In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
Filed: May 27, 2021
* * * * * * * * * * * * * UNPUBLISHED
ALAN ARCHER, *
* No. 15-656V
Petitioner, *
v. * Special Master Gowen
*
SECRETARY OF HEALTH * Entitlement; Ruling on the Record;
AND HUMAN SERVICES, * Tetanus, diphtheria, and
* acellular pertussis (“Tdap”);
* Transverse Myelitis; Onset.
*
Respondent. *
* * * * * * * * * * * * *
Diana L. Stadelnikas, Maglio Christopher & Toale, Sarasota, FL, for petitioner.
Sarah C. Duncan, U.S. Department of Justice, Washington, D.C., for respondent.
DECISION ON ENTITLEMENT1
On June 24, 2015, Alan Archer (“petitioner”) filed a petition in the National Vaccine
Injury Compensation Program.2 Petition (ECF No. 1). Petitioner alleges that as a result of
receiving the tetanus, diphtheria and acellular pertussis (“Tdap”) vaccine on August 7, 2012, he
suffered transverse myelitis. Id. at ¶¶ 1-6. On March 3, 2020, petitioner filed a motion for a
ruling on the record. Petitioner’s (“Pet.”) Motion (“Mot.”) (ECF No. 76). Respondent filed a
response to petitioner’s motion on June 29, 2020. Respondent’s (“Resp.”) Response to
Petitioner’s Motion for a Ruling on the Record (ECF No. 89). On July 27, 2020, petitioner filed
1
Pursuant to the E-Government Act of 2002, see 44 U.S.C. § 3501 note (2012), because this decision contains a
reasoned explanation for the action in this case, I am required to post it on the website of the United States Court of
Federal Claims. The court’s website is at http://www.uscfc.uscourts.gov/aggregator/sources/7. This means the
decision will be available to anyone with access to the Internet. Before the decision is posted on the court’s
website, each party has 14 days to file a motion requesting redaction “of any information furnished by that party:
(1) that is a trade secret or commercial or financial in substance and is privileged or confidential; or (2) that
includes medical files or similar files, the disclosure of which would constitute a clearly unwarranted invasion of
privacy.” Vaccine Rule 18(b). “An objecting party must provide the court with a proposed redacted version of the
decision.” Id. If neither party files a motion for redaction within 14 days, the decision will be posted on the
court’s website without any changes. Id.
2
The National Vaccine Injury Compensation Program is set forth in Part 2 of the National Childhood Vaccine
Injury Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755, codified as amended, 42 U.S.C. §§ 300aa-10 to 34 (2012)
(hereinafter “Vaccine Act” or “the Act”). Hereinafter, individual section references will be to 42 U.S.C. § 300aa of
the Act.
a reply to respondent’s response. Pet. Reply (ECF No. 91).
After fully reviewing all of the evidence presented in this case and in accordance with the
applicable legal standards, I hereby GRANT petitioner’s motion for a ruling on the record and I
find that petitioner has not established entitlement, thus his petition shall be dismissed.
I. Procedural History
On June 24, 2015, petitioner filed his claim alleging that the Tdap vaccine administered
on August 7, 2012 caused-in-fact the development of transverse myelitis. Petition at Preamble.
On September 2, 2015, I held an initial status conference, ordering petitioner to file additional
medical records to verify the date the vaccine was administered. Scheduling Order (ECF No. 8).
After petitioner filed updated medical records, respondent filed a status report on November 9,
2015 stating, “Based on the review of this case by the Division of Injury Compensation
Programs, Department of Health and Human Services, respondent does not believe that engaging
in settlement discussions with petitioner is appropriate at this time.” Resp. Status Report (ECF
No. 12). As such, the parties were ordered to file expert reports. See Scheduling Order (Nov. 9,
2015).
On October 24, 2016, petitioner filed an expert report by Dr. Agnes Jani-Acasdi3 and
supporting medical literature. Pet. Exs. 18-45 (ECF Nos. 23-47). On April 7, 2017, respondent
filed an expert report by Dr. Peter D. Donofrio4 and supporting medical literature. Resp. Exs. A-
B). Respondent also filed the Rule 4(c) report the same day. Resp. Report (“Rept.”) (ECF No.
31). In the Rule 4(c) report, respondent stated that “petitioner has yet to establish that he has
transverse myelopathy or auto-inflammatory myelopathy…or ‘longitudinally extensive TM or
neuromyelitis optic spectrum disorder (“NMOSD”). Resp. Rept. at 10. Additionally,
respondent also argued that petitioner’s expert, Dr. Jani-Acsadi’s theory is not supported by a
“ ‘reputable’ or ‘reliable’ scientific or medical explanation.” Id. at 11. Respondent further
argues that petitioner has not provided evidence establishing that there was a proximate temporal
relationship between his Tdap vaccination and his alleged injury. Id. at 12. Specifically,
respondent states that petitioner’s expert, “does not specify when the onset of petitioner’s
3
Dr. Agnes Jani-Acsadi, M.D., was a neurologist at the University of Connecticut School of Medicine. Pet. Ex. 19
at 1. Dr. Jani-Acsadi received an undergraduate degree in 1981 and a medical degree from the University Medical
School Pecs in Hungary. Id. While she worked at the University of Wisconsin, she cloned the gene for Duchenne
muscular dystrophy. Id. Dr. Jani-Acsadi completed her residency training in neurology at Wayne State University,
servicing as chief resident and following a neuromuscular fellowship, she was a staff neurologist at Wayne State
University until 2010. Id. She became the Interim Chair for the Department of Neurology at UConn and Hartford
Hospital. Id. Dr. Jani-Acsadi had published multiple articles in the field of neurology, including about chronic
demyelinating polyneuropathy (“CIDP”). Id. at 2-3. Finally, she had a Neuromuscular Medicine Board
Certification. Id. at 2. Unfortunately, Dr. Jani-Acsadi passed away in 2018.
4
Dr. Peter Donofrio is a professor of neurology and Director of Neuromuscular Division at Vanderbilt University
School of Medicine, and Director of the EMG lab at Vanderbilt University Medical Center. Resp. Ex. B. Dr.
Donofrio received his medical degree from Ohio State University School of Medicine in 1975, and completed his
internal medicine residency at Good Samaritan Hospital in Ohio. Id. Dr. Donofrio completed a neurology residency
at the University of Michigan Medical Center and a neuromuscular fellowship at the University of Michigan. Id. He
is board certified in internal medicine, neurology, electromyography and neuromuscular science. Id. Dr. Donofrio
has experience in evaluating and caring for patients with neurological conditions, including transverse myelitis,
Guillain’-Barre syndrome (“GBS”) and CIDP, among others. Id.
2
symptoms occurred and that Dr. Jani-Ascadi notes that “there is uncertainty regarding the
‘proper onset interval at the margins’ such that several days to three months or longer would be
an appropriate latency between vaccination and the onset of symptoms. Id. at 13; Pet. Ex. 18 at
6.
On October 12, 2017, I held another status conference in the case. Order (ECF No. 39).
During this status conference, petitioner stated that he had retained another expert in the case, as
his original expert was no longer able to continue due to a medical disability. Id. The parties
were ordered to file supplemental expert reports. Id.
On March 12, 2018, petitioner filed a supplemental expert report by Dr. Matthew
Imperioli5 and supporting medical literature. Pet. Exs. 52-57. Respondent filed a supplemental
expert report by Dr. Donofrio on August 9, 2018. Resp. Ex. C (ECF No. 66)6. Pursuant to
Vaccine Rule 5, I held a status conference, indicating that the onset of petitioner’s symptoms in
relation to the Tdap vaccination was outside the “generally expected time frame for vaccine
reactions,” but that according to medical literature, “post-vaccination onset of TM could take as
long as three months.” Scheduling Order at 1 (ECF No. 53). I also explained that the 2-3 month
period between the onset and nadir of symptoms presents another challenge with petitioner’s
claim. Id. I stated that, “This is well outside the 4 hour-21 day timeframe proposed by the TM
Consortium Working Group,” but observed that both petitioner and respondent’s experts agreed
that the “working group’s diagnostic criteria may be too restrictive for clinical practice.” Id.; see
also Pet. Ex. 52 at 5; Resp. Ex. C at 3. Finally, I explained that petitioner’s medical records from
the Mayo Clinic, supported a monophasic inflammatory process, instead of a syrinx. Id. at 2. I
explained that the medical evidence and opinion evidence appeared to be more in favor of
petitioner’s claim, but that any demand made by petitioner should be discounted based on the
litigative risk. Id.
The parties engaged in unsuccessful litigative risk settlement discussions. On February
25, 2019, respondent filed a supplemental report from Dr. Donofrio and a first report from Dr.
Robert Fujinami, Ph.D.7 Resp. Exs. G-H9 (ECF Nos. 61-2). On July 18, 2019, petitioner filed a
responsive report from Dr. Imperioli and supporting medical literature. Pet. Ex. 59 (ECF No. 68).
5
Dr. Matthew Imperioli is a neurologist at the University of Connecticut School of Medicine. Pet. Ex. 53. He
received his undergraduate degree from Massachusetts College of Pharmacy and Health Science and his medical
degree from St. George’s University in 2010. Id. at 1. Dr. Imperioli did his residency in neurology at the John
Dempsey Hospital/Hartford Hospital. Id. at 2. He is board certified in neurology and neuromuscular medicine. Id.
Dr. Imperioli is currently a professor at the University of Connecticut in the Neurology Department. Id.
6
On June 14, 2019, respondent’s exhibits C-F were struck for failure to properly bate stamp and refiled on June 17,
2019.
7
Dr. Robert Fujinami is a professor in the Department of Pathology, Division of Microbiology and Immunology,
and an adjunct progressor in the Department of Neurology at the University of Utah School of Medicine. Resp. Ex.
I. He received his undergraduate degree from University of Utah in 1972 and his Ph.D. in Immunology-
Microbiology from Northwestern University in 1977. Id. at 1. He did his postdoctoral training at the Scripps
Research Institute. Resp. Ex. H at 1. He then went to the University of California as an Associate Professor in the
Department of Pathology and investigated how viruses trigger autoimmune demyelinating disease and the immune
mechanisms that lead to neuroinflammatory disease. Id. Dr. Fujinami investigates neuroinflammation in the
context of CNS autoimmune disease and how infections can initiate seizures and epilepsy. Resp. Ex. H at 1. He has
served on medical panels, including the Worth Health Organization (“WHO”), National Institutes of Medicine,
3
I held another status conference in the case after reviewing the newly filed expert reports
on August 12, 2019. Scheduling Order (ECF No. 69). During the status conference, I explained
that the medical records and statements in petitioner’s affidavit reflect that onset of symptoms
associated with myelopathy occurred after receipt of the Tdap vaccine on August 7, 2012. Id. at
2. I noted that the medical records provide different accounts for onset, but that the initial
symptom was abdominal pain that occurred in September or early October 2012. Id. I also
clarified my opinion relating to petitioner’s diagnosis. Id. at 3. I explained that I agree with
respondent’s expert that petitioner’s symptoms did not reach their nadir within 21 days of onset;
petitioner’s nadir was marked by significant gait impairment; and plateaued by December 2012
or early January 2013. Id. at 2. I noted that based on review of the medical records in particular
the MRIs, I disagreed with Dr. Donofrio’s opinion that there was no evidence of transverse
myelitis in the spinal cord and that a syrinx at the C7-T1 level was the cause of petitioner’s
symptoms, not transverse myelitis. Id. at 2-3. I recommended that petitioner file a supplemental
affidavit regarding his pre-vaccination medical history, if necessary, and the parties propose
further proceedings in this case.
On October 11, 2019, the parties filed a joint status report stating, “After careful
consideration, respondent is not interested in pursuing settlement negotiations. Respondent is
amenable to a ruling on the record or an entitlement hearing; petitioner requests an entitlement
hearing. Accordingly, the parties respectfully request a status conference…” Joint Status Rept.
(ECF No. 73). On October 31, 2019, a status conference was held, where the parties confirmed
that they were amenable to entitlement being adjudicated on the record. Scheduling Order (ECF
No. 74).
II. Legal Standard
The Vaccine Act was established to compensate vaccine-related injuries and deaths. §
300aa-10(a). “Congress designed the Vaccine Program to supplement the state law civil tort
system as a simple, fair and expeditious means for compensating vaccine-related injured persons.
The Program was established to award ‘vaccine-injured persons quickly, easily, and with
certainty and generosity.’” Rooks v. Sec’y of Health & Human Servs., 35 Fed. Cl. 1, 7 (1996)
(quoting H.R. No. 908 at 3, reprinted in 1986 U.S.C.C.A.N. at 6287, 6344).
