresis (weakness)and sensory loss in a brachial plexus distribution with
concomitant involvement of other peripheral nervous system structures.” Pet. Ex. 20, Tab D at
1. The core features include episodes of “extreme pain at symptom onset, rapid multifocal
paresis and atrophy of the upper extremity muscles, and a slow recovery.” Id.
van Alfen explained, “The minimum incidence of neuralgic amyotrophy is 2-3 cases per
100,000 individuals in the general population per year, but under recognition and misdiagnosis
are frequent and the true annual incidence could be 20-30 cases per 100,000 individuals.” Pet.
Ex. 20, Tab D. Neurologic amyotrophy can be misdiagnosed with rotator cuff tendinopathy,
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cervical radiculopathy, glenohumeral bursitis, or muscle strain. Pet. Ex. 32 at 2.22
A distinct feature of neurologic amyotrophy is neuropathic pain at onset. Resp. Ex. C,
Tab 3 at 4,10; Pet. Ex. 20, Tab D at 2. In 96% of patients the pain is characterized as “acute”
and “severe” in the upper extremities, neck and/or trunk. Pet. Ex. 20, Tab D at 2. After the
initial onset of pain, the pain severity increases within hours and can last for four weeks, on
average. Id. at 2; Resp. Ex. C, Tab 3 at 4. After initial pain, weakness then begins to appear
within 24 hours to two weeks. Resp. Ex. C, Tab 3 at 5. In men, the mean time to onset of
weakness from the initial presentation of pain was 13.6 days. Id. In van Alfen’s study of 246
patients, she found that paresis in the distribution of the upper part of the brachial plexus was the
most common. Id.; Pet. Ex. 20, Tab D at 2. Bilateral asymmetric symptoms are seen in one
third of cases. Pet. Ex. 20, Tab D at 2. Additionally, approximately 70% to 80% of patients
have sensory symptoms, such as hyperesthesia and/or paresthesia. Pet. Ex. 32 at 3; see also
Resp. Ex. C, Tab 3 at 5.
Diagnosing neurologic amyotrophy “is based on a patient’s clinical history and physical
examination.” Pet. Ex. 32 at 4. Electrophysiological studies are not often observed in the acute
stage, as “abnormal findings are only manifested after 1 and 3 weeks of onset of neurological
amyotrophy in nerve conduction studies and electromyography, respectively.” Id. Van Alfen
also explained that “many patients are initially diagnosed with shoulder joint pathology…or
cervical radiculopathy (in a neurological setting).” Pet. Ex. 20, Tab D at 4. The review article
explains that cervical radiculopathy can be distinguished from NA “by the fact that all symptoms
and signs can be localized to the distribution of a single root level in a patient with radiculopathy,
but not in patients with NA.” Id.
The van Eijk article explains that nerve conduction studies (NCS) for patients with NA
can “fail to show abnormalities in 80% of patients, even with clinically affected nerves are
studied.” Resp. Ex. C, Tab 1 at 7. The same article also cautions the use of EMG in NA,
because “[m]any of the muscles involved in NA do not belong to the routine set of muscles that
practitioners commonly explore during their EMG evaluation.” Id. However, when nerve
conduction and electromyography studies of patients with NA are done, they have shown axonal
damage, reduced motor conduction velocity, and prolonged F-wave latencies. Pet. Ex. 38 at 3.
The van Alfen, Kim, and van Eijk articles also endorse a “multifactorial etiology,” for
neuralgic amyotrophy, including underlying genetics, mechanical (repetitive strain or strenuous
exercise), or a possible immunological trigger. See Pet. Ex. 20, Tab D; Pet Ex. 32 at 2; Resp. Ex.
C, Tab 1 at 1. All three articles explain that no specific immunological triggers have been
identified for neuralgic amyotrophy, but the fact that “>50% of patients with neuralgic
amyotrophy report an immune event before an attack led to the hypothesis that attacks are
immunologically precipitated.” Pet. Ex. 20, Tab D at 6; see also Resp. Ex. C, Tab 1 at 3.
Different types of immunological events, such as infection, vaccination, surgery, pregnancy,
childbirth, and immunotherapy, have been reported as preceding events. Id.
Treatment for NA consists of oral prednisolone, physical therapy, non-steroidal anti-
22 Kim, T. and Chang, M, Neuralgic amyotrphy: an underrecognized entity, 49 J. of Int’l Med. Research, 1-7 (2021).
[Pet. Ex. 32].
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inflammatory drugs, and immobilization to minimize pain. Pet. Ex. 32 at 4; Pet. Ex. 20, Tab D
at 6. In the acute phase of the disease, a two-week regime of steroids is recommended. Pet. Ex.
20, Tab D at 6. According to the Kim article, patients with NA recover 80% to 90% of their
previous state in 2 to 3 years, but more than 70% of patients experience residual motor weakness.
Pet. Ex. 32 at 5.
2. Diabetic cervical radiculoplexus neuropathy
Diabetic cervical radiculoplexus neuropathy is a neuropathy that arises in persons with
diabetes. Resp. Ex. A, Tab 1; Pet. Ex. 20, Tab N.23 Dr. Callaghan accurately explains that
diabetic lumbosacral radiculoplexopathy is more common that diabetic cervical
radiculoplexopathy, both conditions arise secondary to diabetes. Resp. Ex. F at 1. The Massie
article, cited by Drs. Chen and Callaghan, states, “Diabetes mellitus is widely accepted to be
associated with lumbosacral radiculoplexus neuropathy, but only rarely has the existence of
diabetic cervical radiculoplexus neuropathies (DCRPN) been postulated.” Resp. Ex. A, Tab 1 at
2. The article observes that another study found that 12 out of 44 patients with severe diabetic
lumbosacral radiculoplexopathy also had “upper extremity involvement.” Id. The authors of
Massie explained that their study was the first to explore cervical radiculoplexus neuropathies in
diabetes mellitus and they sought to determine the clinical features, laboratory studies,
neurophysiological findings, neuroimaging, and pathological features independent of this
disease, separate from diabetic lumbar radiculoplexus neuropathy. Id.
