                  In the United States Court of Federal Claims
                                      OFFICE OF SPECIAL MASTERS
                                                No. 13-709V
                                             (to be published)

*************************
KRISTINE R. BELL,             *
                              *                                             Special Master Corcoran
                  Petitioner, *
                              *                                             Filed: December 1, 2016
            v.                *
                              *                                             Decision; Hepatitis B (“Hep B”)
SECRETARY OF HEALTH AND       *                                             Vaccine; Acute Disseminated
HUMAN SERVICES,               *                                             Encephalomyelitis (“ADEM”).
                              *
                              *
                  Respondent. *
                              *
*************************


    Richard H. Moeller, Moore, Heffernan, et al., Sioux City, IA, for Petitioner.

    Althea Walker Davis, U.S. Dep’t of Justice, Washington, DC, for Respondent.

                                  DECISION DENYING ENTITLEMENT1

        On September 12, 2013, Kristine Bell filed this action seeking compensation under the
National Vaccine Injury Compensation Program (the “Vaccine Program”)2, alleging that she
experienced acute disseminated encephalomyelitis (“ADEM”) after receiving the second of three
doses of the Hepatitis B (“Hep B”) vaccine. Petition (“Pet.”) (ECF No. 1) at 1, 4-5. An entitlement
hearing was held in this matter on January 28-29, 2016. After considering the record as a whole, I
find that Petitioner has failed to carry her burden establishing causation, and therefore has not
demonstrated entitlement to compensation under the Vaccine Program. As discussed in greater

1
  Because this decision contains a reasoned explanation for my action in this case, it will be posted on the United States
Court of Federal Claims’ website, in accordance with the E-Government Act of 2002, 44 U.S.C. § 3501 (2012). As
provided by 42 U.S.C § 300aa-12(d)(4)(B), however, the parties may object to the decision’s inclusion of certain kinds
of confidential information. To do so, Vaccine Rule 18(b) permits each party fourteen (14) days within which to request
redaction “of any information furnished by that party: (1) that is a trade secret or commercial or financial in substance and
is privileged or confidential; or (2) that includes medical files or similar files, the disclosure of which would constitute
a clearly unwarranted invasion of privacy.” Vaccine Rule 18(b). Otherwise, the decision will be available to the
public. Id.
2
 The National Vaccine Injury Compensation Program comprises Part 2 of the National Childhood Vaccine Injury Act
of 1986, Pub. L. No. 99-660, 100 Stat. 3755 (codified as amended at 42 U.S.C. § 300aa-10 through 34 (2012)).

                                                             1
detail below, Petitioner’s entire claim hinges on the factual finding that she had ADEM – but the
record, as amplified by both side’s experts, suggests she did not.

    I.      FACTUAL BACKGROUND

           The record in this case consists of Ms. Bell’s medical records, the testimony of four experts,
    and medical or scientific literature submitted by the parties in support of their respective positions.
    I have reviewed the entire record as required by the Vaccine Act. In this ruling I address the
    sufficiency of Petitioner’s evidence in support of an award of compensation.

          A.      Receipt of First and Second Hep B Vaccines

           Petitioner was born on July 7, 1975. Petitioner’s Exhibit (“Pet’r’s Ex.”) 2 at 1. Her prior
    relevant medical history includes migraine headaches, depression, anxiety, adult attention deficit
    disorder (ADD), and two miscarriages. Pet’r’s Ex. 1 at 2. The only prescribed medication
    Petitioner took was Zoloft. Id.

           Ms. Bell was seen at St. Luke’s Hospital on December 6, 2011 for her yearly physical, at
    which time she received the first of three Hep B vaccine doses. Pet’r’s Ex. 1 at 1. There is no
    record evidence of any notable reaction to that dose, and indeed (as was underscored at hearing)
    Petitioner’s experts could not point to any either. See, e.g., Transcript (“Tr.”) at 23, 159-60.

           The second dose of the Hep B vaccine was administered to Petitioner on January 16, 2012.
    Pet’r’s Ex. 1 at 1. Fifteen days later, on January 31, 2012, Petitioner saw an optometrist because
    she was suddenly experiencing blurred vision, burning, tearing, itching, and photophobia. Pet’r’s
    Ex. 2 at 5. Specifically, she reported that she had noticed the blurriness and red eye for one week.
    Id. At this visit, the doctor noted a history of Meniere’s disease,3 and that Petitioner had
    experienced a cold two weeks before. Id. Ms. Bell was prescribed Tobradex4 for possible
    conjunctivitis and a corneal abrasion. A few days later, on February 2, 2012, at her follow up
    appointment, Ms. Bell presented with improved symptoms, allowing her to restart use of her
    contact lenses. Id.

          B.      Symptoms Following Second Hep B Vaccine Dose

          Thirty-three days after receiving the second Hep B vaccine, on February 18, 2012, Ms. Bell

3
  Meniere’s disease consists of hearing loss, tinnitus, and vertigo resulting from non-supperative disease of the
labyrinth with edema. Dorland's Medical Dictionary 539 (32nd ed. 2012) (hereinafter “Dorland’s”).
4
 Tobradex is a combination of an antibiotic and a corticosteroid, used in the eye (as an eye drop) to prevent permanent
eye damage. Drugs and Supplements: Tobramycin And Dexamethasone, Mayo Clinic (Jan. 01, 2016),
http://www.mayoclinic.org/drugs-supplements/tobramycin-and-dexamethasone-ophthalmic-route/description/DRG-
20062827 (last visited Nov. 2, 2016).

                                                          2
    visited Unity Point Urgent Care complaining of left-sided weakness. Pet’r’s Ex. 10 at 1. At this
    visit, the records indicate, Petitioner informed her treater that she believed her symptoms were
    carpal tunnel syndrome, and consequently she had delayed seeking a physician’s opinion until
    her symptoms had progressed over the “last couple of weeks.” Id. The Urgent Care physician
    who examined Ms. Bell noted “definite left-sided weakness, probably 3-4/5 in the left arm, hand,
    left leg and foot,” and therefore instructed Ms. Bell to get a “head scan.” 5 Id. Because Ms. Bell
    worked in billing for St. Luke’s Hospital- where she wanted to go for treatment, she waited until
    Monday, February 20, 2012 to schedule a head scan. Id. On that day, Ms. Bell was first seen by
    a nurse practitioner, Joan Schlenk, who took Ms. Bell’s vitals and reviewed her systems.
    Petitioner reported that her medical history included Meniere’s disease, but she did not disclose
    having received the Hep B vaccine earlier that year. Pet’r’s Ex. 7 at 1. In reviewing Ms. Bell’s
    systems, Nurse Schlenk reported that Ms. Bell presented with a number of symptoms including
    fatigue, “feelings of weakness on exertion,” “inability to cope with daily activities,” and a
    previous history of dizziness. Id. at 2.

           Based on those symptoms, Ms. Bell was instructed to report to the Emergency Room at St.
    Luke’s Hospital in Cedar Rapids, Iowa for an evaluation by a neurologist. Pet’r’s Ex. 7 at 2. She
    did so on February 20, 2012, and saw Laurence Krain, M.D., a neurologist, for an evaluation and
    CT scan. Pet’r’s Ex. 6B at 348. The written record of that evaluation documents Petitioner’s
    verbal report to Dr. Krain that she felt “flulike,” with fatigue, abdominal pain, and nausea, but
    also reported that “it all started with blurred vision in her left eye associated with redness and
    pain about 4 to 5 weeks ago.” Id. at 343, 347. The CT scan was normal, leading Dr. Krain to
    propose that Ms. Bell had a “subtle suggestion of the left spastic hemiparesis…subacute course
    consistent with progressive spastic left hemiparesis. This could be hemispheric or myelopathy.
    Major consideration demyelinating disease.” Id. at 347. Dr. Krain’s treatment plan included an
    MRI6 of the cervical spine and head, along with an evaluation of Petitioner’s B12 levels7. Id.

          An MRI was performed on February 21, 2012, and showed an “abnormal mass-like signal
    centered in the region of the right basal ganglia, caudate nucleus, and centrum semiovale.” Pet’r’s
    Ex. 6B at 369. That finding led Dr. Krain to include in his differential diagnosis low grade
    neoplasm or tumefactive demyelinating disease as possible explanations for Petitioner’s


5
  The treating physician did not specify if the “head scan” would be an MRI or CT scan, however. Mrs. Bell’s first
test once at St. Luke’s Hospital was a CT scan. Pet’r’s Ex. 10 at 1.
6
    MRI stands for Magnetic Resonance Imaging. Dorland’s at 1184.
7
  Dr. Krain’s notes do not explain his rationale for measuring Petitioner’s B12 levels. A B12 deficiency, however,
“frequently causes macrocytic anemia, glossitis, peripheral neuropathy, weakness, hyperreflexia, ataxia, loss of
proprioception, poor coordination, and affective behavioral changes,” and it is therefore likely that Dr. Krain was
trying to rule out B12 deficiency as a cause of Petitioner’s symptoms. Test ID: B12, Vitamin B12 Assay, Serum, Mayo,
http://www.mayomedicallaboratories.com/test-catalog/Clinical+and+Interpretive/9154 (Last visited Nov. 4, 2016).


                                                         3
    condition, whereas cerebritis8 or an area of subacute ischemia were now considered less likely.
    Id. Dr. Krain began treating Ms. Bell with IV steroids, which were to be tapered off with the use
    of oral steroids. Id. at 381. This treatment plan came with a diagnosis of multiple sclerosis
    (“MS”). Id.

           Ms. Bell reported to her follow-up appointment on March 21, 2012, and presented with
    increased stiffness, dystonic posturing on her right upper extremities, and other movement
    impairment, reporting no improvement despite the steroid treatments. Pet’r’s Ex. 6B at 180-81.
    Dr. Krain noted that Ms. Bell’s previously-observed brain lesion was “difficult to categorize
    fully.” Id. at 180. A second MRI he had ordered had been performed the day before, on March
    20, 2012, and it showed that the previous hyper-intense T2 signal in the lentiform nucleus and
    caudate nucleus had diminished, as well as less swelling in the right caudate nucleus. Id. at 185;
    Pet’r’s Ex. 5 at 501. At the same time, the MRI revealed a new, T1 hyper-intensity in the lentiform
    and caudate nucleus, but with no abnormal enhancement (which would show inflammation).9
    Pet’r’s Ex. 6B at 185; Pet’r’s Ex. 5 at 501. The radiologist who performed new MRI, Dr. Glenn
    Hammer, overall noted some “internal improvement in edema and . . . swelling,” and this, plus
    the changes in signal intensity, suggested “petechial hemorrhage or necrosis within a previous
    ischemic infarct,” while deeming MS or neoplasm unlikely. Pet’r’s Ex. 5 at 501.

          Based on the above, Dr. Krain proposed a new diagnosis of extrapyramidal disorder,10
    which required substantiation through blood tests, a lumbar puncture, and a third brain MRI,
    accompanied by occupational and physical therapy and botox injections.11 Pet’r’s Ex. 6B at 180.
    The lumbar puncture was conducted on April 12, 2012 and showed normal results. Id. at 135-
    138. Tests for oligoclonal bands, cryptococcal antigen, IgG and syphilis were also normal. Id.
    The repeat MRI ordered by Dr. Krain was performed on April 30, 2012, and revealed reduced

8
    Cerebritis is inflammation of the cerebrum. Dorland’s at 332.
9
 Lesions revealed by an MRI that are suggestive of ADEM are “hyperintense (have a greater signal) on T2-weighted
and FLAIR sequences,” but “are usually inconspicuous or unenhanced T1-weighted sequences (black holes).”
Waldman, A. and D. Jacobs, Acute Disseminated Encephalomyelitis in Adults, UpToDate, F. Gonzalez-Scarano,
Editor Accessed on February 12, 2015, Wolters Kluwer Health: Waltham MA. Filed as Resp’t’s Ex. I.

When a patient is suspected of having inflammation in the brain, a physician will inject paramagnetic dye in their
veins while the patient undergoes an MRI. Tr. at 221-22. If the dye goes through the blood vessels and gets to the
brain then enhancing lesions will appear on the MRI. Id. at 222. If the dye does not reach the brain, or show up on the
MRI through enhancing lesions, that is a good indicator that the blood brain barrier was not breached – and hence no
inflammation of the brain. Id.
10
  Extrapyramidal disorder constitutes any of a group of clinical disorders considered to be attributable to malfunction
in the extrapyramidal system (a non-anatomical part of the central nervous system that controls motor activities), and
characterized by abnormal involuntary movements, e.g. Parkinsonism, athetosis, and chorea. Dorland’s at 1829, 1859.
11
  The Doctors at the Mayo Clinic who later evaluated Ms. Bell concluded that these botox treatments “caused
worsening weakness in the hands.” Pet’r’s Ex. 9 at 49.


                                                           4
 signal size of the right basal ganglia, but was accompanied by an increased signal in the right
 lentiform nucleus consistent with small vessel ischemia or vasculitis.12 Pet’r’s Ex. 3 at 28. Dr.
 Krain discussed Ms. Bell’s condition with Dr. Mary L. Hlavin.13 Id. at 34. A handwritten note by
 Dr. Hlavin states “tell [Petitioner] scan continues to look better.” Id. at 28.

       In addition to Dr. Krain, Ms. Bell also sought treatment from Dr. David E. Puk, an
 ophthalmologist, on May 5, 2012, for her ongoing vision problems first manifesting after her
 receipt of the second Hep B dose. During that appointment, she complained of diplopia14 that had
 begun two days prior, along with intermittent blurriness. Pet’r’s Ex. 4 at 6. Dr. Puk acknowledged
 the improvement in the brain lesion discussed above, and diagnosed Ms. Bell with hypertropia,15
 which could be helped with an eye patch on one eye. Id.

       Ms. Bell then followed up with Dr. Krain on May 17, 2012, to get his input on the diplopia
 she had been experiencing for two weeks. Pet’r’s Ex. 4 at 17. Dr. Krain’s notes from this
 examination and visit underscore the extent to which Ms. Bell’s treaters were uncertain of the
 cause of her condition – but were slowly but surely moving away from initial concerns about
 demyelination. Thus, Dr. Krain characterized her right basal ganglia lesion as of “indeterminate
 etiology,” and that “[t]he presentation [of Ms. Bell] does not suggest infectious or autoimmune
 encephalitis well . . . [d]emyelinating disease presenting with a single lesion has been entertained,
 but there are lesions in the gray matter and I have felt this is quite unlikely.” Id. at 16 (emphasis
 added). He also noted that the steroidal treatments had not proven effective. Id. at 18.

