Greene v. Secretary of Health and Human Services

In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 11-631V
(to be published)

*************************
ROY GREENE, *
*
Petitioner, * Filed: August 2, 2019
*
v. *
*
SECRETARY OF HEALTH * Tetanus-Diphtheria (“Td”)
AND HUMAN SERVICES, * Vaccine; Evidentiary Support
* for Onset Timeframe; Expert
Respondent. * Opinions; Vaccine Trial
* Risk Intervals
*************************

Richard Gage, Law Offices of Richard Gage, Cheyenne, WY, for Petitioner.

Brittany Ditto, U.S. Dep’t of Justice, Washington, DC, for Respondent.

DECISION DENYING ENTITLEMENT1

On September 29, 2011, Roy Greene filed a petition for compensation in the National
Vaccine Injury Compensation Program (the “Vaccine Program”),2 alleging that he developed
brachial neuritis as a result of his receipt of the tetanus-diphtheria (“Td”) vaccine on July 22, 2009.
Pet. (ECF No. 1). Mr. Greene originally asserted both a Table injury claim and a “non-Table”
causation-in-fact claim (id. at 2), but I dismissed the Table claim after a March 2015 fact hearing,
at which time I determined that Petitioner’s symptoms arose forty-one days after the vaccination,

1
This Decision has been designated “to be published,” and will therefore be posted on the United States Court of
Federal Claims website, in accordance with the E-Government Act of 2002, Pub. L. No. 107-347, § 205, 116 Stat.
2899, 2913 (Dec. 17, 2002) (current version at 44 U.S.C. § 3501 (2014)). As provided by 42 U.S.C. § 300aa-
12(d)(4)(B), however, the parties may object to the published Decision’s inclusion of certain kinds of confidential
information. Specifically, under Vaccine Rule 18(b), each party has fourteen days within which to request 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). Otherwise, the whole Decision in its present form
will be available to the public. Id.
2
The Vaccine Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660,
100 Stat. 3758, codified as amended, 42 U.S.C. §§ 300aa-10 through 34 (2012) [hereinafter “Vaccine Act” or “the
Act”]. Individual section references hereafter will be to § 300aa of the Act.
and thus outside of the twenty-eight-day limit for a brachial neuritis Table claim. 42 C.F.R. §
100.3(a)(I)(B)).

This case has had a tortuous procedural history, but at long last the parties participated in
an entitlement hearing on May 9, 2019, at which time both sides offered expert testimony—
primarily addressing whether Mr. Greene’s brachial neuritis began in a medically acceptable
timeframe as measured from the date of vaccination. After listening to that expert testimony, and
considering the expert reports and literature offered, I find that Petitioner has not met his burden
of establishing by a preponderance that a six-week timeframe for onset of brachial neuritis after
receipt of the tetanus vaccine is medically reasonable—or that the vaccine “more likely than not”
did injure him given the undisputed facts.

Factual History

The facts relevant to the present decision are set forth in my earlier onset fact ruling. See
Greene v. Sec’y of Health & Human Servs., No. 11-631V, 2015 WL 9056034, at *1 - 4 (Fed. Cl.
Spec. Mstr. July 31, 2015) (“Fact Ruling”). They are incorporated by reference herein. The Fact
Ruling was issued after a 2015 hearing at which several witnesses testified, including Petitioner.
For present purposes, the most important of the Fact Ruling’s findings are as follows:

(a) Petitioner received the Td vaccine on July 22, 2009, in his right arm after experiencing
a significant construction-related injury to his hand at his workplace;

(b) Petitioner saw no healthcare providers in connection with his injury until September 7,
2009 (Labor Day of that year), when he went to a hospital emergency room in Houston,
Texas, complaining of sharp pain in his right upper arm that he stated had begun only a
few days before—not any time in the month of July or August;

(c) after hearing witness testimony and comparing it to the medical records filed in the
case, I determined that onset of Petitioner’s subsequently-diagnosed brachial neuritis3 had
occurred no earlier than September 1, 2009 (or 41 days post-vaccination); and

(d) based on this fact determination, I dismissed the Table claim, since Petitioner’s onset
had not been established preponderantly to have occurred within 28 days of administration
of the tetanus vaccine.

See generally Fact Ruling at *1–4, *17.

3
As recognized by the parties and their experts, the term “brachial neuritis” is medically synonymous with the terms
“Parsonage Turner Syndrome” or neuralgic amyotrophy. See, e.g., Tr. at 10, 69. I shall use the former as an overall
descriptor of Mr. Greene’s injury herein, although certain items of literature filed in this case use the other terms in
discussing the condition’s nature and etiology.

2
 Brief Summary of Relevant Procedural History

Between the date of the Fact Ruling and the fall of 2016, the parties could not settle the
non-Table claim. In that period, Petitioner submitted two expert reports from an orthopedist,
Thomas W. Wright, M.D. See Report dated Dec. 18, 2015, filed as Ex. 22 (ECF No. 62); Report
dated Apr. 25, 2016, filed as Ex. 29 (ECF No. 66). But Respondent took issue with the adequacy
of the opinions expressed therein—arguing in particular that more was needed on the third Althen
prong because of the conclusory nature of Dr. Wright’s opinion, which relied heavily on the fact
that a 41-day onset was only about two weeks longer than what the Table contemplates, rendering
the extra time a de minimis difference.

In light of Respondent’s objections, I proposed that Petitioner obtain an additional expert
report addressing the Althen prong three issue. See Status Conference Order, dated Sept. 29, 2016
(ECF No. 72). Mr. Greene thereafter filed an expert report from Dr. Marcel Kinsbourne on January
6, 2017. Respondent, however, deemed this report similarly inadequate and conclusory. In
response (and mindful that the case was now nearly six years old) I proposed that Respondent
either file his own expert report or move for a ruling on the record as it stood. See Status
Conference Order, dated Jan. 26, 2017 (ECF No. 86).

Respondent took the second option, filing a motion to dismiss in March 2017. See Motion
to Dismiss, dated Mar. 31, 2017 (ECF No. 90) (“Mot.”). Respondent argued that the record itself
(which at that time included only the two Wright expert reports plus the supplemental Kinsbourne
report, as well as my fact determination on onset) established “legally insufficient proof” for a
favorable entitlement decision and should therefore be dismissed. Id. at 1. In particular,
Respondent challenged Dr. Wright’s attempt to “piggyback” on the Table timeframes for
appropriate onset, despite clear Program law establishing that non-Table claims could not do so.
Id. at 5–6; (citing Grant v. Sec’y of Health & Human Servs., 956 F.2d 1144, 1147–48 (Fed. Cir.
1992) (“[s]imple similarity to conditions or time periods listed in the Table is not sufficient
evidence of causation”)). Respondent also maintained that Dr. Kinsbourne’s report set forth a
scientifically unreliable opinion, and was just as conclusory as Dr. Wright’s reports in assuming
that a 41-day onset period was within what is “generally recognized” as medically reasonable for
other autoimmune illnesses, without providing reliable scientific or medical substantiation for that
proposition. Id. at 8–9.

After the Motion was fully briefed, I granted it, but Petitioner subsequently filed a motion
for reconsideration on June 16, 2017, along with two new, supplemental expert reports (one from
Dr. Kinsbourne and an additional report from Dr. Vera Byers4) as well as several items of
previously-unfiled medical literature. ECF Nos. 94–97. I subsequently withdrew my initial
dismissal decision in order to evaluate the merits of the reconsideration request, but then denied

4
The Byers report (which was accompanied by five items of literature) was mistakenly filed twice. See Ex. 59. Its
contents were not referenced during the May 2019 hearing, and Dr. Byers did not testify there.

3
entitlement a second time. Greene v. Sec’y of Health & Human Servs., No. 11-631V, 2017 WL
5382856 (Fed. Cl. Spec. Mstr. Sept. 26, 2017) (“Second Dismissal Decision”). The Second
Dismissal Decision arose from my determination that Petitioner’s experts were improperly relying
on the Table timeframes to defend the medical sufficiency of the timeframe for onset of his brachial
neuritis. Second Dismissal Decision at *6–7.

In dismissing Mr. Greene’s claim, I erroneously conflated the standards applied to
evaluating a reconsideration request with the legal standards applicable to entitlement claims
generally. Petitioner thus sought review of the Second Dismissal Decision, and the Court of
Federal Claims granted his motion on February 27, 2018, remanding this matter back to me for a
new disposition of Respondent’s original motion, based on all evidence Petitioner had submitted
and applying the proper legal standards. Greene v. Sec’y of Health & Human Servs., No. 11-631V,
2018 WL 1514440 (Fed. Cl. Feb. 27, 2018). I thereafter determined that, because Petitioner had
now offered sufficient evidence to meet his preponderant burden of proof if unrebutted, I could
not grant Respondent’s request to dismiss the case. Remand Ruling, dated May 7, 2018 (ECF No.
116) (“Remand Ruling”). However, I also found that fairness required that I permit Respondent
(based on a prior request) the chance to submit his own expert report on the timeframe question,
and that I would hold a hearing thereafter. Id. at 11, 16.5

Respondent subsequently filed an expert report from Dr. Eric Lancaster on June 14, 2018
(ECF No. 121-1), with Petitioner filing a report from Dr. Laurence Steinman on November 13,
2018 (ECF No. 128-1). This prompted a supplemental expert report filing from Dr. Lancaster on
April 9, 2019 (ECF No. 133-1), and then a third expert report from Dr. Kinsbourne on April 29,
2019 (ECF No. 134-1). The hearing was held as scheduled on May 9, 2019, with no post-hearing
briefing. The matter is now fully ripe for resolution.

Summary of Expert Testimony

1. Dr. Marcel Kinsbourne

Dr. Kinsbourne filed three written reports and testified at hearing. See Report, dated Jan.
6, 2017, filed as Ex. 38 (ECF No. 82-1) (“Kinsbourne Rep.”); Report, dated June 13, 2017, filed
as Ex. 45 (ECF No. 94-1); Report, dated Apr. 26, 2019, filed as Ex. 73 (ECF No. 134-1); Tr. at 5–
38. Dr. Kinsbourne opined that onset of Mr. Greene’s brachial neuritis occurred in a medically
acceptable timeframe, based upon his characterization of brachial neuritis as a vaccine-caused,
neuropathic autoimmune injury comparable to Guillain-Barré syndrome (“GBS”). Tr. at 8.

5
Petitioner contested my determination to permit Respondent the opportunity to file his own expert report, rather than
simply decide the case based on the existing record, but the Court of Federal Claims ruled that these objections had
no legal merit. See Order, dated May 30, 2018 (ECF No. 119).

