1

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

Filed: October 13, 2015

* * * * * * * * * * * * * * * * * * * * * * * * *

JEREMIAH MEANS, * PUBLISHED

* No. 12-740V

Petitioner, *

v. * Chief Special Master Dorsey

*

SECRETARY OF HEALTH * Entitlement; Tetanus Diphtheria and

AND HUMAN SERVICES, * acellular-Pertussis (“Tdap”) vaccine;

* Influenza (“flu”) vaccine;

Respondent. * Susac’s Syndrome;

* Significant Aggravation. 

* * * * * * * * * * * * * * * * * * * * * * * * *

Donald P. Edwards, Law Office of Donald P. Edwards, Atlanta, GA, for petitioner.

Glenn A. MacLeod, United States Department of Justice, Washington, DC, for respondent.

RULING ON ENTITLEMENT1

I. INTRODUCTION

On November 1, 2012, Jeremiah Means (“petitioner” or “Mr. Means”) filed a petition for 

compensation under the National Vaccine Injury Compensation program (“the Program”)2

alleging that as a result of receiving an influenza (“flu”) vaccination on November 6, 2009, and a 

tetanus, diphtheria, and acellular-pertussis (“Tdap”) vaccination on November 7, 2009, he 

suffered hearing loss, generalized weakness, and gait instability. Petition at ¶¶ 1, 7. Petitioner 

later developed his claim to allege that the vaccinations at issue significantly aggravated his 

 

1 Because this published ruling contains a reasoned explanation for the action in this case, the 

undersigned intends to post this decision on the website of the United States Court of Federal 

Claims, in accordance with the E-Government Act of 2002 § 205, 116 Stat. 2899, 2913 (Dec. 17, 

2002) (codified as amended at 44 U.S.C. § 3501 (2014)). In accordance with the Vaccine Rules, 

each party has 14 days within which to request redaction “of any information furnished by that 

party: (1) that is a trade secret or commercial or financial in substance and is privileged or 

confidential; or (2) that includes medical files or similar files, the disclosure of which would 

constitute a clearly unwarranted invasion of privacy.” Vaccine Rule 18(b). Further, consistent 

with the rule requirement, a motion for redaction must include a proposed redacted ruling. If, 

upon review, the undersigned agrees that the identified material fits within the requirements of 

that provision, such material will be deleted from public access.

2 The Program comprises Part 2 of the National Childhood Vaccine Injury Act of 1986, 42 

U.S.C. §§ 300aa-10 et seq. Hereafter, individual section references will be to 42 U.S.C. § 300aa.
2

Susac’s Syndrome; or alternatively, that the vaccinations caused him to suffer an encephalopathy 

as described in the Vaccine Injury Table (“Table”)3. See Petitioner (“Pet’r”) Prehearing 

Submission at 1; Pet’r Posthearing Brief at 1. Respondent recommends against compensation, 

stating petitioner has not met his burden of showing that the vaccinations at issue significantly 

aggravated his Susac’s Syndrome. Respondent (“Resp’t”) Posthearing Brief at 26. Respondent 

further argues that the evidence does not demonstrate that petitioner suffered a Table 

encephalopathy; or alternatively, respondent argues that the weight of the evidence shows

petitioner’s alleged encephalopathy was caused by his Susac’s Syndrome, a factor unrelated to 

the vaccines. Id. at 17, 24. 

The parties filed expert reports in support of their respective positions. Petitioner filed 

two reports from his treating neuro-immunologist, Dr. John Rinker. See Exhibit (“Ex.”) 9, 16-2. 

Respondent filed a report from a neuro-immunologist, Dr. Subramaniam Sriram. See Ex. A. An 

entitlement hearing was held on December 17, 2014, where Mr. Means and his wife, Ashley 

Means, testified. Dr. Rinker testified as an expert witness on behalf of petitioner, and Dr. Sriram 

testified as an expert for respondent. Additionally, both parties filed respective prehearing 

submissions, a joint prehearing submission, and posthearing briefs. 

The parties agree that petitioner received two covered vaccines, flu and Tdap, and agree

that petitioner experienced headache symptoms prior to receipt of the vaccines. Amended 

(“Am.”) Joint (“J.”) Prehearing Submission (“Sub.”) at 1-2. They also agree that petitioner was 

correctly diagnosed with Susac’s Syndrome and that he suffered residual effects or complications 

of his alleged vaccine injury for more than six months. Id. at 2. At the hearing, petitioner further 

argued that the Tdap vaccine caused him to suffer a Table encephalopathy within seventy-two 

hours of vaccination. Tr. at 108-114. He provided testimony from Dr. Rinker in support of this 

claim and respondent provided testimony from Dr. Sriram in rebuttal. Therefore, the issues to be 

decided are whether petitioner’s Susac’s Syndrome was significantly aggravated by his flu 

vaccination, Tdap vaccination, or a combination thereof; and whether as a result of receiving a 

Tdap vaccination petitioner suffered a Table encephalopathy within the requisite time period. 

Based on a review of the entire record, the undersigned finds by preponderant evidence 

that petitioner suffered a significant aggravation of Susac’s Syndrome under Loving v. Sec’y of 

Health & Human Servs., 86 Fed. Cl. 135 (2009). Accordingly, petitioner is entitled to 

compensation on the significant aggravation claim. Because the undersigned finds that petitioner 

is entitled to compensation, a decision or ruling on the issue of the Table claim is not reached.

 

3 A “Table” injury is an injury listed on the Vaccine Injury Table, 42 C.F.R. § 100.3, 

corresponding to the vaccine received within the specified time frame. 
3

II. BACKGROUND

A. Summary of Relevant Facts4

Mr. Means was twenty-four years old when he received a flu vaccination on November 6, 

2009, and a Tdap vaccination on November 7, 2009. Petition at ¶ 2. Prior to his vaccinations, Mr. 

Means had an unremarkable medical history and lived an active lifestyle. Id. at ¶ 7. He received 

the vaccines while participating in a monthly drill exercise with the United States Air Force 

Reserve (“Air Force”). Hearing Transcript (“Tr.”) at 9-11. As a reserve flight medic, Mr. Means 

regularly engaged in physical activity, as his job required carrying and loading heavy medical 

equipment onto military planes to care for those on board. Tr. 64-65. In the weeks prior to his 

vaccinations, Mr. Means underwent physical training in hopes of becoming an active duty Air 

Force SERE5specialist. Tr. 21-22; 73-74. When not working in the reserve, he was employed 

full time as an emergency medical technician at St. Francis Hospital in Columbus, Georgia. Tr. 

61.

Concerning the events leading up to vaccination, Mrs. Means testified that on the 

afternoon of Sunday, November 1, 2009, petitioner and his father repaired the roof of a shed by 

placing plywood underneath a tin covering. Tr. 12-13, 83. Petitioner testified that he did not wear 

sunglasses while he worked, and as a result developed a “twinge of a headache.” Tr. 83. Mrs. 

Means recalled her husband complaining of a headache later that Sunday and remembers 

reprimanding him for causing his own headache by not wearing sunglasses. Tr. 13. 

According to Mr. and Mrs. Means, Mr. Means’ headache resolved after several days and 

was gone prior to his vaccinations on November 6 and 7, 2009. Specifically, when the 

undersigned asked whether petitioner experienced a headache on Wednesday, November 4, 

2009—the day he arrived at Maxwell Air Force Base for his monthly drill exercise—Mr. Means 

testified that he did not. Tr. 88. When asked whether he had a headache on Thursday, November 

5, 2009, he replied that he did not. Tr. 89-90. Further, Mr. Means testified that he received the flu

vaccine on Friday, November 6, 2009, and that he did not experience a headache on that day. Tr. 

91. Mrs. Means testified that her husband did not complain of a headache until the following 

Sunday, November 8, 2009, after his vaccinations. Tr. 11-12.

On Saturday, November 7, 2009, Mr. Means received the Tdap vaccine. Ex. 1 at 1. 

Although he could not recall the exact time of day he received it, he estimated that he must have 

been vaccinated in the morning, as he remembered being told “to go back to the clinic and get 

another vaccine” when he arrived for drill that day. Tr. 91. 

Petitioner testified that he began to experience a headache sometime after his vaccination

 

4 This Summary of Facts section only contains a review of the most relevant facts, although the 

undersigned has considered the record as a whole in reaching her decision in this ruling. A more 

detailed recitation of the facts may be found in Respondent’s Rule 4 report and in the parties’ 

respective prehearing and posthearing briefs. 

5 SERE is an acronym for Survival, Evasion, Resistance, and Escape specialty training. Tr. 73-

74.
4

on Saturday, November 7, 2009, and that it progressively worsened into the morning of Sunday, 

November 8, 2009. Tr. 92 -93. Petitioner characterized the headache as unlike what he had 

experienced the week before. Petitioner testified that he felt pressure at the base of his head

which “felt like [he] was in a pool and [that he] was drowning.” Tr. 84. At some point on 

Sunday, this pressure became “more of [a] stabbing sensation,” that would not “go away.” Tr. 

94-95. On the drive back home to Columbus, Georgia, the Sunday evening after drill, petitioner 

experienced a severe headache and the onset of “flashes of firecracker light.” Tr. 12; see also Ex.

2 at 37. 

