Court Opinion

ID: 2673445
Source: CourtListenerOpinion
Date Created: 2014-05-10 03:16:04.851591+00
Date Added: 2024-06-11T13:06:51.590224
License: Public Domain

In the United States Court of Federal Claims
                             OFFICE OF SPECIAL MASTERS
                                      No. 08-0266V
                                    Filed: June 6, 2013

* * * * * * * * * * * * * *                      PUBLISHED
MARIA CARRINO, Spouse          *
and Executrix of the Estate of *                 Influenza Vaccine; Alleged
SAMUEL CARRINO,                *                 Guillian-Barré Syndrome;
                               *                 Documented Diagnosis of
             Petitioner,       *                 Coronary Artery Occlusion With
      v.                       *                 Cerebral Infarction; Weight of
                               *                 Record Evidence Contravenes
                               *                 Claimed Injury
SECRETARY OF HEALTH            *
AND HUMAN SERVICES,            *
                               *
             Respondent.       *
* * * * * * * * * * * * * *

Thomas Gallagher, Somers Point, NJ, for petitioner

Darryl Wishard, Washington, DC, for respondent

                                       DECISION1

       On April 14, 2008, Samuel Carrino filed a petition for compensation under the

1
        Because this decision contains a reasoned explanation for the undersigned’s action
in this case, the undersigned intends to post this decision on the United States Court of
Federal Claims’ website, in accordance with the E-Government Act of 2002, Pub. L. No.
107-347, § 205, 116 Stat. 2899, 2913 (codified as amended at 44 U.S.C. § 3501 note
(2006)). As provided by Vaccine Rule 18(b), each party has 14 days within which to
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 entire” decision
will be available to the public. Id.

                                             1
National Childhood Vaccine Injury Compensation Program (the Program).2 He first
alleged that he developed left-sided paralysis and required hospitalization five days after
he received the influenza vaccine on October 6, 2006. Petition; Petitioner’s Exhibit
(Pet’r’s Ex.) 8 at 14. Petitioner amended his claim on February 27, 2009 to allege that
the flu vaccine he had received in October 2006 caused him to develop Guillain-Barré
syndrome (GBS). See Amended Petition. Mr. Carrino died on August 1, 2009.

        Three months later, Mr. Carrino’s widow, Maria Carrino (Mrs. Carrino), filed a
second amended petition as his spouse and the executrix of his estate. She alleged that
the flu vaccine caused her husband’s GBS event as well as his subsequent death. Second
Amended Petition at 1.

       Respondent moved for dismissal of petitioner’s claim, in part, because there was
insufficient proof that Mr. Carrino had suffered a GBS event. See Mot. to Dismiss and
Rule 4(c). The undersigned stayed the motion pending further briefing on the relevant
issues. A telephonic status conference was conducted on November 8, 2010, to discuss
the lack of record support for Mr. Carrino’s claimed injury. Order at 1, Nov. 10, 2010.
Petitioner’s counsel argued that the nature of Mr. Carrino’s injury was a genuine issue of
material fact that precluded dismissal and requested an expert hearing. Id.

       During the pendency of petitioner’s claim, she filed a letter in support of vaccine-
related causation from Joseph DeMayo, M.D., Mr. Carrino’s primary care provider,
Pet’r’s Ex. 12, and three expert reports from Victor Hogen, M.D., a neurologist. Pet’r’s
Exs. 15, 19, 21. Respondent, in turn, filed three expert reports from Martin Bielawski,
M.D., a neurologist. Resp’t’s Ex. A, N, Q.

       An entitlement hearing was held in Washington, D.C., on May 17, 2011. Mr.
Carrino’s treating physician, Dr. DeMayo, and both parties’ experts testified. The parties
disagreed on the nature of Mr. Carrino’s injury and whether the injury was vaccine-
related.

        Following the hearing, the parties were afforded an opportunity to explore the
possibility of informally resolving the claim. Order, June 15, 2011. Unsuccessful in their
efforts, the parties subsequently filed post-hearing briefs. Id. This matter is now ripe for a
ruling.

2
       The Program comprises Part 2 of the National Childhood Vaccine Injury Act of
1986, Pub. L. No. 99-660, 100 Stat. 3755, codified as amended, 42 U.S.C. §§ 300aa-10
et seq. (hereinafter “Vaccine Act” or “the Act”). Hereafter, individual section references
will be to 42 U.S.C. § 300aa of the Act.

                                              2
        At the core of the parties’ dispute regarding entitlement is a disagreement regarding
whether Mr. Carrino developed GBS or suffered a cerebrovascular accident. Mrs. Carrino
maintains that Mr. Carrino endured a debilitating episode of GBS that was caused by the
flu vaccine he received. Respondent contends that Mr. Carrino did not develop GBS, but
suffered a stroke. The preponderant evidence does not support a finding that Mr. Carrino
suffered from a GBS event. There is no diagnosis of GBS in the records from Mr.
Carrino’s hospitalization in the days after his flu vaccination. The mention of a possible
flu-related GBS episode does occur, however, in subsequent hospitalization records as
part of Mr. Carrino’s past medical history. On this record, petitioner has failed to satisfy
her burden of proving that Mr. Carrino suffered a vaccine-related injury and thus, her
claim must be dismissed.

I.     Factual Background

       A.     Mr. Carrino’s Pertinent Medical History
              1.     His pre-vaccination health

        Mr. Carrino was born in March of 1928. Pet’r’s Ex. 1 at 1. His medical history
was significant for non-insulin-dependent diabetes, hypertension, coronary artery disease,3
a lung lobectomy, myocardial infarction,4 multiple cranial neuropathies,5 a stroke with
right-sided weakness, diabetic polyneuropathy,6 and former tobacco use. Pet’r’s Ex. 8 at
1, 27, 32-33, 55; Pet’r’s Ex. 5 at 9.

       In May of 1999, Mr. Carrino was evaluated for a five-day history of double vision.
Pet’r’s Ex. 5 at 12. He was 71 years old. Id. The examining neurologist noted Mr.

3
       Coronary artery disease is caused by hardening of the coronary arteries; the
condition can lead to angina pectoris, myocardial infarction, or sudden death. Coronary
artery disease, http://www.dorlands.com/def.jsp?id=100030680 (last visited June 5, 2013).
4
        Myocardial infarction occurs when the blood supply to the heart is interrupted,
usually as a result of arterial hardening, and heart muscle dies. Myocardial infarcation,
http://www.dorlands.com/def.jsp?id=100053424 (last visited June 5, 2013).
5
        A cranial neuropathy occurs when any of the twelve cranial nerves that exit from
the brain are damaged. Cranial neuropathy,
http://www.emedicinehealth.com/neuropathy/article_em.htm (last visited June 5, 2013).
6
        A diabetic polyneuropathy is diabetes-induced nerve damage that affects either the
sensory, motor, or autonomic nerves, or a combination thereof. Diabetic neuropathy,
http://www.dorlands.com/def.jsp?id=100071988 (last visited June 5, 2013).

                                              3
Carrino’s history of hypertension and diagnosed him with “a probable diabetic right sixth
nerve palsy”7 and “a mild diabetic peripheral neuropathy.”8 Id. at 13.

        Magnetic resonance imaging (MRI) of Mr. Carrino’s brain performed two days
later revealed ischemic changes (which are changes in the blood vessels). Pet’r’s Ex. 5 at
21. Additional testing showed an occlusion of his left vertebral artery. Id. at 20.

       Four months later, a neurologic examination showed that Mr. Carrino was
exhibiting symptoms of diabetic neuropathy. Among the symptoms observed were
missing right ankle reflexes9 and an inability to feel vibrations in his toes. Pet’r’s Ex. 5 at
9.

       Two years later, in January of 2002, Mr. Carrino again developed double vision.
Pet’r’s Ex. 5 at 7. Imaging of his brain showed age-related white matter changes and a
small, old, left-sided cerebellar infarction (an area of tissue death). Pet’r’s Ex. 5 at 15-16.

        Mr. Carrino was evaluated the following year, in April of 2003, by another
neurologist, for an episode of syncope that had occurred a month before his examination.
The neurologist detected right arm weakness and diagnosed a stroke in the left hemisphere
of Mr. Carrino’s brain. An MRI of Mr. Carrino’s brain showed a recent hemorrhage in
the left basal ganglia region and small areas of recent infarction in the left posterior
parieto-occipital region. Pet’r’s Ex. 8 at 58. Also evident from the MRI were old lacunar

7
        Damage to the sixth cranial nerve is described as a sixth nerve palsy; such damage
can cause abnormal movement of the eye and double vision. Sixth nerve palsy,
http://www.hopkinsmedicine.org/healthlibrary/conditions/nervous_system_disorders/multi
ple_cranial_neuropathies_134,48/ (last visited June 5, 2013).
8
        Damage to the peripheral nervous system (known as a peripheral neuropathy)
disrupts the vast communications network that transmits information from the brain and
spinal cord to other parts of the body. See
http://www.ninds.nih.gov/disorders/peripheralneuropathy/detail_peripheralneuropathy.htm
(last visited June 5, 2013). The presenting symptoms are determined by the affected
nerves, and such symptoms develop over a period of days, weeks, or years. Id. Muscle
weakness is the most common symptom of motor nerve damage. Id.
9
       The record indicates that Mr. Carrino’s loss of his ankle reflexes in 1999, seven
years before he received the flu vaccine at issue, was attributed to his pre-existing diabetic
polyneuropathy. Pet’r’s Ex. 5 at 9; Pet’r’s Ex. 8 at 57.

                                               4
infarcts in the basal ganglia and brain softening (encephalomalacia)10 in the lower parietal
lobes, both findings that were consistent with an old ischemic injury. Ischemic changes
also were detected in the brainstem. Pet’r’s Ex. 8 at 39-40.

        Five months later, in November of 2003, Mr. Carrino was admitted to the hospital
with complaints of left upper eyelid pain and a chaotic and irregular heart rate (atrial
fibrillation). Pet’r’s Ex. 8 at 39. Imaging of his brain taken by a magnetic resonance
angiogram,11 Pet’r’s Ex. 8 at 42, 44, showed no acute brain infarcts, Pet’r’s Ex. 8 at 42,
but did show moderate-to-severe stenosis of his left carotid artery and his right mid-
vertebral artery. Pet’r’s Ex. 8 at 44.

