VICP Registry Case Source Bundle Canonical URL: https://vicp-registry.org/case/USCOURTS-cofc-1_11-vv-00077 Package ID: USCOURTS-cofc-1_11-vv-00077 Petitioner: Sherril K. Stillwell Filed: 2011-02-07 Decided: 2015-08-03 Vaccine: influenza Vaccination date: 2008-02-22 Condition: acute demyelinating encephalomyelitis (ADEM) Outcome: denied Award amount USD: AI-assisted case summary: Sherril K. Stillwell filed a petition on February 7, 2011, alleging that an influenza vaccination she received on February 22, 2008 caused her to develop encephalomyelitis, specifically a subacute variant of acute disseminated encephalomyelitis (ADEM) as characterized by her expert, Dr. Marcel Kinsbourne. After an evidentiary hearing, Chief Special Master Campbell-Smith denied compensation on June 17, 2013, applying the Lombardi/Broekelschen injury-first framework. The Chief SM found that petitioner failed to prove by a preponderance of the evidence that she had ADEM, citing six factors: (1) petitioner was in her mid-50s, whereas ADEM primarily afflicts children and young adults; (2) none of her numerous treating physicians diagnosed her with ADEM; (3) the appearance of her brain lesion was inconclusive; (4) her symptom onset was atypically slow and protracted rather than acute; (5) her symptom severity was inconsistent with typical ADEM presentation; and (6) her prolonged clinical course with limited recovery was inconsistent with ADEM, which typically reaches a nadir and then substantially resolves. Because petitioner's ADEM diagnosis was a necessary component of her causation theory, failure to establish the injury was fatal to her claim. In an abundance of caution, the Chief SM also evaluated the Althen causation prongs and found them unsatisfied. Petitioner sought review. On August 21, 2014, Judge Block of the Court of Federal Claims affirmed the Chief SM's decision on both grounds: the Lombardi standard was correctly applied, and the factual findings were not arbitrary or capricious. Petitioner appealed to the United States Court of Appeals for the Federal Circuit, which affirmed without opinion on June 15, 2015. Interim attorneys' fees of $97,500.00 were awarded on June 21, 2013. Following final proceedings, Special Master Hamilton-Fieldman awarded final fees and costs of $57,370.99 ($54,875.00 in fees and $2,495.99 in costs), payable jointly to petitioner and her counsel, Sol P. Ajalat, on July 10, 2015. The petition was found to have been brought in good faith and upon a reasonable basis. Theory of causation field: Flu vaccine Feb 22, 2008 → alleged ADEM variant (subacute onset). Chief SM Campbell-Smith June 17, 2013: DENIED (Lombardi/Broekelschen: failed to prove ADEM on 6 grounds; Althen also failed in abundance of caution). CFC Judge Block Aug 21, 2014: affirmed. Fed. Cir. June 15, 2015: affirmed without opinion. Final fees $57,370.99 (SM Hamilton-Fieldman July 10, 2015). outcome corrected: 'compensated' → 'denied'. award corrected: 57370 → NULL (was fees; no comp awarded). Public staged source text: ================================================================================ DOCUMENT 1: USCOURTS-cofc-1_11-vv-00077-cl-extra-2673439 Date issued/filed: 2013-06-17 Pages: 1 Docket text: Supplementary opinion from CourtListener cluster 2673439 -------------------------------------------------------------------------------- In the United States Court of Federal Claims OFFICE OF SPECIAL MASTERS No. 11-77V Filed: June 17, 2013 *********************************** PUBLISHED SHERRIL K. STILLWELL, * * Influenza (Flu) Vaccine; Acute Petitioner, * Demyelinating Encephalomyelitis * (ADEM); Record Evidence Does Not v. * Support Alleged Injury * SECRETARY OF HEALTH * AND HUMAN SERVICES, * * Respondent. * *********************************** Sol Ajalat, Ajalat & Ajalat, North Hollywood, CA, for petitioner. Alexis Babcock, U.S. Dep’t of Justice, Washington, DC, for respondent. DECISION1 I. Introduction On February 7, 2011, Sherril Stillwell (petitioner) filed a petition for compensation under the National Vaccine Injury Compensation Program (the Program),2 1 Because this published decision contains a reasoned explanation for the action in this case, the undersigned intends to post this decision on the website of the United States Court of Federal Claims, in accordance with the E-Government Act of 2002 § 205, 44 U.S.C. § 3501 (2006). In accordance with the Vaccine Rules, each party has 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). Further, consistent with the rule requirement, a motion for redaction must include a proposed redacted decision. If, upon review, the undersigned agrees that the identified material fits within the requirements of that provision, such material will be deleted from public access. 2 The Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, 42 U.S.C. §§ 300aa-10 et seq. (hereinafter “Vaccine Act” or “the Act”). Hereafter, individual section references will be to 42 U.S.C. § 300aa of the Act. alleging that she suffered from acute demyelinating encephalomyelitis (ADEM) as a result of an influenza vaccination she received on February 22, 2008.3 Respondent recommended against compensation. Respondent challenged petitioner’s claim that she developed ADEM. Resp’t’s Report at 7. Respondent further challenged the vaccine-relatedness of petitioner’s injury. Id. The parties presented expert opinions in support of their respective positions. Dr. Marcel Kinsbourne testified for petitioner. Dr. Jeffrey Cohen testified for respondent. An entitlement hearing was conducted in Washington, D.C., on March 30, 2012. Thereafter, the parties filed post-hearing briefing. The matter is now ripe for a ruling. The question here is whether petitioner’s condition can be characterized as ADEM. The parties and their respective experts focused on this issue in their written submissions and at hearing. Simply stated, petitioner asserts that she suffers from an atypical case of ADEM. Respondent disputes that. Although respondent agrees with petitioner that ADEM can have wide variability in its presentation, respondent contends that numerous aspects of petitioner’s clinical course are too unusual to merit an ADEM diagnosis. As discussed in detail below, the weight of the evidence does not preponderate in favor of a finding that petitioner suffers from vaccine-related ADEM. Accordingly, petitioner is not entitled to Program compensation. II. Factual Background Petitioner was born on October 25, 1954. Pet’r’s Ex. 1 at ¶1. As a child, she had rheumatic fever, but fully recovered. Pet’r’s Ex. 4 at 69.4 Her subsequent medical history was remarkable for smoking, hypothyroidism, gastroesophageal reflux disease, panic and anxiety disorders, and osteoarthritis of the knees. Pet’r’s Ex. 3 at 165. Petitioner also suffered from insomnia. Pet’r’s Ex. 5 at 25. 3 In her petition, petitioner alleged she developed encephalomyelitis as a result of an influenza vaccination. Petition (Pet.) at 3. However, as discussed below, she subsequently defined her injury as acute demyelinating encephalomyelitis (ADEM). 4 All citations to Exhibits 1-7 refer to the pagination adopted by petitioner at the bottom right hand corner of each page. 2 On February 22, 2008, petitioner was evaluated for recurrent pain in her right knee, a discomfort that was attributed to degenerative joint disease. Pet’r’s Ex. 3 at 165. During this office visit, petitioner was treated with injections of steroids and lidocaine in each knee. Id. at 168. She also received the subject influenza vaccination. Pet’r’s Ex. 2 at 2. Petitioner next sought medical treatment two months later, on April 28, 2008. Pet’r’s Ex. 4 at 161. At that time, she presented with dizziness and unsteadiness. Id. She reported that she had suffered for one week with vertigo and nausea, for two weeks with weakness that had worsened, and for three weeks with right ear pain. Id. She further reported that she had “no energy” and that it had been “very difficult to get out of bed in [the morning].” Id. Her treating physician, Chierry Anderson Poyotte, M.D., an internist, diagnosed her with an ear infection (otitis media) and vertigo. Id. at 163. Two days later, on April 30, 2008, petitioner again presented to Dr. Poyotte complaining of ongoing vertigo, malaise, and fatigue. Id. at 154. She also complained of “buzzing [in her] right ear while [lying] on [her] right side.” Id. Dr. Poyotte advised petitioner “to follow up with her [p]sychiatrist for reevaluation.” Id. at 155. Six days later, on May 6, 2008, petitioner saw Natalie Ting, a doctor of osteopathic medicine, with complaints of continuing fatigue and dizziness. Id. at 147. She reported that she felt dizzy “every moment of every day” for the previous three weeks and that her dizziness worsened with movement. Id. She also reported “feeling numb on the right side of her body” during the three week period preceding her office visit. Id. Observing a “[d]epressed mood and affect[,]” Dr. Ting suspected that petitioner’s symptoms “[might] have a psych[iatric] origin” because her “[e]xam [was] not [consistent] with her complaints.” Id. at 148-49. Three days thereafter, on May 9, 2008, petitioner presented to Kijung Paul Sung, M.D., an internist, again complaining of ongoing vertigo, dizziness, and fatigue. Id. at 139-40. Petitioner further complained of “partial numbness [on the] right side of her body.” Id. at 140. Petitioner indicated that she felt “drunk when [she] walk[ed].” Id. She also demonstrated “decreased sensation to light touch over [the] right [side of her] face, right upper extremities, and right lower extremities.” Id. at 141. During this visit, petitioner had a computer tomography (CT) scan and magnetic resonance imaging (MRI) taken of her brain, the results of which were normal. Id. at 142-43. At the end of May, petitioner presented to the emergency room complaining of vertigo, taste disturbance, ataxia, numbness and weakness on her right side, and an 3 inability to find words. Pet’r’s Ex. 4 at 127. She was hospitalized for three days, from May 27 to May 29, 2008. Id. at 127. She showed “no sign of otitis media.” Id. at 128. She had a brain and a cervical spine MRI (with and without contrast), the results of which were normal. Id. at 127. The “etiology of her symptoms [was] unclear,” and she was advised to see a neurologist on June 9, 2008, and to follow up with her psychiatrist. Id. at 129. Petitioner presented to David Shaw, M.D., a neurologist, on June 9, 2008. Id. at 114. She related that she had continuing dizzy spells accompanied by a spinning sensation. Id. She also related that almost two weeks after her hospitalization, she had developed numbness on the right side of her body, fatigue, general weakness, an unsteady gait, nausea, blurred vision, decreased taste sensation, and intermittent neck pain. Id. at 114-15. Dr. Shaw’s diagnostic impression was “[p]ossible or probable multiple sclerosis [(MS)],” but he noted that petitioner’s MRI did not show the “obvious evidence” of the characteristic lesions that are associated with that condition. Id. at 116. Nonetheless, Dr. Shaw prescribed copaxone to treat petitioner’s perceived MS. Id. The next day, on June 10, 2008, petitioner underwent an EEG and a visual evoked response test, the results of which were normal. Id. at 111, 120. Ten days later, on June 20, 2008, she reported no improvement in her symptoms after a ten-day course of copaxone. Id. at 104. Later in the day, petitioner presented to William Miller, M.D., another neurologist. Pet’r’s Ex. 3 at 155. She complained of “progressive dizziness, imbalance, numbness, and weakness” that had lasted several weeks. Id. Petitioner indicated her symptoms had worsened, she had begun to slur her speech, and her legs felt “extremely heavy.” Id. During this office visit, she commented that on further reflection, “she [had] noticed several weeks of feeling that [her] socks seemed too tight on [her] legs . . . prior to the onset of her vertigo.” Id. at 159. Dr. Miller saw “no lesion on [her] MRI to explain [her] symptoms” and noted that it would be “hard to localize [a] lesion that would explain all of her symptoms.” Id. at 158. Among the diagnoses Dr. Miller considered were “neuronitis or other vestibular dysfunction”5 and MS. Id. at 161. Dr. Miller discussed with petitioner’s family the possibility that petitioner was exhibiting the first demyelinating event of MS, but he observed that it would be unusual “for symptoms to 5 Neuronitis is “inflammation of one or more neurons.” Dorland’s Illustrated Medical Dictionary (32d ed. 2012) at 1268 (Dorland’s). Vestibular dysfunction consists of “a single attack of severe vertigo, usually accompanied by nausea and vomiting . . . [which] usually improves within a few days.” Id. 4 be so severe without seeing [a] change on [petitioner’s] MRI.” Id. Although the testing of petitioner’s cerebrospinal fluid (CSF) protein levels showed oligoclonal bands, such findings were “nonspecific and [could] be seen with viral infections and other etiologies.” Id. Dr. Miller did not recommend treatment for MS, but he did recommend “following up with her psychiatrist to make sure treatment of her anxiety [was] maximized as well.” Id. On July 8, 2008, petitioner returned to Dr. Shaw. Pet’r’s Ex. 4 at 90. Dr. Shaw noted that a scheduled MRI of her thoratic spine could potentially confirm a diagnosis of MS, but opined that because some of her “symptoms . . . [could not] be totally explained by” the findings on her MRI, “[s]tress and anxiety . . . [could not] be ruled out.” Id. He also noted that petitioner’s “[m]uscle strength [was] probably normal on all 4 limbs, although she [could not] stand well and she need[ed] assistance to walk.” Id. at 89. Petitioner complained of intermittent dizziness, balance problems, and slurred speech. Id. In addition, she reported numbness on the right side of her face, arm, and leg that had lasted for over a month. Id. A second test of petitioner’s CSF was conducted on July 17, 2008, three months after petitioner first sought treatment for her symptoms. Pet’r’s Ex. 7 at 14-15. That test revealed five oligoclonal bands, which were suggestive of MS. Id. Subsequently, on August 2, 2008, an MRI (without contrast) of petitioner’s brain was performed; it showed “[i]ncreased FLAIR and T2 signal intensity . . . of unclear etiology.” Pet’r’s Ex. 3 at 123. In the reviewing physician’s assessment, petitioner’s MRI exhibited an “unusual lesion.” Id. The lesion was indicative of a demyelinating disease that was “[p]robably inflammatory, [and] atypical.” Id. Petitioner was noted to have non-specific dizziness, gait disorder, anxiety disorder, mild lymphocytic pleocytosis, and oligoclonal bands. Id. at 121-24. Dr. Miller did not find a clear etiology for petitioner’s symptoms. Pet’r’s Ex. 4 at 72. On August 20, 2008, petitioner presented to Christopher Di Stasio, M.D., another neurologist. Id. at 69. Petitioner was referred to Dr. Di Stasio for an additional opinion regarding her suspected MS. Id. at 73. She reported that the general weakness in her legs persisted, but her symptoms of vertigo and numbness on the right side of her body were improving. Id. She also described a “cold/tingly feeling of the right lower face [and] jaw with a pulling sensation that radiate[d] down [the] right side of [her] neck into [her] shoulder . . . [with] episodes of her entire body feeling heavy, difficulty speaking, [and] feeling as though she [might] faint.” Id. She related that she was using a wheelchair “for in-home mobility.” Id. Dr. Di Stasio observed that the result of petitioner’s previous MRIs of the thoracic spinal cord and cervical spine revealed no abnormalities. Id. at 71. 5 He also noted the abnormalities Dr. Miller noted in the results of petitioner’s August 2, 2008 MRI of her brain. Id. Dr. Miller appears to have consulted with Dr. Di Stasio about the unclear etiology of petitioner’s condition. Id. at 74. In Dr. Di Stasio’s view, petitioner was suffering from ataxia. Id. at 71. He “suspect[ed]” her symptoms “[might] represent a post-infectious immune process.” Id. at 71. He noted that her symptoms had begun around April of 2008, but that she seemed to be getting better slowly. Id. Petitioner continued to see Dr. Miller for her neurologic problems. On September 8, 2008, Dr. Miller diagnosed her with demyelinating disease that was “prob[ably] postinfectious,” but was “improving slowly.” Pet’r’s Ex. 3 at 102. Nearly eighteen months later,6 on March 20, 2010, petitioner had another brain MRI. Id. at 61. Compared to her August 2, 2008 brain MRI, this image showed improvement. Id. Dr. Miller reiterated his earlier diagnostic impression that petitioner was suffering from a demyelinating disease, a probable “monophasic demyelinating event.” Pet’r’s Ex. 7 at 7. Dr. Miller noted that although petitioner was reporting “increased weakness now with multiple symptoms,” her “MRI actually look[ed] better.” Pet’r’s Ex. 3 at 65. He stated that the appearance of new lesions would have been consistent with a diagnosis of MS, but he did not find any. See id.; see also Pet’r’s Ex. 7 at 6-7. On April 14, 2010, petitioner presented again to Dr. Sung, who noted that she was “alert and oriented,” and had “normal sensation and normal strength,” but exhibited abnormal coordination and an abnormal gait with noticeable shuffling. Pet’r’s Ex. 4 at 56-57. An MRI of petitioner’s cervical spine (without contrast) was performed on May 23, 2010, to help evaluate petitioner’s worsening gait, as well as the weakness in her arm and left lower extremity. Pet’r’s Ex. 7 at 4. Petitioner’s problems with speech continued until June 2010. See Pet’r’s Ex. 3 at 12. Her problems with coordination, balance, and walking continued through July 2010. See id. at 1. On July 30, 2010, petitioner returned to Dr. Sung complaining of body pain that lasted nearly six months. Pet’r’s Ex. 4 at 22-24. Dr. Sung diagnosed petitioner with, 6 Petitioner did not submit any medical records from the year 2009, presumably because “[s]he lost her job and then lost her . . . insurance [with Kaiser] for one year,” Pet’r’s Ex. 4 at 53, and thus, had no appointments with doctors during that time. 6 among other things, a demyelinating disease of the central nervous system and fibromyalgia. Id. at 25. The pain associated with her apparent fibromyalgia persisted over the next three months, through November 2010. See id. at 4. A few months later, on February 7, 2011, petitioner filed a vaccine claim. Petitioner did not submit any records thereafter that speak to her current condition. As reflected in the opinions of the parties’ experts, the parties disagree about the nature of petitioner’s condition and its vaccine-relatedness. Before evaluating petitioner’s claim, the undersigned turns first to summarize the opinions of the experts. A. Dr. Marcel Kinsbourne, Petitioner’s Offered Expert Petitioner filed an expert report from Dr. Marcel Kinsbourne, a neurologist, to support her claim.7 Pet’r’s Ex. 8. Dr. Kinsbourne holds medical licenses in the United Kingdom, Canada, North Carolina, the Commonwealth of Massachusetts, and the Commonwealth of Virginia. ECF Doc. No. 26, filed Mar. 28, 2012, at 1. He has held numerous teaching positions and hospital appointments in various capacities at universities in each of the aforementioned locations. Id. at 1-2. Additionally, he has authored and edited many medical articles, books, and medically-related literature over his lengthy career as a neurologist. Id. at 5-34. Dr. Kinsbourne is not a currently practicing clinician; he has not had an active clinical neurology practice since 1980. Tr. 61-62. Because his work since 1981 has focused on behavioral disorders, he has not treated a patient with ADEM since 1980. Tr. 62. Before then, he saw “quite a few cases of ADEM.” Tr. 62. Dr. Kinsbourne describes ADEM as “an immune-mediated demyelinating disorder of the central nervous system [(CNS)]” that “commonly presents acutely, with multifocal neurological findings, including motor deficits.” Pet’r’s Ex. 8 at 6. Dr. Kinsbourne 7 Petitioner filed the medical literature on which Dr. Kinsbourne relied as attachments to his initial expert report, Pet’r’s Ex. 8, on a compact disc. See ECF Doc. No. 12, filed May 10, 2011. The 602 pages of the medical literature were divided into eight separate PDF files, seven of which contained more than one medical article. See id. at 2. Petitioner did not provide exhibit numbers for the PDF files or the separate articles. Thus, all citations to the medical literature referenced in Dr. Kinsbourne’s initial expert report correspond to petitioner’s “Index of References” found in her “Notice of Filing of CD,” see id., and the pinpoint page cites refer to the page numbers adopted by petitioner. 