IN THE UNITED STATES COURT OF FEDERAL CLAIMS

Office of Special Masters

CYNTHIA S. SMITH,
Case No. 12-cv-709V
Petitioner,

v.

SECRETARY OF HEALTH AND

HUMAN SERVICES,

Respondent.
_____________________________________________________________________________

MOTION FOR STAY OF PROCEEDINGS AND/OR AN ONSET HEARING

_____________________________________________________________________________

Comes now Cynthia S. Smith, in propria persona and in first-person, stating as follows:

SUMMARY OF THE ARGUMENT

"How often have I said to you that when you have eliminated the impossible, whatever
remains, however improbable, must be the truth?”
—Sherlock Holmes1

Thomas Huxley once observed that the great tragedy of science is “the slaying of a beautiful

hypothesis by an ugly fact.”2 To sustain the Government’s contention that I contracted Guillain-

Barré Syndrome (hereinafter, “GBS”) that manifested itself in December of 2011, and therefore,

that a Fluzone vaccination on August 24, 2011 could not have been the cause of my ailment, it

would have to be able to explain why an otherwise-healthy 54-year-old woman would be taking

~1,200 mg./day of gabapentin—prescribed for nerve pain—in October and November of 2011

1
Arthur Conan Doyle, The Sign of Four 93 (1890) (italics in original).
2
Thomas H. Huxley, "Biogenesis and abiogenesis" (Presidential Address at the British Ass’n for the Advancement
of Science), (1870); reprinted at Thomas H. Huxley 8 Discourses: Biological and Geological Essays 244 (Appleton
Co. 1897).

1
(Exhibit A). Simply put, if I came down with GBS in December, I shouldn’t have had any nerve

pain and thus, any conceivable reason to be taking gabapentin before then.

My argument for causation is rooted in Sherlock Holmes’ famous axiom. The abnormal con-

centration of proteins in my spinal fluid, coupled with the observed symptoms, points to two and

only two possible causes: GBS, or chronic inflammatory demyelinating polyneuropathy (herein-

after, “CIDP”). If it isn’t GBS, it is CIDP, and if it is CIDP, the only open question is whether it

has to manifest itself in dramatic fashion in less than seventeen weeks. And as CIDP is known to

be a heterogeneous condition,3 the answer appears to be no. As it is admitted by the Government

that the influenza vaccine can cause CIDP, and there appears to be no other viable candidate for a

proximate cause, it logically follows that the vaccine probably caused my CIDP.

While GBS is about as delicate as a freight train, CIDP is more subtle; its earliest manifesta-

tions (fatigue, back pain, peripheral neuropathy) are readily attributable to more common causes,

and CIDP is so rare and its presentment so variable that even experienced neurologists often have

difficulty in diagnosing it. For example, my husband has peripheral neuropathy caused by spinal

degeneration requiring a fusion; as Dr. Drewek’s records demonstrate, I have a similar problem.4

The fatigue was initially attributed to over-work and the nerve pain, to a degenerating spine. In a

perfect world, I would have figured this out before the symptoms became pronounced, but this is

not a perfect world, and this Court should not demand more than reasonable diligence.

Cases like this are why Vaccine Court was created in the first place. If the Government were

to tell us that you take flu vaccines at your own risk, and you can’t even sue the manufacturer for

3
Michael P.T. Lum and Kaxim A. Sheikh, “Peripheral Neuropathy,” in The Autoimmune Diseases (Ian R. Mackay
and Noel R. Rose) 641 (4th ed. 2006).
4
See generally, Exh. 5. My husband would testify to this effect if called, with record support.

2
knowingly selling an inherently defective product, no one would get vaccinated, and more people

would end up dying as a result. The legislative solution was to relax a victim’s burden of proof,

in exchange for a severe reduction in damages. I can guarantee Your Honor that you would not

willingly volunteer to go through the living hell I have endured—and will continue to endure for

the rest of my life—for a million dollars or three. I will not be fairly compensated here.

In this submission, I am attempting to preserve what I believe to be a viable claim in the face

of inexplicable indolence by counsel. A competent attorney should have developed a theory of

the case supported by expert testimony before the case was even filed, see Fed. R. Civ. P. 11(b),

but after eighteen months of assurances and facile excuses,5 he appears no closer to discharging

that elementary professional obligation than he was on the day that he rushed this claim to court.

As CIDP doesn’t normally present itself dramatically, and is so rare that few doctors even know

how to look for it, it should have been obvious to everyone that the dispositive issue in this case

was onset, and the evidence would be indirect. I expect that three pieces of the onset puzzle, all

from third-party records and considered in light of other medical evidence formally submitted to

the Court, will be sufficient to establish onset in accordance with its established standards.

While I would like to resolve this claim both quickly and amicably, given his performance to

date, I have lost confidence in Mr. Gallagher’s ability to represent my interests with appropriate

professionalism and zeal. I therefore ask this Court for an extension of time through December

31, 2014 to retain alternate counsel and an expert witness. In the alternative, I ask this Court to

find that there is a question of fact sufficient to warrant an onset hearing.

5
In informing the Court of this fact or any others involving my relationship with Mr. Gallagher, I am not waiving the
attorney-client privilege generally. By way of example, in a message left on my recorder on May 22, he admitted that
he had not even started to write this brief, due a week later. This is one of the natural hazards of compensating coun-
sel from court funds, win or lose: Thomas P. Gallagher’s only real client in this matter is Thomas P. Gallagher.