       One month later, Mr. Carrino was evaluated by a neuro-ophthalmologist, for
complaints of pain near his left eyebrow, a drooping eyelid, and double vision. Pet’r’s Ex.
8 at 32-34. The findings were consistent with a diabetic or microvascular third nerve
palsy.12
              2.     Mr. Carrino’s flu vaccine and his subsequent hospitalization

       Nearly three years later, on October 6, 2006, Mr. Carrino received the seasonal
trivalent flu vaccine, an inactivated, injectable vaccine containing killed influenza virus.
Transcript (Tr.) at 138; Respondent’s Exhibit (Resp’t’s Ex.) W; Pet’r’s Ex. 8 at 14. Dr.
DeMayo, Mr. Carrino’s primary care physician, administered the vaccine in his office. Tr.
at 37.

      Four days later, Mr. Carrino was overcome with sudden dizziness after rising from
bed. Pet’r’s Ex. 10 at 93. Although he was able to walk that morning, he lost his muscle
coordination that evening. Id.

10
       Encephalomalacia is the “softening of the brain,” that results from an infarct.
Encephalomalacia, http://www.dorlands.com/def.jsp?id=100035052 (last visited June 5,
2013).
11
       A magnetic resonance angiogram (MRA) is a type of MRI; it relies on the use of a
magnetic field and pulses of radio wave energy to generate pictures of blood vessels inside
the body. See Mosby’s Manual of Diagnostic and Laboratory Tests (Mosby’s Manual) at
1167 (4th ed. 2010).
12
        Third nerve palsy is a type of cranial neuropathy, associated with sagging or
drooping eyelids, double vision, difficulty with eye movement, and larger pupils than
normal. Third nerve palsy,
http://www.hopkinsmedicine.org/healthlibrary/conditions/nervous_system_disorders/multi
ple_cranial_neuropathies_134,48/ (last visited June 5, 2013).

                                             5
       On October 11, 2006—five days after his flu vaccination—Mr. Carrino was
admitted to Clara Maas Medical Center by his primary care physician, Dr. DeMayo. As
noted in the contemporaneous medical records, he could not walk and was experiencing
“vertigo, nausea, [and] weakness.” Pet’r’s Ex. 11 at 1. The documented diagnostic
impressions at the time of his hospital admission were cerebrovascular accident (stroke),
cerebral infarction,13 and atrial fibrillation.14 See id. at 1.

       Dr. Brand, one of Mr. Carrino’s attending physicians, conducted a neurologic exam
the same day as his hospital admission. Pet’r’s Ex. 10 at 93. Mr. Carrino reported a
spinning sensation, id., and complained of feeling “as if [he were] being pulled to right.”
Id. But, his speech and vision were unaffected. See id. Dr. Brand noted a slight drooping
of Mr. Carrino’s right eyelid, paralysis of his right extremities, and uncoordinated
movements (ataxia). Pet’r’s Ex. 10 at 93. Mr. Carrino’s heartbeat was irregular, and he
felt nauseous. Id. While awake and alert, he needed support to sit. Id.

       A cardiologist also examined Mr. Carrino. The cardiologist diagnosed him with
sudden onset of atrial fibrillation. Pet’r’s Ex. 10 at 94. The day after Mr. Carrino’s
admission, he began to complain of double vision. Pet’r’s Ex. 11 at 3. His ataxia
improved, and by the third day of his hospitalization, he no longer had double vision.
Pet’r’s Ex. 11 at 7. His left-sided numbness also had diminished. Id. at 8.

       Mr. Carrino had three brain MRIs during his hospitalization—two of which were
performed within the first 48 hours of Mr. Carrino’s admission.15 The first MRI,
performed on the same day as his hospital admission, showed “no acute infarctions.”
Pet’r’s Ex. 10 at 55. The second MRI was performed with and without contrast the next
day. As read, this MRI showed no abnormal enhancement. Pet’r’s Ex. 10 at 57.

       Although Mr. Carrino’s first two brain MRIs failed to confirm that he had
experienced a stroke, the medical records indicate that his treating physicians—to include

13
        A cerebral infarction (or cerebral ischemia) is “an ischemic condition of the brain
[that] produc[es] local tissue death . . . usually [presenting as] a persistent focal
neurological deficit in the [distribution] area of . . . one of the cerebral arteries.” Cerebral
infarction, http://www.dorlands.com/def.jsp?id=100053413 (last visited June 5, 2013).
14
        Atrial fibrillation is the most common type of irregular heartbeat. Atrial
fibrillation, http://www.nhlbi.nih.gov/health/health-topics/topics/af/ (last visited June 5,
2013). It can increase the risk of stroke, particularly if another risk factor—such as high
blood pressure—is present.
15
      The third MRI, which was performed more than three weeks later, showed
abnormality that was consistent with a lateral medullary stroke.
                                                6
both Dr. DeMayo and Dr. Brand—continued to view his symptomatology as consistent
with a stroke.

       On October 15, 2006, four days after Mr. Carrino’s hospital admission, Dr. Brand
speculated that Mr. Carrino had suffered a stroke event—that had caused his various
symptoms—in the area of the brain close to the brainstem and cerebellum. Pet’r’s Ex. 11
at 9 (emphasis added) (Dr. Brand remarking: “Patient has neurological signs consistent
[with] posterior fossa ischemia.”). Among the symptoms noted at that time were: (1) a
more pronounced lack of coordination in Mr. Carrino’s right arm than in his right leg; (2)
diminished pain sensitivity on his left-side; (3) dizziness with movement, and (4)
headaches and neck pain. Pet’r’s Ex. 11 at 10.

      Dr. DeMayo evaluated Mr. Carrino on October 16, 2006. Pet’r’s Ex. 11 at 10. Dr.
DeMayo noted that although Mr. Carrino had right-sided numbness and weakness, id., he
was able to move all of his extremities. Id. He continued to experience dizziness with
head movement, but indicated that his “headaches and vertigo” were improving. Id.

      A swallow study performed two days later was normal. Pet’r’s Ex. 11 at 16.

       Many of the physicians who were consulted during Mr. Carrino’s hospitalization
noted that he was undergoing evaluation for a suspected stroke. See Pet’r’s Ex. 11 at 14.
(Dr. Edwin Amirata, an examining surgeon, noted that Mr. Carrino had presented with
lower body paralysis and hiccups after “a new CVA”); Pet’r’s’ Ex. 10 at 95 (Dr. Daniel
Manzi, a consulting gastroenterologist, indicated that Mr. Carrino was “receiving a
neurologic workup for CVA”).
             3.     Mr. Carrino’s weakness worsened when he developed a urinary
                    tract infection during his second week of hospitalization

       Nine days after his hospital admission, Mr. Carrino developed a low-grade fever.
Pet’r’s Ex. 11 at 21. He continued to complain of difficulty swallowing, neck pain, and
weakness in all of his extremities. Pet’r’s Ex. 11 at 25. Dr. DeMayo, his primary care
physician, ordered a urine culture. Id. at 21.

        Dr. Brand, the attending neurologist, examined Mr. Carrino again on October 21,
2006. He detected greater weakness in both of Mr. Carrino’s legs, pain in his right
shoulder, and increasing weakness in his right arm. Pet’r’s Ex. 11 at 27. Mr. Carrino’s
facial sensation and strength were intact. Id. But his eyes moved involuntarily when he
gazed leftward, and he had double vision when he gazed rightward. Id. Noting that Mr.
Carrino had received a flu shot several days before his symptom onset, Dr. Brand
considered the possibility that Mr. Carrino had suffered a parainfectious-induced
radiculopathy presenting as GBS. Pet’r’s Ex. 11 at 32. Dr. Brand initiated a course of
steroids and intravenous immunoglobulin (IVIG), a choice treatment for autoimmune

                                             7
conditions. This documented concern expressed by Dr. Brand is the first mention of
GBS in Mr. Carrino’s medical records. Pet’r’s Ex. 11 at 27.

        That same day, Donald Beggs, M.D., an infectious disease specialist, also
examined Mr. Carrino. He recorded Mr. Carrino’s complaints of “ataxia, dizziness, neck
pain [with] stiffness, [and] vision change,” as beginning two days before his hospital
admission and four days after he had received a flu shot. Pet’r’s Ex. 10 at 99. Mr.
Carrino developed a bilateral “ascending weakness,” id., and lost his left-sided sensation
after his hospital admission. The detection of an “[a]scending paralysis” provoked Dr.
Beggs to consider the possibility of a GBS event—as had Dr. Brand earlier in the day. Dr.
Beggs ordered diagnostic testing for sepsis and prescribed the antibiotic Levaquin.

       Mr. Carrino was transferred to the intensive care unit in “progressively worsening
condition” on October 22, 2006. Pet’r’s Ex. 11 at 28. He had “bilateral leg weakness,”
and pain in his right eye and his neck. Id. at 29. Mr. Carrino began a course of
antibiotics for what was determined later to be a bacterial urinary tract infection. Pet’r’s
Ex. 11 at 28, 39, 41, 49, 52.

       The next day, Mr. Carrino had less pain, was better able to move his neck, and had
no trouble swallowing. Pet’r’s Ex. 11 at 35.

       That same day, Mr. Carrino was evaluated by John Conti, M.D., a specialist in
hematology and oncology. Dr. Conti indicated that Mr. Carrino “had been doing well
[with his neurologic symptoms],” but had developed a “progressive worsening of his
condition,” that was marked—over a two day period—by more “weakness and stiffness.”
Pet’r’s Ex. 10 at 102. Mr. Carrino’s medical records showed that on hospital admission,
he was found to have ischemia in the left parietal lobe of his brain and was deemed to
have suffered a stroke. Id. at 102. Dr. Conti prescribed Coumadin, a blood thinner, for
Mr. Carrino in an effort to reduce the risk of his irregular heartbeat causing another
stroke. See id.

       Later that same day, a lumbar puncture was performed to evaluate whether Mr.
Carrino had an infection and to rule out GBS. Pet’r’s Ex. 11 at 37. As the lumbar
puncture study revealed, Mr. Carrino’s cerebrospinal protein levels were normal and
contained no evidence of infection. Pet’r’s Ex. 10 at 31; Pet’r’s Ex. 11 at 38.

       Dr. Brand, the attending neurologist, ordered needle electromyography16 (EMG)

16
       Electromyography requires the insertion of thin needle electrodes through the skin
into the muscles to evaluate a subject’s muscular health and the health of the nerves that
control the muscles. Electromyography, www.nlm.nih.gov/medlineplus/ency/article (last
visited June 5, 2013).
                                              8
and a nerve conduction test to evaluate Mr. Carrino’s nerve impulses and muscle control.
See Pet’r’s Ex. 11 at 38. The results of this EMG study were not filed into the record.
Dr. Brand’s finding that the EMG results were consistent with a peripheral neuropathy
was filed; but this finding did not exclude the possibility that Mr. Carrino had suffered a
Guillain-Barré type of radiculopathy.

