VICP Registry Case Source Bundle
Canonical URL: https://vicp-registry.org/case/USCOURTS-cofc-1_20-vv-01222
Package ID: USCOURTS-cofc-1_20-vv-01222
Petitioner: Randy Brouette
Filed: 2020-09-17
Decided: 2025-09-02
Vaccine: influenza
Vaccination date: 2017-09-19
Condition: alleged Guillain-Barre syndrome with stroke or opercular-syndrome differential
Outcome: dismissed
Award amount USD: 

AI-assisted case summary:
On September 17, 2020, Randy Brouette filed a petition alleging that an influenza vaccination administered on September 19, 2017 caused Guillain-Barre syndrome. He was 59 years old and had a medical history that included hypertension, hypercholesterolemia, diabetes, sleep apnea, gout, and vascular disease.

Mr. Brouette became acutely ill on November 25, 2017, about 67 days after vaccination. He was found awake but nonresponsive, with aphasia, right facial droop, and a positive right Babinski sign. Imaging initially did not show an acute infarct, but later MRI studies showed bilateral parietal ischemic changes with bilateral internal carotid occlusion. Treating physicians considered different explanations. Some records mentioned Guillain-Barre syndrome and plasmapheresis, while other neurologic opinions found the presentation unusual for GBS and more consistent with stroke or opercular syndrome. EMG findings were not supportive of classic GBS, GQ1b testing was negative, and no lumbar puncture supported the diagnosis.

Petitioner relied on neurologist Dr. David Simpson, who treated GBS as the primary process and interpreted the ischemic findings as secondary. Respondent relied on vascular neurology, neurology, and immunology experts who argued that the presentation fit cerebrovascular disease better than vaccine-caused GBS, that the onset was outside the Table interval of 3 to 42 days, and that a recent respiratory infection was a more plausible immune trigger if GBS were present at all.

On September 2, 2025, Chief Special Master Brian H. Corcoran dismissed the petition. He found that Table GBS was not established because onset was too late, and that off-Table causation was not proven given the diagnostic uncertainty, competing stroke evidence, recent URI, and lack of reliable timing proof. No compensation was awarded. Mr. Brouette was represented by Peter John Wilkes.

Theory of causation field:
Influenza vaccine, September 19, 2017, age 59, alleged Guillain-Barre syndrome with onset on November 25, 2017, about 67 days post-vaccination. DISMISSED. Petitioner relied on Dr. David Simpson, who treated the presentation as GBS and attributed ischemic changes secondarily; respondent's experts Dr. Steven Messe, Dr. Pria Anand, and Dr. Stephen Jameson emphasized bilateral carotid occlusion, bilateral watershed ischemia, normal EMG findings, CNS signs including Babinski, no LP support, recent URI, and timing outside the Table 3-42 day interval. Chief Special Master Corcoran found Table onset not met and off-Table causation not proven. Attorney Peter John Wilkes.

Public staged source text:

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DOCUMENT 1: USCOURTS-cofc-1_20-vv-01222-0
Date issued/filed: 2025-10-02
Pages: 17
Docket text: PUBLIC DECISION (Originally filed: 09/02/2025) regarding 49 DECISION of Special Master. Signed by Chief Special Master Brian H. Corcoran. (cr) Service on parties made.
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Case 1:20-vv-01222-UNJ Document 50 Filed 10/02/25 Page 1 of 17
In the United States Court of Federal Claims
OFFICE OF SPECIAL MASTERS
No. 20-1222V
RANDY BROUETTE, Chief Special Master Corcoran
Petitioner, Filed: September 2, 2025
v.
SECRETARY OF HEALTH AND
HUMAN SERVICES,
Respondent.
Jonathan Joseph Svitak, Shannon Law Group, P.C., Woodridge, IL, for Petitioner.
Rachelle Bishop, U.S. Department of Justice, Washington, DC, for Respondent.
DECISION1
On September 17, 2020, Randy Brouette filed a petition for compensation under
the National Vaccine Injury Compensation Program, 42 U.S.C. § 300aa-10, et seq.2 (the
“Vaccine Act”). Petitioner alleges that he suffered Guillain-Barré syndrome (“GBS”)
resulting from an influenza (“flu”) vaccine received on September 19, 2017. Petition at 1.
The case was assigned to the Special Processing Unit of the Office of Special Masters
(the “SPU”).
1 Because this Decision contains a reasoned explanation for the action taken in this case, it must be made
publicly accessible and will be posted on the United States Court of Federal Claims' website, and/or
at https://www.govinfo.gov/app/collection/uscourts/national/cofc, in accordance with the E-Government
Act of 2002. 44 U.S.C. § 3501 note (2018) (Federal Management and Promotion of Electronic Government
Services). This means the Decision will be available to anyone with access to the internet. In
accordance with Vaccine Rule 18(b), Petitioner has 14 days to identify and move to redact medical or other
information, the disclosure of which would constitute an unwarranted invasion of privacy. If, upon review, I
agree that the identified material fits within this definition, I will redact such material from public access.
2 National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755. Hereinafter, for ease
of citation, all section references to the Vaccine Act will be to the pertinent subparagraph of 42 U.S.C.
§ 300aa (2018).

Case 1:20-vv-01222-UNJ Document 50 Filed 10/02/25 Page 2 of 17
For the reasons set forth below, I find that Petitioner has not established by
preponderant evidence the onset element for a Table flu vaccine-GBS claim – and I find
that the timeframe for onset was otherwise too long to be shown to be medically
acceptable, even under a non-Table version of the claim. Therefore, the case is properly
dismissed.
I. Relevant Procedural History
On July 19, 2021, Respondent stated that he intended to defend this case, and
requested that Petitioner file medical records, including complete EMG/NCS reports with
all relevant data (ECF No. 15). Petitioner requested, and received, numerous extensions
of time to obtain the records (ECF Nos. 16, 17, 19, 20). Following a status conference,
Petitioner obtained some records and moved to subpoena others (ECF Nos. 21-23). The
motion was granted, and Petitioner was directed to file the records by June 16, 2022
(ECF No. 24). When Petitioner missed this deadline, I extended it to September 1, 2022.
Scheduling Order (NON PDF), issued Aug. 25, 2022. Petitioner also missed that
deadline.
I thus directed Petitioner to file the records by December 14, 2022, or to show
cause why the case should not be dismissed for failure to prosecute (ECF No. 25). This
deadline was extended several times (ECF Nos. 26, 28, 29). On March 24, 2023,
Petitioner filed additional records as well as a status report stating that EMG records
remained outstanding, despite countless attempts and receiving thousands of pages of
records (ECF Nos. 32, 33). Over the following months, Petitioner filed records from his
treating neurologist (ECF Nos. 38-40).
Respondent subsequently filed his Rule 4 Report, along with three expert reports
(ECF Nos. 41-44). On February 27, 2024, Petitioner was directed to show cause why
the case should not be dismissed for the reasons identified in Respondent’s Report (ECF
No. 45). On June 25, 2024, Petitioner responded (ECF No. 48).
II. Relevant Factual History
A. Medical Records
Petitioner’s pre-vaccination medical history is significant for hypertension,
hypercholesterolemia, diabetes, sleep apnea, gout, and vascular disease. Ex. 3. On
September 19, 2017, Petitioner (then 59 years old) received a flu vaccine at the office of
his primary care provider, Dr. Pranav Patel. Ex. 3 at 43. On October 24, 2017, 35 days
after vaccination, he returned to Dr. Patel to follow up on labs. Id. at 44. He had no health
complaints at this time, and there were no positive findings other than low vitamin D in his
labs. Id. at 45. Petitioner was advised to restart a medication and return in three months
for labs. Id.
2