        At this point (about four months post-vaccination), Dr. Krain ordered further testing,
 including an MRI and chest X-ray, and also referred Petitioner to specialists in the neurology
 department at the University of Iowa Hospital (“Iowa”). Pet’r’s Ex. 4 at 27. The first of those
 specialists that Ms. Bell saw was Dr. Robert Rodnitzky, a neurologist, on May 23, 2012. Pet’r’s
 Ex. 8 at 24. Dr. Rodnitzky was tasked with evaluating Petitioner for right basal ganglia pathology
 with new cranial nerve palsies. To do so, he reviewed Petitioner’s medical history and
 summarized it as consistent with what is stated above. Id. However, an additional piece of
 information was added to Ms. Bell’s history of migraines: Ms. Bell had experienced paresthesia16

12
  Small vessel ischemia is a deficiency of blood flow in certain smaller vessels, usually due to functional constriction
or actual constriction of the blood vessel, while vasculitis is inflammation of the blood or lymph vessel. Dorland’s at
961, 2026.
13
  Dr. Hlavin’s name is mentioned sporadically throughout the record, mainly by Dr. Krain when he is describing Ms.
Bell’s past medical history, although the medical record does not reveal any instances in which Dr. Hlavin herself
directly examined Ms. Bell. Pet’r’s Ex. 5 at 60. It is also unclear what type of medicine is Dr. Hlavin’s specialty.
14
     Diplopia means double vision. Dorland’s at 525.
15
     Hypertropia is a permanent upward deviation of the visual axis of the eye. Dorland’s at 898.
16
     Paresthesias are the sensations of burning, numbness, tingling, or prickling. Dorland’s at 1383.

                                                             5
 in both hands, expressive aphasia,17 and difficultly writing with her migraines - the most recent
 occurrence of such problems having happened several years before. Id. at 24.

        Dr. Rodnitzky performed several tests, and repeated some that had already been conducted,
 including a cell count, an MS screen, an MRI, and a lumbar puncture. The blood tests revealed
 three oligoclonal bands18, normal protein, and negative tests for histoplasma, cytomegalovirus,
 enterovirus, cryptococcal, and angiotensin-converting enzyme. Pet’r’s Ex. 8 at 40. The newest
 MRI was compared to the MRIs performed in February, March, and April, and the impression in
 the medical records from August 29, 2012, stated “evolution of the signal abnormalities involving
 the gray matter …reflect[ing] evolution of an acute process on the original MRI, the differentials
 of which include viral encephalitis, ADEM19, or autoimmune encephalitis.20” Id. at 41, 160.
 Alongside ADEM, Dr. Rodnitzky also considered “para/post-infectious autoimmune encephalitis
 and mitochondrial disease” as potential diagnoses for Ms. Bell’s condition. Id.

        After completing this testing and evaluation, Dr. Rodnitzky referred Ms. Bell to a neuro-
 ophthalmologist – Dr. Matthew Thurtell. Dr. Thurtell concluded from his examination of
 Petitioner that there was “a broad differential diagnosis, including inflammatory, infectious,
 neoplastic, and paraneoplastic etiologies.” Pet’r’s Ex. 8 at 68. He also noted that Ms. Bell had a
 pattern of misalignment consistent with a fourth nerve palsy and slowing of horizontal saccades
 with impaired gaze-holding. Id. Ms. Bell was prescribed a Fresnel prism for her visual
 disturbance. Id.




17
 Aphasia is any of a large group of language disorders involving defect or loss of the power of expression by speech.
Dorland’s at 115.
18
   “Isoelectric focusing/immunofixation reveals two or more oligoclonal bands in the CSF but no band in the serum.
This is consistent with intrathecal synthesis of immunoglobulin and is considered to be a positive result for oligoclonal
bands. Oligoclonal bands are present in approximately 95 percent of patients with multiple sclerosis.” Pet’r’s Ex. 8 at
30-31.
19
  “Acute disseminated encephalomyelitis (ADEM) is an immune-mediated disorder of the CNS [central nervous
system] characterized by a widespread demyelination that predominantly involves the white matter of the brain and
spinal cord. The condition is usually precipitated by a viral infection or vaccination. The presenting features include
an acute encephalopathy with multifocal neurologic signs and deficits.” S. Tenembaum, et al., Acute Disseminated
Encephalomyelitis, Neurology, Apr. 17, 2007; 68 (Suppl 2), S23-S36 at S23 (filed as Pet’r’s Ex. 16).
20
   These results were in the record labelled “External MRI-store and Interpret.” The record states that the MRI was
reviewed by Aaron D. Berg, MD and Toshio Moritani, MD. Pet’r’s Ex. 8 at 41. Aaron D. Berg appears to be a board
certified radiologist. Aaron Middle Berg, Sanford Health, http://www.sanfordhealth.org/find-a-doctor/aaron-berg (last
accessed on 11/10/2016). Toshio Moritani is the director of the Clinical Neuroradiology at Iowa who is board certified
in medicine and radiology. Toshio Moritani, University of Iowa Carver College of Medicine: Radiology,
https://www.medicine.uiowa.edu/dept primary apr.aspx?appointment=Radiology&id=moritanit (last accessed on
11/10/2016)

                                                           6
        C.       Third Hep B Dose and Further Progression of Symptoms

        Ms. Bell returned to Dr. Krain on June 4, 2012 for a follow-up visit. At this visit, there are
 inconsistencies in the record about her condition. The medical record begins by stating “returns
 today with no new complaints,” but two sentences later states that “her only new complaint today
 is decreased hearing on the right side.” Pet’r’s Ex. 5 at 92. That same paragraph concluded with
 the statement that Petitioner had “not developed any other new problems, nor change in her other
 conditions…she has not had any other new complaints or change in her condition.” Id. (emphasis
 added). Accordingly, this record suggests some concern as of June 2012 on Ms. Bell’s part about
 hearing.

        Several days later, on June 12, 2012, Ms. Bell received her third Hep B vaccine. Pet’r’s
 Ex. 1 at 1. She thereafter reported for occupational therapy on June 19, 2012, where she stated
 that she was experiencing continued decline in balance and the use of her left hand, along with
 further decreased hearing and vision, leading Dr. Krain to order a PET scan.21 Pet’r’s Ex. 6A at
 64. The PET scan revealed unilateral absent 18-FDG22 activity in the right caudate and lentiform
 nuclei, which was termed an unusual result, as in a few reported cases it could reflect an ischemic
 event resulting in parenchymal scaring or hyperglycemic-induced regional metabolic failure.
 Pet’r’s Ex. 5 at 496.

        Ms. Bell was next seen for a follow-up appointment with Dr. Thurtell on July 2, 2012. By
 this point, Ms. Bell noted, she was unable to drive, had onset hearing loss on the right side, gaze
 palsy, and her left hand was not functioning well. Pet’r’s Ex. 8 at 105. Dr. Thurtell concluded
 that “this is a very unusual spectrum of disorders,” and adding his view that “considering her
 progressive symptoms in multiple anatomic locations, an inflammatory cause would be highest
 on the differential.” Id. at 111. Given that Petitioner’s neurologic deficit had worsened since the
 last appointment, Dr. Thurtell recommended an MRI with contrast, a CT with contrast, a
 mammogram, and a pap smear. Id. at 112. Despite his reluctance to recommend steroids, Dr.
 Thurtell also suggested to Ms. Bell that IVIG treatments should be considered again to prevent
 further neurological decline, although she had tried but discontinued their use previously after
 experiencing flu-like side effects (and although they had not proven effective otherwise). Id.

        Following the exam with Dr. Thurtell, Ms. Bell underwent another MRI, plus an additional

21
   A PET scan stands for Positron Emission Tomography, and uses a radioactive drug to show chemical activity in
tissues and organs. Tests and Procedures: Positron Emission Tomography (PET) Scan, Mayo (2014),
http://www.mayoclinic.org/tests-procedures/pet-scan/basics/definition/prc-20014301 (Last visited Nov. 4, 2016).
22
   18-FDG is a radiopharmaceutical used to help measure abnormal glucose metabolism in the brain. Review of F-18
Fluoro-2-Deoxyglucose (F-18 FDG) Positron Emission Tomography in the Evaluation of Malignancy, FDA 1999,
http://www.fda.gov/Drugs/DevelopmentApprovalProcess/Manufacturing/ucm182668 htm (Last visited on Nov. 4,
2016).


                                                       7
 CT and mammogram. The MRI found a largely “stable examination,” with no abnormal
 enhancement or “areas of restricted diffusion.” Pet’r’s Ex. 5 at 495. The radiologist responsible
 for conducting this MRI, after comparing it to the prior MRIs performed on Ms. Bell, proposed
 that the cause of her many symptoms was “a prior focal insult which may have been due to
 vasculitis, encephalitis, or small vessel ischemia.” Id. Dr. Krain reviewed these findings on July
 9, 2012, and stated that he still had difficulty categorizing her disease, but was considering non-
 paraneoplastic autoimmune encephalitis, although the test for paraneoplastic antibodies was
 negative. Id. at 72. In contrast to her improving head MRIs, Dr. Krain noted continuing clinical
 manifestations such as diplopia with opthalmoparesis and hearing loss. Id. Dr. Paulina J.
 Kunecka23 ordered the July MRI and recorded the “pertinent clinical findings and specific
 questions to be answered” as “inflammation (ADEM?) vs. tumor?.” Pet’r’s Ex. 8 at 114.

       Ms. Bell thereafter saw another ophthalmologist, Dr. Mark Granner, who opined that the
 most likely cause of Ms. Bell’s injuries was an autoimmune process because of the evolution of
 her symptoms over time. Pet’r’s Ex. 8 at 134. He noted that Ms. Bell had not responded well to
 IVIG treatments, but because he could not determine the insulting agent for Ms. Bell’s condition,
 he was unsure of the utility of trying more aggressive treatment such as plasmapheresis.24 Id. at
 134-135.

        D.       Alternative Explanations for Petitioner’s Symptoms

        On August 16, 2012, Ms. Bell was seen again by Dr. Krain for another follow-up regarding
 her rigidity and diplopia. Pet’r’s Ex. 5 at 58. This is the first instance evident from the record
 where Ms. Bell (accompanied by her mom) asked if her problems were a result of the Hep B
 vaccines she had received. Id. Dr. Krain stated that given Ms. Bell’s presentation, temporally and
 on imaging, he felt post-vaccinal encephalomyelitis to be unlikely. Id. He noted Petitioner’s
 active problems to be abnormal brain scan, dizziness and giddiness, dystonia musculorum
 deformans idiopathic, extrapyramidal disorders, and inner ear autoimmune disease. Id. Later that
 same month, on August 29, 2012, Ms. Bell saw Dr. Rodnitzky again, who continued to include
 ADEM (specifically, a recurrent form of the condition) as a diagnostic possibility, although it is
 not evident from the record why he did so (and in particular if he was relying on any more recent
 testing for its inclusion in the differential diagnosis). Pet’r’s Ex. 8 at 163.

      Ms. Bell asked if she should seek an opinion at the Mayo Clinic in Rochester, Minnesota,
 and Dr. Thurtell concluded that was a reasonable course of action. Pet’r’s Ex. 8 at 151.

23
  Dr. Kunecka does not appear to be one of Ms. Bell’s treating physicians but rather a Staff, Resident, or Fellow.
Pet’r’s Ex. 8 at 163.
24
  Plasmapheresis is the removal of plasma from withdrawn blood, with re-transfusion of the formed elements into the
donor. Dorland’s at 1456.


                                                        8
 Accordingly, on September 20, 2012, Ms. Bell arrived at the Mayo Clinic for further treatment.
 At this time, Petitioner saw Dr. Andrew McKeon, a neurologist, who oversaw an initial and
 comprehensive evaluation, with numerous tests performed, including an MRA, MRI, EEG, EMG,
 CSF evaluation, echocardiogram, and muscle biopsy of her bicep. Pet’r’s Ex. 9 at 67.

      Dr. McKeon and the associated Mayo treaters who assisted in this testing largely concluded
(consistent with Ms. Bell’s prior testing), based on MRI and MRA findings, that the evidence of
“vascular, infectious or neoplastic projects [was] unlikely.” Pet’r’s Ex. 9 at 78. By contrast, the
EMG showed evidence of a diffuse, distally predominant myopathic process.25 These findings
were most noticeable in Ms. Bell’s arms, and the lack of fibrillation potentials indicated a non-
inflammatory process with no evidence for peripheral neuropathy. As a result, congenital
myopathy and/or a mitochondrial disorder were deemed to be possible causes for her various
symptoms. Id.

        A biopsy of Ms. Bell’s bicep muscle, however, resulted in no evidence indicating a
 mitochondrial, inflammatory, or active-myopathic process, leading Dr. McKeon to conclude that
 his proposition of mitochondrial dysfunction was misplaced. Pet’r’s Ex. 9 at 23, 79. The records
 also reveal Dr. McKeon’s awareness that Ms. Bell had been referred for evaluation of a possible
 autoimmune disease, but that, in his review of the records, there was no evidence pointing to that
 conclusion, noting her lack of response to IVIG or steroids as further supporting the unlikeliness
 of an autoimmune process (for which either treatment would normally be effective). Id. at 49.
 When Ms. Bell prompted Dr. McKeon about possible vaccine causation, he stated that he was
 unaware of a specific relation of her illness to the Hep B vaccine. Id.

        In October 2012, Ms. Bell was seen by four additional doctors at the Mayo Clinic (Drs.
 Lund, Andrea L. Cheville, Lyell K. Jones, and Ralitza H. Gavrilova) some of whom were from
 the medical genetics group at Mayo, to further address whether mitochondrial dysfunction might
 be the cause for Petitioner’s condition despite Dr. McKeon’s initial take. The visit concluded with
 a prescription for a prescriptive “cocktail” intended to help ameliorate the impact of a possible
 mitochondrial disease, and with the recommendation that Ms. Bell obtain a genetics evaluation.
 Pet’r’s Ex. 9 at 35. Dr. Jones performed a neurologic evaluation on Ms. Bell, but in the process
 also determined that although an autoimmune condition was originally considered as a possible
 cause for her symptoms, Ms. Bell did not have the markers for neural autoimmunity that would
 be otherwise expected if the process causing her symptoms were in fact autoimmune. Id. at 29.

