In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 13-993V

(Filed: November 27, 2018)

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

JULIE SULIMAN, * To Be Published

*

Petitioner, * Tetanus-diphtheria-acellular

* pertussis (“Tdap”) Vaccine;

v. * Polymyalgia Rheumatica

 * (“PMR”); Myositis; 

SECRETARY OF HEALTH * Dismissal

AND HUMAN SERVICES, *

 *

 Respondent. *

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

 

Franklin John Caldwell, Esq., Maglio, Christopher, & Toale, Sarasota, FL, for petitioner.

Lisa Watts, Esq., U. S. Department of Justice, Washington, D.C., for respondent. 

DECISION1

Roth, Special Master: 

On December 16, 2013, Julie Suliman (“Ms. Suliman,” or “petitioner”) timely filed a 

petition for compensation under the National Vaccine Injury Compensation Program, 42 U.S.C. § 

300aa-10, et seq.2(the “Vaccine Act” or “Program”), alleging that the tetanus-diphtheria-acellular 

pertussis (“Tdap”) vaccination that petitioner received on April 1, 2011 caused her to develop 

polymyalgia rheumatica (“PMR”) and/or myositis. Petition at 1-2. 

 

1 This Decision has been designated “to be published,” which means I am directing it to be posted on the 

Court of Federal Claims’s website, in accordance with the E-Government Act of 2002, Pub. L. No. 107-

347, 116 Stat. 2899, 2913 (codified as amended at 44 U.S.C. § 3501 note (2006)). This means the Decision 

will be available to anyone with access to the internet. However, the parties may object to the Decision’s 

inclusion of certain kinds of confidential information. Specifically, under Vaccine Rule 18(b), each party 

has fourteen 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 whole Decision will be available to the public. Id.

2 National Childhood Vaccine Injury Act of 1986, Pub. L. No. 99-660, 100 Stat. 3755. Hereinafter, for 

ease of citation, all “§” references to the Vaccine Act will be to the pertinent subparagraph of 42 U.S.C. § 

300aa (2012). 
2

An entitlement hearing was held on January 29 and 30, 2018, in Washington, D.C. For the 

reasons stated herein, I find that petitioner’s evidence is insufficient to demonstrate that the Tdap

vaccine she received on April 1, 2011 more likely than not caused her development of PMR and/or 

myositis. Accordingly, I find that petitioner is not entitled to compensation.

I. Issues to be Determined

The parties agree that petitioner has PMR. Joint Sub. at 1. The parties disagree on the 

timing of onset of petitioner’s PMR, and on whether petitioner also developed myositis. Id. They 

further disagree on whether Tdap vaccine can cause PMR and/or myositis, and, if it can, if it did 

so in this case. Id. at 1-2. Petitioner did not advance a claim that Tdap vaccine significantly 

aggravated a preexisting PMR or myositis. Id. at 1. 

II. Background

A. Procedural History

Petitioner filed her petition on December 16, 2013 and medical records on December 17, 

2013. Petitioner’s Exhibits (“Pet. Ex.”) 1-7, ECF No. 5. On February 28, 2014, respondent filed a 

Rule 4(c) Report (“Rule 4”) stating that compensation was not appropriate. ECF No. 7. 

On July 3, 2014, petitioner filed additional medical records. Pet. Ex. 8-10, ECF No. 10. 

Respondent filed a status report on October 21, 2014, stating that settlement was not feasible. ECF 

No. 19. 

On February 23, 2015, petitioner filed the report of Dr. Raji Grewal, petitioner’s treating 

physician, along with supporting literature. Pet. Ex. 11-18, ECF No. 23. 

On April 24, 2015, respondent filed an expert report from Dr. Mehrdad Matloubian along 

with supporting literature. Resp. Ex. A-F, ECF No. 26. 

Following a status conference on May 20, 2015, petitioner was ordered to file a 

supplemental expert report by July 22, 2015. ECF No. 28. After requesting and receiving six 

extensions of time, petitioner filed a supplemental expert report from Dr. Grewal on February 5, 

2016, along with supporting medical literature. Pet. Ex. 21-37, ECF Nos. 42, 43. 

This case was reassigned to me on January 14, 2016. ECF No. 37.

A Rule 5 conference was held on April 21, 2016. Settlement discussions were encouraged. 

Scheduling Order, ECF No. 45. Petitioner filed a status report on July 20, 2016, stating that the 

parties were not able to resolve this matter, and requested an entitlement hearing. ECF No. 47. A 

status conference was held on August 10, 2016; petitioner was ordered to file a supplemental expert 

report which addressed specific questions about petitioner’s theory of causation, specifically her 

aluminum adjuvant, or “ASIA-like,” theory of causation. Scheduling Order, ECF No. 48. 
3

A prehearing order was issued on October 13, 2016, setting this matter for an entitlement 

hearing on January 29 and 30, 2018 in Washington, D.C. Prehearing Order, ECF No. 51. Petitioner 

filed a second supplemental expert report from Dr. Grewal on December 29, 2016. Pet. Ex. 38, 

ECF No. 53. Petitioner filed updated medical records on March 28, 2017 and January 4, 2018. Pet. 

Ex. 39-40, ECF No. 54; Pet. Ex. 41-42, ECF No. 61.

Petitioner filed her pre-hearing brief on December 7, 2017. ECF No. 58. Respondent filed 

his pre-hearing brief on January 4, 2018. ECF No. 59. 

An entitlement hearing was held in Washington, D.C. on January 29 and 30, 2018. 

At the conclusion of Dr. Grewal’s testimony, the courtroom was cleared and Dr. 

Grewal’s testimony was discussed with counsel as follows: 

The Court: Counsel would you like to tell me how you are going to sustain your 

burden of causation in this case?

Mr. Caldwell: This is a bit surprising, actually. As I sit here, I can’t. But that doesn’t 

mean – what I would like to do is continue with the case since we are here, through 

Dr. Matloubian’s testimony and cross-examination, look at the transcripts and see 

where we go. 

I think that what I watched in this testimony was somebody who was not a typical 

expert witness in these cases. I think a lot of the questions confused him and I think 

he answered them in a way to sort of follow along with what you were both saying 

to him. I think he didn’t have that sort of – the academic backbone to talk about 

what was happening. Because I think when I—what I want to do is go through the 

transcript and compare what he’s talking about with what he’s written and what his 

literature says and what the medical records say. 

