NORA BETH DORSEY, Special Master.
On February 12, 2010, D.S. ("petitioner") filed a petition for compensation under the National Vaccine Injury Compensation Program ("the Program" or "Vaccine Act"),
The parties submitted expert reports in support of their respective positions. Petitioner filed several expert reports from David Axelrod, M.D., an immunologist. Petitioner's Exhibits ("Pet. Ex.") 23, 40, 41, 43. Petitioner also filed expert reports from one of her treating neurologists, Steven H. Schechter, M.D. Pet. Exs. 56, 57. Respondent filed reports from Thomas Leist, M.D., a neurologist and neuroimmunologist. Respondent's Exhibits ("Resp't Ex.") A, G.
A hearing was held on August 20, 2014, during which the parties' experts testified. Petitioner filed a post-hearing brief on December 16, 2014. Respondent filed her post-hearing brief on December 23, 2014. The matter is now ripe for adjudication.
After a review of the entire record, the undersigned finds that petitioner has provided preponderant evidence that she developed the Miller-Fisher variant of GBS after her February 21, 2007 Gardasil vaccination. The undersigned also finds that petitioner has provided preponderant evidence that the Gardasil vaccine caused her to develop the Miller-Fisher variant of GBS, which satisfies her burden of proof under
In their joint prehearing submission filed on September 18, 2014, the parties presented several issues in dispute. To decide the case, the parties request that the undersigned first determine whether petitioner has presented preponderant evidence that she suffered from an onset of the Miller-Fisher variant of GBS or an autoimmune
Second, the parties request that the undersigned determine whether petitioner has presented preponderant evidence that she suffered from an identifiable, underlying medical condition
Third, the parties ask that the undersigned determine whether petitioner has presented preponderant evidence for each factor under
Finally, the parties request that the undersigned decide under
Thus, the parties have asked the undersigned to determine the nature of petitioner's injury and to determine whether the Gardasil vaccine caused or significantly aggravated that injury.
Petitioner filed her petition for compensation on February 12, 2010. Petition (ECF No. 1). Over the next year, petitioner filed the relevant medical records and certified completion of the record on January 28, 2011. ECF No. 30. On March 11, 2011, respondent filed her Rule 4(c) Report "(Resp't Rept.") stating that this case was not appropriate for compensation because petitioner had not presented sufficient evidence of causation under all three prongs of
Thereafter, the case proceeded on a dual litigation/settlement track where the parties proceeded with filing expert reports, while at the same time attempting to informally resolve the case. On November 29, 2011, petitioner filed an expert report from David Axelrod, M.D., and supporting medical literature. ECF No. 39. On February 10, 2012, respondent filed a responsive expert report from Thomas P. Leist, MD, PhD, along with his curriculum vitae and the medical literature references from Dr. Leist's expert report. ECF No. 47. On April 12, 2012, and May 8, 2012, petitioner filed additional supplemental expert reports from Dr. Axelrod. ECF Nos. 49, 52. The special master previously responsible for this case set a hearing for September 14, 2012. ECF No. 58.
Respondent filed another responsive expert report from Dr. Leist on August 13, 2012. Resp't Ex. G (ECF No. 66). A few days thereafter, petitioner's attorney filed a motion to withdraw as counsel due to his termination by petitioner. ECF No. 67. New counsel for petitioner filed a consent motion to substitute as counsel on August 21, 2012. The motion was granted. ECF No. 69. As a result of petitioner's retention of new counsel, the hearing previously set for September 14, 2012, was continued, and new deadlines were set for the filing of additional expert reports. ECF No. 70. The parties worked to resolve petitioner's application for an award of interim attorneys' fees and costs to her prior counsel, and a decision on interim fees was entered on November 16, 2012. ECF No. 78. This case was then reassigned to the undersigned special master on January 14, 2013.
The undersigned special master conducted a status conference with the parties on March 12, 2013. The parties were ordered to discuss whether an informal resolution of the case was appropriate. Petitioner's pending motion to file an additional expert report was also granted. ECF No. 85.
On May 1, 2013, and May 23, 2013, petitioner filed expert reports from her treating neurologist, Dr. Steven Schechter. ECF No. 89, 92. Petitioner also filed her own affidavit in support of her claim on June 6, 2013. ECF No. 93. At a status conference held on June 13, 2013, respondent's counsel indicated that respondent was not interested in pursuing informal resolution of this case and requested that the case be set for hearing. Deadlines were set for the filing of updated medical records and any additional expert reports. ECF No. 94. A hearing was set for March 19-20, 2014. ECF No. 95.
After filing several motions for enlargements of time, petitioner filed a supplemental expert report from Dr. Schechter on October 31, 2013. ECF No. 101. On December 9, 2013, respondent filed a supplemental report from Dr. Leist addressing the most recently filed medical records and Dr. Schechter's most recent report. ECF No. 102.
On March 14, 2014, due to an urgent issue, staff from petitioner's counsel's office contacted the court to request that the March 19-20, 2014 hearing dates be continued. Respondent had no objection. ECF No. 114. The hearing was rescheduled for August 20, 2014, and proceeded as scheduled. Petitioner testified on her own behalf, along with Dr. Axelrod and Dr. Schechter. During the hearing, petitioner's counsel presented a report from Dr. Axelrod (dated August 2012) that had not been filed into the record. Because respondent's counsel and respondent's expert, Dr. Leist, had not had the opportunity to review the report or the literature cited in that report prior to the hearing, the undersigned allowed respondent the opportunity to file a supplemental expert report after the hearing. After the hearing concluded, petitioner was ordered to file Dr. Axelrod's report and a deadline was set for respondent to file a responsive expert report.
A post-hearing status conference was held on August 25, 2014. At the status conference, petitioner's counsel stated that on the basis of the testimony heard at the hearing, petitioner was now interested in pursuing a significant aggravation claim. The undersigned ordered the parties to file an amended joint submission listing the significant aggravation claim as an issue in dispute. The parties were also encouraged to revisit settlement discussions and a deadline of September 24, 2014, was set for the petitioner to file a status report indicating that a demand had been sent to respondent. ECF No. 118. The parties filed the amended joint submission on September 18, 2014. ECF No. 124. Petitioner also filed a status report on September 22, 2014, stating that a demand had been sent to respondent. ECF No. 125.