        On January 16, 2013, Ms. Bell appeared for a follow-up with Dr. Gavrilova, who reviewed
 the testing performed and confirmed that the evidence of an underlying mitochondrial disorder
 remained scant. Pet’r’s Ex. 9 at 11, 16, 18. As a result, Dr. Gavrilova recommended further

25
     Myopathy is any disease of the muscle. Dorland’s at 1224.


                                                          9
 genetics testing, although Ms. Bell was hesitant to participate due to concerns about her insurance
 coverage. At this visit, Ms. Bell also noted that despite the “mitochondrial cocktail” treatment
 intended to address an underlying metabolic disorder, she was now experiencing decreased
 hearing by 50 percent and deterioration in her speech by 25 percent. Id. at 8. The diagnosis for
 Ms. Bell was now “progressive neurological deterioration characterized by dystonia, external
 ophthalmoplegia, hearing loss, gait imbalance, speech dysarthria, and brain MRI abnormalities
 of uncertain etiology.” Id. at 9.

        Dr. Gavrilova referred Ms. Bell to Dr. Patricia J. Best in the cardiovascular diseases group
 at the Mayo Clinic. Pet’r’s Ex. 9 at 13. Dr. Best reviewed the results of Ms. Bell’s September
 echocardiogram, determining that she had “very minimal early signs of cardiac involvement
 likely from her myopathic process.” Id. at 14. As treatment, Dr. Best recommended that Ms. Bell
 start on a low dose of ACE inhibitor (Lisinopril), as well as a low dose of carvedilol.26 Id.

           E.       University of Iowa Treatment and ADEM Diagnosis

         One month later, on February 13, 2013, Ms. Bell went back to the treaters at Iowa. She
 first saw Dr. Rebecca K. Novacek, who reviewed the Mayo Clinic results as well as Ms. Bell’s
 clinical presentation. Dr. Novacek noted that Ms. Bell’s hearing had continued to worsen, while
 her left-side dystonia and vision were stable. Pet’r’s Ex. 8 at 179. Because the etiology of Ms.
 Bell’s condition remained unknown, Dr. Novacek ordered yet another MRI and lab work to
 evaluate copper, ceruloplasmin, ferritin, homocysteine, and a urine screen. Id. at 181. All of her
 lab work returned results within the normal range. Id. at 182-185. The MRI in particular showed
 that the FLAIR signal in the basal ganglia was mostly resolved, there was mild atrophy and iron
 deposition of the right basal ganglia and substantia nigra, and stable minimal wispy enhancement
 in the bilateral basal ganglia. Id. at 199.

        Dr. Bruce J. Gantz, an audiologist at Iowa, also evaluated Ms. Bell. In his clinical notes he
 stated a “coincident finding with onset of symptoms was completion of Hep B vaccine series and
 conjunctivitis,” although the record is silent as to whether Dr. Gantz found reason himself to
 connect the two – indeed, he acknowledged that steroid treatments had not been effective either.
 Pet’r’s Ex. 8 at 191-92. He ultimately concluded that she had severe bilateral asymmetric
 sensorineural hearing loss and facial palsy. Id. at 191.

        On March 29, 2013, Ms. Bell saw Dr. Pedro Gonzalez-Alegre, a neurologist specializing
 in movement disorders, at Iowa. The medical record reveals that, although Dr. Gonzalez-Alegre
 purported to have received the medical history from Ms. Bell and her family and reviewed her
 prior medical records, he misstated certain relevant facts of the progression of her condition.
 Pet’r’s Ex. 8 at 209. For example, he recorded in the medical history section of the treatment

26
     Lisinopril and Carvedilol are medications used to treat hypertension. Dorland’s at 301.

                                                           10
 notes he prepared that she was doing well until December 2012, when she first received the Hep
 B vaccines – when in fact she had received all three doses by June 2012, six months earlier. Id.
 He also incorrectly ordered her symptoms chronologically, reciting that Ms. Bell progressed from
 hearing loss to blurry vision. Id. In fact, Ms. Bell’s first doctor visit after receiving the second
 Hep B vaccine was to an ophthalmologist (15 days after vaccination) (Pet’r’s Ex. 2 at 5), and she
 did not report decreased hearing until June. Pet’r’s Ex. 10 at 1.

        Based on review of testing performed through March 2013, Dr. Gonzalez-Alegre opined
 (like the doctors at the Mayo Clinic) that Ms. Bell did not have a mitochondrial disorder. Pet’r’s
 Ex. 8 at 210. Rather, in his view she likely suffered from an inflammatory disorder that had
 produced permanent brain damage, as suggested by the atrophy in the basal ganglia. Id. He makes
 no mention in these records, however, of earlier contrary determinations – not only by Dr. Krain
 but from the Mayo treaters – that evidence of inflammation was absent, nor does he suggest these
 findings were in error in light of subsequent testing and analysis of Ms. Bell’s symptoms. He also
 noted that Petitioner’s basal ganglia lesion could not account for her visual and auditory
 symptoms. Not long after, in April 2013, Dr. Gonzalez-Alegre wrote a letter to Ms. Bell stating
 that the majority of potential etiologies for her condition had been appropriately ruled out by prior
 providers, with the exception of two rare diseases - - Whipple’s disease and Brucellosis27 - that
 could be tested for through an additional lumbar puncture. Id. at 213.

        Ms. Bell was subsequently admitted to Iowa on May 5, 2013, with a chief compliant of
 “worsening encephalitis.” Pet’r’s Ex. 8 at 683. By this time, Dr. Gonzalez-Alegre had begun to
 pursue more testing, including CSF and brain imaging, in order to look for unusual possible
 additional etiologies such as Nieman-Pick type C.28 Id. at 686. Moreover, he now listed as part
 of Ms. Bell’s differential diagnosis encephalitis, noninfectious acute disseminated
 encephalomyelitis (ADEM), dysphagia, dysarthria, and memory loss. Id. As part of the expansive
 testing performed during the five day stay at Iowa, Ms. Bell saw Dr. Oleg A. Shchelochkov, a
 specialist in genetics. Pet’r’s Ex. 8 at 710. Dr. Shchelochkov listed a multitude of possible genetic
 disorders that present with acute adult onset neuro-metabolic disorders with spasticity,
 recommending further diagnostic testing, especially given the presence of iron in her basal
 ganglia. Id.

       On May 24, 2013, Ms. Bell returned to Iowa for a follow up with Dr. Gonzalez-Alegre.
 After reviewing all the testing results from Ms. Bell’s stay at the Hospital, Dr. Gonzalez-Alegre


27
   Whipple’s disease is a malabsorption syndrome caused by infection with mentation, arthralgia and arthritis,
lymphadenopathy, and sometimes central nervous system involvement with oculofacioskeletal or oculomasticory
dysrhythmia. Dorland’s at 545. Brucellosis is characterized by fever, sweating, weakness, malaise, and weight loss.
Id. at 255.
28
  Nieman-Pick Type C is a lysomal storage disease due to a deficiency of sphingomyelin phosphodiesterase with
sphingomyelin accumulation in the reticuloendothelial system. Dorland’s at 1276.

                                                        11
(based on consultation with other doctors- Drs. Rodnitzky and Shivapour) proposed that the most
likely diagnosis was a monophasic encephalitic process occurring after vaccination. Pet’r’s Ex. 8
at 810. Dr. Gonzalez-Alegre also noted that there was “ongoing inflammation in the central
nervous system from her CSF,” although (other than an increased IgG index from the year
before), the basis of this assertion is unclear and not evident from the records. Dr. Gonzalez-
Alegre also acknowledged that the plasma exchange treatments he had attempted had not been
ameliorative, but proposed to try IV Solu-Medrol for five days, and then consider additional
steroid treatments if Ms. Bell showed even the smallest improvement. Id. As before, Dr.
Gonzalez-Alegre’s notes reference Ms. Bell’s prior treatments but do not grapple with, contest,
or otherwise dispute the determination of earlier treaters that were contrary to his current
impressions.

       Three months later, on August 12, 2013, Ms. Bell returned again to Iowa for another
consultation with a genetics counselor. This visit resulted in extensive clinical notes, including a
chart listing all the medical testing she had undergone in the last year, along with proposals for
yet more new testing and treatment. Pet’r’s Ex. 12 at 21-27. These records also state the remaining
possible diagnoses (including ADEM), both genetic and otherwise, concluding that the etiology
of Ms. Bell’s condition remained unclear. Id. at 29-30. Ms. Bell had a follow up appointment on
September 6, 2013 at the Movement Disorders Clinic with Dr. Gonzalez-Alegre. He noted that
Ms. Bell had been stable (if not slightly better) since her last visit, and his overall impression was
that she had an acquired disorder that had not changed despite the general ineffectiveness of all
the varied treatments she received. Id. at 62. The active symptoms and conditions proposed at
this time as part of the differential diagnosis included basal ganglia disorder, dry eyes, decreased
hearing, gaze palsy, dystonia, noninfectious ADEM, encephalitis, dysphagia, dysarthria, and
memory loss. Id. at 63.

       Dr. Gonzalez-Alegre saw Ms. Bell again on September 25, 2013 to treat her with botulinum
toxin (“Botox”) injections in her left adductor pollicis. Pet’r’s Ex. 13 at 16. Ms. Bell thereafter
requested a visit with a neuro-ophthalmologist because her vision and diplopia were again
worsening, and returned to Iowa for that purpose on December 23, 2013. Id. at 30. Before Ms.
Bell reported for her appointment, Dr. Gonzalez-Alegre noted (in the contemporaneous records
from the time) that Ms. Bell was a “38 yo woman with an episode of suspected basal ganglia and
brainstem encephalitis following Hep B vaccination. She has shown some progression of
symptoms, which is unusual for such a static process.” Id. (emphasis added). Dr. Thurtell also
examined Ms. Bell in December, stating that her condition seemed to be stable since her last visit.
Id. at 45. His treatment plan for her vision was to try aggressive lubrication to help with her dry
eye, and he also proposed surgical correction. Id. at 50.

       Ms. Bell returned for a second Botox treatment on January 8, 2014, because her arm
position had improved from her last visit three months ago. Pet’r’s Ex. 13 at 58; see also Pet’r’s


                                                 12
Ex. 9 at 49. Her encounter diagnoses at this visit no longer included ADEM, however, but instead
listed “encephalitis, postimmunization.” Pet’r’s Ex. 12 at 60. Moreover, the impression of her
status after the MRI performed at this time was deemed most consistent with a neurodegenerative
process involving the bilateral basal ganglia. Id. at 67. The differential diagnoses were
pantothenate kinase associated neuro-generation, multiple system atrophy-parkinsonian, or other
atypical Parkinsonism. Id.

       It appears that Ms. Bell saw Dr. Gonzalez-Alegre one more time, on April 9, 2014. See
generally Pet’r’s Ex. 22 at 2-10. At this visit, Dr. Gonzalez-Alegre characterized her condition as
a “complex neurologic syndrome, likely due to basal ganglia encephalitis that may have been
triggered by a hepatitis B vaccination.” Id. at 9. He informed Ms. Bell that he would be moving
institutions and would no longer be able to provide her care, but introduced her to Dr. Shivapour,
who would be Ms. Bell’s treater at her follow-up visit in six months. Id. at 5. Ms. Bell’s condition
remained largely unchanged for this visit, leading Dr. Gonzalez-Alegre to conclude that she
would benefit from obtaining a “second opinion” at the Mayo Clinic, from an expert in primary
demyelinating disorders of the nervous system. Id. Again, however, Dr. Gonzalez-Alegre’s
impressions and proposed diagnoses showed no awareness of, or grappling with, the Mayo
Clinic’s fall 2012 fairly comprehensive neurologic work-up for Ms. Bell, which had not found
evidence supporting the existence of a demyelinating disorder.

       Ms. Bell then went back to the Mayo Clinic on July 23, 2014 and was seen again by Dr.
McKeon. Pet’r’s Ex. 25 at 46. Dr. McKeon’s history characterized the Petitioner as suffering
from a “multifocal neurological disorder” which seemed most likely attributable to mitochondrial
dysfunction, although he noted that the testing to confirm that hypothesis in later 2012 had been
negative. Id. He also reiterated that her CSF testing had produced normal results in September
2012, but not in the more recent testing in May 2013. Id. Yet the steroidal course prescribed for
Ms. Bell had been unsuccessful (contrary to what would be expected if inflammation relating to
an autoimmune condition were the source of her various symptoms). Dr. McKeon therefore
proposed that the cause for her condition largely remained undiagnosed, and proposed two sets
of further care for Ms. Bell - additional testing to be completed within a few days (including an
MRI, blood work, CSF evaluation, EMG and nerve conduction studies, and a lumbar puncture),
and rehabilitation services, which included seeing a speech pathologist, undergoing a swallow
evaluation, and a consultation with physical medicine and rehabilitation groups. Id. at 47.

      The first of those rehabilitation consultations was with Dr. Joseph Duffy, a speech
pathologist. He noted that Ms. Bell’s speech difficulty had increased over the last six months and
diagnosed her with mixed hypokinetic-ataxic dysarthria, moderately severe. Pet’r’s Ex. 25 at 38-
39. Shortly thereafter, Ms. Bell saw Dr. Margaret A. Moutvic, a specialist in physical medicine
and rehabilitation. Dr. Moutvic performed physical strength testing, concluding that Ms. Bell
would benefit from a rolling walker and more physical therapy. Id. at 34, 36-37. Ms. Bell then


                                                13
 followed up with her Mayo Clinic geneticist, Dr. Gavrilova, who reiterated the views of prior
 treaters that there was no specific etiology for Ms. Bell’s phenotype. Dr. Gavrilova requested
 neurotransmitter analysis of the CSF and a repeat echocardiogram, among other things, while
 also proposing some genetic testing. Id. 30-31.