The Court: I will disagree with you that I don’t think he misunderstood. I think he 

understood full well. I think that he has absolutely no literature or support for what 

he’s saying. He just believes that she got the tetanus, she says she felt worse, and 

he didn’t take into consideration all of the other issues in her medical records, 

including the fact that she has constant infections and had one the week before 

which could more than likely be responsible for the onset of this PMR, if it wasn’t 

already starting with many of the complaints that she had before. So I will disagree 

with you, but I will indulge you. 

Tr. 174-75. 

Respondent moved for a ruling on the evidentiary record, submitting that Dr. Grewal’s 

testimony and concessions did not support a theory causally connecting the vaccine to PMR or 

myositis. Tr. 177. Respondent pointed out that Dr. Grewal conceded that he did not know when 

petitioner’s PMR and/or myositis started and therefore could not marry the alleged injury with the 
4

vaccine. Tr. 177. Respondent stated that petitioner had the burden of proof and was unable to meet 

it. Tr. 177. 

Following a discussion, the decision was made to hear testimony from Dr. Matloubian in 

order to secure the record. Tr. 178. Petitioner requested the opportunity to submit a post-hearing 

brief to address the inconsistencies between Dr. Grewal’s testimony and his written opinions. Tr. 

178. 

At the conclusion of Dr. Matloubian’s testimony, the parties rested. Dr. Grewal had left the 

previous day after the conclusion of his testimony, and was not offered for rebuttal. I confirmed 

with petitioner’s counsel that it was not his intention to secure another expert report in this case. 

He responded that it was not his intention, “[u]nless there’s some smoking gun that I hadn’t seen 

before.” Tr. 285. I pointed out to counsel that it would be unlikely, as the causation theory in this 

case was raised by the original special master assigned to this case and later by me when the case 

was reassigned. Tr. 285. At the pre-hearing conference, I again raised the issue of ASIA as the 

theory of causation and was corrected by counsel that the theory was “ASIA-like.” Order at 1-2, 

ECF No. 68. Following the hearing, I pointed out that Dr. Grewal’s testimony was consistent with 

his reports in putting forth ASIA as the theory of causation. Tr. 285. Petitioner’s counsel agreed, 

stating that the basis was the aluminum in the vaccine. Tr. 285. I responded that Dr. Grewal was 

unable to explain how the aluminum would cause petitioner any injury, other than to say it was 

injected rather than ingested. Tr. 285. 

The parties agreed to submit Post-Hearing Briefs, which were filed April 2, 2018 and May 

31, 2018, respectively. ECF Nos. 74, 76. Petitioner did not attempt to reconcile the written opinions 

of Dr. Grewal with his testimony, but simply stated, “Dr. Grewal’s testimony was not in line with 

his written medical record or his expert reporting. Whether it was his nervousness and confusion 

as a first time testifying expert witness, as undersigned believes is the case, or whether on crossexamination and examination by the Court, Dr. Grewal altered or felt unable to support his opinion, 

is ultimately for the court to decide.” Pet. Post-Hearing Brief at 1-2. 

Dr. Grewal testified that he has provided expert opinions in five other vaccine cases and 

has previously reviewed medical malpractice cases, but has not testified in court in any of those 

cases. Tr. 119-20.

Dr. Grewal was not confused or flustered at any time during the hearing, nor did he lack 

understanding of the questions asked of him. He testified honestly, graciously, and credibly, 

conceding that he had no support for his opinions other than his personal belief that petitioner’s 

PMR and/or myositis was caused by the Tdap vaccine based on timing. Dr. Grewal did not lack 

academic prowess as suggested by counsel, nor was he misled by questions from respondent’s 

counsel or the court. He simply testified honestly with testimony that was adverse to petitioner’s 

case and cannot be rehabilitated. 

In his Post-Hearing Brief, respondent stated that Dr. Grewal conceded having no sound 

scientific basis for his belief that the Tdap vaccination caused petitioner’s PMR or myositis. The 

basis for his theory was that petitioner received the vaccine “and was never quite the same 
5

afterwards.” Resp. Post-Hearing Brief at 4 (citing Tr. 112). Respondent requested that the petition 

for compensation be denied and the case dismissed. Id. at 4. 

This matter is now ripe for decision.

B. Medical History

1. Petitioner’s Health Before Receiving the Tdap Vaccine

Petitioner’s medical history is long standing and complicated. She has been under the care 

of Dr. Allison Faches (primary care), Dr. Fu Bai (rheumatology) and Dr. Richard Gan (neurology) 

for many years. She has a history of multiple sclerosis (“MS”) treated with Copaxone, Avonex, 

and steroids; fibromyalgia treated with amitriptyline, Celebrex, and Lyrica; chronic fatigue 

syndrome, vertigo, recurrent herpes simplex virus II, alcoholism, drug abuse, central vein 

occlusion in the right eye, eczema, panic attacks, migraines, palpitations, allergies, high 

cholesterol, fibroids, right-sided facial numbness, numbness in her feet, hearing loss, insomnia, 

glaucoma, left knee pain, and thirty years of smoking. In the two years prior to, and in the years 

following her Tdap vaccination, petitioner has had repeated gastrointestinal viruses, rashes,

sinusitis, and bronchitis requiring antibiotic treatment with Levaquin3and prednisone. See 

generally Pet. Ex. 2-3, 6, 8, 19-20, 40, 42.

On January 26, 2010, petitioner presented to Dr. Faches for fever, coughing, sinus pain, 

abdominal pain all over, and diarrhea, which had resolved. Pet. Ex. 6 at 88. She was smoking up 

to two packs of cigarettes per day. Id. She was diagnosed with acute sinusitis, prescribed Levaquin, 

guaifenesin,4and a Chantix starter pack. Id. 

On March 9, 2010, petitioner presented to Dr. Gan. Avonex5 was started in January of 

2009, but had to be stopped due to increased blood pressure. Pet. Ex. 8 at 13. She had a left knee 

cartilage repair.6 She was complaining of right facial tingling, drop feet, and diminished 

coordination. Id. Dr. Gan prescribed prednisone and ordered an MRI of the brain and cervical 

spine. Id. 

 

3 Levaquin is the brand name for levofloxacin, an antibiotic used to treat bacterial infections like sinusitis, 

chronic bronchitis, and urinary tract infections. Levofloxacin – Drug Summary, PDR.NET, 

http://www.pdr.net/drug-summary/Levaquin-levofloxacin-271.8231#3 (last visited Oct. 19, 2018).