A petitioner bears the burden of establishing his or her entitlement to compensation from
the Vaccine Program. The burden of proof is by a preponderance of the evidence. § 300aa-
13(a)(1). A petitioner may prevail by proving either that (1) the vaccinee suffered an injury
listed on the Vaccine Injury Table with onset beginning within a corresponding time period
following receipt of a corresponding vaccine (a “Table Injury”), for which causation is presumed
or that (2) the vaccinee suffered an injury that was actually caused by a vaccine. Under either
method, however, the petitioner must also show that the vaccinee “suffered the residual effects or
complications of the illness, disability, injury, or condition for more than six months after the
administration of the vaccine.” Section 11(c)(1)(D)(i).
Institute of Medicine-National Academic of Science, and the National Multiple Sclerosis Society. Id. at 2.
Additionally, he has published multiple articles on molecular mimicry. Id.
4
In the present case, petitioner does not allege a Table injury. Rather, he alleges that the
August 7, 2012 vaccination was the “cause-in-fact” of his development of transverse myelitis.
Petition at Preamble; Pet. Mot. at 1. Thus, he bears the burden of establishing actual causation.
To prove causation-in-fact, the petitioner must “show by preponderant evidence that the
vaccination brought about the injury by providing 1) a medical theory connecting the vaccination
and injury; 2) a logical sequence of cause and effect showing that the vaccination was the reason
for the injury; and 3) a showing of proximate temporal relationship between vaccination and
injury.” Althen v. Sec’y of Health & Human Servs., 418 F. 3d 1274, 1278 (Fed. Cir. 2005).
There must be preponderant evidence for each Althen prong. Caves v. Sec’y of Health & Human
Servs., 100 Fed. Cl. 119, 132 (2011), aff. per curiam, 463 Fed. Appx. 932 (Fed. Cir. 2012).
The preponderance of the evidence standard requires the petitioner to demonstrate that it
is “more likely than not” that the vaccine caused the injury. Moberly v. Sec’y of Health &
Human Servs., 592 F.3d 1315, 1322 n.2 (Fed. Cir. 2010). Proof of medical certainty is not
required. Bunting v. Sec’y of Health & Human Servs., 931 F.2d 867, 873 (Fed. Cir. 1991). A
petitioner must demonstrate that the vaccine was “not only [a] but for cause of the injury but also
a substantial factor in bringing about the injury.” Moberly, 592 F.3d at 1321 (quoting Shyface v.
Sec’y of Health & Human Servs., 135 F.3d 1344, 1352-53 (Fed. Cir. 1999); Pafford v. Sec’y of
Health and Human Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006). Causation is determined on a
case-by-case basis, with “no hard and fast per se scientific or medical rules.” Knudsen v. Sec’y
of Health & Human Servs., 35 F.3d 543, 548 (Fed. Cir. 1994). A fact-finder may rely upon
“circumstantial evidence” which is consistent with the “system created by Congress, in which
close calls regarding causation are resolved in favor of injured claimants.” Althen, 418 F. 3d at
1280.
If the petitioner makes a prima facie case supporting vaccine causation-in-fact, the
burden shifts to respondent to show by a preponderance of the evidence that the injury is instead
due to factors unrelated to the administration of the vaccine. Deribeaux v. Sec’y of Health &
Human Servs., 717 F.3d 1363, 1367 (Fed. Cir. 2013) (citing § 13(a)(1)(B)). Respondent has the
burden of demonstrating that: “[A] factor unrelated to the vaccination is the more likely or
principal cause of injury alleged. Such a showing establishes that the factor unrelated, not the
vaccination, was ‘principally responsible’ for the injury. If the evidence or alternative cause is
seen in equipoise, then the government has failed in its burden of persuasion and compensation
must be awarded.” Knudsen, 35 F.3d at 551.
Additionally, medical records are generally considered trustworthy. Cucuras v. Sec’y of
Health & Human Servs., 993 F. 2d at 1525, 1528 (Fed. Cir. 1993). Where medical records are
clear, consistent and complete, they should be afforded substantial weight. Lowrie v. Sec’y of
Health & Human Servs., No. 03-1585V, 2005 WL 6117475 (Fed. Cl. Spec. Mstr., Dec. 12,
2005). Medical records may be outweighed by testimony that is given later in time that is
“consistent, clear, cogent, and compelling.” Camery v. Sec’y of Health & Human Servs., 42 Fed.
Cl. at 381, 391 (1998).
If there is a dispute as to the nature of the petitioner’s injury, the special master may
opine on the nature of the petitioner’s injury.” Contreras v. Sec’y of Health & Human Servs.,
5
844 F. 3d 1363, 1368 (Fed. Cir. 2017) (citing Hibbard v. Sec’y of Health & Human Servs., 686
F. 3d 1355 (Fed. Cir. 2012); see also Broekelschen v. Sec’y of Health & Human Servs., 618, F.3d
1339 at 1346 (Fed. Cir. 2010). In Broeklschen, the Federal Circuit stated that it was appropriate
for the special master to first determine which injury is best supported by the evidence presented
in the record before applying the Althen test. Broekelschen at 1346.
III. Summary of Relevant Facts
A. Medical Records
Petitioner was 55-years old at the time when he received the Tdap vaccination on August
7, 2012. Pet. Ex. 1 at 1; Pet. Ex. 10 at 7. He had an appointment with Dr. Steven Stiles at St.
Luke’s Internal Medicine in Kansas City, Missouri. Pet. Ex. 10 at 7. Dr. Stiles noted existing
problems of “hyperlipidemia and Type 1 diabetes mellitus.” Id. Petitioner’s physical exam was
normal, and he received the Tdap vaccination. Pet. Ex. 1 at 1.
On October 18, 2012, petitioner presented to KU West Urgent Care for urinary pain and
urinary frequency. Pet. Ex. 6 at 3. Petitioner reported he had urinary pain for five days and
increased dramatically that day. Id. Petitioner informed Dr. Gary Parkhurst that he had been
experiencing urinary hesitancy for several months, but “over the last several days he also begun
experiencing some mild discomfort in the lower abdominal/pelvic area with slight dysuria.” Id.
at 6. Additionally, he was positive for “abdominal pain” and “decreased urine volume and
difficulty urinating.” Id. Dr. Parkhurst noted that petitioner had a slightly enlarged prostate. Id.
On October 23, 2012, petitioner returned to Dr. Stiles with “a week to 10-day history of
upper abdominal discomfort.” Pet. Ex. 10 at 5. Dr. Stiles noted petitioner, “Has a dull
discomfort across the upper abdomen and occasionally gets a sharper pain in a focal area in the
right upper lateral abdomen.” Id. Dr. Stiles also wrote, “His urinary symptoms have become
gradually worse. Having some nocturia issues and also has a delay in bladder emptying.” Id.
Dr. Stiles diagnosed petitioner with “abdominal pain” and “benign prostatic hypertrophy” and
opined, “Abdominal pain-positional nature of symptoms highly suggestive of underlying
thoracic radiculopathy or thoracic spinal stenosis. Lower urinary tract symptoms.” Id. at 6. Dr.
Stiles ordered an MRI of the thoracic spine. Id.
On October 26, 2012, petitioner had an MRI of his thoracic spine. Pet. Ex. 10 at 42. On
the MRI report, it stated, “Indication: mid-abdominal pain and tightness. Difficulty walking.
Tingling in bilateral upper extremities.” The MRI of petitioner’s thoracic spine showed an,
“Incompletely characterized slight expansion of the cervical and thoracic spine to the level of T3
with central T2 hyperintensity.” 8 Id. at 433. The radiologist wrote, “There is a wide differential
for this appearance. Given central cord hyperintensity, ischemic/inflammatory process as well as
an underlying malignancy cannot be excluded. Recommend further evaluation with contrast
MRI of the brain, cervical spine and thoracic spine to better differentiate with these entities.” Id.
Further, he noted, “Incompletely characterized left adrenal lesion measuring up to 1 cm.” Id.
The record also states, “After talking to Dr. Stiles, the patient’s symptoms are relatively mild and
8
This MRI report did not define the level of the cervical spine at which the expansion began and did not note the
subsequently seen small cyst at T1.
6
not acute on onset. As a result, a syrinx9 is suspected and non-contrast and contrast [MRI] c-
spine and post-contrast only T-spine MRI is recommended for further characterization.” Id.
On October 30, 2012, petitioner had an appointment with neurologist, Dr. Steven Arkin.
Pet. Ex. 3 at 20. Petitioner was evaluated for “subacute onset and progression of circumferential
paresthesias and dysesthesias in the thoracic to abdominal region over the past two to three
months or so.” Id. at 20-21. Dr. Arkin wrote that, “[Petitioner]] was in his usual state of health
until about two or three months ago when he started having a sense of pressure tightness in the
abdomen. Since that time, he has had occasional burning sensation…On four or five occasions,
he has difficulty walking if he has been in the recliner for a while…He noticed that his legs have
been a bit jumpier than they have been before. He has a patch of numbness around the right knee
as well as the left thigh. There can be some tingling in the same distributions. He also has some
tingling in his fingers and toes at the same time.” Id. at 21. The physical exam showed
petitioner’s reflexes were brisk, 3/3 at the knees and 2+/2+ at the ankles. Id. Petitioner had a
mild ataxic gait and patches of decreased sensation in the mid-portion of the right calf, normal on
the left side and decreased sensation in the abdomen around T3 to T10. Id. at 21. Dr. Arkin
opined that petitioner “had evidence of cervical thoracic myelopathy in conjunction with slightly
expanded spinal cord with what appears to be centrally located T2 hyperintensities extending
from the lower cervical cord down into the thoracic region….I suspect that this will turn out to
be a syrinx but the other possibilities are inflammatory/autoimmune or demyelinating/multiple
sclerosis.” Id. at 22.
Petitioner had additional MRIs of his brain and cervical and thoracic spine on November
2, 2012. Pet. Ex. 10 at 37. The MRI of petitioner’s cervical spine demonstrated the “central T2
hyperintensity extending from the C6-C7 level to the T3-T4 level which is not significantly
changed compared to the prior exam. There is a focal rounded T2 hyperintense lesion in the left
lateral aspect of the cord at the T1 level measuring 5mm craniocaudal and 3 mm transverse
which was not definitely seen on the prior exam….The cord is mildly expanded at these levels.”
Id. at 38. The radiologist’s impression was, “Intramedullary central T2 signal extending from
the C6-C7 to T3-T4 level as well as a left lateral cystic appearing lesion at the T1 level. Primary
differential considerations include a syringomyelia, sequelae of prior inflammation (transverse
myelitis).” Id. at 38.
Petitioner had a follow-up appointment with Dr. Arkin on November 6, 2012. Pet. Ex. 10
at 22. Dr. Arkin indicated that petitioner was being evaluated for “subacute and progressive
onset of circumferential paresthesia and dysesthesias involving the abdomen associated with T2
lesion in the lower cervical and upper thoracic spinal cord. Pet. Ex. 3 at 18. Dr. Arkin also
noted that petitioner had intermittent difficulty walking after being in a recliner for an extended
period of time, urinary hesitancy and was hyper-reflexive in the lower extremities. Id. at 18. Dr.
Arkin observed that the second MRI “again revealed the T2 hyperintensity…in the spinal cord
between C6-C7 and T3-4.” Id. He also noted a “…tiny 5x3mm T2 lesion just laterally within
9
A “syringomyelia” is a slowly progressive syndrome of cavitation in the central segments of the spinal cord,
generally in the cervical region, but sometimes extending up into the medulla oblongata or down into the thoracic
region. It results in neurologic deficits, usually segmental muscular weakness and atrophy with a dissociated
sensory loss (loss of pain and temperature sensation, with preservation of the sense of touch). Dorland’s Illustrated
Medical Dictionary 33rd ed. (2020) (hereinafter “Dorland’s”) at 1828-29.
7
the cord that looks cystic.” Id. Dr. Arkin opined, “At this point, the situation most likely
represents a syringomyelia involving the spinal cord between C6-7 and T3-4. His symptoms do
match up as well as hyperreflexia and some bowel and bladder dysfunction….One consideration
might be a neurosurgical evaluation if his situation worsens particularly if he starts developing
weakness or gait instability.” Id. Dr. Arkin recommended petitioner undergo a lumbar puncture
to “look for any evidence of [an] inflammatory situation.” Id. He wrote, “This could be
transverse myelitis associated with collagen vascular disease or other type of autoimmune
pathology.” Id. Petitioner had a lumbar puncture performed on November 26, 2012, which
noted that petitioner had 8 white blood cells (WBC), which was noted as “high” and a protein
CSF of 67, also noted as “high.” Pet. Ex. 11 at 186.