        Dr. McKeon reviewed the new findings from Ms. Bell’s July 2014 return visit to the Mayo
 Clinic and associated testing, and concluded that, from a diagnostic standpoint, they were
 unhelpful in identifying the underlying causes of her overall illness. Pet’r’s Ex. 25 at 15. He
 opined that outside of whole exome sequencing (which would be costly), there was no further
 testing that could be done. Id. His listed differential diagnoses as of September 2014 included
 external ophthalmoplegia with diplopia, multifocal central nervous system disorder, myopathy,
 and sudomotor failure – but not ADEM. Id. Overall, however, he opined that even with a correct
 diagnosis, Ms. Bell’s condition was unlikely to improve (although it could become stable). Id.

 II.     EXPERT TESTIMONY

        In this case, both sides offered two experts, but no fact witness testimony. The opinions
and testimony of the relevant experts are set forth below.

       A.     Dr. Thomas F. Morgan – The first of petitioner’s two experts, Thomas Morgan,
M.D., provided an opinion as to the etiology of Ms. Bell’s condition, along with the purported role
the Hep B vaccine played in it.

        Dr. Morgan graduated from Meharry Medical College in 1970 (after completing his
undergraduate degree at St. Louis University). Pet’r’s Ex. 18 at 1. Dr. Morgan went on to complete
his residencies in internal medicine at Brown University School of Medicine (1970-1972) and
neurology at Boston University School of Medicine (1972-1975). Id. at 2. Dr. Morgan is board
certified in psychiatry, neurology, and as a medical examiner. Id. at 3. He is currently with the
Department of Clinical Neuroscience at Brown University as a clinical assistant professor and
maintains a clinical practice at a private office as a disability examiner. Id. at 4. Dr. Morgan sees
about 15 patients a week, but it is uncommon in his practice to treat autoimmune conditions,
including ADEM. Tr. at 17. Additionally, Dr. Morgan could not recall having diagnosed anyone
with ADEM as part of his clinical practice. Id. at 17.

        Dr. Morgan’s opinion was based on his review of Petitioner’s medical records and medical
 or scientific literature (including articles on the methodology of neurology and ADEM). Tr. at
 13-14. He began with testimony about the proper neurologic methodolody employed in coming
 to a diagnosis, explaining how it was used by Dr. Krain and himself to evaluate Ms. Bell’s
 condition. Tr. at 17-24. This evaluation began with describing the changes observed on the MRIs
 performed in 2012, after Petitioner’s second Hep B dose. Id. at 28-29.


                                                 14
       As Dr. Morgan testified, the images from Ms. Bell’s first MRI revealed lesions in the
gray matter of the caudate nucleus region of the brain, along with what appeared to be a tumor
that was producing changes in brain white matter, leading Dr. Krain to characterize it as
evidence of tumefactive demyelination. Tr. at 26-28. Dr. Morgan also relied on Dr. Krain’s
initial conclusions that Ms. Bell’s condition presented as subacute. Id. at 142. The progression
of Ms. Bell’s condition into the brain stem, associated with her reported worsening vision, further
persuaded Dr. Morgan that it was evidence of ADEM – because it affected one side of the brain
and the brainstem. Id. at 24.

      A large portion of Dr. Morgan’s opinion was dedicated to review of Ms. Bell’s symptoms
and the progression of her condition compared to the classical presentation of ADEM. Overall,
Dr. Morgan maintained that ADEM was present (Tr. at 22), relying on the clinical factors for the
disease as set forth in S. Tenembaum, et al., Acute Disseminated Encephalomyelitis, Neurology,
Apr. 17, 2007; 68 (Suppl 2), S23-S36, filed as Pet’r’s Ex. 16 (“Tenenbaum”). In his opinion, Ms.
Bell matched the criteria for ADEM (as stated by Tenembaum) because she had rapid onset of
encephalopathy (problems on the left side of her body affecting deep structures), and because the
MRIs performed in the first half of 2012 showed confluent tumefactive lesions with extension
and edema and mass effect. Tr. at 47.

       Respondent challenged several of these factors on cross-examination. As a preliminary
matter, both Dr. Morgan and Respondent’s primary expert, Dr. Sriram, agreed that a predicate to
ADEM is encephalopathy, although they maintained different definitions for what it meant in this
context. Dr. Morgan defined encephalopathy as any pathology of the brain presenting with either
normal or abnormal mental status, while Dr. Sriram’s position was that encephalopathy
associated with ADEM would present only with behavioral changes or changes in consciousness.
Tr. at 74, 79. Thus, when confronted with Respondent’s definition of encephalopathy (which
relied on Krupp, L.B. and S. Tenembaum, Consensus definitions proposed for pediatric multiple
sclerosis and related disorders, Neurology, 2007, 68 (16 Suppl. 2): p. S7-12, filed as Resp’t’s
Ex. D), Dr. Morgan conceded that Ms. Bell had not presented with any notable behavioral
changes or alterations, but maintained that “they’re saying that’s a requirement, but I’m going to
tell you, in the real world, this [ADEM] is what the lady had.” Tr. at 79.

       Dr. Morgan agreed, however, with Respondent that Ms. Bell’s presentation was otherwise
atypical for the disease, given the absence of other symptoms representative of the condition (as
described by Krupp), and given that it was not until Dr. Krain received the MRI results that he
was able to say there even was a focal problem. Tr. at 77. Dr. Morgan also confronted the errors
in Dr. Gonzalez-Alegre’s (the treater whose ADEM diagnosis is heavily relied upon by
Petitioner) recitation of Ms. Bell’s history from 2013, stating “he may have errors, but I think his
conclusion is right.” Tr. at 115.


                                                15
       Another central issue to Ms. Bell’s diagnosis that was highlighted in Dr. Morgan’s
testimony was the matter of how brain MRIs use enhancement to evaluate the presence of
inflammation as discussed above. Dr. Morgan admitted that the first MRI performed on Ms. Bell
showed no enhancement - meaning there was nothing that would suggest an ongoing
demyelination process, or that the inflammation was so microscopic that it did not appear on the
scan. Id. at 85. He otherwise pointed to no other instances from the time contemporaneous with
the second or third Hep B doses that were contrary.

       Dr. Morgan also conceded that many of Ms. Bell’s normal testing results (none of which
in 2012, for example, corroborated the existence of inflammation) did not support his opinion
about the propriety of the ADEM diagnosis, but maintained that this did not make it less likely
that ADEM was the appropriate explanation, arguing that test results were “great if they’re
positive, but not being there does not by any stretch rule out this condition.” Tr. at 13. He also
proposed that some common testing might not reveal ADEM-related problems. Thus, with
respect to the normal CSF results, Dr. Morgan stated that sometimes there are conditions of the
brain that do not get “spilled over” into the spinal cord, and thus would not be revealed by a
lumbar puncture. Id. at 143. Dr. Morgan also acknowledged that, based on his review of the
medical records, there was no evidence that Ms. Bell had experienced a reaction to her first dose
of Hep B vaccine, but dismissed the significance of that fact. In his view, it was common for
individuals to be unaffected by a vaccine’s initial dose, since many times the first would merely
serve to prime the immune system, leading to a pathologic, inflammatory reaction only after the
second dose. Id. at 13.

       Another debatable aspect of Dr. Morgan’s diagnostic opinion was whether demyelinating
syndromes such as ADEM are established largely on MRI findings of lesions in gray matter
regions of the brain, like the basal stem ganglia. Dr. Morgan proposed that ADEM can so
manifest. Tr. at 94. His proposal arose from Tenenbaum, which states that “the gray matter of the
thalami and basal ganglia are frequently involved” in ADEM. Tenenbaum at S25. Dr. Morgan
supported that statement by discussing how he independently determined that ADEM is the
proper diagnosis. Ms. Bell presented with a subacute demyelinated lesion (seen in the first MRI)
that was tumefactive, she had a lesion in the basal ganglia, and other conditions were excluded.
Tr. at 116.

      Dr. Morgan’s opinion generally strayed away from discussing the causal role the Hep B
vaccine could have played in the development of Ms. Bell’s purported ADEM. Although
throughout his testimony he stated that the cause was post-vaccinal, he also admitted that he is
not an immunologist and relied on molecular mimicry as the mechanism because it is a “touted
medical theory.” Tr. at 36-38, 121. Dr. Morgan did reference some scientific support for the
causal relationship between ADEM and the Hep B vaccine, referencing Langer-Gould, Annette,


                                               16
et al., Vaccines and the Risk of Multiple Sclerosis and Other Central Nervous System
Demyelinating Diseases. JAMA Neurol. 2014; 71 (12):1506-1513, filed as Pet’r’s Ex. 26-1
(“Langer-Gould”). Thus, he opined that based on Langer-Gould, Ms. Bell “fits the bill” for the
results produced in the study. Tr. at 60. Langer-Gould focused on the Hep B and HPV vaccines
and their potential relationship to central nervous system and demyelinating syndromes. Langer-
Gould at 1. Its authors found “no longer-term association of vaccines with MS or any other central
nervous system- acquired demyelinating syndromes (“CNS ADS”) but a “short-term increase in
risk [that] suggests that vaccines may accelerate the transition from subclinical to over
autoimmunity in patient with existing disease.” Id. at 1. In Dr. Morgan’s opinion, Ms. Bell’s
circumstances were comparable to the studied patients who experienced some kind of
demyelinating condition in the first thirty days after vaccination. Tr. at 15.

       Dr. Morgan also proposed, with respect to the period between vaccination and onset of
Petitioner’s symptoms, that “the timing is pretty classic, certainly the first one [vaccine
administered 01/2012], within ten days to two weeks.” Id. at 10. In his view, Ms. Bell’s immune
system was re-challenged when she received the third Hep B vaccine, as evidenced by the fact
that Ms. Bell got worse after receipt. Id. However, when pressed to explain the worsening
symptoms in detail, he conceded that her worsening vision and hearing may have been evident
before she received the third vaccine. Id. at 99.

       Dr. Morgan acknowledged the contrary findings of many of Ms. Bell’s treaters that did not
embrace ADEM as her illness, and instead proposed that there was no explanation yet provided
for the cause of her symptoms, or did not believe that the Hep B vaccination was the most likely
cause. He nevertheless proposed that the opinions offered by some of the Iowa treaters, like Dr.
Gonzalez-Alegre (who, as he noted, had consulted with other Iowa treaters about his views), were
more persuasive on the issue of diagnosis. Tr. at 117. As support for this contention, Dr. Morgan
stated that the Mayo Clinic treaters only focused on the potential genetic aspect of Ms. Bell’s
condition, while only performing a more cursory neurologic review (although, as noted above, the
record belies that assertion). Id. at 145. Dr. Morgan was similarly presented with Ms. Bell’s
condition as of July 2014, and questioned about the implication of the more-recent treater views
that her symptoms did not reflect an acute, monophasic illness like ADEM. Id at 48, 128-129.
When asked if those records indicated a progression in Ms. Bell’s symptoms, Dr. Morgan could
only concede that her symptoms were worse. Id. at 129.

      B.      Dr. David Axelrod

      Petitioner’s second expert, David Axelrod, M.D., provided an immunology opinion about
the theoretical causative role the Hep B vaccine could play in developing ADEM or another
demyelinating condition. He filed one report in this case, and also testified at hearing. See Pet’r’s
Ex. 23, see also Tr. 150-198.


                                                17
       Dr. Axelrod graduated from the University of Michigan Medical School in 1974 (after
completing his bachelor’s degree at the University of Michigan). Pet’r’s Ex. 24 at 1. He
completed two residencies in internal medicine, one at the University of Toronto and one at
William Beaumont Hospital, followed by additional residencies with a fellowship in allergy,
immunology, and rheumatology at McGill University, and then serving as a fellow for the
National Institutes of Health in the laboratory of clinical immunology. Id. Dr. Axelrod is board
certified in medicine, allergy and immunology, adult rheumatology, and medical laboratory
immunology. Tr. at 151. He currently works in private practice, with the vast majority of patients
having allergies, immunologic conditions, or autoimmune rheumatic diseases. Id. at 152. In
particular, he largely treats elderly patients who have suffered an allergic reaction to a medication,
thus dealing with autoimmune diseases only if his existing patients have that as a previously
diagnosed, underlying condition. Id. at 173.

       Dr. Axelrod’s opinions were based mainly on his review of Ms. Bell’s medical records and
scientific literature. Pet’r’s Ex. 23 at 1. He also acknowledged that his opinion assumed that Ms.
Bell in fact had a demyelinating condition. Tr. at 155-56. Indeed, he did not purport to have the
expertise to propose a diagnosis for Petitioner, and did not attempt to do so in providing an expert
report in the case. See generally Id. at 150-75. Thus, he agreed that if the assumption about the
character of her condition were incorrect – that she did not suffer from ADEM or a similar
demyelinating condition affecting her brain - then his testimony would no longer have relevance
to the lawsuit, because he would not be able to offer an opinion with respect to the vaccine’s
causal role in causing a different injury than that alleged. Id. at 180.

       Most of Dr. Axelrod’s opinion focused on the proposed biological mechanism linking the
Hep B vaccine to damage in the central nervous system – molecular mimicry. Dr. Axelrod opined
that the immune response elicited by a vaccine could damage the myelin sheath around nerves in
the brain as a result of homology (which is defined as similarity of nucleotide or amino acid
sequence-protein) between the vaccine and the myelin. Tr. at 156, see also Merriam-Webster,
Definition of Homology, http://www.merriam-webster.com/dictionary/homology (last visited
Nov. 7, 2016). In support of such homology existing, Dr. Axelrod cited Bogdanos, D.P., et al., A
study of molecular mimicry and immunological cross‐reactivity between hepatitis B surface
antigen and myelin mimics. Clinic Dev. Immunology, 2005. 12(3): p. 217‐24, filed as Pet’r’s Ex.
23-12. (“Bogdanos”).

       Specifically, the study referenced in Bogdanos found antibodies that inhibited patients’
response to the recombinant hepatitis B vaccine that contained an antigen identical to the wild
virus. Tr. at 156. In Ms. Bell’s case, Dr. Axelrod proposed, the Hep B vaccine, contained protein
structures homologous to the myelin protein oligodendrocyte glycoprotein; the interaction
between the vaccine homologous antigens and the myelin resulted in the production of antibodies,
and the cytokine production stimulated by the vaccine facilitated movement of the antibodies in


                                                 18
 Ms. Bell’s central nervous system through the blood brain barrier. Pet’r’s Ex. 23 at 6. Once the
 cytokines combined with cells within the brain, damage occurred to her central nervous system.
 Id. And he referenced other literature finding a relationship between the Hep B vaccine and a
 variety of neurologic conditions.29 Id. at 6-7.

