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. 
2

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 (§ 300aa13(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 
3

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. 
4

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. 
5

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 
6

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. 
7

 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. 
8

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. 
9

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. 
10

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 crossreactivity does not even lead to autoimmunity. Tr. at 161-62. 
11

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. 
12

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”]. 
13

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. 
14

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. 
15

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. 
16

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. 
17

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). 
18

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 postvaccination 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 
19

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. 
20

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 MBPspecific 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 
21

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). 
22

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. 
23

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); § 300aa13(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). 
24

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). 
25

 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. 
26

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 & 
27

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 
28

 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”].
29

 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 immunemediated, 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 
30

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. 
31

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 evidencebased 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. 
32

 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 postvaccination 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.
33

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 GuillainBarré which can sometimes have a waxing and waning course . . . I feel that an alternative diagnosis of CIDP is less 

likely”).
34

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 GBSrelated 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 
35

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. 
36

 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, 
37

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. 
38

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 
39

Respondent argued that the FK/FY sequence is too common. Tr. at 313-14. If a twoprotein 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. 
40

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 vaccinecaused 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). 
41

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. 
42

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