7 opined that as a result of receiving the influenza vaccine, petitioner developed “a variant of ADEM,” marked by “[a] subacute onset.” Id. Dr. Kinsbourne acknowledged that in 2011, the Institute of Medicine (IOM) found the evidence insufficient to establish a causal relationship between receipt of a flu vaccine and the onset of ADEM.8 Tr. 78. But, he pointed to the findings of the 2009 Lapphra report,9 which were suggestive of a causal relationship between the administered flu vaccine and the onset of neurologic injuries. Tr. 80-81. Dr. Kinsbourne also pointed to a chapter from the well-regarded textbook of Merritt’s Neurology,10 stating that vaccine-induced ADEM may be a possbility when neurologic signs develop within four to twenty-one days after vaccination. Tr. 86. Adverting to the mention of a causal association between various vaccinations (including flu) and ADEM in the medical literature, Dr. Kinsbourne insisted that, “although rare, [this causal link] is well recognized.” Pet’r’s Ex. 8 at 7 (citing Pet’r’s Ex. 8-6 at 500, Hiroshi Shoji & Mashahide Kaji, The Influenza Vaccination and Neurological Complications, 42:2 The Japanese Soc’y of Internal Med. 1 (2003)). He posited that the flu vaccine can cause ADEM by inducing an autoimmune response through molecular mimicry. Id. at 9. He explained that ADEM occurs when “autoreactive cells enter the [central nervous system] during immune surveillance and . . . encounter homologous myelin protein [to] culminat[e] in a destructive autoimmune process in the [central nervous system].” Id. at 10. He added that the flu vaccine can cause ADEM through another immunologic mechanism of “bystander activation of autoreactive immune T cells.” Id. This process can occur together with and augment the 8 Institute of Medicine, Adverse Effects of Vaccines: Evidence and Causality 308 (Kathleen R. Stratton et al. eds., 2011). Dr. Kinsbourne cited this report in his supplemental expert report, see Pet’r’s Ex. 9 at 6, but petitioner did not file it as an exhibit. 9 Pet’r’s Ex. 8-4 at 383, Keswadee Lapphra et al., Adverse Neurologic Reactions After Both Doses of Pandemic H1N1 Influenza Vaccine With Optic Neuritis and Demyelination, 30:1 The Pediatric Infectious Disease J. 84 (2009). 10 The chapter, Viral Infections, in the textbook Merritt’s Neurology (L.P. Rowland ed., 2005), was authored by Burk Jubelt and James R. Miller. See Pet’r’s Ex. 8-3 at 310. The parties interchangeably referred to the textbook chapter as either “Jubelt” or “Merritt’s.” 8 effect of molecular mimicry. Id. Because there was no evidence of an “event[] . . . capable of causing or triggering ADEM”11 that occurred within the same time frame, id. at 12, Dr. Kinsbourne opined that petitioner’s “ADEM variant was caused by an immune- mediated reaction to [her] influenza vaccine.” Id. at 13. Dr. Kinsbourne averred that the onset of petitioner’s ADEM began “[a]pproximately four weeks after” her February 22, 2008 influenza vaccination, and “progressed for several months before it stabilized.” Id. at 5. He stated that petitioner’s medical records “showed changes compatible with immune activation” in her cerebrospinal fluid and her “[t]reating physicians considered her illness to be inflammatory and postinfectious in nature, but atypical.” Id. Dr. Kinsbourne conceded that none of petitioner’s physicians treated her specifically for ADEM, but he claimed that their treatment of petitioner nonetheless “implied [that her inflammatory condition] was immune[-]mediated” and would respond to the administration of cortical steroids, a prescriptive course that would have been consistent with a finding of ADEM. Tr. 92. Dr. Kinsbourne relied, in part, on the 2007 Sejvar article12 to support his opinion that petitioner suffered from ADEM. See Tr. 30, 50-55, 156. This article set forth “firm guidelines for the diagnosis of ADEM for the specific purpose of assisting in the evaluation of questions of vaccine injury.” Tr. 30. It outlined a number of diagnostic criteria for ADEM that Dr. Kinsbourne posited were applicable in this case, including: (1) a single brain lesion; (2) trouble finding words; (3) cranial nerve abnormalities; (4) motor weakness; (5) sensory abnormalities; (6) ataxia and gait dysfunction; and (7) arm tremors. Tr. 53 (citing Pet’r’s Ex. 9-1 at 8, the 2007 Sejvar article). He asserted that petitioner had exhibited five of the nine criteria discussed in the article—“decreased arousability, aphasia, motor weakness, sensory abnormalities, and ataxia,” Pet’r’s Ex. 9 at 1-2, and he observed that a proper diagnosis of ADEM requires only one of the listed criteria. Tr. 53. The 2007 Sejvar article also identified MRI findings of diffuse or multifocal white matter lesions as necessary criteria for an ADEM diagnosis. Tr. 75-76. Dr. Kinsbourne 11 Dr. Kinsbourne opined that petitioner’s ear infection had no relation to her vertigo or any of her other symptoms. Tr. 94-95. 12 Pet’r’s Ex. 9-1, James J. Sejvar et al., Encephalitis, myelitis, and acute disseminated encephalomyelitis (ADEM): Case definitions and guidelines for collection, analysis, and presentation of immunization safety data, 25 Vaccine 5771 (2007). The parties interchangeably referred to this article as the “Sejvar article” and the “Brighton Group” article. 9 acknowledged that petitioner’s lesion was not multifocal, Tr. 75-76, but he asserted that the description of petitioner’s MRI findings was consistent with a diffused lesion. Tr. 76. As further evidence of the vaccine-relatedness of petitioner’s injury, Dr. Kinsbourne pointed to: (1) the lesion detected on her brain stem; (2) the subacute onset of her disorder; (3) the presence of oligoclonal bands in her cerebrospinal fluid (CSF) test results; and (4) the medically acceptable four-week interval between her vaccination and the onset of her ADEM. Pet’r’s Ex. 8 at 10-11; see also Tr. 22-25. Although Dr. Kinsbourne admitted that “some features of [petitioner’s] case are . . . not typical” for ADEM, he urged that “her condition nonetheless fits within the bounds of [an] ADEM diagnosis.” Pet’r’s Ex. 9 at 1; see also Tr. 38-39 (Dr. Kinsbourne describing petitioner’s subacute onset as “unusual”). Dr. Kinsbourne averred that ADEM “‘usually occur[s] a few days or weeks following vaccine administration or virus-like disease.’” Pet’r’s Ex. 8 at 6 (quoting Pet’r’s Ex. 8-6 at 511, Institute of Medicine, Influenza Vaccines and Neurological Complications 36 (Kathleen R. Stratton et al. eds., 1994)). It “is preceded by an infectious event within a medically reasonable timeframe . . . in the majority of cases.” Tr. 33. But he denied any such infectious event in this case. Based on the documented first appearance of petitioner’s symptoms, and her later recollection that she had “experienced some tightness and numbness around both ankles and began to have an unaccustomed weakness,” Dr. Kinsbourne posited that the onset of petitioner’s demyelinating disorder occurred in the third week of March 2008. Tr. 9; see also Tr. 25. Dr. Kinsbourne described petitioner’s disorder as “monophasic” and non- progressive; he asserted that her condition was marked by “a rise time, a plateau, and then a decline of symptoms.” Tr. 21. In his view, petitioner reached her plateau during her hospitalization at the end of May 2008. Tr. 25. Citing two articles—the 1999 Singh article and the 2004 Leake article13—Dr. Kinsbourne insisted that ADEM can have a subacute onset, such as occurred in this case. Pet’r’s Ex. 9 at 4. Quoting an excerpt from the 1994 IOM report stating that “the latencies for . . . ADEM [may extend] . . . from 5 days to 6 weeks,” Dr. Kinsbourne took the position that the onset of ADEM can take up to forty-two days, even though the most common time frame for the onset of ADEM is one or two weeks. Tr. 34. Although he 13 Pet’r’s Ex. 8-6 at 503, Surendra Singh et al., Acute Disseminated Encephalomyelitis: MR Imaging Features, 173 AJR 1101 (1999); Pet’r’s Ex. 8-4 at 387, John A.D. Leake et al., Acute Disseminated Encephalomyelitis in Childhood: Epidemiologic, Clincal and Laboratory Features, 23:8 Pediatric Infectious Disease J. 756 (2004). 10 recognized that cases with delayed symptom onset were not typical for ADEM, Dr. Kinsbourne noted that such cases were “clearly mentioned in the literature.” Tr. 38. He confessed, however, that he was unaware of any reports in the literature involving the progression of ADEM—as in this case—over the course of multiple months. Tr. 72. B. Dr. Jeffrey Allen Cohen, Respondent’s Offered Expert Respondent filed an expert report from Jeffrey Allen Cohen, M.D., a clinical neurologist, challenging petitioner’s claim. Resp’t’s Ex. A. Dr. Cohen is board certified in neurology, neuromuscular diseases, and clinical neurophysiology. Tr. 104. He has treated patients with ADEM, among other disorders. Tr. 104-05. He is a professor of neurology at Dartmouth Medical School and the chief of the neurology section at Dartmouth Hitchcock Medical Center. Tr. 102. He treats patients and supervises neurology students and fellows about four-and-a-half days per week. Tr. 103. Based on his review of petitioner’s medical records, Dr. Cohen disagreed with Dr. Kinsbourne’s opinion that petitioner developed ADEM as a result of the flu vaccine she received. Resp’t’s Ex. A at 1. Although he agreed that petitioner had “an acquired demyelinating syndrome,” he indicated that—like petitioner’s own treating doctors—he could not affix a more specific diagnostic label to her condition. Tr. 169-70. He was clear, however, that petitioner’s “clinical picture was not consistent with a diagnosis of ADEM.” Resp’t’s Ex. A at 6. He asserted that the medical literature is bereft of “reliable evidence” showing that the flu vaccine can cause ADEM,” 14 id.; see also Tr. 111, but he allowed that a vaccination could cause a demyelinating disorder. Tr. 141. Dr. Cohen outlined the “clinical features of ADEM” with which most subjects present: [an] [a]brupt onset; [s]omnolence, confusion, seizures, headache, meningeal signs,15 fever; [and] 97% [of cases occur in] children and adolescents. Id. [Onset occurs, at most,] four weeks . . . between [the] inciting event and [the] evolution of the neurological picture. Id. [Imaging reveals] confluent diffuse areas of demyelination; a single lesion is not considered to be consistent with the diagnosis of ADEM. Id. [Typically, an afflicted subject is responsive] to steroid therapy. 14 Dr. Cohen described the causation evidence as “very, very scant.” Tr. 111. 15 Meningeal signs are those exhibited when the meninges have been irritated. See Dorland’s at 1132. The meninges are the “three membranes that envelop the brain and spinal cord.” Id. 11 Resp’t’s Ex. A at 2. Dr. Cohen explained that there is no “specific marker” for ADEM; rather, the condition requires “a clinical diagnosis . . . supplemented . . . [by] laboratory examinations.” Tr. 107. Magnetic resonance imaging can assist in making an ADEM diagnosis because such imaging will show the “predominantly white matter lesions . . . [and] the . . . diffused multifocal white matter changes” that are characteristic of the condition. Tr. 108. Dr. Cohen explained that “it would be very unusual” for a patient with ADEM to show no evidence of diffused, multifocal white matter changes on imaging. Tr. 108. Dr. Cohen observed that ADEM is “a disease that is severe and swift in its onset, reaches a nadir, and then . . . gets better . . . to a great degree . . . . [T]he total course [between] illness . . . [and] recovery is measured in months, not years.” Tr. 178. In his clinical experience, the symptoms of ADEM fully manifest, at most, four weeks after the inciting event. Tr. 155-56. Dr. Cohen discussed the aspects of petitioner’s medical history that he believed militated against a finding that she suffered from ADEM. Tr. 152-53, 155; see also Resp’t’s Ex. A at 2-3, 5. He argued that Ms. Stillwell’s symptoms of “decreased arousability, aphasia, motor weakness, sensory abnormalities and ataxia;” are not dispositive of an ADEM diagnosis because they are not “diagnosis-specific neurologic findings;” such symptoms could occur in patients suffering from, among other injuries, either a stroke, a traumatic brain injury, or MS. Resp’t’s Ex. C at 1. In Dr. Cohen’s view, the primary factor that most disfavors a diagnosis of ADEM is the lack of “a markedly depressed level of consciousness” during the course of petitioner’s illness. Id. Dr. Cohen noted that other common indicators of ADEM were absent in petitioner’s case. In particular, he did not see any record of petitioner suffering from facial weakness, a symptom of ADEM readily noticeable to evaluating medical personnel. Tr. 113-14. Nor did he see any evidence of lesions on either petitioner’s May 15, 2008 or May 28, 2008 MRIs. Tr. 114. Dr. Cohen observed that the presence of oligoclonal bands on petitioner’s imaging were features that “can occur in any demyelinati[ng] disease.” Resp’t’s Ex. A at 5. But “they are more representative of MS than ADEM.” Id. Dr. Cohen added that the results of petitioner’s June 10, 2008 EEG were normal. Tr. 114. He testified that if petitioner had the symptoms of impaired speech or a depressed level of consciousness, corroborative evidence would have appeared on her MRI or EEG, to confirm an ADEM diagnosis. Tr. 115. 12 Dr. Cohen elaborated that “the area of demyelination [visible on petitioner’s imaging] was limited to the brainstem which is not the usual location for ADEM.” Resp’t’s Ex. A at 2. “[N]or was the area of [detected] demyelination as extensive as [typically occurs] in ADEM.” Id. Petitioner’s protracted “course [of illness] is [also] very atypical for ADEM— [which generally] progresses over weeks, not months.” Id. at 2. Dr. Cohen asserted that a subacute onset “of over four weeks is very unusual.” Id. at 5. Dr. Cohen explained that as anomalous as petitioner’s symptom onset was, so was her lack of any appreciable recovery. Id. at 2, 5. These features of petitioner’s condition—when considered together—were strikingly uncharacteristic of ADEM. Id. Dr. Cohen disagreed with petitioner’s assertion that her symptoms plateaued during her hospitalization at the end of May 2008. Tr. 116. He pointed to the decision by petitioner’s treating physicians to begin a course of steroid therapy as an indication “that they thought . . . she was getting worse.” Tr. 117. He observed that the steroids had “no clear benefit” to petitioner. See Pet’r’s Ex. 4 at 73. As further evidence of her worsening condition, Dr. Cohen noted that petitioner required a wheelchair in August 2008, but she had not needed one previously. Tr. 117. Dr. Cohen explained that the record evidence of petitioner’s ongoing and unrelenting problems did not support a finding that she suffered from ADEM because symptoms in “the majority of [ADEM] patients . . . tend[] to resolve over a period of . . . two, three, four months. [This] doesn’t mean that they get totally back, but they don’t have [a negative] progression” of their symptoms. Tr. 119. Dr. Cohen took notice that none of petitioner’s treating physicians, including Dr. Miller, the neurologist who treated petitioner for months, considered her demyelination to be vaccine-related. Resp’t’s Ex. A at 3. He took further notice that “[n]one of [petitioner’s] treating neurologists ever suggested a possible diagnosis of ADEM nor did they specifically treat her for ADEM.” Id. at 1; see Tr. 119. Dr. Cohen remarked that “ADEM is a disease [that appears] almost exclusively . . . [in] children and adolescents.” Resp’t’s Ex. A at 3. Petitioner was an adult at the time of her onset, and her records indicate that two months after receiving the flu vaccine, she was diagnosed with an ear infection. Tr. 135. According to Dr. Cohen, that ear infection could have caused her early symptom of vertigo. Tr. 135. Dr. Cohen criticized Dr. Kinsbourne’s reliance on certain medical articles and the conclusions he drew from them, Resp’t’s Ex. A at 4, principally because the subjects 13 presented with a different clinical picture than did petitioner. Id. at 3 (citing the 2003 Shoji article16; see also Resp’t’s Ex. C at 1 (challenging Dr. Kinsbourne’s reliance on the 2007 Sejvar article). Dr. Cohen allowed that the clinical manifestations of ADEM may vary, but insisted that the condition’s onset is almost always acute, involving the “sudden fulminant” appearance of certain symptoms that were notably absent during petitioner’s course of illness.17 Tr. 141-42; see also Pet’r’s Ex. 9 at 2 (defining ADEM “as a first acute fulminant demyelinating episode without any previous neurologic history.”). In his experience, the claim that petitioner experienced a “sub-acute” onset of neurologic symptoms at nearly four weeks (or longer) after vaccination exceeded “the spectrum of [presentation for] ADEM,” particularly when the other distinguishing features of ADEM were missing. Tr. 145. Dr. Cohen opined that petitioner improperly sought to characterize her case as one of atypical ADEM. Tr. 122, 160, 164. III. Discussion A. The Applicable Legal Standard To prevail on a non-Table vaccine claim such as petitioner has asserted here,18 petitioner must show that the vaccine was “‘not only a but-for cause of the injury but also a substantial factor in bringing about the injury.’” Moberly v. Sec’y of Health & Human Servs., 592 F.3d 1315, 1321 (Fed. Cir. 2010) (quoting Shyface v. Sec’y of Health & Human Servs., 165 F.3d 1344, 1352-53 (Fed. Cir. 1999)). Petitioner must prove her 16 Pet’r’s Ex. 8-6 at 500. 