On October 9, 2014, respondent filed a status report stating that respondent would not be filing a supplemental expert report from Dr. Leist, as respondent believed that Dr. Leist's prior reports and hearing testimony addressed the issues raised in Dr. Axelrod's August 2012 report. Respondent also stated that she would file a brief on the significant aggravation claim only if petitioner elected to pursue that issue and filed a brief. ECF No. 127.
On December 16, 2014, petitioner filed a post-hearing brief and a supplemental expert report from Dr. Axelrod in support of petitioner's significant aggravation claim. ECF Nos. 132-33. Respondent filed her post-hearing brief on December 23, 2014. ECF No. 134.
Petitioner was born on [REDACTED\], 1956.
On May 3, 2001, petitioner presented to William M. Leuchter, M.D. (neurologist), with complaints of acute hearing loss and migraine headaches. Pet. Ex. 17 at 209-10. Also in May 2001, petitioner presented to A. Martin Lerner, M.D. (an infectious disease specialist) with symptoms of right facial numbness, blurry eyesight, decreased hearing, and diagnoses of rheumatoid arthritis and fibromyalgia.
In a history provided by petitioner on June 12, 2001, and taken by Jeffrey D. Band, M.D., another infectious disease physician, petitioner noted that she had been in good health prior to 1993, but she thereafter developed fatigue, arthralgias, myalgias, and intermittent swelling of her glands and lymph nodes. Pet. Ex. 17 at 203-04. Petitioner explained that in more recent years, she developed right hearing loss and right visual changes.
An MRI of petitioner's brain and orbits was conducted on October 28, 2002, because of her continuing complaints of right eye pain. Pet. Ex. 17 at 97. The results were normal. On April 1, 2003, petitioner reported severe headaches and right hearing loss. Pet. Ex. 11 at 5. An MRA of petitioner's head on October 15, 2003, was negative for abnormalities. Pet. Ex. 17 at 96.
On January 7, 2004, petitioner reported that she was [REDACTED\] continuing her antibiotic treatment for Lyme disease and [REDACTED\] Pet. Ex. 11 at 4. A Lyme test on March 15, 2004, again did not meet criteria for seropositivity. Pet. Ex. 17 at 59.
On February 24, 2004, petitioner saw Robert W. Ike, M.D., a rheumatologist, who had regularly treated her for years. Pet. Ex. 17 at 211-13. Dr. Ike noted that he had not seen petitioner in nearly three years [REDACTED\]
On October 9, 2006, petitioner treated at the Michigan Ear Institute for complaints of worsening hearing loss, lack of balance with several falls in the past year, facial paresis and numbness, and a history of Lyme disease. Pet. Ex. 19 at 6-7, 17-18. The exam showed slight facial weakness on her right side.
[REDACTED\] Petitioner testified during the hearing that her doctor recommended that she received the HPV vaccine because it was "protective for all women." Transcript ("Tr.") at 9. She received one dose of the HPV vaccine at her next gynecological visit on February 21, 2007, at age 50 years. Pet. Ex. 11 at 2. There were no reported immediate side effects.
Petitioner testified that the onset of her symptoms began on April 1, 2007 (39 days after vaccination), when she started having a twitching sensation in her face and experienced extreme fatigue. Tr. at 9. She explained that the symptoms got "progressively worse" over the next couple of days and she felt like she was "being hit with a ton of bricks."
On April 4, 2007 (42 days after vaccination), petitioner presented to the William Beaumont Hospital ("WBH") ER with complaints that began the day before of a "frozen face," difficulty eating, swallowing, talking, and a headache, and a history of hearing loss, Lyme disease, and migraine. Pet. Ex. 10 at 12-14. On examination, petitioner had facial droop, implicating the right seventh cranial nerve.
Petitioner returned to the ER later that same day on April 4, 2007, with complaints of facial numbness and paralysis, an inability to swallow, and slurred speech, which started the prior day. She was admitted to the hospital at this time. Pet. Ex. 10 at 13-14, 16-17. The impression at admission was cranial nerve palsies.
The Patient Discharge Summary notes (which summarized each date of petitioner's hospitalization), stated for the April 5, 2007 hospitalization date, that petitioner was wearing a hearing aid on both sides, and that she had a history of rheumatoid arthritis, Lyme disease, deafness to her right ear, knee surgery, [REDACTED\] Pet. Ex. 10 at 223-24. In the physician admission history, it was noted that petitioner's symptoms started on April 4, 2007, and that she had a history of migraines [REDACTED\] Pet. Ex. 10 at 54. Facial numbness, very diffuse facial/cranial paresthesia, and dysphasia were all noted. Pet. Ex. 10 at 56.
The progress notes from WBH hospital dated April 5, 2007, state that petitioner [REDACTED\] she had difficulty with her vision, smiling, speaking, and hearing afterwards. Pet. Ex. 10 at 58. Dr. Lerner examined petitioner and noted that he had not seen petitioner in three years.
Saraswati A. Muttal, M.D., a neurologist consulted to evaluate petitioner for cranial nerve palsies, noted that petitioner reported an onset of ear pain and inability to close her eyes followed by loss of taste the day before coming to the hospital (April 3, 2007). Pet. Ex. 10 at 327. Petitioner's vital signs and physical exam were normal, with no motor weakness or sensory changes in her extremities, no ataxia, and normal tandem gait. Her deep tendon reflexes were normal at 2/4 bilaterally. Dr. Muttal mentioned that she was awaiting the results of an MRI of the brain.
A brain MRI, with and without contrast, was performed on April 5, 2007, and the results were compared to previous studies conducted in October 2002 and October 2003. Pet. Ex. 10 at 140-41. The results of the April 2007 MRI were read as within normal limits, [REDACTED\] The results of petitioner's brain MRA and MRV
On April 12, 2007, petitioner was seen by Myron Laban, M.D., a physiatrist, who noted petitioner's bilateral facial paralysis with improving function on the right but absent function on the left. Pet. Ex. 4 at 339-41. Dr. Laban stated that there was no evidence of ataxia and petitioner's proprioception was intact. Petitioner had no lower extremity weakness — her deep tendon reflexes were not tested. Dr. Laban noted that petitioner's EMG study was suggestive of bilateral neuropathy of the facial nerve. Dr. Laban felt that petitioner had a "classic presentation of Guillain-Barré [] syndrome of acute bilateral facial paresis."
Petitioner was discharged from WBH on April 16, 2007, by Dr. Lerner. Pet. Ext. 10 at 347. In the discharge summary, Dr. Lerner noted that petitioner was admitted to the hospital with a sudden inability to speak, close her eyelids, move her face, or swallow. He also noted that petitioner's "abnormalities were real and neurologic," although the CT and MRI scans of her head were normal.
