Valentine v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 17-547V

Filed: January 13, 2025

* * * * * * * * * * * * * * *

MITCHELL VALENTINE, *

*

Petitioner, *

v. *

*

SECRETARY OF HEALTH *

AND HUMAN SERVICES, *

*

Respondent. *

* * * * * * * * * * * * * * *

Joseph Vuckovich, Esq., Mctlaw, Washington, DC, for petitioner.

Eleanor Hanson, Esq., U.S. Department of Justice, Washington, DC, for respondent.

DECISION 1

Roth, Special Master:

On April 18, 2017, a petition was filed on behalf of Mitchell Valentine (“Mr. Valentine”

or “petitioner”)—then a minor 2—for compensation pursuant to the National Vaccine Injury

Compensation Program. 3 Petitioner alleges that he received a Fluvirin influenza (“flu”)

vaccination on August 30, 2015 that caused him to develop transverse myelitis (“TM”). See

Petition (“Pet.”), ECF No. 1. Petitioner further alleged during the course of this matter that his

TM caused him to develop lymphedema of the left leg. Respondent disputed petitioner’s claim,

contending that petitioner did not suffer from TM. The matter was argued through expert reports

and legal memoranda.

1

Because this Decision contains a reasoned explanation for the action taken in this case, it must be made publicly

accessible and will be posted on the United States Court of Federal Claims’ website, and/or at

https://www.govinfo.gov/app/collection/uscourts/national/cofc, in accordance with the E-Government Act of 2002.

44 U.S.C. § 3501 note (2018) (Federal Management and Promotion of Electronic Government Services). This means

the Decision will be available to anyone with access to the internet. In accordance with Vaccine Rule 18(b), the

parties have 14 days to identify and move to redact medical or other information, the disclosure of which would

constitute an unwarranted invasion of privacy. Any changes will appear in the document posted on the website.

2

Once Mitchell Valentine reached the age of 18, the caption was amended to reflect him as the petitioner. ECF Nos.

71-72.

3

National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755. Hereinafter, for ease of

citation, all “§” references to the Vaccine Act will be to the pertinent subparagraph of 42 U.S.C. § 300aa (2018).

Following review of all the evidence and arguments presented, I find that petitioner has

not provided preponderant evidence that the flu vaccine he received on August 30, 2015 caused

him to suffer a compensable injury.

I. Procedural History

The petition was filed on April 18, 2017. Petition, ECF No. 1. Petitioner then filed

medical records and affidavits. Petitioner’s Exhibits (“Pet. Ex.”) 1-12, ECF Nos. 7-8, 10, 13.

On December 22, 2017, respondent filed his Rule 4(c) Report, advising that the matter

was not appropriate for compensation. ECF No. 17. Petitioner was ordered to file an expert

report. Following several motions for extension of time and throughout the next three years, the

parties exchanged expert reports and supporting literature. Pet. Ex. 14-53, ECF Nos. 18-22, 31,

34-35, 37-38, 45-47, 49, 58-64, 78-81; Respondent’s Exhibits (“Resp. Ex.”) A-J, ECF Nos. 39-

43, 51-55, 66-70, 83-85.

Petitioner filed a status report on September 12, 2022, advising that the matter was

appropriate for a ruling on entitlement and filed his Motion for Ruling on the Record (“Motion”)

on December 19, 2022. ECF No. 86; Motion, ECF No. 88. Respondent filed his Response to the

Motion on May 11, 2023. Response, ECF No. 94. Petitioner filed a Reply on June 2, 2023.

Reply, ECF No. 96.

Upon review of the record, issues with some of the evidence filed were found and the

parties were ordered to correct the deficiencies. ECF Nos. 98, 101. Respondent refiled some of

the medical literature relied on by his experts. Resp. Ex. F Tab 13; Resp. Ex. H Tabs 1-4; Resp.

Ex. J Tabs 5-7. Petitioner also refiled medical literature. Pet. Ex. 39; Pet. Ex. 42.

I determined that the parties had a full and fair opportunity to present their cases and it

was appropriate to resolve this issue without a hearing. The parties agreed. See Vaccine Rule

8(d); Vaccine Rule 3(b)(2); Kreizenbeck v. Sec’y of Health & Human Servs., 945 F.3d 1362,

1366 (Fed. Cir. 2020) (noting that “special masters must determine that the record is

comprehensive and fully developed before ruling on the record.”). Accordingly, this matter is

now ripe for resolution.

II. Medical Terminology

Transverse myelitis (“TM”) is a rare acquired demyelinating disorder that presents with

the sudden onset of neurological deficits due to spinal cord lesions. Annual incidence is between

1 and 8 per million with a significant proportion of cases preceded by infectious disease. Pet. Ex.

16 at 2. 4 TM is characterized by acute or subacute motor, sensory, and autonomic (bladder,

bowel, and sexual) spinal cord dysfunction arising typically from an autoimmune phenomenon

after infection or vaccination, with 15-30% of cases being characterized as idiopathic. Pet. Ex. 29

at 1. 5 The pathological hallmark of TM is the presence of a focal collection of lymphocytes and

4

Roger Baxter et al., Acute Demyelinating Events Following Vaccines: A Case-Centered Analysis, 63 CLINICAL

INFECTIOUS DISEASE 1456 (2016), filed as “Pet. Ex. 16”.

5

Elliot M. Frohman, M.D., Ph.D. & Dean M. Wingerchuk, M.D., Transverse Myelitis, 363 N. ENG. J. MED. 564

2

monocytes with varying degrees of demyelination, axonal injury, and astroglial and microglial

activation within the spinal cord. Id. Symptoms of TM generally evolve over the course of hours

to days and are usually bilateral but may be unilateral and asymmetric. Id. at 2. A well-defined

truncal sensory level, below which the sensation of pain and temperature is changed or lost,

distinguishes myelopathy from cerebral lesions and peripheral neuropathies. Urinary

incontinence or retention, bowel incontinence or constipation, and sexual dysfunction are

common but vary in severity in TM patients. The finding of one or more intrinsic cord lesions on

MRI is characteristic of myelitis. Id. TM is a common manifestation of acquired demyelinating

disease of the central nervous system. Id. at 4. “Normal MRI results should prompt a

reconsideration of the diagnosis of myelopathy in favor of other disorders of the central or

peripheral nervous system.” Id.

The lymphatic system “is composed of lymphatic organs, such as lymph nodes, tonsils,

thymus and the spleen”, which are all connected by a network of lymphatic vessels that run

parallel to the venous circulating system. Resp. Ex. F Tab 11 at 2. 6 The lymphatic system has

three main functions: drainage of excess interstitial fluid, fat absorption, and immune

surveillance. Id. The importance of the immune surveillance function is that circulating lymph

transports various antigens and activated antigen-presenting cells into the lymph nodes to

orchestrate the immune response. Id.

Resp. Ex. F Tab 11 at 2, Figure 1. This is a depiction of normal lymphatic circulation. The image

on the left shows lymphatic drainage returning fluid to the bloodstream. The image on the right

shows lymphatic capillaries collecting excess fluid from interstitial space, with about 90% of the

fluid being filtered by the blood capillaries will be reabsorbed and returned to venous

microcirculation. The remaining 10% of the fluid will be drained by the lymphatic capillaries.

Id.

(2010), filed as “Pet. Ex. 29”.

6

Ayman A. Grada, MD & Tania J. Phillips, MD, Lymphedema: Pathophysiology and Clinical Manifestations, 77 J.

AMERICAN ACADEMY OF DERMATOLOGY 1009 (2017), filed as “Resp. Ex. F Tab 11”.

3

Importantly, each limb has its own lymphatic system with a network of lymphatic vessels

and lymph nodes that drain fluid from that specific area of the body. 7 Pet. Ex. 13 at 29-30

(Lymphedema in the leg is dysfunction of the lymphatic system in that leg. An artery delivers

blood flow down the leg, it then goes into the smallest blood vessels where it drops of oxygen

and nutrients and picks up waste that goes into the return vessel, like a French drain system.

When there is excessive swelling in the limb it is a breakdown in that system.)

Lymphedema results from an imbalance between inflow and removal of interstitial fluid

and protein or a malfunction of the lymphatic drainage system. Resp. Ex. F Tab 5 at 6. 8 It is a

progressive disease defined as swelling of a part of the body caused by accumulation of protein-

rich interstitial fluid secondary to a malformation, malfunction, obstruction, or impairment of the

lymphatic drainage system. Pet. Ex. 44 at 1; 9 Resp. Ex. F Tab 5 at 1. Lower extremity

lymphedema, which is usually associated with infection and malignancies, is much more

common than upper extremity lymphedema, which is commonly associated with breast cancer.

Resp. Ex. F Tab 11 at 3. 10

Lymphedema is either primary (hereditary) or secondary (acquired). Resp. Ex. F Tab 11

at 3. 11 Primary lymphedema is divided into three categories: 1) congenital (at or shortly after

birth), 2) lymphedema praecox (around puberty), and 3) lymphedema tarda (late in life). Id. at 3-

4. Secondary lymphedema is much more common, and the result of damage caused by infection,

trauma, surgery, or malignancy and malignancy-associated treatment. Id. at 3; Resp. Ex. F Tab 5

at 1, 6. 12

The etiology of primary lymphedema is unknown. Resp. Ex. F Tab 5 at 5. 13 It develops in

a delayed fashion over years or even decades. Not all patients who experience insult to the

lymphatic system develop disease. Pet. Ex. 44 at 2. 14 “The natural history of primary

lymphedema classically has been stated to be a slow, constant progression from a mild, painless

swelling of an ankle to a huge, swollen extremity.” Resp. Ex. F Tab 5 at 7. 15 Risk factors

including radiation, infection, surgical dissection, and obesity have been identified, but are

insufficient to reliably predict the development of lymphedema. Pet. Ex. 44 at 2. 16 Animal

studies have provided insight into the cellular and molecular mechanisms of inflammation and

7

For example, the fibular lymph node is a lymph node situated along the fibular artery. Fibular lymph node,

Dorland’s Medical Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=93278. Likewise, the

distal deep inguinal lymph node is the most inferior of the deep inguinal lymph nodes, located just distal to the

junction of the great saphenous and femoral veins. Distal deep inguinal lymph node, Dorland’s Medical Dictionary

Online, https://www.dorlandsonline.com/dorland/definition?id=93301. The mandibular lymph node is one of many

facial lymph nodes located near the angle of the mandible. Mandibular lymph node, Dorland’s Medical Dictionary

Online, https://www.dorlandsonline.com/dorland/definition?id=93328.

8

David M. Smeltzer, MD et al., Primary Lymphedema in Children and Adolescents: A Follow-up Study and Review,

76 PEDIATRICS 206 (1985), filed as “Resp. Ex. F Tab 5” and “Resp. Ex. G Tab 3”.

9

Catherine L. Ly et al., Inflammatory Manifestations of Lymphedema, 18 INT’L J. OF MOLECULAR SCIENCES 171

(2017), filed as “Pet. Ex. 44”.

10

Grada & Phillips, supra note 6.

11

Id.

12

Smeltzer et al., supra note 8.

13

Id.

14

Ly et al., supra note 9.

15

Smeltzer et al., supra note 8.

16

Ly et al., supra note 9.

4

changes in lymphedematous tissue. Id. Current evidence suggests that a variety of key players

including T helper cells, T regulatory cells, macrophages, and dendritic cells play complex roles

in the pathology of lymphedema by inflammatory response. Id. at 5-8. “The absence of

lymphedema in some patients despite lymphatic injury and the delayed development in others

indicate that secondary events are likely necessary to elicit these important pathologic

interactions.” Id. at 9. More studies are needed to understand how inflammatory changes regulate

the development of lymphedema. Id.

Primary lymphedema is more frequent in children than secondary lymphedema with

overall female predominance; however, males dominate congenital lymphedema while female

onset is more frequently during adolescence with hormonal influence. Resp. Ex. J Tab 6 at 4. 17

May-Thurner Syndrome is an anatomical variant where the right common iliac artery

compresses the left common iliac vein and can result in iliofemoral deep venous thrombosis 18

(“DVT”). Pet. Ex. 33 at 1, 2; 19 Pet. Ex. 34 at 1. 20 This variant exists in 20% of the population and

can exist without symptomatology. Pet. Ex. 33 at 1; Pet. Ex. 34 at 1. May-Thurner syndrome is

observed in 50% of adult patients with descending iliofemoral DVT. Pet. Ex. 35 at 2.21 It is very

rare in children and usually associated with underlying sepsis, cancer, heart disease,

immobilization, and medications such as oral contraception and asparaginase. Id. at 1-2.