3
 ARGUMENT

The essence of my claim was embedded in the practice notes of Drs. Dianna Quan and David

Saperstein, practicing neurologists with national reputations as experts in GBS/CIDP6:

The clinical course suggests chronic inflammatory demyelization polyneuropathy

syndrome. It is hard to be certain of the precise onset, but it sounds like there was a
prolonged, slow progression followed by a significant deterioration. The patient and
husband fell strongly that she improved with initial IVIG and then worsened again.
This is reflected in the notes of her neurologist in Colorado.7

History and clinical course (with initial episode and subsequent relapse) consistent
with CIDP. Relatively abrupt onset somewhat unusual, but not unheard of.8

Both confirmed Dr. London’s eventual diagnosis of CIDP (Exh. 4 at 14), and taken together,

these statements demonstrate how variable its presentment can be. Importantly, Dr. Saperstein

was not surprised by the “long, slow progression,” and with good reason. In some cases, it takes

many months to manifest in a debilitating fashion,9 and “because of the insidious onset of CIDP,

documenting precipitating illnesses or events is very difficult.”10 CIDP “most frequently starts

insidiously and evolves slowly,”11 but a heterogeneous presentation leads “to underdiagnosis of

6
Phoenix Neurological Associates, Ltd. is recognized as a “Center of Excellence” by the GBS/CIDP Foundation
International (http://www.gbs-cidp.org/home/get-support/centers-of-excellence); Dr. Saperstein serves on its Medical
Advisory Board (http://www.gbs-cidp.org/home/about/medical-advisory-board/). Dr. Quan is a Professor of Neuro-
logy at the University of Colorado (her CV is at http://www.ucdenver.edu/academics/colleges/medicalschool/depart-
ments/neurology/Faculty/Documents/MD_CV%202014/CV.Quan.2014.pdf), consulted on the recommendation of
Dr. London. Dr. Saperstein was consulted for the purpose of confirming Dr. London’s diagnosis and specifically, to
determine whether and how I might eventually be able to discontinue my IVIg treatments.
7
Dr. David Saperstein (Jan. 10, 2013), Exh. 12 at 8.
8
Dr. Dianna Quan (Oct. 18, 2012) Exh. 9 at 15.
9
E.g., Taryn Taylor, Case Report: Chronic Inflammatory Demyelinating Polyradiculoneuropathy In a Remote
Northern Ontario Hospital, Canadian Family Physician Vol. 59, no. 4, 368 (Apr. 2013) (three years from initial
symptoms to catastrophic outcome) (attached as Exhibht B).
10
Chronic Inflammatory Demyelinating Polyradiculoneuropathy Clinical Presentation, Medscape (Richard M. Lewis,
ed., Apr. 3, 2014, at http://emedicine.medscape.com/article/1172965-clinical (Dr. Quan is listed as an editor). Due to
a generally-slow onset, a “trigger” can only be identified in less than 30% of CIDP patients. AF Hahn, et al., Chronic
inflammatory demyelinating polyradiculoneuropathy. in Peripheral Neuropathy 2221 (PJ Dyck PJ, and PK Thomas,
ed.) (4th ed. 2005).
11
Id.

4
the disorder.”12 There is even the “acute-onset” form of CIDP Dr. Quan appears to be alluding to,

but it is regarded as a distinct and rare13 variant, resulting in a good outcome for those who suffer

from it.14 GBS, CIDP, sub-acute inflammatory demyelinating polyneuropathy (SIDP), and multi-

focal motor neuropathy (MMN) can best be thought of as a ‘family’ of diseases. What you don’t

know—and often, even the foremost experts in the world may not be able to tell you—is whether

you got the bratty sister or the obnoxious little brother.

Given the amorphous nature of this family of diseases, and the fact that no one actually knows

their pathology, all you can do is speak in terms of probability. But all I have to do is establish

that it is “more likely than not” that the vaccination with preservative-laden Fluzone15 caused my

illness. As there are strong reasons to conclude that I did not suffer from either GBS or the (rare)

acute form of CIDP, and there was no other possible “trigger” that could have caused my CIDP,

invoking Sherlock Holmes’s famous axiom, it logically follows that the vaccination caused it.

A. Why I Did Not Contract GBS

Ironically, one of my duties as a retail pharmacist is to administer influenza vaccines. One of

the standard questions we asked candidates for vaccination is whether they have ever had GBS.16

12
JM Vallat, et al., Chronic inflammatory demyelization polyradiculoneuropathy: diagnostic and therapeutic chal-
lenges for a treatable condition, 9 Lancet Neurol. 402 (2010).
13
Paolo Ripellino, et al., Treatment of Chronic Inflammatory Demyelinating Polyneuropathy: From Molecular
Bases to Practical Considerations, in Vol. 2014 Autoimmune Diseases (Article ID 201657) at 1, at http://dx.doi.org/-
10.1155/2014/201657 (“In rare cases, CIDP displays acute onset and fast deterioration in the early phases, followed
by chronic progression.”).
14
SK Chieng, et al., Chronic inflammatory demyelinating polyneuropathy in childhood can present acutely: A report
of three cases, 12 Neurology Asia 97 (2007).
15
Certain forms of Fluzone employ thimerosal as a preservative, which is about 50% mercury by weight. While the
Defendant insists publicly that it is perfectly safe, Centers for Disease Control and Prevention (“CDC”), Thimerosal
(website, undated), http://www.cdc.gov/vaccinesafety/Concerns/Thimerosal/Index.html, it has been removed from all
pediatric versions, see e.g., http://www.immunize.org/thimerosal/, and concerns remain. See Coalition for Mercury-
Free Drugs v. Sebelius, 671 F. 3d 1275 (D.C. Cir. 2012) (concerns noted).
16
Exhibit 3 at 2. I only had a vague idea as to what GBS was; all I had to know was that it was a contraindication.