4 Guaifenesin is an expectorant. It is prescribed for coughs, and thins and loosens mucus in the airways. 

Guaifenesin – Drug Summary, PDR.NET, http://www.pdr.net/drug-summary/Mucinex-guaifenesin-1275

(last visited Oct. 19, 2018).

5 Avonex is the brand name for interferon beta-1a. It is prescribed for relapsing-remitting MS. Interferon 

beta-1a – Drug Summary, PDR.NET, http://www.pdr.net/drug-summary/Avonex-interferon-beta-1a-1623

(last visited Oct. 19, 2018).

6 Petitioner did not file any medical records reflecting the surgical repair on her left knee. 
6

On July 12, 2010, petitioner presented to Dr. Faches, complaining of a rash on her ankle 

and arm for a couple of weeks and pain in her right ear. Pet. Ex. 6 at 87. She was diagnosed with 

poison ivy and prescribed prednisone. Id. 

On August 2, 2010, petitioner returned to Dr. Gan with dizziness, right facial numbness, 

and fatigue. Pet. Ex. 8 at 14. Dr. Gan noted her history of MS and the prednisone prescribed in 

March. Id. He wanted to “try Provigil.”7Id. 

On August 11, 2010, petitioner returned to Dr. Faches, with sinus complaints, frequent 

urination, urgency, and urinary incontinence. Pet. Ex. 6 at 86. She was diagnosed with sinusitis, 

prescribed Levaquin, and was advised to stop smoking and lose weight. Id. Dr. Faches noted that 

petitioner needed to get a Tdap vaccination when she was feeling well. Id.

On September 12, 2010, petitioner returned to Dr. Gan with increased vertigo, diplopia, 

clumsiness, numbness on the right side of her face, weakness and rash on her arms. Pet. Ex. 8 at 

12. She was not taking the Lyrica8 or Elavil9as prescribed. Id.

On October 8, 2010, petitioner presented to Dr. Faches, with complaints of being sick for 

a week, more severe “yesterday,” with right ear pain, sinus pain, chest congestion that moved from 

her head into her chest, and a deep productive cough. Pet. Ex. 6 at 85. She reported a stomach virus 

prior to the head cold. Id. She was diagnosed with sinusitis and prescribed Levaquin, rest, fluids, 

Xanax,10 and Valtrex.11 Id. 

On March 4, 2011, petitioner returned to Dr. Faches. She had stopped smoking and gained 

20 pounds since July. She had joined a gym. Pet. Ex. 6 at 83. She had a rash under her breasts and 

complained of shortness of breath, which she attributed to increased weight. Id. She complained 

 

7 Provigil is the brand name for modafinil, a central nervous system stimulant which increases mental 

alertness and decreases fatigue. It is used for narcolepsy and to reduce fatigue or excessive daytime 

sleepiness associated with sleep apnea or circadian rhythm disruptions. Modafinil – Drug Summary, 

PDR.NET, http://www.pdr.net/drug-summary/Provigil-modafinil-2332 (last visited Oct. 19, 2018).

8 Lyrica is the brand name for pregabalin, an anticonvulsant used to treat neuropathic pain associated with 

several conditions, including fibromyalgia. Pregabalin – Drug Summary, PDR.NET, 

http://www.pdr.net/drug-summary/Lyrica-pregabalin-467.8329 (last visited Oct. 19, 2018).

9 Elavil is the brand name for amitriptyline, a tricyclic antidepressant used to treat depression in adults. It 

is also used off-label to treat neuropathic pain. Amitriptyline hydrochloride – Drug Summary, PDR.NET,

http://www.pdr.net/drug-summary/Amitriptyline-Hydrochloride-amitriptyline-hydrochloride-1001 (last 

visited Oct. 19, 2018).

10 Xanax is the brand name for alprazolam, a short-acting benzodiazepine used for the management of 

anxiety. Alprazolam – Drug Summary, PDR.NET, http://www.pdr.net/drug-summary/Xanax-alprazolam1873.31 (last visited Oct. 19, 2018).

11 Valtrex is the brand name for valacyclovir, an antiviral drug used to treat infections caused by herpes 

viruses, including cold sores and herpes zoster. Physicians Desk Reference 1367, 1370 (66th ed. 2012).
7

of “a lot of fibromyalgia pain,” increased blood pressure, and “problems sleeping due to pain.”

She said Lexapro12 had worked for her pain in the past. Id. She reported that Dr. Gan had wanted 

to put her back on Lyrica, but she refused. Id. Dr. Faches prescribed Lexapro, Voltaren,13Lotrisone 

cream,14 and Gold Bond powder for her rash. Id. at 84. She was to follow up in a month. Id.

On April 1, 2011, petitioner returned to Dr. Faches with an injured right great toe; she 

believed it was broken. It was swollen and she could not wear shoes. Pet. Ex. 6 at 82. She also 

reported having a sore throat, and a stomach virus with diarrhea and vomiting the week prior; it 

had since resolved. Id. Her sinuses were painful on palpation. Id. A strep test due to exposure was 

negative. Id. Dr. Faches concluded the sore throat was probably viral. Id. Petitioner received a 

Tdap vaccination in her left deltoid. Id. at 36, 82.

2. Petitioner’s Health After Receiving the Tdap Vaccine

On April 18, 2011, petitioner presented to Dr. Bai, with complaints of a recent flare up of 

“arthralgia/myalgia.”15 Pet. Ex. 3 at 11. She was not taking her medications and had poor function, 

but her MS was stable. Id. She was antalgic16 with a cane. Id. at 10. She reported recent toe trauma 

and a tetanus booster. Id. at 11. She was noncompliant with follow-up visits. Id. She was prescribed 

Celebrex, Lyrica, and Zanaflex. Id. at 10. 

On April 26, 2011, petitioner returned to Dr. Bai reporting significant improvement since 

restarting medication. Pet. Ex. 3 at 9. She had no cognitive or other associated cluster symptoms 

at that time. Id. She did have an antalgic gait and was using a cane. Id. Celebrex, Lyrica, and 

Zanaflex were to be continued. Id.

Petitioner returned to Dr. Bai on May 9, 2011 reporting continued improvement on current 

medications and without any recent fibromyalgia flares. Pet. Ex. 3 at 8. She was tolerating Lyrica 

and Celebrex. Id. She was also taking Valtrex for a recent varicella zoster recurrence. Id. She was 

 

12 Lexapro is the brand name for escitalopram oxalate, a selective serotonin reuptake inhibitor (“SSRI”) 

used to treat depression and anxiety in adults. Escitalopram oxalate – Drug Summary, PDR.NET, 

http://www.pdr.net/drug-summary/Lexapro-escitalopram-oxalate-2214.2561 (last visited Oct. 19, 2018).

