Roach-Yohey v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

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

AUSTIN ROACH-YOHEY, as * No. 17-1744V

representative of the Estate of * Special Master Christian J. Moran

ANGELA ROACH, *

*

Petitioner, *

* Filed: October 17, 2025

v. *

*

SECRETARY OF HEALTH *

AND HUMAN SERVICES, *

*

Respondent. *

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

Sean Greenwood, The Greenwood Law Firm, PLLC, Houston, Texas, for

petitioner;

Madelyn E. Weeks, United States Dep’t of Justice, Washington, DC, for

respondent.

DECISION DENYING ENTITLEMENT TO COMPENSATION1

The petition alleges that an influenza (“flu”) vaccine harmed Angela Roach.

This allegation is supported by a doctor whom petitioner retained, Lawrence

Steinman. Petitioner is proceeding on three causes of action: (1) Ms. Roach

suffered Guillain-Barré syndrome (“GBS”) as defined in the Vaccine Injury Table,

1

Because this Decision contains a reasoned explanation for the action taken in this case,

it must be made publicly accessible and will be posted on the United States Court of Federal

Claims’ website, and/or at https://www.govinfo.gov/app/collection/uscourts/national/cofc, in

accordance with the E-Government Act of 2002. 44 U.S.C. § 3501 note (2018) (Federal

Management and Promotion of Electronic Government Services). This means the Decision will

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

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

of which would constitute an unwarranted invasion of privacy. Any changes will appear in the

document posted on the website.

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(2) the flu vaccine was the cause-in-fact of Ms. Roach’s development of non-

regulatory Guillain-Barré syndrome, and (3) the flu vaccine significantly

aggravated an underlying disorder. The Secretary opposes compensation. The

Secretary’s opposition is based, in part, on the reports of a doctor he retained,

Jeffrey Cohen. The parties advocated through briefs.

A review of the evidence and arguments shows that petitioner is not entitled

to compensation. First, Ms. Roach does not meet the regulatory definition of

Guillain-Barré syndrome. This finding defeats the on-Table claim. Second, the

evidence does not preponderantly support a finding that Ms. Roach developed

GBS at all. Third, the development of the significant aggravation claim was

incomplete and misguided. A complete explanation follows.

I. Medical Conditions

As discussed in more detail below, three medical conditions are relevant to

this case: alcoholic neuropathy, GBS, and the Miller-Fisher variant of GBS. A

brief introduction is provided for context, although additional nuances are

presented throughout the decision.

A. Alcoholic Neuropathy

Chronic consumption of alcohol can lead to “neurologic complications

through both direct and indirect effects on the central and peripheral nervous

systems.” Noble & Weimer2 at 624. One consequence in the central nervous

system can be Wernicke syndrome, which “occurs due to thiamine deficiency

[and] develops in an acute to subacute manner over the course of days to weeks,

and is characterized by a cognitive disorder, gait ataxia, and ophthalmoparesis.”

Id. at 626.

Outside the central nervous system, the “association of peripheral nerve

disease and ethanol use has been recognized for centuries.” Noble & Weimer at

632.

When identified, alcoholic neuropathy is

indistinguishable from other distal sensorimotor axonal

2

James M. Noble and Louis H. Weimer, Neurologic complications of alcoholism, 20

CONTINUUM 624 (2014). Filed as Exhibit A-6.

2

processes. As with many other etiologies, symptoms

typically begin with distal paresthesia in the feet and

slowly progress proximally. In most cases, the onset is

typically slow and insidious and may begin to affect the

hands once leg symptoms ascend well above ankle level,

thus yielding the classic symmetric stocking-glove

sensory pattern.

Id. at 633.

Here, the parties agree that Ms. Roach suffered from alcoholic neuropathy.

While not denying that Ms. Roach suffered from alcoholic neuropathy, petitioner

and Dr. Steinman maintain that she also suffered from Guillain-Barré syndrome.

B. Guillain-Barré syndrome --- Acute Inflammatory Demyelinating

Polyneuropathy

According to the Secretary, GBS “is an acute monophasic peripheral

neuropathy that encompasses a spectrum of four clinicopathological subtypes.” 42

C.F.R. § 100.3(c)(15)(i). Here, Ms. Roach is alleged to have suffered from the

subtype that is the most common in North America, acute inflammatory

demyelinating polyneuropathy (often abbreviated “AIDP”). AIDP is characterized

by “symmetric motor flaccid weakness, sensory abnormalities, and/or autonomic

dysfunction caused by autoimmune damage to peripheral nerves and nerve roots.”

42 C.F.R. § 100.3(c)(15)(ii). The regulatory diagnostic criteria is discussed in

section V below.

A basis for the claim that the flu vaccine harmed Ms. Roach is that she

suffered from the AIDP form of GBS. However, at least one doctor considered

that she might suffer from another form.

C. Guillain-Barré Syndrome --- Miller Fisher Syndrome

According to the Secretary, Miller Fisher syndrome is another subtype of

GBS. Miller Fisher syndrome is “characterized by ataxia, areflexia, and

ophthalmoplegia.” 42 C.F.R. § 100.3(c)(15)(iii). As of the filing of the Third

Amended Petition on September 27, 2024, there is no claim that Ms. Roach

suffered from Miller Fisher syndrome.

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II. Events in Ms. Roach’s Medical History

A. Before and Through Vaccination

Ms. Roach had a lengthy medical history. The earliest medical record filed

is dated January 22, 2013. Exhibit 11 at 5. Ms. Roach saw her primary care

provider, Andrew Swanson. She presented with depression, and described it as

chronic and ongoing with some sleep disturbance. Id. Ms. Roach also presented

with sores on her scalp and reported that the onset had been associated with stress.

Id.

On July 30, 2014, Ms. Roach visited the emergency room at Northern

Nevada Medical Center (NNM). Exhibit 14 at 94. At this time, she was 39 years

old. Ms. Roach reported a two-month history of abdominal pain, nausea, and

vomiting. She stated that she vomited nearly every day, occasionally with specks

of blood, and had lost twenty pounds due to her inability to eat. Ms. Roach stated

that she had “2 cocktails every night,” and she “denie[d] excessive drinking or

drinking to the point of intoxication.” Id.

Labs revealed sludge in Ms. Roach’s gallbladder and an enlarged liver.

Exhibit 14 at 97, 106. The doctor who reviewed the results, Gina Dapra, opined

that “some of her LFT [liver function test] elevation may be related to alcoholic

hepatitis or other hepatitis, but we will get her for possible cholecystitis.” Id. at

97.3 Dr. Dapra expressed concern that Ms. Roach “may have a cholecystitis/biliary

colic given the location of her tenderness, the increased pain with eating, [and her]

vomiting.” Id. She also noted that the AST to ALT ratio suggested alcohol abuse.

Id. at 97-98. Dr. Dapra stated, “I suspect that some of the patient’s hepatic

enlargement . . . and LFT elevation may be related to alcohol, perhaps she drinks

more than she is leading us to believe.” Id. at 98.

Ms. Roach was discharged on July 31, 2014 with the following diagnoses:

1. Abdominal pain with no findings to suggest acute cholecystitis,

unsure etiology.

3

The stem “cholecyst(o)” refers to the gallbladder. Dorland’s Illus. Med. Dictionary 343

33rd ed. Thus, “cholecystitis” is inflammation in the gallbladder. Id. “Cholecystectomy,”

which is used later means the removal of the gallbladder. Id. at 343.

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2. Anemia, macrocytic in nature. Elevations in alkaline

phosphatase as well as AST and ALT with negative hepatitis panel.

Likely nonalcoholic steatohepatitis.

3. Also history of alcohol use, likely dependence, likely alcohol

liver disease as well.

Exhibit 14 at 111. It was noted that her pain “could be secondary to alcohol liver

hepatitis” and she was advised to discontinue any drinking and consult with a

surgeon, Dr. Swanson, about gallbladder removal. Id.

Ms. Roach returned to the NNM emergency department on August 5, 2014

with a complaint of severe upper abdominal pain and vomiting. Exhibit 14 at 82.

It was noted that her LFTs had much improved since her last visit, and that she did

not have active cholecystitis or cholelithiasis. Id. at 85. She was discharged the

same day.

On August 13, 2014, Ms. Roach again presented to the NNM emergency

department with abdominal pain. Exhibit 14 at 73. Ms. Roach stated that “she was

supposed to follow up with a surgeon for possible removal” of her gallbladder. Id.

Her LFTs were “similar to those in the past, and according to GI, more consistent

with alcohol use.” Id. at 76. She was discharged and stated that she would follow

up with surgery and GI. Id.

Two days later, Ms. Roach consulted with Dr. Wynter Phoenix about her

gallbladder. Exhibit 14 at 58. Dr. Phoenix assessed her as having biliary sludge

and hepatosplenomegaly likely attributable to alcohol and acetaminophen use. Id.

at 59. Dr. Phoenix explained to Ms. Roach that removing her gallbladder “may not

alleviate all of her problems,” but scheduled her for a cholecystectomy and

prescribed a small number of narcotics until the surgery. Id.

Ms. Roach underwent the laparoscopic cholecystectomy on August 22, 2014

at NNM. Exhibit 14 at 68. “Her liver biopsy intraoperatively did not show any

signs of cirrhosis or fibrosis; however, did show fatty enlarged liver, which was

definitely seen intraoperatively.” Id. She was discharged on August 25, 2014.

On September 3, 2014, Ms. Roach presented to the emergency department at

Renown Regional Medical Center with complaints of numbness and pain in her

hands and feet, starting about two weeks prior and predating her cholecystectomy,

although the symptoms became worse after that point. Exhibit 13 at 4, 11. The

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numbness was “progressively worse each day” and it had “become very painful to

put any pressure on her hands and feet.” Id. at 4. Ms. Roach reported that she had

lost approximately 30 pounds over the past two months, and denied routine alcohol

use. Id. She described her vision as a bit blurry, and noted that her hair seemed to

be falling out more than usual. Id. at 11.