4
 As his curriculum vitae (“CV”) indicates, Dr. Kinsbourne is a pediatric neurologist. CV,
filed as Ex. 39 (ECF No. 82-2) (“Kinsbourne CV”). He received his medical degree in England,
and he has been licensed to practice medicine in North Carolina since 1967. Id. at 1. From 1967 to
1974, Dr. Kinsbourne served as an associate professor in pediatrics and neurology and a senior
research associate at Duke University Medical Center before holding a series of academic
positions, including professorships in pediatrics, neurology, and psychology. Id. at 2. His clinical
experience includes serving as a senior staff physician in Ontario from 1974–80, and as a clinical
associate in neurology at Massachusetts General Hospital from 1981–91. Id. at 2–3.

Dr. Kinsbourne has published several articles examining neurological diseases (though
none directly addressing brachial neuritis), and he is on the editorial board of several journals, such
as Brain and Cognition and Archives of Clinical Neuropsychology. Kinsbourne CV at 4, 7–40. His
focus has been on teaching cognitive and behavioral neuroscience for twenty years, retiring from
his teaching position at the New School a few years ago. Tr. at 28–29. Although a neurologist, and
although he claims to see patients occasionally, Dr. Kinsbourne has not had a regular clinical
practice for over twenty-five years, and has no specialized expertise in studying or treating
peripheral neuropathies like brachial neuritis (although he asserts that he has encountered it in his
patients). Id. at 6, 28, 36. Accordingly, the opinion Dr. Kinsbourne offered in this case was rooted
not in his personal experience (whether from clinical or research exposure) with brachial neuritis,
but arose from his own knowledge of neurology generally plus research performed specifically for
the purpose of offering an expert opinion for Petitioner.

Dr. Kinsbourne began with a general discussion of what brachial neuritis is, noting that it
usually presents abruptly in the shoulder and upper arm, with pain that can last for days or weeks,
and which can be accompanied by limb weakness and muscle atrophy. Tr. at 10. Because it is
heterogeneous in nature, its etiology can include both mechanical and immunologic causes,
although in either situation its symptoms follow a similar course. Id. at 11. When immunologic in
origin, brachial neuritis occurs because of an attack by autoantibodies, generated in response to
some external signal (i.e., infection), against either the outer myelin sheath of peripheral nerves in
the arms or the nerve axons (although Dr. Kinsbourne acknowledged that attack on the axon was
the main feature of brachial neuritis). Id.

In so maintaining, Dr. Kinsbourne analogized brachial neuritis to a different autoimmune-
in-origin peripheral neuropathy, GBS. Tr. at 12–15. He deemed GBS the most common
autoimmune peripheral neuropathy, stating that it “comes in two variants,” with one primarily
featuring demyelination of the nerve sheath, while the other, acute motor axonal neuropathy
(AMAN)6 involves attack on the nerve axon itself. Id. at 12, 14. He noted in particular that,
regardless of the variant and situs of nerve attack, medical literature supports the conclusion that

6
AMAN is a GBS subtype commonly seen in China, generally caused by the campylobacter virus. Dorland’s
Illustrated Medical Dictionary 1268 (32nd ed. 2012) [hereinafter “Dorland’s”]. It features motor axonal degeneration
with little inflammation or demyelination. P. Dyck & P.K. Thomas, 2 Peripheral Neuropathy 2200 (4th ed. 2005)
[hereinafter “Dyck & Thomas”].

5
the same antiganglioside autoantibodies are involved in the pathologic process leading to GBS
(thus allowing the inference that these autoantibodies might also be part of the process leading to
brachial neuritis). See R. Yu, et al., Ganglioside Molecular Mimicry and its Pathological Roles in
GBS and Related Diseases, 74 Infection & Immunity 6517 (2006), filed as Ex. 54 (ECF No. 95-1)
(AMAN and acute motor and sensory axonal neuropathy both associated with antibodies against
the ganglioside component of nerve membrane). GBS variants otherwise present with the same
symptoms and course, proceeding in a monophasic manner and peaking within thirty days at most
from onset (although the timeframe from instigation to onset can be longer). Id. at 13.7

To support his contention that GBS was sufficiently comparable to brachial neuritis to
apply the former’s timeframe for onset, Dr. Kinsbourne referenced several pieces of medical or
scientific literature. E.g., R. Verma, et al., Neuralgic Amyotrophy Associated with Dengue Fever:
Case Studies of Three Patients, 57 J. Postgraduate Med. 329 (2011), filed as Ex. 52 (ECF No. 94-
8) (“Verma”). Verma considered three patients who presented with brachial neuritis associated
with dengue infection (as opposed to vaccination). Verma at 329; Tr. at 51. All three developed
brachial neuritis in days to a week after experiencing an acute fever and/or rash brought on by the
instigating infection, suggesting to Verma’s authors that immune-mediated mechanisms explained
each case. Verma at 331. Dr. Kinsbourne felt Verma supported the possibility that brachial neuritis
could have a similar mechanism as GBS, such as molecular mimicry. Tr. at 19–20.

Other literature was offered to establish the existence of certain autoantibodies common to
both GBS and brachial neuritis – thus strengthening the idea that they have a common
pathogenesis. See, e.g., N. Van Alfen, The Clinical Spectrum of Neuralgic Amyotrophy in 246
Cases, 129 Brain 438, 448 (2006), filed as Ex. 51 (ECF No. 94-7) (“Van Alfen I”). Van Alfen I
observed that a certain percentage of individuals with brachial neuritis tested positive for
antiganglioside antibodies comparable to those associated with GBS. Tr. at 20–21; Van Alfen I at
444 (nine of thirty-four patients tested, or 26 percent). Van Alfen I itself, however, acknowledges
(consistent with what is understood about brachial neuritis generally in the medical community)
that “motor symptoms are said to predominate” in the condition, with sensory symptoms (which
would reflect impact on sensory nerves) secondary. Van Alfen I at 447–48.

To further support the contention that GBS and brachial neuritis are analogous autoimmune
conditions (making it reasonable to use the same timeframes for onset in both), Dr. Kinsbourne
also offered three Japanese case studies. Tr. at 22–23, 24–27, 33–34 (discussing K. Naito, et al.,
Intravenous Immunoglobulin (IVIg) Therapy with Methylprednisolone Pulse Therapy for Motor
Impairment of Neuralgic Amyotrophy: Clinical Observation in 10 Cases, 51 Internal Med. 1493

7
Dr. Kinsbourne also endeavored to identify record evidence suggesting that Mr. Greene had experienced
demyelination rather than simply an axonal attack. See, e.g., Tr. at 9–10 (citing Ex. 4 at 15 (notes from October 5,
2009 testing indicated presence of “a focal demyelinating process”)). However, Dr. Lancaster forcefully disputed that
this particular evidence established the presence of demyelination, allowing at best that the interpreting physician’s
comment “was an extremely indirect inference based upon very limited data,” and opining instead, based upon his
own reading of the same test results, that they did not establish demyelination. Id. at 96–97.

6
(2012), filed as Ex. 74 (ECF No. 134-2) (“Naito”); R. Morishima, et al., Chronic Brachial Plexus
Neuritis that Developed into Typical Neuralgic Amyotrophy and Positively Responded to
Immunotherapy, 57 Internal Med. 1021, filed as Ex. 75 (ECF No. 134-3) (“Morishima”); K.
Moriguchi, et al., Four Cases of Anti-Ganglioside Antibody-Positive Neuralgic Amyotrophy with
Good Response to Intravenous Immunoglobulin Infusion Therapy, 238 J. Neuroimmunology 107
(2011), filed as Ex. 76 (ECF No. 135-1) (“Moriguchi”)).

Naito and Morishima both examined the efficacy of immunotherapy treatments (common
to the treatment of GBS) such as intravenous immunoglobulin (“IVIG”)8 for brachial neuritis. In
Naito, for example, nine of ten brachial neuritis patients who received a form of IVIG treatment
showed improvement in motor impairment. Naito at 1499; Tr. at 22–23. Dr. Kinsbourne felt Naito
therefore supported his overall contention about GBS and brachial neuritis’s similarities—
although Naito’s authors were careful to limit their conclusions to the concept that only those
experiencing a severe form of brachial neuritis characterized by a prolonged autoimmune response
might benefit from immunosuppressive treatments like IVIG, adding that the overall efficacy of
such treatments for brachial neuritis as a whole remained unresolved—similar to the contention
(central to Petitioner’s theory herein) that antiganglioside antibodies are commonly a component
of brachial neuritis’s pathogenesis. Naito at 1499.

Morishima is a single-patient case study involving a fifty-five-year-old man who developed
brachial neuritis after a marine sports accident that caused direct injury to his arm and shoulder.
Morishima at 1021. After an initial acute response, the man’s pain and related symptoms subsided
for three months, but reappeared thereafter, proving resistant to treatment even a year later. Id. at
1021–22; Tr. at 24, 37. Lab tests revealed the man possessed the kind of antiganglioside antibodies
discussed above (suggesting to treaters that he was experiencing an ongoing autoimmune process),
leading them to employ IVIG effectively. Morishima at 1023. Morishima’s authors thus proposed
that this kind of treatment might also be of use in cases of chronic brachial neuritis. Id. at 1024–
25. Dr. Kinsbourne acknowledged that the lengthy, approximately twelve-week onset for the
patient’s brachial neuritis was an outlier, but maintained nonetheless that Morishima’s authors
appeared to have accepted it as reasonable. Tr. at 33–34.

Moriguchi considered four brachial neuritis patients, three of whom were believed to have
developed it from an antecedent infection (while the fourth had a history of symptom complaints
in connection with arm surgery). Moriguchi at 107; Tr. at 26. All of the studied individuals tested
positive for increased levels of antiganglioside antibodies, and two of the three patients whose
condition was associated with infection showed improvement after IVIG treatment—more
support, Dr. Kinsbourne maintained, for the similarities between GBS and brachial neuritis as
common autoimmune conditions with a similar pathogenesis. Moriguchi at 107–08; Tr. at 26–27.

8
IVIG is a blood product used to treat patients with antibody deficiencies. Caruso v. Sec’y of Health & Human Servs.,
No. 15-200V, 2017 WL 5381154, at *4 n.11 (Fed. Cl. Spec. Mstr. Oct. 18, 2017) (citing Clinical Uses of Intravenous
Immunoglobulin, NCBI (2005), https://www ncbi.nlm.nih.gov/pmc/articles/PMC1809480). Because it increases the
effectiveness of a patient’s immune response, IVIG is commonly employed to treat autoimmune conditions. Id.

7
Significantly, however, the individuals believed to have developed brachial neuritis after infection
(and hence those most analogous to a person, like Mr. Greene, whose brachial neuritis is posited
to have been vaccine-caused) experienced onset between one day and two weeks after infection—
not six weeks, as alleged is reasonable herein. Moriguchi at 107–08.