Case 1:20-vv-01222-UNJ Document 50 Filed 10/02/25 Page 3 of 17
On the morning of November 25, 2017 – now nine and a half weeks (67 days) after
vaccination – an ambulance was dispatched to Petitioner’s home for a possible stroke,
and paramedics found Petitioner awake but non-responsive. Ex. 4 at 219. His family
members reported that he had been “normal” the evening before. Id. at 219, 227. He was
transported to Silver Cross Hospital emergency department (“ED”) and admitted. Id. at
139, 219. In the ED, he was noted to have “complete expressive aphasia, R lower facial
droop . . . [and] +right babinski.”3 Id. at 228.
Neurologist Dr. Nitin Nadkarni evaluated Petitioner on the date of his hospital
admission (November 25th). Ex. 4 at 213. Dr. Nadkarni noted that Petitioner was having
difficulty speaking and finding words. Id. at 214. On examination, Petitioner displayed
bilateral facial weakness that was worse on the right side. Id. His reflexes and sensory
examination were normal. Id. Dr. Nadkarni stated that Petitioner had experienced a left
hemispheric ischemic event and ordered imaging. Id. at 214. A brain MRI done on the
day of admission showed no evidence of acute infarct. Id. at 473. A speech therapist
noted that Petitioner exhibited congestion and a cough, and Petitioner’s relative reported
that Petitioner had a head cold prior to arrival at the hospital. Id. at 615.
On November 26, 2017, Dr. Nadkarni noted Petitioner to have bilateral lower motor
neuron facial weakness, bilateral upper extremity weakness, and distal sensory
impairment. Ex. 4 at 416. Because his brain MRI showed no evidence of a brainstem
stroke, Dr. Nadkarni treated Petitioner for “[e]volving GBS.” Id. at 413, 416. IVIG was
deferred due to vascular risk factors, and Petitioner was transferred to the intensive care
unit and started on plasmapheresis. Id. He was noted to be a “poor historian” because he
initially insisted that he had recently been on a particular medication, but after his spouse
brought in his medications from home, he acknowledged that he had been mistaken. Id.
at 413, 423.
On November 27, 2017, Petitioner reported his recent vaccination to Dr. Nadkarni.
Ex. 4 at 412. On examination, his arm reflexes were absent, but he had normal deep
tendon reflexes in his legs. Id. at 412-13. He exhibited bilateral facial weakness and
slurred speech, and complained of numbness and tingling to both arms, but no pain. Id.
Dr. Nadkarni treated him for “likely GBS,” noting that his brain MRIs4 had not shown
abnormalities that would explain his clinical findings. Id.
3 A positive Babinski result refers to dorsiflexion of the big toe when the sole of the foot is stimulated.
Babinski reflex, DORLAND’S ONLINE, https://www.dorlandsonline.com/dorland/definition?id=102809 (last
visited Sept. 2, 2025). This reflex is normal in infants, but in adults is a sign of a lesion in the central nervous
system. Id.
4 Petitioner had a second brain MRI on November 26, 2017. Ex. 4 at 472. This MRI showed a mass “most
consistent with meningioma” as well as white matter foci that “could be due to the demyelinating process
or focal inflammatory lesions,” with white matter changes of vasculitis also a consideration. Id.
3

Case 1:20-vv-01222-UNJ Document 50 Filed 10/02/25 Page 4 of 17
However, a repeat brain MRI study done the evening of November 27, 2017, and
compared to the November 25th MRI showed “interval development of confluent areas of
gyriform cortical signal abnormality now noted involving parietal regions bilaterally most
suspicious for developing ischemic abnormality especially in view of the bilateral internal
carotid occlusion.” Id. at 468-69.
The record includes an electromyography (“EMG”)5 report. Ex. 4 at 240-41.
Although the EMG report lists a service date of December 11, 2017 (id. at 240), I find this
date is almost certainly inaccurate. Because the EMG was reviewed and relied upon by
Petitioner’s treating physicians as early as November 28th and 30th (id. at 201, 355), it
was more likely performed on or before November 28, 2017.6 Ex. 4 at 240-41.
The EMG report concludes that “[t]here is electrodiagnostic evidence of
polyneuropathy in upper and lower extremities,” (Ex. 4 at 240), although even Petitioner’s
expert describes this as a likely “typographical error.” Ex. 5 at 3 (stating that the EMG
revealed prolongation of median motor nerve distal latency, but showed no evidence of
generalized peripheral neuropathy, noting that “there appears to be a typographical error
in the written impression, indicating ‘evidence of polyneuropathy in UE and LE’”). The
EMG findings section, which describes test results in more detail, noted prolonged right
median nerve distal latency with normal motor amplitude and conduction velocity, but
otherwise normal amplitudes, distal latencies, and conduction velocities for all tested
nerves.7 Id. Respondent notes the data from this study has never been produced despite
several subpoenas. Respondent’s Report, ECF No. 41, at *5 n.1. The record includes a
5 Electromyography records extracellular activity of skeletal muscles at rest, during voluntary contractions,
and during electrical stimulation. Electromyography, DORLAND’S ONLINE,
https://www.dorlandsonline.com/dorland/definition?id=15854 (last visited Sept. 2, 2025).
6 Respondent states that the EMG report was dictated on December 11, 2017. Respondent’s Rule 4(c)
Report, filed Sept. 20, 2023, at *5 (ECF No. 41). The report was transcribed on December 12, 2017; thus,
Respondent’s explanation for why the report is listed as having been performed on December 11th seems
plausible.
7 The findings section states:
Motor conduction studies were performed of right median and right ulnar nerve, right
peroneal, right tibial, left peroneal, left tibial, left median, and left ulnar nerves. Distal
latency obtained from right median nerve was prolonged with normal motor amplitude
and normal conduction velocity. Left peroneal, left tibial, left median, and left ulnar distal
latencies were normal with normal motor amplitudes and normal conduction velocities.
Sensory nerve conduction studies were performed of median and ulnar nerves and sural
nerves on both sides. Sensory nerve action potential, distal latency, and conduction
velocities were normal in all the sensory nerves tested.
Ex. 4 at 240.
4