        Dr. Axelrod was further questioned on the Bogdanos paper, and especially its conclusions
 that no one studied in it ever manifested the disease even with the presence of homology. Tr. at
 187. He conceded that molecular mimicry is just a theory and there is no practical ability to prove
 that homology can lead to disease. Id. at 187-88.

       Dr. Axelrod’s expert report and testimony briefly discussed several other factors that he
 believes support causation in this case. First was the lack of alternative explanations. Ms. Bell’s
 physicians found no preceding infectious or malignant cause of her neurologic symptoms. Pet’r’s
 Ex. 23 at 4. By contrast, Ms. Bell’s MRI in March of 2013 showed near complete interval
 resolution of her lesions from the time of vaccination, thus establishing that she had experienced
 a de-challenge - the defining aspects of the disorder disappeared with removal of the exposure.
 Id.

        Dr. Axelrod’s testimony also addressed the temporal association of Ms. Bell’s receipt of
 the vaccine and her reaction. He relied particularly on Abbas, A.K., Cellular and Molecular
 Immunology Edition 6. 6th ed. 2010, Philadelphia: Saunders Else Ier, 566, filed as Pet’r’s Ex. 23-
 4 (“Abbas”), as evidence that Ms. Bell’s first reaction was within the proper time frame – 14-21
 days following the vaccination. He also found significant Petitioner’s purported second reaction
 after her third dose of Hep B vaccine, noting that a secondary (memory) immune response is
 known to result more quickly than a first immune response. Pet’r’s Ex. 23 at 3; Tr. at 159. Applied
 to Ms. Bell’s case, Dr. Axelrod averred, Ms. Bell’s reaction to her third vaccine fit squarely within
 the time-frame suggested by Abbas. Dr. Axelrod thus concluded that Ms. Bell’s reaction to her
 second and third Hep B vaccinations established that the vaccine played a causative role in her
 illness. Id. at 160.

       Indeed, Dr. Axelrod proposed that Ms. Bell got worse after the third vaccination, bolstering
 his causation opinion because a re-challenge caused her condition to worsen. Pet’r’s Ex. 23 at 4-
 5. However, when cross-examined about instances in the medical record demonstrating that

29
  Thus, Dr. Axelrod cited the following references to show a connection between Hep B and neurologic conditions:
Geier, D.A, et al., A case‐control study of serious autoimmune adverse events following hepatitis B immunization.
Autoimmunity, 2005. 38(4): pp. 295‐301 (studied subjects suffered neurologic damage after Hep B vaccine); Nam,
T.S., et al., Mononeuropathy multiplex in a patient with chronic active hepatitis B. J. Clinical Neurology, 2010. 6(3):
p. 156‐8; Matsui, M., et al., Recurrent demyelinating transverse myelitis in a high titer HBs‐antigen carrier. J.
Neurologic Science, 1996. 139(2): p. 235‐7 (case study of a patient with recurrent demyelinating transverse myelitis
with antibodies to Hep B antigen); and Vital, C., et al., Postvaccinal inflammatory neuropathy: peripheral nerve
biopsy in 3 cases. J. Peripheral Nervous Syst, 2002. 7(3): p. 163‐7 (two cases of demyelinating disease following Hep
B vaccination).

                                                         19
 Petitioner had experienced worsening prior to the third Hep B dose, Dr. Axelrod conceded that
 his assumptions about worsening might not in fact have substantiation and “maybe the third
 vaccine didn’t do much of anything else.” Tr. at 183.

       C.      Dr. Subramanian Sriram


        Respondent’s first expert, Subramanian Sriram, M.D., testified that it was more likely than
not that the Hep B vaccinations that Ms. Bell received were unrelated to the neurologic syndrome
that she developed. Tr. at 214. He further stated that based on her clinical presentation, he did not
think Ms. Bell had ADEM, characterizing her condition instead as of idiopathic origin. Id. Like
Dr. Morgan, Dr. Sriram filed three expert reports in total. See Resp’t’s Exs. A, Q, and R.
        Dr. Sriram completed his bachelors and medical degrees from the University of Madras in
India, completing his residency in internal medicine at Wayne State University followed by a
neurology residency and at Stanford University. Tr. at 206; Resp’t’s Ex. B. He then went on to
complete a four year neuroimmunology fellowship at Stanford, before becoming director of the
MS Center at the University of Vermont for about 10 years. Resp’t’s Ex. B. Today, Dr. Sriram
directs the Multiple Sclerosis Center at Vanderbilt Medical Center, where he sees patients while
also serving as a Professor of Neurology and Experimental Therapeutics at Vanderbilt. Tr. at 206-
07.

       Dr. Sriram sees approximately 35 patients per week, 80 percent of whom have MS, with the
remainder having some other neurological disease. Tr. at 209. Relying on his experience treating
such patients with autoimmune disorders, Dr. Sriram formulated his opinion in this case after
reviewing Petitioner’s medical records, and pertinent medical or scientific literature. Id. at 215-16.
        Dr. Sriram began by describing the characteristic clinical metrics used to diagnose a patient
 with ADEM. He emphasized that ADEM is a monophasic disorder, typically lasting no more
 than four to six weeks before the patient recovers. Tr. at 210. ADEM occurs most commonly with
 children, usually presenting with multiple abnormal areas on an MRI in the white matter of the
 brain, and with evidence of inflammation (as established by CSF testing). In addition, ADEM
 can be effectively treated with steroids and immunosuppressive agents. Id. at 211-12.

        As stated earlier, Dr. Sriram and Dr. Morgan agreed that encephalopathy is a predicate to
 ADEM. Dr. Sriram, however, took issue with Dr. Morgan’s testimony about what factors would
 establish the existence of an encephalopathy. Tr. at 213-14. In Dr. Sriram’s view, encephalopathy
 manifests as behavioral change, such as irritability, inability to concentrate, loss of consciousness
 or alertness, or lethargy. Id. at 214. He also added seizures to the list of behavioral changes
 consistent with encephalopathy. Id. at 273. He thus firmly disagreed with Dr. Morgan’s
 categorization of encephalopathy as a mere pathology of the brain, stating that “encephalopathy
 can result from the pathology . . . that does not mean every pathology of the brain has
 encephalopathy.” Id. at 215.

                                                 20
        After setting out the characteristics of ADEM, Dr. Sriram referenced Ms. Bell’s clinical
presentation to show how it did not fit the classic clinical factors for the disease. Dr. Sriram
placed the most emphasis on ADEM being a disease of the white matter – whereas, according
to the MRI results, any abnormal findings from Ms. Bell’s first two MRIS appeared only in the
gray matter. Tr. at 216-17. Moreover, he opined, based on Ms. Bell’s MRIs that her brain
abnormalities were located in the deep nuclei or the caudate, the putamen, and the globus
pallidus- all deep neurons not found in the white matter regions of the brain. Id. at 217. Dr.
Sriram admitted that it was possible for ADEM to be present without evidence of white matter
lesions, but that it was unlikely that ADEM would present with only isolated lesions in the gray
matter, as here. Id. at 220-21. He also noted that the lack of evidence of inflammation on both
the MRIs and from the CSF tests as further diminishing the propriety of the diagnosis. Id.
Additionally, Dr. Sriram emphasized that if Ms. Bell’s condition was part of an immunological
process, then he would have expected to see progression in the IgG index and oligoclonal bands,
which was not present for Ms. Bell. Id. at 298.

       Dr. Sriram was confronted on cross-examination with the idea that the criteria for
ADEM, which typically appears in children, could be different for adults. Tr. at 270-73. He
mentioned that the variations between adults and children could be the amount of lesions
appearing on MRIs, and the amount of spinal fluid cells that the patient should have. Id. at 273.
But he maintained that there were certain clinical criteria that would be expected regardless of
the patient’s age, such as presenting with encephalopathy or a monophasic course to the
disease’s symptoms – none of which were evident with respect to Ms. Bell. Id. at 273.

       Outside of the issues stated above, Dr. Sriram stressed that Ms. Bell’s ongoing symptoms
over many years, and inability of her treaters to pinpoint the nature of her illness or its source,
further undercut the conclusion that she ever suffered from ADEM. Tr. at 290. In a typical
ADEM case, Dr. Sriram would expect to see the patient’s condition resolve in a matter of weeks.
Id. He acknowledged the existence of other variations of ADEM that did not adhere to a similar
course, including relapse, recurrent, or multiphasic ADEM, although he did not accept that they
provided possible explanations for Ms. Bell’s illness. Id. at 300. Thus, while Dr. Sriram admitted
that relapse of ADEM symptoms could occur, he argued that this was mostly present when the
demyelinating condition was later determined to be MS, which had a different, more intermittent
course. Tr. at 290. He also proposed that purported ADEM relapses were often nothing more
than evidence that an ameliorative treatment like steroids had been tapered or discontinued,
allowing underlying symptoms to flare back. Id. at 289. He acknowledged as well that in very
rare cases children had been known to get better from ADEM and then show new symptoms,
but distinguished such unusual cases from individuals like Ms. Bell, who could only be said to
be experiencing some kind of ongoing process with some demyelinating features, the source of
which ultimately could not be known. Id. at 290.



                                                21
        Dr. Sriram also referenced portions of the medical record that he believed contained
incorrect speculation or conclusions as to Ms. Bell’s condition. The first such disagreement was
with the differential diagnosis of a tumefactive demyelinating disease after Ms. Bell’s first MRI.
Tr. at 223. Dr. Sriram described a tumefactive demyelinating disease as presenting with lesions
in the white matter that are so large they appear on an MRI much like a tumor. Id. at 222.
Although Dr. Krain included it in his differential diagnosis from February 21, 2012, Dr. Sriram
noted that there was little white matter where the lesions were present in the MRI. Id. at 223.

        Dr. Sriram further offered his own interpretation of the results of the MRIs performed in
May and June 2012. At the time of the May MRI, Ms. Bell was exhibiting horizontal gaze palsy
– the inability to look left or right. Tr. at 242. This condition, he proposed, results from a problem
in the pons region of the brain and not the cranial nerves. Id. at 243. The subsequent June MRI
showed stability – Ms. Bell’s lesions had changed very little. Id. at 244. The findings
documented in that MRI stated an abnormal signal extending to the ventral mesencephalon. Id.
In Dr. Sriram’s view, such a finding was demonstrative of basal ganglia damage, which is seen
in Parkinson’s disease and other similar conditions. Id. at 245-47. It was therefore further
evidence not supportive of the ADEM diagnosis.

       Dr. Sriram also discussed the PET scan Ms. Bell received in June 2012. He described the
process of a PET scan, which allows for the measurement of glucose uptake by the cells by
injecting FDG and observing the reaction. Tr. at 238. In Ms. Bell’s case, there was a total absence
of uptake in the right caudate lentiform nucleus, suggesting to Dr. Sriram that those cells were
already dead. Id. In his opinion, such findings were not consistent with either the presence of a
white matter tumor or inflammation, which in either case would require live brain cells capable
of division, and thus susceptible to inflammation. Id. at 239.

      D.      Dr. Kathleen Collins

      Respondent’s final expert, Kathleen Loretta Collins, M.D., Ph. D., offered an opinion
mostly aimed at rebutting Dr. Axelrod’s assertions about the causal relationship between the Hep
B vaccine and ADEM, based both upon the facts of the case as well as science regarding the
vaccine.

       Dr. Collins received her medical degree and doctorate from Johns Hopkins University
School of Medicine (after receiving an undergraduate degree from Wellesley College) in 1993.
Resp’t’s Ex. G at 1, Tr. at 306-63. She then completed her residency in internal medicine at
Brigham and Women’s Hospital before serving as a clinical fellow of infectious disease at Beth
Israel Hospital and served as a research fellow at Harvard University. Tr. at 307. Dr. Collins was
also a post-doctoral fellow at MIT researching the immune response to viral infections. Id. Dr.
Collins is board certified in infectious disease and currently works as a professor of internal


                                                 22
medicine and microbiology and immunology at the University of Michigan. Tr. at 307. Although
she is on the faculty at Michigan as an assistant professor, 70 percent of her time is spent on basic
science research, leading her to publish over 50 articles. Id. at 311. Her opinion in this case was
based on review of the medical records, the expert report of Dr. Axelrod, and medical or scientific
literature. Id. at 313.

      Dr. Collins’ primary opinion was that the record did not support the conclusion that Ms.
Bell had suffered an immune response to any doses of the Hep B vaccine. Tr. at 316. In order to
conclude that there was an immune response, there would, in Dr. Collins’s experience, need to
be evidence of inflammation from the MRI as well as CSF tests. Id. at 316-17. Here, however,
Ms. Bell showed no enhancement in her MRIs - meaning there was no inflammation. Id. The
CSF test results were similarly unsupportive of the conclusion that inflammation was present. Id.
She also reiterated Dr. Sriram’s contention that if there is inflammation in the brain, CSF tests
would reveal it – and in so doing questioned Dr. Morgan’s contention that CSF tests might not
be so revealing, noting that the spinal column was akin to a “cistern” that would almost always
reveal evidence of inflammatory activity in the brain. Tr. at 304.

       Similarly, Dr. Collins noted the difference between the diagnoses of an infection versus an
autoimmune disorder, proposing that this distinction highlighted a deficiency in Petitioner’s
contentions about the nature of her condition. The former would be treated by antibiotics, while
the latter would call for suppression of the immune system in order to halt the damaging
autoimmune process. Tr. at 312-13. The treatment history here, however, showed that Ms. Bell
was treated with anti-inflammatory steroids to suppress her immune system without positive
effect, thus suggesting her underling problem was not autoimmune in nature. Id.