Upon exam, it was noted that Ms. Roach had “subjectively diminished”

sensation around the left side of her lower face and on the lateral aspect of her

upper left thigh. Exhibit 13 at 12. Her gait was normal, but she had a positive

Romberg test with a loss of balance. She had 5/5 strength in her lower extremities

and 4/5 in her upper extremities proximally and 4-/5 distally, which was described

as “symmetric.” Id. Given her high sed rate, there was concern for an acute

inflammatory process. The doctor ordered an MRI of the cervical spine and brain,

a CT scan of her chest, abdomen, and pelvis, and a hepatitis panel. Id.

Ms. Roach’s September 4, 2014 brain MRI showed “symmetric hazy T1

hyperintensity in the basal ganglia. This has been described in hepato-cerebral

encephalopathy, however, this usually seen in patients with end-stage cirrhotic

liver disease.” Exhibit 13 at 37. The MRI was otherwise unremarkable, “with no

evidence of acute infarction, hemorrhage, or mass lesion.” Id. The cervical spine

MRI revealed “minimal degenerative retrolisthesis,” Id. at 38-39. The CT scan

was unremarkable, with findings consistent with Ms. Roach’s recent

cholecystectomy. Id. at 41.

Ms. Roach then saw Dauod N. Majid, a resident in the Renown neurology

department, on September 5, 2014. Exhibit 13 at 14. Given the MRI results, Dr.

Majid opined that her degenerative joint disease was not causing her symptoms,

but that it was “possible that this could be a porphyria disorder.” Id. at 16. He

recommended an EMG and nerve conduction testing. Id.

Ms. Roach was discharged on September 5, 2014 with a primary diagnosis

of severe bilateral peripheral neuropathy. Exhibit 13 at 9. She was prescribed

gabapentin, ibuprofen, oxycodone, and Norco, and was instructed to follow up

with neurology and neurosurgery. Id. at 18-19. Ms. Roach was noted to be “doing

quite well” upon discharge. Id. at 9. She was given information to follow up with

Dr. Bigley in neurology and Dr. Song in neurosurgery, and it was recommended

that she follow up with an EMG and labs. Id. at 9-10.

Ms. Roach then saw gastroenterologist John Gray on September 9, 2014.

Exhibit 9 at 7. It was noted that, at the time of her admission to the hospital for

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severe abdominal pain, “she was taking frequent handfuls of Advil and Tylenol in

addition to drinking 2 large alcoholic drinks daily.” Id. She had not had alcohol

since then. Id. Upon exam, her liver was enlarged and palpable. Id. at 8. Dr.

Gray’s impression was steatohepatitis, likely on the basis of alcohol, with ridging

fibrosis, alcohol abuse, and chronic back pain with narcotic dependency. Id. at 9.

He wrote that Ms. Roach had “chronic liver disease likely on the basis of alcohol

and chronic excessive Tylenol intake.” Id. Dr. Gray ordered blood work “to rule

out other potential sources of liver disease.” Id. He advised her to abstain from

alcohol completely and to take no more than 6 Tylenols per day. Id.

Ms. Roach saw neurosurgeon Deven Khosla on September 16, 2014.

Exhibit 14 at 114. She had been advised by Dr. Song that she required surgery on

her cervical spine due to bone spurs, and sought a second opinion. She had 5/5

strength, 2+ reflexes, and her gait was antalgic due to the difficulty of putting

pressure on her feet. Id. Dr. Khosla reported that Ms. Roach had “sudden onset of

dysesthetic sensations in both hands and feet that appear to be a peripheral

neuropathy issue,” and opined that she did not require cervical spine surgery. Id. at

115.

On October 3, 2014, Ms. Roach saw a pain management physician, Dan

Snow. Exhibit 14 at 12. She reported bilateral hand and foot numbness from

August 2014, which became worse after her cholecystectomy. Id. She was

referred to a neurologist, Kim Bigley, for further evaluation. Dr. Bigley saw Ms.

Roach on October 15, 2014 and performed an EMG and nerve conduction study.

Id. at 1. Dr. Bigley opined that Ms. Roach’s study did “not have dramatic findings

but the results are not what one would expect for a 39-year-old woman.” Id. Dr.

Kim’s impression was that the results “may be consistent with a mild neuropathy,”

and suggested clinical correction. Id. at 3.

Ms. Roach saw Dr. Snow again on December 29, 2014. Exhibit 7 at 5. She

presented with pain in her feet bilaterally going up into her knees, and pain in both

hands. She stated that her hands would go from completely cold to “so hot that it

feels like they’re on fire.” Id. Her left leg had more numbness than her right leg,

and she felt more sensation laterally on her lower legs than medially. Id. She had

normal strength and gait, but her “lower extremities had symmetric medial

paresthesias from the knee down [and] inconsistent dermatonic paresthesias.” Id.

Dr. Snow assessed Ms. Roach as having peripheral neuropathy, paresthesia of the

foot, and paresthesia of the hand. Id. at 6. Along with medications, he prescribed

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an MRI of the lumbar spine to evaluate the possibility of a radiculopathy causing

the pain. Id.

Ms. Roach next saw Dr. Snow on January 28, 2015 to follow up on her test

results. Exhibit 7 at 7. She had pain in her feet bilaterally radiating up to her

knees and tingling pain in both hands, and again described her hands as feeling icy

to very hot. Ms. Roach also had “pain in her lumbar region with radiation into her

hips that is aggravated by physical activity.” Id. Dr. Snow noted that the MRI

“showed degenerative disc disease with stenosis in the lumbar region.” Id.; see

also Exhibit 4 at 37. Dr. Snow again assessed Ms. Roach as having peripheral

neuropathy, paresthesia of the foot, paresthesia of the hand, and peripheral

neuropathy, as well as a hernia of the abdominal wall. Exhibit 7 at 7-8. He

discussed the benefits of epidurals for her peripheral neuropathy, and Ms. Roach

was to return for a massage and epidural. Id. at 8.

Ms. Roach returned for the epidural on February 11, 2015. Exhibit 7 at 9.

She continued to see Dr. Snow over the next year for medication and pain

management treatment for her degenerative disc disease. She received a

termination letter “as a result of her positive amphetamine [urine drug screening]”

in July 2016. Id. at 38.

Ms. Roach had another lumbar spine MRI on October 13, 2016, which again

showed disc desiccation at L5-S1. Exhibit 6 at 19. Ms. Roach returned to Dr.

Song on December 1, 2016, with complaints of severe low back pain radiating

down her legs, neck pain radiating down both arms, and numbness and tingling in

her legs. The pain was sharp and stabbing. Id. at 5. Dr. Song noted the recent

MRI, and reordered an MRI of her cervical spine with plans to follow up in three

months to decide whether to recommend surgical intervention or let Ms. Roach

continue pain management. Id.

On December 5, 2016, Ms. Roach returned to Renown and was seen by

Joshua Dubansky. Ms. Roach complained of nausea and vomiting and stated that

she had “left sided numbness and worsening back pain.” She and her husband

reported that she had appeared jaundiced since about a week prior. Exhibit 3 at 39-

40. Dr. Dubansky noted that Ms. Roach’s “history and review of symptoms [was]

confusing and not particularly coherent. She [did] not appear intoxicated or

alerted, nonetheless, [Dr. Dubansky found] her history and review of systems to be

unreliable.” Id.

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Lab results revealed that Ms. Roach had elevated LFTs, bilirubin, and white

blood cells, and electrolyte changes consistent with GI losses. Exhibit 3 at 41-44.

A CT of her abdomen showed that Ms. Roach had an enlarged fatty liver, and

findings were consistent with acute appendicitis. Id. at 43-44. Dr. Dubansky was

concerned for liver failure and sepsis if Ms. Roach was not treated, and recorded

his final impression as acute appendicitis, transaminitis, jaundice, leukocytosis, and

metabolic acidosis. Id. at 44.

The following day, December 6, 2016, Ms. Roach was seen by surgeon

Robert Nachtsheim. Ms. Roach told Dr. Nachtsheim that she had experienced

fevers and occasional abdominal pain over the last two weeks, and chills, nausea,

and vomiting for the last three weeks. Her abdomen was nontender in the lower

right quadrant, and she had an enlarged appendix and an enlarged liver. Exhibit 3

at 55-56. She tested positive for benzodiazepines and opiates on a urine screening.

Id. at 57. Although Dr. Nachtsheim opined that it was unlikely that Ms. Roach was

suffering from appendicitis and recommended that she not undergo an

appendectomy, Ms. Roach went through with the procedure that same day. Id. at

58. She also received the flu vaccine. Id. at 329.

B. After Vaccination

Dr. Patrick Woodward saw Ms. Roach after her procedure. Exhibit 3 at 61.

The day after her appendectomy, Dr. Woodward told Ms. Roach that her liver

problems were likely caused by alcohol use. Id. at 65-66. Ms. Roach confirmed

that she drank several vodka drinks each night and had been doing so “for quite

some time,” and perhaps “more over the last month.” Id.

Ms. Roach remained in the hospital overnight. She was seen by a

gastroenterologist, Dr. Erik de Jonghe, on December 8, 2016. Exhibit 3 at 49. Dr.

de Jonghe said Ms. Roach appeared to be a “poor historian,” highlighting that she

believed she was in the hospital for pneumonia, numbness in her left leg, and

kidney pain. He further noted that her liver enzymes had been elevated since at

least 2014 and that she admitted to alcohol abuse, although she also stated that she

“quit last week.” Id. Dr. de Jonghe recorded that her condition was consistent

with alcoholic hepatitis. He recommended complete alcohol cessation and a lab

work-up. Id. at 54. Ms. Roach was discharged that same day. Her diagnoses

were “resolved sepsis, unlikely appendicitis, acute alcoholic hepatitis, alcohol

abuse, thrombocytopenia, acute on [sic] chronic anemia with acute blood loss, and

hyperbilirubinemia, and she was “strongly advised to stop drinking alcohol in

entirety.” Id. at 45.