On November 28, 2012, petitioner had an evaluation with neurosurgeon Dr. Darren
Lovick. Pet. Ex. 5 at 3. Dr. Lovick wrote that, “[Petitioner] has had burning and tingling and
tightness around the rib cage over the last few months now with difficulty with numbness in his
legs and some weakness in his feet and difficulty with his gait. He also has noticed some
troubles with urination.” Id. After performing a physical examination and reviewing petitioner’s
MRIs, Dr. Lovick stated, “He is definitely myelopathic and it fits with his level of function.” Dr.
Lovick recommended a spinal arteriogram “in the case this could be a dural AV fistula.” Id. at 4.
The petitioner underwent a spinal and cervical IR angiogram on December 19, 2012. Pet.
Ex. 11 at 160. The results were normal. Id. at 163. Petitioner had a follow-up appointment with
Dr. Lovick on December 26, 2012. Pet. Ex. 5 at 5. Dr. Lovick noted that petitioner did not have
a dural AV fistula or any type of arteriovenous malformation. Id. Dr. Lovick explained to
petitioner that “the possible etiologies” of his symptoms, included, “inflammatory conditions like
transverse myelitis, sarcoidosis, and a demyelinating process.” Id. He ordered petitioner begin a
trial of prednisone beginning at 60 mg per day. Id.
On January 10, 2013, petitioner returned to Dr. Arkin. Pet. Ex. 3 at 13. Dr. Arkin
repeated petitioner’s medical history, noting petitioner had a normal spinal angiogram. Id.
Petitioner had reported slight improvement, but then worsened on the prednisone taper. Id. The
differential diagnosis continued to be “fistula versus sarcoidosis versus transverse myelitis versus
neoplasia.” Id. Dr. Arkin recommended a repeat lumbar puncture and prescribed Neurontin at
200 mg. Id. The repeat lumbar puncture performed on January 21, 2013 showed elevated protein
in the CSF and mildly elevated pleocytosis. Pet. Ex. 3 at 4. Interestingly, Dr. Arkin continued to
note fistula despite the normal arteriogram and did not mention a syrinx at this point.
Petitioner had an appointment with Dr. Arkin on January 30, 2013. Pet. Ex. 3 at 11. At
this appointment Dr. Arkin noted petitioner had slightly decreased strength in his lower
extremities with increased reflexes and upgoing toes. Id. He observed petitioner “continues to
have decreased sensation, although not to the extent that he has had before.” Id. Dr. Arkin
stated, “This remains a very perplexing situation. This could be still be syringomyelia fairly
stable. This could still be an occult AVM or neoplasia.” Id. Dr. Arkin stated that he would help
facilitate a second opinion at another facility and recommended a repeat MRI in the future. Id.
On March 18, 2013, petitioner sought a tertiary care evaluation of his condition at the
Mayo Clinic and had an appointment with Dr. Joseph Y. Matsumoto for a neurology evaluation.
8
Pet. Ex. 7 at 17. Petitioner explained that in September 2012 he began to feel a tightness in his
abdomen that was recorded as “periumbilical.” Id. Petitioner further explained he also
experienced a “sense of burning.” Id. Dr. Matsumoto reviewed the MRI reports and noted
evidence of central hyperintensity of T2 signal and the results from the lumbar punctures and
noted elevated protein in the CSF from both samples. Id. Petitioner also reported that he was
getting progressively weaker and dragging his feet and falling. Id. Petitioner stated that he had
numbness from his knees to his feet, but that the numbness would sometimes present more
proximally. Id. After performing a neurological exam, Dr. Matsumoto wrote,
[Petitioner] has clear evidence of a predominately thoracic myelopathy at this time. He
has weakness in an upper motor neuron distribution bilaterally. He has vibratory and
joint position loss at the toes. The vibratory sensation loss extends to the knees. He has
clear pinprick sensation loss, worse on the left than the right, that extends all the way up
to approximately the T7 level….Reflexes are increased in the legs, and plantar reflexes
are extensor. He is walking with dragging both feet and unsteadiness on tandem gait.
Pet. Ex. 7 at 18. Dr. Matsumoto diagnosed petitioner with “Myelopathy, predominately thoracic
with some question of cervical myelopathy as well. The cause is uncertain.” Id. at 18. Dr.
Matsumoto also noted that a sarcoid is unlikely given the absent response to steroids. Id. Dr.
Matsumoto ordered repeat MRIs and requested the films from the spinal angiogram. Id.
The same day, March 18, 2013, petitioner had additional MRIs of his cervical and
thoracic spine. Pet. Ex. 7 at 31. The results showed a T2 hyperintensity centrally in the spinal
cord from the C6-C7 interspace to the mid T3 level. Id. It also showed a focal 1-2 millimeter
cystic “appearing component” at the C7-T1 interface, in the left side of the cord. Id. It was noted
that there was no enhancement within or adjacent to the lesion. Id. The radiologist stated that
the lesion was not consistent with a dural AV fistula, but it could represent a demyelinating
process such as neuromyelitis optica or post viral myelitis. Id. The radiologist stated, “the
absence of enhancement would be atypical for a neoplastic process or sarcoidosis.” Id.
On March 20, 2013, petitioner had a follow-up appointment with Dr. Matsumoto
following the MRIs. Pet. Ex. 7 at 14. Dr. Matsumoto ruled out evidence of AVM or AV fistula.
He stated that the MRIs from October 26, 2012 looks “a bit worse than the one we have today.”
Id. Dr. Matsumoto wrote, “The area of T2 signal abnormality looks a bit wider within the cord
than what we see today. Its extent looks about the same, although the films do not go to the
rostral extent of the lesion.” Id. He sent the MRIs for another review to determine if there had
been any interval progression of the lesion and also referred petitioner to the Mayo Clinic’s
demyelinating disease experts. Id. After reviewing the results, Dr. Matsumoto questioned the
petitioner again about his disease progression and noted petitioner stated he had gotten worse
after plateauing in January. Id.
Another radiologist at the Mayo Clinic, Dr. David DeLone, reviewed all of petitioner’s
MRIs, including the MRIs from October 26 and November 2, 2012. Pet. Ex. 7 at 31. Dr.
DeLone noted that the upper thoracic cord central T2 hyperintensity has not changed since
October 26, 2012. He also wrote that the “small cystic appearing focus now present at C7-T1
was not clearly present on 10/26/2012.” Id.
9
Petitioner met with Dr. Mark Keegan, a demyelination expert at the Mayo Clinic on
March 21, 2013. Pet. Ex. 7 at 8-11. Petitioner reported that he was well until August 2012 and
recalled receiving the Tdap vaccine around the same time. Id. at 8. Petitioner indicated that in
September or earlier, he developed a “numb sensation and a tightness and burning sensation in
his abdomen that was positional in nature.” Id. Petitioner explained that in mid-October he
could walk three miles with only abdominal discomfort, however, later he developed gait
impairment that plateaued between December and January. Id. Dr. Keegan noted that the
neuroimaging shows a longitudinally extensive area of abnormal signal centrally within the
spinal cord. Id. After a physical exam, Dr. Keegan stated that, “It seems likely that [petitioner]
had an inflammatory cause for the myelopathy….There was no compressive impairment. It is
not clear, as was the concern, that there has been a definitive progression over time, and it does
appear that it is confirmed that it has plateaued.” Id. at 11. Dr. Keegan explained that repeat
corticosteroids or plasma exchange for symptom resolution would not be beneficial at that time,
but if his tests came back positive for an autoimmune condition like neuromyelitis, then he
would recommend immunosuppressive medications. Id. Additionally, Dr. Keegan indicated that
he would treat petitioner’s condition as a monophasic process if petitioner’s serological
evaluations came back negative and would only recommend chronic immunosuppressive
medications if a definite recurrent inflammatory myelopathy process was found. Id. Dr.
Keegan recommended petitioner obtain a gait aid and pursue physical therapy. Id. Dr. Keegan
diagnosed petitioner with “myelopathy, probable inflammatory cause.” Id.
Petitioner met with Dr. Matsumoto later the same day. Pet. Ex. 7 at 7. Dr. Matsumoto
noted that Dr. Keegan “felt the petitioner had an inflammatory myelopathy,” but was waiting for
serological results to determine next treatment steps. Id. Dr. Matsumoto explained, “If all
serological evaluations come back negative, [Dr. Keegan] would recommend conservative
therapy, considering this is a monophasic illness such as transverse myelitis.” Id. Petitioner’s
autoimmune panel returned normal, including the NMO antibody. Id. at 3-4.
On March 28, 2013, petitioner had an evaluation by Dr. Brad Steinle at Physical
Medicine and Rehabilitation. Pet. Ex. 8 at 3. Petitioner reported progressive difficulties with his
legs since September 2012, erectile dysfunction for two years and urinary hesitancy since June
2012. Id. Dr. Steinle noted an enhancing lesion around C4-T6 was found and petitioner
underwent extensive work-up and it “appears to be transverse myelitis.” Id. During the physical
exam, Dr. Steinle observed that petitioner had “profound proprioceptive loss in the lower limbs,”
and his “sensation is also diminished in a stocking glove fashion in his feet bilaterally.” Id. at 4.
Dr. Steinle assessed petitioner with “transverse myelitis with paraparesis, neuropathic pain,
neurogenic bladder and bowel.” Id. He recommended petitioner increase the dosage of
gabapentin and prescribed Nuvigil, as well as, physical therapy. Id.
Petitioner a physical therapy evaluation on April 3, 2013. Pet. Ex. 11 at 38. The
patient’s medical history (“PMH”) notes that petitioner was diagnosed with transverse myelitis.
Id. During the physical examination, petitioner demonstrated weakness in his lower extremities
bilaterally and decreased sensation in his lower extremities as well. Id. at 39. On May 1, 2013
petitioner was discharged from physical therapy. Id. at 45-46.
10
On May 2, 2013, petitioner had a follow-up appointment with Dr. Steinle. Pet. Ex. 8 at 2.
Petitioner reported that physical therapy helped, and he was compliant with the home exercise
program. Id. Dr. Steinle noted petitioner still had proprioceptive loss in the lower limbs, but he
has a steadier and brisk gait with the use of forearm crutches. Id. Dr. Steinle again diagnosed
petitioner with transverse myelitis with paraparesis, neuropathic pain and neurogenic bladder and
bowel, functionally improved. Id.
On August 15, 2013, petitioner had an appointment with Dr. Steven Stiles for his annual
physical. Pet. Ex. 10 at 2. Dr. Stiles noted that petitioner had gone to the Mayo Clinic and
wrote, “This diagnosis available at this point for his neurologic issues is transverse myelitis.” Id.
During the physical exam, petitioner demonstrated mild weakness in the lower extremities and
his gait was observed as mildly to moderately ataxic. Id. at 3.
On September 26, 2013, petitioner presented to Dr. Jennifer Elliott with the main
complaint of abdominal pain. Pet. Ex. 11 at 22. Petitioner reported chronic abdominal pain that
is predominantly in the right upper quadrant which feels like a “knot type sensation at times.”
Id. Petitioner described it as a “burning and tightness associated with position,” that would go
away when he was laying down. Id. Petitioner rated his pain as a 5-8 out of 10 in seating or
standing positions, but a 0/10 when laying down. Id. During the physical exam, petitioner
demonstrated intact sensation to light touch and “abnormal sensation” to pinprick in the bilateral
lower extremities. Id. at 23. His reflexes were 2+ bilaterally in the lower extremities. Id. Dr.
Elliott diagnosed petitioner with neuropathic abdominal pain secondary to transverse myelitis,
diabetes, and low back pain. Id.
On November 19, 2015, petitioner had an appointment with Dr. James H. McDonald for
an annual wellness exam. Pet. Ex. 50 at 17. Petitioner reported he was experiencing mild
symptoms of neuropathy which was recorded as “stable.” Id. at 18. Petitioner declined the
annual flu shot at this appointment, explaining that he had transverse myelitis from the Tdap
vaccine he received in 2012. Id. at 20. Petitioner stated that, “About 5 weeks after the vaccine
symptoms started. They have remained the same. Symptoms have not gotten better or worse.”
Id. Petitioner continued to be treated by Dr. McDonald for managing diabetes and cholesterol.
See Pet. Ex. 50; Pet. Ex. 71.
On February 21, 2017, petitioner had a neurology consult with Dr. Michael
Schwartzman. Pet. Ex. 50 at 75. Petitioner was referred by his primary care physician, Dr.
James McDonald. Id. Petitioner reported intermittent prickly dysesthesias in his arms and
sometimes radiating to his upper chest. Id. Dr. Schwartzman reviewed petitioner’s past medical
history, noting a history of thoracic transverse myelitis beginning in September 2012 associated
with spastic paraparesis and neuropathic pain. Id. Dr. Schwartzman reviewed petitioner’s
October 2012 MRI and observed that the differential diagnoses included syringohydromyelia,
sequelae of prior inflammation or less likely a low-grade glial tumor. Id. at 76. During the
neurological evaluation, Dr. Schwartzman observed petitioner had “superimposed decreased
pinprick and temperature discrimination in the distal lower extremities with distal proximity
gradient to below the knees.” Id. at 79. Petitioner’s proprioception was normal. Id. Dr.