5
When patients asked what it was, I would tell them, “if you had it, you would know it.”

One of the emblematic characteristics of traditional GBS is that it is almost always preceded

by a “trigger.” Roughly 50-75% of GBS cases are preceded by acute infectious illnesses,17 with

the most common being severe gastroenteritis caused by the Campylobacter jejuni bacillus, typi-

cally appearing within 2-3 weeks of the incident.18 Other potential triggers are still being inves-

tigated,19 but anything that puts serious stress on the immune system (e.g., pregnancy,20 mononu-

cleosis, HIV, and influenza21) seems to serve as a trigger. About the one thing you can safely say

about this laundry list of natural trigger conditions is that if you had one, you would notice. The

typical symptoms of gastroenteritis “include diarrhea, abdominal pain, vomiting, headache, fever

and chills,”22 which would be hard to miss, especially on vacation. While I would have to testify

under oath that I was otherwise quite healthy—one reason for an onset hearing—another famous

Sherlock Holmes axiom applies: Even the dog that does not bark is telling us something.23

Another key factor arguing against a diagnosis of GBS or the acute onset form of CIDP is the

prognosis—generally, it is excellent—and as the Government admits, the recovery period can be

as short as three weeks.24 To understand why this is true, you have to understand what demyeli-

17
Ban M. Allos, Association between Campylobacter Infection and Guillain-Barre´ Syndrome, 12(1) Infect. Dis.
Clin. North Am. 173 (Mar. 1998).
18
Shuji Fujimoto and Kazunobu Amako, Guillain-Barre syndrome and Campylobacter jejuni infection. 35 Lancet
1350 (Jun. 1990).
19
E.g., Helmar C. Lehmann and Hans-Peter Hartung, Varicella-Zoster Virus: Another Trigger of Guillain-Barre´
Syndrome? 51(5) Clin Infect Dis. 531 (2010), at http://cid.oxfordjournals.org/content/51/5/531.full.pdf.
20
A Bahadur, et al. Successful maternal and fetal outcome of Guillain-barré syndrome complicating pregnancy, 63
Indian J Med Sci 517 (2009) (“GBS has also been linked to underlying systemic diseases, certain malignancies,
surgery, pregnancy, trauma, severe infection and tissue transplantation”).
21
Guillain-Barre syndrome: Risk Factors, Mayo Clinic (website, undated), at http://www.mayoclinic.org/diseases-
conditions/guillain-barre-syndrome/basics/risk-factors/con-20025832.
22
Gastroenteritis, Medline Plus (Nat’l Inst. Of Health) (website, undated), at http://www.nlm.nih.gov/medlineplus-
/gastroenteritis.html
23
See Arthur C. Doyle, Silver Blaze (1892), reprinted at https://sherlock-holm.es/stories/pdf/a4/2-sided/silv.pdf.
24
NINDS Guillain-Barré Syndrome Information Page, National Institute of Neurological Disorders and Stroke

6
nation is, and what happens in GBS and CIDP.

Think of our nerves as copper wires. If we don’t insulate the wire and it touches metal, it will

short out. Our nerves have sheaths of myelin, that serve as insulation. GBS and CIDP essentially

cause our immune system to eat the insulation, shorting out the nerves and causing pain. If GBS

is caught and treated promptly—within roughly three weeks of onset—the only actual damage is

to the myelin insulation, which seems to grow back quickly.25 But CIDP is persistent, eventually

attacking the nerves themselves, and once a nerve is damaged, it grows back at the rate of a milli-

meter a day, or a little over an inch per year.26 Worse yet, it doesn’t always grow back where it is

needed.27 Accordingly, whereas the GBS (and acute CIDP patient) can expect a full recovery, the

traditional CIDP patient can expect to have residual deficits, the severity of which appears to be a

function of time that the disease remained untreated.

(website, undated), at http://www.ninds.nih.gov/disorders/gbs/gbs.htm.

25
Not a lot is actually known about the mechanism by which our myelin regenerates, but it regenerates well. Natan
Shaoulian, CIDP-Chronic Inflammatory Demyelinating Polyneuropathy; Causes, Symptoms, Treatments, and Diag-
nosis (website, undated), at http://www.beverlyhillsneurology.com/cidp.html. However, as GBS patients recover
quickly, and we know how fast nerves grow, it logically follows that myelin regenerates faster than nerves.
26
E.g., Nerve Injury, British Soc’y for Surgery of the Hand, at http://www.bssh.ac.uk/patients/commonhandcondi-
tions/nerveinjury (website, undated).
27
Id.