       On examination, Dr. Brand found that Mr. Carrino’s upper limb reflexes were
preserved and his knee reflexes had returned. His ankle reflexes, however, had not
returned. Pet’r’s Ex. 11 at 44. Mr. Carrino began a prescriptive therapy of Neurontin for
pain, and steroids together with IVIG for inflammation and any autoimmune
irregularities. Id.

       Dr. Beggs, the infectious disease specialist, evaluated Mr. Carrino again on
October 24, 2006. Pet’r’s Ex. 11 at 41. He noted Mr. Carrino’s urinary tract infection,
spinal stenosis, and leg weakness. He remarked that a study of Mr. Carrino’s
cerebrospinal fluid did not point to any infection. Id.

       Mr. Carrino’s weakness continued to improve. Pet’r’s Ex. 11 at 50. By October
26, 2006, fifteen days after Mr. Carrino’s hospital admission, Dr. Brand commented that
Mr. Carrino had returned to a condition similar to the state in which he had presented on
admission, but without the dizziness. Pet’r’s Ex. 11 at 64.

        Dr. DeMayo’s notes indicated that Mr. Carrino was able to move his neck and sit
up in bed. Pet’r’s Ex. 11 at 50. His notes also indicated that Mr. Carrino had developed
“chronic” hiccups—which are notable symptoms that tend to present in subjects who have
suffered a lateral medullary stroke. See id., see Resp’t’s Ex. E at 573; see What is
Wallenberg’s Syndrome?
http://www.ninds.nih.gov/disorders/wallenbergs/wallenbergs.htm (last visited on Apr. 30,
2013). Id.

       In the medical assessment plan dated October 27, 2006, Mr. Carrino’s weakness
was attributed to arthritis, not to a GBS event. Pet’r’s Ex. 11 at 62.

       Dr. Brand observed that Mr. Carrino had become “more comfortable” over a period
of several days; but his neurologic findings after treatment with the intravenous gamma
globulin (IVIG) and steroids (Solu-Medrol) were similar to his pre-treatment findings—
which suggested that the treatment had not been effective. See Pet’r’s Ex. 11 at 69.

        The third MRI of Mr. Carrino’s brain was performed on November 1, 2006. That
imaging showed a “small focus of T2 signal abnormality and enhancement in the right
lateral aspect of the brainstem at the cervicomedullary junction, most likely due to
ischemia.” Pet’r’s Ex. 10 at 56. Dr. Brand read the MRI as confirming an “infarct of

                                             9
lateral medulla . . . on admit.” Pet’r’s Ex. 11 at 75. It appears that after discussing the
case further with the radiologist, Dr. Brand wrote:
       Patient’s MRI’s reviewed. There is a clear cut [right] lateral medullary
       infarct seen on several segments. Patient will require on-going [physical
       therapy]. [Out of bed with] help and rehabilitation. . . . Meyer features17
       remain clinically evident.
Pet’r’s Ex. 11 at 77 (emphasis added).

              4.     Mr. Carrino’s medical condition after his hospital discharge in
                     November of 2006

       Mr. Carrino was discharged on November 3, 2006 from the hospital to a continuing
care facility for rehabilitation. See Pet’r’s Ex. 2 at 6; Pet’r’s Ex. 10 at 91-92. The
discharge summary, authored by Dr. DeMayo, listed as the principal diagnosis: cerebral
artery occlusion with cerebral infarction. Id. at 92. The discharge summary contained no
mention of GBS. See Pet’r’s Ex. 10 at 91-92.

       On November 10, 2006, seven days after his admission to the rehabilitation facility,
Mr. Carrino was evaluated for “shortness of breath.” Pet’r’s Ex. 2 at 5. His past medical
history of “CVA, hypertension, coronary artery disease, and arrhythmia” was documented
during the evaluation. Id.

       Mr. Carrino remained in the rehabilitation facility for three months. He was
discharged to his home from the facility on February 10, 2007. See Pet’r’s Ex. 4 at 4.

       The day after his discharge from the rehabilitation facility, Mr. Carrino required an
emergent evaluation after he fell off a chair at home. Pet’r’s Ex. 4 at 4. The hospital
admission record, dated February 11, 2007, indicated that Mr. Carrino had been
hospitalized for “bilateral lower extremity weakness possibly due to receiving a flu shot,
as per patient’s wife.” Id. (emphasis added).

       The next month, Mr. Carrino was admitted to the hospital again after falling away
from his walker while at home and fracturing his right hip. The handwritten medical
history for this admission—which was authored by Mr. Carrino’s primary care physician,

17
        This reference pertains to the Fugl-Meyer Assessment (FMA), a stroke-specific,
performance-based impairment index. It is designed to assess motor functioning, balance,
sensation and joint functioning in patients with post-stroke hemiplegia (the inability to
move a group of muscles in one side of the body). Meyer features refer to a patient’s
Fugl-Meyer Assessment (FMA). Lisa Zeltzer, Fugl-Meyer Assessment of Sensorimotor
Recovery After Stroke(FMA), StrokEngine,
http://strokengine.ca/assess/module_fma_intro-en.html (last visited June 5, 2013).
                                              10
Dr. DeMayo—listed “diabetes, [hypertension (HTN)] [coronary artery disease (CAD)],
[status post (s/p)] Guillain-Barré, hemiparesis[, and] unsteady gait.” Pet’r’s Ex. 10 at
422. Notably, the dictated version of this same admission note, which was also prepared
by Dr. DeMayo, does not list GBS among Mr. Carrino’s prior health conditions. Id. at
421.

       On December 23, 2007, Mr. Carrino presented to the emergency room by
ambulance transport with altered mental status, facial droop, and an inability to provide
any reliable information regarding his condition. Pet’r’s Ex. 4 at 24. On admission, Mrs.
Carrino insisted that Mr. Carrino had not been diagnosed with a cerebral vascular
accident, but she acknowledged that his neurologist had informed her that Mr. Carrino
may have had suffered such an injury in October 2006. Id.

       Mr. Carrino required additional hospital admissions on a number of occasions
between late 2007 and early 2008 after various falling episodes and for diverse
complaints, including abdominal pain, chest wall pain, abnormally slow heart rate
(bradycardia), pneumonia with sepsis, and respiratory failure. These various hospital
admissions periodically listed GBS as a past medical condition. Pet’r’s Ex. 10 at 250,
253, 422, 470.

        Mr. Carrino died on August 1, 2009, at the age of 81. Pet’r’s Ex. 17. GBS is not
listed as an immediate cause of death on the death certificate.18
       B.            The Medical Literature
              1.     Petitioner’s literature

        Petitioner filed seven articles in this case. Only one article spoke to the
pathogenesis of GBS in general; the remaining articles examined the incidence of and
relationship between influenza vaccination and the subsequent occurrence of GBS.19 See
Pet’r’s Ex. 28. None of the articles submitted by petitioner discussed the diagnostic
criteria for or expected clinical presentation of GBS; nor did any of the articles discuss the
recommended treatment for the condition. See generally Pet’r’s Ex. 22-28. The literature
filed by petitioner was of limited assistance to the undersigned in evaluating this claim.
More helpful to the undersigned was the unrebutted literature filed by respondent.

18
       The copy of the death certificate that was filed into this record does not appear to
be the official one because the document is marked as VOID. See Pet’r’s Ex. 17.
19
      R.A.C. Hughes et al., Pathogenesis of Guillain-Barré Syndrome, 100 J. of
Neuroimmunology 74 (1999).

                                               11
              2.     Respondent’s Literature

        Respondent filed literature that specifically addressed the relevant considerations
for a diagnosis of GBS.20 Respondent also filed into the record an article that discussed
the symptoms of lateral medullary syndrome,21 which is characterized by a constellation
of neurologic symptoms caused by a stroke in the vertebral or posterior inferior cerebellar
artery (PICA) of the brain stem. See Resp’t’s Ex. A at 11 (citing Resp’t’s Ex. E22 at 570).
In addition, respondent provided diagrams of the brainstem and transverse views of the
inferior medulla near the cervical junction to depict the neuroanatomic structures
referenced by Dr. Bielawski when he discussed Mr. Carrino’s symptoms and signs. See
Resp’t’s Ex. O.23

       C.     The parties disagree about the condition from which Mr. Carrino
              suffered during his October 2006 hospitalization.

     For perspective before considering the experts’ respective positions, a brief
summary follows of the injuries about which the parties disagree.
              1.     GBS

      GBS is an “acute, immune[-]mediated polyneuropathy with several variant forms,
the most common of which in the United States is acute inflammatory demyelinating
polyneuropathy.” Resp’t’s Ex. A at 7. This variant represents 85 to 90 percent of cases.
Id.

       A diagnosis of GBS is based initially on clinical presentation. The “cardinal
clinical features” of GBS are progressive, mostly symmetric muscle weakness and absent

20
       Francine Vriesendorp, Clinical Features and Diagnosis of Guillain-Barre Syndrome
in Adults, http://www.uptodate.com/contents/clinical-features-and-diagnosis-of-guillain-
barre-syndrome-in-adults?source=search_result&search=guillain-
barre+syndrome&selectedTitle=1%7E150 (last visited June 5, 2013).
21
       Lateral medullary syndrome is also referred to as Wallenberg syndrome or
posterior inferior cerebellar artery syndrome.
22
      Respondent’s Exhibit E is identified as H.J.M. Barnett et al., Lateral Medullary
Syndrome in Stroke: Pathophysiology, Diagnosis, and Management 570 (1986).
23
       R. Trues & M. Carpenter, Human Neuroanatomy 306, 309 (6th ed. 1969).

                                            12
or depressed deep tendon reflexes. Resp’t’s Ex. D at 6 (Vriesendorp article).24 To
confirm a GBS diagnosis, spinal taps and neurophysiology studies routinely are performed
in patients suspected of having the disorder. Id.; see also Resp’t’s Ex. C at 2.

       A GBS diagnosis is appropriate if cerebrospinal fluid and clinical neurophysiology
studies show certain characteristic abnormalities. Id. In GBS patients, the cerebrospinal
fluid surrounding the spinal cord and brain contain elevated protein levels. See id.