Case 1:20-vv-01222-UNJ Document 50 Filed 10/02/25 Page 5 of 17
note stating “NCV [nerve conduction velocity]8 COMPLETED 11/28/17,” (Ex. 4 at 241)
although Respondent states that the NCV results were not recorded. Respondent’s
Report, ECF No. 41, at *5.
Neurologist Dr. Bassel Kazkaz was consulted for a second opinion while Petitioner
was hospitalized on November 28, 2017. Ex. 4 at 198. Dr. Kazkaz noted that Petitioner
woke up the morning of November 25, 2017 throwing up and went to the bathroom. Id. at
199. While there, he developed bilateral hand weakness and speech disturbance, and
was unable to open the door. Id. At the emergency room, he was severely hypertensive,
unable to speak with right-sided lower facial droop, and right Babinski, a reflex which in
adults may indicate central nervous system disorder. Id. A CT angiogram showed
complete occlusion of the internal carotid arteries bilaterally up to the bifurcation within
the neck. Id.
Petitioner was noted to have significant dysphasia, bifacial weakness, and bilateral
distal upper extremity weakness. Ex. 4 at 199-200. Petitioner reported some numbness
and tingling in his hands, but no weakness in his lower extremities. Id. On examination,
Petitioner had “rather dramatic and significant bilateral distal hand weakness” and
reduced but present upper and lower extremity reflexes. Id. at 200. Dr. Kazkaz reviewed
the EMG study and data, which he stated “showed completely normal study without any
evidence of conduction slowing, distal latency prolongation, conduction block, [or] F-wave
latency prolongation.” Id. at 201.
Dr. Kazkaz noted that Petitioner’s third brain MRI on November 27th showed
changes that were suspicious for developing ischemic abnormality. Ex. 4 at 201.
Petitioner was noted to have an “unusual presentation” with significant bilateral
pharyngeal and facial weakness and bilateral distal hand weakness with “sparing of lower
extremities and sparing of proximal upper extremities.” Id. Dr. Kazkaz noted Petitioner’s
carotid artery occlusion, and thought his presentation was most consistent with “unusual
stroke syndrome” causing “Opercular syndrome.” Id.
Dr. Kazkaz thought it was reasonable to consider a neuromuscular illness like
GBS, particularly a rare bulbar-cervical-brachial variation, although “it would be unusual
to have a second diagnosis on top of the primary acute stroke diagnosis, which is
consistent with the whole clinical context,” including the EMG, which was “completely
normal.” Ex. 4 at 201. He acknowledged that the EMG was performed early in Petitioner’s
illness course, but stated that given Petitioner’s degree of weakness, he would expect to
see some degree of conduction block in the nerves studied in the hands. Id. He added
that GBS usually involves proximal muscles more than distal ones – not the opposite
8 Nerve conduction velocity studies measure the speed at which impulses move along the largest fibers of
a peripheral nerve. Nerve conduction velocity, DORLAND’S ONLINE,
https://www.dorlandsonline.com/dorland/definition?id=117402 (last visited Sept. 2, 2025).
5

Case 1:20-vv-01222-UNJ Document 50 Filed 10/02/25 Page 6 of 17
pattern Petitioner displayed. Id. He stated that a lumbar puncture could be considered to
confirm Petitioner’s diagnosis, although it does not appear that this test was done. Id.
On November 30, 2017, Petitioner saw endovascular surgical neuroradiology
specialist Dr. Richard Burgess. Ex. 4 at 353. Petitioner reported that the previous Friday
(November 24th) “he felt NORMAL – denies any weakness or paresthesia.” Id. The next
day, he woke up feeling normal. Id. He went out, and felt “weird” when he came back
home. Id. Eventually he went to the bathroom with difficulty; once there, he vomited and
was unable to get up or talk, and could not turn the doorknob with his hands. Id. He was
found several hours later and brought to the hospital; the overall onset of symptoms “was
over minutes.” Id.
Dr. Burgess noted that Petitioner had now undergone plasmapheresis and was
getting better. Ex. 4 at 354. Dr. Burgess commented on the negative EMG and lack of a
lumbar puncture, and described it as a “highly unusual and difficult case that does not
perfectly fit either GBS variant nor typical stroke syndromes.” Id. at 355. Dr. Burgess
thought Petitioner’s risk factors, rapid symptom onset, lack of lower extremity symptoms,
acute to subacute vascular occlusion, and MRI progression led to the conclusion that his
clinical picture was most consistent with . . . a syndrome similar to Foix-Chavany-
Marie/bilateral opercular syndrome.” Id. The differential diagnosis included GBS with
plasmapheresis induced borderzone strokes from hypotension. Id.
On December 1, 2017, Dr. Nadkarni examined Petitioner, finding normal leg
reflexes but absent arm reflexes. Ex. 4 at 352. Dr. Nadkarni’s impression was “likely
GBS,” noting a “very unusual presentation for bilateral parietal lobe stroke,” and that the
MRI findings did not correlate with clinical findings. Id. at 352-53. Plasmapheresis was
continued. Id. Dr. Burgess examined Petitioner that same day. Id. at 335. He stated that
Petitioner was improving daily, and that “[o]ne interpretation is hospitalization began with
GBS but that plasmapheresis lowered [Petitioner’s blood pressure] and in the setting
bilateral carotid occlusion led to strokes seen on MRI.” Id. at 335-36. He ordered that
plasmapheresis be continued, with care taken to avoid hypotension. Id.
On December 4, 2017, Dr. Burgess noted that Petitioner’s weakness was slowly
improving. Ex. 4 at 271. He assessed Petitioner with bilateral carotid artery occlusion and
bilateral parietal strokes that “[s]ignificantly worsened several days into admission after a
couple of rounds of plasmapheresis.” Id. at 272. He found this was most consistent with
“watershed infarcts due to chronic/subacute carotid occlusion and hypotension.” Id.
However, he added, “[w]hile an opercular syndrome from stroke could result in symptoms
similar to this patient’s presentation . . . an unusual superposition of GBS followed by mild
hypotension leading to minimally symptomatic MRI changes seems most likely.” Id. at
272. While hospitalized, Petitioner’s tested negative for GQ1b antibodies. Id. at 455.
6