The authors studied 85 patient cases who had diabetes and a history of upper extremity
pain, paresthesia or weakness and neurological examinations and/or electrophysiological
abnormalities localizing the process to the cervical nerve roots, brachial plexus or upper
extremity nerves. Resp. Ex. A, Tab 1 at 3. They observed that the median age for onset was 62
years and the median duration of diabetes mellitus or impaired fasting glucose was 5.5 years. Id.
Additionally, most patients had Type 2 diabetes. Id. The study observed that pain was the main
initial symptom. Id. Further, Massie explained that the onset was acute and predominantly
affected one side with “subsequent spread to the contralateral side” in 30 out of 85 patients. Id.
Sensory symptoms appeared in 66% of cases, with tingling/paresthesia and numbness as the
predominant sensory symptoms. Id. at 5. Thirty of the 85 patients had experienced weight loss
greater than 10 pounds. Id. Half of the patients with DCRPN had involvement of other regions
of the peripheral nervous system, including thoracic radiculopathy, lumbosacral radiculoplexus
neuropathy, and Horner’s syndrome. Id. Nerve conduction studies performed in 80 of the 85
patients were consistent with a predominantly axonal process. Id. at 6. Further, conduction
velocities and distal latencies were generally only minimally abnormal. Id. Out of the 80
patients with EMG/NCS studies, demyelinating features were only observed in 10 patients and
“consisted most commonly of conduction blocks.” Id. The needle examinations revealed
“frequent fibrillation potentials in almost all patients with decreased recruitment of large
amplitude, long duration polyphasic motor unit potentials.” Id.
The Laughlin article explained that in patients with DCRPN, all levels of the brachial
plexus are involved, compared to nondiabetic brachial plexopathies in which the upper trunk of
23 Massie, R. et al., Diabetic cervical radiculoplexus neuropathy: a distinct syndrome expanding the spectrum of
diabetic radiculolplexus neuropathies, 135 Brain 3074-3088 (2012). [Resp. Ex. A, Tab 1; Pet. Ex. 20, Tab N].
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the brachial plexus is “preferentially involved.” Pet. Ex. 28 at 4.24 This is consistent with the
Massie article, which found that “all three levels of the brachial plexus were involved,” in
DCRPN. Resp. Ex. A, Tab 1 at 7. Massie found that, “The upper plexus was involved in 45 out
of 80 patients, the middle plexus in 39 out of 80 patients, and the lower plexus in 46 out of 80
patients. Pan-plexus electrophysiological involvement (all three levels simultaneously) occurred
in 24 out of 80 patients.” Id.
Treatment for DCRPN consists of immunotherapy, which includes oral or intravenous
steroids, immunoglobulin or plasmapheresis. Resp. Ex. A, Tab 1 at 7; Pet. Ex. 28 at 5. The
neuropathological abnormalities in DCRPN showed “evidence of ischaemic injury…and of
microvasculitis.” Resp. Ex. A, Tab 1 at 12.
The authors of Massie also compared their patient cohort to the patients studied by van
Alfen and van Engelen and stated, “Our patients are generally distinct from patients with
idiopathic and hereditary neuralgic amyotrophy by their autonomic features, more frequent
weight loss, common bilateral upper limb and lower trunk involvements, and co-occurring
thoracic and lumbosacral radiculoplexus neuropathies.” Resp. Ex. A, Tab 1 at 14. Massie
observed that the patients from his study had “more involvement outside of the brachial plexus
(38% versus 17%) and had more involvement of the lower trunk of the brachial plexus (58%
versus 14%)” compared to the patients studied by van Alfen and van Engelen. Id. Further,
Massie explained that “almost all [of our patients] had evidence of autonomic dysfunction,” and
that “The degree of autonomic involvement was more than would be expected from the degree of
glucose dysregulation and is typical of other diabetic radiculoplexus neuropathies.” Id.
3. Analysis and conclusion of petitioner’s injury
Petitioner’s medical records, along with the expert opinions provided by Drs. Chen and
Huffman, provide support for the diagnosis of neuralgic amyotrophy (“brachial neuritis” or
“Parsonage Turner Syndrome”). Further, petitioner’s diagnosis and disease course are most
consistent with the medical literature about NA.
As described in the medical literature above, the first symptom patients complain about
with neuralgic amyotrophy is acute pain. van Alfen explains that “In 96% of patients the pain is
characterized as “acute” and “severe” in the upper extremities, neck and/or trunk. Pet. Ex. 20,
Tab D at 2. In this case, at multiple medical appointments, petitioner reported onset of acute
pain within a few days of receiving the flu shot and he characterized the pain as “knife-like.” Pet.
Ex. 2 at 89. Additionally, the van Alfen study found that patients with NA reported their pain at
an 8 at onset and a 9 out of 10 a maximum intensity. Resp. Ex. C, Tab 3 at 4. At petitioner’s
physical therapy evaluation, he rated his pain as an 8 out of 10 at its “best” but a 9 out of 10 at its
“worst.” See Pet. Ex. 3 at 11. While acute pain is the presenting symptom in patients with
diabetic cervical radiculoplexus and the onset of pain is typically unilateral, in about 35% of
cases, the pain spreads to the other side. Pet. Ex. 20, Tab N at 3. Here, petitioner’s pain
remained restricted to his left arm.
24 Laughlin, R. et al., Diabetic radiculoplexus neuropathies, 126 Handbook of Clin. Neurol. 45-51 (2014). [Pet. Ex.
28, Tab 5].
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After the initial onset of pain in NA, “muscle weakness is [a] conspicuous finding…and
occurs days to weeks after the onset of symptoms.” Pet. Ex. 32 at 3. According to the van Alfen
study, motor weakness appeared more frequently in the upper and middle of the brachial plexus,
which may or may not include the long thoracic nerve. Resp. Ex. C, Tab 3 at 5. Accordingly,
commonly affected muscles would be the infraspinatus, serratus anterior, supraspinatus, biceps
bracii, rhomboids, and pronator teres, but “clinically any muscle could be involved.” Id. When
petitioner initially reported his left shoulder pain to Dr. Barmach on March 12, 2015, petitioner
exhibited proximal and distal weakness in his left arm, compared to his right. Pet. Ex. 2 at 91.
