                          In the United States Court of Federal Claims
                                                          OFFICE OF SPECIAL MASTERS
                                                                  No. 10-410V
                                                                (To be Published)

*************************
                           *                                               Special Master Corcoran
SHEELA BLACKBURN,          *
                           *                                               Filed: January 9, 2015
               Petitioner, *
                           *
          v.               *
                           *                                               Entitlement Ruling; Human Papillomavirus
SECRETARY OF HEALTH        *                                               (“HPV”) Vaccine; Guillain-Barré
AND HUMAN SERVICES,        *                                               Syndrome (“GBS”); Chronic Inflammatory
                           *                                               Demyelinating Polyneuropathy (“CIDP”);
               Respondent. *                                               Molecular Mimicry; Homology; Onset
                           *
*************************

Isaiah R. Kalinowski, Maglio, Christopher & Toale, Washington, DC, for Petitioner.

Ann D. Martin, U.S. Dep’t of Justice, Washington, DC, for Respondent.

                                                               ENTITLEMENT DECISION1

       On June 30, 2010, Sheela Blackburn2 filed a petition seeking compensation under the
National Vaccine Injury Compensation Program3 (the “Vaccine Program”) alleging that she
suffered a variant of Guillain-Barré syndrome (“GBS”) caused by her receipt of the Human

                                                            
1
   Because this decision contains a reasoned explanation for my action in this case, it will be posted on the United
States Court of Federal Claims’ website, in accordance with the E-Government Act of 2002, Pub. L. No. 107-347, §
205, 116 Stat. 2899, 2913 (codified as amended at 44 U.S.C. § 3501 note (2006)). As provided by 42 U.S.C §
300aa-12(d)(4)(B), however, the parties may object to the decision’s inclusion of certain kinds of confidential
information. To do so, Vaccine Rule 18(b) permit each party 14 days within which to request redaction “of any
information furnished by that party: (1) that is a trade secret or commercial or financial in substance and is
privileged or confidential; or (2) that includes medical files or similar files, the disclosure of which would constitute
a clearly unwarranted invasion of privacy.” Vaccine Rule 18(b). Otherwise, the decision will be available to the
public. Id.
2
 The case was originally titled Sheela Roten v. Sec’y of Health & Human Servs., but the caption was changed by
Order dated March 1, 2013 (ECF No. 50) after Petitioner changed her legal name.

3
  The National Vaccine Injury Compensation Program comprises Part 2 of the National Childhood Vaccine Injury
Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755 (codified as amended, 42 U.S.C.A. ' 300aa-10 – 34 (2006))
[hereinafter “Vaccine Act” or “the Act”]. Individual sections references hereafter will be to ' 300aa of the Act.
Papillomavirus (“HPV”) vaccine on July 23, 2009. Petition (ECF No. 1) at 1. An entitlement
hearing in this matter was conducted in Washington, DC on March 25 - 26, 2014.

       The case presents two intertwined questions: (a) whether Ms. Blackburn suffered from
GBS, and (b) whether Ms. Blackburn’s illness began before she received the HPV vaccine. After
hearing the testifying witnesses and reviewing the parties’ various pre- and post-trial
submissions, and based on a review of the entire record as required by the Vaccine Act (§ 300aa-
13(a)(1)), I hereby rule in favor of Respondent, for the reasons set forth below.


I.     Factual Background and Medical History

       A.      Petitioner’s Pre-Vaccination Medical History

        Before Ms. Blackburn ever received the vaccination that is the basis for her claim, she
had visited healthcare professionals complaining of symptoms similar to those she alleges
resulted from the vaccination, although their etiology was at that time unclear.

         On October 24, 2008, Ms. Blackburn visited a chiropractor, Mark Snow, and complained
of left hip and shoulder pain. Pet’r’s Ex. 4 at 2-3. In the course of that examination, she reported
constant numbness in her feet and frequent numbness in her hands. Id. Thereafter, on November
6, 2008, Ms. Blackburn was seen at the Exodus Health Care Magna Clinic in Magna, Utah,
where she reported numbness in her feet over the prior four months, plus more recent numbness
and tingling in her hands. Pet’r’s Ex. 2 at 15-16. Ms. Blackburn also indicated that she was
experiencing nerve pain both in her left shoulder and hip area, which she claimed to be an
ongoing problem. Id. at 15. She received a diagnosis of a “pinched nerve in lower back, neck,
and hip arthritis,” but unspecified polyarthritis and neuralgia/neuritis were listed as other
possible sources of her symptoms. Id. at 15-16.

        A few days later, on November 13, 2008, Ms. Blackburn went back to the Exodus Clinic
and was seen by Dr. Jill McBride. Pet’r’s Ex. 2 at 14. The assessment recorded at the time of this
visit indicated that Ms. Blackburn was believed to be suffering from an unspecified polyarthritis
as well as neuralgia/neuritis. Id.

        Based on Dr. McBride’s referral, Ms. Blackburn saw Dr. Susan Zimmerman in December
of 2008 at the Granger Medical Clinic in Salt Lake City for a neurologic consultation. Pet’r’s Ex.
8 at 18. At that time, Petitioner again represented she had been experiencing shoulder pain and
paresthesias for the past four months. Id. Ms. Blackburn’s neurology examination was significant
for revealing “mild sensory loss and left-side hyperalgesia,” although she presented normal
reflex responses. Id. at 19. Because the precise cause of Ms. Blackburn’s symptoms remained
unclear, Dr. Zimmerman made a number of treatment and diagnostic recommendations. In
particular, Dr. Zimmerman ordered magnetic resonance imaging (“MRI”) of Petitioner’s brain

                                                 2 
 
and cervical spine “[t]o help exclude problems such as demyelination, cervical cord
compression, tumor or other focal lesions,” and raised the possibility of “proceed[ing] to a
lumbar puncture or nerve conduction studies to look for other central or peripheral causes of
numbness as well.” Id. The MRIs ordered by Dr. Zimmerman were performed on December 31,
2008. Id. at 10-12. The brain scan results were essentially normal, and the MRI of Petitioner’s
cervical spine revealed “minimal to mild degenerative changes.” Id.

        Less than a month later, on January 14, 2009, Ms. Blackburn had a follow-up visit with
Dr. Zimmerman. Pet’r’s Ex. 8 at 7-8. Petitioner indicated that she was still experiencing
significant right shoulder pain as well as some numbness and pain down both legs (which she
attributed to sciatica) plus foot numbness. Id. at 7. Upon physical examination, Dr. Zimmerman
found that Petitioner had “very mild distal sensory loss.” Id. He recommended physical therapy
to relieve some of the pain that Petitioner was experiencing. Id. Additionally, Dr. Zimmerman
informed Petitioner about the potential of undergoing nerve conduction studies in an attempt to
identify the source of her pain, but Petitioner decided to wait and see if her symptoms improved
with physical therapy. Id. Accordingly, such testing was never performed until well after Ms.
Blackburn’s vaccination.

       B.      July 2009 HPV Vaccination and Subsequent Medical History

         Petitioner received an injection of the Gardasil vaccination in her left deltoid on July 23,
2009, during a comprehensive medical examination at Exodus Health Care Clinic performed by
Cathy Baxter, APRN. Pet’r’s Ex. 6 at 1. The past medical history section of the records from that
visit, reported that Ms. Blackburn previously experienced an unspecified polyarthritis as well as
neuralgia/neuritis. Pet’r’s Ex. 2 at 11. Ms. Blackburn also reported “in [the] past couple of weeks
having tingling in legs and feet,” although her reflexes were tested and recorded to be within
normal limits, as well as her cranial muscle responses. Id. at 12.

        On August 7, 2009, Ms. Blackburn again presented to Exodus where she was seen by
Nurse Baxter. Pet’r’s Ex. 2 at 9. Petitioner indicated that she had been fine until just recently but
was now experiencing “worsening tingling in legs and weakness,” with her legs feeling heavy as
well. Id. (emphasis added). As the contemporaneous medical records note, there had been “no
findings on all workup last year” as to the source of her condition, although the records again
referenced unspecified polyarthritis as well as neuralgia/neuritis. Id. Ms. Blackburn obtained a
note for light duty at work due to her weakness and discomfort. Id. at 10.

        A few days later, on August 11, 2009, Petitioner returned to Dr. Zimmerman (the
neurologist she had seen at the beginning of the year) for a “semi-urgent follow-up” regarding
her ongoing numbness and pain. Pet’r’s Ex. 8 at 4-5. Petitioner reported that “[s]he was doing
reasonably well until [three] weeks ago,” but that she was now experiencing “complete
numbness from her knees down bilaterally” as well as back pain and muscle spasms and some
less severe right shoulder pain. Id. at 4. Notes from the neurological exam performed by Dr.

                                                 3 
 
Zimmerman indicate that the exam was “notable for areflexia[4] and ankle dorsiflexion weakness
bilaterally.” Id. Dr. Zimmerman also stated that “no cause of her pain has yet clearly been
identified,” but that the onset of Ms. Blackburn’s symptoms occurred in the “context of increased
stress” given that Petitioner worked two jobs. Id.5 No connection between Ms. Blackburn’s July
23rd vaccination and her symptoms was made at this time.

        In order to diagnose the cause of Ms. Blackburn’s symptoms, Dr. Zimmerman
recommended a MRI of the lumbar spine plus a lumbar puncture (in light of her demonstrated
areflexia) to “look for the cyto-albuminologic dissociation that can be seen in Guillain-Barré
syndrome,” but Petitioner refused to undergo the latter. Pet’r’s Ex. 8 at 4-5. The MRI did not
reveal the presence of any abnormalities. Id. at 2-3.

        Ms. Blackburn thereafter went back to her chiropractor, Mark Snow, on August 17, 2009,
complaining of continued pain in her left shoulder as well as the previously-reported numbness
in her hands and feet. Pet’r’s Ex. 4 at 4. Deep tendon reflex (“DTR”) testing performed during
the visit revealed normal reflexes in her upper body limbs, but areflexia in her knees and right
ankle. Id. at 5. Cranial nerve testing, however, revealed no abnormalities, and the record from
this visit specifically indicated that Ms. Blackburn was “able to perform the normal range of
facial movements, no asymmetry or other abnormalities were noted.” Id.

        Ms. Blackburn saw Mark Snow again two days later, at which time she underwent a
nerve conduction velocity study, the results of which were abnormal. Pet’r’s Ex. 4 at 7. Results
from that study and an electromyography (“EMG”)6 were reviewed by Robert A. Sellin, PT,
DSc, ECS, a board certified electromyographer. Id. at 12. Those nerves tested had normal
amplitudes, latencies, and nerve conduction velocities, but there was no measurable sensory
response from any of the sensory nerves tested; the left median motor distal latency was severely
prolonged and the distal nerve conduction velocity was markedly slowed; the left ulnar motor
distal latency was severely prolonged and the segmental nerve conduction velocities were
markedly slowed; bilateral fibular (peroneal) motor responses were not obtainable; bilateral tibial
motor evoked responses were of markedly diminished amplitude and exhibited severe temporal
dispersion; bilateral common fibular (peroneal) and tibial motor F-waves were not obtainable;
and the left median and ulnar motor F-waves were severely prolonged. Id. The remarks included

                                                            
4
   Areflexia is defined as the absence of reflexes. Dorland’s Illustrated Medical Dictionary (32d ed. 2012) at 130
[hereinafter “Dorland’s”].
 
5
   The medical records from this visit with Dr. Zimmerman also reflect that Petitioner reported that “[five] weeks ago
[i.e. some time in July 2009] she had symptoms similar to a friend, who was diagnosed with strep throat,’ although
“[s]he did not seek medical attention at that time.” Pet’r’s Ex. 8 at 4. 
 
6
    Electromyography (“EMG”) is “an electrodiagnostic technique for recording the extracellular activity (action
potentials and evoked potentials) of skeletal muscles at rest, during voluntary contractions, and during electrical
stimulation.” Dorland’s at 602.
 

                                                               4 
 
with the testing results indicated that “[t]hese electrophysiologic findings combined with her
history are strongly suggestive of some form of acute inflammatory demyelinating
polyradiuloneuropathic process (AIDP)[7] such as Guillain-Barre syndrome).” Id. at 8. The
remarks also indicated that “I believe it is important to note that the patients symptoms were very
mild [six] weeks ago and she received immunization about [five] weeks ago and then noticed her
increasing symptoms. Id. at 9 (emphasis added). The EMG results revealed that “[a]ll muscles
tested exhibited normal insertional activity, electrical silence at rest, and had normal motor unit
configuration and recruitment, except: There was reduced interference patterns in all muscles
tested except the left deltoid.” Id. at 9-10.

        On August 24, 2009, Ms. Blackburn went to the University Health Care Emergency
Department at the University Health Care Hospitals and Clinics in Salt Lake City, Utah
complaining of three and a half weeks of progressive ascending weakness and numbness as well
as back pain, and noting that her condition had occurred after receipt of the Gardasil Vaccine.
Pet’r’s Ex. 3 at 19. She specifically reported that she last felt well on July 4th when she became
ill with flu-like symptoms, and then later that month received the Gardasil vaccination. Id.
During this visit, Ms. Blackburn noted that for the first two weeks her symptoms were mild and
that she had seen Dr. Zimmerman, but her symptoms had progressed to the point where she was
having difficulty walking. Id. The contemporaneous medical records from this visit included
GBS and multiple sclerosis (“MS”) as potential differential diagnoses. Id. at 42.

        The next day Ms. Blackburn saw Dr. Jeffrey C. Wagner, a neurologist. Pet’r’s Ex. 12 at
35-36. She informed Dr. Wagner that she had been using a walker since her visit to Dr.
Zimmerman earlier in August, and that she was experiencing more tingling, numbness, and
weakness in her hands and arms. Id. at 35. Petitioner again reported having experienced “strep or
flu-like symptoms at the beginning of July” with “associated neck stiffness,” but she noted that
these symptoms had improved and “she was feeling back to her usual state of health by the end
of July when she presented for a general annual physical exam” and “received the Gardasil
vaccination.” Id. at 35-36. After examination of Petitioner and review of her history, Dr. Wagner
stated that Ms. Blackburn appeared to have a “history on exam consistent with Guillain Barré
syndrome.” Id. at 38.

       Based on this GBS diagnosis, Dr. Wagner recommended that Ms. Blackburn be admitted
to the Inpatient Neurology Service at the University Hospital for a course of intravenous
immunoglobulin (“IVIG”).8 Pet’r’s Ex. 12 at 38-39; Pet’r’s Ex. 7 at 25, 29, 30. Dr. Wagner also

                                                            
7
    AIDP refers to acute inflammatory demyelinating polyradiculoneuropathy, a common GBS variant. P. Dyck &
P.K. Thomas, 2 Peripheral Neuropathy 2199 (4th ed. 2005) [hereinafter “Dyck & Thomas”].
 
8
    IVIG treatments are used with patients suffering from neuropathies like GBS and other illnesses believed to have
an autoimmune character, and help patients maintain sufficient antibody levels. Dyck & Thomas at 642-43. The
exact mechanism of action for IVIG in individuals with GBS is unknown, but the American Academy of Neurology
Practice Parameter Group recommends “consideration of IVIg for patients within [two] weeks and probably within

                                                               5 
 
ordered an EMG, which was performed on August 26, 2009. Pet’r’s Ex. 3 at 45. Dr. Wagner’s
written interpretation of these EMG results stated that “[t]here is electrodiagnostic evidence of a
severe demyelinating peripheral neuropathy consistent with the presumed diagnosis of Guillain
Barré Syndrome (acute inflammatory demyelinating polyradiculoneuropathy, AIDP).” Pet’r’s
Ex. 5 at 124. Dr. Wagner’s notes go on to indicate that “[t]he low compound muscle action
potential amplitude in the median motor response implies significant axonal damages as to the
fibrillations and positive waves in anterior tibialis muscle.” Id.

        During her hospitalization, Petitioner “received 2 g/kg of IVIG treatment over three days
and developed nausea and vomiting, as well as anemia, which was diagnosed as hemolytic
anemia” attributed to the IVIG treatment (not an uncommon occurrence).9 Pet’r’s Ex. 7 at 6-7.
Despite such treatment complications, Ms. Blackburn completed her course of IVIG on August
28, 2009, showing “dramatic improvement in her symptoms” and was therefore discharged from
inpatient neurology care at the University Hospital. Id. at 23, 25, 33. Dr. Wagner indicated upon
discharge that Ms. Blackburn was to undergo physical rehabilitation for further treatment, and
cautioned that “[g]iven the patient’s reaction to Gardasil vaccine, she is not to complete the 3-
step series and is also not to receive further vaccines given her risk of [GBS].” Id. at 24.