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On December 7, 2017, Petitioner was transferred to inpatient rehabilitation, where
he remained until December 17, 2017. Ex. 4 at 141; Ex. 17 at 4. Thereafter, he continued
outpatient care with Dr. Patel and Silver Cross Hospital. Exs. 4; 16.
Petitioner saw Dr. Patel on January 4, 2018, following his hospital discharge. Ex.
16 at 88. Dr. Patel noted that while hospitalized, Petitioner “was diagnosed with GBS post
flu shot.” Id. Petitioner was noted to have recovered “about 80%” from GBS, with a
“slightly sloppy” gait, reduced right upper extremity strength, and lack of fine manipulation
in his right hand. Id. at 88-89.
On November 6, 2019, Petitioner saw Dr. Patel to follow up on labs. Ex. 16 at 54.
He was doing well, with no new complaints. Id. Dr. Patel documented a “history of Guillain-
Barre induced from flu vaccination.” Id at 55. The record does not explain why, however
(and nearly two years after Petitioner’s GBS diagnosis), Dr. Patel concluded that the
condition was caused by vaccination.
B. Affidavit Evidence
Petitioner filed an affidavit in support of his claim. Ex. 6. He states that he was
given a GBS diagnosis at Silver Cross Hospital in November 2017. Id. at ¶ 5. For over a
year after his injury, he required assistance for dressing, eating, and personal hygiene.
Id. at ¶ 8. He is no longer to do his professional work duties. Id. at ¶ 7.
III. Expert Reports
A. Petitioner’s Expert Report, David M. Simpson, M.D.9
Petitioner submitted an expert report from David M. Simpson, M.D., Professor of
Neurology and Director of Clinical Neurophysiology, Neuromuscular Division and the
Neuro-AIDS Program at the Mount Sinai Medical Center. Ex. 5. Dr. Simpson reviewed
Petitioner’s medical records, noting that there was “significant discussion among the
treating providers as to the relative contributions of a central vs peripheral nerve
localization of Mr. Brouette’s symptoms.” Id. at 5. The evolution of MRI changes raised
the question of stroke/opercular syndrome, but Dr. Simpson asserts that “after careful
consideration by the neurologists, radiologists, and neurointerventional surgeons, it was
ultimately concluded that GBS was the primary cause of Mr. Brouette’s symptoms . . . .
[and] the brain ischemic changes were a secondary phenomenon, likely precipitated by
shifts in [blood pressure] induced by plasmapheresis.” Id.
Dr. Simpson states that the onset of neurological symptoms approximately nine
weeks after a flu vaccination is within the reported time onset of post-influenza vaccine
GBS in the literature. Ex. 5 at 6. He relies on a study of GBS following a 1976 swine flu
9 Petitioner apparently obtained the expert report before filing the petition, as it was filed along with the
petition (ECF No. 1-7). As stated in the SPU Initial Order issued on March 19, 2021, experts should not be
consulted without first consulting with Respondent’s counsel and the court (ECF No. 11).
7

Case 1:20-vv-01222-UNJ Document 50 Filed 10/02/25 Page 8 of 17
vaccination program, which he states demonstrates an “increased attributable risk [of
GBS] . . . for the 10 weeks following [flu] vaccination.” Id. (citing L. Schonberger et al.,
Guillain-Barre Syndrome Following Vaccination in the National Influenza Immunization
Program, United States, 1976-1977, 110 Am. J. Epidemiology 105, 111 (1979), filed as
Ex. 12, ECF No. 1-14). He acknowledges, however, that the greatest risk period for GBS
was in the first two to three weeks after vaccination. Id.
Dr. Simpson adds that after treatment with IVIG,10 Petitioner had “both subjective
and objective improvement in symptoms,” although he continued to have residual
neurological symptoms. Ex. 5 at 7. He concludes that “the sequence of events, with
neurological symptoms beginning within 9 weeks of influenza vaccination, followed by
progressive neurological signs of sensory and motor neuropathy, support the diagnosis
of AIDP/Guillain Barre syndrome.”11 Id. at 7 (emphasis added). He states that Petitioner’s
treating physicians documented a causal association between his vaccine and the onset
of GBS, and he had a “clear response to plasmapheresis,” supporting an immune-
mediated pathogenesis. Id. He states that there is no alternative explanation – despite
the evidence of a recent upper respiratory infection – and concludes that, more likely than
not, the flu vaccine was causally related to the development of AIDP/GBS. Id.
B. Respondent’s Expert Reports
1. Steven R. Messé, M.D.
Respondent filed an expert report from Steven R. Messé, M.D., a Professor of
Neurology in the Division of Vascular Neurology at the University of Pennsylvania. Ex. A.
Dr. Messé opined that Petitioner’s November 25, 2017 hospital admission “was not
related to the influenza vaccination that he received over 2 months previously on
September 19, 2017.” Ex. A at 4. Dr. Messé finds it “very clear” that Petitioner’s sudden
onset of symptoms on the day of admission “are attributable to bilateral hemispheric
ischemia from his extensive vascular disease and bilateral carotid occlusions, and I think
it is extraordinarily unlikely that he also had GBS.” Id. In Dr. Messé’s view, “the treatment
he received for the purported GBS likely worsened the brain ischemia.” Id.
Dr. Messé states that “[a]ll aspects of this case strongly favor stroke” as the cause
of the symptoms resulting in Petitioner’s hospitalization. Ex. A at 4. Dr. Messé
emphasizes Petitioner’s history of severe vascular disease, sudden onset of focal
symptoms that indicate central nervous system cortical dysfunction, and MRI findings
confirming bihemispheric stroke “which would explain all of his symptoms.” Id. In contrast,
Dr. Messé states that “there is little to support the idea that he had GBS.” Id. Dr. Messé
states that GBS typically presents with ascending and symmetrical weakness that
10 The reference to IVIG appears to be a typo, as Petitioner was treated with plasmapheresis but not IVIG.
11 AIDP stands for acute inflammatory demyelinating polyneuropathy, a form of GBS.
8