17 Pet’r’s Ex. 9-1 at 2 (“histological confirmation of inflammation of the brain, encephalopathy, decreased or absent response to the environment, decreased or absent eye contact, inconsistent or absent response to external stimuli, decreased arousability, seizure associated with loss of consciousness, visual field defects, fever, EEG findings consistent with encephalitis, neuroimaging consistent with encephalitis.”). 18 If petitioner alleges an injury listed on the Vaccine Injury Table (Table) that occurred within the correlative time frame set forth in the Table, petitioner’s vaccine claim is deemed a Table claim, and a presumption of causation attaches. See § 300aa-14; see also 42 C.F.R. § 100.3. If petitioner alleges an injury that is not listed on the Table, such as the ADEM injury alleged in this case, the vaccine claim is deemed a non-Table case and no presumption of causation attaches. Id. Petitioner must therefore satisfy her burden of proof by proving that her injuries were caused-in-fact by her vaccination. See § 300aa- 13(a)(1)(A). 14 vaccine claim by a preponderance of the evidence. Althen v. Sec’y of Health & Human Servs., 418 F.3d 1274, 1278 (Fed. Cir. 2005). The preponderant evidence standard under the Vaccine Act requires proof that a vaccine more likely than not caused the vaccinee’s injury. Id. at 1279; see also In re Winship, 397 U.S. 358, 371–72 (1970) (Harlan, J., concurring) (quoting F. James, Civil Procedure, 250–51 (1965)) (a preponderance of the evidence standard requires the trier of fact to “believe that the existence of a fact is more probable than its nonexistence before the [special master] may find in favor of the party who has the burden to persuade the [special master] of the fact’s existence.”). But, this evidentiary standard “allows a finding of causation in a field bereft of complete and direct proof of how vaccines affect the human body.” Capizzano v. Sec’y of Health & Human Servs., 440 F.3d 1317, 1324 (Fed. Cir. 2006). Mere conjecture or speculation will not establish a probability. See Snowbank Enter., Inc. v. United States, 6 Cl. Ct. 476, 486 (1984). Petitioner satisfies her burden of showing that the received vaccination brought about her injury by providing (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 proximate temporal relationship between vaccination and injury. Althen, 418 F.3d at 1278. Proof of vaccine causation must be supported by a sound and reliable “medical or scientific explanation that pertains specifically to the petitioner’s case, although the explanation need only be ‘legally probable, not medically or scientifically certain.’” Moberly, 592 F.3d at 1322 (quoting Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 548-49 (Fed. Cir. 1994)); see also Grant v. Sec’y of Health & Human Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992) (requiring that the medical theory must support actual cause). Petitioner may use circumstantial evidence to prove her case, and “close calls” regarding causation may be resolved in favor of petitioner. Althen, 418 F.3d at 1280. Causation can be supported by a treating physician’s opinion that a vaccination was causally linked to the vaccinee’s injury if the special master finds the opinion to be both reliable and persuasive. Moberly, 592 F.3d at 1324-25; see also Capizzano, 440 F.3d at 1326. Mere temporal association is not sufficient to prove causation. Grant, 956 F.2d at 1148. Because the parties dispute the nature of petitioner’s injury here, the undersigned first applies the analytical framework endorsed in Broekelschen v. Sec’y of Health & 15 Human Servs., 618 F.3d 1339 (Fed. Cir. 2010) and Lombardi v. Sec’y of Health & Human Servs., 656 F.3d 1343 (Fed. Cir. 2011). B. The Weight of the Record Evidence Does Not Preponderate in Favor of a Finding that Petitioner Suffers From ADEM Petitioner alleges that she suffers from ADEM. See Pet’r’s Ex. 8 at 6. Petitioner’s own expert, Dr. Kinsbourne, concedes that this case is an “unusual” and “atypical” one for ADEM. The parties do not dispute that petitioner does suffer from some sort of neurologic illness, but they disagree on what her illness is. Respondent contends that petitioner’s condition cannot be characterized as ADEM—or an atypical variant thereof, as petitioner and Dr. Kinsbourne propose. See Resp’t’s Exs. A, C. Special masters are required to evaluate the record as a whole. 42 U.S.C. § 300aa- 13. The record here reveals many extraordinary characteristics of petitioner’s presentation that call into question the appropriateness of a diagnosis of an atypical ADEM variant. The undersigned is persuaded, on this record, that petitioner’s onset, symptoms, and the course of her illness diverge in too many respects and by too great a degree from the presentation of ADEM to even be deemed an atypical form of ADEM. Yet, petitioner does appear to suffer from another, unspecified illness that has bewildered her physicians. Six factors, in particular, weigh against a finding that petitioner has ADEM. The factors are: (1) the statistical improbability that petitioner has ADEM; (2) the absence of an ADEM diagnosis from her treaters; (3) the appearance of her brain lesion; (4) the timing of her symptom onset; (5) the nature and severity of her symptoms; and (6) the protracted course of her illness and her limited recovery. The undersigned addresses these factors in turn. i. The Statistical Improbability That Petitioner Suffers From ADEM Both Dr. Kinsbourne and Dr. Cohen testified that ADEM primarily afflicts children and adolescents. See Tr. 29; see also Tr. 38 (Dr. Kinsbourne explaining that “most of the cases [of ADEM]” occur in children and adolescents); Tr. 175 (Dr. Cohen agreeing that the vast majority of ADEM cases occur in adolescents or children). The condition is much less common in adults, but “has been reported in young and elderly adults.” Pet’r’s Ex. 8-4 at 410. The statistical likelihood that children, rather than adults, would be afflicted by ADEM is well-supported by the literature the experts cited. See, e.g., Pet’r’s Ex. 8-2 at 16 195; Pet’r’s Ex. 8-4 at 410; Pet’r’s Ex. 8-3 at 301; Resp’t’s Ex. A-619; Resp’t’s Ex. A-9 at 6. At the time petitioner developed her symptoms, she was nearly 54 years old. This statistical factor merits consideration, although it is not dispositive. The undersigned turns now to consider the other factors that inform the likelihood of petitioner’s alleged ADEM diagnosis. ii. The Absence of an ADEM Diagnosis From Petitioner’s Treaters The parties do not dispute, and a review of petitioner’s medical records confirms, that none of petitioner’s treating physicians diagnosed her with ADEM. See Tr. 69, 177. Dr. Miller, petitioner’s treating neurologist over the course of several months, did not once suggest ADEM as a possible diagnosis for her various neurologic symptoms in his differential diagnoses. Instead, petitioner’s various treating physicians considered MS as a possible diagnosis, but apparently concluded she did not suffer from it. See Pet’r’s Ex. 3 at 16 (petitioner advised during an office visit dated June 15, 2010, that she had been “told her symptoms are not [MS] but a demyelinating brain disorder”). The parties’ experts also considered the treatment petitioner received from her attending doctors during the course of her emerging illness. Dr. Kinsbourne and Dr. Cohen agreed that the three days of steroid treatment she received was strongly suggestive of her physicians’ suspicion that she had MS. Dr. Kinsbourne testified, however, that three days of administered steroids was not long enough to treat MS. See Tr. 74-75, 177-78. He maintained that the treatment “is classically used for ADEM” as well, but confessed that he was “not sure what the [treating physicians’] thought process was” because they never documented a diagnosis of ADEM for petitioner. Tr. 74. Dr. Cohen countered Dr. Kinsbourne’s testimony, insisting that a three-day course of steroids was insufficient to treat the onset of ADEM, Tr. 109, but was appropriate for the treatment of an acute MS attack. Tr. 109. In Dr. Cohen’s view, petitioner’s symptom presentation—that is, the onset, type, duration, severity, and course of her symptoms— was too atypical for a diagnosis of, and treatment for, ADEM. Tr. 154. That none of the physicians who regularly examined and treated her contemplated the illness that petitioner now claims she has does not support a finding in her favor. 19 Respondent did not file the medical articles on which Dr. Cohen relied as separate exhibits. Rather, she filed nine separate PDF files as part of an “Appendix” to his expert opinion. See ECF Dkt. No. 14, July 19, 2011. All citations to the medical literature referenced in Dr. Cohen’s report refer to these filings. 17 iii. The Appearance of Petitioner’s Brain Lesion The parties agree that petitioner’s brain imaging shows demyelination has occurred in her brainstem and has created a single lesion in the area of her pons. The lesion was first detected on an MRI conducted in August 2008. See Pet’r’s Ex. 3 at 123- 24; Tr. 72, 117, 164-165. What the parties dispute is the nature of the lesion. The parties disagree on whether the lesion is diffuse or focal and whether the appearance of the lesion is supportive of a finding of ADEM. See Resp’t’s Ex. A at 2. Dr. Kinsbourne argued that diffuse or multifocal lesions are a necessary criterion to diagnose ADEM. Tr. 75. He described the lesion detected in petitioner as “single” and “diffused,” Tr. 22, which—he asserts—would comport with the “classical descriptions of ADEM” lesions. Pet’r’s Ex. 8 at 10. Dr. Kinsbourne cited six sources to support this proposition,20 three of which described “ADEM [lesions that were] confined to the brainstem” only.21 But, he acknowledged that multiple lesions throughout the central nervous system are a much more common finding in cases of ADEM than is a solitary lesion located in the brainstem, such as presented in petitioner’s case. Tr. 69. Nonetheless, Dr. Kinsbourne asserted that petitioner’s presenting symptoms and the finding of a single diffused lesion in petitioner’s brainstem were sufficient to support a diagnosis of ADEM. See Tr. 21, 23-24, 37-38, 53-58, 71, 75, 89. 20 Pet’r’s Ex. 8-1 at 1, Helga Almeida Silva et al., Magnetic resonance imaging in five patients with a tumefactive demyelinating lesion in the central nervous system, 57 Arq. Neuropsychiatric 921 (1999); Pet’r’s Ex. 8-2 at 194, Jin Hwan Cheong et al., Acute disseminated encephalomyelitis associated with influenza vaccination, 35 J. Korean Neurosurgical Soc’y 223 (2004); Pet’r’s Ex. 8-5 at 442, J. I. O’Riordan et al., Long term MRI follow-up of patients with post infectious encephalomyelitis: evidence for a monophasic disease, 167 J. Neurological Sciences 132 (1999); Singh et al., supra note 13; Pet’r’s Ex. 8-2 at 594, A.J. Barkovich, Pediatric Neuroimaging (4th ed. 2005); Pet’r’s Ex. 8-8 at 592, Recai Turkoglu & Erdem Tuzun, Brainstem encephalitis following influenza vaccination: Favorable response to steroid treatment, 27 Vaccine 7252 (2009). 21 K. Tateishi et al., Acute disseminated Encephalomyelitis Confined to Brainstem, 12 J. Neuroimaging 67 (2002); Zhengqi Lu et al., Comparative Brain Stem Lesions on MRI of Acute Disseminated Encephalomyelitis, Neuromyelitis Optica, and Multiple Sclerosis, PLoS ONE 6(8) (2011); Singh et al., supra note 13. 18 Dr. Cohen cited the 2009 Callen article22 to support his claim that the confinement of petitioner’s demyelination to the brainstem was notably unusual for ADEM subjects, who more generally present with extensive lesions on brain imaging. Resp’t’s Ex. A at 2; see also Tr. 117-118, 161, 164-165 (Dr. Cohen testifying that a solitary lesion located in the brainstem was atypical for an ADEM subject). The 2009 Callen article provided MRI “diagnostic criteria . . . that [might] be useful in differentiating children experiencing the first attack of [MS] from those with monophasic [ADEM].” Resp’t’s Ex. A-2 at 1. The authors compared and analyzed MRI data from subjects suffering from MS with those suffering from ADEM and found that the “[d]iffuse, bilateral lesions [more prevalent in ADEM subjects]. . . emerged as an important differentiating feature between the . . . groups.” Id. at 6. Dr. Cohen also cited the 2006 Wingerchuk article,23 id. at 5, which described the MRI results in ADEM subjects as “typically reveal[ing] multifocal, bilateral, often large white matter lesions.” But, the article’s authors did recognize the reporting of “[a] wide spectrum of exceptional findings . . . including [the detection of a] normal initial brain scan, lesion development only during the clinical recovery stage, [and] a solitary lesion restricted to an area such as the brain stem.” Id. In the 2000 Dale article,24 the authors discussed the MRI findings performed in thirty-five individuals with ADEM. The imaging uniformly showed “disseminated [central nervous system] lesions,” the majority of which were large. Pet’r’s Ex. 8-2 at 205. In another study of forty-two ADEM patients, the imaging showed demyelination, with “[l]esions typically number[ing] 3-8,” but only “rarely” did a “solitary” lesion appear. Pet’r’s Ex. 8-4 at 391. Although ADEM can present with a solitary diffused lesion, see Pet’r’s Ex. 8-8 at 596, the medical literature on which the parties relied consistently reported that individuals suffering from ADEM generally have multiple lesions in their CNS. See, e.g., Pet’r’s Ex. 8-3 at 305 (“Cerebral lesions are usually disseminated but solitary lesions [do] occur in about 10% and 30% of cases. Lesion 22 Resp’t’s Ex. A-2 at 1, D.J.A. Callen et al., Role of MRI in the differentiation of ADEM from MS in children, 72:11 Neurology 968 (2009). 23 Resp’t’s Ex. A-9 at 2, Dean M. Wingerchuk, The clinical course of acute disseminated encephalomyelitis, 28 Neurological Research 341 (2006). 24 Pet’r’s Ex. 8-2 at 198, R.C. Dale et al., Acute disseminated encephalomyelitis, multiphasic disseminated encephalomyelitis and multiple sclerosis in children, 123 Brain 2407 (2000). 19 patterns often seen in ADEM includ[e] widespread, multifocal or extensive white matter lesions . . . [that] may evolve over several weeks.”); Pet’r’s Ex. 8-8 at 596 (“ADEM is characterized [by] multiple lesions distributed all over the CNS.”); see also Resp’t’s Ex. A-1 (“[W]idespread MRI lesion pattern[s] [are] characteristic of ADEM.”). The parties’ experts admitted that interpreting petitioner’s MRIs here was difficult because neither expert had the opportunity to review the imaging results personally. See Tr. 76, 117. Instead, they relied on the description of the imaging results documented in the notes of petitioner’s treating neurologist, Dr. Miller. See Pet’r’s Ex. 3 at 123. Dr. Kinsbourne construed Dr. Miller’s notations to describe a diffused lesion because Dr. Miller wrote that it “cover[ed] a fair amount of territory” in petitioner’s brain. Tr. 76 (discussing Pet’r’s Ex. 3 at 123-24). Dr. Cohen disagreed with Dr. Kinsbourne’s interpretation, pointing out Dr. Miller did not describe the lesion using either of the terms “diffuse” or “multifocal.” Tr. 117-18. Whether petitioner’s brain lesion bore the appearance of the type of lesion usually seen in ADEM subjects is not clear from the record. The medical records do not indicate whether her detected lesion was either diffuse or multifocal, the characteristic presentations for ADEM lesions. None of her treating physicians—who did have the opportunity to review the results of her MRIs—described her discovered lesion using those terms. But her treating neurologist, Dr. Miller, did describe her lesion in plain language that indicated that the lesion was spread over a moderate space in her brain. Notwithstanding this recorded description, the undersigned is not persuaded by Dr. Kinsbourne’s assertions that petitioner’s lesion was sufficiently diffuse to be suggestive of an ADEM lesion because petitioner’s own treating physicians were not persuaded of an ADEM diagnosis based on her radiologic evidence. See Perreira v. Sec’y of Health & Human Servs., 33 F.3d 1375, 1376 n. 6 (Fed. Cir. 1993) (“An expert opinion is no better than the soundness of the reasons supporting it.”); Burns v. Sec’y of Health & Human Servs., 3 F.3d 415, 417 (Fed. Cir. 1993) (“The special master concluded that the expert based his opinion on facts not substantiated by the record. As a result, the special master properly rejected the testimony of petitioner's medical expert.”). Moreover, the weight of the medical literature on which the parties’ respective experts relied supports a finding that the pattern of petitioner’s observed demyelination was not representative of ADEM cases. Petitioner’s presenting symptoms also militate against a finding that she suffered from ADEM. Her symptom onset was too protracted, she did not present with the kind of symptoms that are characteristic of ADEM, and the duration of her clinical course and the lack of improvement of her neurologic condition would be unusual for ADEM. 20 iv. The Timing of Her Symptom Onset Petitioner received the subject flu vaccine on February 22, 2008. Pet’r’s Ex. 2 at 1. Dr. Kinsbourne opines petitioner’s symptom onset began “[a]pproximately four weeks after [her] influenza vaccination.” Pet’r’s Ex. 8 at 5. Dr. Kinsbourne based this calculation on petitioner’s comment to Dr. Miller on June 20, 2008, that “on reflection . . . she [had] noticed several weeks of feeling that socks seemed too tight on [her] legs or that [there] was numbness in her leg prior to the onset of her vertigo.” Pet’r’s Ex. 3 at 159; see also Pet’r’s Ex. 4 at 73 (petitioner reported to Dr. Di Stasio on August 20, 2008, that her initial symptoms included a “feeling that socks or underwear were too tight (mainly on left side)”). Petitioner first complained of her vertigo during an office visit in April 2008, nearly eight weeks after she received the flu vaccine. She reported during that office visit in the third week of April that she had developed vertigo “several weeks” earlier, had begun to feel abnormally fatigued, and had developed numbness in her lower legs (primarily around her ankles) that ascended over the ensuing weeks. Pet’r’s Ex. 3 at 159- 60. By the end of April 2008, petitioner was afflicted by increasingly worsening vertigo, which significantly affected her performance at work. Id. at 118-19; Pet’r’s Ex. 1 at 2. When she presented to the hospital on April 28, 2008, she reported a one-week history of vertigo and a two-week history of progressive weakness and loss of energy. Pet’r’s Ex. 4 at 162. Petitioner’s own accounts of her symptom onset were inconsistent. Based on her related complaints to her doctors, her symptom onset appears to have begun between the end of March 2008 and the second week of April 2008. 