        Petitioner was thereupon transferred to Acute Rehabilitation Service at the University of
Utah for comprehensive treatment, as she was still experiencing difficulty in movement. Pet’r’s
Ex. 7 at 29-30. Petitioner nevertheless continued to be followed by the hospital’s Neurology
service. Id. at 19. A few weeks later, on September 5, 2009, Petitioner was discharged from her
rehabilitation, having “made significant functional gains during her stay,” with discharge
diagnoses of “(1) [a]cute inflammatory demyelinating polyradiculoneuropathy; (2) [n]europathic
pain; [and] (3) [h]emolytic anemia secondary to IVIG.” Id. at 18, 20.

              C.             Petitioner’s Ongoing Symptoms and Eventual Change in Diagnosis

       Ms. Blackburn continued to undergo physical and occupational therapy throughout
September of 2009. See generally Pet’r’s Ex. 1. Despite her general progress and nascent
recovery, results from a September 18, 2009 EMG study were interpreted by Dr. Wagner as
abnormal due to “electrodiagnostic evidence of a primary demyelinating neuropathy with
secondary axonal damage” as well as “evidence of early reinnervation.”10 Pet’r’s Ex. 5 at 363.


                                                                                                                                                                                                
[four] weeks of the onset of symptoms” even though “[a]ccording to a Cochrane systematic review, there are no
adequate trials comparing IVIg to placebo” in patients with GBS. Id.
9
  Petitioner’s medical records contain the observation that “[t]here are multiple case reports describing hemolysis in
the setting of high-dose IVIG treatment.” Pet’r’s Ex. 7 at 27.
10
 Reinnervation is defined as the restoration, by regrowth or by grafting, of nerve supply to a part of the body from
which it has been lost. Dyck & Thomas at 1421-22.


                                                                                              6 
 
        As of early October, Ms. Blackburn appeared to be recovering and reported a
diminishment of her symptoms. Pet’r’s Ex. 3 at 61. By October 22, 2009, however, when Ms.
Blackburn was seen by Katarina Waters, PNP,11 she had begun to experience increased bilateral
numbness below her knees, weakness in bilateral lower extremities, and was also having trouble
walking, making Petitioner concerned that she was suffering a relapse. Pet’r’s Ex. 3 at 58. A
physical examination revealed that her reflexes were (again) absent in both knees and ankles, and
that she had decreased bilateral sensation from her knees down. Id. at 59. Because a neurologic
evaluation could not be immediately scheduled, Ms. Blackburn was sent to the emergency room.
Id. at 60.

        At the hospital emergency department, Ms. Blackburn complained of “worsening
weakness and numbness the onset of which had been gradual” but which had flared in the prior
one and a half weeks. Pet’r’s Ex. 3 at 39; Pet’r’s Ex. 7 at 14-15. She reported that she had
previously spoken to Dr. Rosenbluth about her symptoms and he indicated that she may need
more IVIG, so she was told to come to the Emergency Department for possible admission.
Pet’r’s Ex. 7 at 15. A physical examination performed at this time revealed decreased sensation
to touch of her lower extremities below her knee, no pain sensation of her feet, decreased
temperature sensation to her bilateral feet, and loss of proprioception of her toes. Pet’r’s Ex. 3 at
39-40. The doctors who evaluated her, however, did not conclude that inpatient admission for
IVIG treatment was appropriate despite her symptoms. Pet’r’s Ex. 7 at 16.

        In the following days, Ms. Blackburn continued to experience the recurrence of many of
the severe symptoms she had just received treatment for in August (i.e., bilateral and ascending
limb weakness), leading her to see Dr. Jackie J. Whitesell in the Neuromuscular Disease Clinic
on October 29, 2009. Pet’r’s Ex. 3 at 64-65. A physical examination confirmed the areflexia in
her arms and legs (as observed at her emergency department visit earlier that month) as well as
some numbness in her legs. Id. at 66. Dr. Whitesell indicated in her notes that “I feel that this
likely still represents slowly improving Guillain-Barré which can sometimes have a waxing and
waning course . . . I feel that an alternative diagnosis of CIPD [chronic inflammatory
demyelinating polyneuropathy] is less likely.” Id. Dr. Whitesell did not, however, explain why
she discounted the possibility of CIDP, indicating only her conclusion that based on the
examination, Petitioner had “AIDP with continued weakness and numbness in her extremities.”
Id.

        Ms. Blackburn’s symptoms did not dissipate (as had been anticipated when she first
completed her IVIG treatment in late August 2009) in the months that followed. However, her
condition did not impel her to visit another doctor again until the spring of 2010 – nine months
after the vaccination. At that time, on April 22, 2010, Ms. Blackburn presented to Mark B.
Bromberg, M.D. in the Neuromuscular Clinic at the University of Utah Hospitals and Clinic in

                                                            
11
     Medical notes from that visit were electronically signed by Dr. Rosenbluth. Pet’r’s Ex. 3 at 58.


                                                               7 
 
Salt Lake City, Utah with complaints of limb weakness that had for the past six months
fluctuated on an almost daily basis. Pet’r’s Ex. 7 at 6-7. Although Petitioner reported that she
was doing better, she indicated that she had not returned to baseline and was still experiencing
“aches and pains, with neuropathic pain, as well as muscle spasms.” Id.

       Dr. Bromberg’s notes state that Ms. Blackburn was “here for another evaluation for her
history of AIDP with a question of if there is a component of chronic involvement or just
delayed and incomplete recovery.” Pet’r’s Ex. 7 at 8. However, given Petitioner’s history of
unresolved, waxing-and-waning symptoms, Dr. Bromberg questioned whether the prior AIDP
diagnosis was in fact correct. Id. As he specifically indicated:

              [h]er overall history does fit a monophasic illness, given the vaccine-related symptoms,
              as well as the lack of true exacerbation throughout her course in the past couple months.
              However, she still has significant disability from her arm and leg weakness, as well as
              pain. At this point, we would like to give her a trial of prednisone,12 given that she has
              had more side effects with IVIG in the past. [] We would expect significant and
              noticeable clinical benefit if this were CIDP and if she does not have significant
              response, then this steers us towards this being a monophasic AIDP with prominent
              axonal injury and delayed and perhaps incomplete recovery.

Id. (emphasis added). Accordingly, Ms. Blackburn was prescribed prednisone and instructed to
come in for a follow-up appointment within five to six weeks. Id. at 8-9.

       By the time of Ms. Blackburn’s follow-up visit on June 24, 2010, Dr. Bromberg was able
to observe that since beginning prednisone two months prior, Petitioner exhibited “subjective
and objective improvement.” Pet’r’s Ex. 7 at 2-3. He thus indicated in his notes that Petitioner
“was thought initially to have AIDP. However, given her lack of complete improvement and now
improvement on prednisone, this suggests that she has rather CIDP as explanation of her
symptoms.” Id. at 4 (emphasis added).

              D.             Ms. Blackburn’s More Recent Treatment History

       Since Ms. Blackburn’s diagnosis was changed to CIDP, she has (consistent with that
diagnosis) continued to experience symptoms on a waxing and waning basis, and has thus been
seen regularly by a number of providers to follow-up on and attempt to manage her symptoms.
But nothing in the subsequent record contradicts the consensus among Ms. Blackburn’s treating
physicians that the initial diagnosis of AIDP had been in error. See, e.g., Pet’r’s Ex. 12 at 6 (Dr.
Bromberg’s notes from her February 2011 visit). Consistent with that, any initial efforts to take
Ms. Blackburn off prednisone lead to a recurrence of her symptoms such as numbness in her
upper and lower extremities. Id.
                                                            
12
  Prednisone is “a synthetic glucocorticoid derived from cortisone, administered orally as an anti-inflammatory and
immunosuppressant in a wide variety of disorders.” Dorland’s at 1509.


                                                               8 
 
        In a May 2011 follow-up visit with Dr. Bromberg, it was noted that Petitioner was
continuing to take prednisone and was doing well since her last visit other than experiencing
some mild paresthesias in her limbs and fatigue – symptoms that Dr. Bromberg characterized as
natural fluctuations commonly experienced by CIDP patients. Pet’r’s Ex. 11 at 2-3. Petitioner
thereafter continued to follow-up with Dr. Bromberg and other treatment providers to gauge her
progress, and also to evaluate whether IVIG could ever be tried again in the event of another
relapse (leading to a determination that future IVIG treatment was not contraindicated). Pet’r’s
Ex. 29 at 79-80, 85-88. Ms. Blackburn saw Dr. Bromberg again in the spring of 2012 to address
the treatment management of her CIDP, and he concluded that her illness appeared to be in
remission despite the tapering off of her steroid treatment. Id. at 77-78. The remaining medical
records filed in this case indicate that Petitioner has not subsequently experienced a severe
recurrence of her CIDP and has not required ongoing prednisone treatment.13



II.           Expert Testimony

        Three experts testified at hearing: one for Petitioner and two for Respondent. The
qualifications and testimony of each side’s respective experts are summarized below.

              A.             Petitioner’s Expert – Dr. Steinman

       Lawrence Steinman, M.D. is a professor in Stanford University’s Departments of
Neurology, Pediatrics, and Genetics, and the chair of Stanford’s Immunology Program. Pet’r’s
Ex. 17 (Dr. Steinman’s curriculum vitae). He has been elected to the Institute of Medicine
(“IOM”) and has published more than 400 articles, including articles related to his research on
autoimmune disease and molecular mimicry. Id. Dr. Steinman’s primary focus is on MS, but
during the thirty-two years that he has been a board-certified neurologist he has treated
approximately 400 patients with GBS (although, unlike Ms. Blackburn, approximately sixty-five
percent of these patients that he has treated were children). Tr. at 144-46. Of those 400 patients,
Dr. Steinman indicated that approximately twenty-five percent could be characterized as having
CIDP. Id. at 146.


                                                            
13
   On June 18, 2012, Petitioner presented for her six-month follow-up appointment. Pet’r’s Ex. 29 at 7. Even without
steroid treatment at that time, she generally appeared to be doing well, although she complained of some lingering
upper and lower body bilateral weakness as well as occasional fevers the cause of which could not be identified by
tests. Id. On November 26, 2012, Petitioner was again seen for a follow-up appointment and reported that she was
doing well. Id. at 19. Thereafter, on April 18, 2013, Petitioner was seen for a follow-up appointment, and it was
noted that she was “pregnant for 9 weeks now” and reported that she was doing well – although because she had
decreased her doses of medication during her pregnancy, she was occasionally experiencing some of the old
symptoms. Id. at 48-49.



                                                               9 
 
        Dr. Steinman admitted that due to his focus on research, he has seen considerably fewer
patients in the last five years than he saw earlier in his career, but he still sees patients (including
approximately eighty patients as of March 2014, which he estimated to be less than the number
of patients that he saw in 2013). Tr. at 144-45. During the last five years, Dr. Steinman has only
seen patients approximately one month out of the year when he serves as an inpatient attending
physician, and during this time he has been called to diagnose an individual with GBS or CIDP
no more than about sixteen or seventeen times (including once in 2014 as of March of that year).
Id. at 147. Additionally, Dr. Steinman has not conducted nerve conduction studies or interpreted
the results from such studies since his initial training. Id. at 149. Moreover, Dr. Steinman
acknowledged that no patients with CIDP have been referred to him for management of their
long-term care in the last five years. Id. at 147.

       Dr. Steinman offered an opinion on two topics: (1) a theory by which he proposed the
HPV vaccine Ms. Blackburn received could have caused an autoimmune response leading to her
purported GBS, and (2) whether, based upon his review of Ms. Blackburn’s medical records, he
believed her illness was AIDP or CIDP.

                1. Dr. Steinman’s Molecular Mimicry Theory – Dr. Steinman proposed the theory
of molecular mimicry to explain how the HPV vaccine could cause GBS (including the AIDP
variant of GBS). Molecular mimicry has been defined to be a “sequence and/or conformational
homology between an exogenous agent (foreign antigen) and self-antigen leading to the
development of tissue damage and clinical disease from antibodies and T cells directed initially
against the exogenous agent that also react against self-antigen.” Institute of Medicine, Adverse
Effects of Vaccines: Evidence and Causality at 70 (Stratton K. et al., eds. 2011) [hereinafter
“Adverse Effects of Vaccines”]; see also Tr. at 21-24; Steinman L., Autoimmune Disease, 269
Scientific America 106-14 (Sept. 1993) (Pet’r’s Ex. 19). As Dr. Steinman explained in his
testimony, invading microbes mimic the structure of host proteins. Tr. at 21. Because of these
shared structures, when certain hosts develop an immune response to the invading microbes,
their immune systems confuse self with foreign proteins, attacking both. Id. at 22-23. For
molecular mimicry to occur, sufficient homology (a term Dr. Steinman defined broadly as
“similarity” (Id. at 36)) must exist between self and foreign antigens. Id. at 35, 38, 192.14

       All forms of GBS, Dr. Steinman testified, are autoimmune diseases occurring after the
body mounts an immune response to a foreign agent that accidently targets the body’s own nerve
tissue – through molecular mimicry. Tr. at 19. One of the most well-known examples of
molecular mimicry as the mechanism for GBS, he stated, involves a structure shared between a
                                                            
14
   Though homology is necessary to trigger molecular mimicry, Dr. Steinman conceded that the existence of
homology alone does not lead automatically to the conclusion that molecular mimicry has or will occur. Tr. at 56-
57. Indeed, homology occurs frequently without any clinical effect. Adverse Effects of Vaccines at 71. Most cross-
reactivity does not even lead to autoimmunity. Tr. at 161-62.


                                                               10 
 
bacterium called Campylobacter jejuni and gangliosides, sugar structures found on the surface of
myelin (which is present in large quantities in human peripheral nerve tissue). Id. at 25. Thus, an
antecedent Campylobacter jejuni infection can, through molecular mimicry, lead to a particular
GBS variant called acute motor axonal neuropathy (“AMAN”).15 Id. Dr. Steinman opined that it
is medically accepted (while not fully understood) that certain vaccines can also cause GBS,16
initiating an autoimmune process the same way another microbe (like the Campylobacter
bacterium) might. Id. at 35. The components of the wild viruses contained in many vaccines
actually share molecular homologies with myelin structures present in the human body, and thus
could produce the same reaction as a wild virus alone. Id.

        Dr. Steinman proposed a specific means by which molecular mimicry occurs within an
autoimmune reaction between the HPV vaccine and the body. Dr. Steinman contended that the
HPV virus (portions of which the Gardasil vaccine contains17) shares “molecular similarities”
with certain amino acid peptides making up myelin basic protein (“MBP”), which he defined as
“the most common protein in central and peripheral nervous system myelin.” Tr. at 29, 39-40.
After receipt of the HPV vaccine, in the course of the human body’s adaptive immune response
the host’s immune system would be “tricked” into attacking MBP, the putative target antigen of
the autoimmune response. Id. at 51, 162, 192-93.

       Dr. Steinman’s conception of homology was specifically based on structural similarities
between components of the HPV vaccine and host tissues, and he applied that paradigm to
explain how MBP would be putatively attacked. Tr. at 36, 38. In his testimony, he repeatedly
employed the metaphor of a “catcher’s mitt” (a groove formed on the host tissues by the human
leukocyte antigen (“HLA”))18 holding a peptide from the vaccine which would then be presented
to a host T cell.19 Id. at 18-22, 156-57. The peptide would “fit” into the catcher’s mitt due to its
                                                            
15
  AMAN is an autoimmune neuropathy that principally targets motor nerve axons. Dyck & Thomas at 575; Tr. at
16. Because there is a much higher incidence of Campylobacter jejuni infection in China than the United States,
AMAN is rarer here. Tr. at 34-35.
16
   Dr. Steinman specifically cited the epidemiologic evidence derived from the 1976 swine flu outbreak (as outlined
in the Schonberger article (Schonberger, L.B. et al., Guillain-Barré syndrome Following Vaccination in the National
Influenza Immunization Program, United States, 1976-1977, 110(2) Am. J. Epidemiol. 105–23 (1979) (Pet’r’s Ex.
25) and the Langmuir article (Langmuir, A.D. et al., An Epidemiological and Clinical Evaluation of Guillain Barre
Syndrome Reported in Association with the Administration of the Swine Influenza Vaccine, 119 Am. J. Epidemiol.
841-79 (1984) (Pet’r’s Ex. 26)) to support this proposition. Pet’r’s Ex. 19 at 13.
17
  Gardasil is a recombinant (as opposed to live virus) quadrivalent vaccine prepared from virus-like particles of the
major capside (L1) protein of HPV Types 6, 11, 16, and 18. Centers for Disease Control and Prevention,
Quadrivalent Human Papillomavirus Vaccine: Recommendations of the Advisory Committee on Immunization
Practices (ACIP), 56(RR-2) MMWR 8 (2007) (Pet’r’s Ex. 38 at 3, 10-11); Tr. at 40-42.
18
  HLA or “human leukocyte antigens” are “histocompatibility antigens governed by genes of the HLA complex (the
human major histocompatibility complex [MHC]).” Dorland’s at 105.
19
  T cells are lymphocytes carrying their own unique receptors, some of which recognize the foreign peptide, while
others recognize the self MHC molecule. Dyck & Thomas at 560-61.