The evaluation by Dr. Gracie revealed a positive impingement sign, which is indicative of
problems with the supraspinatus and the long head of the biceps brachii. See Pet. Ex. 3 at 5.
Further, petitioner’s strength was reduced in all directions during his initial physical therapy
evaluation, demonstrating weakness upon elbow flexion, elbow extension, flexion, abduction,
external rotation and internal rotation. Pet. Ex. 3 at 11. These movements which tested
petitioner’s strength are indicative of weakness in the muscles that are most affected by a
brachial plexus injury. For example, the primary flexors of the elbow are the biceps brachii.
Here, petitioner demonstrated decreased strength on both elbow flexion and extension.
When petitioner presented for the NCS/EMG on August 18, 2015, five months after
physical therapy, petitioner continued to have weakness in his biceps. Pet. Ex. 23 at 12. The
EMG confirmed “severe chronic denervation in the left biceps muscle.” Id. After reviewing the
EMG/NCS and performing a physical examination, petitioner’s treating neurologist, Dr. Zager
noted severe left, chronic musculocutaneous neuropathy with weakness in multiple muscles in
the left arm, scapular winging, and decreased sensation in the left upper extremity. He diagnosed
petitioner with Parsonage-Turner syndrome. Id. at 10.
Dr. Callaghan asserts that petitioner’s left upper extremity disorder is more likely DCRN
than brachial neuritis, because of petitioner’s “concomitant adhesive capsulitis is also likely
caused by diabetes.” Resp. Ex. F at 1. However, this argument is unpersuasive because van
Alfen reported that many patients with NA developed “subsequent persisting musculoskeletal-
type pain,” and that in approximately 17% of the patients van Alfen studied developed true
frozen shoulder (glenohumeral adhesive capsulitis) during the course of the attack. Resp. Ex. C,
Tab 3 at 4. Further, van Alfen explains that “29% [of patients with NA] developed, chronic,
usually therapy-resistant, continuous pains in the previously affected region.” Id. Consistent
with the van Alfen article, petitioner’s arm pain and weakness preceded what developed into
adhesive capsulitis. Petitioner saw orthopedist, Dr. Huffman after attending physical therapy and
was diagnosed with adhesive capsulitis after the onset of acute pain and weakness. See Pet. Ex.
6 at 29. When petitioner was evaluated by neurologist Dr. Eric Zager, he noted in petitioner’s
history of present illness, that petitioner’s pain following the flu shot was “so severe with
movement he ultimately had frozen shoulder.” Pet. Ex. 23 at 10. Further, petitioner’s pain and
weakness continued not only after physical therapy, but after he received a steroid injection, and
underwent a shoulder arthroscopy. Thus, petitioner’s clinical course of developing acute pain,
followed by weakness, which resulted in him developing adhesive capsulitis is consistent with
the diagnosis of neuralgic amyotrophy.
Finally, petitioner’s pain and weakness were limited to his left arm, which is more
consistent with NA, than a diagnosis of DCRN. Dr. Chen stated that, “[petitioner’s] examination
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and EMG does not show any evidence of further neuropathy in other body parts. [Petitioner’s]
examination and EMG does not show evidence of further neuropathy in other body parts.” Pet.
Ex. 25 at 1. The literature submitted in this case explains that DCRN “is an acute upper limb
neuropathy…which begins focally but often spreads to involve the contralateral limb, thoracic,
and lumbosacral segments.” Pet. Ex. 20, Tab N at 10. Further, petitioner’s EMG and NCS of
the left upper limb showed “evidence of severe, chronic denervation in the left biceps muscle.”
Pet. Ex. 23 at 12. The impression of Dr. Bird was “severe, chronic left musculocutaneous
neuropathy.” Id. Throughout the record, consistent with Dr. Chen’s opinion, shows that
petitioner’s pain, weakness, and neuropathy is contained to his left arm. Dr. Callaghan does not
dispute this fact.
Thus, consistent with the medical literature, and with the diagnosis of petitioner’s treating
neurologist, Dr. Zager, petitioner has demonstrated by preponderant evidence that he suffered
from brachial neuritis (neuralgic amyotrophy).
B. Vaccine causation
1. Althen prong one
Under Althen prong one, the causation theory must relate to the injury alleged. Thus, a
petitioner must provide a “reputable” medical or scientific explanation, demonstrating that the
vaccine received can cause the type of injury alleged. Pafford, 451 F.3d at 1355-56. The theory
must be based on a “sound and reliable medical or scientific explanation.” Knudsen v. Sec’y of
Health & Human Servs., 35 F.3d 543, 548 (Fed. Cir. 1994). It must only be “legally probable,
not medically or scientifically certain.” Id. at 549. However, the theory still must be based on a
“sound and reliable medical or scientific explanation.” Knudsen at 548. The Federal Circuit
explained in Althen that “while [that petitioner’s claim] involves the possible link between
[tetanus toxoid] vaccination and central nervous system injury, a sequence hitherto unproven in
medicine, the purpose of the Vaccine Act’s preponderance standard is to allow the finding of
causation in a field bereft of complete and direct proof of how vaccines affect the human body.”
Althen, 418 F.3d at 1280 (emphasis added).
I find that petitioner has provided preponderant evidence of a sound and reliable medical
theory explaining how the intradermal flu vaccine can cause brachial neuritis. This finding is
supported by the expert opinions and medical literature filed in this case.
Petitioner’s experts credibly explained that the intradermal flu vaccine takes advantage of
the skin’s unique and complementary immune activation pathways to rapidly process vaccine
antigen while upregulating proinflammatory cells which infiltrate blood vessels, leading to
vasculitis, damaging the underlying nerves. See Pet. Ex. 9 at 5; Pet. Ex. 19 at 2-3. Their opinion
of how the intradermal flu vaccine can lead to vasculitis resulting in brachial neuritis is
supported by the medical literature.