13 Voltaren is the brand name for diclofenac sodium, a nonsteroidal anti-inflammatory drug (“NSAID”) 

used to treat pain. Diclofenac sodium – Drug Summary, PDR.NET, http://www.pdr.net/drugsummary/Voltaren-XR-diclofenac-sodium-2033.6043 (last visited Oct. 19, 2018).

14 Lotrisone is the brand name for betamethasone dipropionate/clotrimazole, a combination of 

corticosteroids and antifungals. It is used to treat skin infections. Betamethasone dipropionate/clotrimazole 

– Drug Summary, PDR.NET, http://www.pdr.net/drug-summary/Lotrisone-betamethasone-dipropionateclotrimazole-2276 (last visited Oct. 19, 2018).

15 “Myalgia” is muscle pain; “arthralgia” is joint pain. Myalgia, DORLAND’S ILLUSTRATED MEDICAL 

DICTIONARY 150, 1214 (32d ed. 2012) [hereinafter DORLAND’S].

16 “Antalgic” means counteracting or avoiding pain; an “antalgic gait” is a limp adopted so as to avoid pain 

on weight-bearing structures, as in hip injuries. Antalgic, DORLAND’S at 97, 753. 
8

noted to be well and clinically unchanged. Id. Dr. Bai’s assessment was fibromyalgia, chronic 

fatigue syndrome, varicella, and MS. Id. Petitioner was prescribed Elavil, Lyrica, Celebrex, and 

Soma. Id.

On June 30, 2011, petitioner returned to Dr. Bai, with complaints of increased pain with 

stiffness in her lower extremities. Pet. Ex. 3 at 7. She was working two jobs, which she was usually 

able to handle, but now felt partially incapacitated. Id. She had 18 out of 18 classic fibromyalgia 

tender points, bilaterally.17 Id. Dr. Bai’s assessment was fibromyalgia and chronic fatigue 

syndrome; rule out MS flare. Id. Lyrica dosage was increased and she was advised to consult with 

her neurologist as soon as possible. Id. 

On July 5, 2011, petitioner returned to Dr. Faches. She reported that, after her tetanus shot, 

her fibromyalgia “kicked in” and “I can’t move.” Pet. Ex. 6 at 80. She could not raise her arm 

above her head. Id. She reported that Dr. Bai gave her medications, but did not order blood work. 

Id. She complained of myalgias and arthralgias in all joints, with lower back pain causing pain 

when walking, but she could walk in her pool for exercise. Id. She was taking Lyrica, Celebrex, 

Elavil, Soma, Provigil, pantoprazole, Valtrex, and Xanax. Id. Dr. Faches noted no obvious joint 

swelling, redness, or warmth. Id. at 81. Her assessment was fibromyalgia, MS, and 

arthralgia/myalgia. Id. Petitioner was instructed to follow up with Dr. Bai and Dr. Gan. Id. Blood 

work was ordered. Id.

Blood work performed on July 6, 2011 showed an elevated C-reactive protein18 (“CRP”).

 

17 Fibromyalgia patients must have pain in all four quadrants of their body for a minimum of 3 months and 

at least 11 of the 18 specific tender points, according to the classification criteria for fibromyalgia syndrome 

(FMS) published by the American College of Rheumatology (ACR) in 1990. See M. Fitzcharles et al., 2012 

Canadian Guidelines for the diagnosis and management of fibromyalgia syndrome: Executive summary, 

18 PAIN RES MANAG 3: 119-26 (2013), filed as “Pet. Ex. 17.” 

18 C-reactive protein (“CRP”) is a protein used to indicate an inflammatory illness. It is elevated in patients 

with a bacterial infectious disease, tissue necrosis, or an inflammatory disorder. A positive test result 

indicates the presence, but not the cause, of the disease. See Mosby’s Manual of Diagnostic and Laboratory 

Tests 165-66 (Pagana eds., 6th ed. 2018) [hereinafter Mosby’s].
9

Pet. Ex. 6 at 76. Erythrocyte sedimentation rate19 (“ESR”), ALT/AST,20 and CK enzymes, or 

muscle enzymes,21 were normal. Id. at 74-76. 

On July 11, 2011, petitioner underwent MRIs of the brain, thoracic spine, and cervical 

spine. An MRI of the thoracic spine did not show any cord lesions or significant changes. Pet. Ex. 

8 at 10. An MRI of the cervical spine showed facet arthrosis and C5-6 bulge overall but no spinal 

cord lesions. Id. An MRI of the brain showed unchanged punctate white matter foci of signal 

alteration, with no new lesions or infarct. Id. at 9. 

On July 13, 2011, petitioner returned to Dr. Gan complaining of pain. She had stopped 

taking Lyrica. Pet. Ex. 8 at 11. She was noted to be alert, cranial nerves were within normal limits, 

and sensory examination was 5/5. Id. Dr. Gan wrote “questionable fibromyalgia,” and suggested 

a new medication and follow up for “TM.” Id. It is unclear what “TM” refers to.

On July 18, 2011, petitioner returned to Dr. Bai with complaints of “incapacitating pain.” 

Pet. Ex. 3 at 5. Her MS was stable, without exacerbation. Id. Petitioner “insist[s] she be treated 

w/steroids.” Id. On examination, she had no “overt synovitis,” but fibromyalgia tender points were 

18 out of 18. Her CRP was elevated. Id. She also needed calcium and vitamin D supplements. Dr. 

Bai concluded that petitioner was having a flare up of fibromyalgia, and prescribed a trial of low 

dose steroids. Id. 

On July 20, 2011, petitioner presented to Wade Toma, M.D., for a second opinion. Dr. 

Toma noted a 53 year old woman with complaints of pain in her hands, wrists, elbows, shoulders, 

hips, knees, lower back, and leg muscles. Pet. Ex. 5 at 3. She said her pain started after a tetanus 

shot in April. She stated after the shot, she had fever, flu-like symptoms, and arthralgia, then 

stiffness in her muscles, especially her neck, arms, and thighs, with difficulty getting up from a 

chair and with lifting her arms. Id. She had a history of MS, which was inactive. Id. She had 

fibromyalgia, and was treated with Lyrica, Soma, and Elavil, but did not feel better. Id. She 

described aching pain associated with morning stiffness lasting for one hour. Id. She experienced 

 

19 Erythrocyte sedimentation rate (“ESR”) is a non-specific test used to detect illnesses associated with 

acute and chronic infection, inflammation, and tissue necrosis or infarction. Mosby’s at 199.