Petitioner underwent EMG and NCV studies on April 19, 2007, which showed dysfunction in her bilateral fifth and seventh cranial nerves. Pet. Ex. 17 at 75-76. The study was interpreted by Kirsten Gruis, M.D., a neurologist, who stated that petitioner's normal cerebral spinal fluid ("CSF") analysis and CSF Lyme Western blot results "argue against an infectious process or demyelinating polyneuropathy variant." Pet. Ex. 17 at 75-76. Dr. Gruis noted that idiopathic cranial neuropathies or autoimmune collagen-vascular disease could explain the multiple cranial mononeuropathies.
In a separate office note, dated April 19, 2007, Dr. Gruis recounted petitioner's medical history including her longstanding history of rheumatologic symptoms, joint swelling, intermittent sharp pain in her right eye since the late 1990s, sensory neural hearing loss since 2001, and chronic headaches. Pet. Ex. 17 at 156-57. Dr. Gruis noted that earlier on April 1, 2007 (the day of onset of petitioner's symptoms), petitioner was at a garden party and ate salmon and spinach and began developing neurologic symptoms later in the day. Petitioner told Dr. Gruis that her symptoms began with a sensation on the left side of her face of twitching without any associated numbness or tingling.
On April 23, 2007, petitioner presented to Dr. Lerner for a consultation. Upon examination, Dr. Lerner commented that petitioner was "remarkably better." Pet. Ex. 21 at 9. He noted that petitioner's enunciation was clear and that she could close her right eye.
Dr. Ike (a rheumatologist) saw petitioner on April 30, 2007, noting that it was petitioner's first visit to him in two years. Pet. Ex. 17 at 136-38. Dr. Ike noted that petitioner had a consultation and examination with Dr. Gruis who noted that petitioner did have facial nerve palsy but that he did not see evidence of Lyme disease.
On May 1, 2007, petitioner was seen by Justin C. Riutta, M.D., a physiatrist, who noted that petitioner's previous evaluations at the University of Michigan did not support a diagnosis of Lyme disease. Pet. Ex. 2 at 19-20. Dr. Riutta's impression was bilateral cranial nerve VII palsy.
Petitioner next presented to Dr. Steven Schechter for neurologic evaluation on May 14, 2007. Pet. Ex. 3 at 24. Petitioner told Dr. Schechter that she believed she developed Lyme disease while on a cruise in Great Britain at age 36, and that she was diagnosed eight years later.
On May 23, 2007, petitioner consulted with Dr. Sandro K. Cinti, an infectious disease physician. Pet. Ex. 17 at 175-78. Dr. Cinti noted that he had previously consulted with petitioner in 2001 because of a concern petitioner had about Lyme disease.
Petitioner underwent a brain MRI and an MRI of her internal auditory canal (with and without contrast) on May 30, 2007, which noted an "enhancement [of the] bilateral facial nerve at labyrinthine segment and geniculate ganglia portion. These findings are stable." Pet. Ex. 17 at 71-72. The impression stated "stable appearances of enhancement of bilateral facial nerves. . . ."
Petitioner returned to Dr. Gruis on June 14, 2007. Dr. Gruis took into consideration petitioner's previous visit, where there was not enough objective evidence to support a Lyme disease diagnosis. Pet. Ex. 17 at 151. Due to petitioner's continued concerns, Dr. Gruis stated that petitioner was being referred to Dr. Nadelman, a Lyme disease specialist in New York, who would conduct a further evaluation for neuro-Lyme disease.
Petitioner returned for a follow-up consultation with Dr. Riutta on June 15, 2007. Pet. Ex. 2 at 17. Dr. Riutta noted that petitioner had recently been seen at the University of Michigan and diagnosed with idiopathic bilateral Bell's palsy with involvement of the seventh cranial nerve only.
Petitioner underwent another brain MRI on June 19, 2007. Pet. Ex. 17 at 70. The MRI showed previously noted enhancement of the distal internal auditory canals. Pet. Ex. 17 at 70.
On July 26, 2007, petitioner had an evaluation with Dr. Robert B. Nadelman, an infectious disease specialist, regarding a possible Lyme disease diagnosis. Pet. Ex. 46 at 57. Dr. Nadelman noted that petitioner "has a complex illness. I am uncertain of the etiology. I am also uncertain whether if she has ever had Lyme disease. . . . It would be extremely unlikely for American Lyme disease not to have a positive IgG Western blot with all of her neurologic and rheumatologic findings. . . . Vasculitis of some sort seems to make the most sense as a unifying diagnosis." Pet. Ex. 46 at 57. Petitioner underwent a repeat lumbar puncture on August 9, 2007, which showed normal results. Pet. Ex. 3 at 5-6; Pet. Ex. 21 at 70-77.
Petitioner returned to Dr. Gruis on August 23, 2007, for a follow-up consultation. Pet. Ex. 17 at 114-17. Dr. Gruis noted that "an extensive work-up has been done excluding other associated neurological conditions (including multiple sclerosis and atypical Guillain-Barré syndrome) sometimes associated with seventh nerve palsies. This leaves viral neuritis as the likely cause for her seventh nerve palsies." Pet. Ex. 17 at 116.
Petitioner saw Dr. Rebecca M. Kuenzler, a neurologist, at the Cleveland Clinic on October 2, 2007, for an evaluation for facial weakness. Pet. Ex. 12 at 7. Dr. Kuenzler noted that petitioner received an HPV vaccination in February 2007, and that petitioner was concerned that her symptoms were a reaction to the vaccine.
Petitioner also saw Dr. Steven K. Schmitt, an infectious disease specialist at the Cleveland Clinic, on the same day, October 2, 2007. Pet Ex. 12 at 2-5. Dr. Schmitt noted that petitioner received the HPV vaccine in February 2007, and that she had facial nerve palsy with an acute onset afterwards.