According to the Bragazzi and del Pilar Martin articles, the skin provides an optimal site
for vaccination because of its “dense network of antigen presenting cells, including
macrophages, Langerhans cells, and dermal dendritic cells present in the dermis and epidermis,
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which are crucial in the initiation of the adaptive immune response.” Resp. Ex. C, Tab 6 at 1;
Pet. Ex. 20, Tab L at 5. The Bragazzi article, which reviewed the Fluzone intra-dermal vaccine,
states that the “skin harbors immune cellular components (epidermal dendritic cells, different
types of T cells, natural killer cells, B cells, mast cells and macrophages), thus constituting an
immunocompetent, multi-tasking organ or a complex immune system.” Pet. Ex. 20, Tab L at 5.
The Bragazzi article also explains the different mechanisms that take advantage of the
skin’s unique immunological and microvascular properties that can activate both innate and
adaptive immune responses to vaccines. The “exact nature of [the mechanisms of action for
intradermal vaccination] is complex,” but that “the effect of the ID vaccination may be the result
of three concurring complementary pathways.” Id. at 5. Bragazzi refers to the first pathway as
the “dermal dendritic cells-dependent pathway” and Dr. Byers described this pathway in her
report. Id. at 5; see also Pet. Ex. 9 at 5. Dr. Byers described the mechanism, stating, “the
dendritic cells pick up the vaccine antigen or foreign substance, they mature and produce pro-
inflammatory cytokines, which promote the migration of the dendritic cells to the para-cortical
area of the regional lymph nodes, which allows the dendritic cells to present the vaccine peptides
to CD8+ T cells and CD4 lymphocytes.” Pet. Ex. 9 at 5. The Bragazzi article provides
additional detail about this pathway, explaining:
The maturation, the differentiation, the acquisition of adequate immune abilities, and the
migration to the paracortical area of the regional draining lymph nodes as afferent lymph
veiled cells through high endothelial venules, are modulated by different signaling
pathways, including increased expression of MHC antigens, co-stimulatory molecules
and pro-inflammatory cytokines such as IL-1β, IL-6, IL-12 and TNF-α. These events
lead to the subsequent activation of lymphocyte T CD8+, releasing interferon gamma,
TNF-α, granzyme B, among other molecules, and high cytotoxic activity and memory B
cells.
Id. at 6. Bragazzi also explains that “There is also another complementary pathway, independent
of the first: antigens and especially small vaccine components are passively drained by the
unique micro-vascular and lymphatic structures of the skin and transported directly to the lymph
nodes, where they are captured by lymph node resident dendritic cells, medullary macrophages
and subcapsular sinus macrophages.” Id. Dr. Chen describes this complementary pathway in her
first report. See Pet. Ex. 19 at 3. Finally, Bragazzi states that the actual needle injection
“generates localized transient stresses invoking cell necrosis and apoptosis around each injection,
favoring the release of damage associated molecular patterns (DAMPs).” Pet. Ex. 20, Tab L at
6. Dr. Chen, consistent with Bragazzi, opined that the “local skin injury generates molecular
signals that cause inflammatory cascades via damage associated molecular signals that reside in
the skin.” Pet. Ex. 19 at 3.
Both Drs. Byers and Dr. Chen opined that because of the skin’s unique immunological
mechanisms, the intradermal flu vaccination can cause a heightened innate immune response,
which leads to a rapid upregulation of cytokines to the area of the injection site. Pet. Ex. 9 at 4;
Pet. Ex. 19 at 3. Respondent’s expert, Dr. Tompkins agreed with Drs. Byers and Chen about the
different immune mechanisms activated after an intradermal vaccination. Resp. Ex. C at 5.
However, he argued that there is no evidence that the intradermal flu vaccine causes increased
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cytokine responses compared to the intramuscular vaccination, and that the adaptive immune
responses between the intradermal and intramuscular flu vaccines are comparable, thus the
intradermal flu vaccine “is not more inflammatory than the intramuscular” vaccine. Id. at 6. He
asserted that “the improved immunogenicity of the intradermal vaccination may be the result of
improved antigen delivery to the draining lymph node.” Id. at 5.
The medical literature filed in this case supports petitioner’s experts’ opinion that the
intradermal flu vaccine causes a “heightened initial inflammatory immune response.” The
Bragazzi article explains, “….Fluzone ID seems to elicit temporary transcriptional changes in the
circulating myeloid compartment. Vaccination upregulates modules linked to NF-kB-driven
inflammation, IFN-γ response, TNF and CD40 signaling. These pathways are involved in T-cell
activation and the development of adaptive immunity.” Pet. Ex. 20, Tab L at 6. The del Pilar
Martin article, referenced by Dr. Tompkins, examined local responses to microneedle influenza
vaccinations, found “significant increases in the levels of cytokines IL-β, macrophage
inflammatory protein 1 alpha, macrophage inflammatory protein 2, TNF-α, and monocyte
chemoattractant protein 1 (MCP-1)” after a microneedle injection without the flu vaccine into the
skin of mice. Resp. Ex. C, Tab 6 at 2. When the mice were injected with microneedles coated
with flu vaccines, the cytokine levels “were further increased” and “enhanced at the 12-hour
point.” Id. The researchers wrote, “…these findings indicate that a rapid increase of cytokines
at the insertion site was induced by [microneedle] mechanical skin penetration, which was
enhanced upon antigen delivery. The skin cytokine profile analysis shows that skin
immunization induces a local innate immune response and a release of chemokines in the skin
suggestive of the activation and recruitment of immune cells to the site of vaccination.” Id. at 2.
In the discussion, del Pilar Martin explained, “Our analysis of cytokine expression in the skin
following insertion of antigen-coated microneedles indicated the upregulation of IL-1β, TNF-α,
and MIP-1α and supports the current models of Langerhans cell migration. The induction of the
chemotactic proteins…suggests that following antigen-coated needle vaccination, the production
of IL-1β and TNF-α in the skin is reinforced by recruitment of neutrophils and macrophages to
the site of vaccination.” Resp. Ex. C, Tab 6 at 5.