25 As discussed in further detail below, even assuming petitioner’s neurologic symptoms did, in fact, begin around the third week of March of 2008, such a symptom onset is toward the tail end of the recognized time frame for the onset of post-vaccinal ADEM. In the months after her symptom onset, petitioner’s neurologic problems persisted and appeared to worsen. Pet’r’s Ex. 3 at 112. In August 2008, she reported some 25 Petitioner saw her treating physicians on numerous occasions between April and June of 2008, and did not mention the sensations she apparently felt in her legs in March of 2008 until she did so “on reflection” during her June 20, 2008 visit to Dr. Miller. The undersigned finds it unlikely that petitioner would have failed to mention these noteworthy symptoms during her late April and early May visits to her treating physicians during which she reported numerous other neurologic complications she had been experiencing in the weeks prior. 21 improvement in her symptoms, although her gait and balance problems were ongoing. Id. Dr. Kinsbourne conceded that the subacute presentation of petitioner’s symptoms (that is, over the course of a number of weeks after her vaccination—without overt expression) was “unusual” for ADEM. See Tr. 38. He described ADEM as a “monophasic [condition] in almost every case.” Tr. 40. He explained “that it came[,] . . . reached a peak[,] . . . reached a plateau, and then . . . got to some extent better.” Tr. 39. Yet, he added that “ADEM has an unusually wide variability of presentation,” Tr. 28, and there is “a subacute variant [of ADEM],” which has a “more gradual beginning . . . [with] a more prolonged course,” Tr. 39. But neither Dr. Kinsbourne nor the literature he filed specifically addressed how subacute the presentation of ADEM could be. Tr. 38. Dr. Cohen provided important perspective on this issue. Observing that petitioner’s symptom onset—as described in her contemporaneous medical records— reflected an irregular case of ADEM, Tr. 164, he explained that, in his experience, ADEM is “a sudden fulminant . . . illness” that presents with “an abrupt onset,” Tr. 141, and the entire course of the illness “progresses over [a period of] weeks, not months”--as in petitioner’s case. Resp’t’s Ex. A at 2. Although he agreed that cases of ADEM do occur where the symptom presentation might be described as “subacute,” he explained that onset in such cases would occur over--“at most[--]weeks, [but] not months.” Tr. 145. Here, he asserted, the onset of petitioner’s symptoms after vaccination was beyond the “spectrum” of onset for ADEM. Id. A review of the parties’ submitted medical literature also indicates that petitioner’s course was, in the best but unlikely case, an atypical form of ADEM. In the 2004 Cheong article,26 the authors explained that “[p]atients with ADEM usually have a monophasic clinical course [that is marked by an] abrupt onset, [and that] last[s] . . . 2 to 4 weeks.” Pet’r’s Ex. 8-2 at 195. Similarly, in the 2000 Dale article, the authors reported in their study of twenty-eight children with ADEM that the “presentation [of symptoms] varied from an acute explosive onset, with a maximum neurological deficit attained within 1 day, to a more indolent progression with maximum deficit at 31 days (mean 7.1 days).” Id. at 202. “The mean latency between predemyelinating illness 26 Pet’r’s Ex. 8-2 at 195, Jin Hwan Cheong et al., Acute disseminated encephalomyelitis associated with influenza vaccination, 35 J. Korean Neurosurgical Soc’y 223 (2004). 22 and the onset of neurological signs [for the children] was 13.0 days (range 2-31 days).” Id. at 201. Dr. Kinsbourne referred to a case report of four individuals with ADEM,27 in which the authors found that “[a] common feature for all the patients . . . was a rapid deterioration in their condition within a few days after being admitted to the hospital.” Pet’r’s Ex. 8-3 at 293. “During the . . . weeks [following their admission], the conditions of [three of the individuals] gradually improved,” and the fourth patient died seven weeks later. Id. at 292. Dr. Kinsbourne pointed to the 2008 Huynh study28 to support his theory that vaccines—and not just illnesses—can cause ADEM. Pet’r’s Ex. 8 at 8. The authors of the Huynh study found that in cases of alleged vaccine-related ADEM, “the onset of symptoms may vary slightly: from 1 to 14 days . . . less than one week . . . [or] 1 to 3 weeks . . . after vaccination . . . [with] [s]ymptom onset [that] is usually rapid with progression over hours to a peak in days . . . .” Pet’r’s 8-3 at 305 (emphasis added). Then citing the 1994 IOM report—apparently for its comment on the timing of ADEM onset—Dr. Kinsbourne drew attention to the statement that “ADEM is characterized by acute depression of consciousness and multifocal neurological findings that usually occur a few days or weeks following vaccine administration . . . .” Pet’r’s Ex. 8-6 at 511;29 see also Pet’r’s Ex. 8-8 at 575, Olafa Stuv & Scott Zamvil, Pathogenesis, diagnosis, and treatment of acute disseminated encephalomyelitis, 12:4 Current Opinion in Neurology 395 (1999) (“Neurologic symptoms [of ADEM] usually follow between 1 and 20 days [after the inciting event]”); Pet’r’s Ex. 8-5 at 474, Louis Reik, Immune-Mediated Central Nervous System Disorders in Childhood Viral Infections, 2:2 Seminars in Neurology 106 (1982) (“Symptoms [of ADEM] usually begin 4 to 21 days after the inciting event”). 27 Pet’r’s Ex. 8-3 at 291, Jari Honkaniemi et al., Delayed MR Imaging Changes in Acute Disseminated Encephalomyelitis, 22 Am. J. Neuroradiology 1117 (2001). 28 Pet’r’s 8-3 at 301, William Huynh et al., Post-vaccination encephalomyelitis: Literature review and illustrative case, 15 J. Clinical Neuroscience 1315 (2008). 29 Institute of Medicine, Adverse Events Associated with Childhood Vaccines: Evidence Bearing on Causality (Kathleen R. Stratton et al. eds., 1994). 23 Respondent filed the 1985 Murphy article30 in which the authors found that ADEM manifests abruptly. Resp’t’s Ex. A-6 at 1. As reported in the article, the authors studied 805 vaccinated subjects and found that the probability of developing post- vaccinal ADEM in 28 days (or more) was less than one percent (0.6%). Id. at 5-6. The medical literature the parties’ referenced makes clear that ADEM most commonly manifests abruptly, although several of the articles Dr. Kinsbourne cited furnished the barest of support for his proposition that petitioner’s subacute onset was an appropriate—even if aberrant—presentation for ADEM. Pet’r’s Ex. 8 at 11 (citing Pet’r’s Ex. 8-4 at 374). In the 2005 Khurana study, the authors reported that of the 13 individuals they studied, “7 . . . evolved subacutely over 5 to 10 days,” but “[s]ix of 13 . . . had rapid progression of symptoms that required prolonged care in the ICU.” Pet’r’s Ex. 8-4 at 376. Similarly, in the 2007 Menge study,31 the authors described reports of ADEM where the afflicted patients “developed [symptoms] subacutely over a period of days, . . . [that] led to hospitalization within a week.” Pet’r’s Ex. 8-4 at 412; see also Pet’r’s Ex. 8-4 at 419 (“Neurologic manifestations [of ADEM] begin 3 days to 4 weeks (mean 12 days) following a precipitating event”); Pet’r’s Ex. 8-5 at 474 (“Symptoms [of ADEM] usually begin 4 to 21 days after the inciting event.”). In the 2001 Schwarz article,32 the authors studied forty individuals with ADEM and found that “[t]he duration of symptoms before admission was shorter in patients with ADEM [than those with MS and they exhibited] . . . a more abrupt onset of symptoms.” Pet’r’s Ex. 8-5 at 490. In addition, a number of the case studies Dr. Kinsbourne cited reported an onset of neurologic symptoms in subjects with ADEM within two days to one week of the precipitating event. Id. at 479 (subjects’ neurologic injuries manifested five and seven days after a flu vaccine); Pet’r’s Ex. 8-5 at 484 (subject’s neurologic symptoms manifested four days after a flu vaccine); Pet’r’s Ex. 8-8 at 600 (symptom onset five days after a flu vaccine); Pet’r’s Ex. 8-2 at 194 (injury manifested two days after a flu vaccine). 30 Resp’t’s Ex. A-6 at 1, James Murphy & James Austin, Spontaneous Infection or Vaccination as Cause of Acute Disseminated Encephlomyelitis, 4 Neuroepidemiology 138 (1985). 31 Til Menge et al., Acute disseminated encephalomyelitis: an acute hit against the brain, 20 Current Opinion of Neurology 247 (2007). 32 Pet’r’s Ex. 8-5 at 487, S. Schwarz et al., Acute disseminated encephalomyelitis: A follow-up study of 40 adult patients, 56 Neurology 1314 (2001). 24 The weight of the record evidence before the undersigned establishes that the symptoms of ADEM appear abruptly—that is, between one and two weeks after the triggering event—in the overwhelming majority of cases. The timing of petitioner’s symptom onset was unusually protracted. Petitioner’s symptom onset occurred slowly and well beyond the typical time frame for the vast majority of subjects afflicted with ADEM. Petitioner’s symptom onset—even if it occurred approximately four weeks after her flu vaccine, as she and Dr. Kinsbourne assert—does not fit within the recognized time frame for most cases of ADEM. At best, petitioner’s symptom onset occurred at the outer reaches of the recognized time frame for the onset of post-vaccinal ADEM. This factor provides only meager support for petitioner’s claim. v. The Nature and Severity of Petitioner’s Symptoms The parties’ experts agreed that certain symptoms are characteristic of ADEM, and petitioner’s expert conceded that petitioner’s presentation “deviated” from the usual presentation of most cases of ADEM. Pet’r’s Ex. 9 at 1. Nonetheless, Dr. Kinsbourne asserted that petitioner’s condition could be regarded as an atypical variant of ADEM because the condition “has . . . unusually wide variability . . . [in] presentation.” Tr. 28. A review of the medical literature filed by the parties, however, persuades the undersigned that petitioner did not exhibit symptoms that were suggestive of ADEM— even an atypical variant—either in nature or in severity. ADEM “is an uncommon inflammatory demyelinating disease of the central nervous system.” Pet’r’s Ex. 8-2 at 192. The disease “is believed to be a manifestation of an autoimmune attack on the myelin of the [CNS].” Dorland’s at 613. Because the “symptoms and signs of [the condition] . . . are related to the portion of the nervous system that is most severely damaged[,] . . . variable clinical syndromes may occur.” Resp’t’s Ex. A-4 at 4. Thus, “ADEM has no [defined] diagnostic criteria.” Pet’r’s Ex. 8- 2 at 209. But, the main symptom of ADEM is a noticeably decreased level of consciousness, “varying from lethargy to coma.” Pet’r’s Ex. 8-3 at 291; see also Pet’r’s Ex. 8-2 at 202 (69% of subjects with ADEM in one study experienced an “[a]lteration in mental state and level of consciousness”); Pet’r’s Ex. 8-4 at 375 (“The typical presentation is that of multifocal neurologic disturbance accompanied by change in mental status.”). Symptoms suggestive of meningeal involvement, such as headaches and neck stiffness, also “are common early in the course of all types [of ADEM].” Resp’t’s Ex. A-4 at 4. Both Dr. Kinsbourne and Dr. Cohen agreed that individuals afflicted with ADEM typically suffer from a significantly lowered level of consciousness and, in some cases, 25 coma. See Tr. 28, 52. The parties also agree that petitioner did not exhibit any clear signs of impaired consciousness.33 Other symptoms of ADEM include “fever . . . and vomiting; sometimes tremor, seizures, and paralysis.” Dorland’s at 613; see also Pet’r’s Ex. 8-2 at 209 (signs of meningism, which include headache, fever, stiff neck, light sensitivity, disorientation, and—occasionally seizures—are common in ADEM patients). Other neurologic signs or symptoms typically associated with ADEM are “weakness, sensory changes, [and] ataxia.” Resp’t’s Ex. A-9 at 5; see also Pet’r’s Ex. 8-2 at 209 (ADEM subjects usually present “with multifocal neurologic disturbance such as ataxia, hemiparesis, cranial nerve palsies, and altered conscious state.”); Pet’r’s Ex. 8-8 at 578 (The “neurologic signs and symptoms [of ADEM] include parathesias, pain, motor weakness, spasticity, incoordination, dysarthia and dysphagia.”). Individuals with ADEM also typically develop complications with their vision. See Pet’r’s Ex. 8-2 at 202. Moreover, “[s]ystemic symptoms [of ADEM] including fever, malaise . . . headache, [and] nausea [with] vomiting often precede neurological symptoms.” Pet’r’s Ex. 8-8 at 578. The parties disputed whether petitioner’s symptoms were sufficiently “severe” to merit an ADEM diagnosis. See, e.g., Tr. 146, 153. The views of the parties’ experts are inconclusive on this issue because neither had the opportunity to observe petitioner and thus, to properly evaluate the severity of her symptoms. The undersigned is informed, however, by the silence of petitioner’s treaters—who did observe her—on the matter of her symptom severity. Although they noted a worsening of her symptoms of discomfort, the symptoms did not appear to have been sufficiently severe to provoke any concern that petitioner might have ADEM. In the view of the undersigned, petitioner did not present with the most characteristic of ADEM symptoms. Nor did her symptoms appear with the type of severity and abruptness that generally occurs in cases of ADEM. Although petitioner exhibited some symptoms associated with ADEM, she did not exhibit the particular 33 Dr. Kinsbourne stated that petitioner’s feelings of confusion when she awakened could have been a sign of depressed consciousness, but he acknowledged that this was not a clear sign of diminished consciousness. See Tr. 52, 70. Dr. Kinsbourne further asserted that symptoms involving consciousness were more common in children afflicted with ADEM whereas adults afflicted with ADEM more commonly exhibited symptoms involving sensory and motor problems. Tr. 28. However, none of the medical literature either party submitted speaks to this proposition. 26 symptoms that the parties agreed are most commonly associated with ADEM, such as a markedly decreased state of consciousness, fever, and headache. This factor does not militate in petitioner’s favor. vi. The Protracted Course of Petitioner’s Illness and Her Limited Recovery The extended duration of petitioner’s clinical course would be unusual for a case of ADEM, further suggesting that petitioner did not suffer from that condition. As Dr. Cohen explained, a typical clinical course of ADEM includes a “severe and swift . . . onset,” a “nadir,” and then improvement over the course of a period of months. Tr. 178. Dr. Kinsbourne agreed that the onset of ADEM generally does not present over the course of multiple months, Tr. 72, although the course of recovery might require a period of months. A review of the medical literature submitted by the parties corroborates Dr. Cohen’s description of the clinical course of ADEM. The disease manifests in an abrupt, fulminant manner; the symptoms are severe, and then reach a plateau. Shortly thereafter, the individual begins a gradual recovery. See Pet’r’s Ex. 9-1 at 3 (a study of seventeen ADEM patients finding the range of disease duration to fall between one and ten months, with an average length of disease duration of four months); Pet’r’s Ex. 8-4 at 378 (“All 4 patients in [an] adult [case] series . . . ha[d] rapid deterioration followed by gradual improvement.”); Pet’r’s Ex. 8-2 at 195 (“Recent studies suggest a more favorable prognosis with rapid recovery.”). Moreover, “[r]ecovery is often . . . complete among those who survive,” Pet’r’s Ex. 8-5 at 474, and individuals afflicted with ADEM generally recover within months of onset. Pet’r’s Ex. 8-2 at 198 (“The outcome in the ADEM patients was mixed; 57% of patients made a complete recovery.”); Pet’r’s Ex. 8-4 at 377 (“Seven of 13 children [with ADEM] had complete recovery.”); see also Pet’r’s Ex 8-2 at 207 (“Despite the often dramatic presentation [of subjects with ADEM], the[ir] outcome was surprisingly good, with recovery completed between 0.25 and 6 months[.] 