        Nerve conduction studies (NCS) and needle electromyographs (EMG), that
measure nerve signaling to muscles, provide important information that assists in
diagnosing GBS. See id. at 7. Because the abnormalities detected by nerve conduction
tests progress over time, serial clinical and neurophysiologic studies are also helpful. Id.

       Among the clinical features most commonly observed in patients with fully
developed GBS are: abnormal needle electromyography (99 percent), weakness in legs
(95 percent), areflexia25 (90 percent), weakness in arms (90 percent), protein levels in
cerebrospinal fluid exceeding 55 grams/dl (90 percent), paresthesias (85 percent), sensory
loss (75 percent), and weakness in face (60 percent). Resp’t’s Ex. A at 9.
              2.     Lateral Medullary Syndrome

       This syndrome is characterized by a constellation of neurologic symptoms
triggered by a stroke in the vertebral or posterior inferior cerebellar artery (PICA) of the
brain stem. See Resp’t’s Ex. A at 11 (citing Resp’t’s Ex. E at 570).26

       Symptoms include difficulties with swallowing, hoarseness, dizziness,
       nausea and vomiting, rapid involuntary movements of the eyes (nystagmus),
       and problems with balance and gait coordination. Some individuals will
       experience a lack of pain and temperature sensation on only one side of the
       face, or a pattern of symptoms on opposite sides of the body – such as
       paralysis or numbness in the right side of the face, with weak or numb limbs

24
       Francine Vriesendorp, Clinical Features and Diagnosis of Guillain-Barré Syndrome
in Adults, http://www.uptodate.com/contents/clinical-features-and-diagnosis-of-guillain-
barre-syndrome-in-adults?source=search_result&search=guillain-
barre+syndrome&selectedTitle=1%7E150 (last visited June 5, 2013).
25
        Areflexia refers to the absence of reflexes. Areflexia,
http://www.dorlands.com/def.jsp?id=100007742 (last visited June 5, 2013).
26
      Respondent’s Exhibit E is identified as H.J.M. Barnett et al., Lateral Medullary
Syndrome in Stroke: Pathophysiology, Diagnosis, and Management 570 (1986).

                                              13
       on the left side. Uncontrollable hiccups may also occur, and some
       individuals will lose their sense of taste on one side of the tongue, while
       preserving taste sensations on the other side.

Wallenberg’s Syndrome,
http://www.ninds.nih.gov/disorders/wallenbergs/wallenbergs.htm (last visited May 2,
2013); see also Resp’t’s Ex. E 4-8.

       The prognosis for subjects with lateral medullary syndrome depends on the size
and location of the brain stem segment damaged by the stroke. See id.

       D.     The opinions of petitioner’s medical witnesses

       Mr. Carrino’s primary care physician, Dr. DeMayo, states in the letter he drafted on
petitioner’s behalf in this vaccine action, that his patient received a flu vaccine on October
6, 2006 and shortly thereafter, “developed weakness, loss of balance, unsteady gait and
confusion.” Pet’r’s Ex. 12 at 2. Admitted to the hospital five days after his vaccination,
Mr. Carrino’s “neurological status deteriorated.” Id. Dr. DeMayo indicated that the CAT
scans taken of Mr. Carrino’s head did not reveal any bleeding or lesions that were
suggestive of a cerebrovascular accident (CVA); he did not address, however, the MRI,
performed on November 1, 2006, that confirmed the diagnostic impression of stroke held
by Mr. Carrino’s treating physicians during his hospitalization. Pet’r’s Ex. 10 at 56; Id.

        Petitioner’s expert neurologist, Dr. Hogen, opined that Mr. Carrino became unable
to rise from bed or walk or sit independently because he had suffered a GBS event. As
evidence that Mr. Carrino suffered a vaccine-related GBS, Dr. Hogen pointed to Mr.
Carrino’s presentation to the hospital with symptoms of “extensive weakness of his arms
and legs,” within one week of his receipt of the flu vaccine. Pet’r’s Ex. 19 at 2.
According to Dr. Hogen, Mr. Carrino “had a thorough work-up to rule out other causes of
[his] weakness,” id., and “was given a diagnosis of Guillain-Barré Syndrome to account
for [his] . . . diffuse[] weakness.” Id. Dr. Hogen reasons that Mr. Carrino must have
suffered from GBS because his attending physicians in the hospital treated him with Solu-
Medrol and IVIG, both of which therapies are routinely administered to GBS patients. Id.
As further support for his opinion, Dr. Hogen relied on the notations of Mr. Carrino’s past
history for GBS, which were contained in subsequent medical records dated more than
one year after Mr. Carrino’s hospital discharge. Pet’r’s Ex. 21 at 1.

       Respondent’s neurology expert, Dr. Martin Bielawski, challenged petitioner’s
claim that Mr. Carrino suffered from GBS. Dr. Bielawski asserted that Mr. Carrino’s
signs and symptoms at hospital admission were “consistent with right lateral medullary
syndrome, a vascular ischemic event.” Resp’t’s Ex. A at 9. Dr. Bielawski pointed to the

                                             14
findings on Mr. Carrino’s brain MRI, which was performed on November 1, 2006 (three
weeks after Mr. Carrino’s hospital admission), as confirmation of the stroke event.

       The November 2006 MRI findings did show a right lateral medullary infarct.
Resp’t’s Ex. N at 2. Dr. Bielawski explained that the location of Mr. Carrino’s brain
injury had determined what his clinical symptoms and signs were on presentation to the
hospital. Id. at 1.

       Dr. Bielawski observed that notwithstanding certain of his symptoms, Mr. Carrino
did not “fulfill the diagnostic criteria for GBS.” Resp’t’s Ex. A at 9. Nor did his
discharge summary reflect a diagnosis of GBS, but rather of a cerebral artery occlusion
with cerebral infarction. Id. at 6.

       Unlike the conclusory reports and circular arguments regarding vaccine-related
injury prepared by Dr. DeMayo and Dr. Hogen, Dr. Bielawski’s expressed opinion was
amply supported by detailed references to Mr. Carrino’s hospitalization records from his
October 2006 admission—which did not include a diagnosis of GBS—and to the literature
he filed. See generally Resp’t’s Ex. A, N, and Q.

       Before turning to evaluate petitioner’s claim, the undersigned first sets forth the
applicable legal standard.

II.    STANDARDS OF ADJUDICATION

       A.     Elements of petitioner’s claim

        If petitioner alleges that an injury listed on the Vaccine Injury Table (Table)
occurred within the correlative time frame set forth in the Table, petitioner’s vaccine claim
is deemed a Table claim, and a presumption of vaccine causation attaches. See § 300aa-
14; see also 42 C.F.R § 100. If petitioner alleges an injury that is not listed on the Table
(such as the GBS injury alleged in this case), the vaccine claim is deemed a non-Table
case, and no presumption of causation attaches. In such circumstances, petitioner must
satisfy her burden of proof. See § 300aa-13(a)(1)(A).

        To prevail on a non-Table vaccine claim, such as petitioner has asserted here, she
must allege: (1) that the vaccinee “sustained, or had significantly aggravated any illness,
disability, injury, or condition not set forth in the Vaccine Injury Table;” and (2) that the
injury “was caused by a vaccine.” 42 U.S.C. § 300aa-11(c)(1)(C)(ii)(I). Petitioner must
show that the vaccine was “‘not only a but-for cause of the injury but also a substantial
factor in bringing about the injury.’” Moberly v. Sec’y of Health & Human Servs., 592
F.3d 1315, 1321 (Fed. Cir. 2010) (quoting Shyface v. Sec’y of Health & Human Servs.,
165 F.3d 1344, 1352-53 (Fed. Cir. 1999)).

                                              15
        As required by the Federal Circuit, petitioner must prove that the flu vaccine given
to Mr. Carrino caused his injury and death by preponderant evidence that shows: (1) a
medical theory causally connecting the vaccine and Mr. Carrino’s injury; (2) a logical
sequence of cause and effect showing that the vaccine was the reason for his injury; and
(3) a showing of a proximate temporal relationship between the vaccine and his injury.
Althen v. Sec’y of Health & Human Servs., 418 F.3d 1274, 1278 (Fed. Cir. 2005); 42
U.S.C. § 300aa–13(a)(1) (requiring proof by a preponderance of the evidence).

       Because the causation theory must relate to the injury alleged, a petitioner must
provide a reputable medical or scientific explanation that pertains specifically to the
vaccinee’s case—although the explanation need only be “legally probable, not medically
or scientifically certain.” Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 548–
49 (Fed. Cir. 1994); Moberly, 592 F.3d at 1322. To be clear, “the function of a special
master is not to ‘diagnose’ vaccine-related injuries, but instead to determine ‘based on the
record evidence as a whole and the totality of the case, whether it has been shown by a
preponderance of the evidence that a vaccine caused the [claimed] injury.’” Andreu v.
Health & Human Servs., 569 F.3d 1367 at 1382 (Fed. Cir. 2009) (quoting Knudsen v.
Sec’y of Health & Human Servs., 35 F.3d 543, 549 (Fed. Cir. 1994)).

        The preponderance of the evidence standard has been interpreted to mean that a
fact is more likely than not. Moberly, 592 F.3d at 1322 n.2 (Fed. Cir. 2010). A petitioner
who satisfies this burden is entitled to compensation unless the government can prove, by
a preponderance of the evidence, that the vaccinee’s injury is “due to factors unrelated to
the administration of the vaccine.” 42 U.S.C. § 300aa-13(a)(1)(B).
       B.     Establishing the nature of petitioner’s injury

       When—as in this case—the parties dispute the nature of the injury at issue, the
special master must first determine which injury is best supported by the evidence before
applying the Althen test to determine whether the vaccine caused the injury.
Broekelschen v. Sec’y of Health & Human Servs., 618 F.3d 1346, 1350 (Fed. Cir. 2010);
see also Locane v. Sec’y of Health & Human Servs., 685 F.3d 1375 (Fed. Cir. 2012);
Lombardi v. Sec’y of Health & Human Servs., 656 F.3d 1343 (Fed. Cir. 2011). A special
master’s findings regarding the nature of petitioner’s injury may be sufficient to resolve
the case because the special master determines, from the record evidence, that the injury
petitioner suffered was not the injury that was contemplated in petitioner’s theory of
causation. See Lombardi, 656 F.3d at 1356; Broekelschen, 618 F.3d at 1350. To assist a
special master in evaluating a claim, the Federal Circuit has provided guidance that
evidence of an injury other than the one alleged can be relevant—not only to the “factors
unrelated” defense on which the government bears the burden of proof—but also to the
showing petitioner must make that the vaccine was a substantial factor in causing the
claimed injury. Stone v. Sec’y of Health & Human Servs., 676 F.3d 1373, 1380 (2012).