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Ms. Roach returned to Renown on December 26, 2016. Exhibit 3 at 329.

She reported numbness in her face, chest, and bilateral lower extremities that had

started a couple days prior. Id. at 332. An emergency department provider, Dr.

Andrew Abrass, examined Ms. Roach on December 27, and noted that she had

“extensive jaundice,” mild asterixis, decreased sensation and a “mild questionable

facial droop” on the left side of her face, and decreased sensation in her left

forearm, calf, and foot. Id. at 334. Her white blood cell count was “grossly

elevated,” and Dr. Abrass put Ms. Roach on an antibiotic to cover for a possible

infection from her appendectomy. Id. at 346. He ordered CTs of her abdomen and

lumbar spine to rule out an epidural abscess, and admitted Ms. Roach to the

hospital. Id. at 346-47.

Ms. Roach was next seen by a D.O., Dr. Natalie Lewman. Exhibit 3 at 349.

Ms. Roach reported that she noticed leg weakness two to three days prior, as if

“her legs were going to collapse.” Id. She estimated that she had fallen about 15

times over the last three days. Id. Ms. Roach also described “left-sided jaw, left

neck and left shoulder numbness” that had started earlier that day and had been

constant and had not improved with rest. Id. at 350. Ms. Roach reported that she

had stopped drinking alcohol three weeks prior. Id.

Ms. Roach was seen by surgeon Dr. Paul Stumpf on December 27, 2016.

Exhibit 3 at 353. Although Ms. Roach had a high white blood cell count and a

diagnosis of sepsis, Dr. Stumpf stated that she had hepatic dysfunction and

potentially hepatic failure. Id. at 354. He recommended GI medicine and

repeating the hepatitis panel. Id. Dr. Stumpf saw no evidence of a surgical

problem. Id.

Dr. Stumpf discussed Ms. Roach’s condition with another doctor, David

Julian. Exhibit 3 at 356. Dr. Stumpf again questioned whether Ms. Roach was

actually septic. Id. Ms. Roach was positive for malaise/fatigue, abdominal pain,

itching, and weakness, and she was “markedly jaundiced.” Id. Dr. Julian

suspected that her weakness was cirrhosis related. Id. at 358. On December 28,

2016, Dr. Julian confirmed that Ms. Roach was ready for discharge. Id. at 354.

Her final diagnosis included acute alcoholic hepatitis, resolved leukocytosis,

alcoholic cirrhosis, paresthesias, hyperkalemia, and Grade I diastolic dysfunction.

Id. at 347. It was reported that she was feeling “much better” and that her

paresthesias had largely resolved. Id. at 348. Ms. Roach was advised to

discontinue alcohol use, which she promised she would. Id.

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Ms. Roach returned to the Renown emergency department on January 1,

2017. Exhibit 3 at 512. She reported weakness and stated that she had been

having difficulty walking. She had been “unsteady on her feet since her

hospitalization and it seem[ed] to be worsening,” and she was “almost wheelchair

bound and require[d] full-time assistance from family members.” Id. at 517. She

denied drinking or drug use. Her lower extremities felt weaker than her upper

extremities. She did not have slurred speech, but was “occasionally confused.” Id.

Emergency department provider Dr. Brian Trimmer conducted an exam, and

diagnosed her with back pain, spinal stenosis, neuropathy, and liver disease.

Exhibit 3 at 517. He noted jaundice and muscle atrophy, and wrote that Ms. Roach

had “Remarkable ataxia with hand flapping, poor finger to nose, poor heel to shin.

Generalized weakness throughout. Paresthesias lower extremities primarily.

Unable to ambulate. Lack of DTR at Achilles and patellas bilaterally.” Id. at 519.

Dr. Trimmer stated that Ms. Roach’s exam was consistent with Wernicke’s

encephalopathy and ordered a detox bag with thiamine. Id. at 522. She also had

significant hypokalemia4, which was likely contributing to her weakness. Id. Dr.

Trimmer’s final impression was ataxia, generalized weakness, leukocytosis,

electrolyte disturbances, alcoholic hepatitis, abnormal CT scan of the abdomen and

pelvis, and ascites. Ms. Roach was admitted to the hospital, and Dr. Trimmer

ordered “the highest level of care” with instructions to rule out bacteremia and

spontaneous bacterial peritonitis. Id.

Dr. Susan Marron saw Ms. Roach upon admission and recorded her history

and complaints of severe ataxia, numbness in her extremities, and left facial

numbness. Exhibit 3 at 523. Dr. Marron observed that Ms. Roach was “obviously

quite jaundiced” but noted no obvious motor deficits in her face. She had severe

ataxia and some paresthesias in her bilateral upper extremities, and was able to

move her lower extremities on the gurney. She could not hold herself up at all, and

appeared to be ataxic with generalized bilateral weakness. Id. at 524-25. Dr.

Marron did not note any encephalopathy, and Ms. Roach did not have slurred

speech but answered questions “with difficulty.” Id. at 525.

MRIs of Ms. Roach’s brain and cervical spine, thoracic spine, and lumbar

spine were taken on January 2, 2017. Exhibit 3 at 705. The brain MRI showed

4

Hypokalemia is the “presence of an abnormally low concentration of potassium ions in

the circulating blood.” Hypokalemia, STEDMANS MEDICAL DICTIONARY 429130 (2014).

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“stable symmetric signal abnormality in the basal ganglia which can be seen in the

setting of hepatic encephalopathy.” Id. The spinal MRIs showed stable

degenerative changes. Id.

Dr. Omar Ashraf saw Ms. Roach on January 3, 2017. Exhibit 3 at 702. He

recorded that Ms. Roach “was found to be septic on admission and started on

empiric antibodies.” Id. She had back pain, focal weakness, abdominal distention,

edema, and pallor. Id. at 702-03. Dr. Ashraf had concern for GBS due to her ataxia

and progressive neurological deficit. He consulted with neurology and ordered a

lumbar puncture. Id. at 706.

Ms. Roach was seen by neurologist Dr. Jonathan Spivack on January 4,

2017. Exhibit 4 at 606. He recorded that she had “progressive quadriparesis

beginning about 2 weeks prior to admission,” which had been “preceded by a 1-2

week course of progressive coughing and a possible pneumonitis treated with

antibiotics.” Id. at 607. She did not describe “actual weakness, but fatigue and

incoordination.” Ms. Roach could usually walk with minimal assistance and

occasionally a cane, but she eventually required the use of a walker and then lost

the ability to stand as her ataxia progressed. Id. Dr. Spivack also noted her

“chronic neuropathy, presumably related to alcohol,” and a “constant burning

paresthesias in the feet and hands, [and] some loss of sensation.” Id. Upon exam,

Dr. Spivack observed bilateral facial droop and bilateral ptosis, but Ms. Roach’s

smile was symmetric and there was no nystagmus. Id. at 608. She had strength

almost intact throughout, although with some possible weakness distally in her

hands. Ms. Roach had bilateral biceps and triceps reflexes but otherwise was

areflexic. She had “consistent appendicular dystaxia in both upper and lower

extremities out of proportion to the degree of weakness.” Id.

Dr. Spivack’s impression was “a progressive ataxia with

hyporeflexia/areflexia and no evidence of ophthalmoplegia.” Exhibit 3 at 609. He

also noted bilateral ptosis and “questionable fatigable weakness with the shoulder

girdles bilaterally” and diminished tone throughout. Id. Dr. Spivack wrote:

Consideration would be for an acute inflammatory

demyelinating polyneuropathy such as Guillain Barre,

but also a Miller Fisher variant with the significant limb

ataxia and a proportion to the degree of weakness, though

there is absent ophthalmoplegia. Patient's weakness is

minimal, the ataxia out of proportion. The areflexia again

could be related to a progressive polyneuropathy, but

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again she has a history of chronic neuropathy that I

assume is related to alcohol and this is serving to muddy

the waters. Myasthenia gravis is the other possibility.

Id. Dr. Spivack ordered serum serologies for myasthenia reflex and for anti-GQ1b

antibodies. Id.

Ms. Roach was also seen by a resident in the gastroenterology department,

Dr. Htwe Yin, on January 4, 2017. Exhibit 3 at 610. Dr. Yin noted Ms. Roach’s

history of alcohol use and stated that she was confused upon admission but now

appeared alert and oriented. Id. at 611. After reviewing her labs, Dr. Yin’s

presumptive diagnosis was “alcoholic hepatitis (with or without cirrhosis) with

portal hypertension.” Id. at 617. She also noted that Ms. Roach had possible

hepatic encephalopathy upon admission, but it had since resolved. Id. Dr. Yin

recommended prednisolone upon approval from neurology and alcohol cessation.

Id. Dr. Yin’s report was attested to by Dr. Thomas Caves, who wrote that Ms.

Roach’s clinical picture was consistent with alcohol induced hepatitis. Id. at 610.

Antibody treatment was discontinued on January 5, 2017, but restarted on

January 6 when Ms. Roach tested positive for C. difficile.5 Exhibit 3 at 672.

Dr. Spivack saw Ms. Roach again on January 6, 2017. Exhibit 3 at 684. Her

symptoms were “essentially unchanged,” and the protein, glucose, and cell count

values from her lumbar puncture were all normal. Id. Ms. Roach had tingling and

focal weakness, abnormal reflex, abnormal muscle tone, and abnormal

coordination and gait. Id. at 685. Her quadriparesis was unchanged, and her upper

extremity weakness was more profound distally than proximally, while her lower

extremity weakness was more of a proximal issue than a distal issue. Id. Ms.