III. Background

A. Petitioner’s History Prior to the Subject Flu Vaccination

Petitioner had a normal childhood with uneventful childhood illnesses and seasonal

allergies. He received all his vaccinations without event. See generally Pet. Ex. 3.

Petitioner received the subject seasonal flu vaccine at Walgreen’s Pharmacy on August

30, 2015. Pet. Ex. 1; Pet. Ex. 3; Pet. Ex. 25 at 7-12 (noting in 2019 a “transverse myelitis-like

reaction 3 weeks after flu shot 2012”).

B. Petitioner’s History Following the Subject Flu Vaccination

Twenty-two days later, on September 21, 2015, petitioner presented to the pediatrician

reporting one day of left leg numbness. Pet. Ex. 3 at 5-6. He played soccer on Saturday and was

stumbling on Sunday. Id. He had a stuffy nose but no fever. On examination, his right leg was

17

Caroline Colmant et al., Pediatric Lymphedema: Study of 180 Patients Referred to a Tertiary Lymphedema Clinic,

26 J. CUTANEOUS MEDICINE AND SURGERY 502 (2022), filed as “Resp. Ex. J Tab 6”.

18

Deep vein thrombosis is thrombosis of one or more deep veins, usually of the lower limb, characterized by

swelling, warmth, and erythema. Deep vein thrombosis, Dorland’s Medical Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=113602.

19

Matthew Peters, MD et al., May-Thurner Syndrome: A Not So Uncommon Cause of a Common Condition, 25

PROC (BAYL UNIVERSITY MEDICAL CENTER) 231 (2012), filed as “Pet. Ex. 33”.

20

Melina R. Kibbe, MD et al., Iliac Vein Compression in an Asymptomatic Patient Population, 39 J. VASCULAR

SURGERY 937 (2004), filed as “Pet. Ex. 34”.

21

Martin Olivieri, MD et al., Ultrasound Assisted Endovascular Thrombolysis in Adolescents: 2 Case Reports, 138

PEDIATRICS e20160022 (2016), filed as “Pet. Ex. 35”.

5

normal, but his left leg had minimal strength. The pediatrician wrote “…suspect spinal lesion, ?

Tumor vs. infection. Recent flu vaccine but [symptoms] do not fit GBS.” Id. The pediatrician

called a neurologist at Children’s Hospital of Pittsburgh (“CHP”) who agreed further evaluation

was necessary. Id.

Petitioner was taken to CHP that day and admitted. His admission history included

playing soccer on Saturday without issue and waking Sunday morning with tingling in his right

lower extremity, numbness in his left lower extremity, and his left leg “not working” well.

Symptoms continued throughout the day on Sunday with trouble walking because his knee

would “buckle underneath” him. This morning he awoke with the same symptoms. Upon

presentation he complained of shooting pain from his left calf to behind his knee that did not

radiate up his leg. When he laid down, the weakness was more pronounced on the left. He had a

flu vaccine three weeks ago and mild upper respiratory infection-like symptoms but no fever 2

weeks ago. He was otherwise healthy. Pet. Ex. 5 at 39.

Neurological exam revealed slightly decreased motor strength in the left lower extremity

with normal strength in the right lower extremity. Pet. Ex. 5 at 40, 42. He had increased clonus 22

in the left ankle with upgoing toes on the left foot. Id. Although it was difficult to assess with

consistency, he had diminished pinprick and light touch sensation in both feet. Id. at 41-42. His

left leg was notably unstable when walking. Id. He had no bladder or bowel changes. Id. at 100.

Primary concerns were cortical lesion, cord lesion, mass, or vascular malformation. Id. at 42.

Petitioner was hospitalized until September 25, 2015 and underwent extensive testing all

of which was normal or negative. More specifically, MRI of the brain was normal. Pet. Ex. 5 at

24-25, 31, 139. MRI of the spine showed Schmorl’s nodes 23 at T11-T12 and L1, disc narrowing

and desiccation at T11-T12 and T12-L1 but was otherwise normal. Id. at 26, 137-38. EMG was

normal with no evidence of large fiber peripheral neuropathy. Id. at 166-69. Cerebral spinal fluid

(“CSF”) studies were negative for Epstein Barr virus (EBV), cytomegalovirus (CMV), varicella

virus (VZV), and enterovirus. White blood cell levels were within normal limits. Id. at 80, 150-

154. “A presumptive diagnosis of early transverse myelitis was made based on his symptoms and

his recent URI symptoms. He was treated with IV methylprednisolone [for] 5 days and was

started on an oral prednisone taper…”. Id. at 31. “His left leg weakness improved throughout

admission but did not disappear completely” by the time of discharge. Id.

One month later, petitioner presented to his pediatrician for a yearly check-up and follow

up for “transient myelitis.” Pet. Ex. 3 at 3. His dad expressed concern that the flu vaccine was to

blame. The pediatrician advised that it was an “unfortunate possibility that we may not know for

sure what the true cause was.” Id. She advised she would speak with petitioner’s neurologist Dr.

Alper about reporting the event to VAERS. Id. at 4. Petitioner’s examination was normal on that

date, and he was noted to be a well child with “[i]mproving transient myelitis.” Id. at 3-4.

22

Clonus is a continuous rhythmic reflex tremor initiated by the spinal cord below an area of spinal cord injury, set

in motion by reflex testing. Clonus, Dorland’s Medical Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=10153&searchterm=clonus.

23

Dr. McCormick described Schmorl’s nodes as the lymph nodes that are located in the thoracic spine. It is defined

as an irregular or hemispherical bone defect in the upper or lower margin of the body of the vertebra. Schmorl node,

Dorland’s Medical Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=93112.

6

Petitioner presented to Dr. Alper for a follow up visit on December 3, 2015. His parents

reported that he was “completely fine” with no tingling, buckling, or strength complaints. He

was playing soccer with no complaints. Pet. Ex. 5 at 422-23. Dr. Alper noted on examination that

petitioner had some swelling of the left ankle with a few beats of clonus raising concern for

arthritis. Id. at 422-24. Dr. Alper asked petitioner about the swelling and petitioner said the

swelling may have been there since Monday after a family hunting trip. He also reported some

heel pain after playing soccer in November. Id. at 423. He was sent to CHP for further evaluation

of the ankle swelling. Id. at 424.

Petitioner presented that day to CHP for painless left ankle swelling. Pet. Ex. 5 at 44. Ten

beats of clonus and asymmetric reflexes of the left leg were noted. Neurological consult was

ordered. Id. Neurology exam showed no significant abnormalities and no further neurological

testing needed. Id. at 45. X-ray showed some diffuse swelling of the left ankle and knee but no

bone or joint abnormality. Id. at 105-07. A venous doppler conducted on the left leg was normal.

Id. at 108.

Petitioner had no further medical visits until February 20, 2016 when he presented to

CHP for left leg swelling. Pet. Ex. 5 at 10. The record documented that since he was last seen in

December, he has had mild intermittent swelling around his left toes and ankle especially at the

end of the day. Two weeks ago, his parents noticed increased swelling of his left leg. Two days

ago, there was a marked increase of swelling involving his entire left leg up to the groin. His

parents called Dr. Alper who recommended MRI of the spine. Petitioner reported left knee pain

that day after playing in two soccer games. Petitioner reported the swelling was only of his left

leg, never anywhere else and there was no numbness, weakness, tingling, or incontinence. Id. He

was admitted with a differential of “obstructive malignancy including bone cancers vs

lymphoma, testicular cancer, post infectious/viral/recurrence of transverse myelitis though w/out

any overt neurological symptoms, autoimmune process, myxedema (though would expect more

widespread).” Id. at 26. There was lesser concern for venous abnormality due to localization and

lack of pitting edema. Ultrasounds done in December were normal. Id. The unilateral

presentation made it less likely to be a systemic syndrome such as cardiac, renal, or hepatic

abnormality. Systemic inflammatory arthritis was also being considered. Id.

Imaging studies for deep vein thrombosis were negative. Scrotal ultrasound was normal.

Pet. Ex. 5 at 10, 13-15. An MRI of the pelvis showed left iliac vein compression by the right iliac

artery. Id. at 10, 15. MRIs of the thoracic and lumbar spine were normal/negative with no

evidence of transverse myelitis. Id. at 10, 127-28. Petitioner had 5/5 strength in all extremities,

grossly intact sensation, and normal reflexes in the lower extremities with normal gait and

balance throughout his admission and discharge. Id. at 10-11. The discharge diagnosis was

swelling of the lower extremity. He was to follow up at the vascular clinic and wear compression

stockings. Id. at 10-11, 13.

Petitioner presented to Dr. McEnaney at the UPMC Vein Center on February 26, 2016.

Pet. Ex. 6 at 2. Examination revealed normal lower extremity motor strength and reflexes, but 1+

pitting edema of the left lower extremity. Id. at 3-4. Dr. McEnaney’s impression was venous

compression from the iliac artery (May Thurner syndrome) v. primary lymphedema.

7

Conservative treatment with compression therapy was recommended. He advised petitioner to

remain active and continue playing soccer to assist in drainage. Id. at 4. A discussion about doing

a lymphoscintigraphy 24 and “venogram to transduce a pressure across the segment of the vein in

order to confirm diagnosis” was had in the event there was no improvement. Id.

On March 9, 2016, petitioner presented to the pediatrician with left knee pain since

February 20, 2016. He thought it was from playing in multiple soccer games, but he now had

increased leg swelling. Pet. Ex. 3 at 2. Examination of the knee was normal. The pediatrician

questioned if the pain may be due to mechanical injury and made a referral to a sports medicine

specialist/orthopedic. Id.

Petitioner presented to the orthopedist the next day and reported knee pain since playing

in a soccer tournament on February 28, 2016. 25 Pet. Ex. 4 at 2. He reported being fine in the first

game but had increasing pain in the second game then had to stop playing due to knee

discomfort. He went to the ER for lower leg swelling and was discharged with compression

stockings from thigh to toes. Id. at 2-3. His history included “left lower extremity

swelling…initially began in September of 2015” with numbness and weakness diagnosed as TM

and treated with steroids and PT. Id. at 3. Petitioner had diffuse swelling from left thigh to toes,

including his left knee, though he had full range of motion of his left hip and knee. The

impression was left “patellofemoral syndrome and Sinding-Larsen-Johansson syndrome[ 26],

status post injury on February 20, 2016.” Id. PT for stretching and strengthening was

recommended along with a knee brace. He could participate in sports as tolerated. Id. He

attended nine physical therapy sessions through April 2016 for juvenile osteochondrosis of the

patella. See generally Pet. Ex. 7.

At his April 1, 2016 physical therapy visit, he was noted to be a 12 year old boy with a

history of “myelitis (LLE numbness, tingling and weakness) 9/2015, increased LLE

(lymphedema) 12/2015” who was seen in the neuroimmunology clinic. He had improving

lymphedema and felt his outpatient physical therapy was helping. Pet. Ex. 10 at 6. Examination

was within normal limits, but ankle clonus was still present. A physical therapist that specialized

in lymphedema was suggested. Id. at 6-7.

That same day, petitioner returned to Dr. Alper for follow up. His neurological

examination was normal, with subtle 1-2 clonus in the left foot. Pet. Ex. 10 at 14-15. Dr. Alper

noted that she had treated petitioner since his hospitalization in September of 2015 and that the

lower leg swelling/edema is possibly lymphedema without explanation and no underlying

diagnosis. Id. at 15. She noted the possibility that his mild edema started in September, expressed

initially as numbness; however, this would not explain the few beats of clonus or right-sided

complaints at that time. The September examination showed most symptoms to be left-sided

with left leg weakness, more proximal with knee buckling, so there could have been some soft

24

Lymphoscintigraphy has been described as the “ideal imaging technique to evaluate lymphatic flow and confirm

the diagnosis of lymphedema.” Resp. Ex. J Tab 6 at 4.

25

All other records refer to February 20, 2016 as the date his pain began, so this likely a typographical error.

26

Sinding-Larsen-Johansson syndrome, also called Larsen disease, is traction apophysitis in the lower pole of the

patella, an overuse injury seen most often in children between the ages of 10 and 16, characterized by pain and

tenderness, often with inflammation. Larsen disease, Dorland’s Medical Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=70515.