Dr. Kinsbourne subsequently addressed in more direct form the timeframe issue central to
Petitioner’s claim. Because of GBS’s “prototypical” nature as an autoimmune peripheral
neuropathy, Dr. Kinsbourne reasoned that the timeframe “risk intervals” that the scientific and
medical community uses for evaluating when GBS onset might properly be associated with a
vaccination could also be applied to a similar neuropathy like brachial neuritis. Tr. at 15. He thus
considered a number of items of literature he felt supported a longer timeframe—some, but not all,
of which involved brachial neuritis. E.g., H. Tseng, et al., Safety of a Tetanus-Diphtheria-Acellular
Pertussis Vaccine When Used Off-Label in an Elderly Population, 53 Clinical Infectious Diseases
315 (2012), filed as Ex. 49 (ECF No. 94-5) (“Tseng”).

Tseng, for example, considered 119,573 adults over the age of sixty-five who received the
tetanus-diphtheria-aceullar pertussis (“TDaP”) vaccine, following them over a four-year period to
evaluate the risk of adverse events (including GBS and brachial neuritis) after vaccination, in
comparison to the whole-cell form of vaccine that was previously in wide use. Tseng at 315; Tr.
at 30. Tseng’s authors noted that there was reliable evidence (derived from Institute of Medicine
(“IOM”) publications) supporting a possible causal relationship between TDaP and brachial
neuritis, thus justifying consideration of it as a possible adverse event. Tseng at 316 (citing K.R.
Stratton, et al., Adverse Events Associated with Childhood Vaccines Other Than Pertussis and
Rubella, 271 J. Am. Med. Ass’n 1602 (1994), filed as Ex. A (ECF No. 91-1) (“Stratton”)). They
found that brachial neuritis was no more common after Tdap vaccination than after Td. Id. at 316,
319; Tr. at 15–16, 30–31. In so doing, however, Tseng’s authors utilized a one to forty-two day
risk interval to look for brachial neuritis or GBS, although they did not explain why this interval
was used. Id. at 4.9

Van Alfen I included in its studied subject group individuals whose brachial neuritis was
considered hereditary or idiopathic, observing that a little over half (53.2 percent) reported an
antecedent event, with less than 5 percent of that subgroup reporting having been vaccinated before
symptoms arose. Van Alfen I at 440, 443. Although the time between vaccine administration and
onset was not reported, other onset times (after infection, exercise, or surgery) were measured as
under twenty-four hours, one to seven days, one to two weeks, and over two weeks, with most

9
In prior filings in this action, Respondent has observed the incongruity of Petitioner’s reliance on the IOM
determination of a causal association between tetanus-containing vaccines and brachial neuritis (see, e.g., Kinsbourne
Rep. at 3) and the fact that the IOM—which Tseng also relied upon as a basis for including it as a possible adverse
event—goes only to three or four weeks in proposing what a reasonable timeframe under such circumstances might
be. Mot. at 5–6, 8.

8
cases seeing onset within a week (although 10 percent of post-infection cases occurred more than
two weeks later). Id. at 443.

Other articles offered on the risk interval period said nothing about brachial neuritis
specifically. W. Yih, et al., An Assessment of the Safety of Adolescent and Adult Tetanus-
Diphtheria-Acellular Pertussis (Tdap) Vaccine, Using Active Surveillance for Adverse Events in
the Vaccine Safety Datalink, 27 Vaccine 4257 (2009), filed as Ex. 53 (ECF No. 94-9) “(Yih”); Tr.
at 30. Yih considered five categories of potential adverse events after TDaP vaccination:
encephalopathy-encephalitis-meningitis; paralytic syndromes, seizure, cranial nerve disorders, and
GBS. Yih at 4258. Nearly 700,000 TDaP recipients ten to sixty-four years old were followed for
145 weeks, relying on a forty-two-day risk interval for all potential adverse outcomes save seizure.
Id. at 4259, 4261. In doing so, Yih’s authors explained that, “not knowing the true window of risk
and not wanting to miss late events,” they relied on the same six-week period known to be
applicable to GBS, in a desire to be intentionally over-inclusive. Id. at 4259. Dr. Kinsbourne
deemed Yih significant despite its failure to include brachial neuritis as an adverse event because
it demonstrated the range of possible adverse outcomes involving possible autoimmune-mediated
conditions. Tr. at 17.

Another article discussed by Dr. Kinsbourne at hearing explored the larger question of what
kind of risk intervals should be used as a general matter in vaccine safety studies. See generally A.
Rowhani-Rahbar, et al., Biologically Plausible and Evidence–Based Risk Intervals in
Immunization Safety Research, 31 Vaccine 271 (2012), filed as Ex. 48 (ECF No. 94-4) (“Rowhani-
Rahbar”); Tr. at 17–18. Rowhani-Rahbar discussed the process for identifying and defining
biologically plausible and evidence-based risk intervals (the period of time after vaccination) for
adverse events following vaccination. Rowhani-Rahbar at 272. Risk intervals allow researchers to
study the incidence of a potential adverse effect by following risk and control intervals, and should
be determined by considering features of the adverse event, presumed or known pathologic
mechanism, and the vaccine itself. Id. at 272–73. The researchers cautioned against a too-long
interval, noting that the risk of adverse events is likely concentrated in a short period of time, and
that applying a long interval could dilute results pointing to the actual period of highest risk
(although a too-short period could also underestimate risk). Id. at 275. For these reasons, the
researchers emphasized the need to identify the most biologically-plausible timeframes possible.
Id.

Rowhani-Rahbar specifically proposed risk intervals for only two adverse events following
vaccine administration—febrile seizures and acute disseminated encephalomyelitis (“ADEM”).
Rowhani-Rahbar at 273. For ADEM (which, like brachial neuritis, is neurologic in nature, but is a
central nervous system disease rather than peripheral), Rowhani-Rahbar concluded that the most
trustworthy time period from vaccination to onset “best substantiated by available biological and
epidemiologic data” was five to twenty-eight days. Rowhani-Rahbar at 274. A secondary, longer

9
interval of two to forty-two days was also deemed “biologically plausible,”10 and therefore worthy
of consideration in order to fully assess a potential safety problem, but was more uncertain, since
“there might be reason to suspect that most of the excess risk, if any, is concentrated in a much
shorter period of time.” Id. at 275; Tr. at 18–19.

Based on the above, Dr. Kinsbourne opined that onset of Petitioner’s brachial neuritis forty-
one days after vaccination was medically reasonable. He noted that he would actually support a
similar six-week period for virtually any autoimmune disease with “no hesitation,” adding that
although he was aware of reliable scientific support for even longer onsets in the case of other
autoimmune conditions like GBS, he was not comfortable proposing a timeframe beyond forty-
two days. Tr. at 31–33. He admitted, however, that even if such a six-week period was reliable,
the probability of developing brachial neuritis diminished as the tail end of the temporal “curve”
was reached. Id. at 38. He also acknowledged that none of the evidence offered for the timeframe
question directly involved cases measuring onset from vaccination, as opposed to a different cause
(although he emphasized that some evidence, like Van Alfen I, did support the more general
proposition that vaccines could cause brachial neuritis). Id. at 37; Van Alfen I at 443.

2. Dr. Laurence Steinman

Dr. Steinman prepared one brief written report for this case and testified at hearing. Tr. at
39–71, 135–43; Report, dated Nov. 12, 2018, filed as Ex. 68 (ECF No. 128-1). He offered an
opinion that largely overlapped with what Dr. Kinsbourne presented.

Dr. Steinman obtained his medical degree from Harvard Medical School, where he
completed a fellowship in chemical neurobiology. Tr. at 39; see also CV at 1, filed as Ex. 77
(ECF No. 136-1) (“Steinman CV”). After medical school, Dr. Steinman went on to complete both
a pediatrics and neurology residency at Stanford University. Tr. at 39; Steinman CV at 1. He then
joined the faculty at Stanford in 1980, where he presently serves as the George A. Zimmerman
Professor of Neurological Sciences, Neurology, Genetics and Pediatrics. Tr. at 39; Steinman CV
at 1. Dr. Steinman claimed to have encountered brachial neuritis at least one hundred times in his
career (although he did not specify when he most recently encountered it—or whether his
encounters came via his role as professor overseeing the work of medical residents, as opposed
to his own treatment of patients). Tr. at 136. Dr. Steinman has also published extensively in peer-
reviewed journals on topics including neuroimmunology and GBS. Steinman CV at 5–45. He has
demonstrated expertise in both a wide variety of central nervous system diseases (multiple
sclerosis in particular) and immunologic issues, and claimed great familiarity in treating brachial
neuritis, although he does not appear to have focused on it over other central nervous system

10
The only support for this timeframe offered in Rowhani-Rahbar is the statement that “[b]ased on prior reports of
the onset of ADEM following immunization, the occurrence of such events appears to decrease substantially beyond
6 weeks.” Rowhani-Rahbar at 274. This statement is footnoted in turn by nine items of literature—all involving
ADEM, however, and some of which appear to discuss passive surveillance reports of post-vaccine cases rather than
to weigh actual biologic risk.

10
 diseases (such as multiple sclerosis).

Dr. Steinman characterized brachial neuritis as a kind of neuropathic autoimmune disease.
Although his testimony on this point was mostly indistinguishable from Dr. Kinsbourne’s, he did
attempt to refine some of Dr. Kinsbourne’s earlier assertions. Thus, Dr. Steinman emphasized that
brachial neuritis is in his opinion likely an inflammatory autoimmune condition, similar to GBS in
pathophysiology, although more focal (i.e., restricted to an arm and shoulder as opposed to having
an impact bilaterally/symmetrically). Tr. at 43–44. He allowed that it has different triggers than
GBS, although Dr. Steinman emphasized its immunologic character, based on his experience as
well as existing literature. Tr. at 135–36 (referencing Van Alfen I in support of his contention that
the most common cause for brachial neuritis is not trauma but an immunologic trigger, such as
vaccination or infection), 138 (noting that based upon his experience “at grand rounds or some
teaching conference,” the etiology of brachial neuritis can be identified half of the time).

Consistent with Dr. Kinsbourne’s testimony, Dr. Steinman asserted that brachial neuritis
involves attacks on myelin and nerve axon equally. Tr. at 56–57. He admitted, however, that
brachial neuritis is not exclusively immunologic in origin, but can also be the result of some direct
trauma (like the case study discussed in Morishima), although the subsequent pathogenesis in all
cases would be “autoimmune or at least inflammatory,” concepts he contradictorily claimed were
the same but also distinguishable. Id. at 70–71.