Both the Bragazzi and del Pilar Martin articles suggest an increase in proinflammatory
cells after an intradermal vaccination, and that different complementary pathways are activated
by the intradermal vaccination, which can lead to a more rapid and robust immune response. As
Bragazzi observes, “muscle [is] quite inefficient to capture antigens and the IM route is therefore
inferior to ID route in terms of biological mechanism and action.” Pet. Ex. 20, Tab L at 6.
Additionally, Dr. Chen correctly observed that both injection site reactions and systemic
reactions were higher compared to the intramuscular vaccination. See Pet. Ex. 19 at 3. The
Fluzone Intradermal package insert provided that injection-site erythema, induration, swelling,
and pruritus were all higher compared to the intramuscular flu vaccine. Resp. Ex. C, Tab 8 at 10.
More people also reported headaches, shivering, malaise, and fever after receiving the
intradermal flu vaccine compared to the intramuscular vaccination. Id.
The rapid upregulation of a pro-inflammatory response generated by the different
immune cells resident between the intradermal layers leads to infiltration of the blood vessels at
the site, leading to vasculitis that results in an ischemic injury, like brachial neuritis. Dr. Chen
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explained the “presence of immune cells in the blood vessel of the injured nerve indicates that
the mechanism of immune-mediated injury is a vasculitic process.” Id. at 3. While Dr.
Callaghan did not dispute Dr. Chen’s characterization of brachial neuritis being a vasculitic
neuropathy, Dr. Tompkins argued that “immune mediated brachial neuritis is mediated by an
adaptive immune response,” rather “than the innate response proposed by Dr. Chen.” See Resp.
Ex. E at 1; Resp. Ex. C at 4. He asserted that the biopsies of the brachial plexus from four
patients found, “infiltrates [that] were predominately T and B cells, suggesting an adaptive
immune response contributed to neuronal disease.” Resp. Ex. C at 4.
Contrary to Dr. Tompkins’ characterization of Drs. Chen and Byers’ opinions, they did
not assert that the vasculitic brachial neuritis was solely caused by the innate immune system’s
cells. Rather, as discussed above, Dr. Chen characterized brachial neuritis as inflammatory in
nature. Dr. Chen explained that the initial rapid response by the non-specific cells of the innate
immune system, such as the dendritic cells, macrophages, or natural killer cells, facilitates the
recruitment of proinflammatory cells and T cells to the site of injury. Further, the Suarez article,
cited by Dr. Tompkins, supports Dr. Chen’s opinion. After examining four biopsies of patients
with brachial neuritis, the authors wrote, “The main observation from this series of patients with
[brachial neuritis] was the presence of prominent collections of inflammatory cells (especially T
lymphocytes) within the brachial plexus.” Pet. Ex. 38 at 1. Dr. Chen appropriately noted that
within her area of specialty, neurology, as opposed to that of Dr. Tompkins it is easy to
understand that neurologists do not biopsy nerves at the outbreak of a condition such as brachial
neuritis but rather do so only after the condition has persisted for some time at which point the T
cells may be more prominent. As Dr. Tompkins is not medically trained, and his opinions that
verge into the specific neurologic processes are given little weight.
Finally, I have accepted that the influenza vaccine can cause brachial neuritis in Echols.
In that case, the petitioner received an intramuscular flu vaccine, resulting in immediate pain
followed by weakness that developed over a few days. Echols v. Sec’y of Health & Human
Servs., No. 17-838, 2021 WL 4891589 (Fed. Cl. Spec. Mstr. Sept. 14, 2021), mot. for review
denied, 165 Fed. Cl. 9 (Mar. 9, 2023). In Abels, Special Master Dorsey, also accepted that the
influenza vaccine can result in brachial neuritis due to both the activation of the innate and
adaptive immune system. See Abels v. Sec’y of Health & Human Servs., No. 18-558, 2022 WL
2036101 (Fed. Cl. Spec. Mstr. May 6, 2022). The opinions offered in this case as to how the
intradermal flu vaccine can result in brachial neuritis is consistent with Echols and Abels.
Petitioner’s experts in this case have proposed a sound and reliable theory, showing how
the intradermal flu vaccine can result in brachial neuritis, thus satisfying Althen prong one.
2. Althen prong two
Under Althen prong two, petitioner must prove by a preponderance of the evidence that
there is a “logical sequence of cause and effect showing that the vaccination was the reason for
the injury. Capizzano, 440 F.3d at 1324 (quoting Althen, 418 F.3d at 1278). “Petitioner must
show that the vaccine was the “but for” cause of the harm or in other words, that the vaccine was
the reason for the injury.’” Pafford, 451 F.3d at 1356 (internal citations omitted).
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In evaluating whether this prong is satisfied, the opinions and views of the vaccinee’s
treating physicians are entitled to some weight. Andreu, 569 F.3d at 1367; Capizzano, 440 F. 3d
at 1326 (“[M]edical records and medical opinion testimony are favored in vaccine cases, as
treating physicians are likely to be in the best position to determine whether a ‘logical sequence
of cause and effect show[s] that the vaccination was the reason for the injury.’” (quoting Althen,
418 F.3d at 1280)). The petitioner need not make a specific type of evidentiary showing, i.e.,
“epidemioligc studies, rechallenge, the presence of pathological markers or genetic
predisposition, or general acceptance in the scientifici or medical communities to establish a
logical sequence of cause and effect.” Capizzano, 440 F.3d at 1325. Instead, petitioner may
satisfy his burden by presenting circumstantial evidence and reliable medical opinions. Id. at
1325-26.
I find that petitioner has provided preponderant evidence of a logical sequence of cause
and effect. This finding is based on expert opinion, petitioner’s clinical course, petitioner’s
treating physician’s opinion, and lack of evidence to support an alternative cause.