                                                               11 
 
structural homology with the host protein. Id. at 21-22. It would thereupon give instructions to
the T cell, which would in turn migrate to MBP on the host’s peripheral nerves and attack,
causing the demyelination that characterizes GBS. Id. at 17, 155-57, 160-62.

        Dr. Steinman contended that the molecular mimicry process by which MBP was attacked
could involve T cells, antibodies produced from B cells, or both, with neither being predominant.
Tr. at 17-18, 24, 155, 161.20 However, although T cells and B cells recognize similar antigens,
they play different roles in the adaptive immune system; T cells can only recognize structures
that are bound to the HLA, while antibodies are not so constrained. Id. at 17, 24-25. Dr.
Steinman’s theory ultimately relied on T cells as playing the primary role in the destruction of
myelin. Id. at 156-58.

        In support of his assertion that MBP was the target antigen for the molecular mimicry
process he outlined, Dr. Steinman relied upon the Cornblath study (David R. Cornblath et al.,
Immunoreactive Myelin Basic Protein in Cerebrospinal Fluid of Patients with Peripheral
Neuropathies, 20 Annals of Neurol. 370 (1986) (Pet’r Ex. 32)). Tr. at 162. The Cornblath study
found increased MBP in the spinal fluid of patients with GBS, although it did not find that MBP
was the target antigen in GBS. Pet’r’s Ex. 32 at 3741. He also relied heavily on an article – Kai
W. Wucherpfennig et al., Recognition of the Immunodominant Myelin Basic Protein Peptide by
Autoantibodies and HLA-DR2-Restricted T Cell Clones from Multiple Sclerosis Patients, 100 J.
Clinical Investigation 1114 (1997) (Pet’r’s Ex. 18) [hereinafter “Wucherpfennig”] – which
studied cross-reactivity between MBP peptides, on the one hand, and antibodies and T cells, on
the other, in multiple sclerosis patients. Id. at 28-29, 37.

        Dr. Steinman next attempted to identify the precise homology involved in the purported
cross-reaction between an epitope21 of MBP and the components of the HPV vaccine. Tr. at 48,
55-56, 155. Relying on two laboratory studies in which an autoimmune disease (experimental
autoimmune encephalomyelitis (“EAE”))22 has been induced in mice using peptides from HPV
40, 32, or the HPV L2 protein23, Dr. Steinman specifically identified HFFKN24 as the critical
                                                                                                                                                                                                
20
  Indeed, not only did Dr. Steinman not substantially distinguish the structural requirements for T cell and B cell
mimicry, but at some points he conflated the two despite the differences in the way each functions. See Tr. at 17, 46.
21
  An epitope is the “antigenic determinant.” Dorland’s at 637. “[O]nly the portion of the protein or polysaccharide
molecule known as the antigenic determinant (q.v.) combines with antibody or specific receptor on a lymphocyte.”
Id. at 103.
22
  EAE is an experimental model for MS. Steinman, L., Autoimmune Disease, 269 Scientific American 109 (1993)
(Pet’r’s Ex. 19).
23
  See Ruiz P.J. et al., Microbial Epitopes Act as Altered Peptide Ligands to Prevent EAE, 189 J. of Experimental
Medicine 1275-84 (1999) (Pet’r’s Ex. 21) [hereinafter “Ruiz”]; Ufret-Vicenty et al., In Vivo Survival of Antigen
Specific T Cells that Induce EAE, 188 J. of Experimental Medicine 1725-38 (1998) (Pet’r’s Ex. 23) [hereinafter
“Ufret-Vicenty”].

                                                                                             12 
 
sequence sharing homology with these HPV strains. Id. at 55-57, 168. Within this sequence,
FKN is the “core motif” for MBP mimicry, but (based on Dr. Steinman’s view of the structural
character of homology) an FK or FKN sequence would be sufficient for the cross-reactive
process to occur. Id. at 48, 168, 192-93; see also Pet’r’s Mem. at 6.

         As Dr. Steinman admitted on the witness stand, however, the homology analysis set forth
in his written expert report was premised upon an error.25 Tr. at 47. Dr. Steinman’s report had
described homology between MBP and the L2 protein of HPV (strains 7, 13, and 40). Id. at 48-
49; Pet’r’s Ex. 16 at 8. However, Gardasil is manufactured from the L1 protein of HPV (strains
6, 11, 16, and 18) – not the L2. Pet’r’s Ex. 38 at 8. The sequences he described are thus not
included as components of the Gardasil HPV vaccine, and therefore (as Dr. Steinman admitted)
his initial analysis was “not germane” to the actual formulation of the relevant HPV vaccine. Tr.
at 48-49, 135.26

       Dr. Steinman attempted to correct his mistake through his live testimony, supported by
additional medical literature filed before the March hearing. Tr. at 48-49; Pet’r’s Ex’s 41-44
(medical literature); Pet’r’s Pre-Hr’g Reply Mem. (ECF No. 60) at 6-10; Pet’r’s Ex. 46 at 1
(demonstrative exhibit). To do so, he indicated that after he discovered the error, he conducted
what he termed “an experiment done, if you will, in silico [meaning performed on a computer] at
my desk with publicly available databases.” Tr. at 47. In effect, he looked up on the Internet the
published genome sequences relevant to the actual components of the Gardasil vaccine and then
compared them to the protein sequences found in MBP.

        In so doing, Dr. Steinman determined that the L1 proteins contained in the Gardasil HPV
vaccine included the amino acid sequences “YKN” and “FK.”27 Tr. at 52. Dr. Steinman then
asserted that F and Y are “pretty much interchangeable,” due to their shape and spatial position
in the overall protein sequence, illustrating his point with visual charts representing how the


                                                                                                                                                                                                
24
   “H” refers to the amino acid histidine, “F” refers to phenylalanine, “K” refers to lysine, and “N” refers to
asparagine. Tr. at 39-44; Pet’r’s Ex. 46 at 1. The amino acids in this sequence may be referred to as H88, F89, F90,
K91, and N92. Wucherpfennig at 1117.
25
  Dr. Steinman’s written report was filed in July 2012. ECF No. 36. Respondent pointed out in her January 28, 2014
pre-hearing memorandum (ECF No. 62), however, that Dr. Steinman had not compared the proteins actually
contained in the relevant formulation of the HPV vaccine in this case to MBP. Because the hearing was held in late
March of 2014, Petitioner had ample forewarning of the need to respond to this criticism of Dr. Steinman’s
reasoning, and did so during Dr. Steinman’s testimony.
26
  Dr. Steinman attributed this error to the fact that when he wrote his report, he “stuck to the viruses that we had
addressed in this paper by Wucherpfennig.” Tr. at 48.
27
     “Y” refers to the amino acid tyrosine. Tr. at 43.


                                                                                             13 
 
sequences appear in three dimensions after magnification. Tr. at 47, 43, 52-54.28 From a
homology standpoint, both “keys” would still fit the “lock” represented by the MBP peptide
sequences, thereby inducing an autoimmune response. Accordingly, Dr. Steinman testified that
he was still able to maintain the opinion that there is sufficient homology between the actual
HPV vaccine received by Ms. Blackburn and MBP. Id. at 135, 192-93. Indeed – it was his
opinion that the homology was even stronger than before, because now there were two possible
sequences – FK and YKN – to provide a basis for molecular mimicry. Id. at 52, 143.

                2. Dr. Steinman’s Diagnostic Opinion – Dr. Steinman also offered an opinion on
the nature of Ms. Blackburn’s illness based on a review of her treatment history. Dr. Steinman
challenged the concept that when Ms. Blackburn presented to Dr. Zimmerman between
December of 2008 and January of 2009, her symptoms were consistent with the expected
presentation of an individual suffering from CIDP. Tr. at 70, 92-96,123, 130-31. If an individual
were suffering from CIDP, he reasoned, a treating physician would expect to observe numerous
abnormalities from their neurologic exam. Id. at 92. However, Dr. Steinman pointed out that
diagnostic testing, such as her December 2008 MRI, displayed essentially normal results,29 or
were logically consistent with the physical demands of her job. Id. at 88-89. He also observed
that she displayed asymmetric pain and no areflexia.30 Id. at 89-92. And the typical patient with
CIDP, Dr. Steinman opined, would not be able to continue to work two jobs (one in the nursing
profession and the other in housecleaning) without seeking treatment, yet Ms. Blackburn had
done so. Id. at 70; 93-94. In the same vein, Dr. Steinman also noted the gap in Ms. Blackburn’s
medical records from January of 2009 to July of 2009 – a long time, in his view, for an
individual with CIDP to not seek medical treatment. Id. at 90-92.

       Dr. Steinman further testified that he considered the post-vaccination AIDP diagnosis to
be especially reliable and improperly revised to CIDP in 2010. Tr. at 74-75, 123. For example,
Ms. Blackburn’s neurologist, Dr. Zimmerman, first observed areflexia on August 11, 2009, but
not before. Id. at 95. In Dr. Steinman’s reading of the records, this was a significant presenting
symptom, and the fact that it was not seen before vaccination was very important. Id. at 96. He
                                                            
28
   In support, Petitioner offered a blown-up x-ray diffraction photograph of the relevant portion of MBP in order to
illustrate precisely where on the HLA “catcher’s mitt” the homologous portion of the HPV vaccine peptide would
bind by showing the shapes or structure of the relevant peptide sequences. Tr. at 39-40, 42-44 (referencing Pet’r’s
Ex. 46).
29
  In addition Ms. Blackburn’s cranial/cerebellar/sensory motor responses and reflexes (as tested in December 2008
and January 2009) were within normal limits. Tr. at 91-92. Dr. Steinman further observed that Ms. Blackburn had
normal reflexes with intact sensation, which he opined was not supportive of a diagnosis of ongoing inflammatory
demyelination. Id. at 87-88.
30
  Ms. Blackburn was experiencing shooting pain down one leg, which in Dr. Steinman’s view was not consistent
with an ongoing process of CIDP where pain would normally be symmetrical. Tr. at 89. Nor did he consider the
physical therapy treatment prescribed for Petitioner at that time normal treatment recommended for a patient with
CIDP. Id. at 89-90.


                                                               14 
 
also considered it important that her subsequent lumbar puncture revealed the anticipated
albumin dissociation that is a clinical hallmark of GBS. Id. at 105. He questioned whether certain
symptoms that Respondent argues are critical for a GBS diagnosis that were absent (such as
cranial facial muscle weakness, respiratory weakness, and autonomic instability) were in fact
critical. Id. at 71. Dr. Steinman deemed particularly significant the abnormal results obtained
from the EMG performed on September 18, 2009, which revealed secondary axonal damage31 –
something he considered uncommon in the case of CIDP. Id. at 66, 112-13.32

       Dr. Steinman also stressed those instances in the treating record where Ms. Blackburn’s
physicians linked the Gardasil vaccination to her GBS. Tr. at 108. He discounted the possibility
that Ms. Blackburn’s treating physicians had not taken her prior medical history into account in
so concluding. Id. at 109. He admitted, however, that to some extent his conclusion arose from
his assumption that in a “teaching hospital” such as where Ms. Blackburn was treated any
diagnosis could be assumed to have taken into account a patient’s medical history. Id. at 109-
10.33

        Dr. Steinman explained the waxing and waning quality of Ms. Blackburn’s symptoms
after her hospitalization as the product of an incomplete recovery from her initially acute GBS.
He attributed some of her relapse (which he admitted was “pretty big” (Tr. at 116)) to her having
received an incomplete series of IVIG treatments due to the hemolytic anemia she developed. Id.
at 115. This new phase of her disease thus did not negate the AIDP diagnosis, as recurrence is
not unknown to AIDP patients. Id. at 115-16, 119. Dr. Steinman also emphasized Ms.
Blackburn’s neurology consult with Dr. Whitesell (who rejected a CIDP diagnosis), and the
subsequent follow-up EMG and nerve conduction studies, the results of which confirmed
Petitioner’s recovery (showing reinnervation). Id. at 118-120. Had Ms. Blackburn been suffering

                                                            
31
  As Dr. Steinman explained, secondary axonal damage refers to the fact that after the overlying myelin sheath gets
damaged, the axon within can also become damaged from the consequences of the initial process. Tr. at 112. He
noted that the AMAN form of GBS is more commonly associated with secondary axonal damage, but distinguished
Ms. Blackburn’s case by observing that motor and sensory axons were involved (which would not be true for
AMAN). Id. at 112-13.
32
     In support of this part of his opinion, Dr. Steinman referenced an article (L. Ruts, M.D. et al., Distinguishing
Acute-Onset CIDP From Fluctuating Guillain-Barré Syndrome, 74 Neurol. 1680-86 (2010) (Resp’t’s Ex. H)) citing
a study of GBS and CIDP which found signs of axonal damage were “rare in acute onset CIDP group, while more
than half of the patients in the GBS treatment-related fluctuations group show signs of axonal damage in the acute
phase.” Tr. at 66.  
 
33
     Dr. Steinman testified that in his experience, a teaching hospital (such as the University of Utah where Ms.
Blackburn received care) is typically staffed with extremely bright interns, residents, and faculty members who are
challenging every diagnosis. Tr. at 74. Accordingly, Dr. Steinman opined that “for the doctors and professors at a
major university teaching hospital to have made the diagnosis of acute inflammatory demyelinating polyneuropathy
based on clinical presentation, spinal fluid examination, electrophysiology and all the challenges that go on from the
team, to me, chances are [ninety-nine] percent that that diagnosis was correct.” Id. at 75.


                                                               15 
 
from ongoing CIDP, Dr. Steinman testified, he would have expected to see the opposite (less
reinnervation, and more dennervation). Id. at 120-21.

        Dr. Steinman specifically disputed the accuracy of changing Ms. Blackburn’s diagnosis
to CIDP. He believed the improvement in her overall health by the spring of 2010 supported the
conclusion that she merely suffered from a waxing and waning form of AIDP. Tr. at 124. He
further noted that in his experience, AIDP patients often had incomplete recoveries – and that
therefore this was an insufficient reason to alter a patient’s initial diagnosis. Id. at 62-63, 127-28,
131. Dr. Steinman went on to observe that reflexes were present during this visit and continued
to be present at every bodily site (including her ankles) at subsequent visits in the months to
follow. Id. at 128-30. He admitted, however, that based on the very same treatment history, many
of his colleagues would likely change a patient’s diagnosis to CIDP. Id. at 62-63.

        Finally, Dr. Steinman questioned the significance of Ms. Blackburn’s responsiveness to
prednisone, asserting that steroids such as prednisone would inherently tend to make a patient
feel less depressed and even “ebullient.” Tr. at 126-28. He added that he was not in favor of
prednisone as a treatment due to its “nasty side effects.” Id. at 130. He later admitted, however,
that prednisone was in fact indicated for CIDP34, but asserted that it represented a disfavored,
last-ditch treatment when more standard treatments like IVIG had failed. Id. at 181-83. At
bottom, Dr. Steinman felt that the mere temporal coincidence of corticosteroid treatment and
continued recovery from a demyelinating episode was insufficient to establish CIDP as the
correct diagnosis. Id. at 72.