Schwartzman’s impression was “history of idiopathic transverse myelitis; probable diabetic
peripheral neuropathy of bilateral lower extremities; probable cubital tunnel syndrome; and
11
upper extremity dysesthesias extending into this arms and anterior chest of unclear etiology.” Id.
An EMG/NCS and repeat MRI of the cervical and thoracic spine with and without contrast was
ordered. Id.
The EMG/NCS tests performed on February 23, 2017 showed evidence of bilateral ulnar
motor neuropathies at the elbows and chronic motor axonal loss without evidence of chronic
reinnervation or denervation. Pet. Ex. 50 at 82. The MRI of petitioner’s cervical spine taken on
March 4, 2017 noted the T2 hyperintense signal involving the cervical thoracic cord from C7-T2
with a focal 5 mm syrinx in the left aspect of the cord at the level of T1. Pet. Ex. 51 at 21. The
radiologist’s impression was, “Persistent abnormal cord signal at the cervicothoracic junction
with overall decrease T2 signal compared to the 2012 examination, without enhancement. This
suggests remote demyelinating or remote infectious/inflammatory process.” Id.
Petitioner had a follow-up visit with Dr. Schwartzman on March 14, 2017. Pet. Ex. 51 at
8. Petitioner reported prickly dysesthesias in his chest and hands, along with intermittent
numbness involving the bilateral fourth and fifth digits. Id. Dr. Schwartzman stated that he
reviewed the Mayo Clinic’s assessment and his impression was, “It was felt that [petitioner] had
idiopathic transverse myelitis.” Id. After a physical exam, Dr. Schwartzman’s impression was,
“History of idiopathic transverse myelitis. I suspect that his sensory symptoms are reemergence
of his prior transverse myelitis; probable diabetic neuropathy; and bilateral cubital tunnel
syndrome.” Id. at 10. Petitioner was prescribed a trial of Cymbalta and referred to a
neurosurgeon for potential ulnar nerve transposition. Id.
Petitioner underwent bilateral ulnar decompression in the fall of 2017. See Pet. Ex. 51 at
11-16. Petitioner reported that his chronic pain was completely resolved, and numbness
significantly decreased in his upper extremities. Id. at 16.
On November 28, 2017, petitioner had an annual wellness exam and routine diabetic
maintenance visit with Dr. McDonald. Pet. Ex. 71 at 24. It was noted that petitioner’s diabetes
and dyslipidemia were stable, and he was exercising at least thirty minutes a day a few days a
week. Id. It was recorded that he had a normal gait and was able to stand without difficulty at
this appointment. Id. at 29. He was diagnosed with controlled diabetes mellitus with
neuropathy. Id. at 30. Petitioner continued to have medical appointments focused on his
diabetic maintenance. See Pet. Ex. 71 at 36-54. Transverse myelitis was noted in petitioner’s
past medical history. Id.
B. Petitioner’s Affidavit
Petitioner submitted a supplemental affidavit on December 12, 2017. Pet. Ex. 49. In this
affidavit, petitioner stated that prior to the administration of the Tdap vaccine on August 7, 2012,
he had full mobility with reasonable fortitude and could walk eighteen holes of golf. Pet. Ex. 49
at ¶ 1. He stated that he was in same condition until “late September to early October,” when he
began to notice minor pain near his bladder. Id. at ¶ 2. Petitioner also wrote that he was having
trouble urinating and abdominal pain. Id. He described that the pain was located mostly on his
right side and “the pain was like a band, with pressure across my abdomen.” Id. The pain had
built up so much, that by October 18, 2012, he sought medical assistance. Id.
12
Petitioner stated that after a second medical appointment on October 23, 2012, he
continued to have pain but also experienced weakness and difficulty walking any significant
distance. Id. at ¶ 3. Additionally, petitioner stated that he was unable to urinate and felt a sense
of urgency without being able to empty his bladder. Id. Eventually his primary care physician
arranged an MRI and an appointment with Dr. Arkin. Id.
Petitioner indicated that by the end of October he found it increasingly difficult to walk
and the sensation in his legs were diminished. Id. at ¶ 4. Petitioner stated that he lost some sense
of his balance which contributed to further issues with walking. Id.
Petitioner wrote that on the day of the vaccination, he had been seeking treatment for an
enlarged prostate. Id. at ¶ 5. He stated that his urinary symptoms became significantly worse
after vaccination. Id. Petitioner clarified that the progression of symptoms after the vaccination
were abdominal tightness and banding sensation, pain, constipation and bladder urgency, which
he stated, “began in late September.” Id. Petitioner explained that the pain was what initially
caused him to seek assistance at the Acute Care Center, then his primary care physician, which
resulted in an MRI all in the month of October. Id. He stated that his symptoms of decreased
sensation in his legs, loss of balance, pain and urinary disruption have continued since October
2012. Id. at ¶ 6. He continues to take Gabapentin and Tramadol daily, in addition to using a
TENS unit. Id. at ¶ 7.
IV. Consideration of Petitioner’s Diagnosis
In this case, the parties dispute whether petitioner has transverse myelitis. Pet. Mot. at
17-19; Resp. Response at 17. Petitioner’s experts, Drs. Jani-Acsadi and Imperioli contended that
petitioner suffered monophasic transverse myelitis following the receipt of the Tdap vaccine.
Pet. Ex. 18 at 8; Pet. Ex. 52 at 2. Respondent’s expert, Dr. Donofrio, contended that petitioner
did not have transverse myelitis and petitioner most likely had a syrinx, which was the cause
petitioner’s symptoms. Resp. Ex. A at 11; Resp. Ex. C at 7. Accordingly, I find it appropriate
for first determine which injury is best supported by the evidence presented.
If the existence and nature of the [petitioner’s] injury itself is in dispute, it is the special
master’s duty to first determine which injury was best supported by the evidence presented in the
record before applying the Althen test to determine causation of that injury. Lombardi v. Sec’y of
Health & Human Servs., 656 F.3d 1343, 1352 (Fed. Cir. 2011) (citing Broekelschen v. Sec’y of
Health & Human Servs., 618 F.3d 1339, 1346).
The Vaccine Act provides that Special Masters are to consider any medical diagnosis
contained in the record. §300aa-13(b)(1). A special master must weigh and evaluate opposing
expert opinions, medical and scientific evidence and the evidentiary record in deciding whether
petitioners’ have met their burden of proof. Id. The function of a special master is not to
‘diagnose’ vaccine-related injuries, but instead to determine based on the evidence as a whole
and the totality of the case, whether it has been shown by a preponderance of the evidence that a
vaccine caused the petitioner’s injury. Lombardi v. Sec. of Health & Human Servs., 656 F.3d
1343, 1351 (citing Andreu, 569 F.3d at 1382) (Fed. Cir. 2011). In Capizzano, the Federal Circuit
13
provided additional guidance as to how special masters should weigh evidence, placing emphasis
on the statements of treating doctors. 440 F.3d at 1320 (Fed. Cir. 2006). The Federal Circuit
stated, “Althen III explained that medical records and medical opinion testimony are favored in
vaccine cases, as treating physicians are likely to be in the best position to determine whether a
‘logical sequence of cause and effect’ shows that the vaccination was the reason for the injury.’”
Capizzano at 1326 (quoting Althen, F. 3d at 1280).
Additionally, medical records are generally considered trustworthy. Cucuras v. Sec’y of
Health & Human Servs., 993 F. 2d at 1525, 1528 (Fed. Cir. 1993). Where medical records are
clear, consistent and complete, they should be afforded substantial weight. Lowrie v. Sec’y of
Health & Human Servs., No. 03-1585V, 2005 WL 6117475 (Fed. Cl. Spec. Mstr., Dec. 12,
2005). Medical records may be outweighed by testimony that is given later in time that is
“consistent, clear, cogent, and compelling.” Camery v. Sec’y of Health & Human Servs., 42 Fed.
Cl. at 381, 391 (1998).
A. Transverse Myelitis
Inflammatory diseases of the spinal cord are collectively described as myelitis and can
either be infectious or immune mediated (autoimmune). Pet. Ex. 23 at 6.10 According to the
article by Frohman et al., “Transverse myelitis syndrome may arise from various causes, but it
most often occurs as an autoimmune phenomenon after infection or vaccination (accounting for
60% of cases in children)…” Pet. Ex. 64 at 1. 11 The same article states that, “Estimates of the
annual incidence of idiopathic or postinfectious transverse myelitis range from 1.3 to 8 cases per
million.” Id. at 1.
Petitioner’s expert, Dr. Jani Acsadi explained that transverse myelitis “is a rare clinical
syndrome in which an immune-mediated process causes neural injury to the spinal cord,
resulting in varying degrees of weakness, sensory alterations and autonomic dysfunction.” Pet.
Ex. 18 at 3. Respondent’s expert, Dr. Donofrio agreed with Dr. Jani-Acsadi’s description of
transverse myelitis, adding that transverse myelitis, “may arise from many causes but most occur
as an autoimmune phenomena after an infection, an underlying systemic autoimmune disease, or
an acquired demyelinating disease such as the first presentation of multiple sclerosis or spectrum
disorders of central nervous system demyelinating disease.” Resp. Ex. A at 6.
The article by Karussis and Petrou explained that, “Transverse myelitis is characterized
by inflammation and demyelination across both sides of one level, or segment, of the spinal cord
resulting in symptoms of neurological disconnection and dysfunction below the level of the
demyelinating area.” Pet. Ex. 23 at 6. The article by the Transverse Myelitis Consortium
Working Group (“TMCWG”), submitted by the respondent, explained that transverse myelitis is
characterized “clinically by acutely or subacutely developing symptoms and signs of neurologic
dysfunction in motor, sensory, and autonomic nerves and nerve tracts of the spinal cord.” Resp.
10
Karussis, D. & Petrou, P., The spectrum of post-vaccination inflammatory CNS demyelinating syndromes,
Autoimmune Review (2013). [Pet. Ex. 23]
11
Frohman, E. & Wingerchuk, D., Transverse Myelitis, 363 N. Engl. J. Med. 564-72 (2010). [Pet. Ex. 64].
14
Ex. A Tab 1 at 1. 12 Further, the TMCWG explained that there is “often a clearly defined rostral
border of sensory dysfunction and spinal MRI and lumbar puncture often show evidence of acute
inflammation.” Id.
An article by Goh et al., regarding MRI imaging in transverse myelitis, submitted by
petitioner, stated that idiopathic transverse myelitis is a diagnosis of exclusion. Pet. Ex. 63 at
1.13 The article also explained the distinction between “longitudinally extensive transverse
myelitis” and “acute partial transverse myelitis.” Id. at 2. The article states that longitudinally
extensive transverse myelitis” extends over more than three segments and involves all or most of
the cross-section of the cord and “acute partial transverse myelitis” has less than two segments of
eccentric or asymmetric cord involvement. Id. Further, this article stated, “The typical MRI
appearance in transverse myelitis is a central T2 hyperintense spinal cord lesion extending over
more than two segments, involving more than two-thirds of the cross-sectional area of the cord.
Although any cord level can be affected, the classic description includes a preference for the
thoracic cord.” Id. Finally, this article states that enhancement is present in only 37-74% of
cases. Id.
Both parties submitted articles that explained the Transverse Myelitis Consortium
Working Group’s (“TMCWG”) inclusion criteria for diagnosis of transverse myelitis (idiopathic
or disease associated). See Pet. Ex. 63; Resp. Ex. A. The TMCWG proposed the following
diagnostic criteria for transverse myelitis:
Resp. Ex. A Tab 1 at 2. Further, the TMCWG states that to be diagnosed with idiopathic acute
transverse myelitis “all of the inclusion criteria should be met and none of the exclusion criteria
are fulfilled.” Id. The same article identifies limitations to the proposed criteria. Id. at 3. The
article explains that the exclusion of cases based on the “interval between symptom onset and
12
Transverse Myelitis Consortium Working Group, Proposed diagnostic criteria and nosology of acute transverse
myelitis, 59 Neurol. (2002). [Resp. Ex. A Tab 1].
13
Christine Goh et al., MRI in Transverse Myelitis, 40 Journal of Magnetic Resonance Imaging, 1267-1279 (2014).
[Pet. Ex. 63].