The contemporaneous medical records reflect that on Monday afternoon, November 9, 

2009, petitioner visited his primary care physician, Dr. Terry Cone, complaining of a “headache,

since Sunday.” Ex. 2 at 37. Dr. Cone noted that petitioner felt as though his head would 

“explode” when he bent down below his chest. Id. Dr. Cone also noted petitioner’s complaints of 

photophobia and blurring vision. Id. He ordered an MRI of the brain, which was performed on 

that Monday evening at an outpatient radiology center. Id. at 13. Petitioner was accompanied by 

his wife to obtain the MRI. Tr. 48-49. Mrs. Means testified that in the moments leading up to the 

scan, petitioner was “really restless and irritable,” “agitated” and behaved uncharacteristically. 

Tr. 48-49. She further testified that he complained about “how much the sound and the light in 

the MRI [bothered] him.” Tr. 48. Petitioner testified that “every sound was hurting his head,”

and as a result he had a difficult time lying still. Tr. 98-99. The MRI report noted that part of his 

study was “technically unreadable because of motion and/or artifact or both.” Ex. 2 at 13.

Otherwise, the study was unremarkable and revealed normal results. Id.

At 7:00 p.m. Monday evening, November 9, 2009, petitioner went to work a twelve hour 

shift in the emergency department (“ED”) at St. Francis Hospital. He testified that while at work, 

his colleagues encouraged him to “lie down and put on oxygen” in response to his complaints of 

a severe headache. Tr. 99-100. Although petitioner treated himself with nasal cannula of oxygen,

this did not alleviate his headache symptoms. Tr. 100. Petitioner returned home from his shift at

7:00 a.m. Tuesday morning, November 10, 2009. Petitioner does not recall any events from after 

he returned home or leading up to his hospitalization later that day. Id.

Mrs. Means testified that she did not notice anything unusual about Mr. Means on 

Tuesday morning, November 10, 2009, as she only saw him in passing when she was leaving 

their home to go to work. Tr. 16. When she returned around 3:00 p.m. in the afternoon, she put 

their one-year old child down for a nap and sat in the living room. Id. She assumed Mr. Means 

was sleeping, as this was his usual routine, so she minimized any disturbances. Id. Mrs. Means 

testified that on this afternoon, Mr. Means’ behavior was dramatically unusual, in that:

[he] would get up and come storming into the living room cussing, which was 

very out of character, very unusual for him. [He] was cussing, was yelling, was 

angry, was telling me why was I being so loud, what is all the noise for, I can’t 

take it, you’ve got to stop. And then would go back in [their] room, and he would 

be curled up in a ball rocking back and forth holding his head. ‘I can’t take it 

anymore. I can’t take it. It’s just got to end. It’s just got to stop. I can’t do this 

anymore.’ And then two seconds later, he’d be quiet like he was sleeping. And ... 

then it would start all over again. He’d come back out yelling and cussing and 
5

going on about so much noise. [However,] I wasn’t making any noise. The baby 

was sleeping, and I was sitting at the kitchen table reading a book. 

Id.

Mrs. Means testified that this cycle progressively worsened. Tr. 17. Around 6:30 p.m.,

she called Dr. Cone’s office to ask whether the MRI results revealed any abnormalities, but they 

replied that it had not. Id. Mrs. Means was then instructed to obtain Stadol pain medication from 

the nearest pharmacy. Tr. 17-18. She left with their baby for the pharmacy and while there

received a telephone call from Mr. Means’s father inquiring as to his son’s well-being. Tr. 18. 

Mr. Means testified that he apparently called his father while his wife was away, a fact Mr. 

Means does not recall but was later told by his father. Tr. 76. Mr. Means also testified that his 

father told him that when he arrived at his son’s home that night, Mr. Means did not know how 

to unlock the dead bolt on the front door and that it took him a long time to comprehend what 

was being asked of him. Tr. 76-77.

Mrs. Means testified that when she got home from the pharmacy with the medication, 

petitioner’s parents were there. Tr. 18. She stated that at that point, petitioner recognized his 

father, but he did not recognize her or his mother. Id. He could not tolerate any sound or light, 

and he was still swearing, crying, rocking, and holding his head. Id. They decided to take him to 

the ED, but he could not walk down the stairs to get into the car, so they called an ambulance. Id.

The paramedics that arrived recognized petitioner from his work at the ED, however, he did not 

recognize his colleagues. Tr. 19. The paramedics used a lift chair to move petitioner from his 

upstairs bedroom to the ambulance. Tr. 20. 

Petitioner was then transported to the St. Francis Hospital ED. Mrs. Means described 

petitioner’s behavior at the hospital as “very combative, very aggressive, angry, irritated, very 

disoriented, confused,” and he did not recognize his co-workers. Tr. 20. Mrs. Means testified that 

prior to this episode, petitioner “was a very friendly guy.” Tr. 19. “He never met a stranger” and 

“knew everybody.” Id. He was admitted to St. Francis Hospital on Tuesday, November 10, 2009.

See Ex. 3.

The medical records reveal that petitioner was admitted to the hospital for headache, 

dizziness, scotoma, seeing flashing lights, nausea, and vomiting. Ex. 3 at 2. The hospitalist noted 

that the intake examination was incomplete due to petitioner’s “combativeness.” Id. Petitioner’s 

parents reported to the hospitalist that he had been experiencing these symptoms over the 

previous five days. Id. at 2, 13. However, as Mrs. Means testified, this report was inaccurate with 

respect to the fact that petitioner’s parents did not visit with their son after Sunday, November 1, 

and before Tuesday, November 10, and thus would not have been in the position to report a

medical history of the five days leading up to his hospitalization on November 10. Tr. 38. 

The consulting neurologist at the ED, Dr. Jagdish Sidhpura, incorporated the hospitalist’s

and Dr. Cone’s histories into his own neurology evaluation on November 10, 2009. Ex. 3 at 13. 

Dr. Sidhpura noted petitioner’s CAT scan of the brain was unremarkable. Id. He also noted, 

although erroneously, that petitioner received a flu vaccine two weeks prior to his 
6

hospitalization. Id.

6 Dr. Sidhpura further noted that petitioner had no history of migraines or 

seizures and that this episode was very unusual for him. Id. Physical examination revealed 

“intense photophobia.” Id. at 14. A cerebrospinal fluid (“CSF”) analysis revealed elevated 

protein levels. Id. at 15. Dr. Sidhpura diagnosed a “[one] week history of continuous headaches 

with acute encephalopathy, especially confusion and combative behavior.” Id. at 14.

An electroencephalography (“EEG”) performed on Wednesday, November 11, 2009, was 

“grossly abnormal,” showing “an acute encephalopathic process, most likely of toxic metabolic 

etiology.” Ex. 2 at 10. An MRI of the brain, performed on November 13, 2009, suggested 

possible “edema associated with recent trauma, including diffuse axonal injury” in both 

hemispheres and a large lesion in the splenium of the corpus callosum. Ex. 3 at 23; Tr. 213. 

Mr. Means was transferred to the University of Alabama Birmingham Hospital (“UAB”) 

on November 15, 2009. Ex. 2 at 16. The attending neurologist diagnosed probable acute 

disseminated encephalomyelitis (“ADEM”)7based on demyelinating white matter lesions visible

on the MRI. Ex. 4 at 3. The doctor prescribed an intravenous corticosteroid, called IV-SoluMedrol. Id. A repeat EEG on November 17, 2009, indicated “a severe encephalopathic process . . 

. affecting both [brain] hemispheres.” Id. at 47. The EEG revealed frontal intermittent rhythmic 

delta activity (“FIRDA”), which the physician noted “often implies a metabolic or toxic cause, 

but could also indicate subfrontal lesions.” Id. An MRI performed on November 19, 2009,

produced limited images due to Mr. Mean’s inability to keep still. Id. at 24. The MRI confirmed 

brain lesions, although the lesions appeared “less conspicuous” compared to prior studies. Id.

Lumbar punctures performed on November 17, 2009, and November 20, 2009, revealed that his 

CSF had elevated protein levels and myelin based proteins. Id. at 47, 49.

Petitioner was discharged from UAB on November 24, 2009, with a diagnosis of ADEM 

with cognitive and gait impairments. Ex. 4 at 44. The discharge summary noted that petitioner

was “profoundly encephalopathic upon presentation,” and that he showed “significant clinical 

improvement after a five day course of IV Solu-Medrol, but that his gait and movements were 

abnormal and uncoordinated. Id. at 45. He was transitioned to Spain Rehabilitation Center for 

further physical and occupational therapies. Id. at 46-47. He was prescribed oral steroid 

medication, as well as Keppra for seizure prevention. Id. at 46.

Mr. Means received therapy at Spain Rehabilitation Center until November, 27, 2009, 

when he was transferred back to UAB after becoming unresponsive in the shower. Ex. 4 at 50. 

During his relapse, he was noted to have experienced tonic clonic movements in his left lower 

extremity, as well as decreased consciousness with a left-preferred gaze. Id. He was also noted to 

be drooling and experiencing difficulty hearing. Id.; Tr. 80-81. A November 27 MRI of the brain

showed worsening periventricular and corpus callosum lesions, consistent with diffuse 

encephalitis. Ex. 4 at 72. He was started on a seven day course of IV Solu-Medrol, to no avail. 

Id. at 80. He then completed five days of plasma exchange treatments. Id. He experienced some

 

6

In fact, petitioner received a flu vaccination four days prior to his hospitalization and received a 

Tdap vaccination a day after the flu vaccine, three days prior to hospitalization. See Ex. 1 at 1.

7

“ADEM is an initial inflammatory, demyelinating event with multifocal neurologic deficits, 

typically accompanied by encephalopathy.” Nelson Textbook of Pediatrics 2079 (19th ed. 2011).
7

improvement in his condition after the second exchange treatment. Id. Petitioner was discharged 

from UAB and sent back to Spain Rehabilitation Center on December 17, 2009. 