Also consistent with Dr. Kinsbourne’s prior testimony was Dr. Steinman’s overarching
presumption that GBS, and what is known about it in terms of vaccine causation, provides an
analog to brachial neuritis for purposes of determining timeframe in this case. Thus, he deemed
significant the fact that brachial neuritis has been shown (in case reports like Naito and Moriguchi)
to respond to immune-modulating treatments like IVIG,11 and that the specific antiganglioside
antibodies allegedly associated with GBS were observed to be present for the patients considered
by these case studies, thereby confirming its autoimmune character and/or similarity to GBS—
along with the fact that (reflecting the role the immune system writ large plays in its pathogenesis)
brachial neuritis does not always occur in the same arm that receives trauma. Tr. at 57–64. He also
maintained, like Dr. Kinsbourne, that “host factor” variations in how an individual reacts to an
event triggering an autoimmune response would impact that individual’s course. Id. at 44–45.

Based upon the foregoing, Dr. Steinman echoed Dr. Kinsbourne’s conclusion that
timeframes viewed as medically reasonable for onset of GBS were equally applicable to brachial
neuritis. In so maintaining, he relied on the fact that both illnesses are directed at the peripheral
nerves and (in his view) likely involve similar mechanistic paths. Tr. at 45. He also invoked a
seminal item of medical literature (not directly relevant to brachial neuritis) from the swine flu

11
Dr. Steinman went so far as to assert that IVIG is used at his own hospital at Stanford to treat brachial neuritis,
although he did not substantiate this assertion with any independent evidence. Tr. at 138.

11
epidemic in the 1970s. L. Schonberger, et al., Guillain-Barré Syndrome Following Vaccination in
the National Influenza Immunization Program, 110 Amer. J. Epidemiology 105 (1979), filed as
Ex. 69 (ECF No. 128-2) (“Schonberger”). Schonberger, Dr. Steinman observed, supported up to a
ten-week timeframe for onset of GBS, but suggested risk was highest in the shorter, six to seven-
week interval (although Schonberger itself expressly states that GBS risk “was concentrated
primarily within the 5-week period after vaccination”). Schonberger at 105; Tr. at 47, 49. Because
Schonberger was “based on an enormous data set of surveillance,” he felt it was a particularly
reliable epidemiologic study that had applicability herein. Id. at 47, 55.12

As a result, Dr. Steinman (like Dr. Kinsbourne) endorsed a six-week timeframe for onset
of brachial neuritis after vaccination as medically reasonable. Tr. at 53. He claimed that, in his
own clinical experience, he had seen a variety of onsets ranging throughout the proposed six-week
period, but that onset toward the end of that period “would not worry me.” Id. at 141. In explaining
this conclusion, Dr. Steinman repeated many of the same points made by Dr. Kinsbourne,
commenting on the same items of literature reviewed during Dr. Kinsbourne’s testimony. He was
thus asked about Verma (Tr. at 50–51), Yih (id. at 52–53), Rowhani-Rahbar (id. at 54–56), Naito
(id. at 58–59), Morishima (id. at 60–61), and Moriguchi (id. at 62–63). He acknowledged,
however, when asked generally about the utility of risk intervals, that they were often primarily
the product of what a particular study’s authors wanted to achieve in a particular study, rather than
a reflection of biological plausibility for a given potentially adverse event. See, e.g., Tr. at 52–53,
55 (“where you set the dial is in the hands of the person or teams turning the dial”).

On cross examination, Dr. Steinman admitted some limitations to the bases for his
conclusions regarding timeframe for onset herein. He allowed that case studies like Naito
equivocated as to the efficacy of immunotherapies for brachial neuritis, although he maintained
nonetheless that such evidence pointed in the direction of the utility of such treatments, even if
more formal scientific corroboration was still absent. Tr. at 67–68. He agreed that such treatments
were not uniformly called for either, especially since certain individuals suffering from brachial
neuritis might see improvement absent IVIG treatment (although he stressed the medical
importance of doing whatever possible to aid patients). Id. at 68. And he conceded that one of the
articles referenced in his own expert report only supported a three-week timeframe for post-
vaccination onset of brachial neuritis. Id. at 65–66 (discussing P. Tsairis, et al., Natural History of
Brachial Plexus Neuropathy, 27 Arch. Neurol. 109, 111–12 (1972), filed as Ex. 58 (ECF No. 95-
5) (“Tsairis”)).

12
Dr. Steinman also noted that the tetanus vaccine package insert indicates that individuals with GBS are advised
against getting a second vaccine within six weeks of the disease’s appearance as further bulwarking the reliability of
the six-week timeframe. Tr. at 49–50. Petitioner did not, however, file this document—and even if he had, the fact
that it applies to GBS (coupled with existing sound Vaccine Program caselaw suggesting that package inserts deserve
little evidentiary weight) greatly reduces the value of this argument (especially given the existence of several more
reliable items of evidence that were filed in this action and which support the timeframe argument (e.g., Rowhani-
Rahbar)).

12
3. Dr. Eric Lancaster

Dr. Eric Lancaster provided two expert reports in this action on Respondent’s behalf, and
also testified at hearing. See Report, dated May 25, 2018, filed as Ex. B (ECF No. 121-1)
(“Lancaster Rep.”); Report, dated Mar. 28, 2019, filed as Ex. D (ECF No. 133-1) (“Supp. Lancaster
Rep.”). Dr. Lancaster opined that the tetanus vaccine did not likely cause Petitioner’s brachial
neuritis, and that the timeframe in which Petitioner’s injury began was not a medically acceptable
period for post-vaccination causation. In so proposing, he disputed the assumption of Petitioner’s
experts that what is known about GBS onset and timeframe can be applied equally to brachial
neuritis.

Dr. Lancaster is a clinical physician at the Center for Autoimmune Neurology at the
University of Pennsylvania, as well as an assistant professor of neurology at the University of
Pennsylvania. Ex. C at 1 (ECF No. 121-11) (“Lancaster CV”). He completed a neurology
residency at the University of Pennsylvania from 2004–07, and is board certified in neurology,
with subspecialties in neuromuscular medicine and electrodiagnostic medicine. Id.; Tr. at 73–74.
His research focuses on antibody-mediated neurological disorders, and he sees patients with
complex autoantibody disorders on a regular basis. Lancaster CV at 1; Tr. at 75. He has
considerable expertise performing the tests used to evaluate peripheral neuropathies (e.g., EMGs,
nerve conduction studies)13, and devotes half his time to a clinical practice, although he estimates
only to have treated ten to twenty patients with brachial neuritis over his career. Tr. at 74–75;
Lancaster Rep. at 1.

Dr. Lancaster’s description of brachial neuritis was mostly consistent with that provided
by Petitioner’s experts, although it diverged in a few significant respects. He characterized the
condition as “inflammation in a particular area of the nervous system called the brachial plexus,”
located in the shoulder near the neck. Tr. at 76–77. It has a monophasic course, with a sudden
onset followed by a slow recovery over weeks or months, although patients often recovery fully.
Id. at 77. He was less confident than Petitioner’s experts that brachial neuritis is primarily
autoimmune in nature, however, noting that although “it certainly involves inflammation,” not
enough is known about its pathophysiology and the mechanisms driving it (for example, whether
it is solely antibody-mediated or the result of a T-cell response) to firmly state that it is primarily
an autoimmune condition. Id. at 107. But several items of literature filed by Respondent seem to
accept that autoimmunity plays a role in brachial neuritis’s pathogenesis. See, e.g., N. Van Alfen,
Clinical and Pathophysiological Concepts of Neuralgic Amyotrophy, 7 Nat. Rev. Neurol. 315, 320

13
An EMG, or electromyography test, is a diagnostic procedure used to assess the health of muscles and the nerve
cells that control them (motor neurons). Dorland’s at 602. A nerve conduction study, or “nerve conduction velocity
test,” measures the speed of conduction of an electrical impulse through a nerve, to evaluate the presence of nerve
damage or destruction. Nerve Conduction Studies, Health Library, Johns Hopkins Medicine,
https://www.hopkinsmedicine.org/health/treatment-tests-and-therapies/nerve-conduction-velocity-ncv (last visited
July 23, 2019).

13
(2011), filed as Ex. B-1 (ECF No. 121-2) (“Van Alfen II”) (acknowledging that brachial neuritis
“is thought to be autoimmune in origin”).

Dr. Lancaster nevertheless stressed (in contrast to Drs. Kinsbourne and Steinman) that
brachial neuritis is primarily an “axonal” injury to the nerves, readily ascertainable via an EMG
study, rather than one featuring multifocal demyelination—and in fact it is this axonal
characteristic that causes recovery after onset to take time. Tr. at 77, 96–97; Lancaster Rep. at 6;
J. Feinberg, et al., Parsonage-Turner Syndrome, 6 Hosp. for Spec. Surg. 199, 202 (2010), filed as
Ex. B-2 (ECF No. 121-3) (“Feinberg”); see also Van Alfen II at 319 (“[a]s in other [peripheral
nervous system] disorders, the amount of axonal damage provides a fair prediction of the
possibility for nerve recovery,” adding that subsequent reinnervation can take months or years).
He indicated no awareness, based on existing literature or medical community views, that brachial
neuritis should be considered primarily a demyelinating injury, noting that testing (such as nerve
conduction studies) used to diagnose brachial neuritis does not usually reveal “severe conduction
slowing or reversible conduction blocks”—either of which would reflect the existence of
demyelination. Tr. at 79.

Dr. Lancaster similarly took issue with the efforts of Petitioners’ experts to borrow GBS
onset timeframes for this case, stressing the differences in the two conditions: the focal and
localized nature of the inflammation present in brachial neuritis, as opposed to the multifocal,
bilateral character of GBS, and the demyelination featured most often in GBS, as opposed to the
“axonal process” in brachial neuritis. Tr. at 87–88, 89 (“these are very different disorders and it
isn’t that hard to tell them apart”), 94–95 (referencing Van Alfen II). He also disputed the efficacy
of immunosuppressive treatments for brachial neuritis, arguing that although such treatments have
been medically established to be effective for GBS, there is a lack of persuasive and reliable
scientific data establishing their utility for brachial neuritis, and that he had not in his experience
encountered the use of such treatments for this condition (or the testing of brachial neuritis patients
for the presence of autoantibodies). Id. at 88–89, 124–26. And he noted that given what is known
about the two diseases and their differing courses (with brachial neuritis having a higher likelihood
of a fast onset after triggering event than GBS), it made sense to him that the latency period
relevant to one would be inapplicable to the other. Id. at 89–91. In fact, he felt it far more medically
likely that brachial neuritis would have a shorter, post-trigger onset than GBS. Id. at 91–92.