15
maximal deficit is arbitrary….[the authors] remain committed to distinguishing ATM from a
rapidly evolving vascular myelopathy (< 4-hour progression), a slowly progressive or stuttering
hereditary myelopathy, spinal cord tumor, myelopathy due to a dural arteriovenous fistula and a
chronic progressive form of MS (all longer than 21 days of progression).” Id. Further, the
authors explained that the proposed criteria represent a useful framework for future studies but
will need to be prospectively validated to determine whether they appropriately categorize
individuals and whether the criteria is useful in terms of treatment strategies. Id. at 3-4.
Significantly, the TMCWG states, “Although the criteria may be perceived as restrictive, we
believe the use of these criteria will lead to the identification of more homogeneous groups of
individuals for clinical studies.” Id. at 4.
B. Petitioner’s experts’ opinions regarding the diagnosis
Dr. Agnes Jani-Acsadi opined that petitioner developed “a monophasic illness affecting
his cervical and thoracic spinal cord consistent with a longitudinally extensive transverse
myelitis lesion (“LETM”) seronegative for aquaporin 4 antibodies.” Pet. Ex. 18 at 8. She
explained, “When the inflammatory lesion extends across more than three vertebral segments
longitudinally, it is commonly referred to as ‘longitudinally-extensive transverse myelitis.’” Id.
at 3.
In his first report, Dr. Matthew Imperioli opined that petitioner “developed a monophonic
illness affecting his cervical and thoracic spinal cord consistent with transverse myelitis within 4-
6 weeks following the Tdap vaccination.” Pet. Ex. 52 at 4. He stated that petitioner’s
“symptomology and documented neurological exams…is consistent with a predominantly
thoracic myelopathy due to transverse myelitis.” Id. He noted that petitioner was evaluated by
neuroimmunologist, Dr. Mark Keegan at the Mayo Clinic, who “felt it was likely that [petitioner]
had an inflammatory cause for the myelopathy.” Id.
Additionally, Dr. Imperioli referenced the TMCWG’s proposed inclusionary criteria and
stated that “[petitioner] has none of the exclusion criteria” and “meets all the inclusion criteria
except for the proposed time frame of progression to nadir of 4 hours to 21 days following the
onset of symptoms.” Id. at 5. Dr. Imperioli then argued that the TMCWG’s proposed criteria
were designed to be applied for recruitment of patients into research studies and therefore may
be restrictive for clinical practice. Id.
He asserted, “Transverse myelitis is a heterogenous inflammatory disorder and not all
patients may follow the same clinical course.” Id. To support his assertion, Dr. Imperioli
referenced an article by Kim et al., which provided a case report about a 51-year old woman
whom developed progressive weakness in her upper and lower extremities over a four month
period and was eventually diagnosed with neuromyelitis optica (NMO). Pet. Ex. 54 at 1.14 The
authors of this case report note that the patient’s disease course did not meet the diagnostic
criteria for idiopathic acute transverse myelitis, in which progression time to nadir from
symptom onset is usually between four hours to three weeks. Id. at 2. The authors concluded
14
Jun-Soon Kim et al., A case of chronic progressive myelopathy, 16(10) Multiple Sclerosis, 1255-1257 (2010).
[Pet. Ex. 54].
16
that this case report demonstrates that patients with progressive myelitis over a period of several
months can also have a limited form of NMO. Id.
Dr. Imperioli indicated that petitioner met the other inclusion criteria proposed by the
TMCWG. Pet. Ex. 52 at 5. He stated that petitioner experienced sensory, motor and autonomic
dysfunction attributable to the spinal cord, consistent with the TMCWG’s inclusion criteria. Id.
at 5. He also wrote, “In regards to the other inclusion criteria of transverse myelitis published by
the TMCWG, [petitioner] had bilateral symptoms as well as a clearly defined sensory level on
exam. MRI imaging excluded an extra-axial compressive lesion to account for his symptoms,
i.e., there was no significant degenerative change of the spine or tumor to cause his myelopathy.
There was evidence of inflammation within the spinal cord demonstrated by CSF pleocytosis.”
Id. Dr. Imperioli explained that petitioner had 8 cells in his first spinal fluid assessment and
elevated CSF protein in his first spinal fluid assessment that occurred on November 26, 2012, as
evidence of inflammation. Id. at 6; see also Pet. Ex. 11 at 186.
Dr. Imperioli stated that petitioner’s MRIs “assist in narrowing the diagnosis to
transverse myelitis.” Pet. Ex. 52 at 6. He explained that the November 2, 2012 MRI of
petitioner’s cervical and thoracic spine revealed a T2 hyperintensity centrally in the spinal cord
from C6-C7 interspace to the mid T3 level. Id.; see also Pet. Ex. 10 at 38-39. Dr. Imperioli
stated, “This pattern is consistent with longitudinally extensive transverse myelitis as the lesion
spans over 3 or more vertebral segments.” Id. He also noted a “focal 2mm cyst area in the left
side of the cord at T1.” Id. Dr. Imperioli indicated that the petitioner’s MRI in 2017 did not
demonstrate any interval progression of the lesion over time, increased T2 hyperintensity within
the cord and/or the development of contrast enhancement, which would be expected if the lesion
was a neoplasm. Id. Importantly, he observed that the Mayo Clinic radiologist compared the
2017 MRI to petitioner’s prior scans and reported a decrease in the T2 hyperintensity of the cord
“which suggests interval improvement and is consistent with the expected evolution of imaging
in transverse myelitis.” Id.
Dr. Imperioli also stated that the entirety of the lesion is not consistent with that seen in a
syringomyelia as there was “no dilation of the central spinal canal or significant expansion of the
cord at the level of the lesion as would be expected.” Id. Dr. Imperioli explained that
syringomyelia are commonly associated with developmental disorders, such as Chiari
malformations, or spinal cord trauma, spinal cord tumors and spinal cord infarction. Pet. Ex. 52
at 6. Dr. Imperioli suggested that the syrinx identified on petitioner’s MRI could be caused by
an inflammatory myelitis. Id. at 6. He cited an article by S. Ravaglia et al., which studied the
development of syringomyelia in four patients with myelitis and found that the spinal cord
cavitation developed in association with the myelitis and their “spatial coincidence suggested a
causal relationship between the two conditions.” Pet. Ex. 57 at 2.15 The authors explained:
Inflammatory diseases of the central nervous system (CNS) are characterized by the
blood-brain barrier breakdown and abnormalities of the microvascular permeability,
leading to edema. The accumulation of extracellular fluid increases the interstitial
15
Sabrina Ravaglia et al., Pathogenetic role of myelitis for syringomyelia, 109 Clinical Neurology and
Neurosurgery, 541-546 (2007). [Pet. Ex. 57].
17
pressure in the spinal cord, leading to extension of the edema, and eventually,
coalescence into syringomyelia.
Id. at 5. The authors concluded, “…our observations suggest that myelitis alone can induce the
formation of syrinx as a result of intrinsic mechanisms, leading to accumulation of intra-spinal
fluid.” Id. at 6.
In Dr. Imperioli’s second report, he expounded upon his initial opinion regarding
petitioner’s diagnosis after reviewing the petitioner’s MRIs from the Mayo Clinic taken in 2017
and the respondent’s experts’ reports. Pet. Ex. 59. Dr. Imperioli stated that, “[Petitioner’s]
myelopathic symptoms reached a nadir at approximately 3-4 months based on the available
records. Id. at 2. He conceded that the TMCWG’s diagnostic criteria of acute transverse
myelitis are the best criteria published to date and can apply to the majority of patients with acute
transverse myelitis, but it is also common place to evaluate patients with a medical condition
manifesting in an atypical manner from what is described in published literature. Id. at 2. But
added that the TMCWG explained that proposed interval between symptom onset and maximal
deficit is arbitrary. Id. at 2; see also Resp. Ex. A Tab-1 at 3. Dr. Imperioli referenced the article
by Barreras et al., to demonstrate that some patients with inflammatory myelitis have a chronic
progression of symptoms. Pet. Ex. 59 at 2.16 Barreras et al. article reviewed 457 cases of
patients with presumptive diagnosis of transverse myelitis to differentiate the clinical and
paraclinical features of inflammatory myelopathy versus other causes of myelopathy (including
vascular and spondylotic causes). Id. The authors classified 247 cases with inflammatory
myelopathy. Id. They noted that those patients with inflammatory myelopathy had lesions that
“more frequently occurred in the posterolateral spinal cord relative to other myelopathy groups
and were located more often in the cervical and upper thoracic spinal cord (C1-T6).” Id. at 11.
Additionally, Barreras et al. found that inflammatory myelitis presented more often with a
subacute temporal profile, but that sixty-seven patients had a chronic progression of symptoms of
21 days or greater. Pet. Ex. 55 at 4. Further, of the 247 patients identified with inflammatory
myelitis, 81% experienced sensory abnormality; 65% had demonstrated weakness during the
neurologic examination; and 53% were found to be hyperreflexic. Id. at 12.
Dr. Imperioli stated that based on petitioner’s records it was his opinion that, “causes of
chronically progressive myelopathies, including hereditary myelopathy, spinal cord tumor,
myelopathy due to a dural arteriovenous fistulas, and a chronic progressive form of multiple
sclerosis were all sufficiently excluded.” Id. at 2. He reiterated that petitioner’s clinical
presentation meets all the inclusionary criteria proposed by the TMCWG, except for the
proposed time frame of progression and has none of the exclusion criteria. Id. at 3. Dr.
Imperioli stated that the first lumbar puncture petitioner had on November 26, 2012
demonstrated evidence of inflammation as shown by elevated CSF protein and pleocytosis of 8
cells in the CSF, both were flagged as “high” on the lab report. Pet. Ex. 59 at 3; Pet. Ex. 11 at
186.
Dr. Imperioli again addressed the identification of the “small, focal cystic area in the left
side of the cord at the T1 level,” opining that the focal area is a small syrinx that was formed
16
Barreras, P. et al., Clinical biomarkers differentiate myelitis from vascular and other causes of myelopathy, 90
Neurol. 12-21 (2018). [Pet. Ex. 55].
18
secondary to the myelitis and subsequent degenerative changes. Pet. Ex. 59 at 3. He explained
that the “small, focal cystic area at the T1 level of the cord had a hyperintense signal different
than the area of the myelitis, and has a similar signal intensity of the CSF. This cystic area does
not appear to be communicating with the central canal as would typically be seen in
syringomyelia.” Id. Significantly, Dr. Imperioli observed that the small focal area was not
identified on petitioner’s initial MRI taken on October 26, 2012. Id.; Pet. Ex. 10 at 43. The
neuroradiologist at the Mayo Clinic, Dr. David DeLone, reviewed petitioner’s MRIs from
October and November 2012, compared them to the MRI taken on March 18, 2013 and stated
that a “small cystic appearing focus now present at C7-T1 was not clearly present on
10/26/2012.” Pet. Ex. 7 at 33. Further, Dr. Imperioli wrote, “Dr. Brian Chin, the neurologist
who read [petitioner’s] 2017 MRI felt that the small focal cystic lesion was likely a syrinx but
overall the cord lesion was suggestive of demyelination or an infectious inflammatory cause.”
Pet. Ex. 59 at 4. Dr. Imperioli stated that petitioner had no conditions commonly known to cause
syringomyelia, such as Chiari malformations, Dandy-Walker cysts, basilar invaginations, spinal
arachnoiditis, cord compression, spinal cord intramedullary hemorrhage and neoplasm, that
could explain the appearance of the syrinx at the T1 level, other than it forming secondary to the
myelitis that was demonstrated on petitioner’s MRI. Id.
He concluded that petitioner developed a severe, monophasic immune mediated disease
of his spinal cord consistent with transverse myelitis. Pet. Ex. 59 at 5.
C. Respondent’s experts’ opinions regarding petitioner’s diagnosis
Dr. Donofrio opined that some of petitioner’s treating physicians, “other than the
neurologists,” used the term “transverse-myelitis” without having a full understanding of the
criterion used to establish a diagnosis of transverse myelitis. Id. at 7. He stated that neurologists
are the most knowledgeable in the criteria for transverse myelitis and in differentiating the types
of conditions that can cause a myelopathy (a generic term to describe all forms of spinal cord
disease). Id. In his second report, he acknowledged that “the diagnosis of transverse myelitis
was rendered in this case, even though petitioner’s presentation did not meet the full criteria for
transverse myelitis as outlined by the TMCWG in 2002.” Resp. Ex. C at 4. Dr. Donofrio also
agreed with Dr. Imperioli that the TMCWG’s criteria was created for recruitment of patients into
research studies and the criteria may be too restrictive for clinical practice. Resp. Ex. C at 3.
However, he explained that he used the TMCWG’s criteria to diagnose TM in his daily
neurology practice and it is his opinion that “this is the practice of most of my colleagues.” Id. at
1.