8

tissue problems causing those symptoms. But swelling was not noticed or diagnosed until

December at his follow up and only involved his left lower leg and ankle. Dr. Alper referred

petitioner to specialists in diagnostics. Id.

Petitioner returned to Dr. McEnaney on May 20, 2016 with persistent and somewhat

worsened lower left extremity swelling. Pet. Ex. 6 at 6. He reported that the swelling was

significantly worse when he did not wear the compression stocking. He saw an orthopedist for

his knee pain and tenderness. Examination revealed swelling from the hip to the toes of the left

leg. Lymphoscintigraphy was recommended. He was to wear the compression stocking. Id.

Dr. McEnaney discussed the results of the lymphoscintigraphy with petitioner and his

parents at a June 3, 2016 visit, advising that the testing demonstrated a lack of radiotracer transit

in the left lower extremity consistent with obstructed lymphatic flow, reinforcing the diagnosis of

lymphedema. Pet. Ex. 6 at 7, 8-9. Aggressive manual lymphatic drainage was anticipated. Id.

On September 22, 2016, petitioner presented to Dr. McCormick for a second opinion on

the diagnosis of lymphedema. Dr. McCormick noted a history of hospitalization in the fall of

2015 for left leg weakness, tingling, and numbness. Despite negative imaging and normal CSF,

TM was thought to be the best diagnosis. Petitioner received 5 days of high dose steroids with a

6-week oral taper, got better very quickly, and remained neurologically asymptomatic. Pet. Ex. 8

at 19. In December of 2015, he had left ankle and foot swelling but no other symptoms. The

swelling then became acutely worse in February of 2016 with the swelling up to the groin. He

was admitted to the hospital and diagnosed with May-Thurner syndrome. After discharge,

petitioner saw a vascular specialist who diagnosed petitioner with congenital lymphedema not

May-Thurner syndrome. Id. at 19-20. Lymphoscintigraphy testing was consistent with

lymphedema. Id. Dr. McCormick recommended an MRI/A of the lower left extremity with

vascular anomaly protocol to evaluate for underlying lymphatic malformation. Id. at 22. He

noted a concern that the underlying lymphatic malformation “accelerated after puberty/steroid

treatment vs. May-Thurner syndrome developing after steroid with loss of fat pad between iliac

venous and arterial system.” Id. The MRI performed on October 18, 2016 revealed diffuse left

lower leg edema consistent with history of lymphedema and no lymphatic or vascular

malformation. Id. at 27-28. Lower extremity arteries and veins were patent. There was a

nonspecific finding of partial bone marrow edema. Id. at 28.

Petitioner underwent unrelated bilateral hydrocele surgery in December of 2019 without

event and was treated for a pilonidal cyst in 2022. See Pet. Ex. 46. He was otherwise a healthy

teenager who continued to play soccer. Pet. Ex. 50.

C. Affidavits by Petitioner’s Father, Kary Valentine 27

Kary Valentine is petitioner’s father. In his initial affidavit, he affirmed petitioner’s

receipt of a flu vaccine as set forth in the Vaccine Injury Table, which was administered in the

U.S. and caused transverse myelitis and sequelae in excess of six months. Pet. Ex. 9.

Mr. Kary Valentine was initially the named petitioner in this matter until Mitchell Valentine reached the age of

27

majority. See Pet.

9

Mr. Valentine submitted another affidavit five years later dated December 15, 2022. Pet.

Ex. 54. In his second affidavit, Mr. Valentine affirmed that petitioner was healthy and did not

have any abnormal swelling of his left leg or elsewhere prior to his August 30, 2015 vaccination.

Id. at 1. Mr. Valentine further affirmed that petitioner showed no signs of puberty in the year

before or after the subject flu vaccine. Id.

Mr. Valentine noticed something was not right with petitioner’s left foot and ankle in the

fall of 2015. Pet. Ex. 54 at 1. “By January or February of 2016, it was evident that the

lymphedema has progressed and now encompassed his entire left leg.” Id. at 1-2.

According to Mr. Valentine, he and his wife sought medical treatment for petitioner for

“his neurological symptoms” very quickly. The steroids he was given were very effective in

controlling his symptoms. Mr. Valentine was convinced that petitioner’s TM would have

progressed if not for the steroids. Pet. Ex. 54 at 2.

Mr. Valentine affirmed that he noticed petitioner’s left ankle and foot swelling around the

time he was losing the weight gained from the steroid treatment. As his parent and “caregiver

who observed him every day, it seems almost certain that the lymphedema which followed the

TM was caused by it.” Pet. Ex. 54 at 2. Prior to the vaccine, he had no signs of lymphedema or

other health conditions. Id.

D. Deposition Testimony of Andrew McCormick, M.D.

Dr. McCormick was deposed on November 27, 2018. Pet. Ex. 13.

Dr. McCormick 28 is a pediatrician with a specialty in pediatric hospital medicine and a

subspecialty in children with vascular anomalies and Down Syndrome. Pet. Ex. 13 at 6-7. He

described himself as the pediatrician for children admitted to the hospital for everything from

asthma to complex medical needs. Id. at 7.

Dr. McCormick described vascular anomalies as a “unique field of medicine” that is

multidisciplinary because the patient will need more than one subspecialist to assist in their care.

Pet. Ex. 13 at 10-11. Dr. McCormick does the diagnostic evaluation at admission and then

decides who the patient needs as a subspecialist going forward. Id. at 11.

Dr. McCormick explained that vascular anomalies are divided into vascular tumors and

vascular malformations with vascular tumors being the most common and treatable requiring

only management because they usually resolve over time. Pet. Ex. 13 at 11, 13. Vascular

28

Dr. McCormick graduated from University of Pittsburgh Medical School, did his residency at University of

Pittsburgh Medical Center (“UPMC”), and has been a hospitalist at the Paul C. Gaffney Hospital Medicine Division

for eight years. He has worked in the Vascular Anomaly Center at UPMC for the last five years and has been the

medical director for the past three years. Pet. Ex. 13 at 8. He is an associate professor of pediatrics through UPMC

and faculty clinician at the Paul C. Gaffney Pediatric Hospital Medicine Division. Id. at 9. He said 75% of his time

is spent as a clinician and 25% as medical school faculty. He does research on the side. Id. Dr. McCormick teaches

the residents and medical students in the hospital. Outside of the medical system, he teaches both vascular anomalies

and Down Syndrome care. Id. at 10. He teaches an advanced physical examination course for first- and second-year

medical students on how to take histories from the family and complete physical exams. Id.

10

malformations are congenital abnormalities, typically lifelong, and require multidisciplinary

treatment. Id. at 11-13. Dr. McCormick stated that data shows “vascular malformations

accelerate during puberty and during pregnancy . . .”. Id. at 42. He said that clinicians “see

lymphedema show up in teenagers all the time because of” puberty. Id. There are also arterial

and venous system malformations purposefully created for dialysis, those that are traumatically

induced, or are due to error in correction when the injury occurs. Id. at 14-15.

Dr. McCormick saw petitioner once on September 22, 2016. He was questioned at length

about his record for that visit. He explained that the first portion of his office record contains the

history provided by the parents including the hospitalization and the treatment provided to

understand what may have caused the lymphedema. Pet. Ex. 13 at 15-18; Pet. Ex. 8. His “write

up of the case” included his review of the medical records prior to meeting the family,

confirmation of the history with the family, and his thoughts about what was occurring with the

patient. Id. at 19, 55-56. He included Dr. Alpers’s findings because petitioner’s hospitalization in

September of 2015 and follow up visits were not for lymphedema; rather, the lymphedema was a

new finding and was why he was evaluating petitioner. Id. at 21-22.

He discussed the facts that informed his thinking about petitioner’s case, including

petitioner’s presentation of only one swollen leg, no joint swelling, no fever, no rash, no

shortness of breath, no loss of appetite, etc. The general screening questions are designed to

ascertain whether the unilateral leg swelling was part of a larger process like a systemic illness, a

rheumatological disorder, or an oncologic disorder for example. Pet. Ex. 13 at 22-23. Petitioner’s

presentation, in combination with earlier testing, effectively ruled out those other conditions. Id.

at 23-24. He included the MRI results as well and explained that Schmorl’s nodes are lymph

nodes seen at T11, T12, and L1 and were non-enhancing and not inflamed, indicating that the

neurological disease petitioner presented with earlier had since resolved and was thus not the

etiology of his leg swelling. 29 Id. at 24-25. He further explained the significance of seeing the

Schmorl’s nodes on petitioner’s MRI, stating that they could have been enlarged for a “run-of-

the-mill virus”, bacterial infection, or even cancer but that their enlargement alone “doesn’t

necessarily tell you anything other than we know that they’ve been stable over time…”. Id. at 26-

27. He added that the enlarged Schmorl’s nodes were likely not connected to the swelling of

petitioner’s left leg, explaining that unilateral extremity swelling is an abnormality of the

lymphatic tract like a unilateral malformation or an obstruction of flow to one side. A central

channel would not cause obstruction to an entire leg. Id. at 27-28. He agreed that DVT was ruled

out before he saw petitioner. Id.

Dr. McCormick explained that “left iliac vein compression by the right iliac artery”

means that there is a blockage of the fluid draining into the veins. Pet. Ex. 13 at 28-30. He

explained that each leg has arteries and veins that run next to each other. An artery delivers blood

down the leg and a vein drains fluid and waste product. If there is compression, the return

through the veins is blocked and the system becomes inefficient which may cause excessive

swelling in a limb or lymphedema. Id. at 29-30.

29

Dr. McCormick stated that if the nodes were enhancing, that would indicate a change in blood flow which could

be related to an inflammatory or oncologic process. Pet. Ex. 13 at 26. Enlarged lymph nodes, on the other hand, may

be present for several reasons, including upper respiratory infection, a virus, bacterial infection, or lymphoma in the

location. Enlargement alone cannot indicate etiology and can exist for a long time after infection. Id. at 26-27.

11

Dr. McCormick explained that May-Thurner syndrome is the compression of the outflow

system because of either lymphedema or a blood clot. Pet. Ex. 13 at 30, 32. May-Thurner

syndrome can either be congenital or can develop during life. Id. at 33. For those that develop

later in life, there is a fat pad that exists between the two systems that can be lost in childhood,

leading to the compression of venous outflow. Id. at 31, 33. High-dose steroids can also

redistribute fat, causing someone to lose some protective fat pads. Id. at 40.

Petitioner’s testing showed both a venous outflow obstruction consistent with May-

Thurner syndrome and dysfunction in the lymphatic system. Pet. Ex. 13 at 33-34. It is possible

for a person to have both May-Thurner syndrome and a dysfunctional lymphatic system, both

occurring together but the two are not necessarily connected. Id. at 34-35.

Dr. McCormick’s “Impression” included his concern for possible underlying lymphatic

malformation of the left lower leg present all of petitioner’s life that may have changed over time

due to age and the pressures of puberty. Pet. Ex. 13 at 36-37. He stated that May-Thurner

syndrome and the loss of fat pad can develop from an illness, but there was insufficient

information to make that determination. Id. at 36-38. His thought was not May-Thurner

syndrome because of the lack of varicosities, so he ordered an MRA to look at petitioner’s

vasculature system. Id. at 38-39, 43. Petitioner’s MRA was normal, apart from diffuse swelling

suggestive of lymphedema, with no congenital malformation of the major arteries, veins, or

lymphatic tissue to cause it, which ruled out both May-Thurner syndrome and congenital

lymphatic malformation. Id. at 44-45. Rather, “this child fits the category of primary

lymphedema.” Id. at 45.

A classic picture for primary lymphedema in teenagers is praecox lymphedema which is

puberty driven. Pet. Ex. 13 at 41-42, 46, 48. However, the mechanism for how the production of

steroids in puberty (and in pregnancy) can accelerate an underlying lymphatic malformation is

unknown and is only an association. Id. Therefore, it is referred to as idiopathic requiring system

management with compression garments and lymphedema therapy. There is no medication to

prescribe. Id. at 45-46. Dr. McCormick thought that high-dose steroids can have the same effect

on the body as puberty, which itself is driven by steroids in the form of estrogen and testosterone

but was unaware of any case reports pointing to high dose steroids as a cause of primary

lymphedema. Id. at 48-49. Thus, while puberty is a well-defined disease process for praecox

lymphedema, there is little data to suggest that external steroid use could cause progression or

changes in lymphatic disease. Id.