              B.             Respondent’s Experts

               1.    Dr. Chaudhry – Respondent’s expert, Vinay Chaudhry, M.D., received his
medical degree from All-India Institute of Medical Services in New Delhi, India. Tr. at 194;
Resp’t’s Ex. B (Dr. Chaudhry’s curriculum vitae). He then went to England for secondary
training where he obtained Membership in the Royal College of Physicians (M.R.C.P). Tr. at
194. Thereafter, Dr. Chaudhry completed a residency in neurology at the University of
Tennessee Center for the Health Sciences and the University of Alabama in Birmingham,
followed by a two-year electromyography (“EMG”) and neuromuscular disease fellowship
training program at Johns Hopkins University. Id. Dr. Chaudhry joined the faculty at John
Hopkins in 1989, where he currently works as a professor of neurology, teaching and working on




                                                            
34
    Dr. Steinman also attacked Dr. Chaudhry’s contention that steroids are never to be used for treatment of GBS,
arguing instead that they were in fact commonly used until it became clear that IVIG and plasmapheresis treatments
were more successful. Tr. at 73-74.
 

                                                               16 
 
clinical trials.35 Id. at 194, 196. He is board-certified in clinical neurophysiology, neuromuscular
medicine, and electrodiagnostic medicine. Id. at 199. He has also published articles on a variety
of topics, including GBS, with most of his publications pertaining to some aspect of peripheral
neuropathy. Id.

        Despite his academic duties, Dr. Chaudhry spends the majority of his time caring for
patients, including patients suffering from GBS, CIDP, and other neuromuscular diseases. Tr. at
196-97. Most of Dr. Chaudhry’s outpatients suffer from CIDP, and he assists such individuals
with diagnosis and management of long-term care. Id. at 196-98. Patients with GBS, by contrast,
are typically so acutely ill that they require inpatient hospitalization (and then rarely return to the
hospital thereafter because they have recovered), but one month a year Dr. Chaudhry sees GBS
patients as well in conjunction with his work as an attending physician. Id. at 169, 208. Dr.
Chaudhry also sees GBS patients for diagnostic purposes in the EMG laboratory at Johns
Hopkins (where his responsibilities include acting as co-director of the laboratory, which is
responsible for conducting about 5,000 of such studies per year), and he is directly experienced
in conducting such tests and interpreting their results. Id. at 196-98, 218-19. Dr. Chaudhry
estimated that over the course of his twenty-five year career, he has seen close to 30,000 patients
with either GBS or CIDP. Id. at 197.

        Consistent with the opinions expressed in his written reports (see Resp’t’s Ex. A at 5;
Resp’t’s Ex. XX at 2), Dr. Chaudhry testified that Petitioner’s CIDP diagnosis was correct.36 Tr.
at 201-02, 209-41; See also Resp’t’s Ex’s E-J (medical or scientific literature relied upon by Dr.
Chaudhry in formulating this opinion). While acknowledging that CIDP is a difficult diagnosis to
make, even under the best circumstances (Tr. at 197-98), Dr. Chaudhry expressed the opinion
that this is the diagnosis that all of Ms. Blackburn’s providers would have eventually made –
even those who initially surmised that she suffered from AIDP – had they had the benefit of
reviewing the totality of her medical records (including the clinical, electrophysiological,
laboratory, and therapeutic features of her disease). Id. at 222-23, 249-51.

       Dr. Chaudhry reached his conclusion that Petitioner had CIDP largely based on the
evidence of waxing and waning of her symptoms over a large period of time (including before
her receipt of the HPV vaccination). Tr. at 239-41. Thus, he viewed the symptoms Ms.
Blackburn exhibited in late 2008 as initial evidence of her CIDP. Id. at 210. Indeed, Ms.
                                                            
35
   Dr. Chaudhry’s involvement in clinical research includes serving as an investigator on research trials; for
example, he was involved in the clinical trials that recently lead the FDA to approve IVIG for treatment of CIDP. Tr.
at 200.
36
   Dr. Chaudhry also opined that, given the diagnosis and the onset of symptoms that preceded the vaccination, he
did not believe that the HPV vaccine played a significant role in Ms. Blackburn’s alleged injury. Tr. at 202. My
decision does not, however, rely on this portion of his testimony (which was in fact mooted by Dr. Chaudhry’s
testimony about the pre-vaccination course of Ms. Blackburn’s CIDP).


                                                               17 
 
Blackburn’s initial symptoms were referred to as neuropathic or neuralgic several times in the
contemporaneous medical records, and she was prescribed medications typically given to
patients who are experiencing neuropathic or neuralgic conditions. Id. Dr. Chaudhry also found it
significant that Dr. Zimmerman suggested performing tests aimed specifically at ruling out nerve
injury, nerve damage, or neuropathy of some sort, such as nerve conduction studies.37 Id. at 228.
And that Mr. Blackburn reported experiencing tingling in her legs and feet on the date of her July
2009 vaccination (at which time she was still taking medication for her prior neuropathic
symptoms). Id. at 211-12. Based on all of the above, Dr. Chaudhry concluded that Petitioner’s
CIDP had likely begun in the second half of 2008. Id. at 227, 249-50.

        Dr. Chaudhry found further support for his opinion that Ms. Blackburn’s CIDP predated
her vaccination in Petitioner’s August 19, 2009 EMG and nerve conduction study results (based
on tests performed within a month of her vaccination). Tr. at 216-18. Having conducting
hundreds of such tests over the years, Dr. Chaudhry indicated that he would expect a typical
GBS patient to have EMG results displaying relative preservation (sparing) of sensory nerve
action potentials. Id. at 216. Ms. Blackburn’s test results, however, showed no response in any of
her sensory nerves. Id. He also observed reduced recruitment in her EMG results,38
demonstrating to him that Ms. Blackburn already had a severe demyelinating neuropathy. Id. at
217. Assuming Ms. Blackburn’s GBS began as a result of her July 2009 vaccination, it would be
highly unusual for a patient to display such extensive damage in so short a time, whereas it
would be common for CIDP (which would have progressed over a much greater length of time
and begun many months before). Id. at 216, 218.

       On the other hand, Dr. Chaudhry opined that Ms. Blackburn did not display post-
vaccination the kind of symptoms that he believed were consistent with a GBS diagnosis. Tr. at
220. For instance, Ms. Blackburn presented with complaints of three-and-a-half weeks of
ascending weakness and numbness on August 24, 2009, but when examined, Ms. Blackburn did
not exhibit any facial weakness – her cranial facial nerve appeared normal. Id. at 219-22. Her
upper extremities were also close to normal, which in Dr. Chaudhry’s view would be unusual for
someone suffering from an acute disease like GBS that purportedly began about a month earlier
(and should be at its most severe point by that time). Id. at 219-21.39 And he questioned Dr.

                                                            
37
  Even if her symptoms were not severe enough at this point for the doctor to order a lumbar puncture or nerve
conduction studies, they still suggested to Dr. Zimmerman that he do preliminary testing, and start treating Ms.
Blackburn with amitriptyline. Tr. at 226-28.
38
   “In a normal recruitment pattern, the number of discharging motor units increases appropriately for the muscle
force generated by the effort. In neuropathy, a loss of functional motor units results in late or decreased recruitment
associated with rapid firing of discharging units to compensate for the reduced number.” Dyck & Thomas at 952-53
(citations omitted).
39
  Based on his review of the contemporaneous records and test results from Ms. Blackburn’s August 24th doctor’s
visit, Dr. Chaudhry actually concluded that even if he accepted the GBS diagnosis, the time from onset at this point

                                                               18 
 
Steinman’s belief that Ms. Blackburn’s post-hospitalization relapse was attributable to her not
receiving a full course of IVIG treatment, since (based on the medical records) it appeared to Dr.
Chaudhry that she had received a full course of treatment despite her anemic reaction. Id. at 224-
25, 233-34.40

       The success of the prednisone course that Dr. Bromberg prescribed was in Dr.
Chaudhry’s view particularly strong evidence that CIDP was the correct diagnosis. Tr. at 235-36,
238-39. In discussing the benefit of prednisone for CIDP patients, Dr. Chaudhry took issue with
Dr. Steinman’s suggestion that Ms. Blackburn felt better after receiving it simply because of its
“euphoric effect.” Id. at 239. Dr. Chaudhry emphasized that Ms. Blackburn’s intervening
medical history corroborated the benefit of the prednisone treatment, since her symptoms got
worse whenever her dosage was removed or reduced. Id. In fact, when Dr. Bromberg began a
slow taper of the prednisone, he started Ms. Blackburn on CellCept41 – a very strong steroid
sparing agent that (in Dr. Chaudhry’s experience) would never be given to a patient believed to
have GBS. Id. at 237. Nothing Dr. Chaudhry saw in Ms. Blackburn’s medical history suggested
to him that the diagnosis change was in error, nor did any of her subsequent treating physicians
believe that CIDP was a mistaken diagnosis in light of additional findings or data pertaining to
her progress. Id. at 239-40, 249-50.

        Dr. Chaudhry addressed some of Petitioner’s arguments that Ms. Blackburn did not
display any CIDP symptoms pre-vaccination. He acknowledged that Ms. Blackburn’s reflexes
were recorded as normal when she received the vaccination as well as before, but opined that her
other symptoms, viewed together, likely represented the beginning of a neuropathy. Tr. at 212-
13. In his experience, however, it was typical for CIDP patients to experience a variety of mild
neuropathic symptoms over a long period of time before receiving a CIDP diagnosis, despite the
presence of normal reflexes.42 Id.

        He did not find significant the long gap between Ms. Blackburn’s early 2009 doctor’s
visits and the post-vaccination flare-up she experienced, since in his view it was common for

                                                                                                                                                                                                
would have to have been longer than four weeks and closer to sixty days (six weeks or thereabouts), which is well
outside the clinical definition for the disease’s four-week progression. Tr. at 221-22.
40
  See Pet’r’s Ex. 7 at 25; Tr. at 224. Dr. Chaudhry’s understanding of what a full IVIF course would be is consistent
with prominent medical literature on the subject. See, e.g., Dyck & Thomas at 642 (the standard course of IVIg “first
used for autoimmune thrombocytopenia was 0.4g/kg daily for [five] days, and this has been adopted in
neuromuscular diseases” (although the dose may be different for recurrent courses)).
41
  CellCept (mycophenolate mofetil) is an immunosuppressive agent (Dorland’s at 1216) more commonly used for
renal transplant patients. Tr. at 237.
42
   Dr. Chaudhry speculated that Ms. Blackburn’s initial treatment providers may not have been as comprehensive in
testing her reflexes (given the other warning signs present) as he would have given his experience. Tr. at 213.


                                                                                             19 
 
CIDP patients to go a long time with low grade or intermittent symptoms while still being able to
work. Id. at 206, 226. Dr. Chaudhry found it unlikely that a twenty-six year old would
experience this type of nerve pain and tingling as the result of mere “physical stress” (Resp’t’s
Ex. A at 6-7; Tr. at 227), and pointed to Dr. Zimmerman’s suspicion of neuritis or neuralgia as
supportive of this view. Resp’t’s Ex. A at 6; Tr. at 228.

               2.      Dr. Whitton - James Lindsay Whitton, M.D. is an immunologist at
Scripps, a nonprofit private research institution. Tr. at 269; Resp’t’s Ex. D (Dr. Whitton’s
curriculum vitae). He serves on the editorial boards of several medical journals. Tr. at 272. Dr.
Whitton has “only worked a little in molecular mimicry,” though he has had professional
colleagues with greater expertise in the topic. Id. at 269, 362. Dr. Whitton’s testimony was
offered in response to Dr. Steinman’s proposed theory by which the HPV vaccine could cause
GBS. Dr. Whitton proposed that Dr. Steinman’s theory relied upon two core premises: (1)
homology between the protein components of the HPV vaccine and the relevant target sites on
the peripheral nerves; and (2) the induction of an immune response against MBP. Id. at 278-79.
Dr. Whitton’s disputed both premises, arguing that (1) MBP is not the target antigen in GBS; and
(2) Dr. Steinman’s homology theory is not scientifically valid.

        Dr. Whitton agreed with Dr. Steinman that molecular mimicry is a biologically plausible
theory under certain circumstances. Tr. at 362-63. He similarly did not challenge Dr. Steinman’s
general explanation for how molecular mimicry would occur. Id. at 281, 362. And he did not
seriously question the assertion that GBS could be caused by molecular mimicry. See Resp’t Ex.
C (Dr. Whitton’s Expert Report) at 4. Instead, Dr. Whitton challenged Dr. Steinman’s invocation
of molecular mimicry in this particular case. Tr. at 306.

        First, Dr. Whitton questioned the application of Dr. Steinman’s homology theory to the
autoimmune response specifically resulting in GBS. Tr. at 295. Dr. Whitton explained that
peripheral nervous system diseases are generally thought to be driven by antibody responses
rather than T cell mediated. Id. at 327. He acknowledged the literature establishing that MBP-
specific T cells induce EAE in mice via molecular mimicry (Id. at 283-86), but asserted that such
studies were of limited applicability here, as they involved an artificial stimulation of animal
immune systems intended to produce a central nervous system disease that nevertheless did not
also cause the test subject laboratory animals to develop peripheral nerve diseases. Id. at 281-83.
In Dr. Whitton’s view, the “pathology and parthogenesis” of central nervous system neuropathies
could not be properly conflated with peripheral nervous system neuropathies. Id. at 283.

       Importantly, Dr. Whitton argued, the MBP-specific T cells that have been shown in the
EAE studies to target MBP have not been shown to have the same effect in causing peripheral
nervous system diseases. Id. at 286. This, he elaborated, was due to the fact that there is no
evidence that MBP is a possible target antigen in causing GBS. Id. at 287. Rather, he noted that


                                                20 
 
there are many other potential structures in peripheral myelin (of which MBP is a component)
that could be the target of a demyelinating autoimmune response. Id. at 291. In particular, nerve
gangliosides43 have been demonstrated to be the target in autoimmune-induced GBS via the
process of molecular mimicry between the infectious agent and the ganglioside. Id. at 289-91;
Tomoko Komagamine & Nobuhiro Yuki, Ganglioside Mimicry as a Cause of Guillain-Barré
Syndrome, 5 CNS & Neurological Disorders 391-400 (2006) (Rep’t’s Ex. R at 6-7) [hereinafter
“Komagamine”].

        Second, Dr. Whitton questioned the scientific validity of Dr. Steinman’s revised theory of
homology. Dr. Whitton asserted that F and Y are in fact not generally interchangeable. Tr. at
310. Moreover, Dr. Whitton argued that there is “nothing special about FK” (Tr. at 317),
pointing out that the probability that a protein of 500 amino acids contains at least one FK
sequence is about seventy-one percent. Id. at 314. Thus, according to Dr. Whitton, if, as Dr.
Steinman proposed, a sequence of that short length were sufficiently homologous with MBP to
induce an autoimmune response, then it would be reasonable to expect autoimmune diseases to
be far more common than they actually are. Id. at 315-17.44

III.          Medical Literature

       Both sides offered substantial scientific and medical literature.45 Petitioner submitted
twenty-five articles relied upon by her expert in formulating an opinion in this case. This
included ten articles initially relied upon by Dr. Steinman to provide a mechanistic explanation
of how the HPV vaccine could cause neurological damage, and to support his opinion that Ms.
Blackburn’s GBS was caused by her receipt of the vaccination in question.


                                                            
43
  The term ganglioside refers to any of a group of glycosphingolipids (ceramide and oligosaccharide) occurring in
nervous system tissues. Dorland’s at 760,794.
44
  Dr. Whitton also addressed whether it appeared from Ms. Blackburn’s medical history that she had suffered from
GBS as a result of the vaccine rather than an antecedent infection, and also whether the proposed theory by which
the HPV vaccine had caused Ms. Blackburn’s purported AIDP occurred in a medically-acceptable timeframe. See
generally Tr. at 319-40. Because my decision turns on other aspects of Dr. Whitton’s testimony, however, or matters
that he did not specifically address (such as the propriety of the GBS diagnosis), I do not review these additional
portions of his testimony herein.
45
  Although I do not reference or discuss in this decision every item of medical or scientific literature offered by the
parties, I have read all of the submitted articles. Hazlehurst v. Sec'y of Health & Human Servs., 604 F.3d 1343, 1352
(Fed. Cir. 2010) (indicating that on review it is not necessary to rely on the presumption that the finder of fact has
reviewed all presented evidence unless he specifically states otherwise, where the opinion of the special master
specifically refers to that evidence). See also Andreu v. Sec'y of Health & Human Servs., 569 F.3d 1367, 1379 (Fed.
Cir. 2009) (“Although Althen and Capizzano make clear that a claimant need not produce medical literature or
epidemiological evidence to establish causation under the Vaccine Act, where such evidence is submitted, the
special master can consider it in reaching an informed judgment as to whether a particular vaccination likely caused
a particular injury”) (emphasis added).