On October 15, 2007, Dr. Schechter noted that the physicians at the Cleveland Clinic felt that petitioner had "possible Guillain-Barré [Miller-Fisher] variant." Pet. Ex. 3 at 19. A neuro-ophthalmic exam by Edward M. Cohn, MD, on October 22, 2007, noted a resolving seventh nerve palsy and paresthesia in the region of her left cheek. Dr. Cohn stated that petitioner had associated her symptoms to her receipt of the HPV vaccine. Pet. Ex. 38 at 14-15. Another MRI of the brain was performed on petitioner on December 7, 2007, showing stable enhancement along the seventh nerve since the June 19, 2007 study, but the enhancement also appeared decreased when compared to a study performed on May 30, 2007. Pet. Ex. 2 at 7-8; Pet. Ex. 3 at 3-4. Petitioner underwent a SPECT brain scan on December 28, 2007, that did not show significant interval changes when compared to a study performed on December 15, 2004. Pet. Ex. 17 at 64.
In a report by Dr. Riutta, dated February 21, 2008, she noted that petitioner's condition was suggestive of an intermittent immune condition most consistent with chronic inflammatory demyelinating polyneuropathy. Pet. Ex. 2 at 13-15. During that same visit, petitioner inquired as to her initial diagnosis of Guillain-Barré syndrome. Dr. Riutta noted that the GBS diagnosis was made by Dr. Laban while petitioner was hospitalized, and that the only abnormalities identified by Dr. Riutta were consistent with bilateral cranial nerve VII palsy.
On March 19, 2008, petitioner saw Dr. Schechter in a follow-up visit. Pet. Ex. 3 at 15. Dr. Schechter noted that petitioner "wonders if Gardasil has induced some of her symptoms," but stated that her symptoms "could be related to her prior history of Lyme disease. She is on IVIG, which is helping, Mobic and Lyrica."
On April 20, 2011, petitioner presented to Robert C. Erickson, M.D., an ophthalmologist, who noted that petitioner continued to have facial paralysis since having GBS. Pet. Ex. 38 at 3. He also noted left facial weakness, double vision, vertical diplopia, and ocular hypertension,
Petitioner was examined by Steven A. Telian, M.D., a neurologist, on May 24, 2011. Pet. Ex. 38 at 1. Dr. Telian noted that petitioner had a normal ear exam and that her facial nerve function was normal on the right and Grade 3/6 on the left, with residual spasm and synkinesis.
On May 8, 2013, petitioner underwent an EMG/NCV study because of complaints of progressive weakness on the left side of her face with numbness and tingling. Pet. Ex. 55 at 3-4. It was noted that petitioner had marked asymmetry between the two facial sides.
On July 3, 2013, Dr. Schechter ordered a second EMG/NCV of petitioner's bilateral facial motor nerves which showed prolonged distal latencies and low amplitudes bilaterally, worse on the left, consistent with bilateral facial neuropathy. Pet. Ex. 55 at 5-6.
At the hearing, petitioner testified that she still struggles to speak. Tr. at 6. She speaks with one side of her mouth because of bilateral facial nerve damage.
To receive compensation under the Vaccine Act, 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 injury was actually caused by a vaccine (a "non-Table injury").
Petitioner bears the burden of demonstrating actual causation by a preponderance of the evidence.
Causation is determined on a case by case basis, with "no hard and fast
In Vaccine Act cases, expert testimony is usually evaluated according to the factors for analyzing scientific reliability set forth in
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."
Three experts testified at hearing: two for petitioner and one for respondent. The qualifications and testimony of each party's respective experts are summarized below.
Steven H. Schechter, M.D., is a neurologist and one of petitioner's treating physicians. Tr. at 31. He is board certified in neurology and is currently in private practice in West Bloomfield, Michigan. Tr. at 32. Dr. Schechter attended medical school at the Chicago Medical School in North Chicago, and graduated in 1987.
Dr. Schechter testified that he first saw petitioner on May 14, 2007, when she presented to him with complaints of facial weakness. Tr. at 32, 34. It was his understanding that petitioner had a complex of symptoms mainly consisting of a facial diplegia or bifacial weakness.
Dr. Schechter offered an opinion regarding the nature of petitioner's injury based on his clinical experience with petitioner and a review of her treatment history. During his testimony, Dr. Schechter explained that the Miller-Fisher variant of GBS is "a clinical variance of Guillain-Barré syndrome which has distinct clinical features, ataxia,
Dr. Schechter discussed the basis for his opinion that the Miller-Fisher variant of GBS was likely the proper diagnosis, as he explained that the cerebrospinal fluid can be normal with the Miller-Fisher variant of GBS during the first few days of the illness. Pet. Ex. 54 at 1. He further stated that the results of nerve conduction studies may also be normal, and F-wave responses (which are sometimes affected in GBS, Tr. at 70) may not be prolonged.
Dr. Schechter testified that he believed it was more likely than not that the Gardasil vaccine triggered petitioner's symptoms. In his report, Dr. Schechter stated that "it is more probable than not, that [petitioner's] facial diplegia and associated symptoms have resulted from GBS syndrome, or variant which presented in 2007, following Gardasil vaccine." Pet. Ex. 56 at 1-2. He further stated that "[g]iven the time course of vaccine followed by the onset of her clinical symptoms, with ongoing residual symptomatology, symptom complex may be consistent with a Miller-Fisher variant of GBS syndrome."
Dr. Schechter explained how Gardasil could have triggered petitioner's condition as his report states, "[i]t appears that the vaccine triggered an autoimmune type response resulting in a form of acute inflammatory demyelinating neuropathy, which has produced permanent symptoms which have persisted to this time. . . ." Pet. Ex. 54 at 2; Pet. Ex. 56 at 2. Dr. Schechter stated that "with a reasonable degree of medical certainty, [petitioner] appears to have sustained an immune mediated type of reaction which has left her with ongoing residual focal neurological deficits."
In his expert report, Dr. Schechter explained that the Gardasil vaccine "triggered an autoimmune type response resulting in a form of acute inflammatory demyelinating neuropathy, which has produced permanent symptoms which have persisted to this time. . . ." Pet. Ex. 54 at 2. Dr. Schechter noted that Dr. Laban had indicated that petitioner had a classic presentation of GBS with facial diplegia and bilateral cranial nerve conduction delays.
On cross examination, Dr. Schechter explained that petitioner had a complex medical history and clinical presentation, and that "there was a temporal time course where she had a clear onset of symptoms, a complex of symptoms following the vaccine, within that temporal time frame, it was helpful in terms of thinking about what the ultimate cause may be for her symptoms." Tr. at 59. Dr. Schechter also testified that there was no particular article or case study that led him to his opinion on causation in this case, but rather "there is evidence in the literature of . . . post-vaccine induced GBS, including Gardasil." Tr. at 60.