Dr. McCormick opined that petitioner had primary lymphedema with abnormalities in the

peripheral lymphatic drainage system seen on imaging. It would be hard to know the etiology

unless you saw what the trigger was. Pet. Ex. 13 at 58-60. Dr. Yilmaz, an interventional

radiologist with specialized training in reading vascular anomalies, saw petitioner after Dr.

McCormick and had the same impression after reading the test results. Id. at 54-55, 58-59.

When asked what the timeframe for onset would be between steroids (either through

puberty or medication) and clinically significant lymphedema, Dr. McCormick relied on the

12

onset of praecox lymphedema in puberty in girls to say that it would be weeks or months, not

years. Pet. Ex. 13 at 60-62.

E. Expert Reports

Petitioner submitted expert reports from Dr. Allan Rubenstein and Dr. Tejas Shah. Pet.

Ex. 14; Pet. Ex. 27; Pet. Ex. 30; Pet. Ex. 31; Pet. Ex. 47. Respondent submitted reports from Dr.

Michael Sweeney and Dr. Caitlin Hicks. Resp. Ex. A; Resp. Ex. C; Resp. Ex. D; Resp. Ex. G;

Resp. Ex. H; Resp. Ex. I; Resp. Ex. J. All expert reports were considered and are referenced and

discussed in the analysis of this Ruling.

IV. Standard for Adjudication

A petitioner is required to establish his case by a preponderance of the evidence. 42

U.S.C. § 300aa-13(1)(a). The preponderance of the evidence standard requires a “trier of fact to

believe that the existence of a fact is more probable than its nonexistence before [they] may find

in favor of the party who has the burden to persuade the judge of the fact’s existence.” Moberly

v. Sec’y of Health & Human Servs., 592 F.3d 1315, 1322 n.2 (Fed. Cir. 2010) (citations omitted).

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

867, 873 (Fed. Cir. 1991).

Distinguishing between “preponderant evidence” and “medical certainty” is important

because a special master should not impose an evidentiary burden that is too high. Andreu v.

Sec’y of Health & Human Servs., 569 F.3d 1367, 1379-80 (Fed. Cir. 2009) (reversing a special

master’s decision that petitioners were not entitled to compensation); see also Lampe v. Sec’y of

Health & Human Servs., 219 F.3d 1357 (Fed. Cir. 2000); Hodges v. Sec’y of Health & Human

Servs., 9 F.3d 958, 961 (Fed. Cir. 1993) (disagreeing with the dissenting judge’s contention that

the special master confused preponderance of the evidence with medical certainty).

A. Legal Standard

The Vaccine Act provides two avenues for petitioners to receive compensation. First, a

petitioner may demonstrate a “Table” injury—i.e., an injury listed on the Vaccine Injury Table

that occurred within the provided time period. 42 U.S.C. § 300aa-11(c)(1)(C)(i). “In such a case,

causation is presumed.” Capizzano v. Sec’y of Health & Human Servs., 440 F.3d 1317, 1320

(Fed. Cir. 2006); see § 13(a)(1)(B). Second, where the alleged injury is not listed on the Vaccine

Injury Table, a petitioner may demonstrate an “off-Table” injury, which requires that the

petitioner “prove by a preponderance of the evidence that the vaccine at issue caused the injury.”

Capizzano, 440 F.3d at 1320; see § 11(c)(1)(C)(ii); see also Wright v. Sec’y of Health & Human

Servs., 22 F.4th 999, 1006 (Fed. Cir. 2022) (defining the term “residual effects” in the Act, as

“detrimental conditions within the patient, such as lingering or recurring signs and symptoms” of

the alleged vaccine injury, which are compensable). A petitioner need not show that the

vaccination was the sole cause, or even the predominant cause, of the alleged injury; showing

that the vaccination was a “substantial factor” and a “but for” cause of the injury is sufficient for

recovery. Pafford v. Sec’y of Health & Human Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006);

Shyface v. Sec’y of Health & Human Servs., 165 F.3d 1344, 1352 (Fed. Cir. 1999). Petitioners

13

are not required “to eliminate alternative causes as part of establishing [their] prima facie case.”

Doe v. Sec’y of Health & Human Servs., 601 F.3d 1349, 1357-58 (Fed. Cir. 2010); see Walther v.

Sec’y of Health & Human Servs., 485 F.3d 1146, 1152 (Fed. Cir. 2007) (holding that a

“petitioner does not bear the burden of eliminating alternative independent potential causes”).

Once a petitioner has proven causation by preponderant evidence, “the burden then shifts to the

respondent to show by a preponderance of the evidence that the injury is due to factors unrelated

to the administration of the vaccine.” Deribeaux ex rel. Deribeaux v. Sec’y of Health & Human

Servs., 717 F.3d 1363, 1367 (Fed. Cir. 2013) (citing 42 U.S.C. § 300aa-13(a)(1)(B)).

To prove causation, a petitioner must satisfy the three-pronged test established in Althen

v. Sec’y of Health & Human Servs., 418 F.3d 1274 (Fed. Cir. 2005). Althen requires that a

petitioner show by preponderant evidence that a vaccination they received caused their injury

“by providing: (1) a medical theory causally connecting the vaccination and the injury; (2) a

logical sequence of cause and effect showing that the vaccination was the reason for the injury;

and (3) a showing of a proximate temporal relationship between vaccination and injury.” Id. at

1278. Together, these prongs must show “that the vaccine was ‘not only a but-for cause of the

injury but also a substantial factor in bringing about the injury.’” Stone v. Sec’y of Health &

Human Servs., 676 F.3d 1373, 1379 (Fed. Cir. 2012) (quoting Shyface, 165 F.3d at 1352-53).

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).

Petitioners are not required to identify “specific biological mechanisms” to establish causation,

nor are they required to present “epidemiologic studies, rechallenge, the presence of pathological

markers or genetic disposition, or general acceptance in the scientific or medical communities.”

Capizzano, 440 F.3d at 1325 (quoting Althen, 418 F.3d at 1280). “[C]lose calls regarding

causation are resolved in favor of injured claimants.” Althen, 418 F.3d at 1280.

Each Althen prong requires a different showing. Under the first prong, a petitioner must

provide a “reputable medical theory” demonstrating that the vaccine received can cause the type

of injury alleged. Pafford, 451 F.3d at 1355-56 (citation omitted). To satisfy this prong, a

petitioner’s “theory of causation must be supported by a ‘reputable medical or scientific

explanation.’” Andreu, 569 F.3d at 1379 (quoting Althen, 418 F.3d at 1278). This theory need

only be “legally probable, not medically or scientifically certain.” Id. at 1380 (emphasis omitted)

(quoting Knudsen, 35 F.3d at 548). Nevertheless, “petitioners [must] proffer trustworthy

testimony from experts who can find support for their theories in medical literature.” LaLonde,

746 F.3d at 1341.

The second Althen prong requires proof of a “logical sequence of cause and effect.”

Capizzano, 440 F.3d at 1326 (quoting Althen, 418 F.3d at 1278). Even if the vaccination can

cause the injury, a petitioner must show “that it did so in [this] particular case.” Hodges v. Sec’y

of Health & Human Servs., 9 F.3d 958, 962 n.4 (Fed. Cir. 1993) (citation omitted). “A reputable

medical or scientific explanation must support this logical sequence of cause and effect,” Id. at

961 (citation omitted), and “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,” Paluck v. Sec’y of Health & Human Servs., 786 F.3d 1373, 1385 (Fed. Cir. 2015)

(quoting Andreu, 569 F.3d at 1375).

14

The third Althen prong requires that a petitioner establish a “proximate temporal

relationship” between the vaccination and the alleged injury. Althen, 418 F.3d at 1281. This

“requires preponderant proof that the onset of symptoms occurred within a timeframe for which,

given the medical understanding of the disorder’s etiology, it is medically acceptable to infer

causation-in-fact.” De Bazan v. Sec’y of Health & Human Servs., 539 F.3d 1347, 1352 (Fed. Cir.

2008). Typically, “a petitioner’s failure to satisfy the proximate temporal relationship prong is

due to the fact that onset was too late after the administration of a vaccine for the vaccine to be

the cause.” Id. However, “cases in which onset is too soon” also fail this prong; “in either case,

the temporal relationship is not such that it is medically acceptable to conclude that the

vaccination and the injury are causally linked.” Id.; see also Locane v. Sec’y of Health & Human

Servs., 685 F.3d 1375, 1381 (Fed. Cir. 2012) (“[If] the illness was present before the vaccine was

administered, logically, the vaccine could not have caused the illness.”).

Finally, although this decision discusses some but not all the literature in detail, I have

reviewed and considered all of the medical records and literature submitted in this matter. See

Moriarty ex rel. Moriarty v. Sec’y of Health & Human Servs., 844 F.3d 1322, 1328 (Fed. Cir.

2016) (“We generally presume that a special master considered the relevant record evidence

even though [s]he does not explicitly reference such evidence in h[er] decision.”); Simanski v.

Sec’y of Health & Human Servs., 115 Fed. Cl. 407, 436 (2014) (“[A] Special Master is ‘not

required to discuss every piece of evidence or testimony in her decision.’” (citation omitted)),

aff’d, 601 F. App’x 982 (Fed. Cir. 2015).

B. Law Regarding Diagnosis

In Broekelschen v. Sec’y of Health and Human Servs., 618 F.3d 1339, 1346 (Fed. Cir.

2010), the Federal Circuit recognized that in some circumstances, the special master may “first

determine which injury was best supported by the evidence in the record before applying the

Althen test.” This principle also means that a petitioner must establish that the vaccinee suffers

the injury allegedly linked to the vaccination. Lombardi v. Sec’y of Health & Human Servs., 656

F.3d 1343, 1353-54 (Fed. Cir. 2011).

V. Discussion

The outcome of petitioner’s case is based on three different findings. First, petitioner

must establish that TM was the appropriate diagnosis. Second, he must present persuasive

evidence that the flu vaccine was the cause in fact of his TM. Finally, if he proves that TM was

the appropriate diagnosis and that the flu vaccine was the cause in fact of his TM, he must show

that his TM caused lymphedema in his left lower extremity.

A. Diagnosis

Petitioner alleges that he suffered from TM as a result of the flu vaccine he received on

August 30, 2015. Respondent disagrees that TM was the appropriate diagnosis. This dispute

involves several issues including the value of published diagnostic criteria, how the pieces of

evidence preponderate, and the legal significance of petitioner’s lack of success in proving TM.

15

a. Diagnostic Criteria for TM

The diagnostic criteria for TM includes: 1. Bilateral, not necessarily symmetric,

sensorimotor and autonomic spinal cord dysfunction; 2. Clearly defined sensory level; 3.

Progression to nadir of clinical deficits between 4 hours and 21 days after symptom onset; 4.

Demonstration of spinal cord inflammation through cerebrospinal fluid pleocytosis, elevated IgG

index, or MRI revealing a gadolinium-enhancing cord lesion; and 5. Exclusion of compressive,

post-radiation, neoplastic, and vascular causes. Pet. Ex. 28 at 6, Table 4; 30 Pet. Ex. 29 at 2, Table

1; 31 Resp. Ex. A Tab 3. 32

Spinal cord disorders are generally “classified as ‘syndromes’ due to typical signs and

symptoms produced because of the location of the lesion and specific tract involvement.” Pet.

Ex. 28 at 1-2. 33 Transverse myelitis specifically typically arises as an autoimmune phenomenon

after infection, vaccination, systemic autoimmune disease, or acquired demyelinating disease;

anywhere from 15% to 30% are classified as idiopathic. Pet. Ex. 29 at 1; 34 Pet. Ex. 28 at 9.

Although idiopathic TM can arise at any age, the peak incidence is between 10 and 19 years of

age and 30 and 39. Pet. Ex. 29 at 1.

b. Evidence regarding petitioner’s health

Petitioner developed tingling in his right lower leg, with numbness of his left lower leg

and his left leg “not working” three weeks after his receipt of the flu vaccine, two weeks after

mild cold symptoms without fever and following a competitive day of soccer. Pet. Ex. 3 at 5;

Pet. Ex. 5 at 39. Neurological exam revealed slightly decreased motor strength in the left lower

extremity with normal strength in the right lower extremity. Pet. Ex. 5 at 40, 42. He had

diminished pinprick and light touch sensation in both feet. Id. at 41-42. His left leg was notably

unstable when walking. Id. Primary concerns were cortical lesion, cord lesion, mass, or vascular

malformation. Id. at 42.