57% had no impairments on follow-up . . . [while 17%] had motor disability.”). The parties agree that petitioner’s clinical course did not follow the expected clinical course for subjects afflicted with ADEM. Tr. 98, 130. In July of 2008, more than four months after her symptom onset, petitioner reported that her symptoms had worsened; she reported again one month later, in August of 2008, that her symptoms had continued to worsen. Pet’r’s Ex. 3 at 121. Petitioner’s physical therapist noted that her symptoms—particularly her feelings of weakness—had continued on a downward slope for a four-month period. Pet’r’s Ex. 3 at 115. Toward the end of August 2008—nearly five months after her symptoms first appeared—petitioner reported that she was 27 beginning to feel better with some slow improvement in her condition. Pet’r’s Ex. 3 at 109-10. While some of her symptoms began to abate over the ensuing months, her symptoms of dizziness, imbalance, numbness, and weakness persisted through March of 2009—seven months after she first showed signs that her symptoms were improving. Pet’r’s Ex. 3 at 81, 86-87; see also id. at 63 (Petitioner “last seen on 3/09, at that time [she had] . . . some improvement . . . [but] over last 2-3 months has had worsening of gait, feels weak all over, feels like knees will give out. Feels more fatigued.”) In April of 2010, petitioner returned to her neurologist, Dr. Miller, and reported a “significant[ly] worsening gait and [left extremity] weakness, [and] arm weakness,” which led Dr. Miller to evaluate petitioner for a potential cervical cord lesion. Pet’r’s Ex. 7 at 5. The record indicates that petitioner’s condition did not plateau and then gradually improve—as would be expected with a case of ADEM. Instead, petitioner struggled— after the gradual onset of her symptoms—with a protracted clinical course marked by many periods of exacerbation. The course of petitioner’s illness strongly suggests that she did not suffer from ADEM. The lack of appreciable recovery within a year after her symptom onset further suggests that she did not suffer from ADEM. Petitioner’s overall clinical course was inconsistent with the well-recognized course of ADEM. Although petitioner and her expert, Dr. Kinsbourne, relied heavily on case reports discussing the wide variability of symptom presentation in subjects with ADEM, none of the cases involved subjects with the extraordinary combination of atypical features present in petitioner’s case. The undersigned cannot credit petitioner’s position on the assertions of her expert alone, Snyder ex rel. Snyder v. Sec’y of Health & Human Servs., 88 Fed. Cl. 706, 742-43 (2009) (special masters are not required to accept the ipse dixit of an expert) (citing Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997)), and must decline petitioner’s urging that she do so. C. Petitioner did not suffer from the injury for which she seeks a Program award In conformance with the statute’s direction to evaluate the record as a whole, 42 U.S.C. § 300aa-13, the undersigned finds on the record here—that includes the contemporaneous medical records, petitioner’s undiagnosed condition, and the testimony of Drs. Kinsbourne and Cohen—that petitioner has failed to prove by preponderant evidence that she developed ADEM. This determination precludes a finding of causation in petitioner’s favor because the evidence does not support a finding that the vaccinee suffered from the injury for 28 which petitioner she seeks Program compensation. In such a circumstance, an Althen causation analysis may not be required. See Lombardi, 656 F.3d at 1356 (affirming the special master’s decision to forego an Althen analysis after determining that petitioner did not suffer from any of his alleged injuries). Out of an abundance of caution, however, the undersigned evaluates petitioner’s theory under the Althen standard. Because petitioner’s injury is yet undefined, it cannot be identified on the Vaccine Injury Table, see 42 C.F.R. § 100.3. Thus, petitioner cannot establish a Table injury. Instead, she must establish that the vaccine she received caused her neurologic complications. See Cedillo v. Sec’y of Health & Human Servs., 617 F.3d 1328, 1335 (Fed. Cir. 2010). To do so, petitioner must show by preponderant evidence that the vaccines brought about her injury by providing: (1) a medical theory causally connecting the vaccination and her injury; (2) a logical sequence of cause and effect showing that the vaccination was the reason for her injury; and (3) a showing of a proximate temporal relationship between the vaccination and her injury. Althen, 418 F.3d at 1278. 1. Althen Prong One: Petitioner’s Medical Theory Under Althen Prong 1, petitioner must put forth a biologically plausible theory explaining how the received vaccines could have caused the sustained injury. Andreu v. Sec’y of Health & Human Servs., 569 F.3d 1367, 1375 (Fed. Cir. 2009). Under this prong, petitioner must make a showing that the received vaccines “can” cause the alleged injury. Pafford, 451 F.3d at 1355-56. The offered medical theory must be supported by either the vaccinee’s medical records or the opinion of a competent physician. Grant v. Sec’y of Health & Human Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992). Support for the offered medical theory must also include an explanation that “pertains specifically to the [claim made in] petitioner’s case.” Moberly, 592 F.3d at 1322. See Veryzer v. Sec’y of Health & Human Servs., No. 06-0522V, 2010 WL 2507791, at * 24 (Fed. Cl. Spec. Mstr. 2010) (noting that the relevant inquiry is whether, based on facts known to medical science and logical inferences drawn by a qualified expert, the vaccine at issue is more than likely to have caused the alleged injury), aff’d, 100 Fed. Cl. 349 (2011), aff’d, 475 F. App’x 765 (Fed. Cir. 2012). Petitioner’s theory of causation need not be medically or scientifically certain, Knudsen, 35 F.3d at 548-49, but it must be informed by “sound and reliable medical or scientific explanation,” id. at 548; see also Veryzer v. Sec’y of Health & Human Servs., 98 Fed. Cl. 214, 223 (2011) (noting that special masters are bound by both 42 U.S.C. 29 § 300aa-13(b)(1) and Vaccine Rule 8(b)(1) to consider only evidence that is both “relevant” and “reliable”). If petitioner relies upon a medical opinion to support her theory, the basis for the opinion and the reliability of that basis must be considered in the determination of how much weight to afford the offered opinion. See Broekelschen, 618 F. 3d at 1347 (“The special master’s decision often times is based on the credibility of the experts and the relative persuasiveness of their competing theories.”); Perreira v. Sec’y of Health & Human Servs., 33 F.3d 1375, 1377 n.6 (Fed. Cir. 1994) (citing Fehrs v. United States, 620 F.2d 255, 265 (Ct. Cl. 1980)) (“An expert opinion is no better than the soundness of the reasons supporting it.”). Petitioner’s medical records do not support her theory that the vaccine she received on February 22, 2008, caused her neurologic condition. There is no indication from her treating physicians that they considered her problems to be vaccine-related. Thus, petitioner must rely on Dr. Kinsbourne’s expert opinion to prevail on her claim. Because Dr. Kinsbourne has failed to persuade the undersigned that petitioner suffers from an ADEM variant, the undersigned does not evaluate whether petitioner put forth a biologically plausible theory explaining how the received flu vaccine could have caused ADEM. Petitioner’s claim that she developed ADEM as a result of the receipt of a flu vaccine necessarily fails on Prong One. An Althen analysis for petitioner’s undefined neurologic condition, however, is attempted. The record establishes that Dr. Sung affirmatively diagnosed petitioner with fibromyalgia. See Pet’r’s Ex. 4 at 25. But Dr. Kinsbourne did not mention petitioner’s fibromyalgia in either of his reports. Nor did the parties address the relevance of this diagnosis,34 and petitioner has not put forth any evidence that the flu vaccine could have caused her fibromyalgia. To the extent that petitioner claims that the received flu vaccine caused her fibromyalgia, the claim fails for lack of proof. The medical professionals who examined petitioner during the course of her protracted illness have yet to define or diagnose her neurologic condition. Although her treating neurologist initially considered a diagnosis of MS, no such formal diagnosis was made, and petitioner does not allege she suffers from MS. The parties do not dispute that petitioner has a lesion in her brain that appears to have resulted from a demyelinating process and is responsible for a measure of her neurologic symptoms. Because the potential spectrum of injuries that petitioner’s 34 Dr. Cohen mentioned this diagnosis once in his testimony, but he declined to discuss whether it had any relevance to petitioner’s vaccine claim. See Tr. 181. 30 symptoms suggest is too broad to evaluate for a vaccine-related injury, the undersigned cannot assess Dr. Kinsbourne’s theory of causation adequately. Petitioner has not satisfied Prong One. 2. Althen Prong Two: Logical Sequence of Cause and Effect Under Althen Prong Two, petitioner must establish “a logical sequence of cause and effect showing that the vaccination was the reason for the injury.” Althen, 418 F.3d at 1278. Under this prong, petitioner must show that the received vaccine “did” cause the alleged injury. Pafford, 451 F.3d at 1354. Petitioner need not make a specific type of evidentiary showing. That is, petitioner is not required to offer “epidemiologic studies, rechallenge, the presence of pathological markers or genetic disposition, or general acceptance in the scientific or medical communities to establish a logical sequence of cause and effect.” Capizzano, 440 F.3d at 1325. Instead, petitioner may satisfy her burden by presenting circumstantial evidence and reliable medical opinion. See id. at 1325-26. Here, the entirety of Dr. Kinsbourne’s opinion regarding the causal relationship between petitioner’s flu vaccine and her injuries turned on a finding that petitioner suffers from ADEM. But the evidence does not preponderate in favor of a finding that petitioner suffers from ADEM, the undersigned cannot evaluate whether petitioner’s illness is vaccine-related in the manner proposed by Dr. Kinsbourne. Petitioner does not prevail on Prong Two. 3. Althen Prong Three: Timing Under Althen prong three, petitioner must establish that her injury occurred within a time frame that is medically appropriate for the alleged mechanism of harm. See Pafford, 451 F.3d at 1358 (“Evidence demonstrating petitioner’s injury occurred within a medically acceptable time frame bolsters a link between the injury alleged and the vaccination at issue under the ‘but-for’ prong of the causation analysis.”). Petitioner may satisfy this prong by producing “preponderant proof that the onset of symptoms occurred within a time frame for which, given the medical understanding of the disorder’s etiology, it is medically acceptable to infer causation-in-fact.” de Bazan, 539 F.3d at 1352. Petitioner may discharge her burden by showing: (1) when the condition for which she seeks compensation first appeared after vaccination and (2) whether the period 31 of symptom onset is “medically acceptable to infer causation.” Shapiro v. Sec’y of Health & Human Servs., No. 99-552V, 2011 WL 1897650, at *13 (Fed. Cl. Spec. Mstr. Apr. 27, 2011), aff’d in relevant part, vacated in non-relevant part, 101 Fed. Cl. 532, 536 (2011), aff’d 503 F. App’x 952 (2013). The appropriate temporal association will vary according to the particular medical theory advanced in the case. See Pafford, 451 F.3d at 1358. Dr. Kinsbourne opined that petitioner’s symptoms first appeared approximately four weeks after her flu vaccine, and he asserted that this timing was appropriate based on his theory of causation. Pet’r’s Ex. 8 at 11. In particular, Dr. Kinsbourne advanced the theory that petitioner suffered from immune-mediated neurologic injuries that were caused by the biological mechanism of molecular mimicry, and that mechanism was augmented by bystander activation. Pet’r’s Ex. 8 at 9-10. In his initial report, Dr. Kinsbourne averred that [t]he accepted temporal relationship between influenza vaccination and the onset of immune-mediated neurological disorders is generally accepted as extending to at least 42 days, and there is evidence for even longer latencies between vaccination and disease onset. So the [four week] temporal interval between Ms. Stillwell’s vaccination and her first neurological symptoms fits comfortably into this time frame. Pet’r’s Ex. 8 at 11. Dr. Kinsbourne provided no medical literature to support this assertion. None of the articles he referenced in his initial report speak to the timeframe of symptom onset associated with immune-mediated neurologic injuries induced by molecular mimicry and/or bystander activation. To support his postulate that petitioner’s symptom onset occurred within an appropriate temporal interval, Dr. Kinsbourne quoted the 1994 IOM report in his supplemental expert report. Pet’r’s Ex. 9 at 4. He claimed that the 1994 IOM report “summarized the range of latencies as follows ‘a conservative estimate of the limits of the latencies for both GBS and ADEM is considered to be from 5 days to 6 weeks.’” Id.35 35 Dr. Kinsbourne quotes from Institute of Medicine, Adverse Events Associated with Childhood Vaccines: Evidence Bearing on Casuality 45 (Kathleen R. Stratton et al. eds., 1994) (emphasis added). Although petitioner filed another excerpt of this report, see Pet’r’s Ex. 8-6 at 511, petitioner did not file this quoted portion of this report as an exhibit. However, it is available in full online at http://www.nap.edu/catalog.php? record_ id=2138. 32 Dr. Kinsbourne again relied on this excerpted passage during his testimony at hearing. See Tr. 85. What Dr. Kinsbourne failed to address, however, is the preceding part of the excerpted paragraph, which states: . . . the expected latency between an antecedent event . . . and the first symptoms of [Guillain-Barré Syndrome (GBS)] is mainly between 7 and 21 days. Occasional cases appear to have latencies of between 22 and 42 days . . . [this] allow[s] a range of latencies to be stated for GBS, that is, 5 days to 6 weeks. Similarly, ADEM is widely believed to be the human counterpart of experimental allergic encephalomyelitis [(EAE)], and EAE has an observed latency of about 10 to 20 days. ADEM has a similar clinical latency.36 The full excerpt from the 1994 IOM report suggests that ADEM has a much shorter latency period than GBS, and this shorter period of latency undercuts Dr. Kinsbourne’s assertion that petitioner’s symptom onset was medically appropriate for ADEM. This IOM reference provides support for the proposition that petitioner’s neurologic complications occurred within the six-week time frame that may be appropriate for the onset of immune-mediated condition of GBS. But that is not the condition that petitioner here has developed. Petitioner has not offered preponderant evidence that her injuries occurred in a timeframe consistent with the proposed theory of causation. Snyder, 88 Fed. Cl. at 742- 43 (special masters are not required to accept the ipse dixit of an expert) (citing Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997)). Because petitioner has failed to meet her burden under the Althen prongs, she is not entitled to compensation, and her petition must be dismissed. de Bazan, 539 F.3d at 1354. IV. Conclusion 36 Institute of Medicine, Adverse Events Associated with Childhood Vaccines: Evidence Bearing on Casuality at 45, available at http://www.nap.edu/openbook.php?record_id= 2138&page=45. 33 For the foregoing reasons, petitioner’s claim for Program Compensation fails. The petition SHALL BE DISMISSED, and the Clerk of Court shall enter judgment consistent with this decision.37 IT IS SO ORDERED. s/ Patricia E. Campbell-Smith Patricia E. Campbell-Smith Chief Special Master 37 Pursuant to Vaccine Rule 11(a), entry of judgment is expedited by the parties’ joint filing of notice renouncing the right to seek review. 34 ================================================================================ DOCUMENT 2: USCOURTS-cofc-1_11-vv-00077-0 Date issued/filed: 2014-09-05 Pages: 16 Docket text: REISSUED, REPORTED VACCINE OPINION--Filed this date. Signed by Judge Lawrence J. Block. (smm) -------------------------------------------------------------------------------- Case 1:11-vv-00077-LB Document 47 Filed 09/05/14 Page 1 of 16 United States Court of Federal Claims No. 11-77 V (Filed Under Seal: August 21, 2014) (Reissued: September 5, 2014) _________________________________________ SHERRIL K. STILLWELL, Vaccine Act; Vaccine Injury; Petitioner, Motion for Review; ADEM; Diagnosis; Influenza; Flu Vaccination; Preponderance of v. Evidence SECRETARY OF HEALTH AND HUMAN SERVICES, Respondent. _________________________________________ Sol P. Ajalat, Esq., Ajalat & Ajalat, North Hollywood, CA, for petitioner. Alexis B Babcock, Esq., United States Department of Justice, Vaccine/Torts Branch, Civil Division, Washington, DC, for respondent. OPINION Block, Judge. This case is before the court on a motion to review (“Pet’r’s Mot.”) then Chief Special Master (“CSM”) Campbell-Smith’s decision to dismiss petitioner’s claim for compensation under the National Vaccine Injury Compensation Program (the “Vaccine Program” or “Vaccine Act”), 42 U.S.C. § 300aa-1 to -34, which provides compensation to individuals who can establish, by a preponderance of the evidence, that they have suffered “a vaccine-related injury.” § 300aa-11(c)(1)(C). Petitioner, Sherril K. Stillwell, alleges that she developed acute demyelinating encephalomyelitis (“ADEM”) as a result of an influenza (“flu”) vaccine she received on February 22, 2008.1 Pet. at 1. After holding an evidentiary hearing on the matter, the CSM concluded, on June 17, 2013, that petitioner had failed to prove by a preponderance of the evidence that she was suffering from ADEM, and denied compensation. Stillwell v. Sec'y of Health & Human Servs., (“Stillwell I”) 2013 WL 4540013 (Sp. Mstr. Fed. Cl. June 17, 2013).  This opinion originally was issued under seal on August 21, 2014. The court afforded the parties an opportunity to propose redactions in the opinion prior to its reissue. No such redactions were proffered. Accordingly, herewith is the reissued opinion without redactions. 