Case 1:20-vv-01222-UNJ Document 50 Filed 10/02/25 Page 9 of 17
progresses over many hours or days, reaching a nadir at around two to four weeks; in
contrast, Petitioner presented with sudden and dramatic central nervous system
symptoms. Id.
Dr. Messé adds that “GBS is typically associated with findings of demyelination or
axonopathy on EMG, neither of which were present on either of [Petitioner’s] studies. Ex.
A at 4. While there are rare variant forms of GBS that present differently, such as Miller-
Fisher, in such cases “there is still a progression of symptoms over time related to
peripheral nerve injury” that was not present in this case. Id. Instead, Petitioner had
“fluctuating symptoms related to blood pressure variability,” commonly seen in patients
with stroke and large vessel occlusions. Id. Also important is that Petitioner’s testing for
anti-GQ1B antibodies – associated with the Miller-Fisher form of GBS – was negative. Id.
Petitioner’s bilateral arm weakness is “easily explained by the bilateral strokes seen on
MRI, attributable to the bilateral carotid occlusions.” Id. The absence of apparent infarct
on the MRI taken on the day of Petitioner’s admission “likely is due to the fact that he was
experiencing ischemia, but the infarct may not yet have been completed.” Id. In Dr.
Messé’s view, Petitioner’s bilateral upper and lower face weakness, cited by Dr. Nadkarni
as evidence that Petitioner had GBS, is also explained by bilateral strokes. Id.
Dr. Messé thinks it is “very likely that [Petitioner] did not even have GBS, and
instead, his primary and only issue was bihemispheric strokes.” Ex. A at 5. Dr. Messé
notes that Petitioner had reflexes documented by both neurologists who saw him early in
his course, and neither of two EMGs were indicative of a demyelinating polyneuropathy.
Id. at 6. There was no monophasic progression of worsening over days and weeks, but
instead a sudden onset of focal symptoms, “the hallmark of stroke.” Id. Although Petitioner
had absent reflexes in his face and arms on November 28, 2017, “[t]he MRI the day before
clearly demonstrated bilateral strokes and it is well known that strokes may initially cause
hyporeflexia.” Id. Overall, Petitioner’s “medical history, presentation, diagnostic testing,
and subsequent clinical course are all consistent with bihemispheric strokes from bilateral
carotid occlusions,” and there is “no feature of this case that provides a credible argument
that he also had GBS.” Id.
2. Pria Anand, M.D.
Respondent filed an expert report from Pria Anand, M.D., Chief of the Division of
Hospitalist Neurology and Assistant Professor of Neurology at the Boston University
School of Medicine/Boston Medical Center. Ex. C. Dr. Anand opines that Petitioner’s
clinical course is not typical of a GBS diagnosis, and the timing of onset of his symptoms
is not typical for GBS provoked by vaccination. Ex. C at 4-5. Moreover, in Dr. Anand’s
view, Petitioner’s records “do not show any of the objective findings required to make a
diagnosis of GBS.” Id. at 5.
Dr. Anand explains that there are seven “Brighton criteria” for a GBS diagnosis,
and of the seven, Petitioner meets just two, suggesting that he did not have GBS at even
9