5

Clostridium difficile is “a species [of bacteria] that is part of the normal colon flora in

infants and some adults; it produces a toxin that can cause pseudomembranous enterocolitis in

patients receiving antibiotic therapy.” Dorland’s at 368. Pseudomembranous enterocolitis is “an

acute type [of inflammation involving both the small intestine and the colon] with formation of

pseudomembranous plaques that overlie superficial ulcerations and pass out in the feces; it may

result from ... aftereffects of antibiotic therapy.” Id. at 618.

13

Roach was still areflexic except for her biceps, and she required maximum

assistance to stand. She also had a negative Tensilon test.6 Id. at 684, 687.

For his plan, Dr. Spivack wrote:

Clinically, with a negative Tensilon test, and despite

normal protein and white blood cell count in CSF, I still

suspect that this is the Miller-Fisher variant of GBS.

Absent ophthalmoplegia, she has the hypo-to areflexic

throughout and the profound appendicular and gait

ataxia. There is a percentage of patients with this

condition that do have normal CSF protein value, the

anti-GQ 1B antibody titers are positive in almost 85% of

patients with this condition, these are still pending. She

does require steroids sooner rather than later because of

her liver disease, I think empiric treatment with IVIG is

appropriate since this will cover all the bases including

myasthenia gravis in crisis as well as GBS and its

variants.

Exhibit 3 at 687. He prescribed steroids for her alcohol liver disease and

neuropathy. Although steroids “are known to worsen myasthenic crises initially,”

Dr. Spivack stated that IVIG would “hopefully protect her from this if she in fact

has myasthenia.” Id.

Ms. Roach recovered her strength over the next few days, but continued to

have difficulty with ataxia. Exhibit 3 at 650-68. Her ataxia was recorded as

“likely from Guillain Barre Syndrome-Miller-Fisher variant vs alcohol.” Id. at

655. Ms. Roach also continued to be seen by gastroenterology. On January 10,

Dr. de Jonghe opined that she had end stage liver disease secondary to alcoholic

hepatitis. Id. at 631. On January 11, Ms. Roach was discharged to a skilled nursing

facility. Id. at 601. Her primary diagnoses were Guillain-Barre syndrome,

clostridium difficile colitis, alcoholic cirrhosis and related hepatitis, acute delirium

secondary to her other diagnoses, iron deficiency anemia, and peripheral

neuropathy. Id.

6

A “Tensilon test” helps determine whether a person suffers from myasthenia gravis.

Dorland’s at 1871.

14

From January 23 to January 26, 2017, Ms. Roach was again hospitalized at

Renown. Exhibit 3 at 1129, 1137. She stated she felt “totally fine” but had a fever

of 100.9 and an elevated white blood cell count. Id. at 1132. The emergency

department provider, Dr. Suzanne Larson, recorded an impression of a heart

murmur and fever. Id. at 1136. Dr. Letitia Anderson examined Ms. Roach upon

admission, and did “not hear a real heart murmur, but rather a hyperdynamic

state,” and ordered an echocardiogram. Id. at 1145. Ms. Roach was started on

lactulose and rifaximin “to prevent encephalopathy.” Id. at 1143. She was still

somewhat ataxic but was able to walk short distances with a walker. Id. at 1221-

22. Ms. Roach was discharged back to the skilled nursing facility in stable

condition on January 26, with medications including lactulose, rifaximin,

prednisone, gabapentin, oxycodone, and trazodone. Id. at 1137.

On January 30, 2017, Ms. Roach underwent an upper GI endoscopy with Dr.

de Jonghe. Exhibit 2 at 31. His impressions were: normal esophagus, portal

hypertensive gastropathy, and normal examined duodenum. Id. She was

discharged on February 10, 2017. Id. at 11.

Ms. Roach saw Dr. Mohsen Tamasaby at the Reno Family Medical Center

on February 23, 2017. Exhibit 4 at 1. She stated that she had been diagnosed with

GBS two months prior after receiving the flu vaccine. She reported joint pain,

weakness all over, and an inability to walk by herself. Id. Dr. Tamasaby assessed

her as having GBS, insomnia, and low back pain. Id. at 2. He prescribed

trazodone and Percocet, and had her follow up with her neurologist and with him

in two weeks. Id. Ms. Roach continued to see Dr. Tamasaby for refills of her pain

medication every few weeks until September 28, 2017. See Exhibit 4 at 1-28.

On April 3, 2017, Ms. Roach returned to Dr. de Jonghe to follow up about

her alcoholic hepatitis and probable cirrhosis. Exhibit 4 at 30.7 It was reported

that she had been sober since her December 2016 hospitalization. Dr. de Jonghe

stated that she did not look frankly jaundiced anymore, and noted that there was

some uncertainty as to whether Ms. Roach had cirrhosis since her scans did not

reveal a small or nodular liver. Id. Still, given other findings, he opined that she

“probably has a degree of cirrhosis,” but could “potentially regain significant

function” since she was detoxing from alcohol. Id. He also noted that Ms.

Roach’s “hospitalization was complicated by extreme lower extremity weakness”

7

This scanned record is difficult to read.

15

and that she was treated for GBS. Although she was not walking with crutches,

her overall recovery could take years. Id.

Ms. Roach’s next appointment was on April 26, 2017 for a physical therapy

evaluation with Marc Magstadt, MPT. Exhibit 5 at 21. Her chief complaint was

decreased motor control, standing balance, and overall functional mobility due to

GBS. She reported that, shortly after her flu shot in December 2016, she “began

having decreased motor control, balance, and coordination causing a fall every

once in a while, to the point where she was hospitalized for approximately 2

months.” Id. Ms. Roach reported that she had:

Pain that is generalized, primary due to the peripheral

neuropathy from the nerve issues with tingling and

burning. Patient reports recently she had decreased gait

tolerance, decreased standing balance, as well as

decreased motor control and coordination in her bilateral

lower extremities, resulting in decreased ambulation

tolerance and ability to complete all functional mobility.

Patient also reports numbness in her hands as well as

decreased grip and coordination resulting in difficulty

writing, pretty much being unable to write at this time, as

well as dropping things often, resulting in decreased

cooking ability and ability to complete IADLs.

Id. She had 4+/5 strength bilaterally on her upper and lower extremities; impaired

sensation all over secondary to the numbness from her recent diagnosis; a grip

strength test on the left to 12 pounds and the right to 20 pounds; and a moderate

risk for falls with a 20/28 on the Tinetti Balance Assessment. Id. at 22. It was

recommended that she attend physical therapy 2-3 times per week for 4-6 weeks to

decrease pain and improve overall quality of life. Id. at 23.

Ms. Roach next saw Dr. Spivack on May 31, 2017. Exhibit 10 at 2. He

described her as having a “slow and steady improvement.” Dr. Spivack noted that

Ms. Roach “never developed ophthalmoplegia to a notable degree, so the Miller

Fisher variant of this disorder was difficult to establish.” Her nerve pain had

improved, although she was still taking pain medication. Overall, the gait ataxia

had stabilized. She had numbness in her lower extremities in their entirety. Dr.

Spivack wrote that Ms. Roach’s hepatitis had stabilized and she was no longer on

steroids. Id. In his assessment and plan, Dr. Spivack wrote:

16

She is recovering slowly and steadily, it will take more

time, but she also has a bit of a neuropathy related to the

chronic alcohol use by history. In any case, I would

expect steady improvement over the next several months,

though I would expect a plateau after about one year. I

did recommend that Neurontin be increased, the dose can

be up to 1200 mg, 3 times a day. Caution needs to be

maintained since the higher doses of the drug can often

make people feel unsteady, and she already has a

problem with this related to the [GBS] and maybe some

effect of chronic alcohol overuse. Still she seems to be

tolerating the drug at this time. I will defer these

decisions to her primary care physician. There is no need

for neurologic follow-up at this time.

Id. at 3.

Ms. Roach continued with physical therapy between April 26, 2017 and June

1, 2017. Exhibit 5 at 19. A progress note from June stated that her pain had

consistently remained at about a 4 to 5 out of 10 throughout the sessions. It was

described as “a generalized pain, kind of a numb and tingling type pain with an

occasional shooting pain.” Id. Her low back pain had improved since Ms. Roach

had become more active. Overall, Ms. Roach felt that her motor control and

strength and stability in her bilateral lower extremities was improving, but she

continued to have trouble with prolonged walking, walking on uneven terrains, and

difficulty with her grasp, carrying objects, and writing. She reported that she was

“70% improved.” Id. The physical therapist, Mr. Magstadt, stated that Ms. Roach

was progressing well regarding her overall motor control of bilateral upper and

lower extremities and had improved ambulation tolerance and gait pattern, but

continued to demonstrate a compensatory gait pattern and strategies, particularly

hyperextension of the left knee with decreased motor control. Id. at 20. He

recommended that she continue with physical therapy.

Ms. Roach’s next physical therapy evaluation was on July 6, 2017. Exhibit

5 at 17. She reported pain at a 6 to 7 out of 10, attributed to increased walking and

walking on uneven terrain over the weekend. Mr. Magstadt noted that, prior to this

appointment, Ms. Roach “did have multiple sessions where she had a 0 out of 10

pain rating.” Id. At her next evaluation on August 9, 2017, Ms. Roach reported a

0 out of 10 pain level and stated that she noticed an improvement in overall

17

strength, endurance, and function. Id. at 15. The physical therapist assessing her,

Jared Pugmire, DPT, noted that Ms. Roach had “shown great progress” so far with

physical therapy, and recommended that she continue 2-3 times per week for 4-6

weeks. Id. at 16. It appears that Ms. Roach attended four more sessions through

September 6, 2017. Id. at 7-8.