Petitioner’s experts, Drs. Huffman, Byers, and Chen, all opined that petitioner’s brachial
neuritis began shortly after he received the flu vaccine. Pet. Exs. 8-10; 19, 25. Dr. Chen
observed that petitioner had been diagnosed with diabetes for “up to two years prior to the flu
vaccination…and had not developed any neurological complications.” Pet. Ex. 19 at 3. Dr.
Huffman, petitioner’s treating orthopedist, outlined petitioner’s clinical course and found it to be
consistent with brachial neuritis. Dr. Huffman explained that when he first treated the petitioner
on May 28, 2015, the petitioner described having immediate pain, swelling and the sensation of
heat in his left shoulder following the flu vaccination. Pet. Ex. 8 at 2. Dr. Huffman stated that
after petitioner underwent the circumferential capsular release and repair of the small rotator
cuff tear in his left shoulder, petitioner’s pain did not subside. Id. Dr. Huffman wrote, “While I
was able to restore [petitioner’s] passive shoulder motion, his pain did not subside and had a
largely neurogenic component to it. Combined with focal weakness in his musculocutaneous
nerve distribution, I ordered a neurologic evaluation.” Id. The EMG on August 8, 2015
documented a severe, chronic musculocutaneous nerve neuropathy. Id. When petitioner was
evaluated by neurologist, Dr. Zager, he was diagnosed with Parsonage Turner Syndrome. Id.;
see also Pet. Ex. 23 at 10.
Respondent argued that petitioner cannot establish Althen prong two because the medical
records do not demonstrate the temporal association between the October 2014 vaccination and
the onset of his left arm pain and weakness. Resp. Brief at 19. More specifically, respondent
argues that the January 19, 2015 medical appointment does not document that petitioner had left
arm pain. Id. at 17; see also Pet. Ex. 2 at 84.
However, as Dr. Huffman observed, multiple medical records document the onset of
petitioner’s left arm pain and weakness as occurring shortly after the flu vaccination. See Pet.
Ex. 2 at 89 (reporting left arm pain that started “back in Oct. a few days after got the flu shot);
Pet. Ex. 6 at 29 (complaints of left shoulder pain which has been ongoing since
October..2014…he had an influenza injection, that night he started having pain); and Pet. Ex. 23
at 10. Further, the record from March 2, 2015 actually documents that petitioner showed Dr.
Peet a lump at the injection site. Pet. Ex. 2 at 89. Finally, the January 19, 2015 appointment
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appears to be a diabetes follow-up, where the purpose of the visit was to review labs. Medical
records are not presumed to be accurate and complete to document all physical conditions. Kirby
v. Sec’y of Health & Human Servs., 997 F.3d (Fed. Cir. 2021). Thus, it does not seem
appropriate to ignore all the other medical records which document an association between the
onset of petitioner’s pain in his left arm and the flu vaccine because one intervening record failed
to document petitioner’s symptoms accurately.
Respondent also argues that petitioner’s course is more likely consistent with diabetic
cervical radiculoplexopathy. Resp. Brief at 20. As discussed above, I found that petitioner’s
injury was brachial neuritis, and not diabetic cervical radiculoplexopathy. supra at 28-29. Dr.
Chen acknowledged that petitioner had poorly controlled diabetes for nearly two years prior to
the vaccination but had not developed any neurological complaints. Pet. Ex. 19 at 5. Dr. Chen
credibly explained that petitioner’s brachial neuritis clinical presentation was more consistent
with immune-mediated brachial neuritis than a diabetic radiculoplexus. Id. at 2.
Dr. Chen stated that “the prominent associated feature that is seen with diabetic
radiculoplexus neuropathy…is the presence of weight loss (typically 15-30 lbs.) coinciding with
the development of the neuropathy.” Pet. Ex. 25 at 1. She observed that the medical records do
not document any weight loss between April 2014 and March 2, 2015. Id. Additionally, Dr.
Chen stated that petitioner’s neuropathy was limited to his left arm, whereas diabetic
radiculoplexus neuropathy there is often involvement of other body regions. Id. at 2.
Petitioner’s clinical course was consistent with that of patients who experienced post-
vaccination brachial neuritis as described in the medical literature submitted in this case. The
Shaikh article describes a 46-year-old woman who described acute onset of pain a “few days
after an influenza vaccination.” Pet. Ex. 20, Tab E. Within a week of the onset of pain, she
developed left-upper limb weakness with difficulty performing her usual activities. Id. The
woman’s cervical MRI ruled out cervical radiculopathy, but an EMG and NCS revealed severe
axonal denervation of the left deltoid and supraspinatus muscles with mild involvement of the
infraspinatus muscle and evidence of renervation. Id. at 1. The woman was diagnosed with
post-vaccination acute brachial neuritis. Id. The authors explained that the “temporal pattern in
our patient, of pain followed by weakness, is classic of brachial neuritis.” Id. Further, the
authors note that brachial neuritis is an uncommon condition that is often misdiagnosed. Id. at 1.
As explained by Van Alfen, brachial neuritis has “core features that include episodes of extreme
pain at symptom onset, rapid multifocal paresis (weakness) and atrophy of the upper extremity
muscles, and a slow recovery requiring months to years.” Pet. Ex. 20, Tab D at 1. In another
article by Van Alfen, she explains that many patients with brachial neuritis also develop
glenohumeral joint pathology after a brachial neuritis attack with weakness of the rotator cuff
muscles or decreased glenohumeral excursions due to weakness, that can lead to frozen shoulder.
Resp. Ex. C, Tab 3 at 4. Further, Van Alfen explains “misdiagnoses are frequent” in brachial
neuritis cases. Id.