20 ALT stands for “alanine aminotransferase” and is also known as serum glutamic-pyruvic transaminase. 

Mosby’s at 36-37. ALT is an enzyme found predominantly in the liver. Id. Injury or disease affecting the 

liver will cause elevated ALT levels; therefore, this test is used to help identify liver diseases. Id. A mildly 

elevated ALT is one indicator of myositis. Id. AST stands for “aspartate aminotransferase” and is also 

known as serum glutamic oxaloacetic transaminase. Mosby’s at 107-09. AST is an enzyme found in the 

heart muscle, liver, and skeletal muscle. Id. Injury or disease affecting any of these organs will cause 

elevated AST levels. Id. If the injury or disease is chronic, the levels will be persistently elevated. Id. 

Increased AST levels are an indicator of primary muscle diseases like myopathy and myositis. Id.

21 Creatine kinase (“CK”) is an enzyme found in muscles. Mosby’s at 167-68. CK levels are elevated when 

muscle or nerve cells are injured. Id. It is used to support the diagnosis of myocardial muscle injury and 

can also indicate neurologic or skeletal muscle diseases. Id.
10

gelling22 throughout the day. Id. Her pain was steady all of the time, but worse in the morning. Id. 

She did not sleep well or feel rested in the morning. Id. She stated her blood work showed possible 

PMR. Id. She had stopped taking Lyrica, as advised by her neurologist. Id.

Dr. Toma noted a steady gait, intact coordination, and negative straight leg raising. Pet. Ex. 

5 at 4. She had tenderness and fullness of the first and second MCP joints23 and second, third, and 

fourth PIP joints24 on the right side, and second, third, and fourth MCP joints and second, third, 

and fourth PIP joints on the left side. Id. There was pain on flexion of the wrist joints, pain on 

hyperextension of the elbows, and limited range of motion of the shoulders with diffuse tenderness. 

Id. There was crepitus of the knees and tenderness of the MTP joint.25 Id. The rest of the joints 

revealed no synovitis and good range of motion. Id. She had multiple tender points of fibromyalgia, 

but no spinal tenderness, no sacroiliac joint tenderness, and no proximal muscle weakness or 

tenderness. Id. Blood work showed a normal CPK26 and normal aldolase,27 negative ANA, negative 

rheumatoid factor, CRP at 16.3 and uric acid at 7.2. Id. Dr. Toma’s impression was fibromyalgia 

and osteoarthritis, but noted that it did not explain all of her presentation. “It is unlikely she has 

polymyalgia rheumatica given her age but she does have evidence of inflammatory process 

probably involving the joints given the involvement of the small joints of the hand and limited 

range of motion of the shoulders with the elevated CRP.” Id. at 5.

 

On July 30, 2011, petitioner had x-rays of her left and right hands and wrists, which were 

normal. Pet. Ex. 5 at 8-9. An x-ray of the left shoulder was unremarkable except for slight AC 

joint28 arthritic changes suspected. Id. at 10. An x-ray of the right shoulder was normal. Id. at 11. 

 

22 “Gelling” or “gel phenomenon” is rheumatological stiffness after rest, typical of rheumatic diseases. R. 

Manno, Osteoarthritis: Signs and Symptoms, JOHNS HOPKINS ARTHRITIS CENTER, 

https://www.hopkinsarthritis.org/arthritis-info/osteoarthritis/signs-and-symptoms/ (last updated Aug. 16, 

2017).

23 The “MCP joints” are the metacarpophalangeal joints, which connect the metacarpal bones in the hand 

to the phalanges, the bones in the fingers. DORLAND’S at 1142, 1424. 

24 The “PIP joints” are the proximal interphalangeal joints, which connect the proximal and intermediate 

phalanges (the lower finger bone to the middle finger bone). DORLAND’S at 950, 1424.

25 The “MTP joint” is the metatarsophalangeal joint, which connects the metatarsal bones in the foot to the 

bones in the toes. DORLAND’S at 1145, 1424. 

26 “CPK” is an abbreviation for creatine phosphokinase. Mosby’s at 167. It is the same test as the test for 

creatine kinase (CK) levels. Id.

27 Aldolase is an enzyme used in the breakdown of glucose. Mosby’s at 38. This test is used to diagnose and 

monitor skeletal muscle diseases. Id. Elevated aldolase levels can indicate muscular dystrophy, 

dermatomyositis, or polymyositis. Id. 

28 The “AC joint” is the acromioclavicular joint. It connects the clavicle, or collarbone, to the scapula, or 

shoulder blade. STEDMAN’S POCKET MEDICAL DICTIONARY 10 (1st ed. 1987) [hereinafter STEDMAN’S].
11

On August 16, 2011, petitioner returned to Dr. Toma reporting significant improvement 

taking prednisone, but upon tapering, she had recurrence of pain in her hands, but not as bad as it 

used to be. Pet. Ex. 5 at 6. She noted occasional swelling in her hands. Id. She continued to 

complain of pain in her thumbs and knees and diffuse muscle pain. She did not sleep well or feel 

rested in the morning, and was tired during the day. Id. She had tenderness in the first CMC joint,29

and her knees had crepitus with no warmth or effusion, but the rest of the joint exam revealed no 

synovitis with good range of motion. Id. at 7. She had several tender points of fibromyalgia, but 

no spinal tenderness, no sacroiliac joints tenderness, and no proximal muscle weakness or 

tenderness. Id. Dr. Toma concluded that petitioner had fibromyalgia and osteoarthritis. Id. Since 

there was evidence of inflammatory arthritis at petitioner’s last visit but no synovitis on physical 

exam on that date, Dr. Toma felt rheumatoid arthritis was unlikely. Id. Dr. Toma wrote, “[A]lso, 

her presentation is not consistent with polymyalgia rheumatica.” Id.

According to the record, petitioner presented to Dr. Faches on September 8, 2011. Pet. Ex. 

6 at 30. However, there is no reason or treatment contained in the record for that visit. 