                                                               21 
 
        Respondent cites certain pieces of literature submitted by Petitioner as well as forty-seven
additional articles relied upon by her experts in formulating their opinion in this case.
Respondent initially submitted six articles used to support Dr. Chaudhry’s expert opinions,
which consisted of literature addressing the possible competing diagnoses as well as whether the
vaccination in question triggered Ms. Blackburn’s alleged illness. Respondent then submitted
one additional article regarding the molecular pathogenesis of GBS. Respondent also submitted
forty articles relied upon by Dr. Whitton to address the timing of the first onset of Petitioner’s
neurological disease in relation to her receipt of vaccination, as well as the likelihood that Ms.
Blackburn’s neurological disease was triggered by a prior infection rather than the HPV
vaccination.



IV.           Procedural History

        As noted above, Ms. Blackburn filed this petition in June 2010. Petition (ECF No. 1) at 2-
3. Over the ensuing six months, she filed relevant medical records and an affidavit that she
intended to rely upon to establish her entitlement to compensation, certifying completion of the
record on January 13, 2011. ECF No. 17. Thereafter, on March 9, 2011, Respondent filed her
Rule 4(c) Report (ECF No. 20 (“Resp’t’s Rep’t”)), asserting in it that Petitioner could not satisfy
the test for establishing entitlement to a Vaccine Program award as set forth in Althen v. Sec’y of
Health & Human Servs., 418 F.3d 1274, 1278 (Fed. Cir. 2005). Resp’t’s Rep’t at 14. Among
other things, Respondent argued that the medical records did not themselves establish causation
because none of Petitioner’s treating physicians provided a medical theory. Id. Respondent also
proposed that onset occurred before the vaccination, and/or was related to an antecedent
infection, and further questioned the accuracy of the GBS diagnosis. Id. at 15.

        Ms. Blackburn subsequently filed additional medical records in support of her claim, and
then filed a second statement of completion on August 21, 2011. ECF No. 25. A status report
filed on that same date indicated that Petitioner’s counsel was preparing a demand letter to send
on Petitioner’s behalf to Respondent with the aim of resolving this case through settlement. ECF
No. 25. Such initial settlement efforts were unsuccessful, however.

        Petitioner requested and was granted a number of extensions of time to file an expert
report in support of vaccine causation46 before she did so on July 30, 2012. ECF No. 36. On
September 25, 2012, Respondent filed an unopposed motion requesting an extension of time to
file her expert reports, which was subsequently granted. ECF Nos. 38-39. Thereafter, on
November 27, 2012, Respondent filed two expert reports. ECF Nos. 40-45. The special master
                                                            
46
  On October 31, 2011, January 30, 2012, March 30, 2012, and May 30, 2012, Petitioner requested and was
subsequently granted requests for an extension of time for filing an expert report in support of vaccine causation.
ECF Nos. 27-31, 34-35.


                                                               22 
 
formerly responsible for this case next conducted a telephonic status conference on December
20, 2012, to discuss the merit of each party’s position in this case. ECF No. 46. During the
conference, the parties again expressed the desire to explore the possibility of resolving this case
through informal settlement negotiations prior to setting a date for an entitlement hearing. Id. But
these additional settlement discussions proved unsuccessful, and so during a status conference on
June 6, 2013 the case was set for hearing and the parties were instructed to complete the filing of
relevant medical records as well as pre-trial briefs. ECF Nos. 55, 58.

       In early 2014, the parties filed some additional medical literature, prehearing memoranda,
and other supplemental materials. Thereafter, in March of 2014 the matter was assigned to me
(ECF Nos. 69-70) but the previously-scheduled hearing dates (March 25-26, 2014) were
maintained and the matter was tried as scheduled. Both parties filed post-trial briefs in June (ECF
Nos. 77-78) and then responded to each other’s filings in July (ECF Nos. 79-80). This matter is
now ripe for adjudication.



V.            Standards for Entitlement Award in Vaccine Program Cases

        To receive compensation under the Vaccine Program, a petitioner must prove either: (1)
that she suffered a “Table Injury” – i.e., an injury falling within the Vaccine Injury Table –
corresponding to one of the vaccinations in question, or (2) that her illnesses were actually
caused by a vaccine (a “non-Table injury”). See §§ 300aa-13(a)(1)(A),11(c)(1); § 300aa-14(a), as
amended by 42 C.F.R. § 100.3; 300aa-11(c)(1)(C)(ii)(I); see also Moberly v. Sec’y of Health &
Human Servs., 592 F.3d 1315, 1321 (Fed. Cir. 2010); Capizzano v. Sec’y of Health & Human
Servs., 440 F.3d 1317, 1320 (Fed. Cir. 2006).47 No table injury is alleged in this case, so Ms.
Blackburn must prove causation-in-fact.

        Petitioners bear the burden of demonstrating actual causation by preponderant evidence.
Cedillo v. Sec’y of Health & Human Servs., 592 F.3d 1315, 1321 (Fed. Cir. 2010); § 300aa-
13(a)(1). To do so, a petitioner must provide: “(1) a medical theory causally connecting the
vaccination and the injury; (2) a logical sequence of cause and effect showing that the
vaccination was the reason for the injury; and (3) a showing of a proximate temporal relationship
between vaccination and injury.” Althen, 418 F.3d at 1278. The preponderance standard requires
a petitioner to demonstrate that it is “more likely than not” that the vaccine at issue caused his
injury. Moberly, 592 F.3d at 1322 n.2. Proof of medical certainty is not required. Bunting v.
Sec’y of Health & Human Servs., 931 F.2d 867, 873 (Fed. Cir. 1991). In particular, a petitioner
                                                            
47
   Decisions of special masters (some of which I reference in this ruling) constitute persuasive but not binding
authority. Hanlon v. Sec’y of Health & Human Servs., 40 Fed. Cl. 625, 630 (1998). By contrast, Federal Circuit
decisions are binding on special masters. Guillory v. Sec’y of Health & Human Servs., 59 Fed. Cl. 121, 124 (2003),
aff’d, 104 F. App’x 712 (Fed. Cir. 2004); see also Spooner v. Sec’y of Health & Human Servs., No. 13-159V, 2014
WL 504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014).


                                                               23 
 
must demonstrate that the vaccine was “not only [the] but-for cause of the injury but also a
substantial factor in bringing about the injury.” Moberly, 592 F.3d at 1321 (quoting Shyface v.
Sec’y of Health & Human Servs., 165 F.3d 1344, 1352-53 (Fed. Cir. 1999)); Pafford v. Sec’y of
Health & Human Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006). To determine if Petitioner has
carried her burden, I must assess “the record as a whole” and may not make an entitlement
decision in her favor based solely on her own claims “unsubstantiated by medical records or by
medical opinion.” § 13(a)(1).

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

        Petitioners may satisfy Althen prong one without resort to medical literature,
epidemiological studies, demonstration of a specific mechanism, or by offering a theory that has
general acceptance in the medical or scientific communities. Andreu v. Sec’y of Health & Human
Servs., 569 F.3d 1367, 1378-79 (Fed. Cir. 2009) (citing Capizzano, 440 F.3d at 1325-26). Special
masters, despite their expertise, are not empowered by statute to conclusively resolve what are
essentially thorny scientific and medical questions, and thus scientific evidence offered to
establish Althen prong one is viewed “not through the lens of the laboratorian, but instead from
the vantage point of the Vaccine Act’s preponderant evidence standard.” Andreu, 569 F.3d at
1380.

       Often, however, establishing a sound and reliable medical theory requires that the parties
present expert testimony in support of their claims. Lampe v. Sec’y of Health & Human Servs.,
219 F.3d 1357, 1361 (Fed. Cir. 2000). Vaccine Program expert testimony is usually evaluated
according to the factors for analyzing scientific reliability set forth in Daubert v. Merrell Dow
Pharm., Inc., 509 U.S. 579, 594-96 (1993). Cedillo, 617 F.3d at 1339 (citing Terran v. Sec’y of
Health & Human Servs., 195 F.3d 1302, 1316 (Fed. Cir. 1999)). “The Daubert factors for
analyzing the reliability of testimony are: (1) whether a theory or technique can be (and has
been) tested; (2) whether the theory or technique has been subjected to peer review and
publication; (3) whether there is a known or potential rate of error and whether there are
standards for controlling the error; and (4) whether the theory or technique enjoys general
acceptance within a relevant scientific community.” Terran, 195 F.3d at 1316 n.2 (citing
Daubert, 509 U.S. at 592-95).



                                               24 
 
        In other federal judicial fora (such as the district courts), the Daubert factors are
employed by judges (in the performance of their evidentiary gatekeeper roles) to resolve
admissibility questions, excluding evidence that is unreliable and/or could confuse a jury. In
Vaccine Program cases, by contrast, these factors are used in the weighing of the scientific
evidence actually proffered and heard. Davis v. Sec’y of Health & Human Servs., 94 Fed. Cl. 53,
66-67 (Fed. Cl. 2010) (“uniquely in this Circuit, the Daubert factors have been employed also as
an acceptable evidentiary-gauging tool with respect to persuasiveness of expert testimony
already admitted”), aff’d, 420 F. App’x 923 (Fed. Cir. 2011). The flexible use of the Daubert
factors to determine the persuasiveness and/or reliability of expert testimony in Vaccine Program
cases has routinely been upheld. See, e.g., Snyder v. Sec’y of Health & Human Servs., 88 Fed. Cl.
706, 742-45 (2009).48

         Where both sides offer expert testimony, a special master’s decision may be “based on
the credibility of the experts and the relative persuasiveness of their competing theories.”
Broekelschen v. Sec’y of Health & Human Servs., 618 F.3d 1339,1347 (Fed. Cir. 2010) (citing
Lampe, 219 F.3d at 1362). However, nothing requires the acceptance of an expert’s conclusion
“connected to existing data only by the ipse dixit of the expert,” especially if “there is simply too
great an analytical gap between the data and the opinion proffered.” Snyder, 88 Fed. Cl. at 743
(quoting Gen. Elec. Co. v. Joiner, 522 U.S. 146 (1997)). Weighing the relative persuasiveness of
competing expert testimony, based on a particular expert’s credibility, is part of the overall
reliability analysis to which special masters must subject expert testimony in Vaccine Program
cases. Moberly, 592 F.3d at 1325-26 (“[a]ssessments as to the reliability of expert testimony
often turn on credibility determinations”); see also Porter v. Sec’y of Health & Human Servs.,
663 F.3d 1242, 1250 (Fed. Cir. 2011) (“this court has unambiguously explained that special
masters are expected to consider the credibility of expert witnesses in evaluating petitions for
compensation under the Vaccine Act”).

        The second Althen prong requires proof of a logical sequence of cause and effect, usually
supported by facts derived from a petitioner’s medical records. Althen, 418 F.3d at 1278; Andreu,
569 F.3d at 1375-77; Capizzano, 440 F.3d at 1326; Grant, 956 F.2d at 1148. In evaluating
whether this prong is satisfied, the opinions and views of the injured party’s treating physicians
are entitled to some weight. Andreu, 569 F.3d at 1367; Capizzano, 440 F.3d at 1326 (“medical
records and medical opinion testimony are favored in vaccine cases, as treating physicians are
likely to be in the best position to determine whether a ‘logical sequence of cause and effect
show[s] that the vaccination was the reason for the injury’”) (quoting Althen, 418 F.3d at 1280).
Medical records are generally viewed as trustworthy evidence, since they are created

                                                            
48
   Petitioner argued at length in her pre-trial submissions that Daubert had been incorrectly cited by Respondent
because it is a tool for determining only if evidence was admissible, and therefore has less utility in evaluating the
reliability, persuasiveness, or adequacy of expert testimony. See, e.g., Pet’r’s Pre-Hr’g Reply Mem., dated February
18, 2014 (ECF No. 68) at 10-20. This is plainly against relevant controlling authority.


                                                               25 
 
contemporaneously with the treatment of the patient. Cucuras v. Sec’y of Health & Human
Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993).

        However, medical records setting forth a treating physician’s views do not per se bind the
special master to adopt the conclusions of such an individual, even if they must be considered
and carefully evaluated. § 300aa–13(b)(1) (providing that “[a]ny such diagnosis, conclusion,
judgment, test result, report, or summary shall not be binding on the special master or court”);
Snyder, 88 Fed. Cl. at 745 n.67 (“there is nothing . . . that mandates that the testimony of a
treating physician is sacrosanct—that it must be accepted in its entirety and cannot be rebutted”).
Rather, as with expert testimony offered to establish a theory of causation, the opinions or
diagnoses of treating physicians are only as trustworthy as the reasonableness of their
suppositions or bases. The views of treating physicians should also be weighed against other,
contrary evidence present in the record – including conflicting opinions among the treating
physicians themselves. Hibbard v. Sec'y of Health & Human Servs., 100 Fed. Cl. 742, 749 (Fed.
Cl. 2011) (not arbitrary or capricious for special master to weigh competing treating physicians’
conclusions against each other), aff'd, 698 F.3d 1355 (Fed. Cir. 2012); Caves v. Sec'y of Health
& Human Servs., 100 Fed. Cl. 119, 136 (Fed. Cl. 2011), aff'd, 463 F. App'x 932 (Fed. Cir. 2012);
Veryzer v. Sec'y of Health & Human Servs., No. 06-522V, 2011 WL 1935813, at *17 (Fed. Cl.
Spec. Mstr. Apr. 29, 2011), mot. for review den’d, 100 Fed. Cl. 344.

        The third Althen prong requires establishing a “proximate temporal relationship” between
the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been equated to
the phrase “medically-acceptable temporal relationship.” Id. A petitioner must offer
“preponderant proof that the onset of symptoms occurred within a timeframe which, given the
medical understanding of the disorder’s etiology, it is medically acceptable to infer causation.”
de Bazan v. Sec’y of Health & Human Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The
explanation for what is a medically acceptable timeframe must also coincide with the theory of
how the relevant vaccine can cause an injury (Althen prong one’s requirement). Id.; Shapiro v.
Sec’y of Health & Human Servs., 101 Fed. Cl. 532, 542 (Fed. Cl. 2011), recons. den’d after
remand, 105 Fed. Cl. 353 (2012), aff’d mem., 2013 WL 1896173 (Fed. Cir. 2013); Koehn v.
Sec'y of Health & Human Servs., No. 11-355V, 2013 WL 3214877, at *27 (Fed. Cl. Spec. Mstr.
May 30, 2013), aff’d, No. 2014-5054, 2014 WL 6804880 (Fed. Cir. Dec. 4, 2014).

         The law pertaining to the parties’ respective burdens of proof also merits brief mention.
Petitioner has suggested that because Respondent argues that Ms. Blackburn actually suffered
from CIDP rather than GBS, it is Respondent’s burden to establish Petitioner’s CIDP as a “factor
unrelated” cause of Petitioner’s illness. See, e.g., Pet’r’s Pre-Hr’g Reply Mem. (ECF No. 68) at 2
(citing Walther v. Sec’y of Health & Human Servs., 485 F.3d 1146, 1152 (2007)). It is correct
that in cases where a petitioner successfully satisfies her initial burden of proof, the burden then
shifts to Respondent to establish (also by the same preponderance of the evidence standard) that
the petitioner’s injuries are due to “factors unrelated” to the vaccines. C.K. v. Sec’y of Health &

                                                26 
 
Human Servs., 113 Fed. Cl. 757, 766 (2013) (citing Knudsen, 35 F.3d at 547); Deribeaux v.
Sec’y of Health & Human Servs., 105 Fed. Cl. 583, 587 (2012), aff’d, 717 F.3d 1363 (Fed. Cir.
2013); 42 U.S.C. § 300aa–13(a)(1)(B).