Petitioner completed rehabilitation and was discharged and returned home on January 7, 

2010. Ex. 4 at 144-48. Upon discharge, a neuro-psychological evaluation revealed evidence of 

decreased attention, severe hearing loss in his right ear, problems with fine motor dexterity, and 

severe global cognitive deficits, including poor memory, poor processing speed, and poor use of 

language. Id. at 145-46. His treating physicians recommended that he not return to work and that 

he receive daily supervision. Id. at 146. 

On March 25, 2010, Mr. Means began treatment with a neurologist, Dr. John Rinker. Ex.

4 at 188. Based on a history provided by Mr. Means and his wife, Dr. Rinker recorded that on 

November 1, 2009, Mr. Means experienced an unrelenting and atypical headache. Id. Dr. Rinker 

further noted, “About a week later, [Mr. Means] had his regular seasonal flu vaccination,” and 

about three days later, due to persistent headaches, he obtained a routine MRI. Id.

Concerning Mr. Means’ condition at that time, Dr. Rinker noted that Mr. Means was 

“quite a bit better,” and he was able to walk, although he had some ongoing balance and 

coordination difficulties. Ex. 4 at 188. He also noted that Mr. Means continued to have hearing 

loss and cognitive difficulties. Id. At the time, Dr. Rinker believed Mr. Means experienced “an 

episode of ADEM,” however, he later opined that “the ADEM label was an incorrect diagnosis” 

in light of petitioner’s subsequent diagnosis of Susac’s Syndrome. Tr. 132. In March 2010, Dr. 

Rinker recommended that petitioner continue physical and occupational therapies, and to refrain 

from resuming work. Ex. 4 at 190.

Mrs. Means testified that petitioner’s mobility, balance and coordination was poor in the 

months following his release from the hospital. Tr. 28. She further testified that petitioner was 

forgetful and would get confused over simple daily activities, such as getting dressed, showering 

and brushing his teeth. Id. He would easily become “very angry” and lacked self-control in 

“dealing with everyday life.” Tr. 28, 31. She testified that “his mentality seemed like he reverted 

to . . . a ten-or-[twelve] year old.” Tr. 28-29. According to Mrs. Means, petitioner was in speech, 

physical and occupational therapies three to four days per week, and his physical and speech 

therapies continued over the next two years. Tr. 30; see also Ex. 5, 13. 

A neuro-psychological evaluation on April 26, 2010, noted, “[W]hile Mr. Means 

show[ed] a lack of improvement in some areas of neuropsychological functioning, he [had] 

improved significantly in his daily functioning.” Ex. 4 at 213. “His stable performance across 

two months in some areas suggest[ed] that the prognosis for further improvement [was] guarded, 

and he may continue to experience residual deficits in processing speed, memory, and executive 

function.” Id. The evaluation further noted that his reasoning skills were variable. Id.

Mr. Means had a follow-up evaluation with Dr. Rinker on May 27, 2010. Dr. Rinker 

noted that Mr. Means had tapered off prednisone since his March 2010 visit and that his 

condition had since stabilized, although his hearing continued to suffer. Ex. 4 at 191. Petitioner’s 

May 2010 MRI showed improvement with residual atrophy. Id. at 193. Dr. Benjamin McGrew, 

an otolaryngologist, fitted Mr. Means with a hearing aid in August 2010 and anticipated that his 
8

hearing would continue to improve “if his demyelination process improves.” Id. at 226. 

On November 11, 2010, Mr. Means visited Dr. Rinker “on an urgent basis for follow-up 

of presumed ADEM.” Ex. 14-3 at 23. Mr. Means reported that “a little over a week” prior, he 

began having a new onset headache, increasing somnolence, and had been sleeping for days at a 

time. Id. By way of a telephone communication the week prior to his visit, Dr. Cone prescribed 

Prednisone for petitioner’s headache. Ex. 12 at 1. Mr. Means reported that the prednisone 

afforded him some relief but that he was also experiencing some vision difficulties in both eyes. 

Ex. 14-3 at 23. Dr. Rinker believed petitioner was experiencing new neurological symptoms; 

particularly optic neuritis in his right eye and possibly an increase in gait ataxia.8Id. at 24. He 

noted that petitioner’s disease “could be [evolving] into a different demyelinating condition, such 

as recurrent ADEM or more atypically, ... neuromyelitis optica, or Susac’s Syndrome.” Id.

Upon review of petitioner’s November 2010 MRIs, Dr. Rinker noted new areas of abnormality. 

Id.

Several days after his visit with Dr. Rinker, petitioner was hospitalized for worsening

symptoms. Ex. 14-3 at 24. A subsequent ophthalmological evaluation revealed retinal artery 

occlusions. Id. As a result, he was diagnosed with Susac’s Syndrome, based on the triad of 

encephalopathy, hearing loss, and retinal artery occlusions. Id. Mr. Means was initially treated 

with daily immunosuppressants, CellCept and Prednisone; however, when that course of 

treatment failed, he was then started on six cycles of a chemotherapeutic agent, 

cyclophosphamide. Ex. 10 at 3. Mr. Means responded well to this therapy, and presently, his 

condition has been largely stabilized, although he continues to have severe deficits in hearing, 

balance, memory, reasoning, and emotional maturity. Id.; Tr. 32, 172. 

As a preliminary matter, the undersigned notes that petitioner aptly testified concerning 

the events leading up to his vaccinations and the onset of his symptoms, despite the fact that due 

to his health condition, his memory failed him with regard to the immediate events after receipt 

of the vaccines. Moreover, Mrs. Means provided credible testimony as to critical events in the 

days before and after petitioner’s vaccinations. As such, the undersigned fully credits their 

testimony, particularly when corroborated by the contemporaneous medical records.

B. Susac’s Syndrome

Susac's Syndrome (“SS”) is a condition diagnosed in patients who experience an 

identifiable triad of symptoms: an encephalopathy, branch retinal artery occlusion (“BRAO”), 

and hearing loss (“HL”). Ex. E at 86.

9 This condition is an autoimmune endotheliopathy,10

usually affecting young women ages twenty to forty. Id. SS was first reported by Dr. John O. 

Susac in 1979, when he treated two women who presented with encephalopathic symptoms, 

 

8 Ataxia is a “failure of muscular coordination; irregularity of muscular action.” Dorland’s 

Illustrated Medical Dictionary 170 (32d ed. 2012) [hereinafter “Dorlands”].

9 Some of the referenced documents are not numbered. In those cases, the undersigned 

references the PDF page number.

10 A pathology affecting the blood vessels. See Dorlands, supra note 8, at 621.
9

vision loss, and hearing loss caused by small strokes in the brain, retina and cochlea. Ex. 20 at 1. 

As of 2010, there have been over 200 cases reported. Ex. E at 86. An article published by Dr. 

Robert Rennebohm and Dr. Susac,11 among others, notes: 

When only the encephalopathy is present—or when the other [two] components 

of the triad are not recognized—some clinicians fail to consider SS. Instead, a 

mistaken diagnosis of multiple sclerosis (“MS”) or acute disseminated 

encephalomyelitis (“ADEM”) is made and the patients are treated with a 

relatively brief course of corticosteroids. Initial improvement may seemingly reenforce the misdiagnosis, but relapse occurs when corticosteroids are tapered or 

stopped.

Id.

According to respondent’s expert, Dr. Subramaniam Sriram, since the initial discovery of 

the disease in 1979, the triad of symptoms necessary to make the diagnosis has evolved to a 

tetrad, and evidence of MRI abnormalities in the corpus callosum of the brain is used to confirm

the diagnosis. Tr. 193. The Rennebohm and Susac article notes, “In the encephalopathic form of 

SS, the corpus callosum is always involved. Usually, callosal microinfarctions are the 

predominant findings . . . .” Ex. E at 86. Rennebohm and Susac assert that the “diagnosis of SS 

can be made with certainty in an encephalopathic patient when the [] pathognomonic corpus 

callosal findings are present, even in the absence of BRAO and HL . . . .” Id. at 87.

Rennebohm and Susac also note:

It is important to distinguish between the ‘encephalopathic form of SS’ and the 

‘recurrent BRAO subset.’ The encephalopathic form is characterized by the 

predominance of encephalopathy at the time of diagnosis, or at the time of peak 

disease severity. BRAO, hearing loss, or both, may precede, accompany, or

follow the encephalopathy, but it is the encephalopathy that dominates the clinical 

picture and dictates the treatment needs. The encephalopathic form is the most 

well-known and probably accounts for the majority of definite cases of SS.

Id. at 89. The BRAO subset of SS is characterized by a less severe and prolonged course of 

recurrent episodes of active retinal vasculopathy, with “symptomatic BRAO at one end of the 

spectrum and asymptomatic [arteriolar wall hyperfluorescence] at the other.” Id. at 89-90. 

Dr. Sriram, and petitioner’s expert, Dr. Rinker, both agree that information regarding the

pathogenesis and natural history of the disease is lacking. Tr. 124, 193. Indeed, Rennebohm and 

Susac state, “Much remains to be learned about the immunopathogenesis, natural history, clinical 

characteristics, optimal treatment, and ultimate outcome of SS.” Ex. E at 91. However, there is a 

working consensus that the disease is immune-mediated, as patients respond well to 

immunosuppressive treatment. Id.; see also Tr. 121-22, 191. 