       Finally, Dr. Collins challenged Dr. Axelrod’s opinion that molecular mimicry is a
mechanism by which the Hep B vaccine can cause ADEM. Tr. at 338. In particular, one of the
primary studies he relied upon addressing cytokines opening the blood brain barrier did not relate
to the proteins in the Hep B vaccine. Id. at 330; see also Lawson, C.M., Evidence for mimicry by
viral antigens in animal models of autoimmune disease including myocarditis. Cell Molecular
Life Science, 2000. 57(4): p. 552‐60, filed as Pet’r’s Ex. 23-11 (“Lawson”). Dr. Collins described
how the blood brain barrier works to protect the brain, allowing that in rare cases or particular
kinds of viral or bacterial infection (such as meningitis) the barrier will open as a result of
excessive inflammation. Tr. at 333. That did not lead to the conclusion, however, that the barrier
would necessarily open as a result of vaccine-induced cytokine expression, which could not be
shown (and had not been shown by Dr. Axelrod) to have the same inflammatory impact. Id. In
order to have an immune response that could even involve molecular mimicry as a pathologic
mechanism, inflammation was required – but she purports it was completely absent here. Id. at
350.



                                                23
         E.       Supplemental Reports Interpreting Missing MRIs

        During the January 2016 entitlement hearing, it was disclosed that Ms. Bell’s initial 2012
 MRIs had not been reviewed by the experts, because they were never obtained or filed in the
 case. Tr. at 138-39. I therefore ordered them produced and filed, if possible, and allowed both
 sides the opportunity to file a supplemental expert report interpreting the newly-disclosed MRIs.
 See Order dated February 5, 2016; see also Non-PDF Order dated March 22, 2016. The parties
 did so on April 29, 2016.30

        Petitioner’s supplemental report was not merely Dr. Morgan’s opinion, but was also based
 on his consultation with Dr. Roman Klufas, a neuro-radiologist at Brigham & Women’s Hospital
 in Boston, Massachusetts. Pet’r’s Ex. 35; see also Pet’r’s Ex. 35-2. Dr. Morgan stated that the
 newly-disclosed MRIs demonstrated that Ms. Bell had “classic MRI findings for ADEM,”
 noting the improvement seen on the March 20, 2012, MRI after Ms. Bell was treated with
 steroids. Pet’r’s Ex. 35 at 2. He also discussed the new demyelination findings of the July 2,
 2012, MRI and their consistency with a post vaccinal second attack following Ms. Bell’s third
 injection. Id. at 3. However, Dr. Morgan pointed out nothing from the MRIs that was different
 from what the existing contemporaneous record reveals, or that added any shading to his
 previous testimony.

        The supplemental report included a separate piece of correspondence from Dr. Klufas as
 well. Pet’r’s Ex. 35-2. Dr. Klufas noted a large area of T2 abnormality from his review of the
 first February 2012, MRI which nearly resolves by September 24, 2012. Pet’r’s Ex. 35-2 at 2.
 Regarding the July MRI, Dr. Klufas specifically claimed to discern new white matter findings
 within the mid pons. Id. Dr. Klufas ultimately concluded that the MRI findings were consistent
 with a diagnosis of ADEM. Id. at 2. However, he also stated that he saw little to no evidence of
 enhancement that would suggest the presence of inflammation. Id. at 1-2.

        Respondent’s supplemental report from Dr. Sriram reached conclusions consistent with
 his trial testimony about the MRI findings. Thus, Dr. Sriram notes a basal ganglia abnormality
 in the February 2012 MRI (thus a gray matter abnormality, as testified) and an increase in the
 T2 signal without inflammation. Resp’t’s Ex. R. at 2. He emphasized that his review of the
 unfiled MRIs also showed a gradual decrease of the T2 signal as seen on the March, April, and
 July MRIs. Id. In his opinion, the evolution of the T2 signal from hyper to hypo-intense is
 characteristic of metal deposits – something typically seen in degenerative and metabolic
 conditions such as Alzheimer’s and Parkinson’s, rather than a demyelinating condition. Id.
 Overall, and with the benefit of having seen the original MRI, Dr. Sriram reiterated his opinion

30
   This was the second supplemental report for both Drs. Morgan and Sriram. Dr. Morgan previously filed a
supplemental report on February 3, 2015 addressing Respondent’s expert reports as well as attempting to provide
further evidentiary support for causation as ordered by the court on October 8, 2014. See Order dated October 8, 2014.
Dr. Sriram filed his first supplemental report responding to Drs. Morgan’s and Axelrod’s reports on April 1, 2015.

                                                         24
 that there was no evidence of lesions in the white matter, making ADEM unlikely in this case,
 and confirming for him that the true etiology of Ms. Bell’s condition remained unknown. Id.


 III.     PROCEDURAL HISTORY


        Ms. Bell filed her Petition on September 23, 2013. Pet. at 1. In it, she specifically alleged
that she suffers from ADEM, progressive neurological deterioration, gaze palsy, facial palsy,
asymmetric sensorineural hearing loss, and other conditions. Id. at 4-5.
        On January 6, 2014, Respondent filed her Rule 4(c) report denying that Ms. Bell was
entitled to compensation. ECF No. 10. Shortly thereafter, the case was reassigned to me. In the
ensuing 16 months, Petitioner filed medical records, both sides submitted expert reports, and
Petitioner filed an amended petition stating that “regardless of the precise diagnoses of or label of
Kristine’s illnesses, disabilities, injuries, condition, and/or disorder, one or more of them constitute
a vaccine-related injury.” See Amended Petition Filed on December 15, 2014. Thereafter, in May
of 2015, I scheduled a hearing for January 28-29 of 2016, to determine entitlement. ECF No. 43.
        The entitlement hearing was held as scheduled, with both sides filing pre-hearing briefs.
That hearing included testimony from the experts identified above. After the hearing, I instructed
Petitioner to obtain the actual MRI images of Ms. Bell taken during 2012. Both parties were then
to have their neurologists review the images and write supplemental reports. The parties filed these
reports from Drs. Morgan and Sriram on the same day, April 29, 2016. The parties elected not to
file post-hearing briefs.



 IV.      APPLICABLE LEGAL STANDARDS

         A.       Petitioner’s Overall Burden in Vaccine Program Cases
         To receive compensation in the Vaccine Program, a petitioner must prove either: (1) that
she suffered a “Table Injury” – i.e., an injury falling within the Vaccine Injury Table –
corresponding to one of the vaccinations in question within a statutorily prescribed period of time
or, in the alternative, (2) that her illnesses were actually caused by a vaccine (a “Non-Table
Injury”). See Sections 13(a)(1)(A), 11(c)(1), and 14(a), as amended by 42 C.F.R. § 100.3; §
11(c)(1)(C)(ii)(I); see also Moberly v. Sec’y of Health & Human Servs., 592 F.3d 1315, 1321 (Fed.
Cir. 2010); Capizzano v. Sec’y of Health & Human Servs., 440 F.3d 1317, 1320 (Fed. Cir. 2006).31
In this case, Petitioner does not assert a Table claim.

31
  Decisions of special masters (some of which I reference in this ruling) constitute persuasive but not binding
authority. Hanlon v. Sec’y of Health & Human Servs., 40 Fed. Cl. 625, 630 (1998). By contrast, Federal Circuit rulings
concerning legal issues are binding on special masters. Guillory v. Sec’y of Health & Human Servs., 59 Fed. Cl. 121,
124 (2003), aff’d, 104 F. App’x 712 (Fed. Cir. 2004); see also Spooner v. Sec’y of Health & Human Servs., No. 13-

                                                         25
         For both Table and Non-Table claims, Vaccine Program petitioners bear a “preponderance
of the evidence” burden of proof. Section 13(1)(a). That is, a petitioner must offer evidence that
leads the “trier of fact to believe that the existence of a fact is more probable than its nonexistence
before [he] may find in favor of the party who has the burden to persuade the judge of the fact’s
existence.” Moberly, 592 F.3d at 1322 n.2; see also Snowbank Enter. v. United States, 6 Cl. Ct.
476, 486 (1984) (mere conjecture or speculation is insufficient under a preponderance standard).
Proof of medical certainty is not required. Bunting v. Sec’y of Health & Human Servs., 931 F.2d
867, 873 (Fed. Cir. 1991). In particular, a petitioner must demonstrate that the vaccine was “not
only [the] but-for cause of the injury but also a substantial factor in bringing about the injury.”
Moberly, 592 F.3d at 1321 (quoting Shyface v. Sec’y of Health & Human Servs., 165 F.3d 1344,
1352-53 (Fed. Cir. 1999)); Pafford v. Sec’y of Health & Human Servs., 451 F.3d 1352, 1355 (Fed.
Cir. 2006). A petitioner may not receive a Vaccine Program award based solely on her assertions;
rather, the petition must be supported by either medical records or by the opinion of a competent
physician. Section 13(a)(1).

        In attempting to establish entitlement to a Vaccine Program award of compensation for a
Non-Table claim, a petitioner must satisfy all three of the elements established by the Federal
Circuit in Althen: “(1) a medical theory causally connecting the vaccination and the injury; (2) a
logical sequence of cause and effect showing that the vaccination was the reason for the injury;
and (3) a showing of a proximate temporal relationship between vaccination and injury.” Althen,
418 F.3d at 1278.

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

        Petitioners may satisfy the first Althen prong without resort to medical literature,
epidemiological studies, demonstration of a specific mechanism, or a generally accepted medical
theory. Andreu v. Sec’y of Health & Human Servs., 569 F.3d 1367, 1378-79 (Fed. Cir. 2009) (citing
Capizzano, 440 F.3d at 1325-26). Special masters, despite their expertise, are not empowered by
statute to conclusively resolve what are essentially thorny scientific and medical questions, and
thus scientific evidence offered to establish Althen prong one is viewed “not through the lens of
the laboratorian, but instead from the vantage point of the Vaccine Act’s preponderant evidence
standard.” Id. at 1380. Accordingly, special masters must take care not to increase the burden
placed on petitioners in offering a scientific theory linking vaccine to injury. Contreras v. Sec’y of
Health & Human Servs., 121 Fed. Cl. 230, 245 (2015) (“[p]lausibility . . . in many cases may be

159V, 2014 WL 504728, at *7 n.12 (Fed. Cl. Spec. Mstr. Jan. 16, 2014).

                                                       26
enough to satisfy Althen prong one” (emphasis in original)), appeal docketed, No. 2015-5097 (Fed.
Cir. June 19, 2015). But this does not negate or reduce a petitioner’s ultimate burden to establish
her overall entitlement to damages by preponderant evidence. W.C. v. Sec’y of Health & Human
Servs., 704 F.3d 1352, 1356 (Fed. Cir. 2013) (citations omitted).32

        The second Althen prong requires proof of a logical sequence of cause and effect, usually
supported by facts derived from a petitioner’s medical records. Althen, 418 F.3d at 1278; Andreu,
569 F.3d at 1375-77; Capizzano, 440 F.3d at 1326; Grant v. Sec’y of Health & Human Servs., 956
F.2d 1144, 1148 (Fed. Cir. 1992). In establishing that a vaccine “did cause” injury, the opinions
and views of the injured party’s treating physicians are entitled to some weight. Andreu, 569 F.3d
at 1367; Capizzano, 440 F.3d at 1326 (“medical records and medical opinion testimony are favored
in vaccine cases, as treating physicians are likely to be in the best position to determine whether a
‘logical sequence of cause and effect show[s] that the vaccination was the reason for the injury’”)
(quoting Althen, 418 F.3d at 1280). Medical records are generally viewed as particularly
trustworthy evidence, since they are created contemporaneously with the treatment of the patient.
Cucuras v. Sec’y of Health & Human Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993).

        However, medical records and/or statements of a treating physician’s views do not per se
bind the special master to adopt the conclusions of such an individual, even if they must be
considered and carefully evaluated. Section 13(b)(1) (providing that “[a]ny such diagnosis,
conclusion, judgment, test result, report, or summary shall not be binding on the special master or
court”); Snyder v. Sec’y of Health & Human Servs., 88 Fed. Cl. 706, 746 n.67 (2009) (“there is
nothing . . . that mandates that the testimony of a treating physician is sacrosanct – that it must be
accepted in its entirety and cannot be rebutted”). As with expert testimony offered to establish a
theory of causation, the opinions or diagnoses of treating physicians are only as trustworthy as the
reasonableness of their suppositions or bases. The views of treating physicians should also be
weighed against other, contrary evidence also present in the record – including conflicting opinions
among such individuals. Hibbard v. Sec’y of Health & Human Servs., 100 Fed. Cl. 742, 749 (2011)
(not arbitrary or capricious for special master to weigh competing treating physicians’ conclusions
against each other), aff'd, 698 F.3d 1355 (Fed. Cir. 2012); Caves v. Sec’y of Dep't of Health &
Human Servs., 100 Fed. Cl. 119, 136 (2011), aff'd, 463 F. App'x 932 (Fed. Cir. 2012); Veryzer v.
Sec’y of Health & Human Servs., No. 06-522V, 2011 WL 1935813, at *17 (Fed. Cl. Spec. Mstr.
Apr. 29, 2011), mot. for review den’d, 100 Fed. Cl. 344, 356 (2011), aff’d without opinion, 475
Fed. App’x 765 (Fed. Cir. 2012).

32
   There is ample contrary authority for the more straightforward proposition that the first Althen prong, like the overall
test itself, simply applies a preponderance standard when evaluating if a reliable and plausible causal theory has been
established. Broekelschen v. Sec’y of Health & Human Servs., 618 F.3d 1339, 1350 (Fed. Cir. 2010). For purposes of
the present analysis, I am stressing those cases focusing on the plausibility of the causal theory proposed, as opposed
to whether preponderant evidence supports it, in order to avoid imposing on Petitioners a greater evidentiary burden
than the law requires. This does not, however, change the fact that any theory’s plausibility, for purposes of satisfying
the Althen test, is properly analyzed by subjecting its components to the Daubert tests for scientific reliability. Terran
v. Sec’y of Health & Human Servs., 195 F.3d 1302, 1316 (Fed. Cir. 1999).