7
 Finally, there is the definitional argument. In an article written for the GBS/CIDP Foundation

and aimed at the layman, Dr. Saperstein writes that these autoimmune disorders are distinguished

by their aggressiveness and persistence, and that the most common form of GBS

…may also be referred to as acute inflammatory demyelinating polyneuropathy (AIDP).

This emphasizes the acute nature of this disorder: symptoms come on abruptly and pro-
gress rather quickly. Symptoms stop progressing, often within 2 weeks, and usually not
more than 4 weeks. After a period of weeks to months, patients then begin to experience
improvement. Although the majority of patients with GBS will do rather well, not all
patients will recover fully and may experience chronic weakness, numbness, fatigue or
pain. Once symptoms stabilize, there is rarely any further deterioration.28

By stark contrast, CIDP

…produces manifestations similar to GBS, but there are important differences. Symptoms
tend to come on more slowly and progress for a longer period of time. Patients may stabi-
lize and recover, but then experience a return of symptoms in the future (this is referred to
as the relapsing form of CIDP). Alternatively, patients may experience progressive CIDP
wherein there is slow, continuous progression without a period of stabilization. By defi-
nition, if there is progression of symptoms beyond 8 weeks, the patient has CIDP.29

B. Acute Onset vs. Slow Onset CIDP

As every neurologist who has examined me agrees,30 the elevated protein levels in my spinal

fluid,31 coupled with my observed symptoms, indicate that I suffer from either GBS or CIDP, and

literally by definition,32 if it isn’t GBS, it is CIDP. As we have seen, there appear to be two kinds

of CIDP: the acute-onset version and slower-onset version. The available evidence suggests that

it is more likely than not that I contracted the slower-onset version, on the grounds that: (1) I had

28
David S. Saperstein, What’s In a Name? Important Differences Between GBS, CIDP and Related Disorders,
GBS/CIDP Foundation Newsletter (Summer 2006) at http://www.gbs-cidp.org/newsletters/2006summerwhats-
inaname.htm
29
Id.
30
Exh. 4 at 3-4 (London), Exh. 9 at 15 (Quan), Exh. 12 at 8-10 (Saperstein).
31
As noted at, e.g., Exhibit 4 at 9.
32
Saperstein, What’s In a Name, supra n. 28.

8
symptoms consistent with early stages of slower-onset CIDP within two months of vaccination,

(2) the acute-onset version is rare, even for CIDP, and (3) there were no other “triggers” associ-

ated with GBS/CIDP during the relevant period. In addition, studies purporting to establish the

safety of flu vaccines are fatally flawed, as even the government concedes that the data they rely

on is essentially worthless. But I’ll start with the numbers, because the numbers make everything

else about this case make sense.

1. “It’s Safe. Trust Us. Would Your Government Lie To You?”

According to the federal Centers for Disease Control, somewhere between 3,000 and 6,000

Americans contract GBS annually, and “two studies suggested that approximately 1 additional

person out of 1 million vaccinated people may be at risk for GBS associated with the seasonal

influenza vaccine.”33 Given that roughly 40% of all Americans are vaccinated against the flu,34

that works out to 120 cases per year, or 2-4% of all cases, attributable to the influenza vaccine

alone.

But even that number may be wildly understated, as it is dependent on compliance with the

Vaccine Adverse Event Reporting System (VAERS), which can only be described as abysmal.

As former Food and Drug Administration (FDA) Commissioner David Kessler conceded in the

Journal of the American Medical Association, those adverse reaction reports the FDA receives

“probably represent only a fraction” of the actual number encountered by providers.35 He goes

33
Centers for Disease Control and Prevention (CDC), General Questions and Answers on Guillain-Barré syndrome
(GBS), Dec. 15, 2009, at http://www.cdc.gov/h1n1flu/vaccination/gbs_qa.htm.
34
CDC, Final state-level influenza vaccination coverage estimates for the 2010–11 season (website, undated), at
http://www.cdc.gov/flu/fluvaxview/coverage_1011estimates.htm (~130 million vaccinations).
35
David Kessler, Introducing MEDWatch, 293(21) JAMA 2765, 2765 available at http://www.fda.gov/downloads/-
Safety/MedWatch/UCM201419.pdf.

9
on to cite one study claiming that only “1% of serious [adverse] events” are ever reported,36 but

even if we assumed 20% compliance, it logically follows that as many as 20% of GBS cases

were caused by the influenza vaccine.

In the proposed onset hearing in Denver, I expect to call my neurologist, Dr. Scott London,

to testify that a VAERS report wasn’t filed in my case because the paperwork burden is onerous

and, as a general rule, no one ever bothers.37 I further expect him to testify to the exception that

proves the rule: In a swine-flu (H1N1) year, the academy pushed for increased compliance, and

he and his colleagues “watched a little more closely.”

Whereas GBS is rare, it is common when compared to CIDP. According to the GBS/CIDP

Foundation, between 500-1100 Americans contract GBS annually.38 And almost by definition,

you could never find a statistically significant causal link39 between it and vaccines in a universe

where 80-90% of adverse events remain unreported.