Case 1:20-vv-01222-UNJ Document 50 Filed 10/02/25 Page 10 of 17
the lowest level of diagnostic certainty. Ex. C at 5. Dr. Anand adds that Petitioner also
does not meet the published criteria for the rare pharyngeal-cervical-brachial variant GBS
mentioned in Dr. Kazkaz’s notes. Id. at 5-6. In Dr. Anand’s view, Petitioner’s presentation
is most consistent with an unusual stroke syndrome causing ‘Opercular syndrome.’ Id. at
6. Dr. Anand adds that Dr. Kazkaz and the physicians who saw Petitioner in the
emergency department noted that he had a right-sided Babinski sign (Ex. 4 at 200, 228),
which is a foot reflex suggesting an injury to the brain or spinal cord. Id. at 7. The Babinski
sign is not seen in GBS patients, as GBS is an injury of the peripheral nerves and nerve
roots that does not involve the brain or spinal cord. Id. The Babinski sign is, however,
characteristically seen in patients with stroke causing weakness. Id. Furthermore, the
Babinski sign is 98% specific meaning that when it is present, “the likelihood of a disorder
of the brain or spinal cord is nearly guaranteed.” Id.
Dr. Anand concludes that the hyperacute nature of Petitioner’s symptoms, his
examination, including a Babinski sign, and his MRI findings “are all consistent with a
diagnosis of stroke causing all of his symptoms.” Ex. C. at 7. While Petitioner attributes
difficulty speaking to GBS, Dr. Anand states that “[t]here is no mechanism by which GBS,
a disorder of the peripheral nerves and nerve roots that does not involve the brain at all,
could cause stuttering or another problem of language.” Id. However, stuttering “has been
extensively reported in the literature as a presenting symptom of stroke.” Id.
Finally, Dr. Anand states that GBS symptoms typically progress over a two week
period, and symptoms that reach maximal severity within 24 hours are considered
“fundamentally inconsistent with a diagnosis of GBS and should prompt a search for an
alternative diagnosis.” Ex. C at 8. In contrast to this typical course, Petitioner’s symptoms
were maximal at onset and rapidly progressed over a course of hours. Id. Symptoms that
are maximal at onset and progress over the course of hours rather than days or weeks
are not consistent with GBS and are more consistent with alternative neurologic
diagnoses such as stroke. Id. Petitioner’s symptoms improved over the course of just 11
days during his hospitalization, which is “not consistent with either the natural history of
GBS or the response to treatment.” Id.
Dr. Anand acknowledges the 1979 paper cited by Petitioner’s expert as supporting
the plausibility of an increased GBS risk up to ten weeks after vaccination. Ex. C at 9.
However, that paper also found that the attributable risk of GBS post-vaccination declined
beginning the fourth week after vaccination. Id. Further, more recent studies “suggest a
narrower window of increased risk of up to 42 days, with the highest risk period during
the 21 days following vaccination.” Id. Dr. Anand concludes that the medical records,
literature, clinical features, timing, and objective data in this case “do not support a
diagnosis of GBS,” and alternative etiologies such as stroke are more consistent with the
time course and clinical features of Petitioner’s symptoms. Id.
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3. Stephen C. Jameson, Ph.D.
Respondent filed an expert report from Stephen C. Jameson, Ph.D., a Professor
in the Center for Immunology, Masonic Cancer Center, and Department of Laboratory
Medicine and Pathology at the University of Minnesota Medical School. Ex. E. He
explains that, although Petitioner’s negative antibody testing does not definitively rule out
GBS, it does not support that diagnosis. Id. at 3.
Dr. Jameson explains that the time course of GBS aligns with a typical adaptive
immune response by T and B lymphocytes. Ex. E at 2. Adaptive immune responses “take
several days to become apparent, peak at 1-3 weeks after infection or vaccination, then
gradually decline – kinetics that align with the typical progression of GBS, when an
initiating cause is known.” Id. He explains that GBS disease progression matches the
typical adaptive immune response, peaking 1-2 weeks after onset, followed by a plateau
for a few weeks and slow decline over months. Id. at 6. In Petitioner’s case, “[t]hese
kinetics were not evident . . . making it doubtful that these symptoms were caused by an
immune response to the influenza vaccine that he received.” Id.
Dr. Jameson notes that the onset of Petitioner’s symptoms on November 25, 2017
occurred more than nine weeks after vaccination – well outside the 3-42 day range on the
Table – and his symptoms rapidly progressed to a maximum over a span of a few hours.
Ex. E at 6. Dr. Jameson is “unaware of a situation in which T and B cell responses to
vaccines begin after a delay of more than 2 months.” Id. Additionally, adaptive immune
responses typically build in magnitude over several days or weeks, which is “inconsistent
with such an acute onset and peak of symptoms” as that seen in Petitioner’s case. Id.
Thus, it is “difficult to envisage how the types of immune response that are associated
with GBS can be aligned with the time course observed for Mr. Brouette’s symptoms.” Id.
Dr. Jameson opines that “it is unlikely that Mr. Brouette developed GBS as a result of his
influenza vaccination,” explaining that “the late onset of Mr. Brouette’s symptoms are
inconsistent with the proposed link to his influenza vaccination.” Id. at 7. He adds that “the
characteristics and time course of Mr. Brouette’s symptoms are difficult to reconcile with
a typical progression of GBS at all.” Id.
IV. Parties’ Arguments
Respondent argues that the Petition, Petitioner’s expert report, and multiple
medical records state that his GBS symptoms began more than nine weeks after
vaccination – far longer than the three to forty-two days required for a Table injury.
Respondent’s Report at *10 (“Resp.”) (citing Pet. at 1, Ex. 4 at 199, 214; Ex. 5 at 5).
Respondent adds that Petitioner “does not meet the Table criteria for any of the GBS
subtypes.” Id. at *10-11 Respondent explains:
[P]etitioner did not have a nadir of weakness between twelve hours and
twenty-eight days after onset; his symptoms were maximal at onset and he
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had a sudden presentation of dramatic central nervous system symptoms,
including aphasia, facial weakness, and bilateral arm weakness. Ex. 4 at
199, 219. Second, petitioner’s more likely alternative diagnosis is stroke.
Petitioner had a longstanding history of vertebral artery steal syndrome and
recent bilateral carotid endarterectomies due to complete occlusion, among
co-morbidities that put him at a significantly increased risk for stroke. Ex. 3
at 19, 36; Ex. 4 at 199; Ex. 16 at 163-64. Petitioner initially presented to the
ED with a NIHSS [National Institutes of Health Stroke Scale] of 10. Ex. 4 at
228, 230. His initial presentation also included a positive right Babinski,
indicative of central nervous system dysfunction. Id. Brain MRI studies on
November 26 and 27, 2017 showed that petitioner suffered a stroke. Id. at
468-69, 472. Additionally failing to support FS [Fisher Syndrome, a GBS
subtype], petitioner did not have bilateral ophthalmoparesis, ataxia, an
absence of limb weakness, or lack of alteration in consciousness.
Resp. at *11-12.
In addition, Respondent contends that Petitioner’s EMG findings were not
consistent with a GBS diagnosis. Resp. at *12 (citing Ex. 4 at 240-41). Petitioner did not