Another distinction between GBS and brachial neuritis that Dr. Lancaster deemed
significant was the fact that the latter can be initiated by “different triggering events” not associated
with the former. Tr. at 77. Brachial neuritis can be caused by injury from exertion or other arm
trauma, infection, or vaccination—although half of the time in his experience no causal factor
could be identified. Id. at 77, 104 (discussing vaccination as possible cause). Regardless, the
presentation and progression of most cases of brachial neuritis was the same. Id. at 78. He also
emphasized that direct injury to the nerve itself was not a requirement for triggering of brachial

14
neuritis. Id. at 78, 83–84. On the contrary, “relatively minor events” could produce brachial
neuritis, from overexertion after exercise to maintaining the same body position on a lengthy
airplane flight. Id. at 99–100, 111–12; Lancaster Rep. at 7. He particularly stressed that unlike
GBS, brachial neuritis could have direct arm trauma as its triggering event. Tr. at 90 (“[t]his has
not, to my knowledge, ever been accepted as the cause of [GBS]”).

Turning to the present record, Dr. Lancaster agreed that Petitioner has brachial neuritis. He
did not, however, see evidence that would suggest Mr. Greene’s immune system was undergoing
an autoimmune process in the forty-one-day period between receipt of the tetanus vaccine and
onset of his symptoms in September 2009. Tr. at 80. Indeed, he disputed that such a long timeframe
was reasonable for onset of brachial neuritis after any inciting event.

Relying on Van Alfen I as well as Tsairis, along with his personal clinical experience, Dr.
Lancaster observed that half of studied cases in those items of literature began within a week of
the putative trigger,14 with 90 percent occurring in two weeks. Tr. at 81, 85–87; Tsairis at 111–12;
Van Alfen I at 443 (nearly 70 percent of all studied cases reporting an antecedent event involved
symptom onset within a week or less). He therefore deemed an onset beyond three to four weeks
of the triggering incident as “increasingly implausible.” Tr. at 81. He also disputed the validity of
employing a single timeframe for all neuroimmune disorders attributable to vaccination, as
Petitioner urges. Id. at 82. He did, however, acknowledge that certain items of literature, like Van
Alfen I, seemed to allow for the possibility that brachial neuritis could still occur at a timeframe
beyond two weeks (even though his reading of the data from that item of literature suggested that
the syndrome was “very heavily concentrated” on the immediate two to three weeks after a trigger).
Id. at 117–19; Van Alfen I at 443 (approximately 10 percent of forty-nine studied cases involved
onset of post-infection brachial neuritis occurring more than two weeks after the infection, with
the remaining 90 percent occurring two weeks or less after infection).

Dr. Lancaster noted several findings in the medical record that he deemed significant to his
opinion. The electrodiagnostic test results for Mr. Greene suggested to him the presence of “severe
axonal injury,” with far less convincing evidence of demyelination, and nothing that would suggest
the presence of GBS either. Tr. at 96–97; Lancaster Rep. at 10–11. Such results were therefore
consistent with brachial neuritis. Tr. at 97. He also observed no treater support for the tetanus
vaccine being causal. Id. at 98. And overall, based on his view of the totality of the record, he
thought it most likely that in Mr. Greene’s specific case physical exertion close in time to onset in

14
Dr. Lancaster acknowledged that it might be difficult in cases of infection-induced brachial neuritis to pin down the
date of the inciting event, but noted that incidents involving arm trauma (whether from exertion, accident, or surgery)
were a different matter—and in such cases latency was often very short. Tr. at 81.

15
early September was the most likely trigger15 —otherwise the cause was idiopathic (although he
did not discount the initial hand injury that Petitioner suffered, which caused him to receive the
tetanus vaccine in the first place, as also possibly causative). Id. at 98–104; Ex. 12 at 19 (September
7, 2009 ER record with handwritten note referencing Petitioner’s exertion in the days prior to onset
as a possible “recent injury” explanation for pain).16

Dr. Lancaster went on to review the literature and evidence offered in the case to support,
or refute, a forty-one-day timeframe for onset of post-vaccination brachial neuritis. While articles
like Tsairis did allow that a vaccine might be causative, they lent support for a timeframe for onset
of no more than four weeks. Tr. at 82–84; Tsairis at 111. Rowhani-Rahbar also did not consider
brachial neuritis in proposing the two risk intervals it discusses, and in fact its authors were in Dr.
Lancaster’s view “extremely careful” to highlight that any selected interval needed “to be
customized to the specific disease in question.” Tr. at 85. Schonberger similarly only involved
GBS, and in Dr. Lancaster’s reading underscored the fact that brachial neuritis and GBS have
distinguishable pathophysiologies. Id. at 92–93.

Dr. Lancaster also directly questioned the significance of the three Japanese case studies
(Naito, Morishima, and Moriguchi) filed by Petitioner and commented upon by his experts. He
challenged their findings about the efficacy of immunosuppressive treatments for brachial neuritis
(which, Petitioner argues, corroborates the similarity of the condition to more purely autoimmune
neuropathies like GBS), allowing that even if those articles suggested IVIG might be effective in
treating brachial neuritis, “the jury is still out” on the mechanism by which brachial neuritis occurs
(and in particular whether it is mediated by autoantibodies at all, let alone the same ones implicated
in GBS). Tr. at 94, 121–22. He also did not deem significant the fact that some evidence of
autoantibodies also relevant to GBS was identified in tests performed in these case reports, noting
that he could not exclude the possibility that they were merely false positive findings, reflecting
the fact that many people in the population might also possess them (but not establishing that their
presence meant the patient’s brachial neuritis had been mediated by the autoantibody). Id. at 108–
09.

15
See, e.g., Lancaster Rep. at 9. Because this Decision does not turn on identifying an alternative cause, but instead is
the product of my determination that the proposed forty-one-day onset has not been established with sufficient
preponderant evidence, I do not analyze Respondent’s success in establishing such factual contentions.
16
Mr. Greene was called at hearing to testify to rebut this point, and he maintained that he had not in fact overexerted
or otherwise harmed his arm or shoulder in the days immediately prior to his ER visit in September 2009—and that
he did not so inform treaters at the time, despite what the contemporaneous medical document states. Tr. at 127–29,
130–31. Respondent, however, offered a later-in-time medical record, filled out by Petitioner, in October 2009 (a
month after the ER visit) in which he himself again identified “hard work” around Labor Day of that year triggering
a “neuro explosion.” Id. at 132; see also Ex. 2 at 4; Ex. 12 at 19. Petitioner could not credibly explain these medical
record references and their contradiction of his recollection, other than by asserting that the degree of pain he was in
at the time (coupled with his lack of knowledge about what brachial neuritis was) somehow impacted his judgment or
what he told treaters. Tr. at 133–34.

16
 On cross examination, Dr. Lancaster granted the medical plausibility of a causation theory
relying on vaccination as initiating brachial neuritis, even if the absence of evidence of the correct
autoantibodies relating to the process resulting in the condition. Tr. at 110. He also acknowledged
(in response to questions that seemed aimed at establishing that Dr. Lancaster’s standard for
medical acceptability was far too high for purposes of a Vaccine Program case) that he personally
would not accept a forty-one-day timeframe for onset of brachial neuritis without some kind of
corroborative scientific or medical study specific to brachial neuritis and vaccination. Id. at 107.

Applicable Legal Standards

A. Claimant’s Burden in Vaccine Program Cases

To receive compensation in the Vaccine Program, a petitioner must prove either: (1) that
he suffered a “Table Injury”—i.e., an injury falling within the Vaccine Injury Table—
corresponding to one of the vaccinations in question within a statutorily prescribed period of time
or, in the alternative, (2) that his illnesses were actually caused by a vaccine (a “Non-Table
Injury”). See Sections 13(a)(1)(A), 11(c)(1), and 14(a), as amended by 42 C.F.R. § 100.3;
§ 11(c)(1)(C)(ii)(I); see also Moberly v. Sec’y of Health & Human Servs., 592 F.3d 1315, 1321
(Fed. Cir. 2010); Capizzano v. Sec’y of Health & Human Servs., 440 F.3d 1317, 1320 (Fed. Cir.
2006).17 As already noted, Petitioner’s Table claim was dismissed after issuance of the Fact Ruling.

For both Table and Non-Table claims, Vaccine Program petitioners bear a “preponderance
of the evidence” burden of proof. Section 13(1)(a). That is, a petitioner must offer evidence that
leads the “trier of fact to believe that the existence of a fact is more probable than its nonexistence
before [he] may find in favor of the party who has the burden to persuade the judge of the fact’s
existence.” Moberly, 592 F.3d at 1322 n.2; see also Snowbank Enter. v. United States, 6 Cl. Ct.
476, 486 (1984) (mere conjecture or speculation is insufficient under a preponderance standard).
Proof of medical certainty is not required. Bunting v. Sec’y of Health & Human Servs., 931 F.2d
867, 873 (Fed. Cir. 1991). In particular, a petitioner must demonstrate that the vaccine was “not
only [the] 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., 165 F.3d 1344,
1352-53 (Fed. Cir. 1999)); Pafford v. Sec’y of Health & Human Servs., 451 F.3d 1352, 1355 (Fed.
Cir. 2006). A petitioner may not receive a Vaccine Program award based solely on his assertions;

17
Decisions of special masters (some of which I reference in this ruling) constitute persuasive but not binding
authority. Hanlon v. Sec’y of Health & Human Servs., 40 Fed. Cl. 625, 630 (1998). By contrast, Federal Circuit rulings
concerning legal issues are binding on special masters. Guillory v. Sec’y of Health & Human Servs., 59 Fed. Cl. 121,
124 (2003), aff’d, 104 F. App’x 712 (Fed. Cir. 2004); see also Spooner v. Sec’y of Health & Human Servs., No. 13-
159V, 2014 WL 504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014).

17
rather, the petition must be supported by either medical records or by the opinion of a competent
physician. Section 13(a)(1).

In attempting to establish entitlement to a Vaccine Program award of compensation for a
Non-Table claim (which is the kind of claim asserted in this matter), a petitioner must satisfy all
three of the elements established by the Federal Circuit in Althen v. Secretary of Health & Human
Services, 418 F.3d 1274 (Fed. Cir. 2005): “(1) a medical theory causally connecting the
vaccination and the injury; (2) a logical sequence of cause and effect showing that the vaccination
was the reason for the injury; and (3) a showing of a proximate temporal relationship between
vaccination and injury.” Althen, 418 F.3d at 1278.

Each of the Althen prongs requires a different showing. Under Althen prong one, petitioners
must provide a “reputable medical theory,” demonstrating that the vaccine received can cause the
type of injury alleged. Pafford, 451 F.3d at 1355–56 (citations omitted). To satisfy this prong, the
petitioner’s theory must be based on a “sound and reliable medical or scientific explanation.”
Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 548 (Fed. Cir. 1994). Such a theory
must only be “legally probable, not medically or scientifically certain.” Id. at 549.