                                             16
       C.     Evaluating the presented evidence

        Petitioner cannot establish entitlement to Program compensation based solely on
the claims of petitioner alone. Rather, a vaccine claim must be supported either by the
medical records or by the opinion of a competent physician. 42 U.S.C. § 300aa-13(a)(1).
In determining whether petitioner is entitled to compensation, a special master shall
consider all material contained in the record, 42 U.S.C. § 300aa-13(b)(1), including “any .
. . conclusion, [or] medical judgment . . . which is contained in the record regarding . . .
causation . . . of the petitioner’s illness.” 42 U.S.C. § 300aa-13(b)(1)(A) (emphasis added).

              1.     Reliability of medical records

       Medical records, in general, warrant consideration as trustworthy evidence. The
records contain information supplied to or by health professionals to facilitate diagnosis
and treatment of medical conditions. With proper treatment hanging in the balance,
accuracy has an extra premium. These records are also generally created
contemporaneously to the medical events. Cucuras v. Sec’y of Health & Human Servs.,
993 F.2d 1525, 1528 (Fed.Cir.1993) (citing United States v. U.S. Gypsum Co., 333 U.S.
364, 396 (1947). The Federal Circuit’s decision in Cucuras v. Secretary of Health &
Human Services clearly supports the view that medical records are favored over oral
testimony in circumstances when there is a conflict between the former and the latter and
when the prepared medical records are internally consistent and complete. Id.

              2.     The experts’ opinions

       The persuasiveness of the experts’ testimony must be evaluated, and the testimony
of one side’s expert may be rejected when there is a reasonable basis for doing so. Burns
v. Sec’y of Health & Human Servs., 3 F.3d 415, 417 (Fed. Cir. 1993).27

27
                In the Vaccine Program, an expert’s opinion may be evaluated according to
the factors identified by the United States Supreme Court in Daubert v. Merrell Dow
Pharms., Inc., 509 U.S. 579 (1993). Terran v. Sec’y of Health & Human Servs., 195 F.3d
1302, 1316 (Fed. Cir. 1999). As recognized in Terran, the Daubert factors for analyzing
the reliability of testimony are:

       (1) whether a theory or technique can be (and has been) tested; (2) whether
       the theory or technique has been subjected to peer review and publication;
       (3) whether there is a known or potential rate of error and whether there are
       standards for controlling the error; and, (4) whether the theory or technique
       enjoys general acceptance within a relevant scientific community.

                                             17
       When evaluating the reliability of an expert’s opinion, it is important to ascertain
whether the information on which the doctor is relying is accurate because inaccuracies in
the expert’s factual assumptions compromise the reliability of the view offered. See
Perreira v. Sec’y of Health & Human Servs., 33 F.3d 1375, 1377 (Fed. Cir. 1994) (an
expert opinion is no better than the soundness of the reasons supporting it).

        Applying these standards to determine whether petitioner has established that she is
entitled to compensation for Mr. Carrino’s alleged vaccine-related injury of GBS, the
undersigned finds that she has not. Therefore, she is not entitled to compensation. The
undersigned’s reasoning is explained, in detail, below.

III.   ANALYSIS

       The contemporaneous medical records reflect a general and consistent consensus
about the nature of Mr. Carrino’s injury. His attending physicians recorded the same
diagnostic impression, and the testing and clinical evaluations supported the treating
neurologist’s diagnostic conclusion. The difficulty with petitioner’s vaccine claim is that
the vaccine-related injury she asserts her husband suffered is not the injury with which he
was diagnosed in the medical records. Petitioner’s experts have offered opinions in
support of petitioner’s claim that rely on selectively chosen aspects of the medical records,
while disregarding the consistent diagnostic conclusions reached by Mr. Carrino’s
attending physicians. Remarkably, Mr. Carrino’s primary care physician now offers an
opinion of causation that contradicts his earlier, contemporaneously recorded impressions
of Mr. Carrino’s condition.

       In vaccine cases, expert testimony is helpful when the medical records are unclear.
But, when—as here—the medical records speak plainly about the injury at issue, the value
of the experts’ testimony is somewhat diminished.

       Apparently, petitioner has offered expert testimony to support her vaccine injury
claim because the contemporaneous medical records of Mr. Carrino’s October 2006
hospitalization contain a diagnosis of a condition other than the GBS event petitioner

Terran, 195 F.3d at 1316 n.2 (citing Daubert, 509 U.S. at 592-95). After Terran, decisions
issued by of the Court of Federal Claims have consistently cited to Daubert. E.g. De
Bazan v. Sec’y of Health & Human Servs., 70 Fed. Cl. 687, 699 n.12 (2000) (“A special
master assuredly should apply the factors enumerated in Daubert in addressing the
reliability of an expert witness’s testimony regarding causation.”), rev’d on other grounds,
539 F.3d 1347 (Fed. Cir. 2008); Campbell v. Sec’y of Health & Human Servs., 69 Fed. Cl.
775, 781 (2006); Piscopo v. Sec’y of Health & Human Servs., 66 Fed. Cl. 49, 54 (2005).

                                             18
alleges. Petitioner presented the medical testimony of Mr. Carrino’s primary care
physician, Dr. DeMayo, and an expert neurologist, Dr. Hogen. Their opinions, which
were developed in the context of this litigation conflicted with the contemporaneous
medical records and thus, failed to persuade.

        In contrast, the testimony of respondent’s expert neurologist, Dr. Bielawski,
effectively relied on and was consistent with the medical records and the referenced
literature.

       The undersigned reviews the experts’ positions in turn.
       A.     The opinion of the parties’ experts
              1.     Mr. Carrino’s primary care physician, Dr. Joseph DeMayo28

       In his written report and at hearing, Dr. DeMayo asserted that Mr. Carrino suffered
a flu vaccine-related GBS event that precipitated his October 2006 hospitalization. This
opinion, however, contradicted his diagnostic assessment (and treatment) of Mr. Carrino
during that hospitalization.

        Dr. DeMayo administered Mr. Carrino’s flu vaccination five days prior to his
hospitalization, and served as his admitting physician at the hospital. The
contemporaneous medical records do not indicate that Dr. DeMayo contemplated a
diagnosis of GBS; instead, Dr. DeMayo indicated that Mr. Carrino’s presenting symptoms
on hospital admission were consistent with a cerebrovascular accident. Pet’r’s Ex. 11 at 1.
In fact, prior to the initiation of this Vaccine Program claim, the record is devoid of any
evidence that Dr. DeMayo diagnosed Mr. Carrino with GBS.

       In the opinion he has offered on petitioner’s behalf here, Dr. DeMayo outlined the
symptoms of “weakness, loss of balance, unsteady gait, and confusion” that Mr. Carrino
developed five days after he received the flu shot. Pet’r’s Ex. 12 at 2. He reasoned that
Mr. Carrino must have suffered a GBS event because he developed neurologic symptoms
within a medically acceptable time period after receiving the flu vaccine, and because the
performed “diagnostic testing. . . [had] eliminate[d] other causes.” Id.

28
        Consistent with the guidance from the Federal Circuit in Capizzano, Dr. DeMayo’s
earlier prepared medical records are accorded more weight than his later-developed
medical opinion of vaccine-related causation because while he was acting as a “treating
physician” contemporaneous to the events at issue, he was better positioned to determine
whether “a logical sequence of cause and effect show[s] that the vaccination was the
reason for the injury.” Capizzano v. Sec'y of Health & Human Servs., 440 F.3d 1317,
1326 (Fed. Cir. 2006) (internal citations omitted).

                                            19
        Although at hearing, Dr. DeMayo expressed agreement with respondent’s expert,
Dr. Bielawski, that the combination of clinical symptoms and the results of cerebrospinal
fluid testing and needle electromyography is important to consider when making a
diagnosis of GBS, he had difficulty identifying the predicate factors that led to the change
in his view of Mr. Carrino’s medical condition.

       Because the medical records were clear and consistent, the undersigned accords
more weight to Dr. DeMayo’s impressions recorded in his contemporaneous treatment
notes than to his later-offered opinion of causation.

              2.     Petitioner’s expert neurologist, Dr. Victor Hogen

      The reliability and persuasiveness of Dr. Hogen’s expert opinion were significantly
diminished by his lack of familiarity with critical details in the medical records from Mr.
Carrino’s October 2006 hospitalization.

       Further diminishing the reliability and persuasiveness of Dr. Hogen’s offered
opinion was his reliance on Mr. Carrino’s later medical records (for treatment after Mr.
Carrino’s 2006 hospitalization) to support the theory that Mr. Carrino developed GBS in
the days following his flu vaccination. Petr’r’s Ex. 21 at 2 (citing numerous medical
records from various health care providers in 2008—the year this vaccine claim was
filed—and noting a past history of GBS for Mr. Carrino).

        With only light record support for his opinion, Dr. Hogen asserted that a subject’s
clinical symptoms, without more, are sufficient to make a diagnosis of GBS. He posited
that the sole two features required for a GBS diagnosis are (1) ascending weakness, and
(2) missing or diminished reflexes. Pet’r’s Ex. 21 at 2-3. He testified that Mr. Carrino
had roughly symmetrical, ascending paralysis, and diminished or lost reflexes. Tr. at 87.
He wholly ignores the fact that Mr. Carrino did not present to the hospital with these
symptoms, but briefly manifested the symptoms after he acquired a urinary tract infection.

        Dr. Hogen disregarded the well-established diagnostic criteria for GBS, urging that
neither cerebrospinal fluid testing or nerve electromyography are necessary to confirm a
GBS diagnosis after a patient’s clinical symptoms have raised a treating physician’s
suspicions. Tr. at 79. His view concerning the proper diagnostic criteria for GBS
conflicted with the opinions of Mr. Carrino’s treating physician, Dr. DeMayo, and
respondent’s expert, Dr. Bielawski. The undersigned did not accord significant weight to
Dr. Hogen’s opinion because it was a singular perspective lacking adequate support in
either the medical records or medical literature.
              3.     Respondent’s expert neurologist, Dr. Martin Bielawski

                                             20
       Dr. Bielawski’s testimony offered a more clear and cogent explanation of the
contemporaneously created medical records than did the testimony of petitioner’s experts
Drs. DeMayo and Hogen. Dr. Bielawski filed literature regarding the relevant
considerations in diagnosing GBS. A GBS diagnosis is established by the presence of
certain clinical features, and the results of cerebrospinal fluid testing and an EMG. Tr. at
125; Resp’t’s Ex. D at 6-7 (the Vriesendorp article).29 Dr. Bielawski agreed with Dr.
Hogen that the clinical symptoms of “progressive weakness in both arms and legs” and
“areflexia” or missing reflexes are required for a GBS diagnosis. Resp’t’s Ex. A at 7.