Dr. Schechter stated that to a "reasonable degree of medical probability and/or certainty that the onset of petitioner's injury occurred during an appropriate temporal time period, that being between 1 week to 6 weeks." Pet. Ex. 57 at 1. He testified during the hearing that the timing can be variable, occurring "within a few days to several weeks." Tr. at 39.
Petitioner underwent a number of MRIs prior to and soon after her Gardasil vaccination. The pre-vaccination MRIs include an MRI conducted on April 1, 2001 (not included in the record), a brain MRI conducted on October 28, 2002 (Pet. Ex. 17 at 97), and an MRA/MRI of petitioner's head conducted on October 15, 2003 (Pet. Ex. 17 at 96). The first MRI report that was filed in this case, an October 28, 2002 MRI, conducted on the brain, showed, as compared with a study performed on September 15, 2001 (not included in the record), "[t]he internal auditory canals and orbital contents are within normal limits. . . . There is no evidence for enhancing lesions within the brain, abnormal signal intensity within the brain parenchyma or orbits and the CSF spaces are unremarkable. . . . Impression: Unremarkable evaluation of the brain and orbits without change since prior study." Pet. Ex. 17 at 97. Dr. Schechter testified that the results of this MRI appeared to be normal. Tr. at 86. The MRA conducted on October 15, 2003, also yielded normal results. Pet. Ex. 17 at 96; tr. at 86-87.
Post-vaccination MRIs/MRAs were conducted on April 5 and 14, 2007, May 30, 2007, June 19, 2007 and December 7, 2007. Tr. at 80. A brain CT scan was conducted on April 4, 2007, which showed normal results. Pet. Ex. 17 at 77. The April 14, 2007 MRI references an MRI/MRA that was conducted on April 5, 2007 (Pet. Ex. 10 at 155), for comparative purposes. Tr. at 90. The MRI report dated April 14, 2007, states that "there is mild, symmetric enhancement of the distal intracanalicular acoustic nerve complexes, the bilateral geniculate ganglia, and the descending portion of the facial nerves bilaterally. This is slightly more enhancement than would be expected for physiologic vascular enhancement." Tr. at 90; Pet. Ex. 10 at 155. Dr. Schechter testified that the description of enhancement on this MRI is consistent with his opinion that there was an acute inflammatory reaction occurring post-vaccination. Tr. at 92. According to Dr. Schechter, an enhancement on an MRI demonstrates a newer "active process" and "active inflammation" which means that there is a breakdown of the blood-brain barrier. Tr. at 81.
Dr. Schechter testified that the May 30, 2007 MRI conducted on petitioner's brain and internal auditory canal, as compared to the MRI performed on April 13, 2007, showed a stable appearance of the enhancement of the bilateral facial nerve, i.e., the seventh cranial nerve. Tr. at 80-81; Pet. Ex. 17 at 71. The December 7, 2007 MRI showed decreased enhancement which, according to Dr. Schechter, meant that the inflammatory process was "settling down." Tr. at 82; Pet. Ex. 17 at 66. In summary, Dr. Schechter testified that this enhancement process demonstrated a change in the MRIs before and after petitioner's Gardasil vaccination. Tr. at 87.
Regarding the facial nerve EMG study, Dr. Schechter testified that it is a test that is "done to check the integrity of the facial nerve." Tr. at 73. He explained that demyelination can affect the outer casing of a nerve, while at other times, "the actual axon or the wiring of the nerve is affected."
David Allen Axelrod, M.D., is a clinical immunologist trained at McGill University (Montreal) and the National Institutes of Health. Pet. Ex. 80 at 1. He obtained his medical degree at the University of Michigan Medical School. Tr. 96. Dr. Axelrod trained in internal medicine at the University of Toronto and then at William Beaumont Hospital. Tr. 96-97. He completed a fellowship in allergy, immunology and rheumatology at McGill University and another two years at the National Institutes of Health.
Dr. Axelrod opinioned that petitioner suffered from either a
Dr. Axelrod proposed the theory of molecular mimicry to explain how the HPV vaccine could cause GBS (including the Miller-Fisher variant of GBS). Tr. at 149. 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."
To support his theory, Dr. Axelrod relies on an article by Wucherpfenning
On cross-examination, Dr. Axelrod was asked whether there were any animal models to support his theory that the HPV vaccine or any component of the HPV vaccine could cause either GBS or the Miller-Fisher variant of GBS. Tr. at 143. Dr. Axelrod explained that he would not expect to see any animal studies on those specific issues because the increase in risk would be "incredibly small" and it would "be very hard to have enough sample sizes of anything to sort that out, which is . . . . why the epidemiologic studies don't help us."
Dr. Axelrod testified that based on the timing of petitioner's onset of symptoms and her receipt of the Gardasil vaccination, "it made sense" from an immunologic standpoint, that the vaccine contributed to petitioner's injuries as has been reported in the medical literature. Tr. at 108-09. And because "there were antigens — structures on the vaccine that were similar to structures on the human body. And if the — you make an immune response to those same structures that are common to both, you may end up with damage to the normal tissues in the human being."
When asked about what type of reaction he would expect to see, as an immunologist, when a reaction occurs in response to a vaccine, Dr. Axelrod testified that he would expect to see the development of a problem, such as an inflammatory response, and then he would expect that problem to "taper off" unless the problem caused permanent damage. Tr. at 150-51. He stated, however, that there was no way to measure whether petitioner had an inflammatory reaction to the Gardasil vaccine in this case.
When questioned about petitioner's prior symptoms, which have indicated that there was possibly a prior immune process occurring, Dr. Axelrod testified that the presence of that process would not change his opinion. Tr. at 156. His opinion would be that the vaccine exacerbated any preexisting condition.
In his expert report, Dr. Axelrod stated that "[a]t least 14 days may be required for a vaccine to produce a measurable primary or secondary immune response, which may be followed by the development of disease. In fact, Guillain-Barré Syndrome may occur up to at least 6 weeks, following vaccination with Gardasil." Pet. Ex. 80 at 2-3. Dr. Axelrod similarly testified that it would take at least two to three weeks to look at an immune response to a vaccination, such as Gardasil. Tr. at 105-06. He testified that at least one of the articles he cited in his report that discussed vaccine reaction stated that the reaction occurred six weeks later. Tr. at 146. And because this was petitioner's first and only Gardasil vaccine (she did not receive the boosters), he testified that such a reaction "will take longer." Tr. at 147. Dr. Axelrod stated that the expected response for a secondary reaction is much sooner than for a primary reaction. Tr. at 147-48.