Ms. Roach’s liver disease progressed, and she was hospitalized several times

for complications of her liver disease. See generally Exhibit 50; see also Resp’t’s

Br. at 32 (summarizing Ms. Roach’s hospitalization course). Ms. Roach passed

away on June 23, 2021, at age 46. Exhibit 50 at 147. Her cause of death was listed

as “cardiopulmonary arrest due to or as a consequence of fulminant hepatic failure

due to or as a consequence of alcoholic cirrhosis.” Exhibit 48.

III. Procedural History

Attorneys at the Greenwood Law Firm submitted the petition on November

7, 2017. At this time, Ms. Roach was alive and was the petitioner. The November

7, 2017 petition alleged that the flu vaccine caused her to suffer from Guillain-

Barré syndrome. Pet. at Preamble. Because the Vaccine Table associates the flu

vaccine with GBS, the case was assigned to the special processing unit of the

Office of Special Masters. Order, issued Nov. 7, 2017. Medical records were

periodically filed.

The Secretary reviewed the material and recommended against

compensation. Resp’t’s Rep., filed Dec. 21, 2018. The Secretary addressed the

claim that Ms. Roach suffered GBS as defined for both AIDP and Miller Fisher

syndrome. The Secretary maintained that she did not qualify. Id. at 9-11. In the

Secretary’s view, Ms. Roach was not entitled to compensation pursuant to a

causation-in-fact claim. Id. at 11-12. Finally, the Secretary contended that Ms.

Roach did not meet the Vaccine Act’s severity requirement. Id. at 12.

The first report from Dr. Steinman was filed on May 15, 2019 as Exhibit 15.

Dr. Steinman acknowledged that Ms. Roach suffered from chronic alcoholism. Id.

at 4. This chronic alcoholism contributed to Dr. Steinman’s view that the case was

“complex” and “sift[ing] the impact of the influenza vaccine” on the chronic

alcoholism was “challenging.” Id. at 1.

Dr. Steinman’s report begins with a summary of his qualifications. Exhibit

15 at 1-4. His summary of pertinent medical facts contains quotes from the

Secretary’s report. Id. at 4-7. In the section discussing the relevant diseases, Dr.

18

Steinman asserted that Ms. Roach “had alcoholic neuropathy and GBS.” Id. at 7.

Citing the Vandenbulcke & Janssens8 article, Dr. Steinman stated that a person can

suffer from alcoholic neuropathy and GBS. Id. at 8. Notably absent in this section

is an explanation as to why Ms. Roach should be diagnosed with GBS. In the

remainder of his report, Dr. Steinman presented an opinion as to why the flu

vaccine was the cause-in-fact of Ms. Roach’s GBS. Id. at 8-18. He also asserted

that the flu vaccine “significantly aggravated the alcoholic neuropathy by

triggering GBS.” Id. at 19.

The Secretary responded to Dr. Steinman’s report by obtaining opinions

from two people. The first is Dr. Cohen. Exhibit A. The second is Robert

Fujinami. Exhibit C. Dr. Fujinami generally addressed the assertions that the flu

vaccine can cause GBS. But, given that this case is being resolved on the issue of

diagnosis, neither Dr. Fujinami’s opinion nor portions of Dr. Steinman’s opinions

relating to causation are particularly relevant. Thus, although those reports have

been reviewed, this decision does not summarize them.

In contrast to causation, diagnosis is very important to this decision and the

Secretary’s arguments regarding causation are mostly based upon opinions

presented by Dr. Cohen. Dr. Cohen’s report begins with his qualifications.

Exhibit A at 1. In approximately one single-spaced page, Dr. Cohen summarized

Ms. Roach’s medical records. Id. at 2. He then explained why, in his opinion, Ms.

Roach did not suffer from Miller Fisher syndrome. Id. at 3-4. Dr. Cohen

maintained that the Vandenbulcke & Janssens article “confirms that alcoholic

neuropathy can appear identical to acute Guillain-Barre [] syndrome.” Id. at 4.

Given the dispute over whether Ms. Roach suffered from Guillain-Barré

syndrome, adjudication through the special processing unit seemed infeasible. The

case was assigned to a special master. Order, issued Oct. 18, 2019. The new

special master directed petitioner to obtain a report from Dr. Steinman addressing

Dr. Cohen’s opinion that Ms. Roach did not suffer from Miller Fisher syndrome.

Order, issued Oct. 23, 2019.

Dr. Steinman’s second report addressed opinions from both Dr. Cohen and

Dr. Fujinami. (Again, however, the details of the debate between Dr. Steinman

8

M. Vandenbulcke and J. Janssens, Acute axonal polyneuropathy in chronic alcoholism

and malnutrition, 99 ACTA. NEUROL. BELG. 198 (1999). Filed as Exhibit 22.

19

and Dr. Fujinami do not affect the resolution of the case.) Dr. Steinman wrote:

“Both Dr. Spivack and Petitioner indicated that the differential is large and

explained why they both arrived at Miller Fisher Syndrome as a tenable and correct

diagnosis.” Exhibit 36 at 1 (emphasis removed).9 Quoting his first report, Dr.

Steinman states that “Careful reading of Dr. Spivack’s notes indicate that he

considered a spectrum of diagnoses ranging from inflammatory neuropathy

including the ‘Miller Fisher’ variant, myasthenia, ADEM and even motor neuron

disease.” Id. at 2. Dr. Steinman quoted one of Dr. Spivack’s reports in which Dr.

Spivack wrote: “Consideration would be for an acute inflammatory demyelinating

polyneuropathy such as Guillain Barre, but also a Miller Fisher variant.” Id. at 2,

quoting Exhibit 10 at 11.

The Secretary responded with a second report from Dr. Fujinami on May 26,

2020. Exhibit E. At this time, the Secretary did not submit a second report from

Dr. Cohen. Dr. Steinman addressed Dr. Fujinami’s opinions in a report filed on

August 27, 2020. Exhibit 41, filed Aug. 27, 2020. This report did not add any

information regarding diagnosis.

The Secretary requested that petitioner submit updated medical records.

Resp’t’s Status Rep., filed Oct. 27, 2020. Ms. Roach stated that she did not have

any updated medical records as she had not received any medical care due, in part,

to the Covid-19 pandemic. Pet’r’s Status Rep., filed Nov. 30, 2020. The Secretary

planned to file more reports from Doctors Cohen and Fujinami. Resp’t’s Status

Rep., filed Feb. 2, 2021.10

The next round of reports does not meaningfully advance the analysis. Dr.

Cohen wrote essentially one page, asserting that Ms. Roach’s post-vaccination

symptoms “could be explained by her alcoholic neuropathy.” Exhibit F. Dr.

9

Dr. Steinman’s statement that “Petitioner” asserted Miller Fisher syndrome is curious in

at least two respects. First, it is not readily apparent that Ms. Roach alleged that she suffered

from Miller Fisher syndrome. When Dr. Steinman wrote his second report, the operative petition

alleged that the flu vaccine caused Guillain-Barré syndrome. Pet., filed Nov. 7, 2017, at

Preamble. Second, and more importantly, it is not readily apparent why the assertion of the

petitioner, who appears not to have any medical training, should influence the opinion of a

trained neurologist.

10

The Secretary’s plan to obtain another report from Dr. Cohen was unusual in the sense

that Dr. Steinman’s most recent report (Exhibit 41) did not address diagnosis.

20

Steinman maintained his opinion. Exhibit 45. Dr. Steinman’s comments on

diagnosis largely repeated information from Dr. Spivack and again quoted from the

Vandenbulcke & Janssens article.

The Secretary stated that petitioner’s attorney learned on July 22, 2021 that

Ms. Roach had died. Resp’t’s Status Rep., filed Sep. 13, 2021.11 In due course,

Austin Roach-Yohey, who is Ms. Roach’s son, became the administrator of her

estate and was substituted as the petitioner. Order, issued Oct. 8, 2021.

Mr. Roach-Yohey was directed to obtain updated medical records. He

submitted them via compact disc on February 2, 2022.

For the Secretary, Dr. Cohen reviewed the more recent medical records,

which continued to show that Ms. Roach was consuming too much alcohol. For

example, Dr. Cohen cited hospitalizations in 2019 and June 2020. Exhibit H at 2,

citing Exhibit 50 at 1226 and 905.12 Overall, Dr. Cohen maintained that “None of

her diagnostic studies were consistent with GBS.” Exhibit H at 2. He concluded

that “Dr. Steinman has said nothing new or given any new proof that Ms. Roach

had GBS.” Id. at 3. This report (plus the report from Dr. Fujinami) appeared to

complete the disclosure of opinions from the expert. The case was scheduled for a

hearing to take place in April 2024. Order, issued Aug. 1, 2022. However, the

Secretary stated that Dr. Cohen was not available for unspecified reasons. Resp’t’s

Status Rep., filed Jan. 30, 2024. The hearing was canceled. Non-PDF order, issued

Jan. 30, 2024. The case was reassigned to the undersigned. Order, issued Feb. 15,

2024.

The undersigned attempted to understand the claims and the defenses to

whatever claims were being asserted. Order, issued Feb. 23, 2024. This order also

advised that the parties may want to seek additional information from Dr. Spivack.

The order directed Mr. Roach-Yohey to file an amended petition, potentially

pleading alternative causes of action.

11

It is not readily apparent why nearly two months passed during which both attorneys

were aware that Ms. Roach had died yet neither informed the special master.

12

These hospitalizations contradict the statement in petitioner’s November 30, 2020

status report that Ms. Roach did not have any additional medical care.

21

Although Mr. Roach-Yohey duly filed an amended petition on March 18,

2024, the amended petition is not a model of clarity. It asserted that the flu vaccine

“is both the cause-in-fact for Petitioner’s [actually Ms. Roach’s] GBS and the

cause-in-fact of significant aggravation of Petitioner’s [actually Ms. Roach’s] pre-

existing symptoms and conditions.” First Am. Pet., filed Mar. 18, 2024, at

Preamble. Mr. Roach-Yohey also requested an opportunity to seek more

information from Dr. Spivack. Mr. Roach-Yohey recounted that Dr. Steinman was

interested in knowing whether Dr. Spivack thought Ms. Roach’s progression of

symptoms was more consistent with GBS or more consistent with alcoholic

neuropathy. Pet’r’s Status Rep., filed March 20, 2024.