       Dr. Bielawski asserted that Mr. Carrino did not have GBS because his symptoms at
the time of his hospital admission were not consistent with that condition. Dr. Bielawski
acknowledged, however, that for a brief period during Mr. Carrino’s hospitalization, his
neurologic symptoms worsened in a manner that triggered concern for a GBS event. His
attending physicians proactively ordered treatment for his suspected GBS with steroids
and IVIG, but that particular treatment did not prove effective.

        At the same time that his neurological symptoms began to worsen, Mr. Carrino was
treated for a urinary tract infection. As the infection resolved, the symptoms that
provoked concern that he might have had a GBS event also resolved. Dr. Bielawski
testified that the rapid resolution of Mr. Carrino’s symptoms after the treatment of his
urinary tract infection was appropriate for a stroke patient who had developed an
infection. Resp’t’s Ex. N at 4; see also Tr. at 116.

        The parties’ experts made reference to Mr. Carrino’s medical records to support
their respective positions. Because a review of the records indicates that Mr. Carrino was
not diagnosed with GBS during his October 2006 hospitalization, the undersigned turns
now to evaluate Mr. Carrino’s reported symptoms in accordance with the diagnostic
criteria for GBS upon which Mr. Carrino’s treating physician, Dr. DeMayo, and
respondent’s expert, Dr. Bielawski, agreed.
       B.     Mr. Carrino’s clinical symptoms during his October 2006
              hospitalization did not meet the diagnostic criteria for GBS.

29
       Francine Vriesendorp, Clinical Features and Diagnosis of Guillain-Barre Syndrome
in Adults, http://www.uptodate.com/contents/clinical-features-and-diagnosis-of-guillain-
barre-syndrome-in-adults?source=search_result&search=guillain-
barre+syndrome&selectedTitle=1%7E150 (last visited June 5, 2013). Dr. Bielawski
indicated that this diagnostic guidance was available and relevant in October 2006, when
Mr. Carrino was hospitalized several days after his receipt of the flu vaccine. Tr. at 127-
28.

                                             21
      The parties agreed that there are a number of clinical symptoms that would be
diagnostic of GBS.
              1.     Lost or significantly diminished deep tendon reflexes30

        The parties agreed that deep tendon reflexes must be lost or significantly
diminished to merit a GBS diagnosis. See Tr. at 24 (Dr. DeMayo); Tr. at 73 (Dr. Hogen);
Tr. at 166-7 (Dr. Bielawski); Resp’t’s Ex. A at 7-8.

       Dr. Brand conducted several neurologic examinations of Mr. Carrino during his
hospitalization and documented in his notes the state of Mr. Carrino’s “preserved reflexes in
his knees and in his arms.” Tr. at 117 (Dr. Bielawski). The “preserved” condition of Mr.
Carrino’s reflexes during the early days of his hospitalization in October of 2006 “was. . . a
sign pointing against GBS as a diagnosis” Tr. at 116-17 (Dr. Bielawski).

        During his hospitalization, Mr. Carrino did briefly lose his knee reflexes when he
contracted a urinary tract infection. See Pet’r’s Ex. 11 at 32; Pet’r’s Ex. 11 at 35; Pet’r’s
Ex. 11 at 44; Tr. at 117. With antibiotic treatment of that urinary tract infection, Mr.
Carrino’s reflexes returned within two days. Tr. at 117. Dr. Bielawksi explained that the
“rapid recovery” of Mr. Carrino’s reflexes was not unusual for a stroke patient “who has
had a superimposed toxic metabolic or infectious event”—such as Mr. Carrino
experienced with his acquired urinary tract infection. Resp’t’s Ex. N at 4. Had Mr.
Carrino suffered a GBS event, his knee reflexes would not have returned so quickly. See
Tr. at 116 (Dr. Bielawski).

        Although petitioner’s expert, Dr. Hogen, argued that most of Mr. Carrino’s treating
physicians had identified missing or absent reflexes that were consistent with a GBS
diagnosis, Tr. at 74, he did not provide any record citations for his assertions. The records
do consistently make reference to Mr. Carrino’s absent ankle reflexes; but his missing
ankle reflexes had been attributed to his diabetic neuropathy years before the flu vaccine
at issue.

30
        Normally, when a muscle tendon is tapped briskly, the muscle contracts
immediately due to a two-neuron reflex arc involving the spinal or brainstem segment that
innervates the muscle. Any asymmetry of reflexes suggests that an abnormality is present.
H. K. Walker. Deep Tendon Reflexes, in Clinical Methods: The History, Physical and
Laboratory Examinations 365, 368 (H.K. Walker et al. eds., 3rd ed. 1990), available at
http://www.ncbi.nlm.nih.gov/books/NBK396/#A2362 (last visited June 5, 2013).
                                              22
      The undersigned finds that apart from a brief loss of reflexes in connection with his
urinary tract infection, Mr. Carrino did not lose or have significantly diminished deep
tendon reflexes after his flu vaccination in October 2006.
              2.     Progressive weakness

        The parties agreed that a hallmark symptom of GBS is progressive weakness or
ascending paralysis. Resp’t’s Ex. A at 7-9; Resp’t’s Ex. N at 4; see also Tr. at 22 (Dr.
DeMayo); Pet’r’s Ex. 21 at 1 (Dr. Hogen). Such ascending paralysis, which “is a roughly
symmetric, progressive paralysis,” typically peaks within fourteen days of symptom onset.
Tr. at 57 (Hogen).

       At the time of Mr. Carrino’s hospital admission, he did not have progressive
weakness. Nor did he exhibit any exacerbations of his symptoms during the first nine
days of his hospitalization. Resp’t’s Ex. A at 7-9; Resp’t’s Ex. N at 4; Tr. at 162-63.
Instead, the records reflect that within a few days, his symptoms were better. Mr.
Carrino’s attending neurologist, Dr. Brand, specifically noted an improvement in Mr.
Carrino’s ataxia three days after his hospital admission. Pet’r’s Ex. 11 at 7.

        Nonetheless, petitioner’s expert, Dr. Hogen, asserted that Mr. Carrino had
“progressive weakness in both arms and both legs.” Tr. at 80. A review of Mr. Carrino’s
medical records show two documented instances of Mr. Carrino’s “ascending weakness.”
Tr. at 119 (Bielawski). The significance of these notations, however, is not entirely clear
because they were made by two different consulting physicians—but not Mr. Carrino’s
attending neurologist, Dr. Brand—and neither provided clinical support for the notation.
See Tr. at 156, 157, 162 (Dr. Bielawski); Resp’t’s Ex. A at 10 (Dr. Bielawski asserting
that Dr. Beggs’s notation in the medical records that Mr. Carrino “ha[d] [experienced]
ascending weakness bilaterally” since his hospitalization was “wrong”).

       These two notations of ascending weakness were not documented in the hospital
records until October 21, 2006, when Mr. Carrino complained to Dr. DeMayo of neck
pain, weakness in all of his extremities, and difficulty swallowing. Pet’r’s Ex. 11 at 25.
Dr. Brand, the attending neurologist, evaluated Mr. Carrino that same day and noted there
was more weakness in his legs and pain in his right shoulder with weakness in his right
arm. Pet’r’s Ex. 11 at 27.

       Mr. Carrino’s worsening condition resulted in his transfer to the intensive care unit
the next day. Pet’r’s Ex. 11 at 28. On examination of Mr. Carrino, Dr. Brand found an
absence of “knee jerks and ankle jerks with preserved upper extremity deep tendon
reflexes.” Pet’r’s Ex. 11 at 32. This decline in Mr. Carrino’s condition provoked his
treating doctors to consider a diagnosis of GBS. Tr. at 119-20.

                                             23
       Dr. Bielawski acknowledged in his testimony that Dr. Brand had become
concerned about the possibility of a GBS event when Mr. Carrino developed significant,
new symptoms of generalized weakness more than one week after his hospitalization. Tr.
at 126. Dr. Bielawski also acknowledged that Mr. Carrino received a course of Solu-
Medrol and IVIG, which was intended to treat what seemed to be an emerging GBS
episode. Tr. at 150-51. However, Dr. Bielawski cogently explained:

       [T]he reason [Mr. Carrino] became weak was because he had a systemic
       illness which was the urinary tract infection. He had a low grade fever. And
       we see this all the time in patients who have stroke syndromes, that they
       have unmasking of various neurological signs, and they can become
       generally weak, they can become confused. And once the urinary tract
       infection . . . is treated, they get back to or close to their baseline.

Tr. at 151.

       Once treated with antibiotics, Mr. Carrino’s infection did resolve—as did his
symptoms of pronounced weakness. Pet’r’s Ex. 11 at 62. A subsequent neurologic exam
indicated that he had returned to a state “similar to that on admi[ssion].” Id.

       The undersigned finds that Mr. Carrino briefly exhibited, in association with his
urinary tract infection, a progressive weakness that resolved within a five-day period.

              3.     Paresthesia

       A very common symptom of GBS is paresthesia. Tr. at 117 (Bielawski). About 80
percent of affected subjects experience pins and needles (paresthesia) in their hands and
feet. Resp’t’s Ex. A at 6-9, Tr. at 117-18, 141, 166 (Dr. Bielawski).