Dr. Axelrod testified that he does not interpret MRI films. Tr. at 153. He stated that if the EMG studies and MRIs/MRAs showed demyelination, it would be consistent with his theory that an immune response had occurred.
Dr. Thomas Leist is a neuroimmunologist and is currently employed at the Thomas Jefferson University in Philadelphia, Pennsylvania. Tr. 160; Resp't Ex. O. He holds a doctoral degree in biochemistry and immunology from the University of Zurich.
Dr. Leist opined that petitioner did not suffer from GBS, a variant of GBS, or a demyelinating injury, and that an appropriate diagnosis was never confirmed in her case. Tr. at 163-65. Dr. Leist stated that he relied on the medical records to reach his opinion, including the contemporary medical records from Dr. Schechter. Tr. at 164. Dr. Leist noted that petitioner had evidence of normal deep tendon reflexes and an absence of ataxia, ophthalmoplegia, and areflexia.
Regarding petitioner's theory of molecular mimicry, Dr. Leist states that "it is always possible to find sequence homologies, short sequence homologies between peptides. . . . the mere occurrence of these homologies doesn't, in itself, indicate that such a homology will give rise to a cross-reactive immune response."
Dr. Leist conducted an extensive critique of the other medical literature on which petitioner's experts relied. In his view, none of the medical literature supports petitioner's theory that the HPV vaccine can cause GBS or the Miller-Fisher variant of GBS via molecular mimicry.
Dr. Leist also testified that he believed that the injuries that petitioner alleges were caused by her February 21, 2007 Gardasil vaccine all pre-date her vaccination. Tr. at 168. He stated that the medical records document petitioner's hearing loss/impairment as early as 2001. Tr. at 168-69. Dr. Leist also testified that the medical records document petitioner's facial weakness as early as 2001 with worsening in 2003 and 2004.
Regarding the timing issue, Dr. Leist opined that a time interval of over 40 days between vaccine administration and the occurrence of symptoms further weighs against the vaccine as a cause of petitioner's clinical presentation. Resp't Ex. A at 13. However, he admitted during his testimony that if the proof of an appropriate temporal association is extrapolated from studies involving the swine flu vaccine, although on the outer limits, the 41 day time period between Gardasil vaccination and onset of symptoms in petitioner's case would fall within the appropriate time frame. Tr. at 189. Dr. Leist testified, however, that the likelihood of vaccine causation goes down from the fourth to sixth week after vaccine administration.
In summary, Dr. Leist stated that the bases for his opinion are: (1) that petitioner had a history of similar medical events occur prior to her Gardasil vaccination, (2) that forms of the human papillomavirus are not recognized as commonly associated with Guillain-Barré syndrome, (3) that petitioner's negative anti-ganglioside antibodies and her cerebrospinal fluid findings were not supportive of Guillain-Barré syndrome or the Miller-Fisher variant, and (4) that the time interval between petitioner's vaccination and the onset of petitioner's symptoms was too long.
In his written reports, Dr. Leist stated that petitioner's MRI films did not show evidence of a demyclinating injury post-vaccination, and that the pre- and post-vaccination MRI films he reviewed showed comparable, non-specific findings. Resp't Ex. G at 2. Dr. Leist stated that in reviewing petitioner's MRIs, the "absence of new lesions in the brain parenchyma and the lack of motor and sensory findings below the neck essentially rule out diagnoses of a demyelinating central nervous system disorder including ADEM, transverse myelitis, and MS." Resp't Ex. A at 15.
During his testimony, however, Dr. Leist offered a slightly different opinion. Dr. Leist confirmed that he also reviewed and interpreted the MRI films in addition to the MRI reports. Specifically, in reviewing each MRI, Dr. Leist testified that in petitioner's April 1, 2001 brain MRI, he found some "nonspecific white matter changes" which are indicative of "small vascular injury" but are not "emphatically indicative or supportive of [petitioner's] disease process." Tr. at 172. With the October 28, 2002 MRI study, Dr. Leist testified that he found "comparable abnormalities or signals." Tr. at 173. The October 15, 2003 MR angiogram was a "normal MR angiogram."
A threshold issue in this case is whether petitioner had GBS. A determination of what afflicted petitioner "is a prerequisite to . . . [a causation] analysis."
The preliminary questions to be resolved are: (1) whether petitioner suffered from the Miller-Fisher variant of GBS or an autoimmune demyelinating disorder
In determining petitioner's diagnosis, the undersigned reviewed and relied on statements in the medical records, as medical records are generally viewed as trustworthy evidence, since they are created contemporaneously with the treatment of the patient.
Upon careful examination of petitioner's medical records, the undersigned notes that petitioner's treating physicians did not reach a consensus in reaching a diagnosis for petitioner. However, the undersigned finds that the medical records and the testimony of the respective experts suggest that petitioner more likely than not suffered from the Miller-Fisher variant of GBS.
A brief description of Guillain-Barré Syndrome (GBS) is helpful to understand the Miller-Fisher variant of the condition. Clinically, GBS is characterized by the acute or subacute onset of varying degrees of weakness in limbs associated with hypo- or areflexia, and a characteristic profile in the cerebrospinal fluid.
The Miller-Fisher variant of GBS is a "clinical syndrome characterized by a triad of ataxia, ophthalmoplegia, and areflexia. . . ." Resp't Ex. N at 7. While the "classic triad is often clinically recognized and occurs in the absence of limb weakness, in some cases there is clinical overlap with GBS, with limb weakness present; such cases are considered to be GBS-[Miller-Fisher syndrome] overlap syndromes. Certain features of Miller-Fisher syndrome, including the general interval between onset and clinical nadir and presence of cytoalbuminologic dissociation,
A review of petitioner's records demonstrates that the range of possible diagnoses considered by her treating physicians included the Miller-Fisher variant of GBS, Lyme disease, chronic inflammatory demyelinating polyneuropathy, and a viral neuritis. While petitioner did not present with the classic triad of symptoms for the Miller-Fisher variant, at least five of petitioner's treating physicians considered her history and clinical presentation of symptoms, and either considered the Miller-Fisher variant of GBS as a diagnosis or actually diagnosed petitioner with that condition. In a consultation on April 11, 2007, Dr. Ernstoff, a neurologist, considered a possible diagnosis of Miller-Fisher syndrome as a diagnosis. Pet. Ex. 10 at 155-56. On April 12, 2007, Dr. Laban stated that petitioner had a "classic presentation of Guillain-Barré [] syndrome of acute bilateral facial paresis." Pet. Ex. 4 at 340. In October 2007, after reviewing petitioner's medical records and history, Dr. Kuenzler at the Cleveland Clinic assessed that petitioner's "history is most compatible with a Miller-Fisher variant of Guillain-Barré syndrome." Pet. Ex. 12 at 8. Also in October 2007, Dr. Schmitt noted that petitioner's "[h]istory and testing data support a diagnosis of Guillain-Barré syndrome, [Miller-Fis[]her variant." Pet Ex. 12 at 2-5. On October 15, 2007, Dr. Schechter noted that the physicians at the Cleveland Clinic felt that petitioner had "possible Guillain-Barré [Miller-Fisher] variant." Pet. Ex. 3 at 19.