Dr. Donofrio summarized the TMCWG inclusion and exclusion criteria. Resp. Ex. A at
8-9. Dr. Donofrio stated that petitioner only met three of the six inclusionary TMCWG’s
criteria. Id. at 5. He explained:
First, an extra-axial compressive etiology by neuro imaging was not excluded. Most
physicians would consider a syrinx or intra-axial tumor as a compressive etiology.
Second, inflammation within the spinal cord was never demonstrated by appreciable
cerebral spinal fluid pleocytosis, an elevated IgG index or gadolinium enhancement.
19
Third, the petitioner did not progress to the nadir of his illness within 4 hours to 21 days
following the onset of symptoms.
Resp. Ex. A at 8. In his final report, Dr. Donofrio corrected himself, stating that “the imaging
did exclude extra-axial compressive etiology.” Resp. Ex. G at 2. Dr. Donofrio focused heavily
on how petitioner’s symptoms progressed, and, in his opinion, the lack of inflammation
demonstrated in petitioner’s CSF. Resp. Ex. A at 7-9; Resp. Ex. C at 3-6; Resp. Ex. G at 3.
In his first report, Dr. Donofrio stated that, “the petitioner was not found to be weak until
four and half months after the Tdap vaccination or four months after the onset of the symptoms
of pressure and burning over the abdomen.” Resp. Ex. A at 7. Dr. Donofrio asserts that
petitioner’s first sign of weakness is on December 13, 2012. Id. However, in the same report,
Dr. Donofrio acknowledged that when petitioner was evaluated by neurosurgeon, Dr. Darren
Lovick on November 28, 2012, petitioner had difficulty with numbness in the legs, weak feet and
gait instability. Id. at 7; Pet. Ex. 5 at 3.
In his second report, Dr. Donofrio explained that Dr. Keegan at the Mayo Clinic
documented that petitioner’s gait impairment began sometime after mid-October and “appears to
have plateaued between December and January of this year.” Resp. Ex. C at 3; Pet. Ex. 7 at 8.
He stated that, “The timing of the progression of the disease in the petitioner is so far beyond the
timing from the working group (3-4 months vs. 21 days), makes the diagnosis of TM untenable
even if you consider the criteria too restrictive to be applied in all cases. This large difference in
timing means the diagnosis of TM is unsupported.” Resp. Ex. C at 4. Dr. Donofrio wrote,
“Transverse myelitis is not a progressive illness beyond 3 weeks, yet the petitioner in this case
clearly worsened over a much longer timeframe.” Resp. Ex. G at 3. Dr. Donofrio noted that in
May 2013, petitioner was utilizing forearm crutches and stated that, “The need for forearm
crutches by May 2013 would be evidence for the progression of the thoracic myelopathy well
into the year 2013, many months after the 21 days defined in the working group criteria for TM.”
Resp. Ex. G at 3.
Dr. Donofrio also asserted that petitioner did not have inflammation within the spinal
cord demonstrated by laboratory testing, thus the petitioner would not meet the fifth criterion
required by the TMCWG to make the diagnosis of TM. Resp. Ex. A at 9; Resp. Ex. G at 3. He
stated that the petitioner did not have appreciable cerebral spinal fluid pleocytosis, an elevated
IgG index or gadolinium enhancement of the spinal cord. Id. He agreed with Dr. Imperioli that
the lack of gadolinium enhancement seen on petitioner’s MRI may have been related to the
timing of the imaging obtained. Id. Dr. Donofrio wrote that petitioner’s spinal fluid findings
showed 1 WBC and 1 RBC (normal results) on January 21, and the spinal fluid protein was
elevated at 82 mg/dl (normal being less than 50). Resp. Ex. C at 5. He explained that “TM
should cause an inflammatory reaction in the spinal fluid and one would expect a marked
elevation of WBC to well above 5, the lower limit of normal.” Id. While Dr. Donofrio did not
address the petitioner’s elevated WBC of 8 and elevated protein of 67 in his initial spinal fluid
analysis, Dr. Donofrio asserted that petitioner did not have “convincing evidence for
inflammation of the spinal cord by the spinal fluid analysis.” Resp. Ex. G at 4.
20
Instead, Dr. Donofrio opined that petitioner “most likely had a syrinx (syringomyelia) or
a low-grade tumor that began insidiously in August or September 2012 and progressed at least
through 2013 when petitioner required forearm crutches. Resp. Ex. A at 10; Resp. Ex. C at 6.
Dr. Donofrio stated that he had reviewed petitioner’s MRIs from November 2, 2012 and that he
agreed with the differential diagnosis rendered by the radiologist that included syringomyelia, a
low-grade tumor or sequelae of transverse myelitis. Resp. Ex. C at 3. He also reviewed
petitioner’s MRIs performed on March 4, 2017 and stated that a focal 5 mm syrinx in the left
aspect of the cord was noted at the T1 level. Resp. Ex. G at 1. Dr. Donofrio stated that the
syrinx was present to his view in 2012 and 2017, but that “it does not appear that the syrinx is
communicating with the ventricular system.” Id. Dr. Donofrio cited to an article by Milhorat,
which classified syringomyelia into communicating and noncommunicating syrinxes and
possible causes of each, to refute Dr. Imperioli’s position that transverse myelitis is a possible
cause of syrinxes. Resp. Ex. F at 5;17 Resp. Ex. C at 5.
He explained that petitioner’s imaging revealed a syrinx, which is a “cavity within the
spinal cord or lower part of the brain. They are most commonly localized between C2 and T9 of
the spinal cord, the location of the myelopathy in the petitioner.” Id. at 5. He stated that two
months prior to receiving the vaccine, petitioner complained of urinary hesitancy and
constipation, which would be consistent with the presence of a syrinx. Resp. Ex. G at 3. Dr.
Donofrio also observed that petitioner’s treating neurologist, Dr. Arkin, had suspected the
diagnosis of syrinx and included in the differential diagnosis provided by the radiologist reading
petitioner’s MRI from November 2, 2012. Id. Dr. Donofrio stated, “Dr. Arkin assessed the
[petitioner] four times and each time included a syrinx in his differential diagnosis.” Id.; see also
Pet. Ex. 3 at 10-11, 14-15, 20-22; Pet. Ex. 11 at 186, 192-94. However, he acknowledged that
Dr. Mark Keegan, the neurologist at the Mayo Clinic, did not note the syrinx, but it was
acknowledged by the radiologists. Resp. Ex. G at 2. He surmised that, “The Mayo Clinic
neurologists may have not had the MRI scans reviewed by their colleagues in radiology.” Id.
However, the radiologist at the Mayo Clinic, Dr. David DeLone, did review petitioner’s MRIs
from October 2012 and November 2012. Pet. Ex. 7 at 31. Dr. DeLone observed, “The small
cystic appearing focus now present at C7-T1 was not clearly present on 10/26/2012.” Id. The
radiologist, Dr. Kotsenas, who interpreted the MRI taken at the Mayo Clinic on March 18, 2013,
observed, “At the C7-T1 interface there is a more focal-2 mm cystic appearing component in the
left side of the cord.” Id. Even after noting the cyst at C7-T1, Dr. Kotsenas’ impression was,
“Nonspecific T2 hyperintensity in the spinal cord C6-T3 could be secondary to NMO or post
viral myelitis.” Id.
Dr. Donofrio wrote that there are, “Many issues in this case refute the diagnosis of
transverse myelitis.” Resp. Ex. G at 3. He pointed to petitioner’s symptoms of urinary and
hesitancy beginning in June of 2012, two months before the Tdap vaccination, as evidence of
pre-existing spinal cord disease. Id. at 3. Additionally, Dr. Donofrio noted that petitioner stated
in his affidavit that he could walk an 18 hole golf course, carrying clubs, in mid-October which
he did not find surprising as Dr. Arkin had noted normal strength and no weakness at the initial
appointments. Id. He stated that, “Dr. Arkin rendered the diagnosis of possible syringomyelia at
all four visits when he saw the petitioner,” and that, “the petitioner had symptoms of spinal cord
17
Thomas H. Milhorat, M.D., Classification of Syringomyelia, 8 Neurosurgery Focus (Mar. 2000). [Resp. Ex. F].
21
disease for 1-2 months before the August 7, 2012 vaccination.” Id. at 4. He concluded that it
was his opinion that petitioner did not have transverse myelitis. Id.
D. Petitioner has demonstrated that he had suffered transverse myelitis
After reviewing petitioner’s medical records, the experts’ opinions and medica literature,
I have determined that petitioner has provided preponderant evidence that he suffered transverse
myelitis.
1. Diagnosis of Treating Providers
At his first appointment with neurologist Dr. Arkin on October 30, 2012, Dr. Arkin
considers the possibility of petitioner having a syrinx or “inflammatory/autoimmune or
demyelinating multiple sclerosis.” Pet. Ex. 10 at 25. On November 2, 2012, petitioner had a
second MRI of his cervical and thoracic spine. Id. at 37. The radiologist’s impression was,
“Intramedullary central T2 central signal extending from the C6-C7 to T3-T4 level as well as a
left lateral cystic appearing lesion at the T1 level. Primary differential consideration includes a
syringomyelia, sequelae of prior inflammation (transverse myelitis).” Id. at 38. After review of
petitioner’s second MRI, taken on November 2, 2012, Dr. Arkin observed a “tiny 5 x 3 mm T2
lesion just laterally within the cord which looks cystic,” and stated that he suspected a
syringomyelia, but that it “could also be transverse myelitis associated with collagen vascular
disease or other type of autoimmune pathology.” Id. at 23. On November 26, 2012, Dr. Arkin
noted that petitioner had “subacute and progressive onset of circumferential paresthesias and
dysesthesias involving the abdomen with a sense of weakness in the legs,” and that “the
suggestion is inflammation versus syrinx given the midline distribution. I think he probably has
syringomyelia.” Pet. Ex. 3 at 17. After petitioner underwent an arteriogram which ruled out a
dural arteriovenous fistula, neurosurgeon, Dr. Darren Lovick opined that petitioner could have an
inflammatory condition like, “transverse myelitis, sarcoidosis and demyelinating processes….”
Pet. Ex. 5 at 5. He recommended petitioner begin prednisone. Id. As of January 10, 2013,
despite the negative arteriogram petitioner’s differential diagnosis continued to be, “fistula
versus sarcoidosis versus transverse myelitis.” Pet. Ex. 3 at 13.
On March 18, 2013, petitioner sought a tertiary care second opinion from the Mayo
Clinic. Pet. Ex. 7 at 19. He had repeat cervical and thoracic spine MRIs, which again
demonstrated the T2 hyperintensity in the spinal cord at C6-T3 and a small “cystic appearing
component in the left side of the cord.” Pet. Ex. 7 at 31. The radiologist interpreting the March
18, 2013 MRI stated that the observed hyperintensity “could represent a demyelinating process
such as neuromyelitis Optica or post viral myelitis. The absence of enhancement would be
atypical for a neoplastic process or sarcoidosis.” Id. Dr. David LeLone compared petitioner’s
MRIs taken on October 26th and November 2, 2012 and observed that, “The small cystic
appearing focus now present at C7-T1 was not clearly present on 10/26/2012.” Id. On March
20, 2013, Dr. Joseph Matsumoto reviewed petitioner’s neuroimaging from October 26, 2012 and
compared it to the MRI taken on March 18, 2013. Id. at 14. He wrote, “[Petitioner] had a repeat
MRI of the spine. This showed a multi-segment T2 change consistent with a long area of
intrinsic myelopathy…There was no evidence of AVM or AV fistula according to Dr.
Kotsenas….To me, on the films, the scan of October 26, 2012, looks if anything a bit worse than
22
the one we have today. The area of T2 signal abnormality looks a little bit wider within the cord
than what we see today.” Id. Dr. Matsumoto also noted that Dr. Kotsenas also appeared to rule
out a tumor and decided to have petitioner meet with a demyelinating expert, Dr. Mark Keegan.
Id. Dr. Keegan evaluated petitioner on March 21, 2013. Id. at 11. Dr. Keegan stated that he
“personally reviewed the neuroimaging” and after taking petitioner’s history and a physical
exam, stated, “It seems likely that [petitioner] had an inflammatory cause for the
myelopathy….If all the serological evaluations came back negative, this could remain, even if
this is an autoimmune inflammatory cause, a monophasic process.” Id. Dr. Keegan diagnosed
petitioner with “Myelopathy, probable inflammatory cause.” Id.
On March 28, 2013, when petitioner sought an evaluation for his rehabilitation needs, Dr.
Brad Steinle diagnosed petitioner with transverse myelitis with paraparesis, neuropathic pain,
neurogenic bladder and bowel and recommended physical therapy and prescribed Nuvigil.18 Pet.