        The burden of proof does not, however, shift to Respondent merely because (as in this
case) she disputes the factual nature of the alleged injury or its proper diagnosis. On the contrary
– Respondent may offer evidence, or point to existing evidence in the record, that contradicts or
weakens a petitioner’s evidence, and in so doing demonstrate that the petitioner cannot meet her
overall burden. Stone v. Sec’y of Health & Human Servs., 676 F.3d 1373, 1379 (Fed. Cir. 2012)
(“[o]ur decisions support the commonsense proposition that evidence of other possible sources of
injury can be relevant not only to the “factors unrelated” defense, but also to whether a prima
facie showing has been made that the vaccine was a substantial factor in causing the injury in
question”); La Londe v. Sec’y of Health & Human Servs., 110 Fed. Cl. 184, 198 (2013)
(“[r]egardless of whether the burden ever shifts to the respondent, the special master may
consider the evidence presented by the respondent” when determining if petitioner’s initial
burden has been met), aff’d, 736 F.3d 1334 (Fed. Cir. 2014). In this case, Respondent’s challenge
to the proper diagnosis of Petitioner’s illness does not amount to an attempt to establish a causal
“factor unrelated,” and therefore in considering such issues I do not find that Respondent is
burdened with proving them.



VI.           ANALYSIS

              A.             Dispute Over Petitioner’s Diagnosis

       Both sides devoted a substantial portion of the hearing to addressing whether the HPV
vaccine could be shown to cause GBS (or more precisely the AIDP variant of GBS). The
medical records in this case, however, suggest a more immediate question: whether Ms.
Blackburn had GBS at all, and/or whether her illness began only after her receipt of vaccination.
Ms. Blackburn and her counsel did not originally plead a claim based upon significant
aggravation of a pre-existing condition, and have otherwise repeatedly denied that they do so
now. See generally Hirmiz v. Sec'y of Health & Human Servs., No. 06-371V, 2014 WL 7204716,
at *9-10 (Fed. Cl. Dec. 4, 2014) (failure to amend petition before trial to add significant
aggravation was fatal to claim, despite fact that evidence offered at trial incidentally supported
such a claim). Therefore, if the illness Petitioner suffered from was different from what was
alleged, began before she ever received the HPV vaccination, and/or was not itself triggered or
aggravated by the vaccination – then Petitioner’s entire claim cannot succeed.49

                                                            
49
   In his testimony, Dr. Steinman did claim that his theory for how the HPV vaccine could have caused Ms.
Blackburn’s illness still applied even if she suffered from CIDP rather than the AIDP variant of GBS. Tr. at 186-89.
However, he admitted that his theory was heavily focused on AIDP being the correct diagnosis, and he did not
testify that Ms. Blackburn’s pre-vaccination symptoms were aggravated by the Gardasil vaccine – nor did he ever

                                                               27 
 
        As Federal Circuit precedent establishes, in certain cases it is appropriate to determine the
precise nature of a petitioner’s injury before engaging in the Althen analysis. Broekelschen, 618
F.3d at 1346. Indeed, the fact that a claimed injury predates the vaccination can defeat a Vaccine
Program claim entirely. Shalala v. Whitecotton, 514 U.S. 268, 274-75(1995) (Vaccine Act
claimant who demonstrates she experienced symptoms of injury after receipt of vaccination does
not succeed in her claim if the evidence fails to indicate that she had no symptoms of injury
before her vaccination); Locane v. Sec’y of Health & Human Servs., 99 Fed. Cl. 715 (2011)
(petitioner’s Crohn’s disease began prior to her vaccinations and therefore vaccine causation
could not be established). Since “each prong of the Althen test is decided relative to the injury”
(Broekelschen, 618 F.3d at 1346), determining facts relating to the claimed injury can be
significant in a case like this, where the petitioner has symptoms predating her vaccination that
could be consistent with an illness other than that alleged as the injury. Indeed, as another special
master recently noted, “where the respondent presents evidence of an alternative diagnosis, the
special master may consider the respondent’s evidence of that alternative diagnosis as part of the
master’s evaluation of the petitioner’s prima facie showing of an injury, potentially mooting the
Althen causation test.” Hirmiz, 2014 WL 7204716, at *14.

       Thus, before determining whether Ms. Blackburn has met each of the individual Althen
prongs, I address whether she has established by preponderant evidence that she suffered from
the AIDP variant of GBS, and whether her illness began prior to her vaccination.

              1.      GBS/AIDP vs. CIDP – As noted in the Koningsveld article50 included in
the medical literature offered by Petitioner, GBS is an acute variant of an inflammatory
demyelinating polyneuropathy. Pet’r’s Ex 36 at 1. It is a rapidly progressing and ascending
motor neuron paralysis frequently seen after infection51 (Dorland’s at 1832), and it is typically
monophasic. Pet’r’s Ex. 37 at 1. From a clinical diagnostic standpoint, an individual with GBS
reaches the peak severity of his symptoms (nadir) within four weeks from initial onset.
Koningsveld at 138.



                                                                                                                                                                                                
maintain that her earlier symptoms had anything to do with her post-vaccination illness. More significantly (and in
keeping with the fact that Petitioner does not advance a significant aggravation claim in this case), Petitioner did not
offer any testimony or medical literature explaining how (assuming Ms. Blackburn’s illness predated vaccination)
the HPV vaccine could have worsened a pre-existing condition. I therefore could not find that Petitioner has offered
preponderant evidence to satisfy a significant aggravation off-Table claim, even if such a claim had been alleged.
50
     Ruts, L., Van Koningsveld, R., & Van Doorn, P.A., Distinguishing Acute-Onset CIDP from Guillain–Barré
Syndrome with Treatment Related Fluctuations, 65 Neurol. 1, 138-40 (2005) (Pet’r’s Ex. 36) [hereinafter
“Koningsveld”].
 
51
    Odaka, M., Yuki, Nobuhiro, Y., Hirata, K., Patients with Chronic Inflammatory Demyelinating Polyneuropathy
Initially Diagnosed as Guillain–Barré Syndrome, 250 J. Neurol. 913-16(2003) (Pet’r’s Ex. 35) [hereinafter
“Odaka”].


                                                                                             28 
 
        AIDP is a common GBS variant (and is sometimes thought of as synonymous with the
disease). P. Dyck & P.K. Thomas, 2 Peripheral Neuropathy 2199 (4th ed. 2005) [hereinafter
“Dyck & Thomas”]. It shares the acute and monophasic characteristics of other GBS variants.
Ted M. Burns, M.D., Guillain-Barré Syndrome, 28 Seminars in Neurol. 152-67 (2008) (Resp’t’s
Ex. G at 3) [hereinafter “Burns”]; Dyck & Thomas at 2222. AIDP is considered to be immune-
mediated, meaning that a triggering event (which may or may not be identified) occurs, leading
to an aberrant immune response which in turn causes a breakdown of the blood-nerve barrier and
destruction of the myelin sheath (and secondarily also the axon) resulting in the clinical
presentation seen in an individual with AIDP. Wilson, H. J., The Immunobiology of Guillain–
Barré Syndromes, 10 J. Peripheral Nervous System 94-112 (2005) (Resp’t’s Ex. O). Some of the
symptoms included in the clinical definition of AIDP are: (a) numbness and tingling in the feet
progressing in an ascending fashion to the arms; (b) progressive and ascending weakness; (c)
areflexia; and (d) cranial nerve dysfunction/facial weakness. Amato, A. & Russell, J., 227
Neuromuscular Disorders 213-14 (1st ed. 2006) (Pet’r’s Ex. 33) [hereinafter “Amato”]; Van
Doorn, P.A., Ruts, L., Jacobs, B.C., Clinical Features, Pathogenesis, and Treatment of Guillain–
Barré Syndrome, 7 Lancet Neurol. 939 (2008) (Resp’t’s Ex. F) [hereinafter “Van Doorn”]. Tests
that can confirm or lend support to the diagnosis include a lumbar puncture (to determine
elevation of protein levels in the cerebrospinal fluid) and EMG/nerve conduction studies. Van
Doorn at 940, 950.

       CIDP is also a demyelinating condition with symptoms similar to AIDP, but typically
presents in either a chronically progressive or relapsing-remitting form. Dyck & Thomas at
2221-22. A CIDP patient’s neurologic symptoms develop over weeks and months (with eight
weeks viewed as the minimum clinical period for a CIDP diagnosis), and an antecedent infection
is much less commonly identified as the initiating factor for the illness. Id. Facial muscle
weakness and autonomic nervous system impairment are also less common in CIDP than in
GBS. Id. at 2222-23.

        Despite their differences, distinguishing between the two diseases is difficult – in
particular during their early phases. Koningsveld at 138; Odaka, M., Yuki, N., Hirata, K.,
Patients with Chronic Inflammatory Demyelinating Polyneuropathy Initially Diagnosed as
Guillain–Barré Syndrome, 250 J. Neurol 913-16 (2003) (Pet’r’s Ex. 35) [hereinafter “Odaka”]
(“the difference between GBS and CIDP in some patients may be blurred during the first [four]
weeks” – “physicians could classify patients with CIDP within [four] weeks of onset as GBS”).
Patients whose symptoms are initially believed to be compatible with GBS may later be
diagnosed with CIDP based on the subsequent course of illness. Koningsveld at 138. And when
treatment is administered early in the course of disease, patients may actually experience a
simulated GBS episode within the overall context of CIDP (thus causing further diagnostic
confusion). Odaka at 914.

       It is important for clinicians to attempt to distinguish between CIDP and GBS as early in

                                              29 
 
the course of illness as possible because of differences in treatment and prognoses. Koningsveld
at 138, 140. Although IVIG treatments are utilized successfully in resolving both GBS/AIDP and
CIDP, corticosteroid treatments “provide clear-cut benefit for most patients with CIDP, whereas
they were shown to be ineffective in AIDP.” Dyck & Thomas at 2223; see also Jean-Michel
Vallat et al., Chronic Inflammatory Demyelinating Polyradiculoneuropathy: Diagnostic and
Theraputic Challenges for a Treatable Condition, 9 Lancet Neurol. 403-12 (2010) (Res’p’t Ex. I
at 7-8); Mori, K. et al., Chronic Inflammatory Demyelinating Polyneuropathy Presenting with
Features of GBS, 58 Neurol. 979 (2002) (Pet’r’s Ex. 34) (corticosteroid therapy is not considered
beneficial for GBS); Odaka at 916; Van Doorn at 939-50.

        Recurrences or treatment-related fluctuations have been seen in individuals with GBS.
Hadden, R.D.M., Deterioration After Guillain–Barré Syndrome: Recurrence, Treatment-Related
Fluctuation, or CIDP?, 80 Neurol. Neurosurg. Psychiatry 3 (2009) (Pet’r’s Ex. 37) [hereinafter
“Hadden”]. A treatment-related fluctuation has been defined “as significant deterioration within
[two] months after disease onset, following post-treatment improvement or stabilization,” which
is thought to occur as a result of “relatively prolonged autoimmune activation outlasting the
effect of treatment.” Id. Recurrent GBS is distinguished from CIDP by “very long asymptomatic
periods with return of tendon reflexes, more frequent antecedent illness, rapid onset, frequent
facial weakness and normal CSF protein within [one] week of onset.” Hadden at 3; Odaka at
916.

       Both experts generally agreed on the above, but had slightly different interpretations of
various elements of the two diseases. Dr. Steinman expressed the view that GBS and CIDP are
on the same spectrum – with AIDP simply constituting a more acute form of demyelinating
polyneuropathy than CIDP. Tr. at 61-62, 64; see also Marinos C. Dalakas, Advances in the
Diagnosis, Pathogenesis and Treatment of CIDP, 7 Nature Reviews Neurol. 507-17 (2011)
(Resp’t’s Ex. J) [hereinafter “Dalakas”]. He thus suggested that distinguishing between the two
based on onset and/or length of progression of symptoms reflected an “arbitrary separation from
subacute and chronic demyelinating polyradiculoneuropathy.” Tr. at 65 (quoting Richard A.C.
Hughes & Jeremy H. Rees, Clinical and Epidemiologic Features of Guillain-Barré Syndrome,
176 (Supp. 2) J. Infectious Diseases S92 (1997) (Resp’t’s Ex. L at 2)).52 Nevertheless, Dr.
Steinman acknowledged that “CIDP differs from GBS [] by its time course, mode of evolution,
prognosis, and responsiveness to steroids.” Tr. at 64.

       Dr. Steinman asserted that the presenting symptoms for each disease were different.
Thus, areflexia and symmetry are classic aspects for the presentation of an individual with CIDP,
                                                            
52
  Dr. Steinman elaborated on this point by suggesting that neurologists are famous for wanting to either “lump or
split” (see Tr. at 62), and thus temporal distinctions between the progressions of both conditions reflected a desire by
neurologists responsible for defining clinical facets of each to “draw the line” rather than meaningfully distinguish
what are otherwise closely-related illnesses. Id. at 65.


                                                               30 
 
but not necessarily present in a patient with GBS. Tr. at 66, 68. He further testified that in his
experience it typically takes areflexia approximately one month to six weeks to develop in an
individual with CIDP, after which reflexes would not return. Id. at 66. As a result, Dr. Steinman
indicated that he would be reluctant to diagnose a patient that had reflexes with CIDP – and he
would view a patient whose reflexes recovered, but whose other related symptoms had not
dissipated and appeared chronic, as still recovering from AIDP, rather than as manifesting CIDP.
Id. at 63-64.

        Dr. Chaudhry, by contrast, emphasized that in his view (which he testified was consistent
with the view of “all neuromuscular physicians”), CIDP and GBS represent two separate (if
related) conditions rather than opposing points on the same disease spectrum – and that as such it
would be incorrect to view CIDP simply as a chronic form of GBS. Tr. at 208-09. Rather, they
are distinguishable in terms of their presentation, treatment, and prognosis. Id. at 208. Thus, GBS
(and its most common variant in the Western world, AIDP) is characterized by its rapid and
acute progression, with subsequent slow recovery over a period of time – there is typically no
waxing and waning course.53 Id. at 202-04. He also noted that IVIG is currently the standard
treatment for GBS. Id. at 204-05.

        CIDP patients also experience weakness and numbness, exhibit loss of reflexes, exhibit
high spinal fluid proteins, and demyelination under conduction. Tr. at 206. A distinguishing
characteristic of CIDP, however, is its chronic nature, defined by lengthy relapsing and remitting
phases.54 Id. Dr. Chaudhry expressed the view that the clinical diagnostic definition of CIDP as
needing to last at least eight weeks was misleading – in his experience the course of illness is
typically far longer. Id. at 206-07. Indeed, Dr. Chaudhry testified that he has observed patients
with CIDP see their progression of symptoms take more than a year to get to the point where
treatment was considered or warranted. Id. Dr. Chaudhry also stressed the significance of
prednisone as highly indicated for the successful treatment of CIDP. See generally Id. at 205-
07.55 According to Dr. Chaudhry, Prednisone is not used to treat GBS – and in Dr. Chaudhry’s
opinion it would be malpractice to administer it to a GBS patient. Id. at 236.
                                                            
53
   Dr. Chaudhry acknowledged that there is a subcategory of GBS referred to as “relapsing Guillain-Barré,” but he
testified that in his view this diagnostic classification is limited to those patients who have an attack of GBS, recover
completely, and then have another attack months or years later. Tr. at 257.

54
  In fact, Dr. Chaudhry stated, CIDP typically lasts throughout an individual’s lifetime, with most patients requiring
ongoing treatment, although a few patients do go into remission (approximately one-third probably less). Tr. at 207.
55
   A distinct diagnostic criterion for CIDP (at least in 1975 when it was first described by Dr. Peter Dyck), before the
availability of physiology and nerve conduction studies, was steroid responsiveness to a patient’s symptoms. Tr. ay
205-06. Dr. Chaudhry noted that CIDP was actually termed “steroid responsive chronic relapsing remitting
polyneuropathy” in the landmark 1975 paper in the journal Neurology. Id. at 206. Other medications used for
treatment of CIDP (CellCept, Rituximab, Imuran, and Cyclosporine), Dr. Chaudhry testified, do not have evidence-
based medicine supporting their effectiveness, but are often employed because they can have a steroid-sparing effect
(allowing for a reduction in the amount of steroid that is required to be taken by the patient). Id. at 207.

                                                               31 
 
              2.     Petitioner’s Medical History Suggests Her Actual Illness was CIDP –
Although there is contradictory evidence in the medical records, those record by themselves
(viewed in their totality and without the benefit of expert interpretation) suggest that Ms.
Blackburn more likely than not suffered from CIDP, rather than the AIDP variant of GBS.