1 In her petition, petitioner alleged that she suffered from “encephalomyelitis,” a general term for inflammation of the brain and spinal cord, which includes a wide range of disorders. Dorland's Illustrated Medical Dictionary 608 (31st ed. 2007). Subsequently, however, petitioner’s expert witness, Dr. Marcel Kinsbourne, alleged that petitioner was suffering from acute demyelinating encephalomyelitis or ADEM. See Pet’r’s Ex. 8 at 3, ECF No. 11. Case 1:11-vv-00077-LB Document 47 Filed 09/05/14 Page 2 of 16 Petitioner contends the CSM erred on two fronts. Pet’r’s Mot. at 4-13. First, petitioner argues that the CSM applied an incorrect legal standard. Pet’r’s Mot. at 4-5. In petitioner’s view, the CSM mistakenly applied the standard for determining whether petitioner suffered an actual injury, set forth in Broekelschen v. Sec’y of Health and Human Servs., 618 F.3d 1339 (Fed. Cir. 2010) and Lombardi v. Sec’y of Health and Human Servs., 656 F.3d 1343, 1352 (Fed. Cir. 2011), instead of the three-prong test for causation-in-fact established in Althen v Sec’y of Health and Human Servs., 418 F.3d 1274 (Fed Cir. 2005). Id. Second, petitioner argues that the CSM’s determination that petitioner was not suffering from ADEM and findings in support thereof were arbitrary and capricious. Pet’r’s Mot. at 5-13. For the reasons explained below, the court disagrees and concludes both that the CSM correctly applied the Lombardi standard and that the CSM’s finding that petitioner did not suffer from ADEM was not arbitrary or capricious. Accordingly, the court will affirm the CSM’s decision. I. BACKGROUND A. Petitioner’s Recent Medical History On February 22, 2008, petitioner received an influenza vaccination. Pet’r’s Ex. 2 at 2. In the months following her vaccination, petitioner experienced a series of physical ailments, including vertigo, nausea, dizziness, fatigue, numbness, and others. Pet’r’s Ex. 2, 3, 4, 7. Because physicians could not ascertain the cause of these symptoms, petitioner sought the opinions of practitioners from several fields of medicine. Id. On April 28, petitioner visited Chierry Anderson Poyotte, a doctor of internal medicine, and reported that she was suffering from right ear pain, weakness, and low energy, as well as vertigo and nausea. Pet’r’s Ex. 4 at 161. Dr. Poyotte diagnosed petitioner with “otitis media,” commonly known as an inner ear infection, and vertigo. Id. at 163. On April 30, petitioner returned to Dr. Poyotte, and stated that she continued to experience malaise and fatigue but Dr. Poyotte did not make any further diagnosis. Id. at 154. Petitioner then sought a second opinion from Natalie Ting, a doctor of osteopathic medicine, on May 6. Id. at 147. Petitioner described her symptoms as earache, fatigue, and dizziness. Id. She also stated that she had been experiencing numbness along the right side of her body for the past three weeks. Id. Dr. Ting did not offer a diagnosis but noted that, in her opinion, petitioner’s exam results were not consistent with the described symptoms. Id. at 149. On May 9, petitioner visited a second doctor of internal medicine, Kijung Paul Sung, reporting many of the same symptoms that she had reported to previous doctors, including vertigo, dizziness, fatigue, and numbness along the right side of her body. Id. at 139-140. Dr. Sung recommended, and petitioner underwent, a computer tomography (“CT”) scan and magnetic resonance imaging (“MRI”) of petitioner’s brain, both of which produced “unremarkable,” or normal, results. Id. at 142-3.2 2 Magnetic Resonance Imaging is “a method of visualizing soft tissues of the body by applying an external magnetic field that makes it possible to distinguish between hydrogen atoms in - 2 - Case 1:11-vv-00077-LB Document 47 Filed 09/05/14 Page 3 of 16 On May 27, petitioner checked-in to an emergency room after experiencing vertigo, anomalous tastings, numbness and weakness on her right side, and difficulty speaking and coordinating muscle movements. Pet’r’s Ex. 4 at 128. Attending physicians conducted an MRI of petitioner’s brain and cervical spine. Id. at 127. Neither test revealed a notable physical abnormality and physicians noted that the cause of her symptoms was “unclear” at that time. Id. at 128. Petitioner next sought out a neurologist, David Shaw, on June 9, complaining of unsteady gait, blurred vision, generalized weakness, and intermittent neck pain, in addition to her previous symptoms. Id. at 114. Dr. Shaw suspected petitioner was afflicted with multiple sclerosis (“MS”)3 and ordered a visual evoked response test to confirm his diagnoses. Id. at 115. But, Dr. Shaw noted the lack of lesions or other “obvious evidence” of MS on petitioner’s MRI. On June 10, petitioner underwent an electroencephalogram (“EEG”) test and visual evoked response test, receiving normal results. Id. 111, 120.4 Also on June 10, petitioner visited a second neurologist, William Miller, and relayed similar, but “progressively worsen[ing],” symptoms. Pet’r’s Ex. 3 at 155. During this visit, petitioner mentioned, for the first time, that for “several weeks” prior to the onset of her initial different environments.” Dorland's at 916. Medical professionals use magnetic resonance imaging to observe lesions in the brain of patients that are suspected to have demyelinating diseases such as MS and ADEM. Computer Tomography (also known as “CT scans” or “CAT scans”) “combines a series of X-ray views taken from many different angles and computer processing to create cross-sectional images of the bones and soft tissues inside [the] body.” See Mayo Clinic definition, available at http://www.mayoclinic.org/tests-procedures/ct-scan/basics/definition/prc-20014610. 3 Multiple sclerosis is a disorder of the central nervous system that produces clinical symptoms such as “weakness, incoordination, paresthesia, speech disturbances, and visual complaints.” Dorland's at 1706. It is characterized by “[centers] of demyelination throughout the white matter of the central nervous system, sometimes extending into the gray matter.” Id. Demyelination, in turn, is a medical term for deterioration or damage to the protective coating (i.e., the “myelin sheath”) that surrounds the nerve fibers in the body’s brain and spinal cord. Dorland's at 493. There are three variants of inflammatory demyelination diseases: MS, acute- disseminated encephalomyelitis (“ADEM”), and acute hemorrhagic leukoencephalitis. Id. 4 An electroencephalogram test (“EEG”) is “a recording of the potentials of the skull generated by currents emanating spontaneously from nerve cells to the brain. The normal dominant frequency of these potentials is about 8 to 10 cycles per second and the amplitude about 10 to 100 microvolts. Fluctuations in potential are seen in the form of waves, which correlate well with neurologic conditions and so are used in diagnostic criteria.” Dorland’s at 607. A visual evoked response test, also known as a visual evoked potential study, measures “changes in the evoked cortical potential when the eye is stimulated by light.” Dorland’s at 1496. Stated otherwise, the test uses electrodes to measure the time it takes for nerves to respond to optical stimulation. - 3 - Case 1:11-vv-00077-LB Document 47 Filed 09/05/14 Page 4 of 16 symptoms, she had experienced a sensation that her “socks seemed too tight” against her legs. Id. Dr. Miller considered several diagnoses, including MS, but was puzzled by the lack of a lesion on petitioner’s MRI to explain the symptoms and noted that it was “hard to localize [a] lesion that would explain all of her symptoms.” Id. at 158. On July 17, a test of petitioner’s cerebrospinal fluid displayed indicia of MS. Pet’r’s Ex. 7 at 14-15. On August 2, 2008, an MRI revealed an “unusual lesion” providing evidence of a demyelinating disease. Pet’r’s Ex. 3 at 123. On August 20, petitioner met with a third neurologist, Christopher Di Stasio. Pet’r’s Ex. 4 at 68-72. During her appointment, petitioner conveyed that, while her vertigo and numbness were improving, other symptoms remained constant. Id. at 73. Dr. Di Stasio noted that petitioner was “starting to slowly improve.” Id. at 71. On September 8, petitioner returned to Dr. Miller, who diagnosed her with a demyelinating disease that he believed was “improving slowly.” Pet’r’s Ex. 3 at 102. On March 20, 2010, petitioner underwent another brain MRI. Id. at 61. The results demonstrated improvement and reinforced Dr. Miller’s diagnosis of a probable “monophasic demyelinating event.” Pet’r’s Ex. 7 at 7. This diagnosis was confirmed on July 30, 2010, when Dr. Sung diagnosed petitioner with a demyelinating disease and fibromyalgia. Id. at 25. After visiting more than six different physicians, petitioner was finally diagnosed with a demyelinating disease. B. Proceedings Before the Chief Special Master On February 7, 2011, petitioner filed a request for compensation under the Vaccine Program, 42 U.S.C. §§ 300aa–1 to –34, which allows petitioners to seek compensation if they have “sustained, or ha[ve] significantly aggravated” any “vaccine-related” “illness, disability, injury, or condition.” § 300a-11(c)(1)(C). The parties, however, disagree about the nature of petitioner’s injury, and whether petitioner’s alleged injury can be caused by flu vaccination. Petitioner and respondent each proffered expert reports on this issue. 1. Petitioner’s Expert Petitioner filed the report of Dr. Marcel Kinsbourne, a neurologist and author of many medical books, articles, and other medical-related literature. Pet’r’s Ex. 8. Dr. Kinsbourne’s opinion, petitioner suffered from “a variant of ADEM” distinguished by its “subacute,” or delayed, onset. Pet’r’s Ex. 8 at 6. Dr. Kinsbourne stated that ADEM typically manifests within “a few days or weeks.” Id. Dr. Kinsbourne believed this was consistent with petitioner’s condition, which set in “[a]pproximately four weeks” following petitioner’s vaccination in the third week of March of 2008 and “progressed for several months before it stabilized.” Id. at 5; see also Tr. at 9, 25. In the evidentiary hearing, Dr. Kinsbourne averred that it is possible for ADEM to set in subacutely, taking up to 42 days to surface. Tr. 34. In support of this assertion, Dr. Kinsbourne cited a 1994 Institute of Medicine report, which stated that the latency for ADEM can be between “5 days to 6 weeks,” as well as two other documents,5 referred to as the Singh and Leake articles. Tr. 34; Pet’r’s Ex. 8-6 at 503. 5 Pet’r’s Ex. 8-6 at 503, Surendra Singh et al., Acute Disseminated Encephalomyelitis: MR Imaging Features, 173 AJR 1101 (1999); Pet’r’s Ex. 8-4 at 387, John A.D. Leake et al., Acute - 4 - Case 1:11-vv-00077-LB Document 47 Filed 09/05/14 Page 5 of 16 Dr. Kinsbourne also relied on an article referred to by the parties as the “Sejvar” article.6 Tr. 30, 50-55, 156. The Sejvar article establishes criteria for various levels of “diagnostic certainty” in identifying ADEM. Id. Among others, the Sejvar article cited (1) single brain lesion, (2) trouble finding words, (3) cranial nerve abnormalities, (4) motor weakness, (5) sensory abnormalities, (6) ataxia (uncoordinated movement) and gait dysfunction, and (7) arm tremors as indicia of ADEM. Id. at 5776-79. Dr. Kinsbourne averred that petitioner suffered from five of these symptoms: “decreased arousability, aphasia [or language comprehension difficulty], motor weakness, sensory abnormalities, and ataxia.” Pet’r’s Ex. 9 at 1-2. Notably, the Sejvar article states that an ADEM diagnosis must include discovery of diffuse or multi-focal white matter lesions. Tr 75-76. Dr. Kinsbourne stated that petitioner’s MRI results were consistent with a diffused white matter lesion and, thus, with ADEM. Id. at 76. Dr. Kinsbourne also attested to the causal connection between the flu vaccine and ADEM, calling the link “rare” but “well recognized.” Pet’r’s Ex. 8 at 7-9 (citing Hiroshi Shoji & Mashahide Kaji, The Influenza Vaccination and Neurological Complications, 42:2 THE JAPANESE SOC’Y OF INTERNAL MED. 1 (2003)). He discounted a 2011 study by the Institute of Medicine that determined there was insufficient evidence to establish a causal relationship between the flu vaccine and ADEM. Tr. 78. 2. Respondent’s Expert Respondent presented the report of Dr. Jeffrey Allen Cohen, a clinical neurologist, professor of neurology at Dartmouth medical school, and chief neurologist at Dartmouth Hitchcock Medical Center. Resp’t’s Ex. A; see also Tr. 102. Dr. Cohen averred that petitioner did not suffer from ADEM. Resp’t’s Ex. A at 1. In his opinion, petitioner’s “clinical picture was not consistent with [that] diagnosis.” Id. at 6. Dr. Cohen also stated that the duration of petitioner’s symptoms was “very atypical for ADEM—[a disease which generally] progresses over weeks, not months.” Resp’t’s Ex. A at 2. In Dr. Cohen’s view, onset of ADEM, is almost always acute and even a subacute onset of more than four weeks is “very unusual.” Id. at 5; see also Tr. 141-42. Dr. Cohen testified that in his clinical experience, the outer range for onset of ADEM symptoms is four weeks after the vaccination or infection. Tr. 155-56. Dr. Cohen further noted that ADEM is a disease “that is severe and swift in its onset, reaches a nadir, and then . . . gets better . . . to a great degree.” Tr. 178. Dr. Cohen stated that the majority of ADEM patients’ symptoms “tend[] to resolve over a period of . . . two, three, or four months.” Tr. 119. In Dr. Cohen’s opinion, petitioner’s condition was not consistent with this timetable because her physicians’ treatment choices indicated they believed that “she was getting worse.” Tr. 117. Dr. Cohen also commented that although there is no “specific marker” for ADEM, it would be “very unusual” for a patient not to exhibit diffused or multifocal white matter lesions. Disseminated Encephalomyelitis in Childhood: Epidemiologic, Clincal and Laboratory Features, 23:8 PEDIATRIC INFECTIOUS DISEASE J. 756 (2004). 6 Pet’r’s Ex. 9-1, James J. Sejvar et al., Encephalitis, myelitis, and acute disseminated encephalomyelitis (ADEM): Case definitions and guidelines for collection, analysis, and presentation of immunization safety data, 25 VACCINE 5771 (2007). - 5 - Case 1:11-vv-00077-LB Document 47 Filed 09/05/14 Page 6 of 16 Tr. 107-108. Dr. Cohen did not observe any evidence of white matter lesions on either of petitioner’s MRI exams taken in May of 2008. Tr. 114. He also stated that there was no record of petitioner suffering from facial weakness, a common and readily noted ADEM indicator. Tr. 113-14. Further, Dr. Cohen believed that the lack of a “markedly depressed level of consciousness” indicated petitioner did not suffer from ADEM. Resp’t’s Ex. C at 1. Additionally, Dr. Cohen contended that petitioner’s medical history did not support an ADEM diagnosis because petitioner’s symptoms were not “diagnosis-specific neurologic findings.” Id. Dr. Cohen observed that symptoms such as decreased arousability, aphasia, motor weakness, sensory abnormalities, and ataxia can indicate conditions such as stroke, traumatic brain injury, or MS. Id. He also stated that the location of petitioner’s demyelination, on her brain stem, “is not the usual location for ADEM” and the area of demyelination was not “as extensive” as Dr. Cohen would expect in an ADEM case. Resp’t’s Ex. A at 2. Dr. Cohen also argued that “ADEM is a disease [that appears] almost exclusively . . . in children and adolescents” and noted that petitioner was in her 50’s at the time of vaccination. Id. at 3. Dr. Cohen critiqued Dr. Kinsbourne’s statements, arguing that Dr. Kinsbourne cited to medical articles that were not applicable to petitioner’s clinical picture. Id. at 3; Resp’t’s Ex. C at 1. In Dr. Cohen’s opinion, medical literature does not present “reliable evidence” that the flu vaccine can cause ADEM. Tr. 169-70. C. The Chief Special Master’s Decision On June 17, 2013, the CSM issued a decision denying compensation under the Vaccine Act. The CSM considered the evidence in the record, including Dr. Kinsbourne and Dr. Cohen’s reports and testimony, and disagreed with Dr. Kinsbourne’s assertion that petitioner’s condition was an “atypical ADEM variant.” Stillwell I at 16. Rather, the CSM found that the following six factors “weigh against a finding that petitioner has ADEM.” Id. First, the CSM found that “although it is not dispositive,” the statistics presented by both experts on the typical age of patients who develop ADEM warranted consideration. Id. at 16-17. The CSM noted that Dr. Kinsbourne and Dr. Cohen agreed that ADEM “primarily afflicts children and adolescents.” Id. at 16-17 (citing Tr. 29, 38). Cases of ADEM in adults are less common but have been reported “in young and elderly adults.” Id. at 16-17. Petitioner, 53 at the time of vaccination, does not qualify for either of these groups. The CSM considered the statistical unlikelihood that petitioner suffered from an adult, middle-aged case of ADEM. Second, the CSM observed that none of the petitioner’s numerous physicians diagnosed her with ADEM. Id. at 17. The CSM noted that petitioner’s treating physicians speculated her condition might be due to MS before eventually diagnosing her with a general demyelinating brain disorder. Id. The CSM found that, contrary to Dr. Kinsbourne’s assertions, the treatment prescribed to petitioner by her physicians was not consistent with ADEM. Id. The nature of petitioner’s brain lesion formed the third basis for the CSM’s findings. Id. at 18-20. It is uncontroverted that petitioner suffered from a brain lesion. Id. But, the parties’ experts disagree on whether petitioner’s lesion was diffuse or multifocal, the latter being a necessary condition for ADEM. Id. Dr. Kinsbourne contended that petitioner’s solitary brainstem lesion was both single and “diffused,” and was consistent with “classical descriptions of ADEM” lesions. Id. (quoting from Tr. 22). Dr. Cohen argued that a solitary brainstem lesion - 6 - Case 1:11-vv-00077-LB Document 47 Filed 09/05/14 Page 7 of 16 was atypical, and cited articles describing lesions in ADEM patients as “typically reveal[ing] multifocal, bilateral, often large white matter lesions.” Id. (quoting Resp’t’s Ex. A-9 at 2). The CSM concluded that “[w]hether petitioner’s brain lesion bore the appearance of the type of lesion usually seen in ADEM subjects is not clear from the record.” Id. at 20. The parties’ experts could not interpret petitioner’s test results because the images were not available. Id. Consequently, the CSM determined that Dr. Kinsbourne’s contention that petitioner’s lesion “was sufficiently diffuse” to demonstrate ADEM was not persuasive because “petitioner’s own treating physicians,” who were able to review the image results, “were not persuaded.” Id. Fourth, the CSM found that the timing of petitioner’s symptoms was inconsistent with ADEM. Id. 21-25. Petitioner was vaccinated on February 22, 2008. Pet’r’s Ex. 2 at 1. She reported her initial symptom, vertigo, during an April doctor’s visit, stating that her symptoms dated back “several weeks.” Pet’r’s Ex. 3 at 159-60. On June 20, petitioner told her physicians that “on reflection” she had noticed that her “socks seemed too tight on [her] legs” for several weeks prior to the onset of her vertigo symptoms. Id. The CSM commented that “petitioner’s own accounts of her symptom onset [are] inconsistent.” Id. The CSM then summarized the medical literature presented by the parties’ experts and concluded that it is “clear that ADEM most commonly manifests abruptly, although several of the articles Dr. Kinsbourne citied furnished the barest of support for his proposition that petitioner’s subacute onset was an appropriate—even if aberrant—presentation of ADEM.” Id. at 24. The CSM concluded that “[t]he timing of petitioner’s symptom onset was unusually protracted” and “does not fit within the recognized time frame for most cases of ADEM.” Id. at 25. Fifth, the CSM further noted that the nature and severity of petitioner’s symptoms was not indicative of ADEM. Id. at 25-27. Dr. Kinsbourne and Dr. Cohen agreed that decreased level of consciousness, sometimes resulting in coma, is a common symptom of ADEM. Id. Petitioner did not exhibit this symptom. Id. The parties disputed whether the ADEM symptoms petitioner did exhibit rose to the level of typical ADEM symptoms. Id. The CSM found that “[t]he views of the parties’ experts are inconclusive” because they did not have the opportunity to observe petitioner firsthand. Id. As a result, the CSM was “informed . . . by the silence of petitioner’s treaters—who did observe her— on the matter of her symptom severity.” Id. The CSM determined that the lack of evidence demonstrating decreased consciousness and relatively low symptom severity suggested petitioner did not suffer from ADEM. Id. Finally, the CSM found that the protracted course of petitioner’s injury and limited recovery demonstrated that her condition was not caused by ADEM. Id. at 27-28. The CSM stated that “[t]he record indicates that petitioner’s condition did not plateau and then gradually improve—as would be expected with a case of ADEM. Instead, petitioner struggled . . . with a protracted clinical course marked by many periods of exacerbation.” Id. The CSM concluded that the “course of petitioner’s illness strongly suggests that she did not suffer from ADEM” and that “[p]etitioner’s overall clinical course was inconsistent with the well-recognized course of ADEM.” Id. Weighing these six factors, the CSM determined that petitioner “failed to prove by preponderant evidence that she developed ADEM.” Id. at 28. Rather, the CSM found that petitioner “appear[s] to suffer from another, unspecified illness that has bewildered her - 7 - Case 1:11-vv-00077-LB Document 47 Filed 09/05/14 Page 8 of 16 physicians.” Stillwell I at 16. Relying on precedents set by the Court of Appeals for the Federal Circuit (“Federal Circuit”) in Broekelschen and Lombardi, the CSM concluded that the failure of petitioner to establish the alleged injury of ADEM precluded the CSM from finding that this injury had been caused by petitioner’s flu vaccination. In light of this ADEM failure of proof, the CSM determined that petitioner was not entitled to compensation under the Vaccine Act. Id. Nonetheless, in “an abundance of caution,” the CSM proceeded to apply the Althen test for causation, and concluded that petitioner failed to satisfy this test. On July 9, 2013, petitioner filed a timely motion to review the CSM’s decision. This matter is now ripe for decision. II. STANDARD OF REVIEW FOR VACCINE ACT CASES The Court of Federal Claims has jurisdiction to review the decision of a special master in a Vaccine Act case upon a properly filed petition for review. 42 U.S.C. § 300aa—12(e)(1). When reviewing a special master’s decision, the court must take one of the following three courses of action: (A) Uphold the findings of fact and conclusions of law of the special master and sustain the special master’s decision, (B) Set aside any findings of fact or conclusion of law of the special master found to be arbitrary, capricious, an abuse of discretion, or otherwise not in accordance with law and issue its own findings of fact and conclusions of law, or (C) Remand the petition to the special master for further action in accordance with the court’s decision. 42 U.S.C. § 300aa–12(e)(2). In Vaccine Act cases, the court applies different standards of review to different aspects of a special master’s decision: the court reviews conclusions of law under the “not in accordance with law” standard, findings of fact under the deferential arbitrary and capricious standard, and discretionary rulings under the abuse of discretion standard. Masias v. Sec’y of Health & Human Servs., 634 F.3d 1283, 1287-88 (Fed. Cir. 2011) (construing 42 U.S.C. § 300aa–12(e)(2)(B)); see also Munn v. Sec’y of Dep’t of Health & Human Servs., 970 F.2d 863, 871 no. 10 (Fed. Cir. 1992); Pafford v. Sec’y of Health and Human Servs., 64 Fed. Cl. 19, 27 (2005), aff’d, 451 F.3d 1352 (Fed. Cir. 2006). With regard to a special master’s conclusions of law, such as conclusions regarding legal standards and burdens of proof, the court applies the “not in accordance with law standard.” Doe 93 v. Sec'y of Health & Human Servs., 98 Fed. Cl. 553, 566 (2011). Under this legal standard, a special master’s application of the law is not entitled to any deference. Jarvis v. Sec’y of Health and Human Servs., 99 Fed. Cl. 47, 58 (2011); see also Althen, 418 F.3d at 1278–79 (observing that this court's “not in accordance with law” review of a special master's decision in a Vaccine Act case is de novo); Saunders v. Sec'y of Dep't of Health & Human Servs., 25 F.3d 1031, 1033 (Fed. Cir. 1994) (“Because [the special master’s award of attorneys’ fees] is a legal question, we - 8 - Case 1:11-vv-00077-LB Document 47 Filed 09/05/14 Page 9 of 16 apply the “not in accordance with law” standard. Thus, we review the special master's award de novo . . .”). In contrast, a special master’s findings of fact are reviewed under the arbitrary and capricious standard, which is “well understood to be the most deferential possible.” Munn, 970 F.2d at 870. “Congress assigned to a group of specialists, the Special Masters within the Court of Federal Claims, the unenviable job of sorting through these painful cases and, based upon their accumulated expertise in the field, judging the merits of the individual claims.” Deribeaux ex rel. Deribeaux v. Sec’y of Health & Human Servs., 717 F.3d 1363, 1366 (Fed. Cir. 2013) (quoting Hodges v. Sec’y of Dept. of Health & Human Servs., 9 F.3d 958, 961 (Fed. Cir. 1993) (internal citations omitted)). Accordingly, it is not the role of this court to “reweigh the factual evidence,” “assess whether the special master correctly evaluated the evidence,” or “examine the probative value of the evidence or the credibility of the witnesses.” Lampe v. Sec’y of Health & Human Servs., 219 F.3d 1357, 1360 (Fed. Cir. 2010). “If the special master ‘has considered the relevant evidence of record, drawn plausible inferences and articulated a rational basis for the decision, reversible error will be extremely difficult to demonstrate.’” Hibbard v. Sec’y of Health & Human Servs., 698 F.3d at 1363 (quoting Hines on Behalf of Sevier v. Sec’y of Dep’t of Health & Human Servs., 940 F.2d 1518, 1528 (Fed. Cir. 1991)). In other words, the court is “not to second guess [a] [s]pecial [m]aster’s fact-intensive conclusions; the standard of review is uniquely deferential for what is essentially a judicial process.” Hodges v. Sec’y of Health & Human Servs., 9 F.3d 958, 961 (Fed. Cir. 1993). Finally, the court reviews a special master’s discretionary rulings for “abuse of discretion.” Munn, 970 F.2d at 870 n. 10. Such rulings typically include review of evidentiary rulings. See, e.g. Piscopo v. Sec’y of Health & Human Servs. 66 Fed. Cl. 49, 53 (2005). “An abuse of discretion may be found when (1) the court's decision is clearly unreasonable, arbitrary, or fanciful; (2) the decision is based on an erroneous conclusion of the law; (3) the court's findings are clearly erroneous; or (4) the record contains no evidence upon which the court rationally could have based its decision.” Hendler v. United States, 952 F.2d 1364, 1380 (Fed. Cir. 1991); Woods v. Sec'y of Health & Human Servs., 105 Fed. Cl. 148, 151 (2012). III. DISCUSSION A. Vaccine Act Standards The Vaccine Act, 42 U.S.C. §§ 300aa–1 to –34, established the National Vaccine Injury Compensation Program to compensate individuals injured by vaccines “quickly, easily, and with certainty and generosity.” H.R. Rep. No. 99–908, at 6 (1986), 1986 U.S.C.C.A.N. at 6344. The Vaccine Act allows petitioners to seek compensation if they have “sustained, or ha[ve] significantly aggravated” any “vaccine-related” “illness, disability, injury, or condition” caused by a vaccine. 42 U.S.C. § 300a-11(c)(1)(C). The Act provides petitioners two avenues for obtaining compensation: “table” and “off- table” claims. W.C. Sec’y of Health & Human Servs., 704 F.3d 1352, 1355 (Fed. Cir. 2013). In a table claim, if the petitioner can demonstrate that they received a vaccine listed in the Vaccine Injury Table and that they suffered an injury within the time period defined by the table, the - 9 - Case 1:11-vv-00077-LB Document 47 Filed 09/05/14 Page 10 of 16 petitioner “benefits from a statutory presumption of causation.” Id. But if the injury is not listed in the table, the petitioner must establish actual causation “by a preponderance of the evidence.” Id.; 42 U.S.C. § 300aa-13(a)(1). Stated another way, a petitioner making an off-table claim must present evidence showing that the vaccine “more likely than not” caused the injury. Capizzano v. Sec’y of Health & Human Servs., 440 F.3d 1317, 1326 (Fed. Cir. 2006). Since ADEM is not an injury listed on the Vaccine Injury Table, see 42 C.F.R. § 100.3, this case presents an off-table claim. In order to meet the preponderance of the evidence requirement for successfully bringing an off-table claim, the petitioner has the burden of satisfying the following three-prong test set forth in Althen v. Sec’y of Health & Human Servs.: Concisely stated, [petitioner’s] burden is to show by preponderant evidence that the vaccination brought about her injury by providing: (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. If [petitioner] satisfies this burden, she is entitled to recover unless the [government] shows, also by a preponderance of evidence, that the injury was in fact caused by factors unrelated to the vaccine. 418 F.3d 1274, 1278 (Fed. Cir. 2005). In Althen, the Federal Circuit emphasized that the Vaccine Act does not require exact or conclusive evidence of causation, but a medically credible theory coupled with evidence of a proximate temporal and causal relationship between the injury and the vaccination. See Althen, 418 F.3d at 1281-1282 (stating that “the purpose of the Vaccine Act's preponderance standard is to allow the finding of causation in a field bereft of complete and direct proof of how vaccines affect the human body”). Generally speaking, this standard simply requires the special master to consider whether there is preponderant evidence showing that the vaccine caused the alleged injury. “The function of a special master is not to ‘diagnose’ vaccine-related injuries, but instead to determine based on the record evidence as a whole and the totality of the case, whether it has been shown by a preponderance of the evidence that a vaccine caused [petitioner’s] injury.” Lombardi, 656 F.3d at 1352-53 (quoting Andreu ex rel. Andreu v. Sec'y of Dep't of Health & Human Servs., 569 F.3d 1367, 1382 (Fed. Cir. 2009)). Although the Vaccine Act does not require absolute precision, it does require the petitioner to establish an injury—the Act specifically creates a claim for compensation for “vaccine-related injury or death.” 42 U.S.C. § 300aa-11(c) (emphasis added). Accordingly, the Federal Circuit has held, in a series of recent decisions beginning with Broekelschen v. Sec’y of Health and Human Servs., 618 F.3d 1339 (Fed. Cir. 2010), that if the special master finds, as a preliminary matter, that petitioner has failed to substantiate the alleged injury, the special master need not apply the Althen test for causality. - 10 - Case 1:11-vv-00077-LB Document 47 Filed 09/05/14 Page 11 of 16 In Broekelschen, the petitioner experienced symptoms attributable to either transverse myelitis (“TM”) or anterior spinal artery syndrome, and had received differential diagnoses for those two conditions. Petitioner argued that his flu vaccination caused him to suffer TM, a neurological disorder that has been causally connected with the flu vaccine. Respondent disputed this assertion, and argued that petitioner had suffered anterior spinal artery syndrome, a vascular disorder that is not caused by the flu vaccine. See id. at 1342-44. The Special Master found that the record supported respondent’s position, and denied the petition without applying the Althen test. The Broekelschen court observed that “the instant action is atypical because the injury itself is in dispute, the proposed injuries differ significantly in their pathology, and the question of causation turns on which injury [petitioner] suffered.” Id. at 1346 (emphasis added). The court, in a 2-1 opinion, upheld the Special Master’s approach, stating that “[m]edical recognition of the injury claimed is critical and by definition a ‘vaccine-related injury’ . . . has to be more than just a symptom or manifestation of an unknown injury.” Id. at 1349. The court distinguished the case from Andreu, "where the parties agreed that the petitioner suffered from a seizure disorder . . . or Kelley, where the competing diagnoses were variants of the same disorder . . . . Here, nearly all of the evidence on causation was dependent on the diagnosis of [petitioner’s] injury. Therefore, it was appropriate for the special master to first find which of [petitioner’s] diagnoses was best supported by the evidence presented in the record before applying the Althen test.” Id. at 1346 (discussing Andreu, 569 F.3d at 1378 and Kelley Sec’y of Health and Human Servs., 68 Fed. Cl. 84, 100-01 (2005)). In Lombardi, the Federal Circuit also affirmed a special master assessing the injury claimed by petitioner without applying the Althen test. Lombardi, 656 F.3d at 1352-53. The petitioner in that case was afflicted with pain radiating into her right chest and with chronic fatigue, beginning shortly after she had received a third dose of the hepatitis B vaccine. The petitioner visited a number of doctors, who struggled to identify the etiology of her condition. The petition itself “did not identify any injuries, but claimed that [petitioner] had sought frequent medical treatment following the vaccination.” Id. at 1348. The petitioner’s expert witnesses suggested several possible conditions that had been causally associated with the hepatitis B vaccine but were not listed on the Vaccine Injury Table. Respondent’s witnesses argued that petitioner did not suffer from any of these conditions, but suggested several alternatives not causally associated with the vaccine. See id. at 1345-49. The Special Master in Lombardi analyzed the evidence in the record and concluded that petitioner had “not established that she suffers from any of the three conditions that provide the basis for her experts’ opinions.” Id. at 1349 (quoting Doe 60 v. Sec’y of Health & Human Servs., No. 99–VV–523, 2010 WL 1506010 (Fed. Cl. Mar. 26, 2010)). The Special Master found the cause of petitioner’s condition elusive and denied compensation under the Vaccine Act, without reaching the Althen test. Id. The Federal Circuit affirmed the Special Master’s approach, holding that “[i]n the face of such extreme disagreement among well-qualified medical experts, each of whom had evaluated the petitioner, it was appropriate for the Special Master to first - 11 - Case 1:11-vv-00077-LB Document 47 Filed 09/05/14 Page 12 of 16 determine what injury, if any, was supported by the evidence in the record before applying the Althen test to determine causation. In the absence of any specific injury of which petitioner complains, the question of causation is not reached.” Lombardi, 656 F.3d at 1352-53 (emphasis added) (internal citations removed). Initially, the scope of the Broekelschen and Lombardi opinions was subject to dispute. Previous opinions on this court, for instance, have narrowly characterized Broekelschen and Lombardi as “exceptions to the general rule” that “a special master should not conduct a differential diagnosis, at the outset of the causation analysis, to choose one diagnosis over another, or over a combination of diagnoses.” Contreras v. Sec’y of Health and Human Servs., 107 Fed. Cl. 280, 293 (2012). The court, in Contreras, argued that Broekelschen only applied in cases where “two competing diagnoses of dissimilar diseases” are presented. Id. at 293. That opinion characterized the injury analysis from Broekelschen and Lombardi “as a first step in the causation analysis.” Id. The Contreras court construed Lombardi narrowly, limiting it to “an unusual case where: (1) the petitioner presents conflicting diagnoses of her alleged vaccine injury; (2) the experts have ‘extreme disagreement’ as to the malady suffered; and (3) the diagnoses are not along a continuum of similar conditions.” Id. at 294-95. In the meantime, the Federal Circuit has taken a different approach. Several months after Contreras was decided, the