A study is only as good as your data. This “reality on the ground” explains why some studies

show a causal link between GBS and the flu vaccine, and others do not.40

According to the Defendant, in the past thirty-four years, a little “more than 200,000 reports” of adverse events—
about 6,000 a year, including those for which causal links were not established—have been reported, “most of which
describe mild side effects such as fever.” http://vaers.hhs.gov/about/faqs.
36
Kessler, Introducing MEDWatch, supra n. 35.
37
See Exhibit 4 (no VAERS report in Neurological Associates’ records).
38
All About CIDP, GBS/CIDP Foundation International (website, undated), at http://www.gbs-cidp.org/home/cidp/-
cidp/ (“The incidence of new cases is estimated to be between 1.5 and 3.6 in a million people”). Assuming roughly
310,000,000 Americans, that works out to 465 to 1116 new cases; I rounded the figures to the nearest 100. But while
GBS is usually cured, CIDP is forever; the FDA estimates that it affects about 25,000 Americans. FDA Approves
Treatment for Rare Neurologic Disease (Food and Drug Administration news release), Sept. 12, 2008, available at
http://www.fda.gov/NewsEvents/Newsroom/PressAnnouncements/2008/ucm116946.htm.
39
A general rule of thumb is that you need about 500 participants to reach a conclusion with a 95% confidence level.
See e.g., Sample Size: How Many Survey Participants Do I Need?, Science Buddies.org (website, undated), at
http://www.sciencebuddies.org/science-fair-projects/project_ideas/Soc_participants.shtml. The details, of course, are
far more subtle,
40
See e.g., CDC [HHS], General Questions and Answers on Guillain-Barré Syndrome, Dec. 15, 2009 (website), at
http://www.cdc.gov/h1n1flu/vaccination/gbs_qa.htm (Defendant admission that some studies do show a link)

10
2. There Was Objective Evidence Of Symptoms Consistent With Slow-Onset CIDP

Our “neighbor” was finally spotted a few days ago. We know she has been around for a while

from the paw-prints in the snow, but it took a long time to find her.

Traditional CIDP is a little like a cougar in the woods. You might be able to find it if (a) you

know what to look for, and (b) you are actually looking. But as the odds of contracting CIDP are

about as long as winning $1,000,000 in Powerball,41 only an inveterate hypocondriac would even

be looking.

What makes CIDP so difficult to recognize and diagnose is that it doesn’t present itself in the

same way in every incident, and the earliest symptoms, such as lower back pain,42 unexplained

fatigue,43 weakness, numbness and pain caused by peripheral neuropathy,44 abdominal “bloating”

41
“New Powerball has created 1,014 millionaires in its first two years.” Powerball, Multi-State Lottery Association
(website, undated), at http://www.powerball.com/pb_contact.asp (website copy converted to PDF on May 16, 2014).
The low-end estimate for CIDP cases is actually less than that.
42
G. Di Guglielmo, et al., Low back pain due to hypertrophic roots as presenting symptom of CIDP, 18(5) Ital J
Neurol Sci. 297 (Oct. 1997).
43
Robert G. Miller & Jonathan S. Katz, Fatigue in Guillain-Barre Syndrome, GBS/CIDP Foundation Newsletter
(Summer 2005), at http://www.gbs-cidp.org/newsletters/2005summer.htm.
44
Chronic Inflammatory Demyelinating Polyneuropathy (CIDP), Phoenix Neurological Associates, Ltd. (website,
undated), at http://www.phoenixneurology.com/specialties/cidp.php; Peripheral neuropathy: Definition, Mayo Clinic
(website; undated), at http://www.mayoclinic.org/diseases-conditions/peripheral-neuropathy/basics/definition/con-
20019948 (defining the term for laymen).

11
and even constipation45 can be caused by just about every other ailment under the sun. By way of

example, peripheral neuropathy has been known to have been caused by kidney disease, liver dis-

ease, Lyme disease, vitamin deficiencies, exposure to toxins, diabetes, tumors, and trauma from

sports injuries,46 and even then, in about 30% of cases, neuropathy is classified as “idiopathic,”47

which means that no cause can be identified. Importantly for purposes of this case, my husband

suffers from peripheral neuropathy attributed to spinal degeneration, and can testify to this effect

if called. Even if you have all of these symptoms—and I had all of them, and spinal degeneration

to boot48—CIDP is so rare that you aren’t looking for it. When the symptoms are relatively mild,

you tend to treat the symptoms, for in many instances, you can’t do a lot about the causes.

It is also important to bear in mind that time is of the essence in the treating of CIDP. As Dr.

Natan Shaoulian explains,

In CIDP, it is the myelin that is affected first and in later stages of the disease the nerve
itself is attacked. If we started treatment in the early stages were only the myelin is
damaged, then the chances of recovery are much better as the myelin has very good
regenerative properties.49

GBS can be thought of as a full-scale, Normandy-style invasion of the nerves, but if it is diag-

nosed and treated quickly enough, the actual nerves themselves are not damaged, and the odds of

of a full recovery are high, with an average time to clinical recovery of roughly six months.50 By