Both the First Amended Petition and Mr. Roach-Yohey’s request to seek

more information from Dr. Spivack were discussed in the April 23, 2024 status

conference. Mr. Roach-Yohey’s counsel was again informed that if Ms. Roach

suffered from GBS as defined in the regulations, then Mr. Roach-Yohey was not

required to establish that the flu vaccine was the “cause-in-fact” of the regulatory

GBS. When asked about what type of GBS afflicted Ms. Roach, counsel

responded that it was Miller Fisher, and stated that he would add that specificity to

another amended petition. As to Dr. Spivack, petitioner’s counsel was welcome to

seek additional information from him. See Order, issued Apr. 23, 2024.

Mr. Roach-Yohey amended the petition a second time. This petition alleged

that the flu vaccine “triggered Miller Fisher Syndrome, a variant of Guillain Barré

Syndrome (“GBS”). Alternatively, the vaccine is the cause-in-fact for Angela

Roach’s Miller Fisher variant of GBS which significantly aggravated Angela

Roach’s alcoholic neuropathy.” Second Am. Pet., filed May 1, 2024, at Preamble.

This second amended petition stated that Mr. Roach-Yohey is claiming that Ms.

Roach suffered an injury contained in the Vaccine Injury Table. Id. at ¶ 1.

As to Dr. Spivack, efforts to obtain information from him did not proceed

smoothly for a variety of reasons, none of which affect the outcome of this case.

Eventually, Dr. Spivack answered a series of questions posed to him in writing via

a letter, filed as Exhibit 51 on August 23, 2024. He stated that in his opinion: “The

clinical course including the rate of progression for Ms. Roach’s disease is more

consistent with Guillain-Barré syndrome, not an alcohol-related polyneuropathy.”

Id. at ¶ 4.e. He added: “Based on the data available at the time of her disease

presentation, it is most likely that she did suffer from an atypical presentation of

the Miller-Fisher variant of Guillain-Barré syndrome.” Id. at ¶ 4.f.

22

After Dr. Spivack’s letter was filed, a status conference was held. The

parties suggested that a ruling on the record might be appropriate. Accordingly,

they were instructed to file briefs. The briefing order emphasized that the claims

that Mr. Roach-Yohey was asserting remained unclear. Order, issued Aug. 30,

2024, at 4-13 (discussing three potential causes of action).

Mr. Roach-Yohey obtained relatively short reports from Dr. Steinman. Dr.

Steinman stated that his previous reports “have been clear and unwavering . . . that

the diagnosis is GBS, also known as acute inflammatory demyelinating

polyneuropathy.” Exhibit 57. Dr. Steinman then cited a series of his reports that

use the term “GBS.”13

In Dr. Steinman’s final report, he identified the criteria he uses to diagnose

Guillain-Barré syndrome, including acute inflammatory demyelinating

polyneuropathy and Miller Fisher syndrome. Exhibit 61. Dr. Steinman put

forward an article from the European Academy of Neurology / Peripheral Nerve

Society.14 (The details of these criteria are set forth in section VI.A below). Dr.

Steinman also quoted (again) his previous reports, which used the term “GBS.”

Lastly, Dr. Steinman commented upon the possibility of a significant aggravation

case. He separated the two conditions:

The influenza vaccine triggered a new disease GBS, that

appeared on top of Mrs. Roach’s alcohol neuropathy. The

two diseases are independent. Alcohol neuropathy is

metabolic, and the other disease-GBS- is autoimmune.

This is a significant aggravation case, because both

13

A potential source of ambiguity is that the term “GBS” can be used as an umbrella

term for both acute inflammatory demyelinating polyneuropathy and the Miller Fisher variant.

Although “GBS” is often used interchangeably with “acute inflammatory demyelinating

polyneuropathy,” the possibility that Ms. Roach suffered from the Miller Fisher variant might

have warranted a higher degree of precision. In addition, Dr. Steinman’s second report stated

“Dr. Spivack . . . indicated that the differential is large and explained why [he] arrived at Miller

Fisher Syndrome as a tenable and correct diagnosis.” Exhibit 36 at 1 (emphasis removed). Plus,

it appears that Mr. Roach-Yohey’s attorney might also have been confused as the Second

Amended Petition asserted claims based upon Ms. Roach suffering from Miller Fisher variant.

14

Pieter A. van Doorn et al., European Academy of Neurology/Peripheral Nerve Society

Guideline on diagnosis and treatment of Guillain-Barré syndrome, 30 EUR. J. NEUROL. 3646

(2023). Filed as Exhibit 62.

23

alcohol neuropathy and GBS are peripheral neuropathies,

and the peripheral neuropathy was worsened by vaccine

induced GBS.

Id. at 5.

These reports from Dr. Steinman prompted Mr. Roach-Yohey to revise the

petition again. The third amended petition, which is the operative petition, asserts

three causes of action. These are: (1) Ms. Roach developed acute inflammatory

demyelinating polyneuropathy as defined in the Vaccine Table (Third Am. Pet.,

filed Sep. 27, 2024, at Preamble and ¶ 1); (2) the flu vaccine was the cause in fact

of Ms. Roach’s acute inflammatory demyelinating polyneuropathy (Third Am. Pet.

at Preamble and ¶ 27); and (3) the flu vaccine significantly aggravated Ms.

Roach’s alcoholic neuropathy (Third Am. Pet. at Preamble and ¶ 27).

With the clarification from the Third Amended Petition, the parties could

argue their cases through briefs. Mr. Roach-Yohey presented his arguments in a

35-page entitlement brief, filed October 10, 2024. The Secretary responded on

December 13, 2024 with essentially two relevant submissions. (Again, the

material from Dr. Fujinami is being set aside). The Secretary presented another

report from Dr. Cohen. Dr. Cohen challenged Dr. Steinman’s use of the article

from the European Academy of Neurology and the Peripheral Nerve Society.

Exhibit J at 1-2. In his view, Ms. Roach did not suffer from acute inflammatory

demyelinating polyneuropathy. The Secretary’s other main submission was an 85-

page brief.

As discussed in the analysis below, the Secretary made multiple strong

points challenging the arguments Mr. Roach-Yohey presented in his brief. Thus, a

reply brief would have been appropriate. However, Mr. Roach-Yohey did not file

a reply.

Because the time for submitting a reply elapsed months ago, the case is

ready for adjudication. As both parties have had a fair opportunity to present their

evidence and their arguments, an adjudication based upon the papers is

appropriate. See Kreizenbeck v. Sec'y of Health & Hum. Servs., 945 F.3d 1362,

1365 (Fed. Cir. 2018).

24

IV. Standards for Adjudication

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

evidence. 42 U.S.C. § 300aa–13(1)(a). The preponderance of the evidence standard

requires a “trier of fact to believe that the existence of a fact is more probable than

its nonexistence before [he] may find in favor of the party who has the burden to

persuade the judge of the fact's existence.” Moberly v. Sec’y of Health & Hum.

Servs., 592 F.3d 1315, 1322 n.2 (Fed. Cir. 2010) (citations omitted). Proof of

medical certainty is not required. Bunting v. Sec’y of Health & Hum. Servs., 931

F.2d 867, 873 (Fed. Cir. 1991).

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

important because a special master should not impose an evidentiary burden that is

too high. Andreu v. Sec’y of Health & Hum. Servs., 569 F.3d 1367, 1379-80 (Fed.

Cir. 2009) (reversing special master's decision that petitioners were not entitled to

compensation); see also Lampe v. Sec’y of Health & Hum. Servs., 219 F.3d 1357

(Fed. Cir. 2000); Hodges v. Sec’y of Health & Hum. Servs., 9 F.3d 958, 961 (Fed.

Cir. 1993) (disagreeing with dissenting judge's contention that the special master

confused preponderance of the evidence with medical certainty).

V. Analysis: First Cause of Action – On-Table AIDP

Mr. Roach-Yohey’s first cause of action is that Ms. Roach suffered acute

inflammatory demyelinating polyneuropathy as defined in the regulations. Third

Am. Pet. at Preamble and ¶ 1; see also Pet’r’s Br., filed Oct. 10, 2024, at 3-7. A

petitioner bears the burden of demonstrating that the vaccinee meets the definition

of disease as defined in the regulations. See Waterman v. Sec’y of Health & Hum.

Servs., 123 Fed. Cl. 564, 574 (2015).

The Qualifications and Aids to Interpretation define acute inflammatory

demyelinating polyneuropathy with both inclusive and exclusive factors. The

inclusive factors include:

(A) Bilateral flaccid limb weakness and decreased or

absent deep tendon reflexes in weak limbs;

(B) A monophasic illness pattern;

(C) An interval between onset and nadir of weakness

between 12 hours and 28 days;

25

(D) Subsequent clinical plateau (the clinical plateau

leads either to stabilization at the nadir of symptoms, or

subsequent improvement without significant release;

however, death may occur without a clinical plateau).

42 C.F.R. § 100.3(c)(15)(ii).

The Secretary also requires “The absence of an identified more likely

alternative diagnosis.” 42 C.F.R. § 100.3(c)(15)(ii)(E). The regulations specify a

long list of “[e]xclusionary criteria for the diagnosis of all subtypes of GBS” and

this list includes “hypokalemia” and “hyperkalemia.” 42 C.F.R.

§ 100.3(c)(15)(vi).

In this case, the Secretary presented at least three arguments explaining why

Ms. Roach did not fulfill these criteria. First, the Secretary argued that Ms.

Roach’s course was not monophasic. See Resp’t’s Br. at 34-35. Second, the

Secretary argued that alcoholic neuropathy is a more likely alternative diagnosis.