 

11 Robert Rennebohm, John O. Susac, Robert A. Egan, & Robert B. Daroff, Susac’s Syndrome –

Update 299 J. of Neuro. Sci. 86 (2010).
10

III. EXPERT CREDENTIALS

A. Petitioner’s Expert, Dr. John Rinker II

Petitioner’s treating neurologist, Dr. John Rinker II, testified on petitioner’s behalf as an 

expert witness. Dr. Rinker obtained his undergraduate degree from Wake Forest University and 

his medical degree from the Medical College of Georgia. Tr. 106. He completed his internship 

and residency training in the field of neurology at Washington University in St. Louis. Id. He 

followed his residency training with a two-year fellowship in both neuro-immunology and 

multiple sclerosis at Washington University. Id. In addition to his clinical practice as a neuroimmunologist at the University of Alabama at Birmingham Hospital, Birmingham Virginia 

Medical Center, and Cooper Green Hospital, he is an Associate Professor of Neurology at the 

University of Alabama, Birmingham. Id.; Ex. 9 at 48. He treats patients with a variety of neuroimmunological disorders, including two patients with Susac’s Syndrome (petitioner included). 

Tr. 123; Ex. 9 at 51.

B. Respondent’s Expert, Dr. Subramaniam Sriram

Dr. Subramaniam Sriram is a professor of neurology and microbiology immunology at 

Vanderbilt Medical Center, where he has been on the faculty for approximately eighteen years. 

Ex. B at 1; Tr. at 184. He obtained both his undergraduate and medical degrees from the 

University of Madras in Madras, India. Ex. B at 1. He completed his internship and residency in 

internal medicine at Wayne State University, followed by a residency in neurology at Stanford 

University. Id. He also completed a post-doctoral fellowship at Stanford University in neuroimmunology. Id. He is board certified in internal medicine, neurology and psychiatry. Id. He is 

the associate editor of the Journal of Immunology and has served as a reviewer of several 

neurology and immunology journals. Tr. 184. In 2009, he co-authored an article12 concerning a

series of patients with Susac’s Syndrome treated at the Vanderbilt Medical Center. See generally

Ex. D. Along with his teaching responsibilities at Vanderbilt Medical Center, Dr. Sriram also 

directs its Multiple Sclerosis Clinic. Tr. 185. 

IV. STANDARDS FOR ADJUDICATION

The Vaccine Act was established to compensate vaccine-related injuries and deaths. § 

300aa-10(a). “Congress designed the Vaccine Program to supplement the state law civil tort 

system as a simple, fair and expeditious means for compensating vaccine-related injured persons. 

The Program was established to award ‘vaccine-injured persons quickly, easily, and with 

certainty and generosity.’” Rooks v. Sec’y of Health & Human Servs., 35 Fed. Cl. 1, 7 (1996) 

(quoting H.R. Rep. No. 908 at 3, reprinted in 1986 U.S.C.C.A.N. at 6287, 6344)).

A petitioner’s burden of proof is by a preponderance of the evidence. § 300aa-13(a)(1). 

The preponderance standard requires a petitioner to demonstrate that it is more likely than not 

that the vaccine at issue caused the injury. Moberly v. Sec’y of Health & Human Servs., 592 

F.3d 1315, 1322 n.2 (Fed. Cir. 2010). Proof of medical certainty is not required. Bunting v. Sec’y 

 

12 See Siddharama Pawate et al., The Spectrum of Susac’s Syndrome, 30 Neurol. Sci. 59-64 

(2009) [Ex. D]. 
11

of Health & Human Servs., 931 F.2d 867, 873 (Fed. Cir. 1991). In particular, petitioners must 

prove that 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 who satisfies this burden is 

entitled to compensation unless respondent can prove, by a preponderance of the evidence, that 

the vaccine’s injury is “due to factors unrelated to the administration of the vaccine.” § 300aa13(a)(1)(B).

V. EXPERT OPINION AND CAUSATION ANALYSIS

A. Issue

The issue to be resolved is “whether the influenza or Tdap vaccine[s] that the petitioner 

received on [November 6, and November 7, 2009], substantially contributed to a significant 

aggravation of a pre-existing injury.” See Am. J. Prehearing Sub. at 2.13

B. Legal Framework

To receive compensation under the Program, petitioner must prove one of the following: 

(1) that he suffered a “Table Injury”—i.e., an injury listed on the Vaccine Injury Table within the 

requisite time period—corresponding to a vaccine that he received, (2) that he suffered an injury 

that was actually caused by one or both of the vaccines he received, or (3) that he suffered 

significant aggravation of a preexisting illness as a result of a one or both of the vaccines. See 42 

U.S.C. §§ 300aa-13(a)(1)(A) and 11(c)(1). Petitioner must show that a 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)). If a petitioner 

alleges an injury that is not listed on the Table, the vaccine claim is deemed a non-Table case, 

and there is no presumption of causation. Rather, as in this case, a claim alleging significant 

aggravation must satisfy the burden of proof described in Loving, 86 Fed. Cl. at 144.

To establish that a condition was significantly aggravated by a covered vaccine, 

petitioner must establish, by preponderant evidence: 

(1) the person’s condition prior to administration of the vaccine, (2) the person’s

current condition (or the condition following the vaccination if that is also 

pertinent), (3) whether the person’s current condition constitutes a significant 

aggravation of his condition prior to vaccination, (4) a medical theory causally 

connecting such a significantly worsened condition to the vaccination, (5) a 

logical sequence of cause and effect showing that the vaccination was the reason 

for the significant aggravation, and (6) a showing of a proximate temporal 

relationship between the vaccination and the significant aggravation

 

13 Petitioner has proven significant aggravation, thus it is dispositive of the issue of whether the 

Tdap vaccine caused petitioner to suffer a Table encephalopathy within seventy-two hours of 

vaccination. Accordingly, that issue will not be addressed.
12

Id. (internal quotations omitted).

The causation theory must relate to the injury alleged. Thus, petitioner must provide a 

reputable medical or scientific explanation that pertains specifically to this 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). Petitioner cannot 

establish entitlement to compensation based solely on his assertions. Rather, a vaccine claim 

must be supported either by medical records or by the opinion of a medical doctor. § 300aa13(a)(1). In determining whether petitioner is entitled to compensation, the undersigned shall 

consider all material contained in the record, § 300aa-13(b)(1), including “any . . . conclusion, 

[or] medical judgment . . . which is contained in the record regarding . . . causation.” § 300aa13(b)(1)(A). The undersigned must weigh the submitted evidence and the testimony of the 

parties’ offered experts and rule in petitioner’s favor when the evidence weighs in his favor. See

Moberly, 592 F.3d at 1325-26 (“Finders of fact are entitled—indeed, expected—to make 

determinations as to the reliability of the evidence presented to them and, if appropriate, as to the 

credibility of the persons presenting that evidence”); Althen, 418 F.3d at 1280 (“close calls” are 

resolved in petitioner’s favor).

Another important aspect of the causation-in-fact case law under the Vaccine Act

concerns the factors that a special master should consider in evaluating the reliability of expert 

testimony and other scientific evidence relating to causation issues. In Daubert v. Merrell Dow 

Pharm., Inc., 509 U.S. 579 (1993), the Supreme Court listed certain factors that federal trial 

courts should utilize in evaluating proposed expert testimony concerning scientific issues. In 

Terran v. Sec’y of Health & Human Servs., 195 F.3d 1302, 1316 (Fed. Cir. 1999), the Federal 

Circuit ruled that it is appropriate for special masters to utilize Daubert’s factors as a framework 

for evaluating the reliability of causation-in-fact theories presented in Program cases.

C. Loving Analysis

(1) Loving Prong One: Petitioner’s condition prior to administration of the 

vaccinations.

The first of the Loving factors requires defining petitioner’s condition before he received 

the vaccinations at issue. The parties agree that petitioner’s headache symptoms pre-dated his 

receipt of the flu and Tdap vaccines on November 6 and 7, 2009, respectively. Am. J. Prehearing 

Sub. at 1-2. Additionally, both experts agree that petitioner’s correct diagnosis is Susac’s 

Syndrome and that a headache can be the first symptom of that condition. Tr. 131-33; 191-94. 

Prior to his vaccinations, Mr. Means had an unremarkable medical history and lived an 

active lifestyle. Petition at ¶ 7. Petitioner’s testifying expert and treating neurologist, Dr. Rinker, 

opined, “In November 2009, Mr. Means was a healthy [twenty-four] year old male, with no 

known physical, cognitive, or psychiatric problems . . . .” Ex. 16-2 at 2. As a reserve flight 

medic, Mr. Means regularly engaged in physical activity. Tr. 63-65. When not working in the 

reserve, he was employed full time as an emergency medical technician at St. Francis Hospital in 

Columbus, Georgia. Tr. 59.
13

Petitioner first experienced a headache on the afternoon of Sunday, November 1, 2009,

when he worked on a tin roof with his father. Tr. 12-13, 83. Petitioner attributed this headache to 

not wearing sunglasses to shield his eyes from reflecting rays of sunlight from the tin roof. Tr. 

83. When asked to describe his headache, petitioner described it as unremarkable and 

characterized it as a “twinge of a headache.” Id. On November 4, 2009, petitioner arrived at 

Maxwell Airforce Base with his wife and young child for monthly drill exercises with the Air 

Force Reserve. Tr. 10-11. Petitioner participated in drill exercises from November 4 through 7, 

2009. Id. Petitioner and Mrs. Means testified that petitioner’s headache resolved prior to his 

vaccinations on November 6 and 7, 2009. Tr. 11-12, 88-91 (petitioner testified that he did not 

experience a headache on November 4 through 6, 2009, and petitioner’s wife testified that 

petitioner did not complain to her of a headache until November 8, 2009). On November 8, 2009, 

petitioner experienced severe headache symptoms, which he characterized as a “stabbing 

sensation” that would not “go away.” Tr. 94-95. He visited his primary care doctor, Dr. Terry 

Cone, the next day. Dr. Cone’s records from November 9 and 10, 2009, noted that petitioner 

experienced a “headache since Sunday,” and that he presented on November 9 with a severe 

headache. Ex. 2 at 18, 37. Dr. Cone noted that this headache was ongoing for the previous eight 

days. Id. at 18.