Petitioner consistently reported that his left shoulder pain began within a few days of
receiving the influenza vaccination on October 22, 2014. On March 2, 2015, four months after
the vaccination, petitioner had an appointment with Dr. Barmach with the family medicine
practice Pet. Ex. 2 at 89. Under “Chief Complaint,” it states, “a flu shot on 10/22/2014…the flu
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shot was given in the left deltoid, about three days after injection, there was severe pain, redness
and swelling. Was seen again on 01/19/2015 with Dr. Peet and showed him the lump that had
lasted since [injection].” Id. Petitioner then reported that he had left arm/shoulder pain that was
worse at night and that it had started a few days after he got the flu shot. Id. Additionally,
petitioner reported that he had swelling around the deltoid which resolved, but he has some pain
in the left side of his neck that can radiate down to his elbow, along with numbness in his left
hand. Id. Petitioner stated that it hurt to move his arm in all directions and described the pain as
“knife-like.” Id. The physical exam revealed that petitioner had “palpable muscle spasm along
the left trapezius,” and he was “able to flex left arm about 80 degrees before it becomes too
painful.” Id. at 90. Dr. Barmach diagnosed petitioner with “brachial neuritis or radiculitis,” and
noted, “[patient] believes symptoms started after flu shot but I believe that is more coincidental.
I believe symptoms due to neck pathology and getting radicular pain.” Id. at 90. Petitioner was
referred to an orthopedist for an evaluation and was prescribed methyl prednisone. Id.
On March 16, 2015, petitioner had an appointment with orthopedist, Dr. Diane Gracie.
Pet. Ex. 3 at 5. Petitioner stated that he had been “experiencing left shoulder pain for the past 5
months,” and that “he had a flu shot in October of 2014 and the pain seemed to start after that.
He did have an area that was raised and swollen for awhile…..the pain now radiates down to his
elbow. At times he has numbness in his hands. He took a 6-day Medrol Dosepak with no relief
of his symptoms.” Id. Of importance, Dr. Gracie found no cervical radicular findings, but
petitioner did have a positive impingement sign and tenderness over the deltoid area. Id.
Further, petitioner had restriction on internal rotation with his left thumb only going up to the
sacrum. Id.
Petitioner saw orthopedist, Dr. Huffman, on May 28, 2015, after physical therapy had
failed. Pet. Ex. 6 at 29. Dr. Huffman wrote that petitioner had “complaints of left shoulder pain
which has been ongoing now since October of…2014.” Pet. Ex. 6 at 29. Dr. Huffman also
noted that petitioner “had an influenza injection….that night he started having pain and swelling,
inflammation, and sensation of heat. The symptoms worsened progressively and ultimately, he
was referred to an orthopedist.” Id. Dr. Huffman noted that petitioner had pseudo-winging of
the left scapula and a weak trapezius. Id. Dr. Huffman diagnosed petitioner with adhesive
capsulitis or frozen shoulder “with onset temporally and most likely causally related to the
influenza injection.” Id. at 29-30. Petitioner had a cortisone injection, which apparently offered
little relief. Id. at 31. Eventually, petitioner had a left shoulder arthroscopy on July 15, 2015.
Id. at 39. Again, this surgical intervention did not provide much pain relief and Dr. Huffman
described petitioner’s pain as “neurogenic in nature.” Id.
On August 18, 2015, petitioner underwent an EMG/NCS at the University of
Pennsylvania. Pet. Ex. 6 at 9. Prior to the study, Dr. Shawn Bird performed a neurologic
examination of petitioner’s left shoulder and found that petitioner “appeared to be weak in the
biceps muscle,” and petitioner reported reduced sensation to light touch over all of his fingers in
his left hand and in the anterior left forearm. Id. The nerve conduction study showed that, “The
left lateral antebrachial cutaneous sensory response was absent,” and, “the left median motor
responses were notable for a prolonged distal latency.” Id. Additionally, the EMG found,
“evidence of severe chronic denervation in the left biceps muscle.” Id.
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When petitioner was evaluated by neurologist, Dr. Eric Zager on October 21, 2015, one
year-post vaccination, petitioner again reported that that he had left arm pain and weakness that
began when he received the flu vaccine in October 2014. Pet. Ex. 23 at 10. Dr. Zagar wrote that
“within about a day of getting the injection he complained of left shoulder pain and swelling.
His pain was so severe with movement he ultimately had frozen shoulder.” Id. Dr. Zagar
reviewed petitioner Parsonage-Turner syndrome. Id.
Petitioner’s clinical course began with acute pain close in time to receiving the influenza
vaccine, which developed into weakness shortly thereafter. Additionally, petitioner presented
with a winged scapula, which van Alfen describes as “the most obvious sign of [brachial
neuritis].” See Pet. Ex. 20, Tab D at 1. Petitioner had weakness in his thumb, index and third
digit of his left hand. He also developed a loss of sensation in the fingers of his left hand which
is consistent with van Alfen’s statement that, “Sensory symptoms are usually inconspicuous, but
most patients can recall paresthesia over the radial side of the thumb, index finger and forearm at
onset.” See Pet. Ex. 23 at 10; Pet. Ex. 20, Tab D at 2. Finally, because of petitioner’s condition,
he eventually develop frozen shoulder, which according to the medical literature is common in
patients with brachial neuritis due to the pain being “persistent and more incapacitating.” Pet.
Ex. 20, Tab D at 2. It is common that patients experiencing such pain engage in pain protective
behavior, that is not moving the arm, to minimize the painful symptoms which ultimately results
in adhesive capsulitis which petitioner had developed by the time he saw Dr. Huffman.
Thus, after reviewing the evidence, I have concluded, consistently with the petitioner’s
treating neurologists and orthopedists as well as Dr. Chen, that petitioner developed brachial
neuritis in his left shoulder as a result of receiving the intradermal flu vaccination. Petitioner’s
onset of pain and clinical course progression was consistent with the literature discussed above.
Additionally, I find respondent’s theory that petitioner’s brachial neuritis was more likely
diabetic cervical radiculopathy unpersuasive, as petitioner never experienced complications or
symptoms prior to receiving the vaccination at issue. As such, petitioner has satisfied Althen
prong two.