Ex. 10 at 11. Dr. Steinle maintained petitioner’s diagnosis of transverse myelitis at a follow-up
appointment on August 6, 2013 and on February 19, 2015. Pet. Ex. 14 at 5-7. In February 2017,
at an appointment with neurologist Dr. James McDonald for an evaluation of intermittent prickly
dysesthesias in petitioner’s upper arms, Dr. James McDonald noted petitioner’s history of
transverse myelitis “beginning in 2012” and recommended a repeat MRI. Pet. Ex. 51 at 1. Dr.
McDonald reviewed the March 4, 2017 MRI and compared it to the MRI performed in
November 2012. Id. at 8. Dr. McDonald observed that the overall T2 signal was decreased from
the study performed in November 2012 and he also noted a “multifocal area of T2 hyperintensity
likely a syrinx (at the level of T1),” but concluded, “MRI of the cervical spine without and with
contrast showed an overall decreased T2 signal compared to the last study most likely suggesting
either a remote infectious/inflammatory process or demyelination.” Id. at 8. Dr. McDonald also
stated that he reviewed petitioner’s records from the Mayo Clinic and that, “It was felt that he
had idiopathic transverse myelitis.” Id.
Petitioner’s medical records and treating neurologists establish the diagnosis of transverse
myelitis and they rule out possible other causes, such as sarcoidosis, arteriovenous fistula and a
neoplastic process. Dr. Donofrio puts significant weight on the presence of a 5x3 mm syrinx at
the T1 level, recognized on petitioner’s MRIs from November 2012, March 2013 and March
2017, as the cause for petitioner’s symptoms and disease. However, he also noted that “a
radiologist lists a differential diagnosis of potential disorders, leaving the final decision to the
clinician caring for the patient.” Resp. Ex. G at 3 (emphasis added). Importantly, petitioner’s
interpreting radiologists and treating neurologists acknowledged the syrinx, but concluded that
petitioner had suffered an inflammatory myelopathy that was consistent with transverse myelitis.
For example, Dr. Mark Keegan explained that he had reviewed petitioner’s neuroimaging and
came to the conclusion that petitioner had a myelopathy with a probable inflammatory cause.
See Pet. Ex. 7 at 10-11. Further, Dr. Matusumoto acknowledged the identification of a “small
cystic-appearing focus…at C7-T1,” but his impression was consistent with Dr. Keegan’s-that
petitioner had “an inflammatory myelopathy,” and referred to petitioner’s condition as “a
monophasic illness such as transverse myelitis.” Pet. Ex. 7 at 7. Petitioner’s neurologist Dr.
McDonald did the same, he recognized the existence of a syrinx at the level of T1, but concluded
that the “persistent abnormal cord signal at the cervicothoracic junction with overall decrease T2
18
Nuvigil (armodafinil) is used to treat excessive sleepiness caused by narcolepsy or shift work sleep disorder.
23
signal,” was suggestive of a remote inflammatory process or demyelization. Pet. Ex. 51 at 8.
The
Finally, the Ravalia et al. article, cited by Dr. Imperioli, suggests that the identified syrinx
developed in conjunction with petitioner’s transverse myelitis. The article reviews four cases of
individuals with spinal cord inflammation and syringomyelia and found that “syrinxes associated
with myelitis shared some common features: they developed during the acute phase of myelitis
and disappeared after steroids, were all non-communicating cavitations involving the central
canal and occurred in the same spinal segment affected by myelitis.” Pet. Ex. 57 at 1. The
authors concluded that the myelitis alone can induce the formation of a syrinx as a result of
intrinsic mechanisms, leading to accumulation of intra-spinal fluid. Id. at 6. They also stated
that the, “CSF-flow imbalance can accelerate the development of syringomyelia, especially in
myelitis characterized by discrete focal lesions.” Id. In petitioner’s case, he had a discrete focal
lesion identified on his MRI from C6-7to T3-4 and the small syrinx was identified in the same
area of his spine at T1. Pet. Ex. 51 at 20. Additionally, both experts classified the syrinx as non-
communicating. Resp. Ex. G at 1; Pet. Ex. 59 at 3. Even though petitioner’s syrinx did not
appear to have resolved with steroid treatment, he was treated with a lower dose and shorter
course of oral prednisone than the patients discussed in the Ravalia et al. article. Although
Dr,.Arkin leaned toward a diagnosis of syringomyelia, the later treating neurologists and
radiologist, particularly those at the Mayo Clinic, made a diagnosis of an inflammatory
myelopathy such as transverse myelitis.
2. Application of TMCWG’s criteria for idiopathic acute transverse
myelitis
The main contention between the parties is whether the proposed inclusionary criteria of
acute idiopathic transverse myelitis by the TMCWG should be applied in this case to support the
diagnosis of transverse myelitis. Pet. Brief at 18-19. Resp. Brief at 17.
Dr. Imperioli acknowledge the existence of the proposed diagnostic criteria by the
TMCWG and stated that petitioner had met all of the inclusionary criteria, except for the
proposed frame of progression to nadir of 4 hours to 21 days following the onset of symptoms
and he had none of the exclusionary criteria. Pet. Ex. 52 at 5. However, Dr. Imperioli argued
that the TMCWG proposed criteria was designed for the recruitment of patients into clinical
research studies and therefore may be too restrictive in clinical practice. Pet. Ex. 59 at 2. He
observed that even the authors acknowledged that the “interval between symptom onset and
maximal deficit is arbitrary,” and that “they remain committed to distinguishing ATM from a
rapidly evolving vascular myelopathy or a slowly progressive or stuttering myelopathy, spinal
cord tumor, myelopathy due to a dural arteriovenous fistula, and a chronic form of MS.” Resp.
Ex. A, Tab 1 at 3. Dr. Imperioli stated that, “The proposed criteria applies for the majority of
patients with acute transverse myelitis, but in clinical practice, it is common to evaluate a patient
with a medical condition manifesting in an atypical manner from what is described in text books
and other published literature.” Pet. Ex. 59 at 2.
Dr. Donofrio agreed with Dr. Imperioli that the proposed criteria developed by the
TMCWG was developed for recruitment of patients into research studies and that the criteria
24
may be too restrictive for clinical practice. Resp. Ex. C at 3. He continued, however, and stated
that, “…they are the best inclusion and exclusion criteria thus far,” and that he utilizes the
TMCWG’s criteria in his daily practice to diagnose TM and believes most of his colleagues do
as well. Id.; Resp. Ex. G at 1. Dr. Donofrio initially opined that petitioner only met three out of
the six inclusionary criteria proposed by the TMCWG in his first report, but modified his opinion
by his last report, noting that extra-axial compressive etiology was excluded. Resp. Ex. A at 5;
Resp. Ex. G at 2,4. Specifically, Dr. Donofrio stated that petitioner did not meet the proposed
inclusionary criteria for transverse myelitis because petitioner did not have a monophasic illness
which reached its nadir within 21 days from the onset of symptoms and that he did not have
convincing inflammation of the spinal cord by spinal fluid analysis. Resp. Ex. G at 4.
Dr. Imperioli explained that petitioner’s symptoms reached a nadir at approximately 3-4
months based on the records. Pet. Ex. 59 at 2. Petitioner stated that he first began experiencing
his noticeable symptoms of abdominal pain and difficulty urinating in late September. Pet. Ex.
49 at ¶ 1. He stated that he began to experience pain that was like a band with pressure around
his abdomen that built up over time, resulting in him seeking medical assistance on October 18,
2012. Id. at ¶ 2. Petitioner explained that by the time he was able to see his primary care
physician, Dr. Stiles, he was feeling weak and was unable to walk significant distances. Id. at ¶
3. The “Indication” field on petitioner’s October 26, 2012 MRI states, “Mid abdominal pain and
tightness. Difficulty walking. Tingling in the bilateral upper extremities. PAIN.” Pet. Ex. 10 at
42. This record supports petitioner’s statement that he began to have difficulty walking by late
October 2012. When petitioner saw Dr. Lovick on November 28, 2012, it was recorded that
petitioner had difficulty with his gait and difficulty with numbness in his legs and weakness in
his feet. Pet. Ex. 5 at 3. On December 26, 2012, petitioner returned to Dr. Lovick following the
arteriogram, which was negative for “any type of arteriovenous malformation,” and it was noted
that petitioner “is not getting any worse” and he was “clinically stable.” Id. at 5. When
petitioner presented at the Mayo Clinic for an evaluation, he told Dr. Keegan that “there was no
clear worsening recently,” and Dr. Keegan concluded that petitioner’s symptoms of gait
impairment plateaued between December and January [of 2013]. Pet. Ex. 7 at 8.
Dr. Donofrio asserted that petitioner’s symptoms progressed “at least through 2013 when
the petitioner required forearm crutches.” Resp. Ex. C at 6. In his opinion, the petitioner did not
have a monophasic illness and that petitioner’s nadir was not reached for 3-4 months after the
onset of his symptoms of pressure and burning over the abdomen. Id. However, petitioner
utilizing the forearm crutches in 2013 was the result of him following Dr. Keegan’s
recommended course of action and not evidence that his disease had progressed. See Pet. Ex. 7 at
11 (recommending petitioner utilize a gait aid for fall prevention).
While Dr. Imperioli conceded that petitioner’s disease progression was longer than the
TMCWG’s proposed criteria, he cited to medical literature which supports a longer progression
of symptoms than included in the TMCWG’s criteria. The Barreras article found that 67 patients
out of 247 with inflammatory myelopathy had a progression of symptoms of 21 days or greater.
Pet. Ex. 55 at 5; Pet. Ex. 59 at 2. The authors explained that a hyperacute presentation of
symptoms was suggestive of a spinal cord ischemic stroke and a chronic evolution was
suggestive of a vascular lesion, such as an arteriovenous fistulas or arteriovenous malformation.
Pet. Ex. 55 at 5. In petitioner’s case, the arteriovenous fistulas and arteriovenous malformation
25
were excluded by his treating physicians. See Pet. Ex. 5 at 5 (Dr. Lovick noting petitioner’s
arteriogram was negative for a dural AV fistula or any type of arteriovenous malformation.).
Thus, while not the classic presentation of transverse myelitis as defined by the TMCWG, the
symptom development and imaging in petitioner’s case appeared more likely than not to be the
result of an inflammatory process rather than a dural fistula which was ruled out or the syrinx,
which may well have been secondary to the initiating myelitis. Additionally, petitioner’s
symptoms did not appear to progress after December 2012, when Dr. Lovick noted that
petitioner was “clinically stable,” and petitioner’s symptoms had not progressed since the prior
visit on November 28, 2012. See Pet. Ex. 5 at 5. They appeared to have plateaued by the time
he went to the Mayo Clinic and Dr. Kegan’s recommendation of using a walker was for fall
protection not for progressing symptoms.
The TMCWG’s third criterion is that inflammation is demonstrated in the spinal cord by
CSF pleocytosis or elevated IgG index or gadolinium enhancement. Resp. Ex. A, Tab 1 at 2.
The criterion specifically states, “If none of the inflammatory criteria is met at symptom onset,
repeat MRI and lumbar puncture evaluation between 2-7 days following symptom onset to meet
criteria.” Id. Petitioner’s first MRI, on October 26, 2012, was done without the administration
of intravenous contrast. Pet. Ex. 10 at 42. His second MRI was done with enhancement and
found a “redemonstration of central T2 hyperintensity extending from C6-C7 to the T3-T4
level,” and, “there was no associated enhancement.” Id. at 38. Both Dr. Imperioli and Dr.
Donofrio acknowledged that the lack of gadolinium enhancement on petitioner’s second MRI
may have been due to the timing of the imaging obtained. See Pet. Ex. 52 at 6; Resp. Ex. C at 4.
Dr. Donofrio, however, argued that petitioner’s spinal fluid findings did not demonstrate
pleocytosis, as petitioner’s spinal fluid showed 1 white blood cell and his spinal fluid protein
elevation of 82 mg/dl was non-specific and would not support a diagnosis of TM without an
elevation of WBC count. Resp. Ex. C at 5. However, Dr. Donofrio’s reference is only to
petitioner’s second lumbar puncture, taken on January 21, 2013. Petitioner’s first lumbar
puncture, taken on November 26, 2012, revealed a slightly elevated protein level of 67 in his
CSF and a white blood cell count of 8/ul. Pet. Ex. 10 at 20; Pet. Ex. 11 at 186. The lab report
indicated that petitioner’s WBC count was “high.” Pet. Ex. 11 at 186. Dr. Imperioli stated that
evidence of inflammation within the spinal cord demonstrated by CSF pleocytosis is usually
considered an elevation of greater than 5 leukocytes/ul. Pet. Ex. 59 at 3. Additionally, the article
by Barreras found that 43% of patients who met the criteria for inflammatory myelitis did not
exhibit pleocytosis and 46% of patients had elevated protein (>45 mg/dl) in the CSF. Pet. Ex. 55
at 6. The record demonstrates that petitioner had mild CSF pleocytosis and thus would meet the
TMCWG’s third inclusionary criterion.