       The parties do not dispute that Mr. Carrino made no complaint of tingling in either
his hands or his feet (paresthesia), Pet’r’s Ex. 11 at 27; Tr. at 85-86 (Dr. Hogen); Tr. at
117-18 (Dr. Bielawski), and the undersigned finds that Mr. Carrino did not suffer with
paresthesia.
              4.     Symmetric symptom presentation

         The parties agreed that symmetrical neurologic symptoms are a sign that is
 strongly suggestive of a GBS injury. Conversely, a marked, persistent asymmetric
 presentation of symptoms renders a GBS diagnosis more doubtful. Resp’t’s Ex. A at 7;
 Tr. at 24 (Dr. DeMayo); Tr. at 57, 86 (Dr. Hogen). Mr. Carrino’s motor and sensory
 signs were persistent and notable for their asymmetry. Resp’t’s Ex. A at 9; Resp’t’s Ex.
 N at 4; Tr. at 118 (Dr. Bielawski). In particular, the “numbness and diminished
 sensation [Mr. Carrino] had in his left leg up through [his] rib cage” was inconsistent
                                            24
with the type of symmetric symptoms that are characteristic of GBS. Tr. at 118 (Dr.
Bielawski). The undersigned finds that Mr. Carrino’s symptom presentation was
asymmetric.
             5.     Facial weakness

        Facial weakness is another common indicator of GBS. Dr. Bielawski testified
that roughly 60 percent of GBS patients complain of such weakness. Resp’t’s Ex. A at
9; Tr. at 121 (Dr. Bielawski). Dr. Hogen agreed that facial weakness can be a
“supportive feature” of a GBS finding, but he denied that it is “one of the prime
diagnostic factors.” Tr. at 86.

        That Mr. Carrino did not complain of facial weakness during his hospitalization
is undisputed. Resp’t’s Ex. A at 7-9; Tr. at 24-25 (Dr. DeMayo); Tr. at 86 (Dr. Hogen);
Tr. at 120-21 (Dr. Bielawski). The undersigned finds that he did not develop facial
weakness.
             6.     Elevated protein levels in the cerebrospinal fluid

        Dr. DeMayo and Dr. Bielawski both agreed that the testing of a subject’s
cerebrospinal fluid is important in circumstances involving a “clinical suspicion” of GBS.
Tr. at 21 (Dr. DeMayo), 125 (Dr. Bielawski). Dr. Bielawski testified that 80 to 90 percent
of GBS patients will have “an elevated [protein level in their] cerebrospinal fluid one
week after the onset of symptoms.” Resp’t’s Ex. A at 9; see also Tr. at 125.

       After a week of hospitalization, Mr. Carrino’s neurologic symptoms began to
deteriorate further and he developed difficulty breathing and swallowing. This change in
his condition provoked his treating physicians to order a spinal tap. The spinal tap,
performed twelve days after his admission to the hospital, revealed that Mr. Carrino’s
cerebrospinal protein levels were normal, Tr. at 55 (Dr. Hogen), an unusual finding for a
GBS diagnosis. The undersigned finds that the protein levels in Mr. Carrino’s
cerebrospinal fluid were not elevated.

             7.     EMG abnormalities

         The parties’ witnesses, Dr. DeMayo and Dr. Bielawski, agreed that an abnormal
 EMG is present in 95 to 99 percent of patients with GBS. They also agreed that in
 consideration with a subject’s clinical symptoms and cerebrospinal fluid test results, an
 EMG is a critical aid to diagnosing GBS. See Tr. at 21 (Dr. DeMayo); Resp. Ex. A at 7-
 8; Tr. at 125, 158 (Dr. Bielawski).

      Dr. DeMayo testified at hearing that he did not recall Dr. Brand ever ordering an
 EMG. Tr. at 21-22. Dr. Hogen stated that he did not see an EMG report in the record;
                                            25
 Tr. at 79, nor did he see any notes discussing EMG results in any detail. Id.

       The record indicates that Dr. Brand did order an EMG/NCTS on October 23, 2006,
Pet’r’s Ex. 11 at 38, but the results of the EMG were never filed into the record. Dr.
Brand commented in his notes, the day after he ordered the testing, that the EMG
“findings” were consistent with peripheral neuropathy, but they did not exclude a
Guillain-Barré type of radiculopathy.31 Pet’r’s Ex. 11 at 44; see also Resp’t’s Ex. at 6.

      After careful review of the record as a whole, the undersigned is persuaded that
 an EMG was performed, and the results did not rule out the possibility of GBS.

         The aggregate of Mr. Carrino’s symptoms, however, failed to satisfy the
 diagnostic criteria for GBS upon which the parties’ witnesses agreed. Mr. Carrino’s
 presenting symptoms at the time of his hospital admission and during the course of his
 hospitalization led both his primary care physician and then-treating neurologist to reach
 a different diagnostic conclusion than GBS. Instead, and Mr. Carrino’s diagnosis at the
 time of his hospital discharge was lateral medullary infarct (stroke). Pet’r’s Ex. 11 at
 78.
       C.     The symptoms precipitating Mr. Carrino’s hospitalization were
              strongly suggestive of lateral medullary syndrome

         Mr. Carrino presented for admission to the hospital, five days after receiving a
flu vaccine, with “vertigo, nausea, weakness, [and an inability] to walk.” Pet’r’s Ex.
11 at 1. Over the next ten days, Mr. Carrino’s symptoms of vertigo, nausea,
weakness, inability to walk, headache, neck discomfort, involuntary eye movement,
double vision, slight right eyelid drooping, hiccups, and right cerebellar signs were
well-documented. Resp’t’s Ex. A at 6, 8, 10; Tr. at 25, 31, 33, 45 (Dr. DeMayo); Tr.
at 82 (Dr. Hogen); Tr. at 86-87, 118-19, 121, 130-32, 135-36, 171 (Dr. Bielawski).
The symptoms were all indicative of a stroke. Resp’t’s Ex. A at 6, 8, 10; Resp’t’s Ex.
E at 4 (noting that “[m]oderate or severe headache is common in lateral medullary
infarction” and “vertigo or other feelings of disequilibrium are nearly always
present”); Resp’t’s Ex. E at 5 (finding ataxia “the rule rather than the exception,”
citing diplopia and hiccups as “other frequent complaints,” and identifying nausea and
vomiting as “common symptoms” of vestibular dysfunction). On admission to the
hospital, Mr. Carrino’s primary care physician, Dr. DeMayo, assessed him with a
cerebrovascular accident or a stroke, and four days after his hospital admission, Dr.

31
       The report for this EMG study was never located or filed by petitioner. However,
respondent’s expert, Dr. Biewlaski, characterized Dr. Brand’s notations in the medical
record as consistent with the type of remarks that would follow such testing. See Resp’t’s
Ex. A at 6.

                                             26
Brand was able to speculate where the damage to Mr. Carrino’s brain had occurred
based on neuroanatomy. Pet’r’s Ex. 11 at 1, 9 (Dr. Brand positing that Mr. Carrino’s
presenting symptoms were caused by a stroke in the area of the brain close to the
brainstem and cerebellum).32

      At hearing, Dr. Hogen testified that Mr. Carrino’s symptoms of dizziness, light-
headedness and ataxia were a manifestation of the autonomic dysfunction that can occur
in some cases of GBS. Tr. at 89-90.

      Dr. Bielawski responded by observing that dizziness is not a symptom of GBS
and Mr. Carrino “sudden[ly]” and “acute[ly]” developed dizziness and ataxia. Tr. at
130-31; see also Resp’t’s Ex. E at 5. He added that damage produced by a right lateral
medullary infarct can “compromise one of the tracts called the vestibular ocular tract”
and cause dizziness. Tr. at 130-31. This testimony was unrebutted.

       At hearing, Dr. Bielawski testified that Mr. Carrino’s inability to walk at the
time of his hospital admission, and his subsequent difficulty with his finger-to-nose
neurologic test were signs of a disruption of his right cerebellar connections. Tr. at
130-31. “The cerebellum is [the] organ that . . . [regulates] coordination and [a
disruption of] the cerebellar connections on the right side of the brain stem would . . .
[produce such signs as] finger[-]to[-]nose ataxia.” Tr. at 130-31.

       Dr. Bielawski added that eyelid droop or ptosis can occur when “the
sympathetic fibers [are] compromised [by] . . . ischemic injury.” Tr. at 132. Mr.
Carrino’s initial eyelid droop and later double vision were additional symptoms of a
brain stem stroke. See Tr. at 132.

       Dr. Bielawski commented that because patients with autonomic syndrome are
further compromised by a GBS event, Tr. at 137, other symptoms of autonomic
dysfunction—such as “alternating bouts of high blood pressure and low blood
pressure” would be expected. Id. Mr. Carrino did not have these symptoms, which
militates against a finding that he was suffering from an autonomic syndrome
associated with GBS. Id.

        Dr. Hogen attempted to undercut evidence of the initial impression of stroke
documented in the hospital records by both Dr. DeMayo, Mr. Carrino’s primary care
physician, and Dr. Brand, Mr. Carrino’s attending neurologist. Dr. Hogen urged that
“[a] st[r]oke in [Mr. Carrino’s] parietal lobe would have affected the right side of his
body . . . [m]aybe. . .produced. . .numbness on the right side.” Tr. at 69. Although Dr.

32
       “Patient has neurological signs consistent with posterior fossa ischemia.” Pet’r’s
Ex. 11 at 9 (emphasis added).

                                             27
Hogen did not “really remember exactly” what Mr. Carrino’s complaints were, he
“[thought] that most of [Mr. Carrino’s] complaints were left-sided.” Tr. at 69. A
careful review of the medical records from Mr. Carrino’s hospital admission indicates
that most of his complaints were right-sided.33 See Pet’r’s Ex. 11 at 3-5, 6.

      The medical records and the testimony of respondent’s expert persuade the
undersigned that Mr. Carrino’s symptoms during his October 2006 hospitalization
were consistent with a stroke.

              1.     The absence of evidence of stroke on the initial brain imaging is
                     not determinative because a subsequent MRI confirmed the
                     presence of a stroke

      On the day of Mr. Carrino’s admission to hospital, his brain MRI was read as
showing no acute infarctions. Pet’r’s Ex. 10 at 55. The next day, a second brain MRI also
was read to show no abnormalities. Id. at 57.

       The parties’ expert neurologists, Drs. Hogen and Bielawski, disagreed about the
significance of these initial MRIs.

        Dr. Hogen asserted that the absence of acute infarctions on the brain MRIs is
evidence that Mr. Carrino—who had previously suffered strokes—had not suffered a
“new stroke.” Pet’r’s Ex. 21 at 3; Tr. at 63-65. Dr. Hogen testified, without offering any
supporting references, that “an MRI-scan with diffusion weighted imaging is almost 100
percent sensitive in the first 24 hours of an acute stroke.” Pet’r’s Ex. 21 at 3. Dr. Hogen
further asserted that “it is not likely that the MRI scan of 10/11/2006 missed a stroke[,
and] it is more probable that the stroke seen on 11/01/2006 was acquired during the
hospitalization at a much later date.” Id.