The undersigned credits petitioner and Mrs. Means’ testimony as it suggests petitioner’s 

headache on November 1, 2008, was mild and either resolved or remained mild in the week 

leading up to his vaccinations. It is unlikely that petitioner would have been able to fully 

participate in drill exercises November 4-7 if his initial headache was of the same severity as he 

later experienced following his vaccinations. In the medical record from November 9, 2009, Dr. 

Cone noted that petitioner felt as though his head would “explode” when he bent down below his 

chest. Ex. 2 at 37. This is in stark contrast to what petitioner and his wife described as a “twinge” 

of a headache petitioner experienced on November 1. See Tr. 13, 83. Moreover, petitioner had no 

other signs or symptoms of illness. Accordingly, the undersigned finds that petitioner’s headache 

on November 1, 2009, either resolved prior to his vaccinations, or that it was mild and did not 

impair petitioner’s ability to participate in reserve drill exercises or activities of daily living. 

(2) Loving Prong Two: Petitioner’s condition following the vaccinations.

The second Loving factor to discuss is “the person’s current condition (or condition 

following the vaccination if that is also pertinent).” 86 Fed. Cl. at 144. Here, petitioner’s 

condition following his vaccinations is most pertinent.

Petitioner received a flu vaccination on Friday, November 6, 2009, and a Tdap 

vaccination on Saturday, November 7, 2009. Ex. 1 at 1. Petitioner and Mrs. Means testified that 

petitioner experienced a severe headache, as well as photophobia, on the evening of Sunday, 

November 8, 2009. Tr. 18; see also Ex. 2 at 37. When he visited Dr. Cone on Monday afternoon, 

November 9, 2009, Dr. Cone ordered an MRI of the brain, which was performed on that Monday 

evening. Id. Ex. 2 at 13. During the examination, petitioner was “really restless and irritable,” 

“agitated” and behaved uncharacteristically in the moments leading up to the study. Tr. 48. The 

sound and light of the MRI machine aggravated petitioner’s headache symptoms. Tr. 49, 98-99. 

The MRI report noted that part of his study was “technically unreadable because of motion 
14

and/or artifact or both.” Ex. 2 at 13. The study was unremarkable and revealed normal results. Id.

At 7:00 p.m. on Monday evening, November 9, 2009, petitioner went to work a twelve 

hour shift at the St. Francis Hospital ED. While at work he rested in an unused room at the 

behest of his colleagues due to his unbearable headache. Tr. 99-100. On Tuesday afternoon, 

November 10, 2009, petitioner came “storming into the living room cussing . . . yelling, [and] 

angry,” and he scolded Mrs. Means for making loud noise. Id. at 16. Petitioner would “then [] go 

back in [their] room, and would “curl[] up in a ball rocking back and forth holding his head,” all 

the while shouting “‘I can’t take it anymore. I can’t take it. It’s just got to end. It’s just got to 

stop. I can’t do this anymore.’” Id. Moments later, he would become “quiet like he was sleeping . 

. . and then it would start all over again. He [would] come back out yelling, [] cussing, and going 

on about so much noise . . . .” Id.

Petitioner was hospitalized for approximately two months at St. Francis Hospital. He 

developed severe hearing loss while hospitalized. See Ex. 4 at 146. Dr. Rinker began treating 

petitioner in March 2010, upon petitioner’s discharge from the hospital. Dr. Rinker opined, “The 

dramatic personality changes, physical disability, and hearing loss which followed [petitioner’s] 

initial hospitalization constitute[d] a dramatic and sustained change from the [petitioner’s] 

baseline functional status.” Ex. 16-2 at 2. Dr. Rinker stated, “Following [petitioner’s] initial 

hospitalization, [he] was unfit to return to military service, required cochlear implantation to 

regain hearing, and has been unable to return to meaningful work.” Id. He further stated that 

petitioner “continues to live with substantial disability. [Petitioner] requires a manual wheelchair

for most of his mobility . . . [and] [h]e is a fall risk when standing or attempting to walk.” Id.

Petitioner was re-hospitalized in November 2010 with recurring symptoms and newly 

developed optic neuritis in his right eye. See Ex. 14-3 at 24. An ophthalmological evaluation 

revealed retinal artery occlusions. Id. Although initially diagnosed with ADEM, petitioner was 

re-diagnosed with Susac’s Syndrome based on his presentation of encephalopathy, hearing loss, 

and retinal artery occlusions. Id. While petitioner’s condition has greatly improved over the last 

several months, he has not physically or mentally returned to his pre-vaccination state of health. 

He has diminished hearing which is corrected with the aid of a cochlear device. He currently 

ambulates in a wheelchair due to his general lack of coordination and inability to balance while

standing. Tr. 32-33; Ex. 10 at 2. Ms. Means testified that petitioner’s mental state is altered and 

that he “still has trouble with memory . . . [and] with reasoning, and he’ll still get fixated on 

things.” Tr. 32. 

(3) Loving Prong Three: Whether petitioner’s condition constitutes a 

“significant aggravation” of his condition prior to the vaccinations.

Concerning whether petitioner’s condition constituted a significant aggravation of his 

Susac’s Syndrome, Dr. Rinker acknowledged that some of petitioner’s medical records, 

including his own, noted that petitioner experienced a persistent and unrelenting headache prior 

to his vaccinations. Tr. 127-30. However, Dr. Rinker opined that dating the onset of petitioner’s 

condition cannot be done with certainty. Tr. 132-33. He posited that if we assume the earliest 

symptom of the clinical manifestation of his condition was the week prior to his vaccinations, 

“then the vaccine would certainly prove as an aggravator” based on the testimony and medical 
15

records. Tr. 132-33. Alternatively, according to Dr. Rinker, if the true initiating event of 

petitioner’s disease was the headache symptoms he experienced after his vaccinations, “then the 

disease itself may have actually begun after the administration of the vaccine[s].” Tr. 133. 

Dr. Rinker testified that, with respect to Susac’s Syndrome in general, a typical course 

might be a headache progressing to a personality change, followed by more intense symptoms of 

encephalopathy. Tr. 131. Additionally, a typical case might involve a headache and 

encephalopathy, followed by hearing loss or vision loss. Id. Medical literature14 indicates that 

partial forms of the syndrome have been reported in a number of patients; “for example, [some 

patients present with] cochlear and retinal involvement without cerebral symptoms . . . or 

cerebral and retinal involvement without hearing loss, or retinal involvement only.” Ex. 20 at 17.

With regard to petitioner’s course of the disease, assuming petitioner already had the 

beginning of Susac’s Syndrome “either in the days leading up to the administration of his 

vaccines or immediately following it,” Dr. Rinker opined that petitioner was experiencing mild

symptoms, namely headaches, without cognitive changes. Tr. 132. He further opined that, given 

the timing of the vaccinations, the fact that Susac’s Syndrome is an immune-mediated condition,

“and that vaccines by their nature are meant to provoke the immune system into mounting a 

response . . . [it is] more likely than not the vaccine[s] at least played a triggering role or an 

exacerbating role in the onset of [petitioner’s] disease.” Tr. 134. 

Respondent’s expert, Dr. Sriram, opined that there is no evidence to affirmatively

indicate the medical probability that the vaccines in question could significantly aggravate 

ongoing Susac’s Syndrome. Tr. 200. Dr. Sriram based his opinion on the fact that there is no 

evidence that the Tdap or flu vaccine could worsen an ongoing autoimmune disease. He also 

pointed out that some vaccines, such as tetanus, can actually reduce the incidence of Multiple 

Sclerosis. Id. Dr. Sriram noted that there are not very many cases of Susac’s Syndrome; 

however, of the sixteen patients with Susac’s Syndrome he currently follows, “about five of them 

presented with . . . an acute confusional state.” Tr. 194. About forty percent of his patients 

(approximately six patients) “had headache as a first feature” of the disease, due in part to the 

meninges, which are membranes that envelop the brain. Id. Dr. Sriram further testified that some 

of his patients with Susac’s Syndrome “presented, for example, only with encephalopathy, [and] 

nothing else—like Mr. Means did” and in those instances, he recommended aggressive treatment 

from the outset. Tr. 193-94. Dr. Sriram disagreed with Dr. Rinker’s testimony that symptoms of 

Susac’s Syndrome can resolve without treatment because, according to Dr. Sriram, “we do not 

know the natural history of the disease.” Tr. 193.

In Dr. Sriram’s view, “from the reports of both Dr. Terry Cone who initially saw 

[petitioner], as well as the emergency room physician . . . [petitioner’s headache] was an 

unrelenting, persisting headache in an otherwise healthy man.” Tr. 195. Accordingly, Dr. Sriram

 

14 George W. Petty et al., Retinocochleocerebral Vasculopathy, 77 Medicine 12, 18 (1998) [Ex. 

20]; see also Gennady Landa et al., Multiple Branch Retinal Arteriolar Occlusions Associated 

with Smallpox Vaccination, 52 J. of Infection e7, e8 (2005) (noting that a patient with Susac’s 

Syndrome “showed no evidence of sensory hearing loss,” a symptom “reportedly exhibited only 

by two out of three patients with Susac’s Syndrome”). 
16

believed that the first symptom of petitioner’s Susac’s Syndrome began on November 1, 2009. 