undergo a lumbar puncture, and thus there are no findings of the protein level or white
blood cell count in his cerebrospinal fluid that could support a GBS diagnosis. Id. Other
testing did not indicate an autoimmune process, and GQ1b antibody testing was negative.
Id. (citing Ex. 4 at 443, 451-55). Petitioner never reported neuropathic pain. Id. Thus,
Respondent argues that, even setting aside the onset problem, Petitioner has not
otherwise established a Table GBS claim. Id.
Respondent further asserts that Petitioner has not established that the flu vaccine
actually caused his GBS. Resp. at *12-16. As a threshold matter, Respondent argues that
Petitioner has not established the GBS diagnosis. Id. at *14. Furthermore, Petitioner has
not provided evidence sufficient to meet his burden of proof under Althen v. Sec’y of
Health & Human Servs., 418 F.3d 1274, 1279-80 (Fed. Cir. 2005). Id. Dr. Simpson merely
invokes four potential mechanisms without substantive explanations, but does not apply
these theories to the specifics of Petitioner’s case or provide supporting medical literature.
Id. Respondent argues that invocation of a general medical theory without more is not
enough to satisfy Petitioner’s burden. Id. (citing Broekelschen v. Sec’y of Health & Human
Servs., 618 F.3d 1339, 1345 (Fed. Cir. 2010)).
Respondent adds that Petitioner’s expert “has not meaningfully evaluated and
explained petitioner’s stroke.” Resp. at *15. Dr. Simpson states instead that Petitioner’s
treating providers concluded that GBS was the primary cause of Petitioner’s symptoms
(Ex. 5 at 5), but in Respondent’s view this is not accurate, and in fact during Petitioner’s
hospitalization, his doctors “were divided as to whether petitioner initially presented with
GBS before suffering a stroke.” Id. at *15. Further, “neither petitioner’s expert nor his
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treating providers explained which symptoms or sequelae were attributed to petitioner’s
alleged GBS versus his known stroke.” Id. And “none of petitioner’s treating providers at
Silver Cross Hospital attributed petitioner’s presentation to his flu vaccination.” Id. Only
Dr. Patel, Petitioner’s internist, referenced that Petitioner’s GBS was “induced from flu
vaccination,” well after Petitioner’s hospitalization and without a supporting rationale. Id.
(citing Ex. 16 at 55). Additionally, viral or bacterial infection is a common cause of GBS,
and Petitioner had a head cold with congestion and cough at the time of onset. Ex. 4 at
615. This infection was closer in time to Petitioner’s alleged GBS onset than the flu
vaccination, preponderating against Petitioner’s claim. Resp. at *15.
Finally, Respondent argues that Petitioner “has not shown that nine weeks and
four days is a medically reasonable temporal onset.” Resp. at *16. Petitioner’s lone
support of a 1979 article (Ex. 5 at 5-6, citing Ex. 12) is insufficient to overcome the
numerous cases stating that a GBS onset more than eight weeks after vaccination is not
temporally reasonable. Resp. at *16. Thus, Respondent argues that Petitioner’s causation
in fact claim fails as well.
Petitioner acknowledges that the onset of his symptoms occurred 67 days after
vaccination. Petitioner’s Response to Order to Show Cause, filed June 25, 2024, at *5
(ECF No. 48) (“Pet.”). However, he argues that Dr. Simpson’s expert report “is sufficient
to show that Mr. Brouette’s onset of GBS occurred within a medically reasonable time
period after his flu vaccination.” Pet. at *4. He asserts that Dr. Simpson’s opinion “should
be enough,” and that I should “see and accept that science and medicine show the Table
dates are not sufficiently updated to reflect a more modern analysis such as that
undertaken by Dr. Simpson.” Id. at *5.
Petitioner adds that there is ample evidence that his symptoms were caused by
GBS rather than the alternative cause of stroke offered by Respondent. Pet. at *2.
Petitioner argues that his expert’s opinion is supported by the conclusions of his treating
physicians, noting that two of his neurologists found that GBS was most consistent with
his clinical course and his likely primary diagnosis. Id. at *2-3. Although one of Petitioner’s
treating neurologists, Dr. Kazkaz, thought Petitioner’s clinical picture was most consistent
with a stroke, Dr. Kazkaz’s involvement in Petitioner’s care was limited to a neurology
consult and second opinion just three days into Petitioner’s hospitalization. Id. at *4. By
contrast, Petitioner’s other two neurologists, Dr. Nadkarni and Dr. Burgess, treated him
throughout his admission and concluded that he most likely suffered GBS. Id.
V. Legal Standards
Under Section 13(a)(1)(A) of the Act, a petitioner must demonstrate, by a
preponderance of the evidence, that all requirements for a petition set forth in section
11(c)(1) have been satisfied. A petitioner may prevail on his claim if he has “sustained, or
endured the significant aggravation of any illness, disability, injury, or condition” set forth
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in the Vaccine Injury Table (the Table). Section 11(c)(1)(C)(i). If a petitioner meets the
requirements for a Table Injury, causation is presumed.
If, however, the vaccinee alleges an injury that either is not listed in the Table or
did not occur within the prescribed time frame, the petitioner must prove by preponderant
evidence that the vaccine actually caused the alleged injury. Section 11(c)(1)(C)(ii) and
(iii); Section 13(a)(1)(A). This standard is “one of . . . simple preponderance, or ‘more
probable than not’ causation.” Althen, 418 F.3d at 1279-80 (referencing Hellebrand v.
Sec’y of Health & Human Servs., 999 F.2d 1565, 1572-73 (Fed. Cir. 1993)).
To establish an off-Table injury, a petitioner “must show ‘a medical theory causally
connecting the vaccination and the injury’” to establish that the vaccine was a substantial
factor in bringing about the injury. Shyface v. Sec’y of Health & Human Servs., 165 F.3d
1344, 1351 (Fed. Cir 1999) (quoting Grant v. Sec’y of Health & Human Servs., 956 F.2d
1144, 1148 (Fed. Cir. 1992)). The Circuit Court added that "[t]here must be a ‘logical
sequence of cause and effect showing that the vaccination was the reason for the injury.’”
Id. The Federal Circuit later reiterated these requirements in Althen, explaining that a
petitioner is required
to show by preponderant evidence that the vaccination
brought about her injury by providing: (1) a medical theory
causally connecting the vaccination and the injury; (2) a
logical sequence of cause and effect showing that the
vaccination was the reason for the injury; and (3) a showing
of a proximate temporal relationship between vaccination and
injury.
Althen, 418 F.3d at 1278. All three prongs of Althen must be satisfied. Id.
To resolve factual issues, the special master must weigh the evidence presented,
which may include contemporaneous medical records and testimony. See Burns v. Sec'y
of Health & Hum. Servs., 3 F.3d 415, 417 (Fed. Cir. 1993) (explaining that a special
master must decide what weight to give evidence including oral testimony and
contemporaneous medical records). “Medical records, in general, warrant consideration
as trustworthy evidence.” Cucuras v. Sec’y of Health & Human Servs., 993 F.2d 1525,
1528 (Fed. Cir. 1993). Accordingly, where medical records are clear, consistent, and
complete, they should be afforded substantial weight. Lowrie v. Sec’y of Health & Hum.
Servs., No. 03-1585V, 2005 WL 6117475, at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005).
However, the Federal Circuit has “reject[ed] as incorrect the presumption that medical