Federal Circuit issued Hibbard v. Sec’y of Health and Human Services, 698 F.3d 1355 (2012), a case that expanded the scope of the Broekelschen and Lombardi rulings. Hibbard, unlike Broekelschen and Lombardi, did not feature dueling theories of the nature of the injury afflicting the petitioner. In Hibbard, it was uncontroverted that petitioner suffered from dysautonomia, a dysfunction of the automatic nervous system. Id. The only dispute was whether a flu vaccination caused petitioner to suffer postural orthostatic tachycardia syndrome (“POTS”), a limited form of autonomic neuropathy that manifests itself as dysautonomia, or whether petitioner’s dysauonomia was caused by some other factor. Id. Respondent challenged whether petitioner could prove by a preponderance of the evidence that petitioner had suffered POTS, but in contrast to Broekelschen and Lombardi, did not offer any alternate theory of causation. Id. The Special Master found the evidence for POTS inconclusive, and denied compensation without applying Althen. Id. Petitioner, in response, argued that this approach conflicted with the burden-sharing test set forth in Althen. Id. The Federal Circuit, in Hibbard, upheld the Special Master’s decision, without any of the qualifying language used in Broekelschen and Lombardi. The court held that: “[i]f a special master can determine that a petitioner did not suffer the injury that she claims was caused by the vaccine, there is no reason why the special master should be required to undertake and answer the separate (and frequently more difficult) question whether there is a medical theory, supported by ‘reputable medical or scientific explanation,’ by which a vaccine can cause the kind of injury that the petitioner claims to have suffered.” Hibbard, 698 F.3d at 1365. The court explicitly expanded the scope of the injury inquiry by contrasting the facts of the case with “previous cases” like Lombardi and Broekelschen, in which there was an actual dispute as to which injury afflicted the petitioner. See also Hibbard, 698 - 12 - Case 1:11-vv-00077-LB Document 47 Filed 09/05/14 Page 13 of 16 F.3d at 1370-71 (O’Malley, J., dissenting) (criticizing the majority for extending Broekelschen “well beyond its facts”). This approach also differs markedly from the “general rule” that a special master should avoid selecting among differential diagnoses—the court held that “even assuming the medical plausibility of [petitioner’s] theory of causation—that the vaccine triggered an immune response that damaged her autonomic nerves—her failure to show that she had autonomic neuropathy would be fatal to her case” because “whether [petitioner] suffers from autonomic neuropathy . . . was a necessary component to her theory of vaccine-induced injury.” Id. at 1365. C.f. Andreu, 569 F.3d at 1378 (holding that petitioner was not required to prove whether petitioner had suffered a febrile or afebrile seizure because the parties agreed that toxins in the TBT vaccine can cause seizures, even if there was disagreement in the scientific literature as to whether the vaccine could cause afebrile seizures); Kelley, 68 Fed. Cl. at 100-01 (2005) (holding that petitioner was not required to precisely categorize his injury where the two possible diagnoses were “variants of the same disorder”). B. Review of the Special Master’s Decision 1. The Special Master Correctly Applied the Law Petitioner argues that “the Chief Special Master erred as a matter of law in applying the Lombardi approach to the present case” because this case “involv[ed] a question as to the classification of a disease within an identified disease process, rather than whether an unidentified disease process exists.” Id. at 14. In essence, petitioner contends that the CSM errantly treated the uncertainty as to the sub-type of petitioner’s demyelinating encephalomyelitis (ADEM, MS, or other) as if the cause of petitioner’s injuries was unknown. Id. Petitioner argues that “the sub-classification . . . is of assistance [solely] for medical purposes, in the treatment of the disease process.” Id. at 5. Petitioner asserts that she undisputedly “suffers from an acquired demyelinating encephalomyelitis involving lesions at the pons and mid-areas of her brain.” Pet’r’s Mot. at 4. As explained above, the court reviews legal conclusions, such as the CSM’s decision to apply Lombardi, under the “not in accordance with law” standard. Masias, 634 F.3d at 1287-88 (construing 42 U.S.C. § 300aa–12(e)(2)(B)). Applying this standard, the court affirms the CSM’s application of Lombardi. Petitioner simply misstates the law as it currently stands. Although the Federal Circuit has continued to recite the general principle that it is not the role of a special master to engage in differential diagnosis, the Federal Circuit has increasingly emphasized that a petitioner must, as a preliminary matter, establish a specific injury in order for the Althen test to come into play. Critically, Federal Circuit precedent dictates that the petitioner has the burden of proving, by the preponderance of the evidence, that they are actually afflicted by the injury which, under their theory of vaccine-induced injury, was caused by the vaccine. See Hibbard, 698 F.3d at 1365. A “vaccine-related injury” must be “more than just a symptom or manifestation of an unknown injury[;]” “[m]edical recognition of the injury claimed is critical.” Broekelschen, 618 F.3d at 1349. The court is not persuaded by petitioner’s argument that a precise ADEM diagnosis is not necessary. Petitioner’s ADEM diagnosis is clearly a “necessary component to her theory of - 13 - Case 1:11-vv-00077-LB Document 47 Filed 09/05/14 Page 14 of 16 vaccine-induced injury.” Hibbard, 698 F.3d at 1365. This is demonstrated by the fact that the evidence presented before the CSM related to ADEM, not demyelinating diseases generally or other demyelinating diseases. Petitioner’s expert witness specifically alleged that petitioner suffered from “an atypical example of the subacute onset of demyelinating brain stem encephalitis, a variant of ADEM.” Pet’r’s Ex. 8 at 3. Moreover, petitioner cited studies by Poser (1982), Saito et al. (1980), Shoji and Kaji (2003), Miyamoto et al. (1996), Ravaglia et al. (2004), etc. in support of the proposition that ADEM, in particular, can be triggered by the flu vaccine. Id. at 4-5. As respondent notes, “[t]he theories put forth by petitioner’s expert all relied on a diagnosis of ADEM, and thus this particular diagnosis lies at the very crux of petitioner’s case- in-chief.” Res. at 9. Thus, Hibbard dictates that petitioner’s failure to establish that she has ADEM is fatal to her case. For these reasons, the court finds that the CSM did not err by considering whether petitioner had demonstrated she suffered from a vaccine-caused ADEM injury by a preponderance of the evidence in the record, as a predicate to applying the Althen test. Because petitioner’s arguments and expert testimony centered on a diagnosis of ADEM, the CSM did not err in applying Lombardi once she determined that petitioner had not carried her burden of establishing that she suffered from ADEM. 2. The Special Master’s Factual Findings Were Not Arbitrary or Capricious Petitioner also argues that the CSM acted arbitrarily and capriciously in finding that petitioner had failed to prove, by a preponderance of the evidence, that she was suffering from ADEM. Pet’r’s Mot. at 1. Petitioner insists that the CSM erroneously focused on whether petitioner was actually suffering from ADEM, “rather than whether [p]etitioner’s disease was within the medically accepted guidelines of ADEM.” Pet’r’s Mot. at 14. Petitioner acknowledges that her symptoms do not match those typically exhibited by ADEM patients, but insists that she suffers from an “atypical” variant of ADEM. Id. at 1. As explained above, the CSM cited the following six reasons for finding that petitioner was not suffering from ADEM, or even an “atypical” variant thereof: (1) the statistical probability that petitioner suffers from ADEM, (2) the absence of an ADEM diagnosis from her treating physicians; (3) the appearance of her brain lesion in the MRI; (4) the slow onset of her symptoms; (5) the nature and severity of her symptoms; and (6) the protracted course of her illness and her limited recovery. Stillwell I at 16-28. In short, the CSM found that “petitioner’s onset, symptoms, and the course of her illness diverge in too many respects and by too great a degree from the presentation of ADEM to even be deemed an atypical form of ADEM.” Id (emphasis added). Petitioner disputes the CSM’s finding that Ms. Stillwell was not suffering from ADEM. Petitioner argues that it was improper for the CSM to consider that most victims of ADEM are young children or adolescents because Dr. Kinsbourne introduced evidence that it is possible for ADEM to afflict adults. Pet’r’s Mot. at 5-6. Petitioner also argues that the absence of an ADEM diagnosis by any of petitioner’s treating physicians is irrelevant because “a physician’s purpose in classifying a disease process is to determine a course of medical treatment and prognosis – and not to establish a causative factor which may be necessary in a legal proceeding.” Id. at 6. Additionally, petitioner acknowledges that ADEM usually produces separate, or multifocal, lesions that are visible in MRIs, but insists that several studies cited by Dr. Kinsbourne support - 14 - Case 1:11-vv-00077-LB Document 47 Filed 09/05/14 Page 15 of 16 the possibility that some cases of ADEM may exhibit unifocal lesions. Id. at 6-8. Petitioner also acknowledges that the onset of ADEM symptoms is usually rapid, but argues that an onset of four weeks after the vaccination is nevertheless “within the generally acceptable onset.” Id. at 9- 10. Additionally, petitioner disputes respondent’s argument that the severity of petitioner’s symptoms was inconsistent with symptoms typically caused by ADEM. Id. at 10-12. Finally, petitioner argues that even if petitioner’s protracted course of injury was atypical, it was still within the acceptable range for ADEM. Id. at 12-13. As explained in the preceding section, petitioner has the burden of establishing, by the preponderance of the evidence, that she actually suffers from the specific injury she alleges was caused by the vaccination. Hibbard, 698 F.3d at 1365; see also Broekelschen, 618 F.3d at 1349 (holding that petitioner must establish that she suffers from a “vaccine-related injury,” not merely “a symptom or manifestation of an unknown injury”); Lombardi, 656 F.3d at 1553 (holding that petitioner must successfully establish a “specific injury”). Whether petitioner has successfully satisfied this burden is clearly a factual question, which is reviewed under the arbitrary and capricious standard. See Hibbard, 698 F.3d at 1363, 1365. Under this deferential standard, the court must uphold factual findings if the special master has considered the record and made plausible inferences. Id. at 1363 (quoting Hines on Behalf of Sevier, 940 F.2d at 1528). Plainly, petitioner disagrees with the CSM’s assessment of the evidence. Nevertheless, the court finds that the CSM’s factual findings are clearly supported by the record and therefore are not arbitrary and capricious. As explained above, there is no specific marker for ADEM. Rather, in identifying ADEM, both clinical findings and laboratory evidence must be taken into account. Thus, in considering whether petitioner was suffering from ADEM or some other malady, the court finds that it was reasonable for the CSM to consider a number of probabilistic factors, such as the typical age of individuals afflicted by ADEM, the typical course of illness, severity of symptoms, and others. The CSM summarized the typical characteristics of ADEM, and carefully elucidated six factors that weighed against a finding that petitioner was suffering from ADEM. In light of the fact that petitioner’s symptoms were undisputedly “atypical,” not just in one respect but on multiple levels, the court concludes that the CSM’s finding is substantially supported by the record on the whole. Finally, petitioner’s argument that the CSM should have focused on whether her “disease was within the medically accepted guidelines of ADEM” rather than whether petitioner actually suffered ADEM plainly misstates the law. As explained in the preceding section, petitioner has an affirmative burden of showing, by the preponderance of the evidence, that she actually suffers from the specific injury she alleges was caused by the vaccination. Hibbard, 698 F.3d at 1365. For the foregoing reasons, the court finds that the CSM did not act arbitrarily or capriciously in finding that petitioner does not suffer ADEM. *********** - 15 - Case 1:11-vv-00077-LB Document 47 Filed 09/05/14 Page 16 of 16 The ratio decidendi of the CSM’s decision is that petitioner “failed to prove by preponderant evidence that she developed ADEM.” Stillwell I at 28-29. As the CSM noted, this determination “precludes a finding of causation” and thus obviates any need to apply the Althen test for causation. Id. (citing Lombardi, 656 F.3d at 1352-53). But, in “an abundance of caution” the CSM evaluated petitioner’s claim under the Althen test’s prongs. Stillwell I at 29. Because the CSM decided the case on Lombardi grounds, the CSM’s Althen evaluation is dicta. See e.g. Cohens v. State of Virginia, 19 U.S. 264, 399-400 (1821) (remarking that, with regard to dicta, “[i]t is a maxim not to be disregarded, that general expressions . . . are to be taken in connection with the case in which those expressions are used . . . The reason of this maxim is obvious. The question actually before the Court is investigated with care, and considered in its full extent. . . .”). Accordingly, the court does not reach the question of whether the CSM’s determination that petitioner did not satisfy the Althen test was arbitrary or capricious. IV. CONCLUSION In sum, the court affirms the Chief Special Master’s determination that petitioner’s claim fails under Lombardi. Petitioner has not carried the burden of proving she suffers from a vaccine-related injury. Accordingly, the Special Master’s DECISION is AFFIRMED and petitioner’s MOTION for review of that decision is DENIED. IT IS SO ORDERED. Lawrence J. Block s/ Lawrence J. Block Judge - 16 - ================================================================================ DOCUMENT 3: USCOURTS-cofc-1_11-vv-00077-1 Date issued/filed: 2015-08-03 Pages: 2 Docket text: PUBLIC DECISION (Originally filed: 07/10/2015) regarding 52 DECISION Fees Stipulation. Signed by Special Master Lisa Hamilton-Fieldman. (jb) Copy to parties. -------------------------------------------------------------------------------- Case 1:11-vv-00077-LB Document 56 Filed 08/03/15 Page 1 of 2 In the United States Court of Federal Claims OFFICE OF SPECIAL MASTERS No. 11-77V Filed: July 10, 2015 * * * * * * * * * * * * * * * * * * * * * * * * * UNPUBLISHED SHERRIL K STILLWELL, * * Special Master Hamilton-Fieldman Petitioner, * v. * Attorneys’ Fees and Costs; Reasonable * Amount Requested to which Respondent SECRETARY OF HEALTH * Does Not Object. AND HUMAN SERVICES, * * Respondent. * * * * * * * * * * * * * * * * * * * * * * * * * * Sol P. Ajalat, Ajalat & Ajalat, North Hollywood, CA, for Petitioner. Alexis B. Babcock, United States Department of Justice, Washington, DC, for Respondent. DECISION1 On February 7, 2011, Sherril K. Stillwell (“Petitioner”) filed a petition for compensation under the National Childhood Vaccine Injury Act of 1986, 42 U.S.C. §§ 300aa-1 et seq. (2006) (“Vaccine Act”). Petitioner alleged that the administration of an influenza (“flu”) vaccine on February 22, 2008 caused her to suffer from a demyelinating brain disorder with a lesion. Petition (“Pet.”) at 1-3. On June 17, 2013, then Chief Special Master Campbell-Smith dismissed the Petition. A Motion for Review with the United States Court of Federal Claims was filed on July 9, 2013 and was denied on August 21, 2014. A Notice of Appeal with the United States Court of Appeals for the Federal Circuit was filed on October 10, 2014 and a Notice of Entry of Judgment without Opinion, affirming the decision that was appealed, was filed on June 15, 2015. On July 10, 2015, Respondent filed a Stipulation of Facts Concerning Final Attorneys’ Fees and Costs.2 Pursuant to their Stipulation, the parties have agreed to an award of $54,875.00 1 The undersigned intends to post this unpublished decision 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 Vaccine Rule 18(b), each party has 14 days within which to file a motion for redaction “of any information furnished by that party (1) that is trade secret or commercial or financial information and is privileged or confidential, or (2) that are medical files and similar files the disclosure of which would constitute a clearly unwarranted invasion of privacy.” In the absence of such motion, the entire decision will be available to the public. Id. 2 A Joint Stipulation of Facts regarding Interim Attorney’s Fees and Costs was filed on June 21, 2013; a decision awarding $97,500.00 in interim attorneys’ fees and costs was issued on June 21, 2013. Decision, ECF No. 36. 1 Case 1:11-vv-00077-LB Document 56 Filed 08/03/15 Page 2 of 2 in attorneys’ fees and $2,495.99 in attorneys’ costs. In accordance with General Order Number 9, Petitioner represents that she has not incurred any costs in pursuit of her claim. The undersigned finds that this petition was brought in good faith and that there existed a reasonable basis for the claim. Therefore, an award for fees and costs is appropriate, pursuant to 42 U.S.C. § 300aa-15(b) and (e)(1). Further, the proposed amount seems reasonable and appropriate. Accordingly, the undersigned hereby awards the amount of $57,370.99, in the form of a check made payable jointly to Petitioner and Petitioner’s counsel, Sol P. Ajalat. In the absence of a motion for review filed pursuant to RCFC Appendix B, the clerk of the court SHALL ENTER JUDGMENT in accordance with the terms of the parties’ stipulation.3 IT IS SO ORDERED. /s/ Lisa D. Hamilton-Fieldman Lisa D. Hamilton-Fieldman Special Master 3 Pursuant to Vaccine Rule 11(a), entry of judgment is expedited by the parties’ joint filing of notice renouncing the right to seek review. 2