On December 9, 2011, petitioner returned to Dr. Faches reporting that she had not felt well 

since July, was depressed, and “[H]er mood was much better when on prednisone.” Pet. Ex. 6 at 

27. She had been urinating in bed and having problems getting out of bed due to stiff muscles but

had no weakness. Id. She reported her visits with Dr. Bai, medications, and MRI, stating she had 

“done all that was advised.” Id. She stated that she asked Dr. Bai and Dr. Toma about whether she 

had PMR and neither agreed that she did. Id. She then went to Dr. Gan, who reassured her that she 

did not have muscular dystrophy; but he gave her a steroid and she “felt a million times better 

immediately.” “The prednisone was like a miracle.” Id. Dr. Faches documented fatigue, weight 

gain, headache with facial pain, occasional mild dyspnea, muscle pain, and myalgia, but no joint 

pain or weakness. Id. at 28. Petitioner was taking Provigil, naproxen, and Soma. Id. at 27. Dr. 

Faches’ impression was steroid responsive myalgia and depression with anxiety. Id. at 29. 

Petitioner was referred to Dr. Grewal, a neuromuscular specialist. Id.

3. Petitioner’s Treatment with Dr. Grewal

On January 5, 2012, petitioner presented to Dr. Grewal. On the initial visit questionnaire, 

she documented frequent falls, weight change, appetite change, excessive fatigue, night sweats, 

blurred vision, trouble focusing, double vision, hearing loss, high cholesterol, allergies to milk and 

eggs, shortness of breath, lower back pain, arm and leg pain, headache/migraine on the right side 

of her face, vertigo, concentration problems, weakness, pain, trouble walking, panic attacks, and 

insomnia. Pet. Ex. 4 at 12. She was taking Provigil and naproxen, was sedentary, and had quit 

smoking in September 2010 after 30 years of smoking two packs a day. Id. at 13. Petitioner has 

since resumed smoking. Tr. 29. 

In a letter to Dr. Faches dated January 5, 2012, Dr. Grewal noted petitioner’s past medical 

history including MS, suspected demyelinating disease, and treatment with Copaxone and Avonex, 

from which she developed side effects. Pet. Ex. 4 at 14. He noted episodes of vertigo with facial 

 

29 The “CMC joint” is the carpometacarpal joint. The CMC joint is made up of five smaller joints which 

connect the carpal bones in the wrist to the metacarpal bones in the hand. DORLAND’S at 298, 1142. 
12

numbness which were treated with solumedrol (steroids). Id. She did not take medication for MS 

until 2007, when she was hit by a car while working as a crossing guard after which she developed 

numbness and fatigue associated with vertigo and was treated with steroids. Id. She received a 

tetanus booster in April 2011, after a foot injury, and started having some discomfort involving 

her arms and legs. Since then, she has not been the same. She complained of pain with movements 

of her shoulder and hips, which interfered with her activities of daily living. Id. Dr. Bai prescribed 

Elavil, Celebrex, Savella, Lyrica, and carisoprodol for fibromyalgia. Id. Petitioner reported the 

medication was ineffective. Id. “You” (referring to Dr. Faches) thought she may have developed 

PMR and prescribed steroids. Taking steroids she “felt like a new woman,” until the dose was 

reduced to 10 mg a day, at which point her symptoms recurred. Id. Her current medications 

included Provigil and naproxen. Id. 

Dr. Grewal’s examination revealed bilateral tenderness to palpation in the deltoid and 

biceps muscles, with strength limited due to discomfort in the biceps, deltoid, supraspinatus, and 

infraspinatus muscles. Pet. Ex. 4 at 15-16. Lower arms were strong. Id. at 16. She had weakness 

of hip flexion bilaterally associated with pain, but her knee and lower leg muscles were strong. Id. 

She was able to walk on her heels and toes without difficulty, and her gait was normal. Id. Dr. 

Grewal also reviewed the results of blood work performed on July 6, 2011 noting an elevated white 

blood cell count and C-reactive protein three times higher than normal. Id. Her ESR30 was 32 but 

had been 10 on May 22, 2011. Id. Otherwise, her metabolic panel, testing for rheumatoid factor, 

ANA, Lyme serology, lupus anticoagulant, protein S, anti-cardiolipin antibody, anti-nuclear 

antibody, and homocysteine were all normal. Id. MRIs were unchanged. Id. Dr. Grewal 

acknowledged that he did not have petitioner’s records of prior episodes of MS, but concluded that 

her muscle pain and weakness were not related to MS and it was “interesting that this condition 

occurred after the tetanus vaccination.” Id. He requested an EMG/NCS to determine possible 

inflammatory myositis. Id.

On January 11, 2012, Dr. Grewal issued an addendum to his report, adding that the EMG 

showed mild evidence of myositis in a sampling of the right biceps muscle. Pet. Ex. 4 at 16. He 

recommended a left biceps muscle biopsy. Id. The EMG report stated, “This electrophysiological 

study shows no strong evidence of a neuropathy. The mild abnormalities on needle EMG in the 

right biceps are of unclear significance, but favor a myopathic31 process.” Id. at 8-9. 

On January 18, 2012, petitioner presented to Dr. Gregory Przybylski for an exam in 

preparation for a biopsy of her left bicep. Pet. Ex. 9 at 82. She provided a history of having received 

a tetanus vaccine in April 2011, after which she “became ill with flulike symptoms right away and 

 

30 ESR measures the rate at which red blood cells settle in a solution over an hour. Mosby’s at 199-201. The 

normal range for women is 0-20 millimeters per hour, but the upper threshold may vary from one medical 

practice to another, so petitioner’s 32 is elevated but not grossly out of range. Id. The worse the disease is, 

the higher the ESR will be. Id. A mildly high ESR can indicate anemia, infection, or pregnancy. Id. A very 

high ESR usually has an obvious cause such as chronic renal failure, bacterial infection, necrotic disease, 

or inflammatory disease like PMR or temporal arteritis. Id. 

31 “Myopathic” or “myopathy” is any abnormal condition or disease of the muscular tissues, especially 

involving skeletal muscle. Myopathy, STEDMAN’S at 488. 
13

has since developed severe persistent pain and stiffness in the proximal arms and legs.” Id. 

Petitioner informed Dr. Przybylski that taking prednisone “resulted in substantial improvement,” 

while discontinuing it resulted in recurrent pain. Id. Examination revealed normal upper and lower 

limb strength, tone, sensation, and 2+ upper limb and patellar reflexes without Hoffman’s signs or 

ankle clonus. Id. at 83. Her casual gait and heel and toe walking were normal, but she had mild

trouble with tandem gait. Id. 