Petitioners may satisfy the first Althen prong without resort to medical literature,
epidemiological studies, demonstration of a specific mechanism, or a generally accepted medical
theory. Andreu v. Sec’y of Health & Human Servs., 569 F.3d 1367, 1378–79 (Fed. Cir. 2009)
(citing Capizzano, 440 F.3d at 1325–26). Special masters, despite their expertise, are not
empowered by statute to conclusively resolve what are essentially thorny scientific and medical
questions, and thus scientific evidence offered to establish Althen prong one is viewed “not through
the lens of the laboratorian, but instead from the vantage point of the Vaccine Act’s preponderant
evidence standard.” Id. at 1380. Accordingly, special masters must take care not to increase the
burden placed on petitioners in offering a scientific theory linking vaccine to injury. Contreras v.
Sec’y of Health & Human Servs., 121 Fed. Cl. 230, 245 (2015) (“[p]lausibility . . . in many cases
may be enough to satisfy Althen prong one” (emphasis in original)). But this does not negate or
reduce a petitioner’s ultimate burden to establish his overall entitlement to damages by
preponderant evidence. W.C. v. Sec’y of Health & Human Servs., 704 F.3d 1352, 1356 (Fed. Cir.
2013) (citations omitted).

The second Althen prong requires proof of a logical sequence of cause and effect, usually
supported by facts derived from a petitioner’s medical records. Althen, 418 F.3d at 1278; Andreu,
569 F.3d at 1375–77; Capizzano, 440 F.3d at 1326; Grant, 956 F.2d at 1148. In establishing that
a vaccine “did cause” injury, the opinions and views of the injured party’s treating physicians are
entitled to some weight. Andreu, 569 F.3d at 1367; Capizzano, 440 F.3d at 1326 (“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 show[s] that the

18
vaccination was the reason for the injury’”) (quoting Althen, 418 F.3d at 1280). Medical records
are generally viewed as particularly trustworthy evidence, since they are created
contemporaneously with the treatment of the patient. Cucuras v. Sec’y of Health & Human Servs.,
993 F.2d 1525, 1528 (Fed. Cir. 1993).

However, medical records and/or statements of a treating physician’s views do not per se
bind the special master to adopt the conclusions of such an individual, even if they must be
considered and carefully evaluated. Section 13(b)(1) (providing that “[a]ny such diagnosis,
conclusion, judgment, test result, report, or summary shall not be binding on the special master or
court”); Snyder v. Sec’y of Health & Human Servs., 88 Fed. Cl. 706, 746 n.67 (2009) (“there is
nothing . . . that mandates that the testimony of a treating physician is sacrosanct—that it must be
accepted in its entirety and cannot be rebutted”). As with expert testimony offered to establish a
theory of causation, the opinions or diagnoses of treating physicians are only as trustworthy as the
reasonableness of their suppositions or bases. The views of treating physicians should also be
weighed against other, contrary evidence also present in the record—including conflicting
opinions among such individuals. Hibbard v. Sec’y of Health & Human Servs., 100 Fed. Cl. 742,
749 (2011) (not arbitrary or capricious for special master to weigh competing treating physicians’
conclusions against each other), aff’d, 698 F.3d 1355 (Fed. Cir. 2012); Caves v. Sec’y of Health &
Human Servs., 100 Fed. Cl. 119, 136 (2011), aff’d, 463 F. App’x 932 (Fed. Cir. 2012); Veryzer v.
Sec’y of Health & Human Servs., No. 06-522V, 2011 WL 1935813, at *17 (Fed. Cl. Spec. Mstr.
Apr. 29, 2011), mot. for review denied, 100 Fed. Cl. 344, 356 (2011), aff’d without op., 475 F.
App’x 765 (Fed. Cir. 2012).

The third Althen prong requires establishing a “proximate temporal relationship” between
the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been equated to the
phrase “medically-acceptable temporal relationship.” Id. A petitioner must offer “preponderant
proof that the onset of symptoms occurred within a timeframe which, given the medical
understanding of the disorder’s etiology, it is medically acceptable to infer causation.” 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 (Althen prong one’s requirement). Id. at 1352; 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).

B. Analysis of Expert Testimony

Establishing a sound and reliable medical theory often requires a petitioner to present
expert testimony in support of his claim. Lampe v. Sec’y of Health & Human Servs., 219 F.3d
1357, 1361 (Fed. Cir. 2000). Vaccine Program expert testimony is usually evaluated according to

19
the factors for analyzing scientific reliability set forth in Daubert v. Merrell Dow Pharmaceuticals,
Inc., 509 U.S. 579, 594–96 (1993). See Cedillo v. Sec’y of Health & Human Servs., 617 F.3d 1328,
1339 (Fed. Cir. 2010) (citing Terran v. Sec’y of Health & Human Servs., 195 F.3d 1302, 1316
(Fed. Cir. 1999)). “The Daubert factors for analyzing the reliability of testimony are: (1) whether
a theory or technique can be (and has been) tested; (2) whether the theory or technique has been
subjected to peer review and publication; (3) whether there is a known or potential rate of error
and whether there are standards for controlling the error; and (4) whether the theory or technique
enjoys general acceptance within a relevant scientific community.” Terran, 195 F.3d at 1316 n.2
(citing Daubert, 509 U.S. at 592–95).

The Daubert factors play a slightly different role in Vaccine Program cases than they do
when applied in other federal judicial fora (such as the district courts). Daubert factors are usually
employed by judges (in the performance of their evidentiary gatekeeper roles) to exclude evidence
that is unreliable and/or could confuse a jury. In Vaccine Program cases, by contrast, these factors
are used in the weighing of the reliability of scientific evidence proffered. Davis v. Sec’y of Health
& Human Servs., 94 Fed. Cl. 53, 66–67 (2010) (“uniquely in this Circuit, the Daubert factors have
been employed also as an acceptable evidentiary-gauging tool with respect to persuasiveness of
expert testimony already admitted”). The flexible use of the Daubert factors to evaluate the
persuasiveness and reliability of expert testimony has routinely been upheld. See, e.g., Snyder, 88
Fed. Cl. at 742–45. In this matter (as in numerous other Vaccine Program cases), Daubert has not
been employed at the threshold, to determine what evidence should be admitted, but instead to
determine whether expert testimony offered is reliable and/or persuasive.

The fact that a claimant offers an expert opinion does not render the opinion that expert
espouses scientifically reliable or persuasive. Nothing requires the acceptance of an expert’s
conclusion “connected to existing data only by the ipse dixit of the expert,” especially if “there is
simply too great an analytical gap between the data and the opinion proffered.” Snyder, 88 Fed.
Cl. at 743 (quoting Gen. Elec. Co. v. Joiner, 522 U.S. 146 (1997)); see also Isaac v. Sec’y of Health
& Human Servs., No. 08-601V, 2012 WL 3609993, at *17 (Fed. Cl. Spec. Mstr. July 30, 2012),
mot. for review denied, 108 Fed. Cl. 743 (2013), aff’d, 540 F. App’x 999 (Fed. Cir. 2013) (citing
Cedillo, 617 F.3d at 1339).

C. Review of Medical and Scientific Literature

Both parties filed medical and scientific literature in this case, but not every filed item
factors into the outcome of this decision. While I have reviewed all of the medical literature
submitted in this case, I discuss only those articles that are most relevant to my determination
and/or are central to Petitioner’s case—just as I have not exhaustively discussed every individual
medical record filed. Moriarty v. Sec’y of Health & Human Servs., 844 F.3d 1322, 1328 (Fed. Cir.
2016) (“[w]e generally presume that a special master considered the relevant record evidence even
though he does not explicitly reference such evidence in his decision”) (citation omitted); see also

20
Paterek v. Sec’y of Health & Human Servs., 527 F. App’x 875, 884 (Fed. Cir. 2013) (“[f]inding
certain information not relevant does not lead to—and likely undermines—the conclusion that it
was not considered”).

ANALYSIS

As I have previously noted, the first, “can cause” Althen prong has been met in this case,
given the ample prior decisions associating vaccines containing a tetanus component with brachial
neuritis, as well as the showing made by Petitioner’s experts. Remand Ruling at 11 n.7; Devonshire
v. Sec’y of Health & Human Servs., No. 99-031V, 2006 WL 2970418, at *15 (Fed. Cl. Spec. Mstr.
Sept. 28, 2006) (stating that it is well known that brachial neuritis can occur following a tetanus
vaccination), aff’d, 76 Fed. Cl. 452 (2007); DeGrandchamp v. Sec’y of Health & Human Servs.,
No. 01-413V, 2003 WL 21439670, at *7 (Fed. Cl. Spec. Mstr. May 15, 2003) (relying on IOM
publications to find that in theory, the tetanus toxoid in Td vaccine can cause brachial neuritis).
Literature offered in this case also supports this determination. See, e.g., Van Alfen II at 320. This
case instead turns on the remaining Althen prongs, which I address in order of their significance to
my Decision.

I. Petitioner Has Not Established that his Brachial Neuritis Began in a
Medically-Acceptable Post-Vaccination Timeframe (Althen Prong Three)

There is no dispute in this case that Mr. Greene experienced brachial neuritis, but the
medical reasonableness of the timeframe in which his symptoms began, measured from date of
vaccination forty-one days earlier, is very much contested. I have already determined that
Petitioner cannot meet his preponderant burden of proof merely by relying on the approximately
thirteen-day differential between the end date for a viable Table claim and his own onset. Grant,
956 F.2d at 1147–48.18 Petitioner was thus tasked with establishing the medical reasonableness of
the timeframe herein through resort to expert testimony and whatever other evidence bears on that
question.

Petitioner has offered some literature addressing the amount of time medical science
expects brachial neuritis will occur after an instigating trigger—but it largely does not support a

18
The reasonableness of not allowing a petitioner to rely on the Table claim timeframe for a non-Table claim is
underscored by considering how this is fair to both sides. In this case, for example, Dr. Lancaster has opined that the
defined Table period for a tetanus/brachial neuritis claim is based on the most persuasive medical and scientific
evidence available—thus suggesting to him that anything beyond it would by definition not be medically reasonable.
Tr. at 91 (mentioning that the twenty-eight-day range reflects the “consensus of experts”). If petitioners are permitted
to rely on how close onset in a given case is to the defined Table period in support of a non-Table claim, then
Respondent should be similarly entitled to wield the Table period offensively, as proof that science does not
preponderantly support a longer timeframe. Program law instead requires petitioners (and Respondents in seeking to
rebut a Vaccine Act non-Table claim) to rely on evidence to bulwark the reasonableness of the proposed period—
independent of the Table timeframe (although evidence used to establish that timeframe may still be relevant).