         Dr. Bielwaski disagreed. He contended that the first MRI showed either a
brainstem stroke too small to detect or findings that the radiologist simply missed.
Resp’t’s Ex. N. at 2; see Tr. 161. Supportive evidence for Dr. Bielawski’s claim that the
initial imaging results were simply overlooked or misread is found in the later brain
imaging performed on November 1, 2006. This imaging revealed “a clear cut [right]
lateral medullary infarct seen on several segments,” Pet’r’s Ex. 11 at 74, and Dr. Brand,
Mr. Carrino’s treating neurologist, determined that the neurologic injury had occurred
before Mr. Carrino’s hospital admission. See id. The November 1, 2006 brain MRI
confirmed the location of the infarct about which Dr. Brand, Mr. Carrino’s attending
neurologist, had speculated four days after Mr. Carrino’s hospital admission. The parties’

33
     Dr. DeMayo’s medical evaluations, in particular, consistently reflect right-sided
weakness. See Pet’r’s Ex. 11 at 10, 12, 50.
                                             28
experts, Drs. Hogen and Bielawski, also disagreed regarding the significance of the
November 1, 2006 brain MRI results.

       Dr. Hogen testified that the findings were too small, too late and too
indeterminate to support a finding that Mr. Carrino had suffered a stroke prior to his
hospital admission twenty days earlier. Tr. at 67-69. Dr. Hogen added that the strokes
that were visible on the MRI were in the wrong location to have caused the functional
loss that Mr. Carrino exhibited. See Tr. at 68. In Dr. Hogen’s view, a small stroke at
the cervical medullary junction would not have “produced the quadraparesis” that Mr.
Carrino suffered. Tr. at 60. Nonetheless, Dr. Hogen conceded that Mr. Carrino’s
symptoms of “nausea, vomiting, and stenosis” were all consistent with the damage
caused by a lateral lineal stroke (or a lateral medullary stroke). Tr. 86-87.

       While this imaging evidence alone does not determine the nature of Mr. Carrino’s
evolving condition, it merits consideration with the other record evidence.

              2.     Mr. Carrino’s past medical history of stroke made him
                     vulnerable to further ischemic injury

        Before 2006, Mr. Carrino had suffered at least five ischemic infarctions, including:
(1) two incidents involving sixth nerve palsy; (2) one incident involving third nerve palsy;
(3) a left cerebellar stroke; and (4) a left basal ganglia hemorrhagic stroke. Resp’t’s Ex. A
at 6; Tr. at 128-29; see also Tr. at 76-77 (Dr. Hogen). His prior medical history rendered
him “quite susceptible” to brain stem strokes. Tr. at 129.

              3.     The “progressive” symptoms that provoked concern that Mr.
                     Carrino had developed GBS were unresponsive to a course of
                     IVIG and steroids but did resolve, over the next five days, with
                     antibiotic treatment

        The new symptoms of weakness that emerged ten days after Mr. Carrino’s
hospitalization were treated preventatively, as if they were symptoms of GBS. That
treatment was unavailing, but the course of antibiotics that Mr. Carrino began for
treatment of a urinary tract infection was successful. Resp’t’s Ex. A at 9; Resp’t’s Ex. N
at 4; Tr. at 119-20. Contrary to Dr. Hogen’s assertions otherwise, this prophylactic course
of treatment—and the limited response it provoked—did not point to a GBS episode.

       D.     Mr. Carrino did not suffer from the injury for which petitioner now
              seeks a Program award

                                             29
       As noted previously, special masters are required to evaluate the record as a whole.
42 U.S.C. §300aa-13. The record here—including the contemporaneous medical records
and Mr. Carrino’s brain imaging, the statements of Mr. Carrino’s attending physicians
during his October 2006 hospitalization, and the testimony of Drs. DeMayo, Hogen, and
Bielawski—undercuts petitioner’s claim that Mr. Carrino developed GBS either prior to or
during his October 2006 hospitalization, and militates against a finding that Mr. Carrino’s
injuries were caused by a vaccine-related GBS event.

       This determination precludes a finding of causation in petitioner’s favor. When the
evidence does not support a finding that the vaccinee suffered the injury for which
petitioner seeks Program compensation, an Althen causation analysis may not be required.
See Lombardi, 656 F.3d at 1356 (affirming special master’s decision foregoing Althen
analysis after concluding petitioner did not suffer from any of his alleged injuries). Out of
an abundance of caution, however, the undersigned evaluates petitioner’s theory under the
Althen standard.

              1.     Althen Prong One: Petitioner’s Medical Theory

       Under Althen Prong 1, petitioner must put forth a biologically plausible theory
explaining how the received vaccine “can” cause the injury alleged. Pafford v. Sec’y of
Health & Human Servs., 451 F.3d 1352, 1355-56 (Fed. Cir. 2006). To satisfy this prong,
“a petitioner must provide a reputable medical or scientific explanation that pertains
specifically to the petitioner’s case, although the explanation need only be ‘legally
probable, not medically or scientifically certain.’” Broekelschen, 618 F.3d at 1345
(quoting Knudsen, 35 F.3d at 548-49); see also Moberly, 592 F.3d at 1324 (“[T]he special
master is entitled to require some indicia of reliability to support the assertion of the
expert witness.”).

       The offered medical theory must be supported by either the vaccinee’s medical
records or the opinion of a competent physician. Grant v. Sec’y of Health & Human
Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992). Support for the offered medical theory must
also include an explanation that “pertains specifically to the [claim made in] petitioner’s
case.” Moberly, 592 F.3d at 1322. See Veryzer v. Sec’y of Health & Human Servs., No.
06-0522V, 2010 WL 2507791, at *24 (Fed. Cl. Spec. Mstr. 2010) (noting that the relevant
inquiry is whether, based on facts known to medical science and logical inferences drawn
by a qualified expert, the vaccine at issue is more than likely to have caused the alleged
injury), aff’d, 100 Fed. Cl. 349 (2011), aff’d, 475 F. App’x 765 (Fed. Cir. 2012).

       Petitioner’s theory of causation need not be medically or scientifically certain,
Knudsen, 35 F.3d at 548-49, but it must be informed by “sound and reliable medical or
scientific explanation.” Id. at 548; see also Veryzer v. Sec’y of Health & Human Servs.,
98 Fed. Cl. 214, 223 (2011) (noting that special masters are bound by both 42 U.S.C.
§ 300aa-13(b)(1) and Vaccine Rule 8(b)(1) to consider only evidence that is both
                                             30
“relevant” and “reliable”). If petitioner relies upon a medical opinion to support her
theory, the basis for the opinion and the reliability of that basis must be considered in the
determination of how much weight to afford the offered opinion. See Broekelschen, 618
F.3d at 1347 (“The special master’s decision often times is based on the credibility of the
experts and the relative persuasiveness of their competing theories.”); Perreira, 33 F.3d at
1377 n.6 (Fed. Cir. 1994) (citing Fehrs v. U.S., 620 F.2d 255, 265 (Ct. Cl. 1980)) (“An
expert opinion is no better than the soundness of the reasons supporting it.”).

       The undersigned does not evaluate whether petitioner put forth a biologically
plausible theory explaining how the received flu vaccine could have caused GBS because
petitioner failed to establish by preponderant evidence that Mr. Carrino developed GBS.
And petitioner put forth no evidence regarding whether the flu vaccine can cause stroke.
Thus, petitioner does not prevail on Prong One.

              2.     Althen Prong Two: Logical Sequence of Cause and Effect

        Under Althen Prong Two, petitioner must prove “a logical sequence of cause and
effect showing that the vaccination was the reason for the injury.” Althen, 418 F.3d at
1278. Under this prong, petitioner must show that the received vaccine “did” cause the
alleged injury. Pafford, 451 F.3d at 1354.

        Petitioner need not make a specific type of evidentiary showing. That is, petitioner
is not required to offer “epidemiologic studies, rechallenge, the presence of pathological
markers or genetic disposition, or general acceptance in the scientific or medical
communities to establish a logical sequence of cause and effect . . . .” Capizzano, 440
F.3d at 1325. Instead, petitioner may satisfy her burden by presenting circumstantial
evidence and reliable medical opinions. See id. at 1325-26.

       Here, the record evidence strongly militates against a finding that Mr. Carrino
suffered from GBS, and petitioner’s expert, Dr. Hogen, acknowledged that the flu vaccine
was “less likely than not” to have caused a right lateral medullary infarct, the diagnosis
with which Mr. Carrino was discharged from the hospital in November of 2006. Tr. at 91-
92.

       Petitioner does not prevail on Prong Two.

              3.     Althen Prong Three: Timing

       Under Althen Prong Three, petitioner must establish that Mr. Carrino’s injury
occurred within a time frame that is medically appropriate for the alleged mechanism of
harm. See Pafford, 451 F.3d at 1358 (“Evidence demonstrating petitioner’s injury
occurred within a medically acceptable time frame bolsters a link between the injury
                                              31
alleged and the vaccination at issue under the ‘but-for’ prong of the causation analysis.”).
Petitioner may satisfy this prong by producing “preponderant proof that the onset of
symptoms occurred within a time frame for which, given the medical understanding of the
disorder’s etiology, it is medically acceptable to infer causation-in-fact.” De Bazan, 539
F.3d at 1352.

       Petitioner may discharge her burden by showing: (1) when the condition for which
she seeks compensation first appeared after vaccination and (2) whether the period of
symptom onset is “medically acceptable to infer causation.” Shapiro v. Sec’y of Health &
Human Servs., No. 99-552V, 2011 WL 1897650, at *13 (Fed. Cl. Spec. Mstr. Apr. 27,
2011), aff’d in relevant part, vacated in non-relevant part, 101 Fed. Cl. 532, 536 (2011),
aff’d 503 F. App’x 952 (2013) (per curiam). The appropriate temporal association will
vary according to the particular medical theory advanced in the case. See Pafford, 451
F.3d at 1358.

        Because petitioner failed to establish that Mr. Carrino suffered from the claimed
injury, petitioner cannot prove that the onset of the alleged condition occurred within a
medically acceptable time frame after receipt of the flu vaccine. Thus, petitioner does not
prevail on Prong Three.

IV.    Conclusion
       For the foregoing reasons, petitioner’s claim for Program compensation must fail
and the petition SHALL BE DISMISSED. The Clerk of Court shall enter judgment
consistent with this decision.34
       IT IS SO ORDERED.
                                                        s/Patricia E. Campbell-Smith
                                                        Patricia E. Campbell-Smith
                                                        Chief Special Master

34
        Pursuant to Vaccine Rule 11(a), entry of judgment is expedited by the parties’ joint
filing of notice renouncing the right to seek review.
                                             32