Extensive objective testing including MRIs of the brain and spine were normal (other

than unrelated Schmorl’s nodes on MRI of the spine); a lumbar puncture (performed three days

after onset) was normal, cultures for EBV, CMV, VZV, and enterovirus were negative, and

EMG testing on September 25, 2015 was normal. Pet. Ex. 5 at 24-26, 31, 80, 137-39, 150-54,

166-69. Rheumatology and endocrine workups were normal. Id. at 35.

Despite all normal testing, “[a] presumptive diagnosis of early transverse myelitis was

made based on his symptoms and his recent URI symptoms.” Pet. Ex. 5 at 31. He received 5

days of IV methylprednisolone followed by oral prednisone taper on discharge beginning on

September 26 and ending on November 4, 2015 with symptom improvement. Id. at 31, 34-35. At

30

Anu Jacob, M.D. & Brian G. Weinshenker, M.D., F.R.C.P.(C.), An Approach to the Diagnosis of Acute

Transverse Myelitis, 28 SEMINAL NEUROLOGY 105 (2008), filed as “Pet. Ex. 28”.

31

Frohman & Wingerchuk, supra note 5.

32

Rohit Bakshi, MD & John C. Mazziotta, MD, PhD, Acute Transverse Myelitis After Influenza Vaccination:

Magnetic Resonance Imaging Findings, 6.4 J. OF NEUROIMAGING 248 (1996), filed as “Resp. Ex. A Tab 3”.

33

Jacob & Weinshenker, supra note 30.

34

Frohman & Wingerchuk, supra note 5.

16

the time of discharge, he had a normal physical examination with 4+/5 motor strength in the

proximal lower left leg muscles and 5-/5 on distal. He had normal bulk and tone and 5/5 strength

in the bilateral upper extremities and right lower extremity. Id. at 36. Reflexes were normal, and

sensory was intact to light touch, temperature, pinprick, and proprioception with no sensory

level. Id. at 36, 40. He had 7-8 beats of clonus on the left, equivocal toe on the left, and flexor

plantar response on the right. He had no ataxia or dysmetria, normal rapid alternating

movements, and mild steppage gait with the left foot but able to hop on the left leg with some

difficulty. Id. at 36. The discharge diagnosis was “[w]eakness of left lower extremity.” Id.

A month later he was noted to be a well child with “[i]mproving transient myelitis.” Pet.

Ex. 3 at 3-4.

His parents reported that he was “completely fine” on December 3, 2015, and Dr. Alper

noted there was no tingling, buckling, or strength complaints and he was playing soccer without

issue. Pet. Ex. 5 at 422-23. However, she noted left ankle swelling and a few beats of clonus. Id.

422-24. Petitioner was sent to CHP and underwent further testing, which showed no

abnormalities. Id. at 105-08.

Petitioner was hospitalized again on February 20, 2016 for left leg swelling. Pet. Ex. 5 at

10. Follow up MRIs of the thoracic and lumbar spine performed during his hospitalization were

normal. Id. at 10, 127-28. His September MRIs were referred to as having provided no

explanation for his symptoms. Id. at 10. He had 5/5 strength in all extremities, grossly intact

sensation, and normal reflexes in the lower extremities with normal gait and balance on that day.

Id. at 10-11.

c. Dr. Alper’s Opinions

The opinions of treating doctors can be quite probative. Cappizano v. Sec’y of Health &

Human Servs., 440 F.3d 1317, 1326 (Fed. Cir. 2006). The views of treating doctors about the

appropriate diagnosis are often persuasive because the doctors have direct experience with the

patient whom they are diagnosing. See McCulloch v. Sec’y of Health & Human Servs., No. 09-

293V, 2015 WL 3640610, at *20 (Fed. Cl. Spec. Mstr. May 22, 2015). However, the views of a

treating doctor are not absolute, Snyder v. Sec’y of Health & Human Servs., 88 Fed. Cl. 706, 745

n.67 (2009), even on the question of diagnosis, R.V. v. Sec’y of Health & Human Servs., 127 Fed.

Cl. 136, 141 (2016), appeal dismissed, No. 16-2400 (Fed. Cir. Oct. 26. 2016).

In her February 2016 visit notes, Dr. Alper noted petitioner’s history including September

of 2015 when he presented with lower left leg weakness with sensory changes but normal results

on testing for Lyme disease, NMO-IgG antibody, MRI of brain and spine, CSF, and EMG. Pet.

Ex. 10 at 25. There was no evidence of radiculopathies or neuropathies and no evidence of GBS.

He was treated with IV steroids then oral steroids and did well. Id. Two months later, he was

“completely fine”, playing soccer, and slimming down from the steroid weight gain. Id. at 25-26.

At his December 2015 visit, there was some left ankle swelling with no pain and a few beats of

clonus. Id. at 26. Dr. Alper wrote that based on his symptoms in September, myelitis could not

be ruled out even though all studies were negative, so he was treated for myelitis. However,

today, the swollen ankle is concerning, and she questioned if the Lyme testing may have been a

17

false negative. “He could have had myeloradiculitis before but normal CSF would be unusual” or

arthritis. An evaluation at the ER at CHP and repeat Lyme testing was ordered. Id. at 27.

Petitioner was seen at CHP with no neurological abnormalities noted. X-rays showed

some swelling of the ankle and knee but no bone or joint abnormality. Pet. Ex. 5 at 44, 45, 105-

07. A venous doppler was normal. Id. at 108.

At his return visit on April 1, 2016, Dr. Alper noted no neurological concerns, but

continued left ankle swelling. Pet. Ex. 10 at 14. “Because his diagnosis of myelitis in September

was [a] presumed diagnosis, although his symptoms improved at that time, the CSF findings and

MRI findings were negative.” Id. MRI did not show a tumor or any paraspinal mass that would

cause both symptoms. Vascular studies showed a vascular malformation, and MRI of the

abdominal pelvis showed left iliac vein compression suggestive of May-Thurner syndrome

diagnosed by both vascular and radiology. According to the mother, the specialist thought it was

an incidental finding that did not explain the left leg swelling. Id. Dr. Alper wrote it was “very

interesting” that petitioner had lower left extremity edema, possibly lymphedema with no

explanation for it. Id. at 15. “One possibility in September maybe (sic) he had had mild edema

just starting which may expressed (sic) as numbness feeling, but it is hard to explain he had few

beats of clonus at initial evaluation also he was complaining [of] some right-sided problem[s] at

that time. When I saw the patient the symptoms were more on the left side and he was

demonstrating left leg weakness, more proximal saying that his leg was buckling, so it could be

some soft tissue problems causing symptoms at that time. But his swelling was not noticed or

diagnosed before until December when he came to follow-up with me. It was only involving his

left ankle and lower leg that is why I sent him to ED.” Id.

d. Expert Opinions on Diagnosis 35

Dr. Rubenstein opined that petitioner had mild, early, asymmetric TM 22 days after

receipt of an influenza vaccine, and that petitioner “clearly had an autoimmune event which

caused him to have significant neurologic dysfunction which was successfully treated with IV

and oral steroids.” His subsequent lymphedema was a “direct result of the asymmetric transverse

myelitis.” Pet. Ex. 14 at 3; Pet. Ex. 27 at 1; Pet. Ex. 30 at 1.

In defending his opinion that petitioner suffered from TM despite all objective testing

being normal, Dr. Rubenstein argued that every patient presents differently, and “a diagnosis

must be based on a holistic consideration of all the available evidence.” Pet. Ex. 27 at 3. He

agreed petitioner’s presentation was mild and unusual but relied on Frohman & Wingerchuk to

support that rapid-onset, “unilateral[,] or markedly asymmetric presentations can occur.” Id. at 3-

4; Pet. Ex. 29 at 2. 36 Generally, though, symptoms of TM evolve over the course of hours to days

and are bilateral. Pet. Ex. 29 at 2.

Dr. Rubenstein argued that normal imaging or CSF does not rule out TM, citing a study

wherein roughly 20% of participants had a TM diagnosis with either normal MRI or normal CSF

35

Dr. Shah’s and Dr. Hicks’ opinions assume petitioner had TM and are therefore not relevant to this part of the

Ruling.

36

Frohman & Wingerchuk, supra note 5.

18

findings. In sum, “a lack of abnormal findings on MRI does not undercut a TM diagnosis based

on the patient’s subjective history, objective clinical findings, and response to treatment –

particularly for a mild case.” Pet. Ex. 47 at 1; Pet. Ex. 49. 37

Dr. Rubenstein added that bowel or bladder changes would not be expected in

petitioner’s case because it was mild and most importantly asymmetric, suggesting that the

demyelinating lesions did not cross petitioner’s spinal cord and thus did not interrupt signals to

the bowel and bladder. Pet. Ex. 27 at 5. He further submitted that petitioner’s lack of sudomotor

changes (referring to changes in the ability to sweat) and vasomotor changes (blanching or

atypical redness of the skin) were either not present in petitioner or were overlooked. Id. at 5-6.

In sum, Dr. Rubenstein argued that petitioner’s lack of the characteristic symptoms of TM can be

attributed to how mild his TM was, that not all symptoms are present in every individual, or that

the doctors caring for petitioner missed the signs of vasomotor and sudomotor changes. Id.

However, Dr. Rubenstein also argued that petitioner’s treating physicians were in the best

position to render a diagnosis and diagnosed and treated petitioner for TM. Further, the steroid

treatment was successful in resolving his neurological symptoms which suggested that he

suffered from an autoimmune neuro-demyelination. Pet. Ex. 27 at 2-3.

Dr. Sweeney disagreed that petitioner had TM. He acknowledged that TM following flu

vaccine is rare, and he was unable to find published cases in the literature to support a post-

influenza myelitis without findings on imaging or evidence of inflammation on CSF. Resp. Ex.

A at 3; Resp. Ex. A Tab 1; 38 Resp. Ex. A Tab 2; 39 Resp. Ex. A Tab 3; 40 Resp. Ex. I at 2.

Dr. Sweeney noted that petitioner’s TM diagnosis was based on clinical presentation of

acute onset of weakness and brisk reflexes including positive Babinski in his left leg several

weeks after a flu vaccine. However, there was no evidence of myelitis on MRI of the spine and

no evidence of inflammation on CSF testing which was performed more than two days after

onset. Petitioner awoke with symptoms on September 20 but his symptoms did not progress.

Resp. Ex. A at 3-4. Additionally, petitioner had none of the autonomic changes typically present

in early TM including changes to bowel or bladder, vasomotor, or sudomotor functions. Id. at 4.

Therefore, petitioner’s presentation did not meet the diagnostic criteria for TM. Id. at 5.

Dr. Sweeney argued that the absence of evidence of inflammation within the CSF and

normal MRI of the spine supports that this was not myelitis. Resp. Ex. H at 1. He addressed Dr.

Rubenstein’s opinion that normal imaging or CSF does not rule out TM noting that one study

showed only two out of forty-seven participants with normal imaging and another study showed

two out of thirty-eight subjects with normal imaging, but they had CSF abnormalities consistent

with inflammation. Resp. Ex. H at 1; Resp. Ex. H Tab 2; 41 Resp. Ex. H at 1; Resp. Ex. H Tab

37

J. Sellner et al., Diagnostic Workup of Patients with Acute Transverse Myelitis: Spectrum of Clinical

Presentation, Neuroimaging and Laboratory Findings, 47 SPINAL CORD 312 (2009), filed as “Pet. Ex. 49”.

38

Naoko Nakamura et al., Neurologic Complications Associated with Influenza Vaccination: Two Adult Cases, 42

INTERNAL MEDICINE 191 (2003), filed as “Resp. Ex. A Tab 1”.

39

A.J. Larner & S.F. Farmer, Myelopathy Following Influenza Vaccination in Inflammatory CNS Disorder Treated

with Chronic Immunosuppression, 7 EUROPEAN J. NEUROLOGY 731 (2000), filed as “Resp. Ex. A Tab 2”.

40

Bakshi & Mazziotta, supra note 32.

41

F.S. Pidcock, MD et al., Acute Transverse Myelitis in Childhood: Center-Based Analysis of 47 Cases, 68

19

3. 42 He also addressed Sellner et al., submitted by Dr. Rubenstein, stating that only two out of

sixty-three subjects in the study had normal imaging and normal CSF findings but all had

sensory disturbances. Resp. Ex. I at 1; Pet. Ex. 49. 43 Summarily, Dr. Sweeney opined that the

combination of “the lack of bladder involvement, the absence of sensory abnormalities, the

normal CSF WBC count and protein level, and the normal MRI of the spinal cord” all make a

diagnosis of TM “extremely unlikely.” Resp. Ex. H at 1.