45
Natan Shaoulian, Symptoms of CIDP - Chronic Inflammatory Demyelinating Polyneuropathy (website, undated) at
http://www.beverlyhillsneurology.com/cidp-symptoms.html
46
Peripheral neuropathy: Causes, Mayo Clinic (website; undated) at http://www.mayoclinic.org/diseases-
conditions/peripheral-neuropathy/basics/causes/con-20019948.
47
Jeffrey W. Ralph, Neuropathy 101: Incidence & Causes, Neuropathy Action Foundation (website, undated), at
http://www.neuropathyaction.org/neuropathy_101/incidence_and_causes.htm.
48
See generally, Exhibit 5.
49
Shaoulian, supra n. 45.
50
Ettore Beghi, et al., The prognosis and main prognostic indicators of Guillain-Barre syndrome: A multicentre
prospective study of 297 patients, 119-6 Brain (1996 2053, available at http://brain.oxfordjournals.org/content/-
119/6/2053.full.pdf

12
the same token, the acute onset form of CIDP boasts a similarly optimistic prognosis,51 ostensibly

for much the same reasons. In a slow-onset scenario (of which the example of the Ontario miner

appears to be an extreme example), axonal damage is extensive; the body can’t repair itself prop-

erly, and recovery is poor. In an acute-onset scenario, axonal damage is slight, recovery is virtu-

ally assured and residual deficits, often slight. In my scenario, the axonal damage was moderate;

recovery has been slow and the residual effects, substantial. This is in line with the outcome you

would expect if my CIDP was caused by the Fluzone vaccine in late August: a “prolonged, slow

progression followed by a significant deterioration.”

If I had been lucky enough to find the cougar, I would have received treatment sooner and, in

all likelihood, would not be here seeking compensation. But as was evidenced by the case study

involving the Ontario miner, it can take months and even years for discrete symptoms sufficient

to warrant a diagnosis of CIDP to develop.52 And while this constellation of symptoms might be

unusual enough in a child of 14 to warrant careful investigation, in a woman of 54, they are more

likely to be attributed to a more insidious condition: growing old.

Although their significance is much clearer in the bright light of hindsight, the relevant paw-

prints were there for all to see. The most significant one was that I was taking a ~1,200 mg./day

dose of gabapentin—a medication intended to address nerve pain, and was also prescribed when

51
E.g., Chieng, , supra n. 14.
52
While the article is attached as Exhibit B, the most significant portion of the case history follows:

During a hospitalist locum placement in a small northern Ontario community, I managed the care of a 70-
year-old retired miner with progressive polyneuropathy. In retrospect, he had a history suggestive of
nonspecific peripheral neuropathy going back 1 to 2 years, presenting as numbness of the right foot and
gradually leading to a painful tingling sensation.

CIDP can literally take years to manifest in such a way as to be identifiable. My symptoms quite literally might not
have presented themselves in dramatic fashion for years.

13
I was discharged from the hospital—from some point in October through the catastrophic phase

of my illness around New Year’s Day, as evidenced by the prescription record. Exhibit A.

One of the advantages of being a pharmacist is that you have a pretty good idea as to what a

doctor is most likely to do. For nerve pain, they often prescribe gabapentin (trade name: Neuron-

tin) or pregabalin (Lyrica). For back pain, diclofenac (Voltaren) is commonly prescribed, both in

topical and tablet form. For bloating or swelling, spironolactone or hydrochlorothiazide are often

prescribed, with the former being preferable as it is potassium-sparing. The first order of business

is to address the symptoms, as it often takes time to isolate causes.

As most of these symptoms are idiopathic, the usual course of action is to manage them with

medication. By way of example, in my case, gabapentin had been prescribed to treat symptoms of

bursitis on an as-needed basis,53 as several refills were already authorized; as I already had what I

expected to be prescribed, and I reasonably attributed the problem to known spinal degeneration,

I saw no compelling need to undergo an urgent medical examination. As I have never been in the

habit of running to the doctor at the first sign of a hangnail, that I did not do so here is hardly sur-

prising.

As the diagnostic approach taken by both my Australian and American doctors demonstrates,

even if I had sought treatment more aggressively in late October, it is a veritable certainty that my

ailment would not have been properly diagnosed before acute symptoms manifested. While I can

walk in at any time to see my primary caregiver (Randy Sclar, P.A.), he would not have sufficient

expertise to diagnose a disease only affecting 500 Americans a year on the amorphous symptoms

presented. As evidenced by the fact that the attending physicians on both sides of the Pacific first

53
See Exhibit 2 at 28 (Sclar, P.A.).

14
ordered MRIs even after more acute symptoms had manifested, the next logical step should have

been to consult with the family neurosurgeon to determine whether my neuropathy was caused by

spinal compression. Problem is, as it generally takes 1-2 months to even get an appointment with

Dr. Drewek for non-urgent care, and there was no objective reason for me to begin to suspect that

my symptoms were emblematic of a disease so rare that is diagnosed only by default and after the

fact, all I could do is address symptoms. In short, all I did was save myself a trip to the doctor.

A second paw-print was my gym attendance record. 24-Hour Fitness logs in its member visits

with biometric data provided by a fingerprint reader; records show that the last time that I worked

out there prior to the presentment of catastrophic symptoms was in late September.54 In turn, this

tends to prove that in October of 2011, I was suffering from fatigue sufficient to prevent me from

working out, and that the fatigue was not present earlier.

The last significant paw-print was the record of medications I purchased whilst in Australia.