        Ignoring for the moment Ms. Blackburn’s pre-vaccination medical history,56 the records
establish that Ms. Blackburn began experiencing symptoms no earlier than August of 2009.
Pet’r’s Ex. 2 at 9-11; Pet’r’s Ex. 8 at 4-5. Even after intense treatment in August and September
of 2009, however – about eight weeks after Ms. Blackburn’s HPV vaccination (a period almost
twice as long as the four-week onset of GBS symptoms in most cases (see, e.g., Koningsveld at
138)) – it became evident that Ms. Blackburn was again ill. Pet’r’s Ex. 7 at 14-15; Pet’r’s Ex. 5
at 363.

        Her symptoms continued to wax and wane well into the spring of 2010, nine months
later. Pet’r’s Ex. 7 at 6-7. Indeed, the very fact that Petitioner continued to experience symptoms
despite the initial AIDP diagnosis and immediate treatment specific to that illness was a factor
that lead Dr. Bromberg to conclude that she likely was suffering from CIDP. Id. at 2, 8-9.
Because AIDP and CIDP can be confused in their early stages, it is not surprising that the
treating physicians who first examined Ms. Blackburn between August and October of 2009
reached different conclusions from those treating her six months later.

        The successful alteration of Ms. Blackburn’s treatments also strongly supports the CIDP
diagnosis. By April 2010, the fact that Ms. Blackburn’s symptoms had still not fully cleared
prompted Dr. Bromberg to try a prednisone course, based on the reasonable medical inference
that a demyelinating condition that waxed, waned, and/or relapsed over several months was not
sufficiently acute or monophasic to constitute a GBS variant. Pet’r’s Ex. 7 at 8. The medical
literature strongly associates prednisone with the successful treatment of CIDP. See, e.g.,
Dalakas at 508. And in fact the prednisone worked. Pet’r’s Ex. 7 at 2-4.

       Petitioner unconvincingly objects to the CIDP diagnosis that the medical history reflects.
She argues that I should give great weight to the views of some treating physicians (in particular,
those who treated Ms. Blackburn in the two to three months after her vaccination and/or made
                                                                                                                                                                                                
56
    Ms. Blackburn’s pre-vaccination history lends some support to the CIDP diagnosis. She first reported foot and
hand numbness in October 2008 (see Pet’r’s Ex. 4 at 2-3), and complained of numbness and tingling on the actual
vaccination date in July 2009 (see Pet’r’s’ Ex. 2 at 11-12) – suggesting her condition existed for a long time prior to
its significant flare-up in August 2009 (see Id. at 9-10). Admittedly, however, Ms. Blackburn’s pre-vaccination
treatment history also contains evidence less supportive of CIDP, as certain clinically-significant diagnostic clues (in
particular, areflexia) did not point toward any severe neuropathy (see, e.g., Pet’r’s Ex. 8 at 18), and her post-
vaccination symptoms were self-evidently more severe than what she had experienced in the months before. Pet’r’s
Ex. 2 at 9. I therefore do not find that the pre-vaccination medical history (taken alone, without the assistance of an
expert’s review) is particularly strong evidence for either side’s position – although, when expert interpretation of
that record is added to my analysis, the pre-vaccination history becomes far more significant. 

                                                                                             32 
 
the initial AIDP diagnosis) but not others. Tr. at 118-19, 126-28. Petitioner particularly maintains
that the determinations of Dr. Whitesell (which the record unequivocally establishes were made
within a month or two of Ms. Blackburn’s vaccination) should predominate over a determination
made by Dr. Bromberg – despite the fact that Dr. Bromberg’s evaluations and observations took
into account what had happened during the months that had passed from the time Ms. Blackburn
first complained of post-vaccination symptoms.

        Unquestionably the views of treating physicians are important, but they are also properly
subject to evidentiary weighing. Capizzano, 440 F.3d at 1326. The overall course of Ms.
Blackburn’s treatment history supports giving less weight to the determinations of the treating
physicians who first saw her. Dr. Whitesell and others reached immediate conclusions about the
nature of Ms. Blackburn’s illness without the benefit of the evidence Dr. Bromberg later relied
on, including the results of trying a different medication used almost exclusively for CIDP.
Significantly, there is nothing in the record suggesting that any other treating physicians who
saw Ms. Blackburn after the prednisone’s efficacy was established in treating her symptoms
disagreed with Dr. Bromberg’s conclusion regarding her diagnosis. Dr. Whitesell’s initial
diagnosis of AIDP may, at the time, have been reasonable and supportable based on the
immediate evidence at hand – but ultimately it proved incorrect.57

        All in all, I must consider the treatment record as a whole in evaluating the evidence
offered to establish Petitioner’s illness. § 13(a)(1). Here, the record alone supports the conclusion
that the corrected diagnosis – CIDP – was more accurate, given (a) the relapsing course of Ms.
Blackburn’s symptoms, and (b) the effectiveness of the prednisone treatment.

                3.      Respondent’s Expert Persuasively Confirmed Both the CIDP Diagnosis
and its Pre-Vaccination Onset – In a case such as this, where expert testimony is offered to
interpret medical records and/or contemporaneous tests performed on the petitioner, a special
master necessarily determines the persuasiveness of each competing expert. See, e.g., Carrino v.
Sec’y of Health & Human Servs., No. 08-0266-V, 2013 WL 3328903, at *11-20 (Fed. Cl. Spec.
Mstr. June 6, 2013) (finding Respondent’s expert’s review of medical history and specific test
results more persuasive than Petitioner’s expert’s review, in connection with determination that
Petitioner did not suffer from GBS). This flows naturally from a special master’s duty to evaluate
expert credibility in the process of weighing the evidence. Porter v. Sec’y of Health & Human
Servs., 663 F.3d 1242, 1250 (Fed. Cir. 2011) (“[t]he Federal Circuit has “unambiguously
explained that special masters are expected to consider the credibility of expert witnesses in
evaluating petitions for compensation under the Vaccine Act”).



                                                            
57
   I also note that Dr. Whitesell’s opinion was itself somewhat qualified, conclusory, and not corroborated with any
explanatory basis. See, e.g., Pet’r’s Ex. 3 at 66 (“I feel that this likely still represents slowly improving Guillain-
Barré which can sometimes have a waxing and waning course . . . I feel that an alternative diagnosis of CIDP is less
likely”).

                                                               33 
 
        Both experts were qualified to testify to the matters in dispute generally, but Dr.
Chaudhry was better qualified than Dr. Steinman to opine on the nature and treatment of GBS
and CIDP, and his testimony was more credible. His demonstrated, day-to-day experience in
seeing patients and reviewing the results of tests most relevant to diagnosing demyelinating
diseases rendered his opinion particularly trustworthy. He also persuasively grappled with the
record, acknowledging contrary evidence rather than dismissing it out of hand. Dr. Steinman, by
contrast, has had far less direct experience with GBS or CIDP patients over the past several
years, and less frequently reviews the results of (let alone performs) EMGs and nerve conduction
studies. His core competency is with MS and central nervous system diseases. While such
illnesses have some relationship to the matters in dispute (as they also involve demyelinating
conditions with some common symptoms) they are not equivalent. Petitioner called upon Dr.
Steinman in this case to wear two hats as an expert – that of a diagnostic expert as well as a
theory/Althen prong one expert – but the latter fit him far better than the former, and I found him
less persuasive on diagnostic topics.

        Dr. Steinman’s reduced expertise on matters pertaining to the diagnosis and treatment of
peripheral neuropathies was evident during the hearing (and particularly when he attempted to
minimize the impact of evidence harmful to the Petitioner’s case). For example, Dr. Steinman
strained in arguing that there was nothing notable about the positive results of Ms. Blackburn’s
prednisone treatments, asserting that corticosteroids were simply another option for any GBS-
related illness, and would invariably make a patient feel better regardless of their clinical impact
on the underlying disease. Tr. at 73. But this is contrary to the medical literature submitted by
both parties, all of which strongly suggests that prednisone is indicated only for the treatment of
CIDP. Indeed, Dr. Chaudhry (who plainly possesses substantially more experience in diagnosing
and treating both GBS and CIDP) characterized the use of prednisone for treatment GBS patients
as medical malpractice.

        Dr. Steinman was similarly unpersuasive in his effort to frame CIDP as little more than a
severe, lasting case of AIDP. Tr. at 62. While it is true that the two diseases have much in
common and (especially early in their course) can be easily confused, they are distinguishable –
and, given the difference in treatment and prognosis, need to be distinguished in order to better
assist patients in recovering from either. See, e.g., Koningsveld at 138; Odaka at 913, 916. But
Dr. Steinman did not establish that the recurrence and persistence of Ms. Blackburn’s symptoms,
after her seemingly successful treatment in August through September of 2009, was properly
attributed to either treatment fluctuations or a “recurring” form of AIDP. The medical record in
fact does not suggest that any treatment related fluctuations occurred.58 And beyond some
                                                            
58
   Notations in Ms. Blackburn’s medical records indicate that she received “2 g/kg of IVIG treatment over three
days” (Pet’r’s Ex. 7 at 7) and there is also a notation taken from pharmacy records stating that she “received 35
g[rams] of IVIG on 08/25/2009, 35 g[rams] of IVIG on 08/26/2009, and 30 mg of IVIG on 08/27/2009.” Id. at 25.
Dr. Chaudhry noted that there appeared to be a typographical error in the pharmacy notation – Ms. Blackburn would
have more likely received 30 grams (not milligrams) for her final IVIG dose, adding up to a total dosage of 100
grams. Tr. at 224. In Dr. Chaudhry’s view, this is consistent with the standard dose for someone of her stature (as

                                                               34 
 
medical literature stating that a fluctuating form of AIDP exists, the only support for this
alternative diagnosis is Dr. Steinman’s ipse dixit, rather than evidence drawn from the record.

        Dr. Steinman failed to provide an overarching explanation for Ms. Blackburn’s illness
based on the totality of her medical history. Thus, he placed excessive reliance on Dr.
Whitesell’s October 2009 determination that CIDP was not likely the correct diagnosis for
Petitioner – while giving less weight to the subsequent determination of Dr. Bromberg (as well
as every other treating physician thereafter) that CIDP was in fact the correct diagnosis. Dr.
Whitesell’s opinion itself contains no record support or corroboration explaining why she
discounted the possibility of a CIDP diagnosis. See Pet’r’s Ex. 3 at 66. Dr. Bromberg, by
contrast, had the benefit of months more of evidence regarding Petitioner’s condition, plus the
fact that the test he proposed for determining if CIDP were the correct diagnosis (the prednisone
treatment) worked. Dr. Steinman generally found more significant the initial diagnosis Ms.
Blackburn received – a diagnosis that circumstances, and time, reasonably led her subsequent
treating providers to re-evaluate. See, e.g., Pet’r’s Ex. 7 at 8. Dr. Steinman’s interpretation
favored the position that once AIDP had been diagnosed, it remained the “correct” diagnosis
even if later treatment evidence contradicted it. Tr. at 63.

        Dr. Steinman was also selective in what symptoms he deemed significant versus those he
ignored. Thus, he overemphasized areflexia as a symptom of CIDP (thus rendering its absence
from Ms. Blackburn’s pre-vaccination medical history a telling fact).59 Yet the literature offered
by the parties more definitively identifies areflexia as a presenting symptom of GBS. See, e.g.,
Burns at 3 (in GBS, “[w]idespread areflexia or hypoflexia is the rule”); Amato at 214 (Pet’r’s Ex.
33 at 2). In so doing, Dr. Steinman ignored the fact that Ms. Blackburn did not display upper
limb areflexia as of mid-August 2009 (see Pet’r’s Ex. 4 at 4-5), even though she would then have
reached, if not be approaching, the nadir of her GBS (assuming, as Dr. Steinman opined, that her
illness began with her July vaccination). At the same time, Dr. Steinman consistently
downplayed the importance of cranial nerve weakness or dysfunction as a presenting symptom
of GBS (Tr. at 71) – even though it is considered such (Van Doorn at 939-50) – and thus
sidestepped the fact that Ms. Blackburn never displayed this particular symptom during her
purportedly acute AIDP phase in August and September of 2009. Tr. at 91.



                                                                                                                                                                                                
the medical records indicate that she was five foot four inches and weighed approximately 104 pounds around this
period of time. Id.; see also Pet’r’s Ex. 7 at 12. The medical literature corroborates Dr. Chaudhry’s view. See, e.g.,
Dyck & Thomas at 642-43. Nothing else in the record indicates that Ms. Blackburn did not receive a full course of
IVIG.
59
   In any event, as Dr. Chaudhry later explained, individuals suffering from CIDP often experience a slow, long-term
ramping up of the illness, during which common presenting symptoms might remain mild for a long period of time,
and therefore the absence of clear areflexia before vaccination does not discredit the ultimate conclusion (bulwarked
by a comprehensive review of the record) that CIDP was the correct diagnosis. Tr. at 206-7.
 

                                                                                             35 
 
        Dr. Chaudhry, by contrast, rooted his opinion in a complete view of the record. Having
treated numerous CIDP patients (Tr. at 196-97), he was well qualified to observe that a patient
may experience a number of mild neuropathic symptoms long before they are actually diagnosed
with CIDP (and even before such a diagnosis might be proper). Id. at 206-07, 226. Because of
the chronic nature of their symptoms, CIDP patients can “live” with the condition without
hospitalization for a long time, as opposed to the acute, fast-moving nature of AIDP. Dr.
Chaudhry credibly explained why Ms. Blackburn’s early examinations and test results did not
display all of the formal clinical indicia of CIDP. Id. at 212-13.60 There were enough other signs
to see, in retrospect, a relationship between Ms. Blackburn’s pre-vaccination neuropathic
symptoms and her illness’s subsequent course. Id. at 227, 249-50.

        Dr. Chaudhry was also persuasive in identifying inconsistencies in Ms. Blackburn’s
history from August to September 2009 that undercut the initial AIDP diagnosis. Through his
reading of contemporaneous EMG test results, he pointed out convincingly that early symptoms
and test results actually better supported the CIDP diagnosis – the nerve damage, for example,
evident from Ms. Blackburn’s August EMG (see Pet’r’s Ex. 4 at 7) was too extensive to have
occurred in the weeks immediately after her July 23rd vaccination, but was more likely evidence
of a pre-existing illness that had to have begun before that date. Tr. at 216, 218.

        At bottom, Dr. Chaudhry was more persuasive in commenting on what was (or was not)
relevant in diagnosing GBS and CIDP – based on evidence from contemporaneous medical
records before and after Petitioner’s vaccination. In so doing, he convincingly offered an
interpretation of the medical history that Petitioner has not rebutted – that it is improbable that
Petitioner suffered from AIDP only beginning with her Gardasil vaccination.

              B.             Application of Althen Prongs

        Although my determination that Ms. Blackburn did not suffer from AIDP, and that her
illness began before her vaccination, potentially obviates the need for an extensive Althen
analysis, I nevertheless consider below each of its prongs based on the evidence presented.

                 1.      Prong One: Can the HPV Vaccine Cause GBS and/or CIDP? Petitioner
offered little direct evidence supporting her theory that HPV vaccine can cause GBS, other than
VAERS reports,61 or research and case studies involving other vaccines which Petitioner argues

                                                            
60
     Respondent’s medical literature supported the idea that areflexia is not necessarily a sine qua non symptom of
CIDP even if it is associated with the disease. See, e.g., Dalakas at 2-3 (CIDP characterized generally by “a
progressive, symmetric, proximal and distal muscle weakness, paresthesias, sensory dysfunction, and impaired
balance”).
 
61
     “VAERS” refers to the Vaccine Adverse Event Reporting System. The value of a specific VAERS report as
evidence in proving causation in a Vaccine Program case is extremely limited. As another special master has
observed,


                                                               36 
 
are analogous.62 There is, however, persuasive scientific evidence on the other side of the
question. As Dr. Steinman admitted, the Institute of Medicine (“IOM”) has determined that
“[t]he epidemiologic evidence is insufficient or absent to assess an association between HPV
vaccine and GBS.” Tr. at 81-82; see also Adverse Effects of Vaccines at 512.63 Nevertheless,
there is no specific category of evidence that a petitioner must offer to establish a medical theory
supportive of a causation finding (Althen, 418 F.3d at 1280), and therefore Petitioner’s inability
to marshal this kind of specific scientific proof does not mean she cannot meet the requirements
of the first Althen prong.