Id. at 194.

Dr. Sriram co-authored an article15 on Susac’s Syndrome in which he and his colleagues 

postulated that “it is not important that all three elements (encephalopathy, retinopathy infarcts, 

and cochlear infarcts) be present to make the diagnosis” of Susac’s Syndrome. Tr. 192. Rather, 

he recommended that patients receive treatment even when the full “symptom complex has not 

evolved.” Id. According to Dr. Sriram, “There is a very classical, typical pattern of involvement 

seen in the corpus callosum which makes a physician very suspicious about the diagnosis of 

Susac’s.” Tr. 193. The disease has “very particular features” radiologically, which are sufficient 

to make a diagnosis when one or two elements of the disease are present. Id. This view is echoed 

in an article co-authored by Dr. Susac providing an update on the nature of Susac’s Syndrome. 

See Ex. E. In that article, the authors “contend that a diagnosis of SS can be made with certainty 

in an encephalopathic patient when [] pathognomonic corpus callosal findings are present, even 

in the absence of BRAO and HL.” Id. at 87.

Dr. Sriram’s article, The Spectrum of Susac’s Syndrome, is a report on a series of four 

patients with Susac’s Syndrome. Of the four case reports discussed in the article, “the clinical 

presentations, [] MRI findings, and [] CSF findings were varied, with long temporal intervals 

between symptoms, resulting in delay in the fulfillment of the clinical triad in three of the four 

patients.” Ex. D at 59. In the first case, a thirty year old man presented in February 2006 with 

BRAO in his left eye. Id. “His field loss improved, and in June 2006, [four months later] he 

suffered superior visual field defect, this time in his right eye. Three days later he experienced an 

inferior field loss in his left eye along with tinnitus and HL in his right ear.” Id. BRAO was noted 

in both eyes. Id. An MRI of the brain showed widespread lesions and CSF analysis revealed 

elevated protein. Id. “He was started on oral prednisone 80 mg daily for presumed Susac’s 

syndrome ...” Id. at 60. Two weeks later, he developed confusion, short-term memory loss and 

disinhibition, requiring inpatient hospitalization when his prednisone was reduced. Ex. D. at 60. 

He was started on an immunosuppressive regimen. Id. Thirty months later, “[h]e continue[d] to 

do well . . . with no further episodes of BRAO . . . .” Id. at 61. He had “mild permanent visual 

field defect, normal mentation[,] and no auditory deficits.” Id.

Case two of the series, a thirty-four year old woman, presented in 1991 with intermittent 

vertigo and bilateral hearing loss. Id. at 61. “For the next [ten] years, she continued to have 

intermittent vertigo and depression and her hearing worsened. In 2001, she developed headaches 

and lower extremity stiffness.” Id. In May and August 2006, she experienced visual difficulties. 

Id. “[A]n ophthalmologic evaluation . . . showed a visual acuity of 20/70 and the presence of new 

visual field defects. A presumptive diagnosis of Susac’s syndrome was made” and she was 

treated accordingly. Ex. D. at 6. In December 2007, “[s]he noted improvement in her vision . . .

and her visual acuity in the left eye improved to 20/25 and has since stabilized. 

Immunosuppression was stopped in August 2008.” Id.

In case three of the series, a thirty-four year old woman experienced personality changes 

in 1995. Id. She developed transient diplopia four years later in 1999, along with visual field 

 

15 See Siddharama Pawate et al., The Spectrum of Susac’s Syndrome, 30 Neurol. Sci. 59 (2009) 

[Ex. D].
17

defects, headaches, and intermittent numbness in the right arm. Id. “A brain MRI showed nonspecific lesions in the corpus callosum” and a CSF study showed elevated protein. Id. Six years 

later, “[i]n May 2005 she developed sudden bilateral tinnitus and decrease in hearing.” Id. In 

August 2005, “her major problems continued to be psychiatric and cognitive, with difficulties 

with short-term memory, word-finding, and disorganized thought.” Ex. D at 61. A diagnosis of 

Susac’s Syndrome was made two years later, in February 2007, when she had an acute 

worsening of her vision and bilateral BRAOs were revealed in an ophthalmologic examination. 

Id. “She was started on a regimen of IVIg . . . and slowly tapered oral corticosteroids.” Id. She 

had another episode of BRAO in September 2007 and was treated with Rituximab and 

prednisone. Id. “She had no new problems at her last follow-up in March 2008.” Id.

In case four of the series, a twenty-five year old woman presented in 1999 with episodes 

of diplopia and ataxia. Ex. D. at 61. “In 2001 she had an episode of visual blurring, and lost 

hearing in her right ear.” Id. “A diagnosis of Susac’s syndrome was entertained [in January

2004], but she did not have any features of encephalopathy, and BRAO was not documented. A 

brain MRI in March 2005 showed significant involvement of the corpus callosum . . . .” Id. A 

diagnosis of Susac’s Syndrome was made in October 2006 when an ophthalmologic evaluation 

showed BRAO in the left eye and evidence of old BRAOs in the right eye. Id. at 62. “In 

September 2007, her central visual acuity dropped to 20/70 right eye and 20/40 left eye and has 

remained at this level.” Id. “A regimen of monthly IVIg was added. At the last follow-up in 

August 2008, she had no further problems.” Id.

Dr. Sriram and his colleagues determined that “the clinical triad may not be apparent for 

years, resulting in delays in diagnosis.” Id. at 59. The authors noted, “[P]resentations with only 

one, or two, features . . . and delay in the development of the full clinical triad may delay the 

diagnosis.”16 Id. at 62-63. They stated, “[E]arly diagnosis is key to avoid the development of 

permanent neurological, visual and auditory deficits.” Id. at 59. Additionally, the authors noted

that immunosuppressive treatment is effective, however, “[i]t is still not clear how long to treat [] 

patients with immunosuppression, because symptoms may recur years after remission, and can 

cause considerable neurological damage in a short time.” Id. at 63. They also noted that “there 

may be long periods of quiescence [or inactivity] even with no treatment,” citing a reported case 

of Susac’s Syndrome that recurred after a period of eighteen years. Id. at 63-64.

In the present case, both experts agreed that petitioner’s initial ADEM diagnosis was 

ultimately not the correct diagnosis of his condition. Tr. 132, 195-96. Dr. Rinker believed, “[I]n 

retrospect . . . the ADEM label was . . . a working diagnosis that was subsequently amended once 

the . . . full clinical picture was realized.” Tr. 132. Dr. Sriram explained, “[T]he MRI is the main 

differentiating feature” between ADEM and Susac’s Syndrome. Tr. 196. Dr. Sriram further 

explained that in both conditions, a person may experience encephalopathy, seizures, headache, 

and/or abnormal spinal fluid tests, but that “the picture of what you see in the MRI is what 

differentiates the acute encephalopathy of Susac’s with that of ADEM.” Id. Dr. Sriram believed

petitioner’s correct diagnosis is Susac’s Syndrome. Tr. 191.

 

16 See also Ex. 20 at 7 (noting “97% of patients did not have the clinical triad at the time of the 

onset of symptoms. In some patients, the triad became complete after a delay of weeks to more 

than two years, a factor that contributes to the difficulty in confirming the diagnosis.”). 
18

The testimony of both experts and the supporting medical literature reveal that Susac’s 

Syndrome may be characterized by long temporal intervals between the three major features of 

the disease. See Ex. D at 59; Tr. 131-32, 134, 193-94. The medical literature also shows that 

some patients manifest symptoms of Susac’s Syndrome without positive diagnostic findings to 

confirm a diagnosis. See Ex. D at 60-62. In petitioner’s case, the evidence shows that the course 

of petitioner’s condition was acute and severe, as he developed all three features of the disease 

(encephalopathy, hearing loss, and vision problems), and positive MRI and CSF findings, within 

approximately twenty days of his Tdap vaccination on November 7, 2009. See Ex. 3 at 14 

(noting elevated protein levels in CSF analysis performed on November 10, 2009); Ex. 2 at 10 

(November 11, 2009, EEG showing “an acute encephalopathic process, most likely of toxic 

metabolic etiology); Ex. 3 at 2 (noting scotoma—a partial loss of vision or a blind spot—and 

“flashing lights” upon admission to the ED on November 10, 2009); Ex. 3 at 14 (physical 

examination on November 12, 2009, noting “intense photophobia”); Ex. 3 at 23 (MRI of the 

brain on November 13, 2009, showing a large lesion in the splenium of the corpus callosum); Tr. 

80-81 (noting petitioner had difficulty hearing around November 27, 2009); see also Ex. 4 at 146 

(noting severe hearing loss in petitioner’s right ear and moderate to severe hearing loss in his left 

ear). 

As both experts acknowledge, not much is known about the natural history of the disease. 

Nevertheless, the case reports distinguish petitioner’s case as more acute, more severe, and with 

a poorer clinical outcome in comparison. Dr. Sriram’s article emphasized intervals of several 

years to fully manifest the condition, and the only case report in the article that was characterized

as a relatively rapid manifestation of Susac’s Syndrome took four months to develop. The 

medical literature also suggests that Susac’s Syndrome manifests in partial forms. However, in 

petitioner’s case, the evidence shows petitioner exhibited all three features of the disease in 

approximately twenty days. As such, the undersigned credits Dr. Rinker’s testimony that 

petitioner was experiencing mild symptoms and would have had a mild course of the disease 

absent his vaccinations. The evidence also preponderates in favor of petitioner as to both the 

severity of his condition and the clinical outcome. Compared to the other cases of Susac’s 

Syndrome described in the testimony and the medical literature, petitioner experienced more 

severe symptoms, requiring hospitalization and lengthy physical and occupational therapies. 