                                                           27
        The third Althen prong requires establishing a “proximate temporal relationship” between
the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been equated to the
phrase “medically-acceptable temporal relationship.” Id. A petitioner must offer “preponderant
proof that the onset of symptoms occurred within a timeframe which, given the medical
understanding of the disorder’s etiology, it is medically acceptable to infer causation.” Bazan v.
Sec'y of Health & Human Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). The explanation for what
is a medically acceptable timeframe must also coincide with the theory of how the relevant vaccine
can cause an injury (Althen prong one’s requirement). Id. at 1352; Shapiro v. Sec’y of Health &
Human Servs., 101 Fed. Cl. 532, 542 (2011), recons. den’d after remand, 105 Fed. Cl. 353 (2012),
aff’d mem., 2013 WL 1896173 (Fed. Cir. 2013); Koehn v. Sec'y of Health & Human Servs., No.
11-355V, 2013 WL 3214877 (Fed. Cl. Spec. Mstr. May 30, 2013), mot. for review den’d (Fed. Cl.
Dec. 3, 2013), aff’d, 773 F.3d 1239 (Fed. Cir. 2014).

       B.      Law Governing Analysis of Fact Evidence

        The process for making determinations in Vaccine Program cases regarding factual issues
begins with consideration of the medical records. Section 11(c)(2). The special master is required
to consider “all [] relevant medical and scientific evidence contained in the record,” including “any
diagnosis, conclusion, medical judgment, or autopsy or coroner’s report which is contained in the
record regarding the nature, causation, and aggravation of the petitioner’s illness, disability, injury,
condition, or death,” as well as “the results of any diagnostic or evaluative test which are contained
in the record and the summaries and conclusions.” Section 13(b)(1)(A). The special master is then
required to weigh the evidence presented, including contemporaneous medical records and
testimony. See Burns v. Sec’y of Health & Human Servs., 3 F.3d 415, 417 (Fed. Cir. 1993) (it is
within the special master’s discretion to determine whether to afford greater weight to
contemporaneous medical records than to other evidence, such as oral testimony surrounding the
events in question that was given at a later date, provided that such a determination is evidenced
by a rational determination).

        Medical records that are created contemporaneously with the events they describe are
presumed to be accurate and “complete” (i.e., presenting all relevant information on a patient’s
health problems). Cucuras, 993 F.2d at 1528; Doe/70 v. Sec’y of Health & Human Servs., 95 Fed.
Cl. 598, 608 (2010) (“[g]iven the inconsistencies between petitioner’s testimony and his
contemporaneous medical records, the special master’s decision to rely on petitioner’s medical
records was rational and consistent with applicable law”), aff’d, Rickett v. Sec’y of Health &
Human Servs., 468 F. App’x 952 (Fed. Cir. 2011) (non-precedential opinion). This presumption is
based on the linked propositions that (i) sick people visit medical professionals; (ii) sick people
honestly report their health problems to those professionals; and (iii) medical professionals record
what they are told or observe when examining their patients in as accurate a manner as possible,
so that they are aware of enough relevant facts to make appropriate treatment decisions. Sanchez


                                                  28
v. Sec’y of Health & Human Servs., No. 11-685V, 2013 WL 1880825, at *2 (Fed. Cl. Spec. Mstr.
Apr. 10, 2013); Cucuras v. Sec'y of Health & Human Servs., 26 Cl. Ct. 537, 543 (1992), aff'd, 993
F.2d 1525 (Fed. Cir. 1993) (“[i]t strains reason to conclude that petitioners would fail to accurately
report the onset of their daughter’s symptoms. It is equally unlikely that pediatric neurologists,
who are trained in taking medical histories concerning the onset of neurologically significant
symptoms, would consistently but erroneously report the onset of seizures a week after they in fact
occurred”).

        Accordingly, if the medical records are clear, consistent, and complete, then they should
be afforded substantial weight. Lowrie v. Sec’y of Health & Human Servs., No. 03-1585V, 2005
WL 6117475, at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed, contemporaneously medical
records are generally found to be deserving of greater evidentiary weight than oral testimony –
especially where such testimony conflicts with the record evidence. Cucuras, 993 F.2d at 1528;
see also Murphy v. Sec’y of Health & Human Servs., 23 Cl. Ct. 726, 733 (1991), aff'd, 968 F.2d
1226 (Fed. Cir.), cert. den’d, Murphy v. Sullivan, 506 U.S. 974 (1992) (citing United States v.
United States Gypsum Co., 333 U.S. 364, 396 (1947) (“[i]t has generally been held that oral
testimony which is in conflict with contemporaneous documents is entitled to little evidentiary
weight.”)).

        However, there are situations in which compelling oral testimony may be more persuasive
than written records, such as where records are deemed to be incomplete or inaccurate. Campbell
v. Sec’y of Health & Human Servs., 69 Fed. Cl. 775, 779 (2006) (“like any norm based upon
common sense and experience, this rule should not be treated as an absolute and must yield where
the factual predicates for its application are weak or lacking”); Lowrie, 2005 WL 6117475, at *19
(“[w]ritten records which are, themselves, inconsistent, should be accorded less deference than
those which are internally consistent”) (quoting Murphy v. Sec’y of Health & Human Servs., 23
Cl. Ct. 726, 733 (1991), aff'd per curiam, 968 F.2d 1226 (Fed. Cir. 1992)). Ultimately, a
determination regarding a witness’s credibility is needed when determining the weight that such
testimony should be afforded. Andreu, 569 F.3d at 1379; Bradley v. Sec’y of Health & Human
Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).

       C.      Analysis of Expert Testimony

        Establishing a sound and reliable medical theory often requires a petitioner to present
expert testimony in support of his claim. Lampe v. Sec’y of Health & Human Servs., 219 F.3d
1357, 1361 (Fed. Cir. 2000). Vaccine Program expert testimony is usually evaluated according to
the factors for analyzing scientific reliability set forth in Daubert v. Merrell Dow Pharm., Inc., 509
U.S. 579, 594-96 (1993). See Cedillo v. Sec’y of Health & Human Servs., 617 F.3d 1328, 1339
(Fed. Cir. 2010) (citing Terran v. Sec’y of Health & Human Servs., 195 F.3d 1302, 1316 (Fed. Cir.
1999)). “The Daubert factors for analyzing the reliability of testimony are: (1) whether a theory or


                                                 29
technique can be (and has been) tested; (2) whether the theory or technique has been subjected to
peer review and publication; (3) whether there is a known or potential rate of error and whether
there are standards for controlling the error; and (4) whether the theory or technique enjoys general
acceptance within a relevant scientific community.” Terran, 195 F.3d at 1316 n.2 (citing Daubert,
509 U.S. at 592-95).

         The Daubert factors play a slightly different role in Vaccine Program cases than they do
when applied in other federal judicial fora (such as the district courts). Daubert factors are usually
employed by judges (in the performance of their evidentiary gatekeeper roles) to exclude evidence
that is unreliable and/or could confuse a jury. In Vaccine Program cases, by contrast, these factors
are used in the weighing of the reliability of scientific evidence proffered. Davis v. Sec’y of Health
& Human Servs., 94 Fed. Cl. 53, 66-67 (2010) (“uniquely in this Circuit, the Daubert factors have
been employed also as an acceptable evidentiary-gauging tool with respect to persuasiveness of
expert testimony already admitted”). The flexible use of the Daubert factors to evaluate the
persuasiveness and reliability of expert testimony has routinely been upheld. See, e.g., Snyder, 88
Fed. Cl. at 742-45. In this matter (as in numerous other Vaccine Program cases), Daubert has not
been employed at the threshold, to determine what evidence should be admitted, but instead to
determine whether expert testimony offered is reliable and/or persuasive.

        Respondent frequently offers one or more experts of her own in order to rebut a petitioner’s
case. Where both sides offer expert testimony, a special master’s decision may be “based on the
credibility of the experts and the relative persuasiveness of their competing theories.”
Broekelschen v. Sec’y of Health & Human Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (citing
Lampe, 219 F.3d at 1362). However, nothing requires the acceptance of an expert’s conclusion
“connected to existing data only by the ipse dixit of the expert,” especially if “there is simply too
great an analytical gap between the data and the opinion proffered.” Snyder, 88 Fed. Cl. at 743
(quoting Gen. Elec. Co. v. Joiner, 522 U.S. 146 (1997)); see also Isaac v. Sec’y of Health & Human
Servs., No. 08-601V, 2012 WL 3609993, at *17 (Fed. Cl. Spec. Mstr. July 30, 2012), mot. for
review den’d, 108 Fed. Cl. 743 (2013), aff’d, 540 Fed. App’x 999 (Fed. Cir. 2013) (citing Cedillo,
617 F.3d at 1339).

        Weighing the relative persuasiveness of competing expert testimony, based on a particular
expert’s credibility, is part of the overall reliability analysis to which special masters must subject
expert testimony in Vaccine Program cases. Moberly, 592 F.3d at 1325-26 (“[a]ssessments as to
the reliability of expert testimony often turn on credibility determinations”); see also Porter v.
Sec’y of Health & Human Servs., 663 F.3d 1242, 1250 (Fed. Cir. 2011) (“this court has
unambiguously explained that special masters are expected to consider the credibility of expert
witnesses in evaluating petitions for compensation under the Vaccine Act”). It is in the exercise of
my duties as a special master to weigh competing expert testimony. Copenhaver v. Sec’y of Health
& Human Servs., No. 13-1002V, 2016 WL 6947389, at *5 (Fed. Cl. Oct. 20, 2016) (“Special


                                                  30
Masters may use their discretion in weighing expert testimony, and case law supports that
discretion”).

        In determining whether a particular expert’s testimony was reliable or credible, I may
consider whether the expert offers an opinion that exceeds his training or competence. Walton v.
Sec’y of Health & Human Servs., No. 04-503V, 2007 WL 1467307, at *17-18 (Fed. Cl. Spec. Mstr.
Apr. 30, 2007) (otolaryngologist not well suited to testify about disciplines other than her own
specialty). While (in keeping with the liberality with which evidence offered in Vaccine Program
cases is treated) I heard and have considered all of the testimony of the experts offered at the
entitlement hearing, I may properly evaluate, and give appropriate weight to, whether certain
testimony is beyond a particular expert’s purview. See, e.g., King v. Sec’y of Health & Human
Servs., No. 03-584V, 2010 WL 892296, at *78-79 (Fed. Cl. Spec. Mstr. Mar. 12, 2010)
(petitioner’s expert far less qualified to offer opinion on general causation issues pertaining to
autism than specific issues pertaining to the petitioner’s actual medical history, given the nature of
the expert’s qualifications).

       D.      Consideration of Medical Literature

        Both parties filed medical and scientific literature in this case, including some articles (such
as those discussing molecular mimicry and protein sequences in vaccines) that do not factor into
the outcome of this decision. I have reviewed all of the medical literature submitted in this case,
but I only discuss those articles that are most relevant to my determination and/or are central to
Petitioners’ case – just as I have not exhaustively discussed every individual medical record filed.
Moriarty v. Sec’y of Health & Human Servs., No. 2015-5072, 2016 WL 1358616, at *5 (Fed. Cir.
Apr. 6, 2016) (“[w]e generally presume that a special master considered the relevant record
evidence even though he does not explicitly reference such evidence in his decision”) (citation
omitted); see also Paterek v. v. Sec’y of Health & Human Servs., 527 F. App'x 875, 884 (Fed. Cir.
2013) (“[f]inding certain information not relevant does not lead to — and likely undermines —
the conclusion that it was not considered”).

 V.      ANALYSIS

        Based on consideration of the record and the testimony of both side’s experts, I conclude
that Petitioner has not carried her burden under the Federal Circuit’s test for non-Table causation
claims established in Althen. I address the Althen prongs out of order, in order to highlight the
deficiency in Petitioner’s proof or arguments in order of importance.
       A.      Althen Prong Two

       The Vaccine Act requires a petitioner to show that she has suffered from as least one
defined and recognized injury. Lombardi v. Sec’y of Health & Human Servs., 656 F3d. 1343, 1353


                                                  31
(Fed. Cir. 2011). In the context of Althen prong two, which requires a showing that the vaccine
caused petitioner’s injuries, it follows that “in the absence of a showing of the very existence of
any specific injury of which the petitioner complains, the question of causation is not reached.” Id.
Appellate courts have upheld the decisions of other special masters that focused their inquiry on
determining the injury. Broekelschen, 618 F.3d at 1345. Indeed, where the petitioner cannot show
that she “suffer[s] 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 v. Sec’y of Health & Human Servs., 689 F.3d 1355, 1365 (Fed. Cir. 2012).

        The facts of this case do not permit the conclusion that Ms. Bell “more likely than not”
suffered from ADEM, or any other central nervous system demyelinating condition. Rather, the
evidence allows for no conclusion as to the etiology of her condition – consistent with Dr. Sriram’s
testimony – making it impossible to find preponderant evidence supporting this factual allegation.
Because Petitioner’s theory was heavily dependent upon the finding that she suffered from ADEM
-- for as her immunologic expert admitted, he could not opine to a relationship with any other
condition and the relevant vaccine -- this failure is fatal to Ms. Bell’s entire claim.

         Discussion of the medical records and expert opinions above illustrates the complex nature
of Ms. Bell’s condition, and why ADEM is not the most likely explanation for it. During initial
treatment (between receipt of the second and third Hep B doses), ADEM was not deemed likely.
Ms. Bell did not present with symptoms suggestive of the disease (and the fact that it is typically
an acute and rapidly progressing disease makes those earlier treater views significant). The MRIs
performed on her in the first three months after the January 2012 Hep B dose did not reveal white
matter lesions, demyelination, or inflammation, nor did any of the technicians performing the
MRIs, or neurologists interpreting their result, propose ADEM as part of the differential diagnosis.
Other tests that could have corroborated ADEM, such as the CSF testing (which should have
shown brain inflammation were it occurring), were similarly negative. And treatments that would
be effective if an individual were suffering from a demyelinating condition, such as steroids, did
not assist Ms. Bell either, providing further confirmation that an inflammatory autoimmune
response to some prior insult was not the likely cause of her symptoms. National Institute of
Neurological Disorders and Stroke: Acute Disseminated Encephalomyelitis Information Page,
NIH, http://www.ninds.nih.gov/disorders/acute_encephalomyelitis/acute_encephalomyelitis.htm
(last visited Nov. 3, 2016).

         In the months after the second Hep B dose, and from the time of Ms. Bell’s initial treatment
with Dr. Krain to when she first saw physicians at Iowa (from February to August, 2012), the only
treater to suggest ADEM as part of a differential diagnosis was Dr. Rodnitzky - after the May 2012
MRI, where the radiologist performing the MRI proposed it. Pet’r’s Ex. 8 at 160. It remained a
consideration for Dr. Rodnitzky up until August 2012. At that point, however, Dr. Rodnitzky began
also considering a mitochondrial disorder and wanted to pursue further testing in that area. Id.