3. Althen prong three
Althen prong three requires petitioner to establish a “proximate temporal relationship”
between the vaccination and the injury alleged. Althen, at 1281. That term has been defined as
“medically acceptable temporal relationship.” Id. The petitioner must offer “preponderant proof
that the onset of symptoms occurred within a timeframe which, given the medical understanding
of the disease’s etiology, it is medically acceptable to infer causation-in-fact.” De Bazen, 539
F.3d at 1352. The explanation for what is a medically acceptable time frame must also coincide
with the theory of how the relevant vaccine can cause the injury alleged (due to Althen prong
one). Id.; Koehn v. Sec’y of Health & Human Servs., 773 F.3d 1239, 1243 (Fed. Cir. 2014);
Shapiro v. Sec’y of Health & Human Servs., 101 Fed. Cl. 532, 542 (2011), recons. denied after
remand, 105 Fed. Cl. 353 (2021), aff’d mem., 503 F. App’x 952 (Fed. Cir. 2013).
Prior to the vaccination on October 22, 2014, petitioner had no physical limitation or
injuries to his left shoulder. Petitioner reported that he had pain following the flu shot at multiple
appointments, including one on March 2, 2015 with Dr. Barmach, then again on April 16, 2015
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to Dr. Gracie, and also to Dr. Huffman on May 28, 2015. See Pet. Ex. 2 at 89; Pet. Ex. 3 at 7;
Pet. Ex. 6 at 29. At each of these appointments, petitioner reported that he experienced pain
soon after the flu vaccine was administered, and that he had swelling and a sensation of heat at
the injection site. Further, petitioner consistently reported that his pain progressed over the next
few days post-vaccination. Pet. Ex. 2 at 89. Petitioner’s pain did not subside, and he also
demonstrated weakness in his left arm. Pet. Ex. 3 at 11. Even after a shoulder arthroscopy to
release his frozen shoulder, petitioner’s pain remained. He was diagnosed with brachial neuritis
after an EMG/NCS evaluation by Dr. Shawn Bird. Pet. Ex. 6 at 43.
Petitioner’s medical records consistently record that he experienced an adverse reaction
at the injection site, which consisted of pain and a sensation of heat at the injection site, followed
by progressive pain his left shoulder. Dr. Byers explained that an injection site reaction, such as
swelling or erythema, can often be transient and is “characteristic of vaccines.” Pet. Ex. 9 at 7.
Thus, it appears that petitioner experienced an immediate transient injection site pain, and then
the pain associated with his brachial neuritis developed over two- or three-days post-vaccination.
Drs. Byers, Chen and Huffman all agree that the pain petitioner experienced that was
relatable to his brachial neuritis occurred very close in time to the vaccination. Dr. Chen opined
that the onset of petitioner’s brachial neuritis was three days and is consistent with a rapid
inflammatory response that contributed to the development of a local vasculitic process. Pet. Ex.
19 at 3. Dr. Byers also opined that a rapid initiation of the pro-inflammatory cytokines in the
dermis led to nerve and tissue damage. Pet. Ex. 9 at 5.
Dr. Tompkins acknowledged that the “timing of onset of symptoms [of brachial neuritis]
after events ranged from less than 24 hours to more than two weeks.” Resp. Ex. C at 3. He
stated that “the window between preceding events and onset of [the] disease ranges from hours
to weeks,” however, he argued that the rapid onset of symptoms is not because of an innate
immune response, but rather an adaptive immune response. Id.
I have accepted petitioner’s mechanism as to how the intradermal flu vaccine can cause
brachial neuritis. Petitioner’s experts’ opinions that the onset of petitioner’s pain, two- or three-
days post-vaccination, the first manifestation of brachial neuritis, is consistent with the onset of
immune-mediate brachial neuritis as explained in the medical literature and the findings of an
appropriate temporal association between the flu vaccine and the onset of brachial neuritis.
Additionally, respondent’s expert, Dr. Tompkins does not dispute that the onset of pain, the first
symptom of brachial neuritis can occur rapidly after an inciting event. See Resp. Ex. C at 4
(noting that “the window between preceding event and onset of [brachial neuritis] ranges from
hours to weeks.”).
In the Shaikh article, the authors described the onset of the patient’s pain after the
influenza vaccine as being “acute, developing a few days after an influenza vaccination.” Pet.
Ex. 37 at 1. The authors of that article explained that the exact etiology of brachial neuritis is
unclear, but “is thought to be an immune-mediated inflammatory reaction against brachial plexus
nerve fibers involving complement, anti-peripheral nerve myelin antibodies and T cells.” Id. at
1-2. van Alfen found that 53% of patients reported an antecedent event prior to the onset of the
brachial neuritis, and nearly all of those events, including vaccination or infection, occurred in
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the week preceding the initial attack, with 17.4% of patients reporting that the event occurred
only hours before onset. Resp. Ex. C, Tab 3.
Other cases in the Vaccine Program also have found that an appropriate temporal
association between the flu vaccine and the onset of brachial neuritis is within a few hours post-
vaccination to a few days. For example, in Echols, I found that the onset of symptoms occurring
within hours of the flu vaccination and progressing over several days, was medically acceptable
to infer causation. Echols v. Sec’y of Health & Human Servs., at *23. In Abels, the special
master found that the onset of pain two days after the influenza vaccine, which progressed to
weakness approximately six days later was an appropriate temporal association between the
vaccination and the onset of brachial neuritis. Abels v. Sec’y of Health & Human Servs., No. 18-
558V, 2022 WL 2036101, at *21 (Fed. Cl. Spec. Mstr. May 6, 2022).
I find it acceptable that inflammation would cause the onset of pain within 2-3 days of the
intradermal influenza vaccination, and the progression of pain and weakness over several days to
be an appropriate temporal association between vaccination and the onset of brachial neuritis.
Petitioner has established Althen prong three.
V. Conclusion
For the foregoing reasons, petitioner is entitled to compensation for brachial neuritis and
adhesive capsulitis caused by the October 22, 2014 intradermal influenza vaccine. A separate
damages order will be issued.
IT IS SO ORDERED.
s/Thomas L. Gowen
Thomas L. Gowen
Special Master
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