Further, Dr. Sweeney pointed to Dr. Alper’s record documenting that petitioner’s

bilateral sensory symptoms and left leg weakness did not localize well, meaning that Dr. Alper

felt that a single lesion could not explain the constellation of findings. Resp. Ex. I at 1. Dr.

Sweeney disagreed that a lesion too small to be seen on MRI was capable of causing what Dr.

Rubenstein referred to as significant neurological dysfunction. Further, a lesion responsible for

causing all petitioner’s symptoms “would also be predicted to cause other symptoms that were

not seen [], such as a sensory level and bowel/blader dysfunction.” Id. Dr. Sweeney concluded

that the etiology of petitioner’s weakness and hyperreflexia were unclear but not consistent with

TM. Resp. Ex. A at 5.

e. Summary on Diagnosis

As to whether petitioner suffered from TM, the following conclusions are reached after a

complete review of the evidence filed.

The diagnostic criteria for a diagnosis of TM are clear and include acute or subacute

motor, sensory, and autonomic spinal cord dysfunction. Pet. Ex. 29 at 1. 44 Symptoms evolve

over the course of hours to days and are usually bilateral but can be unilateral and asymmetric.

Id. at 2. The finding of one or more intrinsic cord lesions, which usually enhance with

gadolinium, on MRI is characteristic of myelitis. Id.

Frohman & Wingerchuk describe TM as a “heterogeneous group of inflammatory

disorders characterized by acute or subacute motor, sensory, and autonomic (bladder, bowel, and

sexual) spinal cord dysfunction”. Pet. Ex. 29 at 1. They further document that the “pathological

hallmark of [TM] is the presence of focal collections of lymphocytes and monocytes, with

varying degrees of demyelination, axonal injury, and astroglial and microglial activation, within

the spinal cord.” Id. Clinical symptoms of myelopathy may include urinary incontinence or

retention, bowel incontinence or constipation, sexual dysfunction, altered pain and temperature

sensations, paresthesias, and paroxysmal tonic spasms. Id. at 2. They noted that “[c]linical events

that are consistent with” TM without associated CSF or MRI abnormalities “and that have no

identifiable underlying cause are categorized as possible idiopathic transverse myelitis.” Id.,

Table 1.

NEUROLOGY 1474 (2007), filed as “Resp. Ex. H Tab 2”.

42

Terrence Thomas, MD et al., The Demographic, Clinical, and Magnetic Resonance Imaging (MRI) Features of

Transverse Myelitis in Children, 27 J. CHILD NEUROLOGY 11 (2012), filed as “Resp. Ex. H Tab 3”.

43

Sellner et al., supra note 37.

44

Frohman & Wingerchuk, supra note 5.

20

During his September 2015 hospitalization, petitioner underwent extensive testing, all of

which was normal, including normal MRIs and normal CSF studies. Pet. Ex. 5 at 24-25, 26, 31,

80, 137-39, 150-54, 166-69. He had none of the associated autonomic and sudomotor symptoms

characteristic of TM. Id. at 82, 84, 100, 177. He showed questionable sensory deficit to pinprick

and mild motor dysfunction of the lower left extremity, but reflexes were intact. Id. at 33, 38, 40-

41, 65, 80. Succinctly, petitioner showed none of the “pathological hallmark[s]” of TM. Pet. Ex.

29 at 1-2. 45 His medical records specifically document TM as a presumed diagnosis based on

clinical presentation, which is why he was treated with steroids. Pet. Ex. 5 at 31. Though his

condition improved with the steroids, a response to steroids alone does not support a diagnosis of

or constitute proof of demyelinating disease. As explained by Dr. Shah, steroids are an effective

treatment of a wide variety of conditions, injuries, and illnesses, including lymphedema. Pet. Ex.

31 at 5; Pet. Ex. 41; 46 Pet. Ex. 42. 47

Petitioner’s medical record documents that a “presumptive diagnosis of early transverse

myelitis was made based on his symptoms and his recent URI symptoms.” Pet. Ex. 5 at 31. On

follow up examination one month later, he was referred to as having “[i]mproving transient

myelitis.” Pet. Ex. 3 at 3-4. Three months later, in December of 2015, he was “completely fine”,

had returned to all activities with no neurological symptoms to report. Pet. Ex. 5 at 422-23. Dr.

Alper noted some swelling of the left ankle at that time and began to question the earlier myelitis

diagnosis. Pet. Ex. 10 at 25-27. In April of 2016, Dr. Alper again questioned the “presumed”

diagnosis of TM writing that petitioner’s symptoms in September could have been a result of the

beginning of his edema which manifested as numbness, but that would not explain the clonus or

the right-sided complaints. Id. at 14-15.

Dr. McCormick explained that he included Dr. Alpers’ findings in his notes because the

lymphedema was a new finding and was why he was evaluating petitioner; he noted petitioner

was hospitalized in September of 2015 but it was not for lymphedema. Pet. Ex. 13 at 21-22. He

also included the facts that informed his thinking about petitioner’s case, including petitioner’s

presentation of only one swollen leg, no joint swelling, no fever, no rash, no shortness of breath,

no loss of appetite, etc. The general screening questions were designed to ascertain whether the

unilateral leg swelling was part of a larger process like a systemic illness, a rheumatological

disorder, or an oncologic disorder for example. Id. at 22-23. Petitioner’s presentation and his

earlier testing ruled out those conditions, including systemic illness. Id. at 23-24.

The totality of the evidence does not preponderate in favor of a finding that petitioner

suffered from TM. When objective testing does not meet the diagnostic criteria for the disease,

the impressions of the treating physicians are particularly persuasive. Here, the treating

physicians referred to “presumptive” TM in light of presentation attributing it to a recent URI

and later referred to as “[i]mproving transient myelitis.” Pet. Ex. 5 at 31; Pet Ex. 3 at 3-4. The

September 2015 hospital discharge diagnosis was “[w]eakness of left lower extremity”—not

TM. Pet. Ex. 5 at 30-33. In December 2015, Dr. Alper questioned the TM diagnosis and by April

45

Id.

46

N.C.M. Fyfe, F.R.C.S. et al., Intralymphatic Steroid Therapy for Lymphoedema: Preliminary Studies, 15

LYMPHOLOGY 23 (1982), filed as “Pet. Ex. 41”.

47

Stanley G. Rockson et al., Pilot Studies Demonstrate the Potential Benefits of Antiinflammatory Therapy in

Human Lymphedema, 3 JCI INSIGHT e123775 (2018), filed as “Pet. Ex. 42”.

21

2016, she considered that his September 2015 symptoms may have been early, mild edema

manifesting as numbness rather than TM. Pet. Ex. 5 at 422-24; Pet. Ex. 10 at 14-15. Dr.

McCormick referred to petitioner’s lymphedema as “new” at the time he examined him in

September 2016 and not related to his hospitalization in September 2015 with testing at that time

ruling out other conditions including systemic illness. Pet. Ex. 13 at 21-24.

Dr. Rubenstein submitted that TM is a “diagnosis of exclusion”. Pet. Ex. 27 at 3, quoting

Pet. Ex. 28 at 7. 48 However, the study on which Dr. Rubenstein relied contained this statement in

the context of “[i]nflammatory transverse myelitis” where CSF shows inflammation and in the

absence of a specific cause; here, petitioner had normal CSF findings. Pet. Ex. 28 at 7; Pet. Ex. 5

at 24-25, 26, 31, 80, 137-39, 150-54, 166-69. Dr. Rubenstein’s opinion that petitioner had TM

may have been more persuasive if petitioner met some of the diagnostic criteria or if petitioner’s

treating physicians believed TM was the correct diagnosis. It would not be reasonable to accept

TM as the diagnosis here in the absence of the “hallmark[s]” of the disease, as detailed in the

literature relied on by Dr. Rubenstein. See Pet. Ex. 29. 49 Further, based on the medical records, it

is clear that petitioner’s treaters were not confident that he actually had TM. See Pet. Ex. 5 at 30-

33, 422-24; Pet Ex. 3 at 3-4; Pet. Ex. 10 at 14-15.

I found the opinion of respondent’s expert, Dr. Sweeney, to be more persuasive on the

issue of diagnosis. He agreed that there are reports of TM following flu vaccination but

submitted that there is no support for a post-influenza myelitis without findings on imaging or

evidence of inflammation on CSF. Resp. Ex. A at 3; Resp. Ex. A Tab 1; 50 Resp. Ex. A Tab 2;51

Resp. Ex. A Tab 3; 52 Resp. Ex. I at 2. Without objective findings to support the diagnosis, in

addition to the lack of autonomic or sudomotor changes, it is extremely unlikely that petitioner

had TM. Resp. Ex. A at 3-5.

Based on the totality of evidence filed—the medical records, opinions of the treating

physicians and experts, and the literature—there is not preponderant evidence to support that

petitioner suffered from TM or an inflammatory spinal process.

B. Althen Prongs

Because petitioner does not allege an injury listed on the Vaccine Injury Table, his claim

is classified as “off-Table.” As noted above, for petitioner to prevail on an “off-Table” claim, he

must show by preponderant evidence that his claimed injury resulted from the vaccination at

issue. Capizzano, 440 F.3d at 1320. Doing so shifts the burden to respondent to show that the

injury was caused by factors unrelated to the vaccination. Deribeaux, 717 F.3d at 1367.

Presenting a sound and reliable theory is essential to petitioner’s case. A theory causally

connecting the vaccine to the injury is the first Althen prong. When petitioner fails to establish

this element, compensation is denied. Boatmon v. Sec’y of Health & Human Servs., 941 F.3d

48

Jacob & Weinshenker, supra note 30.

49

Frohman & Wingerchuk, supra note 5.

50

Nakamura et al., supra note 38.

51

Larner & Farmer, supra note 39.

52

Bakshi & Mazziotta, supra note 32.

22

1351, 1360-62 (Fed. Cir. 2019). Moreover, the theory advanced for Althen prong one influences

the remaining two Althen prongs. For the second Althen prong, which addresses whether a

logical sequence connects the vaccine to the injury, special masters may consider whether the

vaccinee responded in a way consistent with the theory being offered. Hibbard v. Sec’y of Health

& Human Servs., 698 F.3d 1355, 1364 (Fed. Cir. 2012); Miller v. Sec’y of Health & Human

Servs., 172 Fed. Cl. 762, 784 (2024) (finding special master did not err in denying entitlement

when petitioner did not establish that she had immune complexes after asserting a theory

involving immune complexes); Dodd v. Sec’y of Health & Human Servs., 114 Fed. Cl. 43, 52-57

(2013); La Londe v. Sec’y of Health & Human Servs., 110 Fed. Cl. 184, 205 (2013), aff’d, 746

F.3d 1334 (Fed. Cir. 2014). Similarly, the third Althen prong, which concerns timing, depends at

least in part upon the theory being offered. Langland v. Sec’y of Health & Human Servs., 109

Fed. Cl. 421, 443 (2013); see also Koehn v. Sec’y of Health & Human Servs., 773 F.3d 1239,

1244-45 (Fed. Cir. 2014) (holding that special master was not arbitrary in finding an onset of

injury seven months after vaccination was incompatible with a theory based upon cytokines).

Without a defined theory, attempting to determine whether preponderant evidence supports the

logical sequence or timing is difficult if not impossible.

The parties never addressed the consequences of a finding that petitioner did not suffer

from TM or an inflammatory myelitis. Rather, they focused on whether petitioner did or did not

have TM, how individual symptoms or subjective complaints did or did not satisfy the diagnostic

criteria of TM, and the various explanations as to why petitioner had TM despite the lack of any

objective findings.

It is undisputed that petitioner suffers from lymphedema of the left leg. The remaining

issues to be resolved is whether a flu vaccine can cause lymphedema and to a lesser extent,

whether petitioner’s lymphedema is primary or secondary lymphedema. To that end, I find that

petitioner’s flu vaccine played no role in his development of lymphedema.

a. Petitioner Has Not Provided a Sound and Reliable Medical Theory

The first Althen prong requires petitioner to provide a “reputable medical theory”

demonstrating that the vaccines received can cause the type of injury alleged. Pafford, 451 F.3d

at 1355-56 (citation omitted). To satisfy this prong, petitioner’s “theory of causation must be

supported by a ‘reputable medical or scientific explanation.’” Andreu ex rel. Andreu v. Sec’y of

Health & Human Servs., 569 F.3d 1367, 1379 (Fed. Cir. 2009) (quoting Althen, 418 F.3d at

1278). This theory need only be “legally probable, not medically or scientifically certain.” Id. at

1380 (emphasis omitted) (quoting Knudsen, 35 F.3d at 548). This standard was recently clarified

by the Federal Circuit. See Boatmon, 941 F.3d at 1359-60 (stating that the correct standard for

Althen prong one is “reputable,” and “sound and reliable” not a “lower reasonable standard”

(internal quotations omitted)). Nevertheless, “petitioners [must] proffer trustworthy testimony

from experts who can find support for their theories in medical literature.” LaLonde v. Sec’y of

Health & Human Servs., 746 F.3d 1334, 1341 (Fed. Cir. 2014).