There, ibuprofen with codeine is available without a prescription, although you have to obtain it

from a pharmacist (in much the same way that pseudoephedrine is controlled here). At the risk

of stating the obvious, these are not medications you take for fun. This evidences my claim that

my condition was deteriorating in December.55

In a short story, Sir Arthur Conan Doyle’s Sherlock Holmes famously solved a murder partly

by recognizing that a dog was not barking. But arguments from silence only carry the day where

54
Exhibit C. Complete records from January of January 1, 2010 establish that I visited our gym on a weekly basis;
although I worked out frequently and was in excellent physical shape despite my weight problems, see Exh. 2 at 28
(reference two-hour workout on elliptical machine), there is little comparable evidence from independent sources to
confirm this fact. At the proposed onset hearing, a records custodian from 24-Hour Fitness could be called to intro-
duce this evidence.
55
Exhibit D. Again, this is evidence that should be developed by counsel, but the records showing what had been
purchased should be available from third parties. As luck would have it, I still had one tablet; a photo with resolu-
tion sufficient to show the lot number (E/NY11405, with an expiration of May, 2014) is at Exhibit D at 3.

15
there actually IS silence. While the noise here was more of a whisper than a thunder, there was

enough of it to be heard. While my testimony could be discounted as self-serving, the evidence

supporting it cannot. And though my attorney has yet to develop it fully, the evidence remains,

and is sufficient to support a finding of causation in an onset hearing.

3. There Are No Alternate “Triggers” Supporting the Government’s Position

As I understand the Government’s argument, they assert that I suffered from GBS or at least,

the acute-onset form of CIDP. Of course, the problem with this theory is that they can’t identify

the “barking dog” they need to support their version of events.

As has been observed previously, the vast majority of GBS cases can be associated with an

identifiable “trigger.” This is owing to the fact that the presentation of GBS is generally prompt

and aggressive. As I have always told customers who asked during consultations, “If you had it,

you would know.” If, as postulated earlier, ~25% of GBS cases can be attributed to reaction to a

vaccination, GBS is always triggered by an illness or other incident stressing the immune system,

even if modern medicine has yet to identify a comprehensive list. This makes intuitive sense, as

our immune system generally lies dormant until needed.

While not a lot is known for certain about CIDP—with only 500 cases a year, it isn’t studied

aggressively—it is believed to be caused by the same mechanism as GBS. Specifically, it strips

the myelin sheaths from our nerves, thereby causing a short-circuit, and then, attacks the nerves

themselves. As Dr. Saperstein and his colleagues explain:

The immune system is supposed to fight off bacteria and viruses, but in some people their
immune system may start to attack their own body. In CIDP the immune system starts to
attack the insulation around the nerves, which is called myelin. Hence the neuropathy
received the name demyelinating. As the myelin around the nerves is damaged, the abil-
ity of the nerves to conduct electricity worsens. Frequently patients will recall a preceding

16
 viral infection a few weeks before the onset of their nerve disease. In some cases we can
identify specific antibodies in a patient’s blood which will allow us to classify the CIDP
more specifically. We also believe that CIDP may be more common in certain other
disease such as diabetes and some forms of cancer.56

It may very well be that, like its more virulent cousin, all CIDP is triggered by stimulation of

the immune system by an illness or more importantly, the illness-like situation intentionally crea-

ted by vaccination. The problem, as illustrated in the case of the Ontario miner, is that CIDP can

take so long to present itself that the ‘trigger’ is almost impossible to identify. It may well be that

his CIDP was caused by a vaccine, as Canadian authorities recommend that everyone over 65 be

vaccinated,57 and it is likely that he was vaccinated. Also, it might have been caused by a case of

the flu he forgot about long ago. Coupled with the rarity of CIDP, it is easy to see why we can’t

identify the complete constellation of causes with reasonable certainty.

For this reason, if the Government insists on arguing that the dog didn’t bark when I needed

it to, it must also explain why the dog didn’t bark when they needed it to. Simply put, I had not

taken a single sick day attributable to illness in five years.58 As Tamiflu is only available by pre-

scription in Australia,59 there is no objective evidence that I had the flu. Nor was there any that I

suffered from gastroenteritis or surgery, and I am really too old to have become pregnant. Their

dog didn’t even whimper. The only argument they can make is that, one fine morning, my body

suddenly decided to attack itself, without warning or provocation.

56
CIDP, Phoenix Neurological Associates, supra n. 44.
57
Public Health Agency of Canada, Statement on Seasonal Influenza Vaccine for 2013-2014 (website, undated), at
http://www.phac-aspc.gc.ca/publicat/ccdr-rmtc/13vol39/acs-dcc-4/index-eng.php. Similarly, the CDC recommends
that American health-care providers receive annual flu shots. http://www.cdc.gov/vaccines/adults/rec-vac/hcw.html.
58
Although I did suffer from bursitis in a hip in early 2011, it is simple joint inflammation, which does not trigger an
immune response. See Exhibit 2 at 28.
59
Australian Dept. of Health and Ageing, Australian Public Assessment Rept. for Oseltamivir Phosphate (Jul. 2011)
62, available at https://www.tga.gov.au/pdf/auspar/auspar-tamiflu.pdf (generic for Tamiflu).