        Molecular mimicry theories have been accepted in other Vaccine Program cases as a
general framework for explaining the development of certain autoimmune diseases (although
such acceptance has not always resulted in entitlement decisions favorable to petitioners).
Tompkins v. Sec’y of Health & Human Servs., No. 10-261V, 2013 WL 3498652, at *22 (Fed. Cl.
Spec. Mstr. June 21, 2013) (“[t]he molecular mimicry theory is the one most widely accepted for
the agents most frequently accepted as causal”), motion for review den’d, Tompkins v. United
States, 117 Fed. Cl. 713 (2014). Dr. Whitton conceded that molecular mimicry may explain
vaccine-induced demyelinating injuries, as long as its basic requirements are met (Tr. at 362),
and Respondent ultimately did not seriously question that this theory offers a potential
explanation for how autoimmune diseases like GBS develop. See Resp’t Mem. at 23-27. But
accepting that molecular mimicry has previously been found to be a reasonable general theory64

                                                                                                                                                                                                
              VAERS is a stocked pond. It only contains reports (many of which are unverified or incomplete) of adverse
              events after vaccinations. VAERS contains no reports or data about the relative rate of these same events in
              individuals who have not been vaccinated. Thus, the number of specific adverse events, such as GBS,
              reported after any vaccine, is meaningless without information about the background rate of that adverse
              event and information about the number of vaccines administered.

Tompkins v. Sec’y of Health and Human Servs., No. 10-261V, 2013 WL 3498652, at *16 (Fed. Cl. Spec. Mstr. June
21, 2013), motion for review den’d, Tompkins v. United States, 117 Fed. Cl. 713 (2014).
62
   Respondent also questioned Petitioner’s reliance on research pertaining to central nervous system diseases, such
as MS in humans and EAE in rodents. Resp’t’s Pre-Hr’g Mem. (ECF No. 62) at n. 7. Respondent further questioned
the evidence showing homology between Y and F in mouse models, arguing that it did not constitute scientifically
reliable evidence that they are interchangeable when dealing with human models. Respondent’s Reply to Pet’r’s
Post-Hr’g Brief (ECF No. 79) at 5. While acknowledging that animal models have been found to be sufficient in
some Vaccine Program cases, I do not specifically address this contention as it does not have a direct bearing on my
decision in this case.
63
   IOM evidence is especially reliable and useful in gauging whether a vaccine “can cause” a given injury. See
generally Crutchfield v. Sec’y of Health & Human Servs., No. 09-0039V, 2014 WL 1665227, at *16 (Fed. Cl. Spec.
Mstr. Apr. 7, 2014) (“[d]uring the 25–year history of the Vaccine Act, special masters have consistently relied upon
the reports of the Institute of Medicine, and reviewing judges have consistently indicated approval of such
reliance”).
64
   I do not mean to say that the molecular mimicry theory is in all cases reasonable. On the contrary – the theory has
at times been misused by certain experts, who have invoked it as a universal mechanism that can explain virtually
any demyelinating or other autoimmune condition. See, e.g., Hennessey v. Sec'y of Health & Human Servs., 91 Fed.

                                                                                             37 
 
does not complete my analysis under Althen prong one – the theory offered must have
application to this case. See Caves, 100 Fed. Cl. at 135 (noting that the Althen requirement to
offer medical theory would be meaningless if petitioner did not need to apply molecular mimicry
specifically to her case); Broekelschen, 618 F.3d at 1345.

       Respondent generally questioned whether Dr. Steinman’s corrected-on-the-witness-stand
homology theory (which posits a mechanism for how the HPV vaccine could result in a
peripheral neuropathy) has been shown to be scientifically reliable. Resp’t Pre-Hr’g Mem. (ECF
No. 62) at 18; Tr. at 168-69. A petitioner need not necessarily demonstrate the precise homology
involved when invoking molecular mimicry as the mechanism for explaining how a particular
vaccine could cause injury. See, e.g., Salmins v. Sec’y of Health & Human Servs., No. 11-140,
2014 WL 1569478 (Fed. Cl. Spec. Mstr. Mar. 31, 2014) (granting entitlement in HPV/GBS case
when petitioner relied on molecular mimicry without showing homology). But because the
homology question was hotly disputed, I will review the evidence on the point pro and con.

        Dr. Steinman’s homology theory is inconsistent – particularly the manner in which he
conflates autoimmune responses involving antibodies produced by B cells with those involving T
cells. See Tr. at 17, 46; Pedro J. Ruiz et al., Microbial Epitopes Act as Altered Peptide Ligands
to Prevent Experimental Autoimmune Encephalomyelitis, 189 J. Experimental Med. 1275 (1999)
(Pet’r’s Ex. 21). The medical literature cited by the parties does not support the notion that this
homology “works” regardless of whether the autoimmune response involves T cells or B cell
antibodies.65 If limited to the context of T cell mimicry, however, there is better support for his F
and Y equivalence argument in the context of an attack on MBP.66 Tr. at 157-60.

                                                                                                                                                                                                
Cl. 126, 134-35 (2010) (noting expert’s overly broad application of the molecular mimicry theory made it
meaningless).
65
   In his expert reports and testimony, Dr. Steinman invoked Wucherpfennig for the proposition that the FKN
sequence is of particular importance to the homology between T cells and B cell antibodies, on the one hand, and
MBP on the other. Tr. at 44. He then immediately jumped to a different study (Grada M. van Bleek & Stanley G.
Nathanson, The Structure of the Antigen-Binding Groove of Major Histocompatibility Complex Class I Molecules
Determines Specific Selection of Self-Peptides, 88 Immunology 11032 (1991) (Pet’r’s Ex. 32) [hereinafter “van
Bleek”]) to support his assertion that F and Y are “pretty much interchangeable.” Tr. at 46-47. The van Bleek study,
however, demonstrates only that Y and F are interchangeable in the specific context of binding T cells to mouse
MHC class I molecules. Van Bleek at 11035.

Dr. Whitton challenged the relevance of this study to humans (Tr. at 305-06), referencing Wucherpfennig (Pet’r’s
Ex. 18 at 1117-18) to demonstrate that substituting Y for F has a “profound effect on immune recognition” in
humans. Tr. at 311. The Wucherpfennig study specifically finds that F and Y are not interchangeable in the context
of human autoantibody recognition. Wucherpfennig at 1116. Indeed, Wucherpfennig suggests that a YKN sequence
is too limited to trigger cross-reactive antibodies (even assuming arguendo that F and Y were interchangeable),
because “autoantibody recognition of microbial peptides required sequence identity over a stretch of four or five
amino acids.” Id. at 1119.
66
  The HFFK sequence of MBP is its “core motif” recognized within the T cell epitope. Pet’r’s Ex. 21 at 1275.
Within this sequence, “K91 is the major TCR contact site, while F90 is a major anchor to MHC.” Id. Thus, the cited
medical literature supports the concept that the two-acid FK sequence is indeed critical, and that limited peptide

                                                                                             38 
 
       Respondent argued that the FK/FY sequence is too common. Tr. at 313-14. If a two-
protein homology is sufficient for cross-reactivity, she asserted, then the majority of microbes
could serve as the basis for molecular mimicry in so many circumstances that the theory would
be “so broad as to be meaningless.” Hennessey, 91 Fed. Cl. at 135; Tompkins, 2013 WL
3498652, at *23. Petitioner responded that because structural similarity is what drives Dr.
Steinman’s molecular mimicry theory, little sequential homology is required for T cell mimicry
to occur. See Rafael L. Ufret-Vincenty, In Vivo Survival of Viral Antigen-Specific T Cells that
Induce Experimental Autoimmune Encephalomyelitis, 188 J. Exp. Med. 1726 (1998) (Pet’r’s Ex.
23).

        Respondent also challenged the precise mechanism offered by Petitioner to explain how
the autoimmune process resulting in GBS would function. Dr. Steinman’s homology analysis
depends upon MBP as the target antigen. See, e.g., Pet’r’s Pre-hr’g Mem. (ECF No. 60) at 15-16;
Tr. at 162-63. But as Dr. Whitton testified, available scientific evidence (reflected in the
literature offered in this case) suggests that MBP is not the target antigen in autoimmune
responses that result in a peripheral neuropathy like GBS. Tr. at 317, 327. Rather, other protein
structures on the peripheral myelin have been demonstrated as far more likely targets of a
demyelinating process. Id. at 290-94. Indeed, the “most solid evidence for a molecular mimicry”
mechanism producing GBS (as Dr. Steinman acknowledged) involves an immune response
against gangliosides. Id. at 162-63 (Dr. Steinman admitting that studies of the “Campylobacter
story” involve attacks against gangliosides, “a different molecular mimic” from MBP);
Komagamine at 394; see also Daily v. Sec’y of Health & Human Servs., No. 07-173V, 2011 WL
2174535, at *3 (Fed. Cl. Spec. Mstr. May 11, 2011) (“[a] large body of literature links
gangliosides and antibodies against certain gangliosides as causal agents of GBS”).

        In support of her contention that MBP is the target antigen, Petitioner offered only the
Cornblath study, which found increased MBP in the spinal fluid of patients suffering from GBS.
Tr. at 162; Cornblath at 370. But the Cornblath study does not conclude that MBP is the target
antigen in GBS – as Dr. Steinman admitted. Id. at 371; see also Tr. at 30-31, 162-63, 288-89.
MBP is simply one of many other proteins and structures contained in peripheral myelin, and has
been found to be released after the destruction of that myelin. Tr. at 180; Steinman, L. &
Oldstone, M.B.A., More Mayhem from Molecular Mimics, 3 Nature Medicine 1322 (1997)
(Pet’r’s Ex. 20). Otherwise, none of the medical literature cited by Petitioner identifies MBP as a
potential target of an immune response that triggers GBS. See Amato at 217 (“[t]he nature of the
epitope is not known but probably is a glycolipid”); Komagamine at 394-95 (listing candidate
target molecules but omitting MBP). Nor has Petitioner offered any instances in which MBP as
the target antigen has been tested (at least in the context of a peripheral neuropathy like GBS).
                                                                                                                                                                                                
substitutions (such as Y for F) would not necessarily hinder the activation of cross-reactive T cells with homologous
protein sequences comprising MBP. Wucherpfennig at 1116, 1119-21.


                                                                                             39 
 
Petitioner otherwise relied on studies establishing attacks on MBP pertaining to MS rather than
peripheral neuropathies like GBS. Tr. at 283-86.67

       Overall (and despite the fact that precise homology has not been required in other cases
to successfully establish a medical theory in satisfaction of the first Althen prong), I found the
evidence offered by Petitioner in support of her molecular mimicry theory to be less persuasive
than Respondent’s arguments to the contrary. However, even if I assume for sake of argument
that Petitioner has offered just enough probative and reliable evidence to establish this first
element of the causation test, such a determination would not aid her case. Hirmiz, 2014 WL
4638375, at *14. Because Ms. Blackburn has not demonstrated that she suffered from a vaccine-
caused injury (give the above-discussed CIDP diagnosis and evidence that it predated her
vaccination), the fact that the HPV vaccine could in theory cause a GBS variant other than the
disease she actively suffered from is irrelevant to meeting her burden of proof.68

                2.      Prong Two: Did the HPV Vaccine Cause Ms. Blackburn’s GBS and/or
CIDP? – There is support in the treatment record establishing a “logical sequence of cause and
effect” between the receipt of the HPV vaccine and the demyelinating symptoms Ms. Blackburn
later suffered – assuming GBS were her illness, and that it arose only after the vaccination. At a
minimum, the record contains statements by Ms. Blackburn’s treating physicians that
Petitioner’s initially-diagnosed AIDP was caused by her vaccination – and although many of
those opinions seem based on the timing between vaccine and injury, that fact alone does not
render their opinions without value.

        My determination that Ms. Blackburn’s illness was more likely than not CIDP rather than
GBS, and that it predated her vaccination, however, precludes a finding that the Gardasil vaccine
likely caused her injury. This determination is based on expert testimony and the treating
records, which clearly reflect that Petitioner’s diagnosis was ultimately changed and has never
been changed back since the time Ms. Blackburn received prednisone. The same evidence
supports the conclusion that her illness more likely than not predated her vaccination, given the
history of the neuropathic symptoms she has suffered.

              Petitioner was unable to rebut the above. Thus, while she pointed out facts from the
                                                            
67
   Those studies were also distinguishable for other reasons. For example, as Dr. Whitton noted, some involved
experimentally-induced immune reactions (Tr. at 281-82) that were intended to produce central nervous system
diseases like MS by significantly amplifying the intensity of the immune response – and therefore it was telling that
they did not also produce a similar response in the peripheral nerves. Id. at 286-87, 325. Dr. Steinman himself
ultimately admitted that EAE is not an acceptable model for GBS. Id. at 27, 169-70. At best, Dr. Steinman
mentioned during his testimony an eighty year-old purported study, in which he claimed EAE-mice were found to
have diseases of both the peripheral and central nervous system. Id. at 58. But that study was not filed in this case
and has not otherwise been identified by Petitioner.
68
   I also note that Petitioner’s Althen one theory does not address the idea of CIDP as being caused by the HPV
vaccine – and indeed, Dr. Steinman strenuously challenged the accuracy of the CIDP diagnosis generally (even
while asserting that his theory worked in either case).

                                                               40 
 
treatment record that reasonably led Ms. Blackburn’s treating providers to assume at the outset
that she suffered from AIDP, she failed to explain the overall thrust of the record – and in
particular the waxing and waning course of the disease she experienced – beyond some general
references to “fluctuating” GBS. Nor did she rebut the effectiveness of the prednisone
treatments, or the changed diagnosis. Dr. Steinman for his part was too selective in his review of
the record, overemphasizing aspects of it that favor Petitioner’s case while not effectively
addressing the fundamental facts that point to CIDP as her real illness.

         My analysis would be the same even if Petitioner had accepted the revised CIDP
diagnosis but still argued that the HPV vaccination caused it. There is no question that Ms.
Blackburn experienced a flare-up of her symptoms temporally after receiving the Gardasil
vaccine – but it is well understood in Program cases that a mere temporal association between
vaccination and illness does not establish causation. Moberly, 592 F.3d at 1323. As CIDP is
clinically understood to involve a longer course, the relatively acute symptoms Petitioner
experienced in the weeks after the vaccination are not consistent with the chronic nature of the
illness, which would be slower to develop. And the neuropathic symptoms she experienced well
before (and even the day of) her July 23rd vaccination also suggest that her disease preceded her
vaccination.

                3.     Is there a Medically-Acceptable Temporal Relationship? – Less than a
month passed between Ms. Blackburn’s vaccination and the severe symptoms initially thought to
be caused by AIDP. See, e.g., Pet’r’s Ex. 8 at 4-5. In addition, the record indicates that a few of
her health care providers between August and October of 2009 believed (based on the
information they possessed at the time) that temporally the vaccine likely had caused the
symptoms they both observed and treated. See, e.g., Pet’r’s Ex. 4 at 9. Certainly there is support
(in both the relevant medical literature as well as the decisions of other special masters) for the
conclusion that the timeframe between vaccination and Ms. Blackburn’s temporally-subsequent
symptoms was medically acceptable – again, assuming she suffered from GBS. See, e.g., Corder
v. Sec’y of Health & Human Servs., No. 08-228V, 2011 WL 2469736, at *27-29 (Fed. Cl. Spec.
Mstr. May 31, 2011) (proposed four-month onset period from vaccination to GBS too long; two
months is longest reasonable timeframe).

        But Petitioner has not established that she more likely than not suffered from GBS. And
even if Petitioner had accepted the CIDP diagnosis and argued that it was caused by the July
2009 vaccination (rather than predating it), there would still be a lack of a medically-acceptable
temporal relationship, due to the fact that (as none of the parties disputed) the course of CIDP is
considerably longer than AIDP. CIDP would less likely become as acute (as the records establish
Ms. Blackburn’s illness was) within a month of vaccination, and no evidence offered by
Petitioner or her expert alters this conclusion. Thus, Petitioner’s claim also founders on her
inability to meet the third Althen prong.



                                                41 
 
                                       CONCLUSION

        I have great sympathy for the medical problems and related suffering Ms. Blackburn has
experienced over the past several years. However, a petitioner who fails to demonstrate by a
preponderance of the evidence that the vaccine she received was more likely than not the cause
of her illness is not entitled to compensation. Such is the case here. Because Ms. Blackburn has
failed to demonstrate that she in fact suffered from injuries caused by her receipt of the HPV
vaccine, I DENY an entitlement award in this case. I instruct the Clerk of Court to enter
judgment dismissing the case unless a motion for review is filed.


       IT IS SO ORDERED.



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




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