Petitioner returned to Dr. Faches on January 20, 2012 and reported that Dr. Grewal was 

“concerned that her myalgia could be related to the tetanus vaccine.” Pet. Ex. 6 at 23. She 

complained of severe pain, and an inability to sleep more than three hours per night or do anything 

without pain. Id. She was taking Provigil and naproxen. Id. Dr. Faches noted complaints of neck 

pain, difficulty breathing on exertion, nasal congestion, anxiety, a change in sleep patterns, and 

depression. Id. at 24. Upper and lower extremity strength and gait were normal. Id. at 25. Reflexes 

were 2+ in both knees. Id. Dr. Faches’s impression was steroid responsive myalgia, 

hypercholesterolemia, and herpes simplex virus II infection. Valtrex was prescribed. Id. A recent

abnormal EKG was sent to petitioner’s cardiologist, Dr. Panebianco, who thought the abnormal 

results were due to improper lead placement or body habitus. Id. at 22.

On January 23, 2012, a left bicep biopsy was performed, finding the “presence of selective 

type 2B fiber atrophy which can be seen in association with muscle disuse or the administration 

of corticosteroids.” Pet. Ex. 9 at 92-93. The impression was “skeletal muscle with non-specific 

abnormalities.” Id.

 

On January 31, 2012, petitioner presented to Dr. Faches with a sore throat and frequent 

urination. She made no other complaints. Examination was normal. Pet. Ex. 6 at 19-20. A strep 

test and urine analysis were both negative. Id. at 18, 21. Rest and fluids were recommended. Id. at 

21. 

Petitioner returned to Dr. Faches on February 1, 2012 with acute sinusitis. She was 

prescribed Levaquin. Pet. Ex. 6 at 17. She returned again on February 7, 2012, for the same 

complaints and was prescribed Proventil. Id. at 16.

Petitioner did not see Dr. Grewal again until March 5, 2012. At that visit he advised her 

that the muscle biopsy showed “there were mild nonspecific abnormalities with no clear evidence 

of an inflammatory myopathy, however, as I informed the patient this does not exclude an 

inflammatory myositis.” Pet. Ex. 4 at 6. Petitioner had “a dramatic response to steroids.” A taper 

was suggested. Id. Dr. Grewal discussed the use of IVIG for conditions like inflammatory 

myopathies, along with its side effects. Id. Petitioner’s most recent blood work was normal.32 Dr. 

 

32 “The following blood tests were ordered and were either negative or normal: CBC and differential, ANCA 

panel, comprehensive metabolic panel, serum protein electrophoresis and immunofixation, ENA, Sjogren’s 

antibodies, B12, folate, ANA, rheumatoid factor, anti-double stranded antibodies, anti-Jo-1, anticentromere B antibodies, anti-scleroderma-70 antibodies, homocysteine, ACE, vitamin B6, vitamin E, 

vitamin B1, anti-gliadin antibody, aldolase, CPK, Lyme serology, cryoglobulin, serum, magnesium, copper, 

zinc and amylase, and anti-GAD antibody.” Pet. Ex. 4 at 6; see also Pet. Ex. 6 at 38, 56-62. 
14

Grewal’s assessment was “[P]ossible inflammatory myositis.” Id. at 7. She was to restart the 

medications that she was on prior to the biopsy, including Elavil. Id. 

On April 12, 2012, petitioner presented to Dr. Faches with complaints of gastroesophageal 

reflux disease (“GERD”) and allergies ongoing for three weeks. Pet. Ex. 6 at 13. She reported 

increased heartburn “over the last week” and she “always needs an acid med [sic] when on a

steroid.” Id. She was taking Valtrex, Proventil, prednisone, Provigil, and omeprazole. Id. Her 

examination was normal. She was prescribed Clarinex. Id. at 14-15. 

On May 8, 2012, petitioner returned to Dr. Faches with bronchitis. Pet. Ex. 6 at 10. She felt 

out of breath and had sinus pressure in her head and pain in her teeth. Id. She complained of sore 

throat with voice change, cough, post-nasal drip, sinus pain, swelling of the neck glands, and ear 

pain that was worse in her left ear. Id. Levaquin was “restarted”. Id. at 12. Petitioner felt her 

dyspnea was worse, and agreed to see both a cardiologist and a pulmonologist. Id. She was referred 

to Dr. Mellilo.33 Id.

On August 13, 2012, petitioner returned to Dr. Grewal with MS and muscle pain. Pet. Ex. 

7 at 39. She was prescribed 20 mg of prednisone every other day, alternating with 15 mg. Id. at 

40.

On October 1, 2012, petitioner returned to Dr. Grewal reporting severe myalgias with joint 

stiffness when prednisone was reduced to 15 mg a day. Pet. Ex. 4 at 17; Pet. Ex. 7 at 20. This was 

the third time a prednisone reduction was attempted. Id. Dr. Grewal increased her dose of 

prednisone to 20 mg a day. Id. He wrote, “[I]n terms of the etiology of her symptoms, it is likely 

that this is a vaccine related rheumatological condition. It was not present prior to the vaccination 

and there is a temporal relationship in the development of symptoms after the vaccination 

suggesting cause and effect.” Id.

Petitioner returned to Dr. Faches on October 16, 2012 with fever, chills, diarrhea, loss of 

appetite, night sweats, sweating, and facial pressure. Pet. Ex. 6 at 7. She had lost some weight and 

felt better “body wise,” but “felt lousey [sic] when [Dr. Grewal] tried to decrease her steroids.” Id. 

Petitioner was diagnosed with probable viral syndrome which was improving. Id. at 9.

Petitioner returned to Dr. Faches on November 30, 2012, complaining of a cold, sore throat, 

cough, facial pain and pressure, headache, ear pain, shortness of breath, fatigue, weakness, chills, 

and body aches. Pet. Ex. 6 at 4. She was diagnosed with acute frontal sinusitis and prescribed 

Levaquin. Id. at 6. 

On February 18, 2013, petitioner returned to Dr. Grewal reporting that she had tried to 

reduce the prednisone but was unable to tolerate less than 20 mg a day. Pet. Ex. 7 at 3. She did not 

have significant muscle or joint pain, and her neuromuscular examination showed 5/5 strength 

both proximally and distally. Id. Imaging studies done on January 29, 2013, showed no new spinal 

cord or brain lesions. Id. Because petitioner reported that her symptoms were worse in cold 

weather, Dr. Grewal suggested reducing her dosage of prednisone once the weather became 

 

33 No records of any treatment with Dr. Mellilo were filed. 
15

warmer. Id. He again discussed IVIG, methotrexate, and Imuran as steroid-sparing medications. 