In addition to the medical records, petitoner's expert and treating neurologist, Dr. Schechter, testified at the hearing and stated that to "a reasonable degree of certainty" the most compatible diagnosis with petitioner's symptoms was the Miller-Fisher variant of GBS. Tr. at 60. In supporting his diagnosis, Dr. Schechter stated that petitioner had coordination difficulties, vision complaints and double vision, which could be related to the ophthalmoparesis aspect, but he agreed that petitioner did not have ataxia. Tr. at 77-78. Dr. Schechter also ordered IVIg treatment for petitioner and noted that she had some improvement with the therapy. Dr. Schechter testified that "the improvement she had was consistent with the [Miller-Fisher] diagnosis; otherwise, why would she improve from it." Tr. at 71-72.
On cross examination, Dr. Schechter agreed that petitioner did not present with all of the classic features of the Miller-Fisher variant. Tr. at 66. However, he still concluded that petitioner sustained a new insult after her Gardasil vaccination and felt that the best diagnosis for petitioner's condition was Miller-Fisher syndrome based on his knowledge of petitioner and her case.
As stated above, Dr. Axelrod testified that he was not a neurologist and was relying on the medical records of petitioner's treating physicians regarding the diagnosis of the Miller-Fisher variant of GBS when reaching his opinions in this case. Tr. at 135-37.
Dr. Leist opined that petitioner did not suffer from GBS, a variant of GBS, or a demyelinating injury, and that an appropriate diagnosis was never confirmed in her case. Tr. at 163-65. Dr. Leist stated that he relied on the medical records to reach this opinion, including the contemporary records from Dr. Schechter that document findings undermining a diagnosis of the Miller-Fisher variant of GBS. Tr. at 164. Dr. Leist noted that petitioner had negative anti-ganglioside antibodies and unsupportive CSF findings. She also had evidence of normal deep tendon reflexes and an absence of ataxia, ophthalmoplegia, and areflexia. Dr. Leist notes in his report that Dr. Schechter first saw petitioner on May 14, 2007, or one month following her WBH discharge. At that visit, Dr. Schechter made no mention of symptoms of extremity weakness. He noted that petitioner had normal extremity strength, sensation, and deep tendon reflexes on exam. He felt that her facial weakness was possibly post-viral or related to Lyme disease.
Regarding the lack of evidence to support a demyelinating injury, Dr. Leist noted that petitioner's MRI films did not show evidence of a demyelinating injury post-vaccination, and that the pre- and post-vaccination films he reviewed showed comparable, non-specific findings. During the hearing, however, Dr. Leist agreed that petitioner did show evidence of bilateral axonal injury to her facial nerve (a loss of nerve cells) and demyelination after the February 21, 2007 Gardasil vaccine as shown by Dr. Schechter's EMG. Tr. at 191-93. Dr. Leist goes on to state that "obviously there was facial weakness and that there was an exacerbation or there was a worsening of the facial weakness," but he states that there is no way to date when that injury occurred, although he does agree that a worsening of the facial nerve injury occurred in April 2007.
The undersigned must consider the record as a whole in evaluating petitioner's injury. § 13(a)(1). Here, the record and testimony supports the conclusion that petitioner more likely than not suffered from Miller-Fisher syndrome after February 21, 2007. This finding is informed by the medical records and the opinions of petitioner's treating physicians, a number of whom diagnosed petitioner with the Miller-Fisher variant of GBS.
In reviewing the medical records, the undersigned notes that although no diagnosis was agreed upon at the time, there is no question that petitioner suffered a significant injury after her Gardasil vaccination which led to a 12-day hospitalization. The record contains documented complaints of petitioner's vision difficulties, coordination difficulties, and bilateral facial weakness after her Gardasil vaccination.
Because the undersigned has found that the evidence supports the conclusion that petitioner suffered from the Miller-Fisher variant of GBS after February 21, 2007, the second issue in dispute, whether petitioner suffered an auto-immune demyelinating disorder after her Gardasil vaccination is answered in the affirmative.
The parties ask the special master to determine whether petitioner suffered from an "identifiable, underlying medical condition before February 21, 2007." Based on the a review of the records filed in this case, the undersigned finds that petitioner did suffer from some symptoms and injuries prior to February 21, 2007, although the exact diagnosis of her condition was never agreed upon by all of petitioner's treating physicians and remains unclear. However, the undersigned is not required to diagnose petitioner's condition. In
In reviewing petitioner's medical records just prior to her vaccination of February 21, 2007, the undersigned notes that petitioner appeared to be doing well with only minor complaints noted. During an exam conducted at the Michigan Ear Institute on October 9, 2006, it was noted that petitioner did have some slight facial weakness on her right side. Pet. Ex. 19 at 16. Petitioner's physical exam was otherwise normal with the exception of some slight instability noted on her balance tests.
Although the undersigned finds that petitioner did suffer from some symptoms and injuries prior to February 21, 2007, the undersigned is not assigning a specific diagnosis to that condition. Furthermore, because the undersigned finds that petitioner suffered from a
Under
As described above, petitioner presented a theory of molecular mimicry to explain how the Gardasil vaccine could cause GBS (including the Miller-Fisher variant of GBS). Petitioner's expert, Dr. Axelrod, explained that the human papillomavirus and the Gardasil vaccine contain structures, to which the human immune response reacts, to protect vaccinated individuals. As Dr. Axelrod explained, the human papillomavirus and the Gardasil vaccine contains structures, to which the human immune response system reacts, to protect vaccinated individuals, including L1 capsid protein. If an individual develops antibodies from the vaccine to these same structures, there may be damage to the normal structures within the nervous system. Pet. Ex. 23 at 3. Dr. Schechter presented a more generalized theory stating that "with a reasonable degree of medical certainty, [petitioner] appears to have sustained an immune mediated type of reaction which has left her with ongoing residual focal neurological deficits." Pet. Ex. 54 at 2; Pet. Ex. 56 at 2.