Petitioner has long-lasting hearing, cognitive, and gait impairments, and he has been unable to 

return to work. Based on this evidence, petitioner has met his burden of proof to show that his 

prior condition was significantly aggravated. 

(4) Loving Prong Four: A medical theory causally connecting such a 

significantly worsened condition to the vaccinations.

The fourth Loving factor requires petitioner to put forth a theory causally connecting his 

significantly worsened condition to the vaccinations. An assessment of whether a proffered 

theory of causation is reputable must be viewed, “not through the lens of the laboratorian, but 

instead from the vantage point of the Vaccine Act’s preponderant evidence standard . . . .” 

Andreu v. Sec’y of HHS, 569 F.3d 1367, 1380 (Fed. Cir. 2009). Petitioner is not required to 

present proof of causation “to the level of scientific certainty,” but rather must provide some 

“indicia of reliability to support the assertion of the expert witness.” Moberly v. Sec’y of HHS, 

592 F.3d 1315, 1324 (Fed. Cir. 2010). A special master is required to consider all other relevant 
19

medical and scientific evidence contained in the record. Id.; § 300aa-13(b)(1).

Dr. Rinker advances two possible theories for how petitioner’s flu and Tdap vaccinations 

significantly aggravated his Susac’s Syndrome. The first theory is molecular mimicry,17 where 

antibodies are directed against healthy tissue creating an aberrant immune response. Ex. 16 at 3. 

“In molecular mimicry, healthy host tissue with some structural similarity to exogenous antigens 

becomes the target of an immune response directed against the host tissue.” Id. Dr. Rinker 

explained that although he cannot state with certainty that molecular mimicry is precisely what 

occurred in petitioner’s case, the theory explains how an individual’s “immune system can go 

from performing a purely beneficial role to also performing a harmful . . . role in an individual’s 

health.” Tr. 136-37.

Dr. Rinker’s second theory is that a non-specific immune response was generated in 

response to the antigens and adjuvants present in the vaccines. Id. at 137. Theoretically, the

vaccinations triggered “activation of toll like receptors, uptake and presentation of antigen by 

dendritic cells, and release of cytokines and chemokines, which signal[ed] upregulation of the 

host immune system, and which are known to lead to systemic symptoms and non-specific 

immune activation.” Id.

Dr. Rinker based his theories on two considerations. First, that there is an immunological 

stimulus that occurs fairly soon after the administration of a vaccine. Tr. 118. Dr. Rinker 

explained:

[W]hen an individual receives a vaccination, the first immunological responses to 

the vaccine [are] generated by the innate immune system, which is kind of a 

nonspecific branch of the immune system. And part of the role of the innate 

immune system is to react to any novel outside antigen or foreign protein matter 

and to try to eradicate it in a very nonspecific way ... I think most people who’ve 

had a vaccination and ever experienced [] muscle aches and flu-like symptoms in 

the day or days immediately following the vaccine are familiar with the effects on 

the innate immune system that result when somebody receives a vaccination.

Tr. 117-18. Dr. Rinker further explained that in the process of an innate immune response, an 

adaptive immune response is stimulated, “which is a more specific and targeted immune 

 

17 The Institute of Medicine defines molecular mimicry as: 

[S]equence or conformational homology between an exogenous agent (foreign 

antigen) and self-antigen leading to the development of tissue damage and clinical 

disease from antibodies and T cells directed initially against the exogenous agent 

that also react against self-antigen. Molecular mimicry as a mechanism that can 

cause pathologic damage and disease has been demonstrated in several animal 

models, most notably experimental allergic encephalomyelitis (EAE) in mice and 

rabbits. 

Institute of Medicine, Adverse Effects of Vaccines: Evidence and Causality 70 (2012)

(internal citations removed).
20

response that takes more time to develop.” Id. at 117.

The second consideration on which Dr. Rinker based his proffered theories is the 

likelihood of an adaptive immune response in a few days following a vaccination. Id. at 118. Dr. 

Rinker stated:

[W]hen someone [has] been exposed to a vaccine for the first time, it can take [] 

upwards of a couple of weeks before the full innate immune response occurs. But 

when someone has already been exposed to a certain infection or vaccine, the 

secondary, or the anamnestic adaptive immune response, is quite a bit shorter, on 

the order of just a few days.

Id. Dr. Rinker relied on a chapter on vaccine immunology written by Claire-Anne Siegrist18 and 

a chapter from an Institute of Medicine (“IOM”) publication19 on the adverse effects of vaccines

to support his contention that an adaptive immune response can form in a few days after a 

subsequent exposure to a given vaccine. Dr. Siegrist stated, “In secondary immune responses, 

booster exposure to an antigen reactivates immune memory and results in a rapid (<7 days) 

increase of IgG antibody titer.” Ex. 23 at 7. The IOM publication indicates:

Due to the development of memory B and T cells during the primary immune 

response, the latency between subsequent exposure to the antigen and 

development of the immune response will usually be shorter. The lag phase [the 

initial activation of B and T cells] is generally 1 to 3 days; the logarithmic phase 

[an increase in serum antibody levels] of the secondary antibody response occurs 

over the next 3 to 5 days.

Ex. 24 at 3. The IOM publication further notes, “While this discussion is not specific to a 

particular antigen, it can be used as a reference point for the latency between antigen exposure 

and the initiation of [] immune-mediated mechanisms . . . .” Id.

Dr. Rinker testified that since petitioner received a Tdap vaccination on several occasions 

in his childhood, a vaccination in 2009 would trigger an “anamnestic adaptive immune 

response.”

20 Tr. 118; see Ex. 1A at 1 (indicating petitioner received “Dtp” or “Dtap”

vaccinations on October 1, 1985, November 26, 1985, January 23, 1986, May 9, 1987, June 20, 

1990, and July 7, 1990). He further testified that Susac’s Syndrome is an immune-mediated 

condition, likely autoimmune. Tr. 122.

Respondent’s expert concedes that Susac’s Syndrome is an immune-mediated disease. In 

 

18 Claire-Anne Siegrist, Vaccine Immunology (2012) in Stanley A. Plotkin et al., Vaccines (6th

ed. 2013).

19 Institute of Medicine, supra note 17, at 70.

20 “[T]he rapid reappearance of antibody in the blood following the administration of an antigen 

to which the subject had previously developed a primary immune response.” The SloaneDorland Annotated Medical-Legal Dictionary 614 (1st ed. 1987).
21

detail, Dr. Sriram opined, “Although the nature of the immune response in Susac’s disease is not 

known, the response of patients to plasma exchange and more recently reports of remission 

following depletion of B lymphocytes with Rituxamab would suggest a role for antibodies as a 

cause for the disease.” Ex. A at 4. Dr. Sriram agreed that the prevailing opinion is that Susac’s 

Syndrome may be “antibody mediated,” or in other words, be an immune-mediated disease, “for 

the simple reason [] that the kind of drugs [used] to treat the disease is [sic] best served by those 

that decrease the antibody levels, or the B lymphocyte . . . .” Tr. 197; accord Ex. 20 at 27 (noting 

that “[t]he etiology of the disease is unknown, but histopathologic and laboratory evidence 

suggests that an immune-mediated mechanism may be involved.”). 

Dr. Sriram agreed that petitioner was correctly diagnosed with Susac’s Syndrome, but he 

opined that petitioner’s condition likely began on November 1, 2009, based on the medical 

records. Tr. 191, 195. He further opined that there is no evidence, “as clinicians,” to suggest that 

vaccinations or any other infection would worsen Susac’s Syndrome. Tr. 198. First, according to 

Dr. Sriram, “[I]f we assume that [petitioner’s course] is an amplification of an immune response, 

then we should have this Susac’s . . . exacerbated not only by vaccines, but also by any other 

exposure to any other infection because . . . [t]he biology of the immune response is the same.” 

Id. “Secondly, if we [] assume . . . that antibodies are related to Susac’s, then we have to have a 

situation or a process by which an infection and/or a vaccine ... somehow amplifies the antibody 

production in the lymph nodes, in the spleen, and targeting them to the end organs to amplify and 

accentuate the damage.” Tr. 189-99. Dr. Sriram testified, “[W]e have no evidence that [] 

exposure to these antigens, viruses or the vaccines do that . . . .” Tr. 199. For those reasons, Dr. 

Sriram felt it was “unlikely that [Dr. Rinker’s theories] are plausible [] mechanisms . . . .” Tr. 

199.

Furthermore, Dr. Sriram stated that he is not aware of any epidemiological or animal 

studies that have concluded that the vaccines in question can cause or exacerbate Susac’s 

Syndrome. Id. According to Dr. Sriram, the only case report of a possible connection between a 

vaccination and Susac’s Syndrome, submitted by petitioner, is “of a gentlemen who developed 

another branch retinal artery occlusion after receiving a small pox vaccination. This gentlemen 

already had Susasc’s because his other eye was already affected by a previous branch retinal 

artery occlusion.” Id. As such, Dr. Sriram opined that it is “difficult to conclude that what 

followed was not otherwise [what] would have happened because that’s the nature . . . of 

Susac’s.” Id.

The undersigned finds petitioner has provided preponderant evidence to establish a 

medical theory causally connecting his significantly worsened condition to his vaccinations. 