21
six-week onset for the illness, instead suggesting more persuasively that the maximum time from
trigger to onset would be no more than two or three weeks. See, e.g., Van Alfen I19, Tsairis. Indeed,
and as Respondent previously argued, one of the same pieces of evidence that supports Petitioner’s
Althen prong one showing—the IOM review of tetanus-caused brachial neuritis—supports at most
a four-week onset risk period. Stratton at 55 (noting that latency period for brachial neuritis after
vaccination “ranges from a few days to 3 or at most 4 weeks”) (emphasis added). And Dr. Lancaster
convincingly explained why a shorter onset timeframe made more sense for brachial neuritis—
and conversely, why a timeframe exceeding four weeks was far less medically acceptable.

Accordingly, what direct proof exists on the topic does not preponderate in Petitioner’s
favor. Of course, petitioners may establish their Vaccine Act claim with circumstantial evidence,
so the absence of sufficient direct proof does not end the analysis. Mr. Greene sought to meet his
preponderant burden through (a) invocation of risk intervals applied to other autoimmune diseases,
and (b) a comparison of the timeframes that reliable scientific evidence establishes for onset of
GBS. Neither argument was ultimately persuasive, however (although both were supported by
some reliable scientific/medical evidence).

A. Risk Intervals for Other Autoimmune Diseases Are Not
Preponderant Evidence Alone of A Reasonable Timeframe

Petitioner relied on some literature involving risk intervals generally, best explained in
Rowhani-Rahbar. This evidence unquestionably has probative value. See generally Rowhani-
Rahbar. The fact that longer risk intervals are often utilized in measuring vaccine safety is
circumstantial evidence supporting the conclusion that it would be medically reasonable to expect
some analogous vaccine-caused neurologic injuries to occur within a similar timeframe. It is for
this reason that the longer risk interval that Petitioner’s experts propose to apply in this case has
also been found persuasive by other special masters in cases alleging autoimmune injuries
comparable to those evaluated in Rowhani-Rahbar. See, e.g., Day v. Sec’y of Health & Human
Servs., No. 12-630V, 2015 WL 8028393, at *22 (Fed. Cl. Nov. 13, 2015) (applying Rowhani-
Rahbar secondary risk interval for ADEM to case alleging that petitioner’s multiple sclerosis
(“MS”) was vaccine-caused).

There are, however, significant countervailing points that weigh against endorsement of a
forty-one-day timeframe herein. First and foremost, not all neurologic injuries with an
autoimmune component are the same, even if they have some common features. Ample Program
authority has noted that, while petitioners may reasonably analogize an injury to other autoimmune
conditions, they cannot prevail solely by doing so. See, e.g., R.V. v. Sec’y of Health & Human
Servs., No. 08-504V, 2016 WL 3882519, at *41 (Fed. Cl. Spec. Mstr. Feb. 19, 2016) (not crediting

19
Although Van Alfen I does allow that 10 percent of studied, infectious-originating cases of brachial neuritis might
have had an onset of greater than two weeks, this finding is too vague to give it significant weight – it does not allow
for the conclusion that an onset of longer than four weeks is acceptable, and it does not involve vaccination directly.
Van Alfen I at 443.

22
petitioner’s reliance on unsupported analogy to other illnesses in proving causation theory), mot.
for review denied, 127 Fed. Cl. 136 (2016); R.K. v. Sec’y of Health & Human Servs., No. 03-
0632V, 2015 WL 10936124, at *105 (Fed. Cl. Spec. Mstr. Sept. 28, 2015) (same), mot. for review
denied, 125 Fed. Cl. 57 (2016), aff’d, 671 F. App’x 792 (Fed. Cir. 2016). And as Dr. Lancaster
noted, brachial neuritis is in fact not congruent with a central nervous system disease like ADEM—
the latter being the basis for the forty-one-day period relied upon in Rowhani-Rahbar (and found
to be analogous to the MS injury considered in Day). It is therefore unpersuasive for Petitioner to
argue that timeframes involving distinguishable neurologic diseases should be applied as a
consistent yardstick to all cases involving nerve-related autoimmune injuries.

A secondary problem posed by Petitioner’s argument is its overreliance on a longer risk
interval as a proxy for preponderant evidence establishing a medically reasonable onset timeframe.
Rowhani-Rahbar addresses the application of risk intervals for epidemiologic studies evaluating
overall vaccine safety. Although they are employed based on some consideration of when an
adverse post-vaccination event might be expected to occur, they are also intentionally “broad nets”
intended to catch as many putative adverse events as possible. Dr. Steinman himself noted that an
adopted interval can mean whatever the study’s author wants it to (although he nevertheless added
that a study would for the most part seek to define an interval based on when a plausible reaction
or illness might occur). Tr. at 52–53, 55.

Thus, a secondary interval explicitly understood to be less specific, and hence medically
accurate, but included nonetheless in a study to avoid missing possible related adverse events is
not particularly robust proof as to the scientific/medical consensus as to when a particular injury
would most likely occur post-vaccination. The fact that a risk interval is selected for a particular
study because its authors deem it to have utility therein does not mean that the same period can be
deemed preponderantly established in the context of a Vaccine Act claim. Thus, while I
acknowledge that Petitioner’s invocation of the risk interval concept generally had some
evidentiary value, it was not by itself enough to preponderantly establish that vaccine-caused
brachial neuritis could reasonably occur within six weeks of vaccination—especially since the
evidence specific to brachial neuritis says otherwise.

B. GBS and Brachial Neuritis Are Not Congruent for Purposes of
Determining Reasonableness of Onset

To bulwark adoption of a six-week timeframe, Petitioner’s experts consistently proposed
that brachial neuritis is analogous to GBS—an autoimmune, peripheral nervous system-affecting
neurologic condition that substantial Program caselaw (based in turn on reliable science) has
determined can reasonably begin in as long as six to eight weeks after vaccination. See, e.g.,
Barone v. Sec’y of Health & Human Servs., No. 11-707V, 2014 WL 6834557, at *13 (Fed. Cl.
Spec. Mstr. Nov. 12, 2014) (eight weeks is the longest reasonable timeframe for a non-Table

23
flu/GBS injury). But this argument was ultimately unpersuasive. Despite some of their common
features, GBS is simply not sufficiently comparable to brachial neuritis to apply the same onset
timeframe to both.

Literature filed in this case relating to brachial neuritis, and the reports and testimony
discussing it, clearly establishes that it is a neurologic injury primarily to the nerve axon—a finding
confirmed by nerve electrophysiologic studies and also consistent with the motor loss associated
with brachial neuritis. Feinberg at 202; see also Lancaster Rep. at 10–11.20 It also can be caused
by direct trauma that would never result in GBS, further suggesting it is highly distinguishable.
And while the same literature also suggests a person with brachial neuritis may have some sensory
symptoms that could reflect secondary nerve demyelination, that is not the fundamental character
of the condition—unlike GBS. See Auch v. Sec’y of Health & Human Servs., No. 12-673V, 2017
WL 1034396, at *9 (Fed. Cl. Spec. Mstr. Jan. 13, 2017) (Dr. Steinman opining that GBS is
characterized by autoimmune attack on nerve myelin sheath, resulting in demyelination).

To establish the contrary, Petitioner’s experts simply asserted that this was not the case—
that brachial neuritis is as characterized by demyelination as GBS. See Tr. at 11 (Dr. Kinsbourne),
56–57 (Dr. Steinman). Alternatively, they attempted to blur the lines between the two conditions
by noting the existence of AMAN, a nerve axon-oriented GBS variant. See, e.g., id. at 21–22.
While this GBS variant clearly exists, Petitioner’s experts did not elaborate on the fact that AMAN
is also (a) uncommon in comparison to other GBS variants, (b) largely confined to a pediatric
population, and (c) mainly occurs outside of the U.S., in eastern Asian countries. Dorland’s
Illustrated Medical Dictionary 1268 (32nd ed. 2012); P. Dyck & P.K. Thomas, 2 Peripheral
Neuropathy 2200–01 (4th ed. 2005). It is also readily distinguishable from brachial neuritis, as Dr.
Lancaster observed. Supp. Lancaster Rep. at 1. The existence of an axonal-impacting GBS variant,
therefore, provides limited assistance to Petitioner’s argument that GBS and brachial neuritis are
comparable for purposes of determining a medically acceptable onset timeframe.

Petitioner also invoked case studies indicating that certain autoantibodies associated with
GBS (antiganglioside antibodies) have been found in testing of brachial neuritis patients. The
significance of the presence of these autoantibodies in individuals with brachial neuritis is far from
determined, however, as more persuasive scientific literature indicates. See, e.g., Van Alfen II at
320 (“some studies have reported antiganglioside [peripheral nervous system] antibodies in
patients, but this finding could well be a consequence of axonal damage rather than its cause”)
(emphasis added). As Dr. Lancaster noted, none of these autoantibodies have been scientifically
demonstrated to drive an autoimmune process resulting in brachial neuritis. And even if it is
assumed that the pathophysiology of brachial neuritis could involve similar autoantibodies, such

20
Well-recognized authorities confirm the same. See, e.g., Dyck & Thomas at 2303 (“most of the currently available
evidence from electrophysiologic studies suggest multifocal or patchy abnormalities consistent with axonal damage
(loss) within the brachial plexus and isolated peripheral nerves of the upper extremities”) (emphasis added).

24
points do not establish, based on existing persuasive science and medical literature about brachial
neuritis specifically, that the timeframes relevant for a different autoimmune disease can simply
be applied wholesale here—that the time in which it would take for brachial neuritis (which Dr.
Lancaster successfully established would usually be an acute process) to manifest would be
consistent with GBS.

The same goes for the Japanese case studies offered to establish that brachial neuritis has
been successfully treated with the kind of immune-modulating treatments long understood to be
effective for GBS. See Naito; Morishima; Moriguchi. It is routinely recognized in the Program that
case reports do not merit significant weight as a class of evidence (see, e.g., Crutchfield v. Sec’y
of Health & Human Servs., No. 09-39V, 2014 WL 1665227, at *19 (Fed. Cl. Spec. Mstr. Apr. 7,
2014), aff’d, 125 Fed. Cl. 251 (2014)), but here the actual reports filed are on their face even less
probative than usual. Indeed, only Morishima involved a lengthy onset (admitted even by Dr.
Kinsbourne to be an outlier under Petitioner’s own theory), with the other case studies observing
post-infectious onset (the most analogous circumstance to vaccine-induced brachial neuritis) in a
timeframe consistent with Respondent’s position of less than four weeks. Accordingly, even if I
give some weight to the suggestion of these case reports that IVIG treatments have been efficacious
for certain cases of brachial neuritis, these articles are greatly outweighed by other evidence
establishing the many accepted differences between GBS and brachial neuritis.