Dr. Leist did not specifically oppose the molecular mimicry theory as a plausible theory other than to state that there is no evidence to demonstrate that molecular mimicry plays a role in explaining how the Gardasil vaccine specifically can cause GBS or Miller-Fisher syndrome. Dr. Leist explained that although there may be homology between the components of the vaccine and part of the human body, there is no evidence to demonstrate that an autoimmune condition is likely to occur.
The undersigned finds that petitioner has provided preponderant evidence that the Gardasil vaccine can cause GBS (or the Miller-Fisher variant) via molecular mimicry. Accordingly, petitioner has satisfied
The second
In his expert report, Dr. Schechter stated that "[g]iven the time course of the vaccine followed by the onset of her clinical symptoms, with ongoing residual symptomatology, [petitioner's] symptom complex may be consistent with a Miller-Fisher variant GBS syndrome." Pet. Ex. 54 at 2. He explained that petitioner had a complex medical history and clinical presentation and that "there was a temporal time course where she had a clear onset of symptoms, a complex of symptoms following the vaccine, within that temporal time frame, it was helpful in terms of thinking about what the ultimate cause may be for her symptoms."
Dr. Axelrod, when asked by the undersigned how, by the concept of molecular mimicry, the vaccine could cause actual damage to the myelin, Dr. Axelrod explained that the body's immune response would recognize antigens that are homologous and then attack the body's myelin through the antigens or antibodies. Dr. Axelrod testified that it was the time interval between the vaccination and the development of petitioner's symptoms that further led him to his opinion that the vaccination was more likely than not the cause of petitioner's symptoms. Tr. at 149-50. Regarding any other explanation of how the vaccine could have caused damage to petitioner's myelin, Dr. Axelrod stated that he would have to defer to the expertise of a neurologist, but he explained that petitioner's treating physicians looked for other possible causes of her symptoms and were unable to find one.
Because Dr. Schechter was one of petitioner's treating physicians, the undersigned has given Dr. Schechter's opinion careful consideration.
The third
Petitioner testified that the onset of her symptoms began on April 1, 2007 (39 days after her February 21, 2007 Gardasil vaccination), and she was admitted to WBH on April 4, 2007 (42 days after vaccination). Tr. at 9; Pet. Ex. 6 at 1-2. Dr. Axelrod and Dr. Schechter testified and state in their respective expert reports that an appropriate temporal association between vaccination and injury can be anywhere from one to six weeks. Dr. Schechter opined that the onset of petitioner's injury occurred during an appropriate time period, "that being between 1 week to 6 weeks." Pet. Ex. 57 at 1. Dr. Axelrod opined that GBS "may occur up to at least 6 weeks following vaccination with Gardasil." Pet. Ex. 23 at 2. Dr. Leist does not dispute that a vaccine reaction can occur as far as six weeks after vaccination. Thus, the undersigned finds that petitioner has satisfied
Because petitioner has established a prima facie case, she is entitled to compensation unless respondent can put forth preponderant evidence "that [her] injury was in fact caused by factors unrelated to the vaccine."
In his report, Dr. Leist opined that the symptoms and the process that led to petitioner's facial weakness after her February 2007 Gardasil vaccine was the same process that led to her facial weakness prior to the vaccination. Tr. at 170. He also hypothesized that petitioner may have had a foodborne illness shortly after the February 2007 vaccination, which may have contributed to the increase of symptoms shortly after vaccination.
As discussed above, a preponderance of the evidence establishes that petitioner's symptoms were of the Miller-Fisher variant of GBS, not symptoms of her pre-existing health issues or a food-borne illness as Dr. Leist suggests. In addition, while several of petitioner's treating physicians speculated about alternative causes of petitioner's condition, none of the physicians settled on any one cause as a more likely diagnosis, as was done for the diagnosis of the Miller-Fisher variant of GBS. At least five of petitioner's treating physicians either considered a diagnosis of the Miller-Fisher variant of GBS or actually diagnosed petitioner with that condition, while there was no consensus as to the other possible causes. Accordingly, respondent has failed to provide preponderant evidence of an alternative cause of petitioner's Miller-Fisher variant of GBS.
A significant aggravation is defined as "any change for the worse in a preexisting condition which results in markedly greater disability, pain, or illness accompanied by a serious deterioration in health." 42 U.S.C. § 300aa-33(4). As confirmed in
In her post-hearing brief, petitioner added a claim of significant aggravation claiming that the Gardasil vaccine caused a "substantial aggravation/exacerbation of an underlying demyelinating disorder." Petitioner's Post-Hearing Brief, filed Dec. 16, 2015 ("Pet. PH Brief"). In support of this claim, petitioner simply stated that: (1) "[a]n increased incidence of GBS has been observed after administration of the Gardasil vaccine," (2) petitioner "suffered GBS" and that the "onset occurred within the right time frame and her doctors have no explanation," and (3) the "onset of petitioner's illness occurred within the time frame after vaccination which is expected when an illness or vaccination causes GBS." Pet. PH Brief 2-3. Respondent filed a post-hearing brief addressing petitioner's significant aggravation claim on December 23, 2014. Respondent's Post-Hearing Brief, filed Dec. 23, 2014 ("Resp't PH Brief"). Respondent disagrees that petitioner had a new post-vaccination demyelinating event. Resp't PH Brief at 5. Respondent argued that based on the record as a whole, petitioner failed to present preponderant evidence that she suffered from GBS, the Miller-Fisher variant of GBS, a de novo demyelinating injury, or a significant aggravation of an underlying demyelinating injury after vaccination.
Because the undersigned has found that petitioner suffered a new event after vaccination, i.e., a development of the Miller-Fisher variant of GBS, and has also found that petitioner presented preponderant evidence to demonstrate the Gardasil vaccine caused her to develop this condition, there is no need for an analysis of petitioner's significant aggravation claim. Her causation-in-fact claim has succeeded.
For the reasons discussed above, the undersigned finds that petitioner is entitled to compensation because she has provided sufficient circumstantial evidence that preponderates in her favor. A separate damages order will issue.