Both experts agree that Susac’s Syndrome is an immune-mediated disease, likely caused by a 

dysregulation of antibodies in an immune response. Both experts provided testimony, and the 

medical literature supports, the proven effectiveness of immunosuppressive therapies in the 

treatment of this condition, which further supports both the expert opinions that Susac’s 

Syndrome is an immune-mediated condition. See Ex. D at 63-64; Ex. E at 91. Accordingly, 

petitioner’s theory of an aberrant adaptive immune response triggered by the vaccinations at 

issue, whereby an innate immune response began upon receipt of a flu vaccination on November 

6, followed by an anamnestic immune response upon receipt of a Tdap vaccine the next morning, 

is supported by reliable evidence in this case. 
22

(5) Loving Prong Five: A logical sequence of cause and effect showing that 

the vaccinations significantly aggravated the petitioner’s condition.

The fifth Loving factor requires petitioner to show a logical sequence of cause and effect 

of how the vaccinations significantly aggravated his Susac’s Syndrome.

Petitioner and Mrs. Means testified that petitioner experienced a mild headache on 

November 1, 2009. Tr. 13, 83. Thereafter, petitioner participated in drill exercises on November 

4 through 7, 2009, and received flu and Tdap vaccinations during that time. Tr. 10-11, 88-91. 

Petitioner and Mrs. Means further testified that petitioner began to experience an intensified 

headache, as well as the onset of a new symptom, photophobia, on November 8, 2009. Tr. 18. 

Petitioner visited his primary care doctor on November 9, 2009, who noted that petitioner had 

experienced a “headache since Sunday . . . [w]ith photophobia and blurring of vision.” Ex. 2 at 

37. 

Dr. Rinker’s opinion is that petitioner’s severe headache on November 8, 2009, was 

related to his Susac’s Syndrome and that the vaccines played an “exacerbating role in the onset 

of his disease” for several reasons. Tr. 127-28, 134. First, according to Dr. Rinker, the timing of 

petitioner’s vaccinations is significant. Tr. 134. Here, petitioner received a flu vaccination two 

days before he experienced symptoms related to his Susac’s Syndrome (on November 6, 2009),

and received Tdap vaccination one day before his symptoms (on November 7, 2009). Ex. 1. 

Second, Dr. Rinker also found it significant that petitioner’s condition, Susac’s Syndrome, “is an 

immune-mediated disease.” Tr. 134. Lastly, he noted “that vaccines by their nature are meant to 

provoke the immune system into mounting an immune response.” Id. In support of his opinion, 

Dr. Rinker provided several medical articles discussing an association between various vaccines 

and certain neuromuscular diseases.21

Alternatively, Dr. Rinker opined,“[I]f we take [petitioner’s] headache a week before to be 

the initial symptom, then . . . the vaccine would certainly prove as an aggravator.” Tr. 133.

According to Dr. Rinker, a headache can be an initial symptom of Susac’s Syndrome. However, 

one cannot establish with certainty that petitioner’s condition began with a mild headache on 

November 1, 2009, especially because “based on the testimony [Dr. Rinker] heard [at the 

hearing], . . . [t]he headache that really stands apart as being distinctly different is the one that 

began . . . the day following [petitioner’s] Dtap [sic] vaccination.” Tr. 127. 

The undersigned is persuaded by Dr. Rinker’s testimony that petitioner’s symptoms on 

November 8 were distinct from the headache he experienced one week prior. Not only do the 

medical records from November 9 and 10, 2009, document the severity of petitioner’s headache 

in the days following his vaccinations, they also note the onset of new symptoms associated with 

petitioner’s Susac’s Syndrome, photophobia and blurring vision. See Ex. 2 at 18, 37. 

Additionally, on November 10, 2009, petitioner was assessed at the ED with a scotoma (partial 

loss of vision), and “flashing light” in his vision. Ex. 3 at 2. While it is not unreasonable to 

 

21 See e.g., H. Orbach & A. Tanay, Vaccines as a Trigger for Myopathies, 18 Lupus 1213-16 

(2009); Joerg-Patrick Stübgen, Neuromuscular Disorders Associated with Hepatitis B 

Vaccination, 292 J. of Neuro. Sci. 1-4 (2010).
23

suggest that petitioner’s Susac’s Syndrome began on November 1, 2009, with a mild headache—

as some of the medical records ascribe ongoing headache symptoms since approximately 

November 1—the testimony and the chain of events, namely petitioner’s participation in reserve 

drill exercises from November 4 through 7, establish that petitioner was experiencing mild 

symptoms of his condition up until two days after his flu vaccination and a day after his Tdap 

vaccination. After his vaccinations, petitioner’s headache symptoms worsened, and he began to 

experience new disease symptoms. Accordingly, the undersigned credits Dr. Rinker’s testimony

that petitioner experienced exacerbated symptoms of Susac’s Syndrome beginning on November 

8, 2009. The undersigned accepts Dr. Rinker’s opinion that petitioner’s vaccinations were one 

substantial factor, among other factors, which contributed to an exacerbation of petitioner’s 

condition. 

(6) Loving Prong Six: A proximate temporal relationship between the 

vaccinations and the significant aggravation.

The last prong in the six-part Loving test is “a showing of a proximate temporal 

relationship between vaccination and [the] significant aggravation.” 86 Fed. Cl. at 144. This 

prong can be informed by the case law relating to Althen prong three. See 418 F.3d at 1280. To 

satisfy this requirement, petitioner must provide “preponderant proof that the onset of symptoms 

occurred within a timeframe for which, given the understanding of the disorder’s etiology, it is 

medically acceptable to infer” that the vaccinations played a triggering role. De Bazan, 539 F.3d 

1347, 1352 (Fed. Cir. 2008) (citing Pafford v Sec’y of Health & Human Servs., 451 F.3d 1352, 

1358 (Fed. Cir. 2006)). 

A major point of contention between the experts is whether vaccinations can trigger an 

exacerbation of an immune-mediated condition twenty-four to forty-eight hours after 

vaccination. Here, petitioner received a flu vaccination on Friday, November 6, 2009, and a Tdap 

vaccination in the morning of Saturday, November 7, 2009. Ex. 1. Dr. Rinker opined that 

petitioner’s Susac’s Syndrome was significantly aggravated beginning on November 8, 2009. Tr. 

126. 

Dr. Sriram disagreed with Dr. Rinker on the likelihood of an adaptive immune response 

forming within just a few days. Dr. Sriram believed that “the kinetics of an immune response to 

induce the development of an antibody response . . . makes [sic] [a] temporal relationship to the 

vaccination unlikely,” because in “virtually all animals and human studies” the earliest immune 

response seen is seven days for IgM antibodies, and two to three weeks for IgG antibodies. Ex. A 

at 4. Dr. Sriram opined that it is unlikely that an adaptive immune response could occur within 

forty-eight hours, even in the case of a subsequent exposure to an antigen, because “it takes time 

for the lymphocytes to become plasma cells; plasma cells to make imunoglobins; imunoglobins 

to be secreted, to circulate[,] and then go into the target.” Tr. 202-03. He thought, “48 hours is 

too short a time frame for the whole maturation process and development process to happen.” Tr. 

203. However, he did not cite any support for this argument. Id.

Dr. Rinker provided reliable evidence to show that in a subsequent exposure to the same 

antigen, an increase of IgG antibody titer can occur in less than seven days. Specifically, the 

Seigrist chapter on vaccine immunology notes, “In secondary immune responses, booster 
24

exposure to antigen reactivates immune memory and results in a rapid (<7 days) increase of IgG 

antibody titer.” Ex. 23 at 7. Additionally, Dr. Rinker provided an IOM publication which notes 

that in a subsequent exposure to an antigen, activation of B cells, of which Dr. Sriram attributes a 

primary role in the pathology of Susac’s Syndrome, is generally one to three days. See Ex. 24 at 

3; Tr. 197. Petitioner provided his childhood vaccination record, indicating several vaccinations 

with the components in a Tdap vaccine, namely tetanus, diphtheria, and acellular-pertussis. See

Ex. 1A at 1. Dr. Rinker opined that because petitioner received Tdap vaccinations on several 

prior occasions, his Tdap vaccination on November 7, 2009, triggered an anamnestic adaptive 

immune response within twenty-four to forty-eight hours of his vaccinations. The Seigrist and 

IOM publications, as discussed above, both support Dr. Rinker’s timeframe.

In this case, the temporal relationship between petitioner’s vaccinations and the onset of 

exacerbated symptoms of Susac’s Syndrome is compelling. The facts here are consistent with 

Dr. Rinker’s testimony and the supportive medical literature, indicating that an anamnestic 

adaptive immune response began twenty-four to forty-eight hours after petitioner’s Tdap and flu

vaccinations, thereby exacerbating his Susac’s Syndrome. Assuming, as Dr. Rinker suggests, that 

petitioner’s symptoms of severe headache and photophobia on November 8, 2009, were the start 

of an exacerbation of his Susac’s Syndrome, the evidence supports petitioner’s significant 

aggravation claim. The same holds true if the undersigned accepts Dr. Sriram’s contention that 

petitioner’s Susac’s Syndrome began on November 1, 2009, as the evidence still supports Dr. 

Rinker’s contention that petitioner experienced an exacerbation beginning on November 8. 

Accordingly, petitioner has provided preponderant evidence to support a temporal relationship 

between his vaccinations and his significantly aggravated condition.

VI. CONCLUSION

For the reasons discussed above, the undersigned finds that petitioner has established 

entitlement to compensation on his claim of a significant aggravation of Susac’s Syndrome. 

Accordingly, petitioner’s Table claim will not be reached. 

A damages order will be issued separately.

IT IS SO ORDERED.

s/ Nora Beth Dorsey

Nora Beth Dorsey

Chief Special Master