C. Respondent Successfully Rebutted Petitioner’s Timeframe
Evidence, as well as his Expert Reports and Testimony

Reliable evidence offered by Respondent and discussed by Dr. Lancaster persuasively
suggests brachial neuritis is more acute in nature, and will likely begin within two or three weeks
of whatever triggers it—not six weeks, as Petitioner argues here. This is consistent with what is
known about the orientation of the injury (to the axon) and its acute nature, and does not rely on
analogy to distinguishable autoimmune conditions. Dr. Lancaster’s opinion stemmed from a
practice-derived understanding of how brachial neuritis presents and what causes it—not just from
research performed for the purpose of offering an opinion herein. He has knowledge of the
condition and regularly performs the EMG and nerve conduction study tests employed to evaluate
its existence and course.

Dr. Lancaster’s opinion is also consistent with my determinations in other cases involving
similar injuries. See, e.g., Garner v. Sec’y of Health & Human Servs., No. 15-063V, 2017 WL
1713184 (Fed. Cl. Spec. Mstr. Mar. 24, 2017), mot. for review denied, 2017 WL 3483352 (Fed.
Cl. July 31, 2017). In Garner, I considered a claim that the Hepatitis A and B vaccines had caused
brachial neuritis. The earliest onset possible in Garner was forty-five days after vaccination, based
on the first record documentation of any complaints by the petitioner about arm or shoulder pain.
Id. at *1. Respondent, however, persuasively argued (also via Dr. Lancaster’s testimony) that the

25
condition was far more acute in nature (and in terms of the causative mechanism as well), making
twenty-eight days the outer limit for latency. Id. at *8. I found this point to be dispositive, even
though the claimant’s Althen prong one showing was (as here) sufficient, and dismissed the case
on the record. Id. at *16. That decision was upheld on review. 2017 WL 3483352. Nothing about
this case distinguishes it from Garner’s analysis or outcome.

Petitioner’s expert testimony, by contrast, was simply less effective and persuasive.21 Both
experts he relied upon are credentialed and competent to testify generally on neurologic injuries
and the potential immunologic triggers for them—and they do so often in the Vaccine Program.
Also, and as discussed extensively above, they offered some reliable items of evidence to support
many of their contentions. And the opinion they jointly voiced -- that similarities between GBS
and brachial neuritis were enough to allow application of the timeframe for onset of the former to
the latter -- was reasonable, and coherently presented as well.

But this does not mean that Drs. Kinsbourne and Steinman offered persuasive expert
opinions that compel a favorable determination for Petitioner on the third Althen prong. Not only
were their contentions effectively rebutted, but these two experts do not possess demonstrated,
specific experience studying or treating brachial neuritis and its causes, even if they may have
intermittently encountered it in their professional lives.22 As a result, their assertions vouching for
the reasonableness of timing in this case lacked the evidentiary heft of an expert who could credibly
explain how his own experience studying or treating the disease in question informed his opinion.

Overall, Petitioner did not offer sufficient evidence to meet his preponderant burden on
this third Althen prong. As the Federal Circuit has noted, establishing the timeframe prong is
dependent upon “the medical understanding of the disorder’s etiology . . . .” Bazan, 539 F.3d at

21
Although Drs. Wright’s and Byers’s expert reports remain in evidence, Petitioner made no reference to their
contentions at hearing, and I do not find that they appreciably assisted Petitioner’s case with respect to the third Althen
prong.

22
Dr. Kinsbourne was particularly deficient in this regard. By his own admission, he has essentially treated almost
no patients for more than twenty-five years (although he routinely seeks to offer opinions in Vaccine Program cases
on an individual’s diagnosis or symptoms course). Tr. at 28; Holmes v. Sec’y of Health & Human Servs., No. 08-
185V, 2011 WL 2600612, at *2 n.9 (Fed. Cl. Spec. Mstr. April 26, 2011) (noting that Dr. Kinsbourne has not had a
clinical neurology practice for thirty-seven years), aff’d, 115 Fed. Cl. 469 (2014). His neurology background cannot
make up for this lack of personal understanding of the condition in question.

Dr. Steinman, by contrast, appears to see patients more regularly, even if a clinical practice is not his main focus. But
he does not possess specific demonstrated expertise with respect to brachial neuritis. Indeed, although he regularly
testifies for Vaccine Act petitioners, by my count he has only offered an expert opinion in cases involving brachial
neuritis twice before. See, e.g., Winterfeld v. Sec’y of Health & Human Servs., No. 15-933V, 2018 WL 2225178 (Fed.
Cl. Spec. Mstr. Mar. 9, 2018) (awarding attorney’s fees and costs in settled case alleging brachial neuritis after receipt
of influenza vaccine). And tellingly, in that case the petitioner claimed an onset of approximately two weeks after
vaccination—not six. See Petition at 2, Winterfeld, 2018 WL 2225178 (ECF No. 1).

26
1352 (emphasis added). The most compelling and reliable evidence offered herein pertinent to
brachial neuritis (the relevant “disorder”) establishes that it proceeds fairly acutely after a trigger,
and is highly unlikely to occur more than three or four weeks after instigation. The fact that other
autoimmune-mediated and somewhat comparable neurologic diseases might reasonably be
understood to have a longer potential onset timeframe does not compel the conclusion that the
same is true for brachial neuritis.

II. Petitioner Has Not Established that his Brachial Neuritis Was Caused
By the Tetanus Vaccine He Received in July 2009

Even if I had found that a forty-one-day timeframe for onset of brachial neuritis was
medically acceptable, the record in this case fails to support the conclusion that the tetanus vaccine
is the most likely explanation for Mr. Greene’s injury.

The record provides no objective evidence whatsoever—direct, circumstantial, or
otherwise—that Petitioner was experiencing an autoimmune-derived injury attributable to
vaccination. Mr. Greene had no symptoms at all before he presented to the ER in early September
2009, and then only reported he had been feeling pain for a few days before—consistent with the
acutely-presenting nature of brachial neuritis.23 There is nothing from the pre- or post-vaccination
record suggesting that an autoimmune reaction was brewing in a subclinical form. And none of
Mr. Greene’s treaters implicated the tetanus vaccine as causative of his injuries—nor did they ever
propose IVIG treatment to remedy it (something that further undercuts the concept that brachial
neuritis is properly deemed congruent with GBS—or that medical science is increasingly viewing
immunosuppressive treatments as effective for brachial neuritis).

I have similarly found in other cases involving a long, silent post-vaccination period before
onset of injury that the “did cause” prong was not met. See, e.g., Bender v. Sec’y of Health &
Human Servs., No. 11-693V, 2018 WL 3679637, at *34 (Fed. Cl. Spec. Mstr. July 2, 2018) (finding
that petitioner’s transverse myelitis, which began forty-two days after receipt of the meningococcal
and Hepatitis A vaccines, could not have been caused by the vaccines when there was no evidence
of subclinical process occurring over that six-week period), mot. for review denied, 141 Fed. Cl.
262 (2019). No evidence was offered here establishing that brachial neuritis would otherwise be
characterized by a subclinical period that could explain the medical record silence. And Petitioner
did not fully rebut Dr. Lancaster’s point that certain medical records seem to contain statements to

23
Although at the 2015 fact hearing Petitioner attempted to establish that he had been experiencing some initial
symptoms in mid-August 2009, I found that these allegations were not corroborated by the medical record, and that
he did not otherwise establish why the presumption of accuracy that attaches to such records under the law should not
control here as well. Cucuras, 993 F.2d at 1528; Doe/70 v. Sec’y of Health & Human Servs., 95 Fed. Cl. 598, 608
(2010) (crediting special master’s decision to rely on contemporaneous medical records over later-in-time statements
from the petitioner to the contrary).

27
providers by Mr. Greene that at the time of onset, he associated his sudden pain with very recent
hard work at his construction job (something Dr. Lancaster deemed as an intervening, possibly
explanatory occurrence).24

Respondent also raised fair questions about whether the true cause of Petitioner’s brachial
neuritis was the injury to his hand in July 2009 that prompted receipt of the tetanus vaccination in
the first place. Based upon the existing record (and although I do not find the burden ever shifted
to Respondent), I cannot find that an alternative cause has been established by a preponderance,
any more than that the vaccine has been established to be causal. This does, however, raise a
reasonable point further undercutting Petitioner’s claim. For, if the tetanus vaccine could explain
Petitioner’s injury forty-one days later, on a medical record devoid of reference to any symptoms
or signs in the intervening period, why would the injury that occurred immediately prior to its
administration not also potentially be causal? Petitioner did not establish that brachial neuritis due
to vaccine is distinguishable in course or presenting symptoms from that caused by trauma, or why
the record otherwise better supports vaccination as the cause.25

CONCLUSION

This claim should have been resolved far sooner. Although some delay was attributable to
the parties’ good faith efforts to settle, Petitioner’s unwillingness to abandon the legally-untenable
position that the Table timeframe applicable to brachial neuritis could be leveraged in a non-Table
context also interfered with its timely resolution. Petitioner did eventually marshal reliable
evidence to support his claim, thus justifying a hearing. But after considering the expert witnesses
and evidence upon which they relied, it is my reasoned conclusion that Petitioner has failed—
despite abundant opportunity—to preponderantly substantiate his contention that a forty-one-day
onset period for his brachial neuritis was medically acceptable, or that the tetanus vaccine more
likely than not “did cause” his subsequent injury.

24
I do not find in this case, however, that Petitioner’s brachial neuritis was “more likely than not” caused by such
trauma close-in-time to the ER visit, since the record does not support that conclusion preponderantly. But this does
constitute evidence undermining Petitioner’s argument that only the vaccine could be causal, and was ineffectively
rebutted.
25
Of course, the causal interplay of hand injury versus vaccine does not solely cut in Respondent’s favor. If this were
a case where Petitioner’s onset had occurred in a more medically-reasonable timeframe, application of the Shyface
“substantial factor” could compel a finding for Petitioner under the present circumstances despite the possible role of
the hand injury in producing brachial neuritis. Heinzelman v. Sec’y of Health & Human Servs., No. 07–01V, 2008 WL
5479123, at *4 (Fed. Cl. Spec. Mstr. Dec. 11, 2008) (vaccine may still be substantial factor in causing injury sufficient
to justify entitlement award, even where “two forces act in concert”). But this only illuminates the significance of my
finding that the timeframe of onset was too remote from either occurrence to even weigh such competing causative
factors.

28
 I accordingly DISMISS Petitioner’s causation claim. In the absence of a timely-filed
motion for review (see Appendix B to the Rules of Court), the Clerk shall enter judgment in accord
with this decision.26

IT IS SO ORDERED.

/s/ Brian H. Corcoran
Brian H. Corcoran
Special Master

26
Pursuant to Vaccine Rule 11(a), the parties may expedite entry of judgment by filing a joint notice renouncing their
right to seek review.

29