                                                 32
However, and as the medical records make clear, the thorough evaluation and testing performed
by the Mayo Clinic treaters essentially ruled out mitochondrial dysfunction – while at the same
time rejecting earlier proposals that a demyelinating condition was to blame. Pet’r’s Ex. 9 at 11,
16, 18. Thus, as Ms. Bell’s condition continued to evolve in a worsening manner, ADEM was
slowly abandoned as an explanation for her symptoms.

        Ms. Bell’s subsequent history only underscores the difficulty with accepting the ADEM
diagnosis proposed by Petitioner. Rather than proceeding in an acute and monophasic pattern, as
would be expected for ADEM, Ms. Bell continued to display a slower progression in a variety of
symptoms from the spring to fall in 2012. Ms. Bell’s treatment and related work-up at the Mayo
Clinic is especially telling. Despite a full neurologic evaluation, the highly-qualified Mayo treaters
found little to no evidence of demyelination or inflammation, and therefore largely rejected
explanations for her state along the lines urged here by Petitioner in favor of an entirely new
diagnosis (also embraced by Dr. Rodnitzky, the treater who first proposed ADEM) – that she had
some kind of mitochondrial disorder. Pet’r’s Ex. 8 at 160. Yet even that diagnosis was later not
found to be supported by test results, and was therefore reasonably abandoned.

        Petitioner places great stock in the subsequent 2013 determinations of Dr. Gonzalez-Alegre
at Iowa, who breathed new life into ADEM as a possible explanation for her condition. As noted
above, however, the mere fact that a treater proposes a possible diagnosis or explanation for a
petitioner’s condition does not require its acceptance. Snyder, 88 Fed. Cl. at 746 n.67. Rather, I
must evaluate such a treater opinion in light of the overall evidence, and conduct an analysis that
properly conforms to the preponderant evidentiary test governing Vaccine Program claims.

        Although Respondent has suggested that errors in Dr. Gonzalez-Alegre’s factual
assumptions about Ms. Bell’s medical history cast doubt on his suppositions, the context for his
analysis is more persuasive grounds for determining that it is not well-founded. Here, it is evident
that Dr. Gonzalez-Alegre’s suppositions were not tested by consideration of Ms. Bell’s prior
medical history, which contained a host of test results and relevant MRI readings that were not
supportive of his proposed diagnosis. It also flies in the face of the understanding, as the literature
offered herein confirms, that ADEM is more often than not acute and monophasic – adjectives that
do not capture the long term, progressive nature of Ms. Bell’s still-undiagnosed condition.

         I thus do not give significant weight to the fact that a year after Ms. Bell first sought
treatment for her initial symptoms, and after numerous relevant tests had been performed that
should have shed light on the diagnosis, another treater began to propose ADEM as Petitioner’s
illness. Indeed, were his after-the-fact view meritorious from an evidentiary standpoint, it should
have been confirmed by additional test results or treatment evidence – but the subsequent treatment
record after Dr. Gonzalez-Alegre first saw Ms. Bell does not provide such confirmation.33 Indeed,

33
  Other special masters have dealt with the issue of treater disagreement as to the existence of ADEM, giving more
evidentiary weight to the diagnoses of early treaters along with the petitioner’s test results. See Carter v. Sec’y of
Health & Human Servs., No. 14-1500V, 2007 WL 415185 at *23 (Fed. Cl. Spec. Mstr. Jan. 19, 2007)( “[t]he treating
doctors saw [petitioner], ran tests, treated him for a virus, noted [his] improvement to the treatment and diagnosed him

                                                          33
as noted above Petitioner returned a second time to the Mayo Clinic, and its subsequent findings
in no way confirm Dr. Gonzalez-Alegre’s diagnosis (which itself only included ADEM as a
possibility, rather than centering on it as likely).

       Petitioner’s experts did not effectively rebut any of the above. Rather, Dr. Morgan offered
a piecemeal reading of the record, emphasizing the facts that helped Petitioner’s claim (for
example, that ADEM can infrequently present with gray matter lesions) while downplaying or
ignoring other facts that called out for evaluation – in particular, both the lack of classic presenting
symptoms suggestive of ADEM, as well as that testing of the CSF did not confirm inflammation
and unsuccessful steroidal treatments. He offered no record support for the contention that Ms.
Bell was experiencing an autoimmune condition, and his acceptance of Dr. Gonzalez-Alegre’s
opinion was conclusory in nature. Dr. Morgan did not grapple with the overarching suggestion the
record makes about the inability of Ms. Bell’s treaters generally to identify her illness.

        While Dr. Morgan was steadfast in his opinion, I gave more weight to Dr. Sriram’s view
(based on frequent patient exposure, and more expertise in evaluating CNS demyelinating
conditions like MS) that Ms. Bell’s presentation was not consistent with ADEM. Among the
problems with her clinical presentation, or lack thereof, was encephalopathy. Dr. Sriram was
persuasive in stating that he would expect to see major behavioral changes as evidence of
encephalopathy. Here, the only slight indication of a behavioral change is the note by Nurse
Schlenk indicating that Ms. Bell was experiencing fatigue and feelings of weakness - symptoms
that are not equivalent to the behavioral changes contemplated by Dr. Sriram. Additionally,
Petitioner’s initial MRIs did not support an ADEM diagnosis. Dr. Sriram was also persuasive in
emphasizing that an individual suffering from ADEM would not have only lesions in gray matter
areas of the brain, without some corresponding white matter lesions. Dr. Axelrod, by his own
admission, lacked the qualifications to offer a diagnostic interpretation of the record.

        Petitioner’s arguments that she experienced a reaction the third Hep B dose in June 2012
are also inadequately supported by the record. That record more persuasively establishes that she
was already experiencing problems with her vision and hearing prior to this date, as discussed
above – and, as Dr. Axelrod admitted, if the record showed prior symptoms, then the Petitioner’s
entire worsening theory was demolished. Tr. at 182. Dr. Collins’s testimony was more consistent
with this record – and as she testified, it revealed that Ms. Bell’s symptoms were simply
progressing on throughout the time of her third Hep B dose, before and afrer, rather than flaring
up in response. Id. at 351. Again – if the third dose had functioned as Petitioner proposed, some




with a viral cause. No doctor, until Dr. Griesemer, diagnosed ADEM. The radiologist did state that the MRI findings
may be seen in processes such as ADEM, but did not diagnose ADEM. Importantly, the treatment of [petitioner] did
not change in light of the MRI scan and interpretation. In the face of this evidence, it is illogical to conclude that
[petitioner] should be re-diagnosed with ADEM and find that the vaccine was its cause”).


                                                         34
evidence of an ongoing autoimmune process, such as inflammation, would be expected, but was
not seen in this case. Id. at 314-18, 326.34

        Other special masters have previously dealt with the propriety of an ADEM diagnosis as a
threshold matter to entitlement. One such claim was determined by former Chief Special Master
Patricia Campbell-Smith in Stillwell v. Sec’y of Health & Human Servs., No. 11-77V, 2013
WL4540013, at *11 (Fed. Cl. Spec. Mstr. June 17, 2013). Stillwell (which involved the flu vaccine
rather than Hep B) set forth six factors for whether ADEM was present, including (1) the statistical
improbability that petitioner has the disease, given its propensity to affect children; (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. Stillwell, 2013 WL 4540013, at *11. Petitioner’s condition
was found to “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 physician.” Id.

        Those same Stillwell factors suggest a similar conclusion herein. The probability that Ms.
Bell developed ADEM - a condition more commonly found in children – in her adulthood makes
the diagnosis unlikely at the outset, although this is not a dispositive factor. Moreover, as
mentioned above, none of Ms. Bell’s treaters firmly opined that ADEM was the proper diagnosis
until Dr. Gonzalez-Alegre a year later, basing that finding primarily on the findings of the MRIs
that were inconsistent with ADEM, while ignoring the rich treatment history that did not support
ADEM as an explanation. Thus, the immediate and initial evidence relevant to the diagnosis, from
the time Ms. Bell first presented with her symptoms in early 2012, did not support the diagnosis.
Finally, the protracted nature of Ms. Bell’s condition further diminishes the likelihood of ADEM.
See also Saunders v. Sec’y of Health & Human Servs., No. 97-808V, 2001 WL 1135035 at *4
(Fed. Cl. Spec. Mstr. Sept. 4, 2001) (the lack of supporting ADEM MRI results and ADEM not
appearing in the differential diagnosis led to the conclusion that ADEM was not a proper diagnosis-
and thus no link to vaccination existed).35
      My decision in this case does not reflect my own judgment as to the proper diagnosis for
Ms. Bell’s condition. Not only is this a task that special masters are not called upon to perform,

34
   I also note again that, as Petitioner’s experts admitted, there is no evidence that Ms. Bell experienced any reaction
at all to the first dose of Hep B vaccine. See, e.g., Tr. at 197-98 (no evidence of immunologic “priming” between first
and second dose). While Petitioner’s experts explained this away as insignificant or commonplace when a vaccine is
administered in multiple doses (Tr. at 160), I find this fact has some bearing on their argument that the second dose
primed Ms. Bell to experience a renewing, or exacerbation, of symptoms after the third. Petitioner did not persuasively
set forth why the first dose would cause no reaction, but the second and third would.
35
  The instant case can also be contrasted with Brown v. Secretary of Health and Human Services, No. 09-426V, 2011
WL 5029865, at *41 (Fed. Cl. Spec. Mstr. Sept. 30, 2011), which found that a petitioner’s flu vaccine did cause his
ADEM. The Special Master in that case relied on the “unwavering” diagnosis of ADEM among the many treaters that
Petitioner saw, unlike here, where ADEM was no more than a brief differential diagnosis until Ms. Bell was seen by
Dr. Gonzalez-Alegre almost a year later.


                                                          35
but it is something that no qualified medical treater in this case has yet to do successfully. Rather,
I have found that Petitioner has failed to meet her burden of offering sufficient preponderant
evidence establishing it more likely than not that she had ADEM.
B.       Althen Prongs One and Three

       Given my finding above, it is unnecessary to discuss Petitioner’s showings under the other
two Althen prongs. See, e.g., Lasnetski v. Sec’y of Health & Human Servs., 128 Fed. Cl. 242, 64
(2016) (not error for special master to forego Althen analysis after determining that a petitioner
had not in fact experienced the disease or illness alleged to have been vaccine-caused), citing
Hibbard, 698 F.3d at 1365. I will nevertheless briefly consider the evidentiary showing made by
Ms. Bell for each of them.

        With respect to the first, “can cause” prong, Petitioner’s theory that Hep B could cause
ADEM has both scientific reasonableness and plausibility. While Respondent identified some
weaknesses in the theory,36 Petitioner has offered sufficient scientific grounding for this aspect of
her claim. Indeed, there are numerous instances in the Vaccine Program in which other special
masters, in cases also involving the Hep B vaccine and similar injuries, have also determined that
a petitioner successfully established a plausible causation theory. See, e.g., Werderitsh v. Sec’y of
Health & Human Servs., No. 99-310V, 2006 WL 1672884, at *26 (Fed. Cl. Spec. Mstr. May 26,
2006) (discussing ADEM’s similarity to MS, and finding that Hep B could cause a demyelinating
disease like MS); Stevens v. Sec’y of Health & Human Servs, No.99-594V, 2006 WL 659525 (Fed.
Cl. Spec. Mstr. Feb. 24, 2006) (Hep B can cause transverse myelitis, a subset of ADEM).
Unfortunately, this does not aid Petitioner – for success in establishing the first prong does not
help her if, as here, her theory applies to an illness the evidence does not suggest she has, as Dr.
Axelrod admitted. Tr. at 180 (“if it turns out she doesn’t have a demyelinating disease, then
whether I’m right or wrong about [causation], it’s irrelevant.”).

        Petitioner’s Althen three arguments were less persuasive, however. Petitioner offered
insufficient evidence, whether record medical documents or literature, supporting the assertion
that the timeframe in which her symptoms developed was medically acceptable. Thus, Dr. Axelrod
assumed that the timing of the development of Petitioner’s symptoms after the second Hep B dose
was medically acceptable, simply because of the temporal relationship between symptom (like left
side weakness) and vaccine (TR. at 175-76, 178), but cited no record evidence that would
corroborate his assertion that an immunologic reaction was occurring in the interval (while again
admitting he lacked the neurologic expertise even to identify what evidence would show the


36
   For example, Dr. Collins noted that Lawson did not involve the Hep B vaccine, and therefore its findings about how
a different vaccine had the capacity to pry open the blood brain barrier could not be assumed to be applicable herein.
Tr. at 328-29. She also proposed that it could not be assumed that inflammation stemming from the upregulation of
cytokines induced by a vaccine would have the same persistent and elevated inflammatory effect as a live virus. Id. at
333, 359-60. And Dr. Axelrod admitted that “we don’t know” if in fact Hep B can cause ADEM (Id. at 183), although
a lack of scientific certainty does not mean that a claimant’s theory is not sufficiently reliable or plausible to satisfy
the first prong of the Althen test.

                                                           36
demyelinating process was occurring). Id. at 185. Dr. Collins, by contrast, both identified what she
would expect to see (e.g. inflammation based on MRIs or CSF testing) were Petitioner’s theory
occurring in “real time,” and established based on the record how this evidence was lacking. Id. at
315-18. Accordingly, even if I had found that Petitioner’s illness was more likely than not ADEM,
and credited her theory as well, I would still find a lack of preponderant evidence on the third
prong.


                                         CONCLUSION


       The Vaccine Act permits me to award compensation only if a Petitioner alleging a
“non-Table Injury” can show by medical records or competent medical opinion that the injury
was more likely than not vaccine-caused. Here, Petitioner’s causation theory depends upon my
finding that she experienced a particular injury, but the weight of the evidence does not support
that conclusion. Thus – and even if the theory itself has plausibility – there is insufficient
evidence to support an award of compensation, leaving me no choice but to hereby DENY this claim.


         In the absence of a timely-filed motion for review (see Appendix B to the Rules of the
 Court), the Clerk shall enter judgment in accord with this decision.


 IT IS SO ORDERED.


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




                                                37