records are always accurate and complete as to all of the patient’s physical conditions.”
Kirby v. Sec'y of Health & Hum. Servs., 997 F.3d 1378, 1383 (Fed. Cir. 2021). Medical
professionals may not “accurately record everything” that they observe or may “record
only a fraction of all that occurs.” Id.
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The association between the flu vaccine and GBS is well-established in the
Vaccine Program. See, e.g., Strong v. Sec'y of Health & Human Servs., No. 15-1108V,
2018 WL 1125666 (Fed. Cl. Spec. Mstr. Jan. 12, 2018); Stitt v. Sec'y of Health & Human
Servs., No. 09-653V, 2013 WL 3356791 (Fed. Cl. Spec. Mstr. May 31, 2013); Stewart
v. Sec'y of Health & Human Servs., No. 06-777V, 2011 WL 3241585, at *16 (Fed. Cl.
Spec. Mstr. July 8, 2011); see also Barone v. Sec'y of Health & Human Servs., No. 11-
707V, 2014 WL 6834557 (Fed. Cl. Spec. Mstr. Nov. 12, 2014). Indeed, GBS was added
to the Table in 2017 for the flu vaccine, although this case does not meet the Table
onset timeframe and thus is analyzed as an off-Table claim. See 42 C.F.R. § 100.3(a).
Accordingly, my resolution of Petitioner's claim does not turn on a finding, under Althen
prong one, that (for purposes of adjudicating a Program claim) the flu vaccine “can
cause” GBS, for that question has been thoroughly examined and answered in the
affirmative.
There are nevertheless limits to the kinds of fact patterns that successfully
establish that the flu vaccine “did cause” a particular petitioner's GBS under the second
Althen prong. In most successful non-Table cases, onset of symptoms is demonstrated
to have occurred no longer than six to eight weeks after vaccination. See, e.g., Barone,
2014 WL 6834557, at *13 (eight weeks is the longest reasonable timeframe for a
flu/GBS injury). And even onsets longer than six weeks are reasonably questioned, with
special masters looking for something about a claimant’s specific health that would
make a slower onset medically acceptable.
Analysis
The record reflects – and Petitioner acknowledges – that onset of his symptoms
occurred 67 days after vaccination. This facially does not meet the Table’s 3-42 day
timeframe. Thus, the matter in dispute is whether Petitioner has established that, more
likely than not, his condition was caused by vaccination. I find that he has not, since
symptoms beginning 67 days after vaccination is simply too late to be credibly associated
with vaccination. Thus, Petitioner cannot demonstrate a “medically acceptable” temporal
relationship between the vaccine and his condition, as required by the third Althen prong.
Althen, 418 F.3d at 1278.
Typically, non-Table cases alleging onset of GBS more than six to eight weeks
after receipt of any vaccine have been unsuccessful.12 See Chinea v. Sec’y of Health &
12 I recognize that other special masters have accepted timeframes that were slightly shorter. See, e.g.,
Cooper v. Sec’y of Health & Human Servs., No. 18-1885V, 2024 WL 1522331, at *20 (Fed. Cl. Spec. Mstr.
Mar. 12, 2024) (ruling the petitioner was entitled to compensation where the onset of symptoms occurred
60 days after vaccination). Spayde v. Sec’y of Health & Human Servs., No. 16-1499V, 2021 WL 686682 at
*18-19 (Fed. Cl. Spec. Mstr. Jan. 27, 2021) (finding claimant entitled to compensation where symptoms
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Human Servs., No. 15-095V, 2019 WL 1873322, at *29 (Fed. Cl. Spec. Mstr. Mar. 15,
2019) (“I am aware of no published Vaccine Program decisions that have found a
timeframe longer than two months to be medically acceptable”), mot. for rev. denied, 144
Fed. Cl. 378 (2019); see also Kindle v. Sec’y of Health & Human Servs., No. 20-1423V,
2025 WL 603690, at *8 (Fed. Cl. Spec. Mstr. Jan. 21, 2025) (dismissing GBS claim where
symptoms began 65 days after vaccination, stating that “a nine-week onset (coupled with
symptoms that have not convincingly been demonstrated to be GBS-specific) is simply
too remote from the date of vaccination to reasonably associate the two”), mot. for rev.
denied, -- Fed. Cl. --, No. 20-1423V, 2025 WL 2251738 (July 17, 2025); Ray v. Sec’y of
Health & Human Servs., No. 20-321V, 2021 WL 778435 (Fed. Cl. Spec. Mstr. Jan. 13,
2021) (dismissing Table GBS claim based on finding that onset of symptoms occurred
over 70 days after vaccination).
Here, the record is devoid of evidence that Petitioner experienced any kind of post-
vaccination reaction, or concerning symptoms within eight weeks of vaccination. Rather,
he experienced his first possibly-neurologic symptoms over nine weeks after vaccination.
To find on this record that such a timeframe is medically acceptable is to rely on a kind of
post hoc ergo propter hoc reasoning that the Program rejects.
The onset insufficiencies in this case are compounded by the uncertainty as to
whether Petitioner even suffered from GBS. And the record reflects that Petitioner had an
upper respiratory infection soon before the onset of his symptoms, representing an
alternative explanation for his condition – one occurring closer in time to onset than
vaccination. See Chinea, 2019 WL 1873322, at *28 (“two-thirds of GBS cases follow an
antecedent infection (typically an upper respiratory or gastrointestinal infection) beginning
a few weeks prior to symptom onset”); Rupert v. Sec’y of Health & Human Servs., No.
10-160V, 2014 WL 785256 (Fed. Cl. Spec. Mstr. Feb. 3, 2014 (dismissing GBS claim
because preponderant evidence established that claimant’s GBS was caused not by
vaccination but by an unrelated factor, an antecedent upper respiratory infection).
In support of his claim, Petitioner offers an expert report from Dr. Simpson.
However, Dr. Simpson posits that Petitioner’s symptoms began within nine weeks of
vaccination – while the record reflects that his first symptoms occurred over nine weeks
after vaccination – nine weeks and four days. With the onset of Petitioner’s symptoms
already at the outside edge of the single study Dr. Simpson relies on to support his
opinion, this factual discrepancy takes on significance, and somewhat undermines Dr.
Simpson’s analysis.
began between 49 and 60 days after vaccination). But these cases involve other factual differences, and
are not binding precedent in any event. By contrast, a decision dismissing a GBS claim asserting an onset
of 65 days after vaccination was recently upheld. Kindle v. Sec’y of Health & Human Servs., No. 20-1423V,
2025 WL 603690, at *8 (Fed. Cl. Spec. Mstr. Jan. 21, 2025), mot. for rev. denied, -- Fed. Cl. --, No. 20-
1423V, 2025 WL 2251738 (July 17, 2025).
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Furthermore, Dr. Simpson ignores an alternative explanation for Petitioner’s GBS,
a recent upper respiratory infection – a known potential GBS trigger. And though Dr.
Simpson’s report suggests that Petitioner’s treating physicians were in agreement that
his primary condition was GBS, I find the record less clear on that matter.
Taking all of these concerns into account, I find that Petitioner has not
demonstrated by preponderant evidence that he suffered GBS caused by his flu
vaccination.
Conclusion
Petitioner has failed to preponderantly establish that his condition meets the
requirements for a Table GBS or off Table claim. Accordingly, this case is
DISMISSED for insufficient evidence. The Clerk of Court shall enter judgment
accordingly.13
IT IS SO ORDERED.
s/Brian H. Corcoran
Brian H. Corcoran
Chief Special Master
13 Pursuant to Vaccine Rule 11(a), entry of judgment can be expedited by the parties’ joint filing of notice
renouncing the right to seek review.
17