Id. at 35-47. Third, the Secretary argued that Ms. Roach suffered from

hypokalemia. Id. at 47-48.

For purposes of resolving the on-Table claim, the third argument about

hypokalemia is dispositive. The arguments about monophasic and alcoholic

neuropathy are reviewed in the context of the off-Table claim below.

The Secretary identified a series of medical records showing that Ms. Roach

suffered from hypokalemia. Resp’t’s Br. at 41-42. The Secretary also pointed out

that Dr. Cohen also raised Ms. Roach’s hypokalemia. Id. at 41. By way of

contrast, Dr. Steinman did not comment upon hypokalemia. See Exhibits 15 and

36.

Thus, an abundance of evidence supports the finding that Ms. Roach had

low potassium. Because hypokalemia excludes an on-Table diagnosis of any form

of Guillain-Barré syndrome (including acute inflammatory demyelinating

polyneuropathy), Ms. Roach does not meet the standards in the regulation.

Therefore, she does not prevail upon her on-Table claim. See Bauer v. Sec’y of

Health & Hum. Servs., No. 18-1451, 2024 WL 4534147, at *30 (Fed. Cl. Spec.

Mstr. Sep. 23, 2024) (finding that a vaccinee who suffered from hyperkalemia,

which is also listed in the exclusionary criteria, did not qualify for Guillain-Barré

syndrome as defined in the regulations).

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from medical professionals who treated Ms. Roach. Although these groups are

separated for purposes of analysis, the opinions from all doctors are ultimately

based upon Ms. Roach's signs and symptoms.

A. Opinions from Doctors Retained in the Litigation

The definition for AIDP that Dr. Steinman proposes is, as already

mentioned, from the European Academy of Neurology and the Peripheral Nerve

Society. This article is relatively long (approximately 20 pages) and cites more

than 250 references. The purposes of the article were “to develop an evidence-

based international guideline on the diagnosis and treatment of Guillain-Barré

syndrome (GBS) . . . and to formulate evidence-based recommendations and

consensus-based good practice points (GPPs) for clinical practice.” Exhibit 62

(van Doorn) at 537. For diagnosis, these authors compiled a list of items for

consideration. They included: “Features required” (3 items); “Features that

support diagnosis” (7 items); “Laboratory findings that support diagnosis” (3

items); and “Findings which make GBS less likely” (15 items). Id. at 539.

Of this group, Dr. Steinman commented upon only the three “Features

required.” Exhibit 61 at 3-5. These required features are:

• Progressive weakness of arms and legs

• Tendon reflexes absent or decreased in affected limbs

• Progressive worsening for no more than 4 weeks

Exhibit 62 (van Doorn) at 539 (footnotes omitted). On pages of 3-5 of his

September 26, 2024 report (Exhibit 61), Dr. Steinman emphasized certain

attributes for Ms. Roach, such as “numbness and tingling [in] her legs” (Exhibit 6

at 5); “progressive quadriparesis” and “bilateral ptosis” (Exhibit 3 at 608);

“progressive quadriparesis beginning about two weeks prior to admission” (Exhibit

3 at 607); “strength [was] actually almost intact throughout, though there may be

some weakness distally in the hands. She was diffusely hypo- to aflexic” (Id.).

As Dr. Cohen maintains, Dr. Steinman’s opinion is incomplete in two

significant respects. First, “Ms. Roach does not meet the third prerequisite due to

the prolonged course of her illness. She suffered from progressive worsening for

much longer than 4 weeks.” Exhibit J at 2; accord Resp’t’s Br. at 50-52. Second,

in Dr. Cohen’s view, neurologists with expertise in peripheral neuropathies do not

stop with the first three factors. Instead, other factors listed in Table 1 should be

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considered. In Dr. Cohen’s assessment, Ms. Roach did not have many of the

features that support diagnosis and conversely, Ms. Roach did have some of the

findings that make a GBS diagnosis less likely. Exhibit J at 2-4.15

Dr. Cohen’s review of the 25 other factors affecting a diagnosis of GBS is

sensible and persuasive for two reasons. First, Dr. Cohen has a great deal of

experience in treating patients with peripheral nerve disorders. Exhibit A (report)

at 1; Exhibit K (curriculum vitae). In contrast, Dr. Steinman’s more specific field

of expertise is diseases of the central nervous system. See Exhibit 53 at 2 (noting

prizes won for his work on multiple sclerosis). As a board-certified neurologist,

Dr. Steinman is certainly qualified to opine on a neurologic diagnosis like Guillain-

Barré syndrome. But, on the narrower question about a disease of the peripheral

nervous system, Dr. Cohen has superior qualifications. A special master may

consider the differences in qualifications in weighing the relative value of

competing opinions. See Depena v. Sec’y of Health & Hum. Servs., No. 13-675V,

2017 WL 1075101 (Fed. Cl. Spec. Mstr. Feb. 22, 2017), mot. for rev. denied, 133

Fed. Cl. 535, 547-48 (2017), aff'd without op., 730 Fed. App'x 938 (Fed. Cir.

2018); Copenhaver v. Sec’y of Health & Hum. Servs., No. 13-1002V, 2016 WL

3456436 (Fed. Cl. Spec. Mstr. May 31, 2016), mot. for rev. denied, 129 Fed. Cl.

176 (2016). Although the Secretary argued this point (Resp’t’s Br. at 66), Mr.

Roach-Yohey did not refute it in a reply.

Second, the consideration of other factors listed in Table 1 of the van Doorn

article aligns with the overall tone of the article. At a basic level, the authors from

the European Academy of Neurology / Peripheral Nerve Society took the trouble

to develop a consensus list of features to consider. If there is a reason not to

consider these features, neither Dr. Steinman nor Mr. Roach-Yohey has provided

one. To take one example, the Taskforce investigated: “In patients with clinically

suspected GBS, does examination of the CSF compared with no CSF examination

influence the diagnostic test accuracy, treatment response and patient outcome?”

Exhibit 62 (van Doorn) at 539 (PICO 2). Laboratory findings that support

diagnosis include a finding of increased protein in the CSF, although “normal

15

Dr. Cohen’s report would have been improved if he cited evidence supporting his

opinions. For example, he wrote “Ms. Roach had asymmetrical weakness,” but did not support

this statement by pointing to an exhibit number and page.

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protein does not rule out diagnosis.” Id. at 540. Ms. Roach’s CSF protein was

normal. Exhibit 3 at 684, 797.

Another example from Dr. Cohen is that van Doorn states another feature

that supports the diagnosis of Guillain-Barré syndrome is cranial nerve

involvement. Exhibit 62 (van Doorn) at 539. When Dr. Spivak examined Ms.

Roach on January 6, 2017, he found no deficits in her cranial nerve. Exhibit 3 at

685.

Neither Ms. Roach’s protein nor the lack of cranial nerve problems are not

diagnostic by themselves. However, when multiple findings tend to point away

from Guillain-Barré syndrome, the collection of findings carry more substantial

weight. Thus, Dr. Cohen’s opinion that Ms. Roach did not suffer from AIDP is

more persuasive than Dr. Steinman’s contrary opinion because Dr. Cohen’s

opinion is more consistent with the medical literature (van Doorn) and more

consistent with Ms. Roach’s medical records.

Ms. Roach’s pre-existing and undisputed alcoholic neuropathy also tends to

weaken the likelihood that Ms. Roach also suffered from AIDP. To start, it is

important to acknowledge that the Secretary recognizes that as a matter of logic, a

person with an alcoholic neuropathy can also develop AIDP. Resp’t’s Br. at 49.

The possibility of co-existing diseases underlies the Vandenbulcke & Janssens

article. See Exhibit 22. But, saying as a theoretical matter that a person could

suffer from two diseases is not the same as saying as a practical matter that Ms.

Roach suffered from both alcoholic neuropathy and AIDP.

The weight of the evidence favors a finding that Ms. Roach suffered from

only alcoholic neuropathy. The Secretary comprehensively and persuasively

argued that Ms. Roach’s course before and after the flu vaccine was better

explained by her alcoholic neuropathy. Resp’t’s Br. at 35-42. Mr. Roach-Yohey

did not rebut any of these arguments through a reply brief.

At best, Mr. Roach-Yohey attempted to anticipate arguments regarding

alcoholic neuropathy in his initial brief. Without citing medical records in this

context, Mr. Roach-Yohey argues that “Ms. Roach’s presentation included new

onset facial numbness, left arm weakness, and bilateral lower extremity numbness,

which were not part of her clinical presentation prior to the vaccination.” Pet’r’s

Br. at 8. But, as the Secretary points out, “Many of Ms. Roach’s post-vaccination

complaints mirror her earlier complaints, further supporting Dr. Cohen’s opinion

that her alcoholic neuropathy is a more likely explanation for her condition than

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GBS. Resp’t’s Br. at 36. For example, for facial numbness, although Ms. Roach

had decreased sensation on the left side of her face after the vaccination (Exhibit 3

at 334 – December 27, 2026), she also had decreased sensation before the

vaccination (Exhibit 14 at 21 --- September 3, 2014).

Overall, Dr. Cohen’s opinion that Ms. Roach suffered from only alcoholic

neuropathy and its sequela is more persuasive than Dr. Steinman’s opinion that

Ms. Roach suffered from alcoholic neuropathy and AIDP. However, Mr. Roach-

Yohey’s argument rests on more than Dr. Steinman’s opinion. Mr. Roach-Yohey

also cites an opinion from a treating doctor, Dr. Spivack.