17
C. You Can’t Beat Something With Nothing

As I understand it, I am entitled to compensation under the VCIP if I can show that it is more

likely than not that the Fluzone vaccination on August 24, 2011 caused my CIDP, and that I am

entitled to fair compensation for lost income, out-of-pocket medical expenses (and that insurers

have no subrogation rights), and pain and suffering (to a maximum of $250,000). And while it is

not by any means conclusive, the objective evidence indicates that I had a fairly ordinary case of

CIDP, with a downhill rollercoaster of symptoms. By contrast, the Government maintains that I

had a case of acute-onset CIDP (rare, even for CIDP60), without any identifiable “trigger” (again,

rare), despite the fact that I had significant axonal damage, and I did not recover in the way that

GBS and acute-onset CIDP patients normally do (again, relatively rare). Therefore, the question

becomes whether I suffered from a variation of CIDP so rare that it may only happen a few times

a year or a fairly normal version. Both are theoretically possible, but the only question this Court

will eventually have to answer is “Which is more likely?”

CONCLUSION

I’m a pharmacist, not a neurologist. I know drugs and interactions. I didn’t know what GBS

was61 before I was first diagnosed with it, or that CIDP even existed until Dr. London let me in

on “the little secret” that there was “a second kind of GBS.”

The Government has already admitted through experts that the flu vaccine can cause CIDP,

60
Ripellino, Treatment of CIDP, supra n. 13. If it even exists at all, acute-onset CIDP is so rare that in one study, the
doctors conducting it could only find eight patients to study. L. Rutz, et al., Distinguishing acute-onset CIDP from
fluctuating Guillain-Barre syndrome: a prospective study, 74(21) Neurology 1680 (May 2010).
61
While I was told was that flu shots can cause GBS, and I would not administer it to anyone with a history of it, the
disease is thought to be rare enough that the Defendant still recommends vaccination in high-risk patients. Guide to
Vaccine Contraindications and Precautions, Centers for Disease Control (Dept. of HHS), 3 and n. 13, available at
http://www.cdc.gov/vaccines/recs/vac-admin/downloads/contraindications-guide-508.pdf.

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Glassberg v. HHS, No. 07-303V (Ct. Cl. 2009) (slip op. at 13), and not being an expert, I agree

with Dr. Kinsbourne’s opinion that initial symptoms of CIDP ought to appear within ten weeks

after vaccination to establish causation, id. at 5, but the initial symptoms are rarely catastrophic.

The Court’s Order of April 14, 2014 indicates that the Government is in basic agreement with

these medical findings. Smith v. HHS, No. 12-709V, Doc. 29 at 1 (Ct. Cl. Apr. 14, 2014).

The only open question—that of onset—is one of fact. And while the factual record is hardly

overwhelming, independent evidence exists. The gym record shows that I stopped working out in

September, consistent with my claim of fatigue. My prescription records show that I was taking

enough gabapentin to need two refills in November, consistent with my claim of the nerve pain

demyelination causes. The catastrophic effects of CIDP in late December are well-documented,

as is evidence of my relapse in mid-February.62 These are classic symptoms of traditional CIDP:

As Dr. Kinsbourne testified, “[T]he onset of CIDP should take at least two months of increasing

disability and symptomatology,” Glassberg, slip op. at 5, and as observed earlier, my symptoms

and progression were both consistent with traditional CIDP. “Close calls are to be resolved in

favor of petitioners [, as] the purpose of the Vaccine Act’s preponderance standard is to allow

the finding of causation in a field bereft of complete and direct proof of how vaccines affect the

human body.” Id. at 11 (emphasis added).

As was the case with Brett Glassberg, my symptoms appeared “within a medically appropriate

time frame to conclude that flu vaccine caused” my CIDP. Id. at 14. “There is no alternate factor

which caused it.” Id. at 13. While “both medical experts and the literature the parties filed agree

62
This is consistent with the diagnosis of CIDP: As a rule, IVIG wears off in about four weeks. See e.g., John-Philip
Lawo, et al., Quantification Of The Wear-Off Effect Towards The End Of The Intravenous Immunoglobulin Infusion
Interval: Pooled Data Analysis (Mar., 13, 2014), abstract at https://aaaai.confex.com/aaaai/2014/webprogram/Paper-
10842.html. See generally, Exh. 4.

19
that the pace and symptomatology of CIDP can vary greatly,” id. at 13, I “had the classic picture

of CIDP, the first word of which is ‘chronic.’” Id. And, as was the case in Glassberg, there were

good reasons why the objective record was not robust.

By stark contrast, the Government’s theories do not fit the facts. The claim that I had GBS is

rendered implausible due to absence of an alternate ‘trigger’, significant axonal damage, my slow

and incomplete recovery, and the February relapse. Also, the notion that I had acute onset CIDP

is rendered implausible due to the lack of an alternate trigger, the axonal damage, poor recovery,

and its extreme rarity.

As I am highly motivated to reach an equitable settlement, the only reason this case is still on

your docket at all is Mr. Gallagher’s unprofessional performance. As near as I can tell, all he has

done is collate papers and beg for delays. But this is not the time or place to discuss that ailment;

in this brief, I seek a cure.

For the above-listed reasons, I respectfully ask that the Court grant my request for an onset

hearing—in the Denver area, if possible—and/or an extension of time until December 31, 2014,

affording me adequate time to retain suitable counsel.

Respectfully submitted this __th day of May, 2014,

________________________________
Cynthia S. Smith, in propria persona
23636 Genesee Village Rd.
Golden, CO 80401-7044
e-mail: 19ranger57@earthlink.net
Telephone: (303) 526-5451

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