The record overall supports a finding that petitioner suffered from transverse myelitis.
Petitioner’s treaters were able to rule out possible alternative causes, such as an arteriovenous
fistula, neoplastic process, or sarcoidosis. Further, the identification of a small syrinx on
petitioner’s MRI did not change the impression of his treating physicians, particularly those at
the Mayo Clinic, that petitioner had an inflammatory myelopathy categorized as transverse
myelitis after the comprehensive evaluation at the Mayo Clinic. Finally, even if petitioner did
not meet all of the proposed diagnostic criteria for idiopathic transverse myelitis, experts from
both parties, along with the authors of the proposed Transverse Myelitis Working Group criteria,
26
agree that there are limitations to the criteria and the purpose of these restrictive criteria was to
“lead to the identification of more homogenous groups of individuals for clinical studies.” See
Resp. Ex. A, Tab 1 at 4. Therefore, based on the clinical judgment of his physicians, particularly
those at the Mayo Clinic who reviewed his history, all of his films and did a comprehensive
evaluation, I find that petitioner presented preponderant evidence that the petitioner’s
appropriate diagnosis is transverse myelitis.
V. Althen Prongs
In order to demonstrate entitlement for an “off-table” injury, petitioner must demonstrate
all three elements established by the Federal Circuit in Althen. 418 F. 3d 1274, 1278. The
petitioner must establish, by preponderant evidence: (1) a medical theory causally connecting the
vaccine and her injury; (2) a logical sequence of cause and effect showing that the vaccine was
the reason for his injury; and (3) a showing of proximate temporal relationship between the
vaccine and his injury. 418 F.3d at 1278.
In this case, the petitioner’s most difficult problem in proving causation is regarding the
acceptable timing criteria of Althen prong three. The third prong requires establishing a
“proximate temporal relationship” between the vaccination and the injury alleged. Althen, 418
F.3d at 1281. A petitioner must offer “preponderant proof that the onset of symptoms occurred
within a timeframe, which, given the medical understanding of the disorder’s etiology, it is
medically acceptable to infer causation. De Bazan v. Sec’y of Health & Human Servs., 539 F.3d
1347, 1352 (Fed. Cir. 2008). The explanation for what is a medically acceptable timeframe must
also coincide with the theory of how the relevant vaccine can cause an injury. Id.; see also
Shapiro v. Sec’y of Health & Human Servs., 101 Fed. Cl. 532, 542 (2011), recons. denied after
remand, 105 Fed. Cl. 353 (2012), aff’d mem., 2013 WL 1896173 (Fed. Cir. 2013); Koehn v.
Sec’y of Health & Human Servs., No. 11-355V, 2013 WL 3214877 (Fed. Cl. Spec. Mstr. May
30, 2013), mot. for review denied (Fed. Cl. Dec. 3, 2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).
Dr. Imperioli opined that there are several mechanisms by which antigens in vaccines can
induce transverse myelitis. Pet. Ex. 52 at 6. Dr. Imperioli referenced an article by Agmon-Levin
et al.19 which reviewed reported cases of transverse myelitis following vaccination, to support his
opinion that vaccines may induce transverse myelitis through molecular mimicry, epitope
spreading or bystander activation. Id. at 6-7. Dr. Imperioli also noted that the Agmon-Levin et
al. article identified 37 cases of post-vaccination transverse myelitis, which included 5 patients
with transverse myelitis following the DTP or DT vaccines and 1 following a pertussis
vaccination. Pet. Ex. 59 at 4; Pet. Ex. 39 at 14. Petitioner’s causation theory offered by Dr.
Imperioli includes molecular mimicry, which has been generally accepted as a reputable and
reliable scientific theory for explaining the pathophysiology of certain immune-mediated
conditions. See White v. Sec’y of Health & Human Servs., No. 15-1521V, 2019 WL 7563239
(Fed. Cl. Spec. Mstr. Dec. 19, 2019); Forrest v. Sec’y of Health & Human Servs., No. 14-1046V,
2019 WL 925495 (Fed. Cl. Spec. Mstr. Jan. 28, 2019); Hargrove v. Sec’y of Health & Human
Servs., No. 05-0694V, 2009 WL 1220986, at *38 (Fed. Cl. Spec. Mstr. Apr. 14, 2009).
19
Agmon-Levin, N. et al, Transverse Myelitis and vaccines: a multi-analysis, 18 Lupus 1198-1204 (2009). [Pet. Ex.
39].
27
As noted above, the petitioner is also required to show how the medically acceptable
timeframe for the onset of symptoms coincides with the theory of causation. The timing of the
onset of the petitioner’s transverse myelitis is a challenging problem, and in this case, is fatal to
the claim.
Dr. Imperioli stated that petitioner’s symptoms began 4-6 weeks after the vaccination,
which is a medically acceptable timeframe for transverse myelitis symptom onset. Pet. Ex. 52 at
7. Dr. Donofrio stated that if petitioner’s symptom began in late September or early October
2012, the symptoms are too delayed to attribute them to the onset of symptoms to the vaccination
of August 7, 2012. Resp. Ex. C at 4. He stated, “One would expect an immune response to
occur within 7-10 days after a vaccination, if implying an immune response modulated by
molecular mimicry, epitope spreading and induced autoimmunity from infectious agents or
vaccination.” Id. Dr. Fujinami also noted that if the Tdap vaccine contained cross-reacting
epitopes with myelin following immunization, the clinical manifestations would likely occur
within 2 weeks following vaccination, which is a very different time course than that
experienced by the petitioner. Resp. Ex. H at 4.
Petitioner received the Tdap vaccination on August 7, 2012. Pet. Ex. 1 at 1. On October
18, 2012, he presented to the University of Kansas Hospital urgent care, reporting mild
discomfort in the lower abdomen and urinary symptoms for “the last several days.” Pet. Ex. 6 at
5. When he sought treatment from his primary care physician on October 23, 2012, he reported,
“a week to 10-day history of upper abdominal discomfort,” and increasing problems of urinary
hesitancy. Pet. Ex. 10 at 5. Thus, based on the history provided at petitioner’s early
appointments in October 2012, and taking the version most favorable to the petitioner, the onset
would have been on or about October 13, 2012, or 67 days post-vaccination
At the Mayo Clinic, on March 18, 2013, or five months after the earlier reported date of
onset, petitioner told Dr. Matsumoto that, “In September he began to feel a tightness in his
abdomen,” and he experienced a sense of burning. Pet. Ex. 7 at 17. Then on March 21, 2013,
petitioner explained to Dr. Keegan that, “In about September or perhaps earlier, he developed a
numb sensation and tightness and burning sensation in his abdomen.” Id. at 10. However, in
petitioner’s affidavit, executed on November 29, 2017, petitioner stated, “….I did not have any
noticeable symptoms until late September to early October.” Pet. Ex. 49 at ¶ 2. He explained
that he was having trouble urinating, along with the abdominal pain. Id. He also described that
his pain felt like a band, with pressure across my abdomen. Id.
In his motion, petitioner argues that a medically appropriate timeframe of the onset of
transverse myelitis following the Tdap vaccination is 2-63 days. Pet. Mot. at 22. Petitioner
references the Agmon-Levin article to support a temporal association as long as three months
between vaccination and the onset of transverse myelitis. Pet. Ex. 39 at 1. It is important to note
that of the 37 cases in the Agmon-Levin study, only nine of the cases occurred more than 21
days post vaccination and three of those were at implausibly long intervals of four, six and nine
years post vaccination. Id. at 4. The three-month timeframe from vaccination to onset was in
relation to one Hepatitis B vaccination. Id. at 4. Id. at 4. Of the DTP, DT or pertussis20
20
The Agmon-Levin study did not report any cases involving TDaP vaccination, but I have considered all of the
vaccines containing component antigens of the TDaP vaccine.
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vaccinations, the intervals from injection to onset of symptoms were between three and
seventeen days. Id.
Dr. Donofrio’s opinion that symptom onset would have to occur between seven and ten
days post-vaccination is considerably shorter than accepted time periods in other vaccine cases,
however, the interval of 67 days for symptom onset falls outside a medically accepted temporal
association with vaccine causation. Even if it is assumed that petitioner’s symptoms began in
late September, the interval would be approximately 54 days post-vaccination, and would l have
begun outside the 4-6 week (28-42 day) window suggested by Dr. Imperioli. At petitioner’s first
medical appointment on October 18, 2012, he reported “several days” of abdominal pain, thus
putting onset of symptoms in mid- October. His second estimate of the date of onset given on
October 23, 2012, as seven to ten days is also consistent with a mid-October onset. Petitioner’s
statements in his supplemental affidavit rendered on November 29, 2017, places the onset of pain
in his bladder in “late September to early October.” Taking the latest time for medically
acceptable temporal association to the vaccine as proposed by Dr. Imperioli of 6 weeks or 42
days post-vaccination, the symptom onset would have had to occur by September 18, 2012.
There was no convincing evidence that the symptoms began on or before that date. The medical
records and petitioner’s statements persuasively put the onset of petitioner’s symptoms in mid-
October but no sooner than the end of September, thus falling outside of Dr. Imperioli’s
suggested timeframe for a medically acceptable temporal association with the Tdap vaccination.
Additionally, for petitioner’s claim an earlier onset for his condition makes transverse
myelitis less likely, in that transverse myelitis usually peaks within 21 days and, as observed at
the Mayo Clinic, his condition did not plateau until late December 2012 or early January 2013.
Even with a mid-October date of onset, the timing from onset to nadir in this case is unusual but
not impossible for transverse myelitis as demonstrated by some of the medical literature
submitted. However, if the onset of petitioner’s symptoms began in mid-September, as
suggested by petitioner to Mayo Clinic physicians, it makes the progression of his symptoms less
likely to fit transverse myelitis.
Special masters have found that a petitioner was entitled to causation where onset
occurred up to two months, or 56 days following the flu vaccination. Spayde v. Sec’y of Health
& Human Servs., No. 16-1499V, 2021 WL 686682 (Fed. Cl. Spec. Mstr. Jan. 27, 2021)
(accepting a 56-day onset for GBS following flu vaccination) (citing to Barone v. Sec’y of Health
& Human Servs., No. 11-707V, 2014 WL 6834557, at *13 (Fed. Cl. Spec. Mstr. Nov. 12, 2014)
(finding a six-week or 42-day interval from vaccination to onset of petitioner’s GBS). However,
these are cases involving the influenza vaccine and Guillain-Barré syndrome, and not the
occurrence of transverse myelitis following a Tdap vaccine. Further, other compensated cases
where petitioners suffered from transverse myelitis following the Tdap vaccination had onset of
symptoms much closer in time to the administration of the vaccine. See e.g. Roberts v. Sec’y of
Health & Human Servs., No. 09-427V, 2013 WL 5314698 (onset of symptoms began four weeks
after Tdap vaccination); Helman v. Sec’y of Health & Human Servs., No. 10-813V, 2012 WL
1607142, at *3 (Fed. Cl. Spec. Mstr. Apr. 5, 2012) (finding onset of symptoms occurring three
weeks after Tdap vaccination); Raymo v. Sec’y of Health & Human Servs., NO. 11-0654V, 2014
WL 1092274, at *19 (Fed. Cl. Spec. Mstr. Feb. 24, 2014) (finding a three to four-day onset of
29
transverse myelitis following administration of Tdap vaccine to medically appropriate temporal
relationship).
The Agmon-Levin article, which examined only 37 cases of transverse myelitis after
vaccination cannot be considered absolutely definitive in establishing an outer time line for
vaccine causation, it is the best evidence presented by the petitioner, and it reported onset of
transverse myelitis at most 17 days post-vaccination for DPT, DT or pertussis. Further, Vaccine
Program cases involving the Tdap vaccine have found vaccine causation where onset has
occurred 28 days post-vaccination. I do not consider four weeks or 28 days for onset to be a hard
line for establishing a medically appropriate timeframe, however, 54 to 67 days post-vaccination
for symptom onset is beyond the time period for which a medically acceptable causal timeframe
can be established based on current medical understanding and the evidence submitted in this
case. Therefore, I find that the petitioner has not established by preponderant evidence that his
symptoms began within a medically acceptable timeframe to satisfy Althen prong three.
VI. Conclusion
The petitioner has not carried his burden of proof, and therefore is not entitled to an
award of compensation. In absence of a motion for review filed pursuant RCFC Appendix B, the
Clerk of the Court shall enter JUDGMENT in accordance with the terms of this decision.
IT IS SO ORDERED.
s/Thomas L. Gowen
Thomas L. Gowen
Special Master
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