Special masters may consider the relative expertise of testifying experts when weighing

the value of their opinion. See Depena v. Sec’y of Health & Human Servs., No. 13-675V, 2017

WL 1075101 (Fed. Cl. Spec. Mstr. Feb. 22, 2017), mot. for rev. denied, 133 Fed. Cl. 535, 547-48

23

(2017), aff'd without op., 730 Fed. App'x 938 (Fed. Cir. 2018); Copenhaver v. Sec’y of Health &

Human Servs., No. 13-1002V, 2016 WL 3456436 (Fed. Cl. Spec. Mstr. May 31, 2016), mot. for

rev. denied, 129 Fed. Cl. 176 (2016).

Petitioner presents two different causation theories. First, Dr. Rubenstein submits that the

flu vaccine caused petitioner’s TM and the damage from TM caused him to develop

lymphedema. Second, Dr. Shah opines that the flu vaccine caused an inflammatory response that

caused petitioner to develop lymphedema.

Petitioner’s first causation theory hinges on the presence of spinal cord myelitis.

Specifically, Dr. Rubenstein’s theory is predicated on petitioner having suffered from TM. He

opined that the flu vaccine caused petitioner’s TM which subsequently resulted in his

development of secondary left leg lymphedema due to the improper functioning of the

sympathetic nervous system, 53 which is a complication of spinal cord myelitis and likely

occurred during the process of sympathetic re-innervation. 54 Pet. Ex. 27 at 4-5; Reply at 8. He

submitted that re-innervation following the nerve damage caused by the TM led to dysregulation

of lymphatic flow in the left lower extremity where the TM symptoms localized, causing

secondary lymphedema. Id. Dr. Rubenstein failed to explain how a flu vaccine could have

caused lymphedema in the absence of TM.

According to Dr. Rubenstein petitioner’s lymphedema was “a complication of

‘dysfunction’ of the sympathetic nervous system. In other words, this was not a matter of a

simple increase or decrease in sympathetic outflow but of improper functioning of the

sympathetic nervous system as a complication of spinal myelitis”. Pet. Ex. 27 at 4-5. Using

complex regional pain syndrome (“CRPS”) as an example, Dr. Rubenstein explained that

“improper ‘wiring’” can cause lymphedema in a patient with re-innervation after spinal myelitis

just as it can cause pain in a patient with CRPS. Id. at 5. He argued that “there is every reason to

think that sympathetic dysfunction in the context of TM could likewise lead to secondary

lymphedema.” Pet. Ex. 30 at 3. Importantly, Dr. Rubenstein failed to propose a theory of

sympathetic dysfunction causing secondary lymphedema outside the context of TM.

Dr. Rubenstein’s opinions for the most part are no longer relevant since they depend on a

finding that petitioner suffered from TM or spinal cord inflammation. As detailed at length

above, there is not preponderant evidence that petitioner suffered from TM or spinal cord

53

The sympathetic nervous system is the portion of the autonomic nervous system that receives its fibers of

connection with the central nervous system through the thoracolumbar outflow of visceral efferent fibers. These

fibers (preganglionic fibers) arise from cells in the thoracic and upper lumbar levels of the spinal cord, leave by way

of ventral roots, and, by way of rami communicantes, enter sympathetic trunks, where some synapse with ganglion

cells. Distal to these ganglia, there are postganglionic fibers that either return to spinal nerves by way of rami

communicantes to supply blood vessels, smooth muscles, and glands of the trunk and limbs, or go as visceral

branches to blood vessels, smooth muscles, glands of the head and neck, and viscera of the thorax, abdomen, and

pelvis. Some preganglionic fibers pass through the sympathetic trunks and synapse in the prevertebral ganglia;

postganglionic fibers from those ganglia supply adjacent viscera. Sympathetic nervous system, Dorland’s Medical

Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=111901&searchterm=sympathetic+nervous+system.

54

Reinnervation is the restoration of nerve function to a part from which it was lost; it may occur spontaneously or

be achieved by nerve grafting. Reinnervation, Dorland’s Medical Dictionary Online,

https://www.dorlandsonline.com/dorland/definition?id=43257&searchterm=reinnervation.

24

inflammation/myelitis. However, even if objective evidence existed that supported TM or spinal

cord inflammation, and assuming Dr. Rubenstein’s theory based on molecular mimicry was

sufficient to prove that flu vaccine can cause TM, there is not preponderant evidence to support

the remainder of Dr. Rubenstein’s theory that petitioner’s left leg lymphedema that developed

three months after his September 2015 symptoms was “a direct complication of dysfunction of

the peripheral sympathetic nervous system” resulting from his TM. Pet. Ex. 14 at 4.

Dr. Shah built his opinion on Dr. Rubenstein’s causation theory “assuming Dr.

Rubenstein’s description of the effects of TM on the sympathetic nervous system is accurate, it

would then follow that this type of sympathetic nervous system dysfunction could cause or

exacerbate lymphedema . . . particularly [in a patient like petitioner] who was already very likely

developing lymphedema as a direct side effect of the vaccine.” Pet. Ex. 51 at 1. He opined that it

is most likely that petitioner had an abnormal inflammatory response to the vaccine, causing both

his TM and lymphedema, “with the lymphedema exacerbated by damage to the sympathetic

nervous system as outlined by Dr. Rubenstein.” Id. at 2; Pet. Ex. 31 at 4, 5. “Since transverse

myelitis is known to result from inflammation of the spinal cord, it is highly probable that the

same inflammatory process that triggered spinal cord inflammation and transverse myelitis

subsequently resulted in an inflammatory process in the lymphatic system thus triggering

lymphedema . . .”. Pet. Ex. 31 at 5.

While conceding that no literature points to causality between lymphedema and flu

vaccines, Dr. Shah argued that “one can largely conclude that [petitioner]’s lymphedema was

secondary lymphedema” in that “his lymphedema was in all likelihood secondary to an external

cause whether that be trauma, surgery, radiation, infection or any other inflammatory cause.” Pet

Ex. 51 at 3. Dr. Shah opined that TM is the result of inflammation of the spinal cord making it

“highly probable” that the inflammatory process that caused petitioner’s TM progressed over

time and slowly caused obstructed lymphatic channels that the body relies on for drainage of

lymph fluid. Pet. Ex. 31 at 5. Even after the inflammatory process ends, obstruction can persist

resulting in edema. The lack of any other factor that could trigger secondary lymphedema is

notable, “as should the consistency of [petitioner’s] vascular symptoms with the theory of post-

vaccinal inflammation.” Pet. Ex. 31 at 5; Pet. Ex. 44. 55

As to the second proposed causation theory, Dr. Shah stated that having ruled out other

obvious causes and “given the well accepted fact that the flu vaccine can cause excessive

systemic inflammation in a small number of patients, it is reasonable to conclude that the flu shot

resulted in a pathological inflammatory reaction resulting in secondary lymphedema.” Pet. Ex.

51 at 3; Pet. Ex. 52. 56 He added that whatever the correct diagnosis for petitioner’s neurological

55

Ly et al., supra note 9.

56

“This study examined the extent to which baseline inflammatory status predicted subjective symptoms and the

extent to which subjective symptoms corresponded with objective inflammatory responses in the days following

receipt of a flu vaccine.” The sample included 56 women, 28 of whom were pregnant. Id. at 6. Previous studies

showed that inflammatory responses to flu infection are more severe in females than in males. Id. at 8. The

researchers found that reports of subjective symptoms following vaccination (like pain or systemic symptoms) are

“accompanied by measurable differences in vaccine-induced serum proinflammatory cytokine responses as well as

some possible associations with body temperature.” Id. Given the study’s conclusion that subjective complaints of

symptoms correspond with objective markers of inflammation, it is not clear how this study supports Dr. Shah’s

proposition that petitioner—who had no subjective symptoms or objective testing indicative of inflammation—had a

25

symptoms, “they provide strong evidence of a systemic inflammatory response to the vaccine

given that they followed it so closely in time.” Pet. Ex. 51 at 3. There is no other “stronger

causation” for petitioner’s unilateral edema of his entire left leg. Id.

Dr. Shah claimed that his inflammation theory of causation was proposed “as an

independent cause of [petitioner’s] symptoms irrespective of the diagnosis of transverse

myelitis.” Pet. Ex. 51 at 3. Dr. Shah contended that his opinion and Dr. Rubenstein’s were

consistent but added that in general, inflammation caused by a vaccine could lead to

lymphedema. Id. at 1. “This process can operate alongside and can be exacerbated by the one

described by Dr. Rubenstein.” Id. at 1-2.

Dr. Shah added that there is “much supporting literature” to support flu vaccines causing

inflammatory reactions citing to only one article. Id. at 4; Pet. Ex. 52. 57 Such an inflammatory

response could result in secondary lymphedema, and petitioner suffered “an episode of systemic

inflammation in the fall of 2015”. Pet. Ex. 51 at 4. Dr. Shah claimed that studies have associated

lymphedema with an inflammatory process, but failed to explain how this can occur. Pet. Ex. 31

at 5.

Dr. Sweeney focused mainly on refuting the diagnosis of TM but also stated that the loss

of sympathetic innervation has not been shown to be a driver of peripheral edema. Resp. Ex. A at

4; Resp. Ex. A Tab 5; 58 Pet. Ex. 53. 59 Dr. Sweeney maintained that lymphedema without the

presence of other autonomic disturbances is unlikely to be caused by alterations in sympathetic

innervation to a limb. Resp. Ex. A at 5. Most importantly, the proposed mechanism of

sympathetic reinnervation elucidated here is not described in any literature. Resp. Ex. C at 3.

Dr. Sweeney added that even if he accepted the TM diagnosis, he could not “find a

plausible link between myelitis and lymphedema”, particularly when the lymphedema presented

three months later. Resp. Ex. H at 2. There is no literature that shows myelitis to be associated

with lymphedema or how it would present three months later. Id.

Dr. Hicks disagreed with Dr. Shah’s opinion that the flu vaccine caused systemic

inflammation that resulted in TM and lymphedema; rather, she believed the two were

coincidental and that petitioner’s lymphedema is likely primary lymphedema. Resp. Ex. G at 3.

Dr. Hicks noted Dr. Shah’s acknowledgment that primary lymphedema affects about 1.2 per

100,000 people and that no reports exist tying TM to secondary lymphedema or that a cause and

effect relationship has ever being observed. Id.; Resp. Ex. G Tab 3. 60 Further, there is no

literature that supports flu vaccine as a cause of lymphedema. Resp. Ex. D at 6. She explained

that “[l]ymphedema is a disease of the lymphatic network, not the nervous system. . . While it is

theoretically possible that sympathetic nervous system dysfunction may somehow be associated

“pathological inflammatory reaction resulting in secondary lymphedema.” Pet. Ex. 51 at 3.

57

See id.

58

Douglas Howarth, M.D. et al., Autonomic Regulation of Lymphatic Flow in the Lower Extremity Demonstrated on

Lymphoscintigraphy in Patients with Reflex Sympathetic Dystrophy, 24 CLINICAL NUCLEAR MEDICINE 383 (1999),

filed as “Resp. Ex. A Tab 5”.

59

Noel McHale, Nervous Control of the Lymphatic System, 4 VASCULAR MEDICINE REVIEW 307 (1993), filed as

“Pet. Ex. 53”.

60

Smeltzer et al., supra note 8.

26

with lower extremity swelling, it is highly unlikely that ‘improper crosstalk among neurons and

neural groups can produce a variety of symptoms, including lymphedema.’” Id.