B. Opinions from Doctors who Treated Ms. Roach

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

of Health & Hum. Servs., 440 F.3d 1317, 1326 (Fed. Cir. 2006). The views of

treating doctors about the appropriate diagnosis are often persuasive because the

doctors have direct experience with the patient whom they are diagnosing. See

McCulloch v. Sec’y of Health & Hum. Servs., No. 09-293V, 2015 WL 3640610, at

*20 (Fed. Cl. Spec. Mstr. May 22, 2015). However, the views of a treating doctor

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

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

Servs., 127 Fed. Cl. 136, 141 (2016), appeal dismissed, No. 16-2400 (Fed. Cir.

Oct. 26. 2016).

During Ms. Roach’s hospitalization that began on January 1, 2017, she saw

Dr. Spivack. Ms. Roach informed him that she developed weakness after her

potential infection the previous month. Exhibit 3 at 606. But, in Dr. Spivack’s

opinion, Ms. Roach did not have “actual weakness, but fatigue and

incoordination.” Id. Dr. Spivack’s examination detected bilateral facial droop and

bilateral ptosis. Id. at 608. Her tone was decreased throughout but her strength

was almost normal throughout.

Dr. Spivack considered that Ms. Roach had a “chronic neuropathy,

presumably related to alcohol.” Exhibit 3 at 606. He also considered that she

could have either the AIDP type of Guillain-Barré syndrome or the Miller Fisher

variant. Id. at 609. He ordered tests of Ms. Roach’s cerebrospinal fluid and tests

for an antibody closely associated with the Miller Fisher variant, GQ1B.

When Dr. Spivack saw Ms. Roach on January 6, 2017, the results on her

cerebrospinal fluid had come back. They showed normal protein, glucose, and cell

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counts. Exhibit 3 at 797. The anti-GQ1B antibody titers were pending. After a

review of the available information and another examination, Dr. Spivack “still

suspect[ed] that this is the Miller-Fisher variant of GBS.” Id. at 687. Dr. Spivack

prescribed IVIG empirically because, in part, IVIG would “cover all the bases . . .

[including] GBS and its variants.” Id.16

Dr. Spivack did not see Ms. Roach for the remainder of this hospitalization.

See Resp’t’s Br. at 25. The next visit was as an outpatient on May 31, 2017.

Exhibit 10 at 2. Dr. Spivack memorialized that Ms. Roach did not develop any

“notable degree” of “ophthalmoplegia.” Thus, establishing the “Miller Fisher

variant” “was difficult.” Dr. Spivack stated that additional follow up was not

needed and Ms. Roach did not return to see him.

In the course of this litigation, Mr. Roach-Yohey sought more information

from Dr. Spivack. Dr. Spivack answered written questions. He wrote that: “Based

on the data available at the time of her disease presentation, it is most likely that

she did suffer from an atypical presentation of the Miller-Fisher variant of

Guillain-Barré syndrome.” Exhibit 51 ¶ 4.f. Relying upon this letter, Mr. Roach-

Yohey argues that “Dr. Spivack ultimately concludes that Ms. Roach’s condition is

consistent with GBS rather than just an exacerbation of her alcoholic neuropathy.”

Pet’r’s Br. at 8.

This argument misconstrues the evidence. Dr. Spivack’s diagnosis is the

Miller-Fisher variant. But, as reviewed in the procedural history, Mr. Roach-

Yohey is not claiming that Ms. Roach suffered the Miller-Fisher variant. The

claim is that Ms. Roach suffered from AIDP. Thus, Dr. Spivack’s August 22, 2024

letter does not preponderantly support an argument that Ms. Roach suffered from

AIDP.

C. Summary regarding AIDP

The evidence does not preponderate in favor of finding that Ms. Roach

suffered from the acute inflammatory demyelinating polyneuropathy form of

Guillain-Barré syndrome. As stated earlier, Dr. Cohen’s opinion weighs more

16

The Secretary emphasizes that “empiric” means “founded on practical experience,

rather than on reasoning alone, but not established scientifically.” Resp’t’s Br. at 44, quoting

Stedman’s Medical Dictionary at 632.

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heavily than Dr. Steinman’s opinion. Dr. Spivack’s work points away from the

AIDP form as an appropriate diagnosis.

Given the finding that Mr. Roach-Yohey did not meet his burden of showing

that Ms. Roach suffered from AIDP, exploring causation via the Althen test is not

necessary. The finding regarding (the lack of) diagnosis suffices to resolve the

Second Cause of Action.

VII. Analysis: Third Cause of Action – Significant Aggravation

The third and final cause of action is that the flu vaccination “significantly

aggravated [Ms. Roach’s] alcoholic neuropathy. Third Am. Pet. ¶ 27; accord

Pet’r’s Br. at 23-32. This cause of action was developed in Dr. Steinman’s

September 26, 2024 report. He stated: “The influenza vaccine triggered a new

disease GBS, that appeared on top of Mrs. Roach’s alcohol neuropathy. The two

diseases are independent. Alcohol neuropathy is metabolic, and the other disease-

GBS- is autoimmune.” Exhibit 61 at 5. He explained why, in his view, there

could be a claim for significant aggravation: “because both alcohol neuropathy

and GBS are peripheral neuropathies, and the peripheral neuropathy was worsened

by vaccine induced GBS.” Id. Mr. Roach-Yohey follows in his footsteps. Pet’r’s

Br. at 26-27. Mr. Roach-Yohey argues: “[t]he flu vaccine does not directly

worsen alcoholic neuropathy but triggers a new autoimmune response (GBS) that

further compromises the peripheral nervous system, thereby significantly

aggravating the existing neuropathy.” Pet’r’s Br. at 28.

The Secretary seizes this language. According to the Secretary, Mr. Roach-

Yohey’s acknowledgment that “the flu vaccine does not significantly aggravate

alcoholic neuropathy” is “fatal to his significant aggravation claim.” Resp’t’s Br.

at 73-74. A response to the Secretary’s argument might have been expected, but

no reply was filed.

A leading case that differentiates initial onset cases from significant

aggravation cases is Paluck. In consideration of granting a first motion for review,

the Court stated: “If [the vaccinee] Karl's neurological, not mitochondrial,

symptoms, however defined, were manifested pre-vaccination, then Karl's case

involves a significant-aggravation claim.” Paluck v. Sec’y of Health & Hum.

Servs., 104 Fed. Cl. 457, 467 (2012). This statement implies that if the vaccinee’s

neurologic problems were not manifest before the vaccination, then the claim is an

initial onset claim. As part of a ruling on a second motion for review, the Court

declined to overturn a determination that the child’s neurologic problems started

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before vaccination. Paluck v. Sec’y of Health & Hum. Servs., 113 Fed. Cl. 210,

228 (2013), aff’d on non-relevant grounds, 786 F.3d 1373 (Fed. Cir. 2015). Thus,

Paluck teaches that in characterizing a claim as an initial onset claim or as a

significant aggravation claim, a critical question is determining whether the

vaccinee suffered the condition before the vaccination. See Lampe v. Sec’y of

Health & Hum. Servs., 219 F.3d 1357, 1362 (Fed. Cir. 2000) (ruling that the

special master did not err in reasoning that because the child-vaccinee’s seizure

disorder started after the second dose of the diphtheria-tetanus-pertussis vaccine,

the petitioners could proceed only on a theory that the third dose significantly

aggravated the seizure disorder); Childs v. Sec’y of Health & Hum. Servs., 33 Fed.

Cl. 556, 559 (1995) (ruling that when the vaccinee did not have a history of a

problem before the vaccination, petitioners could not proceed on a theory of

significant aggravation).

Here, the Secretary’s argument is persuasive and consistent with the cases

cited above. Mr. Roach-Yohey did not present any persuasive evidence that the flu

vaccine worsened the disease from which Ms. Roach suffered before vaccination,

the metabolic alcoholic neuropathy. Indeed, Dr. Steinman actually emphasizes that

alcoholic neuropathy and AIDP are “independent” diseases. Exhibit 61 at 5. This

distinction is, to borrow a word from the Secretary, “fatal” to this cause of action.

VIII. Additional Comments

Through decisions, special masters decide whether compensation should be

awarded. 42 U.S.C. § 300aa–12(d)(3). Appellate authorities expect that the

decision set forth sufficient reasoning to explain the outcome. Stratton v. Sec'y of

Health & Hum. Servs., 138 F.4th 1368, 1371-73 (Fed. Cir. 2025). However,

special masters are not required to address every element of a claim, and they are

not required to detail in the decision each piece of evidence.

This decision complies with those requirements by focusing on the decisive

issues in the case. In doing so, two issues have not been addressed. One of those

depends upon Ms. Roach’s health--- whether any condition caused by the flu

vaccine lasted for more than six months. See Resp’t’s Rep. at 12 (raising the

severity issue); Pet’r’s Br. at 32; Resp’t’s Br. at 74.

The other unaddressed issue, arguably, has potentially more importance for

the Vaccine Program as whole---whether petitioners can persuasively present a

reliable theory as to whether the flu vaccine can cause Guillain-Barré syndrome.

This is the topic on which Dr. Steinman and Dr. Fujinami presented conflicting

34

opinions and contrary evidence. For the parties’ summaries of their arguments, see

Pet’r’s Br. at 9-20 and Resp’t’s Br. at 58-71. Although this issue merits careful

consideration in some future case, an analysis here is not required because Mr.

Roach-Yohey failed to present persuasive evidence that Ms. Roach suffered from

Guillain-Barré syndrome.

IX. Conclusion

Ms. Roach had multiple difficulties in her life and her death is another

reason to extend sympathy to Mr. Roach-Yohey. However, her medical conditions

did not include the AIDP form of Guillain-Barré syndrome. Thus, Mr. Roach-

Yohey cannot prevail upon any claim that the flu vaccine caused her to suffer this

medical condition.

The Clerk's Office is instructed to enter judgment in accord with this

decision unless a motion for review is filed. Information about filing a motion for

review, including the deadline, can be found in the Vaccine Rules, which are

available on the website for the Court of Federal Claims.

IT IS SO ORDERED.

s/Christian J. Moran

Christian J. Moran

Special Master

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