As already noted, petitioner’s theory of causation is largely predicated on a finding that

petitioner had TM and that his TM was caused by the flu vaccine. Thus, my finding that

petitioner did not suffer from TM dramatically undercuts his claim. “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, although the explanation need only be ‘legally

probable, not medically or scientifically certain.’” Broekelschen, 618 F.3d at 1345 (quoting

Knudsen, 35 F.3d at 548-49). The basis of the theory proposed by Dr. Rubenstein and accepted

by Dr. Shah was that petitioner had inflammation of the spinal cord, which caused sympathetic

reinnervation and ultimately lymphedema. Because I found no evidence to support the diagnosis

of TM or inflammation of the spinal cord, this theory fails.

The remaining theory implicating a systemic inflammatory response to the vaccine is

insufficient to meet petitioner’s burden. Vaccines are meant to cause an inflammatory response,

which is how antibodies are generated and what makes vaccines effective. Similar theories

involving excessive inflammation have been accepted as persuasive in other vaccine cases.

However, here, the theory was underdeveloped and insufficient. Conclusory assertions that a

petitioner suffered an abnormal inflammatory response after a vaccine with nothing more are

insufficient to meet petitioner’s burden under Althen prong one. Further, petitioner’s experts

provided no persuasive evidence to support any connection between a flu vaccine, a subsequent

inflammatory response, and lymphedema. Accordingly, petitioner has failed to satisfy prong one.

b. Petitioner Has Not Demonstrated a Logical Sequence of Cause and Effect

The second Althen prong requires proof of a “logical sequence of cause and effect.”

Capizzano, 440 F.3d at 1326 (quoting Althen, 418 F.3d at 1278). In other words, even if the

vaccinations can cause the injury, petitioner must show “that it did so in [this] particular case.”

Hodges v. Sec’y of Health & Human Servs., 9 F.3d 958, 962 n.4 (Fed. Cir. 1993) (citation

omitted). “A reputable medical or scientific explanation must support this logical sequence of

cause and effect,” id. at 961 (citation omitted), and “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,” Paluck v. Sec’y of Health & Human Servs., 786 F.3d

1373, 1385 (Fed. Cir. 2015) (quoting Andreu, 569 F.3d at 1375). Petitioner is not, however,

required “to eliminate alternative causes as part of establishing [their] prima facie case.” Doe v.

Sec’y of Health & Human Servs., 601 F.3d 1349, 1357-58 (Fed. Cir. 2010); see Walther v. Sec’y

of Health & Human Servs., 485 F.3d 1146, 1152 (Fed. Cir. 2007) (holding that a “petitioner does

not bear the burden of eliminating alternative independent potential causes”).

Petitioner here proposed two theories of causation. Not only do I not find either theory to

be sound and reliable, but I also do not find either theory to be consistent with petitioner’s

medical history. Succinctly, without objective proof of a neurological injury as the cause of

petitioner’s September 2015 symptoms, Dr. Rubenstein’s theory of improper functioning of the

sympathetic nervous system as a complication of spinal myelitis, likely occurring during the

process of sympathetic re-innervation resulting in secondary lymphedema, fails on prong two.

27

See Pet. Ex. 27 at 4-5. Dr. Shah’s additional theory that petitioner suffered a systemic

inflammatory process that led to his development of secondary lymphedema also fails as there is

no evidence to support that petitioner suffered from an excessive, abnormal inflammatory

response to the vaccine. See Pet. Ex. 51 at 3; see also Pet. Ex. 13 at 24-27 (Dr. McCormick

explaining that the Schmorl’s nodes seen on petitioner’s MRI were non-enhancing therefore not

inflamed, meaning that they had been “stable” for some time.). Dr. Sweeney pointed out that

there was no evidence of inflammation; rather, petitioner had normal CSF testing and normal

MRI, little reported sensory loss, numbness, and/or weakness, and no bowel, bladder, or sexual

dysfunction, or pain. Resp. Ex. A at 3-4, Resp. Ex. H at 1, 2; Resp. Ex. H Tab 2; 61 Resp. Ex. H

Tab 3; 62 Resp. Ex. H Tab 4. 63

Petitioner developed tingling and numbness of his left lower leg three weeks after his

receipt of the subject flu vaccine. Pet. Ex. 3 at 5; Pet. Ex. 5 at 39. He had slightly decreased

motor strength in the left lower extremity and diminished pinprick and light touch sensation in

both feet. Pet. Ex. 5 at 40-42. All testing was normal. Id. at 24-26, 31, 35, 80, 137-39, 150-54,

166-69. Despite negative testing but because of his presentation and recent upper respiratory

infection, “[a] presumptive diagnosis of early transverse myelitis was made”. Id. at 31. His

symptoms improved with steroid treatment, and he was stable upon discharge. Id. at 31, 34-36,

40. The discharge diagnosis was “[w]eakness of left lower extremity” not TM. Id. at 36.

Thereafter, petitioner was “completely fine” and resumed his regular activities. Pet. Ex. 5

at 422-23. However, on December 3, 2015, at a follow up visit, Dr. Alper noted left ankle

swelling and a few beats of clonus. Id. 422-24. Petitioner underwent further testing, which

showed no significant abnormalities. Id. at 105-08.

Three months later, on February 20, 2016, petitioner was then hospitalized for left leg

swelling since December 2015 that had increased in the last few days. Pet. Ex. 5 at 10. MRIs of

the thoracic and lumbar spine were normal. MRI of the pelvis showed left iliac vein compression

by the right iliac artery. Id. at 10, 15, 127-28. The discharge diagnosis was swelling of the lower

extremity. Id. at 10-11, 13.

Petitioner’s left leg swelling increased throughout the following months. Pet. Ex. 3 at 2;

Pet. Ex. 4 at 2-3; Pet. Ex. 6 at 3-4, 6; Pet. Ex. 8 at 19-20; Pet. Ex. 10 at 6. The lymphedema

diagnosis was confirmed following a lymphoscintigraphy performed in June 2016 and an MRI/A

performed in October 2016. Pet. Ex. 6 at 7, 8-9; Pet. Ex. 8 at 27-28.

Summarily, petitioner’s MRIs did not indicate myelitis or any other inflammatory

process. Likewise, petitioner’s CSF studies refute the notion that there was an ongoing

inflammatory response with the WBC within normal limits. Pet. Ex. 5 at 80, 150-154. Thus, the

objective test results refuted petitioner’s main theory that he had TM which caused lymphedema

61

Pidcock et al., supra note 41.

62

Thomas et al., supra note 42.

63

Thomas F. Scott et al., Acute Partial Transverse Myelitis with Normal Cerebral Magnetic Resonance Imaging:

Transition Rate to Clinically Definite Multiple Sclerosis, 11 MULTIPLE SCLEROSIS 373 (2005), filed as “Resp. Ex. H

Tab 4”.

28

as well as the secondary theory that he had an abnormal inflammatory response to the vaccine

which caused his lymphedema.

Further, none of petitioner’s treating physicians associated his leg swelling with his flu

vaccine or with the symptoms he had in September 2015 other than to question whether he in

fact had the early manifestations of lymphedema in September of 2015. See Pet. Ex. 10 at 14-15

(Dr. Alper questioning whether vascular issues may have been the cause of the neurological

symptoms in September of 2015 rather than the other way around). Instead, petitioner’s treating

providers opined that petitioner had primary lymphedema, which is consistent with respondent’s

position. Pet. Ex. 6 at 4 (noting Dr. McEnaney’s impression of May Thurner syndrome v.

primary lymphedema); Pet. Ex. 10 at 15 (Dr. Alper noting that the lower leg swelling/edema was

possibly lymphedema without explanation and no underlying diagnosis); Pet. Ex. 13 at 21-24, 45

(Dr. McCormick including Dr. Alpers’ findings and petitioner’s hospitalization in September of

2015 not for lymphedema and with larger processes like systemic illness, rheumatological

disorder, or an oncological disorder ruled out; stating that after examining petitioner, that he

believed he “fits the category of primary lymphedema”); see also Resp. Ex. D at 6; Resp. Ex. G

at 3 (Dr. Hicks opining that petitioner most likely had “pre-existing primary lymphedema” that

began to manifest as he entered adolescence).

While there are incidences where vaccines cause excessive inflammatory responses

resulting in injuries through the mechanisms highlighted by Dr. Rubenstein and Dr. Shah, there

is no objective evidence in this case that the flu vaccine administered to petitioner caused an

excessive systemic inflammatory response three weeks after vaccination.

Accordingly, petitioner has failed to provide a logical sequence of cause and effect

connecting the subject flu vaccine to either his symptoms in September 2015 or his leg swelling

ultimately diagnosed as lymphedema. Thus, petitioner has failed to satisfy Althen prong two.

c. Petitioner Has Not Demonstrated a Proximate Temporal Relationship

To satisfy the third Althen prong, petitioner must establish a “proximate temporal

relationship” between the vaccination and the alleged injury. Althen, 418 F.3d at 1281. This

“requires preponderant proof that the onset of symptoms occurred within a timeframe for which,

given the medical understanding of the disorder’s etiology, it is medically acceptable to infer

causation-in-fact.” de Bazan, 539 F.3d at 1352. Typically, “a petitioner’s failure to satisfy the

proximate temporal relationship prong is due to the fact that onset was too late after the

administration of a vaccine for the vaccine to be the cause.” Id. However, “cases in which onset

is too soon” also fail this prong; “in either case, the temporal relationship is not such that it is

medically acceptable to conclude that the vaccination and the injury are causally linked.” Id.; see

also Locane v. Sec’y of Health & Human Servs., 685 F.3d 1375, 1381 (Fed. Cir. 2012) (“[If] the

illness was present before the vaccine was administered, logically, the vaccine could not have

caused the illness.”).

Other than concluding that the “best supported hypothesis” in this case was that

petitioner’s lymphedema was the direct result of his TM which occurred 22 days after a flu

29

vaccine, Dr. Rubenstein did not discuss the medically appropriate timeframe for a flu vaccine

causing TM, TM causing lymphedema, or a flu vaccine causing lymphedema. Pet. Ex. 14 at 4.

Dr. Shah opined that the onset of petitioner’s lower leg edema was on or around

December 3, 2015, consistent with his theory of lymphedema secondary to vaccine-induced

inflammation, “since a systemic inflammatory process affecting the lymphatic system would

require anywhere from several weeks to several months’ time to manifest itself as clinically

significant lower extremity edema.” Pet. Ex. 51 at 2. He further argued that Dr. Alper’s

suggestion that petitioner’s lymphedema may have begun in September 2015 was speculative

with no objective support in the medical records and no treating physician examining petitioner

having noted any left leg swelling. Id.; Pet. Ex. 10 at 14-15.

Dr. Sweeney did not discuss timing. Dr. Hicks wrote that “[w]hile there is a very loose

(months) temporal relationship between vaccination and [petitioner’s] symptoms, temporal

relationships do not mandate causation.” More likely, petitioner developed primary

lymphedema/praecox in the months following the flu vaccine. The onset of petitioner’s

lymphedema is consistent with the literature for onset of lymphedema praecox, “whereas a

causal pathway between vaccination, transverse myelitis, and secondary lymphedema has never

been described.” Resp. Ex. J at 3; see also Resp. Ex. G Tab 6; 64 Resp. Ex. J Tab 5; 65 Resp. Ex. J

Tab 6. 66

Given the findings that petitioner did not have TM and did not meet Althen prongs one or

two, petitioner’s claim necessarily fails on prong three as well. Petitioner failed to present

persuasive evidence regarding any causal association between a flu vaccine, his September 2015

symptoms, and lymphedema—much less a medically appropriate timeframe for onset. As such,

petitioner has failed to prove prong three.

VI. Conclusion

Upon careful evaluation of all the evidence submitted in this matter—including the

medical records, expert reports, medical literature, and other submitted arguments—I conclude

that petitioner has not shown by preponderant evidence that he is entitled to compensation under

the Vaccine Act. The Clerk shall enter judgment accordingly. 67

IT IS SO ORDERED.

s/ Mindy Michaels Roth

Mindy Michaels Roth

Special Master

64

Carolyn C. Schook, B.A. et al., Primary Lymphedema: Clinical Features and Management in 138 Pediatric

Patients, 127 PLASTIC RECONSTRUCTION SURGERY 2419 (2011), filed as “Resp. Ex. G Tab 6”.

65

Isabelle Quere, M.D., Ph.D. et al., Incidence of Cellulitis Among Children with Primary Lymphedema, 378 N.

ENG. J. MEDICINE 2047 (2018), filed as “Resp. Ex. J Tab 5”.

66

Colmant et al., supra note 17.

67

Pursuant to Vaccine Rule 11(a), entry of judgment can be expedited by each party filing a notice renouncing the

right to seek review.

30