Id. 

On May 13, 2013, petitioner returned Dr. Grewal for follow-up of “myositis.” Pet. Ex. 7 at 

35. She was alternating prednisone daily between 20 mg and 15 mg. Id. at 36. Dr. Grewal wrote, 

petitioner has an established diagnosis of MS and inflammatory myositis. “The diagnosis is not in 

doubt and has been made on the basis of a [sic] EMG which showed evidence of an inflammatory 

myositis. She has been responsive to prednisone, but now is becoming intolerant. Previous 

attempts to reduce the prednisone have resulted in increased weakness and inability to walk or 

perform activities of daily living.” Pet. Ex. 9 at 75. Her physical examination showed proximal 

muscle weakness and muscle tenderness. Id. She had 4/5 strength in the deltoids, biceps, and hip 

flexion. Id. IVIG weekly for three months to treat inflammatory myositis was recommended. Id. 

“This can be used in conjunction with the prednisone which can then be slowly withdrawn.” Id.

IVIG infusions consisting of solumedrol34 with IV Benadryl first and Tylenol began. Pet. 

Ex. 9 at 5. Petitioner’s neurological examination on June 30, 2013, prior to starting IVIG was 

normal. Pet. Ex. 7 at 32. Petitioner was also taking prednisone, alternating daily between 20 mg 

and 15 mg. Id. at 34. At the time of hearing, petitioner was still receiving IVIG treatments along 

with daily prednisone.35 Pet. Ex. 10 at 1. 

In a June 21, 2014 letter, Dr. Grewal wrote, petitioner developed a “polymyalgia 

rheumatica like” disorder following a tetanus vaccine. Pet. Ex. 10 at 1. She had a history of MS 

that had been clinically and radiologically stable. Id. She also had preexisting fibromyalgia, but 

her joint and muscle stiffness and pain with movement started after her tetanus shot in April of 

2011. Id. These symptoms interfered with petitioner’s activities of daily living. Id. Petitioner’s 

symptoms improved with steroids, but weaning off steroids caused symptoms to recur. Id. Dr. 

Grewal opined that petitioner’s EMG and muscle biopsy support a co-existing myositis, also an 

autoimmune /inflammatory disease. Id. He noted that the EMG provided evidence of myositis, not 

features of fibromyalgia. Id. “The clinical features and response to steroids are more indicative of 

PMR than of fibromyalgia. Fibromyalgia does not respond to steroids.” Id.

Almost a year later, on May 7, 2015, Dr. Grewal documented that petitioner had 

“deteriorated.” Pet. Ex. 39 at 12. She had documented MS and associated autoimmune 

rheumatological disorder which had features consistent with an inflammatory myositis, sensitive 

to prednisone and to the combination of IVIG and prednisone. Id. 

On November 5, 2015, Dr. Grewal wrote that petitioner required a cardiac workup due to 

shortness of breath, which he suspected was related to deconditioning. Pet. Ex. 39 at 11. She had 

a “polymyalgia rheumatica like” disorder which “possibly” had a component of inflammatory 

 

34 Solumedrol is an anti-inflammatory glucocorticoid, which contains methylprednisolone sodium succinate 

as the active ingredient – a steroid. Solumedrol, DORLAND’S at 1154, 1731. 

35 Petitioner developed a rash due to an albumin allergy and the IVIG was switched without event. Pet. Ex. 

9.
16

myositis. Id. She was receiving weekly IVIG and was taking 10 mg of prednisone per day. IVIG 

reduction to every other week was recommended. Id.

On March 28, 2016, according to Dr. Grewal, petitioner was taking 10 mg of prednisone a 

day, “the lowest dose that she has been on for more than a year.” Pet. Ex. 39 at 9. She was off 

IVIG for several months but felt worse, with discomfort in her joints, muscle tenderness, and 

weakness. Id. Petitioner advised that she slipped, fell, and was unable to get up. Id. On 

examination, she was unable to walk on her heels and toes and had a positive Romberg sign.36 Id. 

Dr. Grewal recommended resuming IVIG every two weeks. Id. He concluded that the recurrence 

of petitioner’s symptoms on 10 mg of prednisone while off of IVIG meant that a component of her 

symptoms was responsive not only to the prednisone, but also to IVIG. Id. He further noted that 

petitioner was intolerant to medications for MS and the IVIG had the additional benefit of being a 

known useful alternative treatment for patients with relapsing-remitting MS. Id. at 10.

In his record of June 13, 2016, Dr. Grewal documented that petitioner had MS and myositis. 

Pet. Ex. 39 at 17. 

Thereafter, Dr. Grewal’s records fluctuate between a diagnosis of myalgia/myositis and 

MS, myositis and MS, and inflammatory myositis and MS. PMR is no longer listed. See Pet. Ex.

39 at 7-39; Pet. Ex. 41 at 2-4. At hearing, Dr. Grewal stated his working diagnosis all along was

“PMR-like” and “myositis-like” disease because petitioner’s “autoimmune process... [is] 

affecting not just the connective tissue but perhaps the muscles as well.” Tr. 105. 

On November 28, 2016, Dr. Grewal wrote that petitioner had an established diagnosis of 

inflammatory myositis and MS. Pet. Ex. 39 at 7. She continued to have double vision in addition 

to weakness and imbalance. Id. Dr. Grewal noted that some of these symptoms were related to 

petitioner’s MS and some to her inflammatory myositis. Id.

The most recent record filed was from Dr. Faches dated August 4, 2017. It documented 

that petitioner was doing well, though “still depressed a little.” Pet. Ex. 42 at 6, 8. She presented 

for management of hyperlipidemia and associated symptoms of decreased exercise tolerance and 

edema. She had GERD, but no chest pain or dysphagia. Id. at 6, 8. She continued to smoke and 

likely had COPD. Id. She was on 10 mg of prednisone daily and IVIG every 10 days. Id. at 6. A

GI specialist was recommended. Id. at 8. 

 

36 A positive Romberg sign occurs when the patient’s balance is more unsteady when his or her eyes are 

closed, and “indicates a loss of proprioceptive control.” Romberg sign, STEDMAN’S at 684.
17

C. Testimony of Petitioner37 Julie Suliman 

Petitioner testified that 23 years ago, she consulted a neurologist38 due to weakness in her 

left arm and loss of balance. She was diagnosed with MS. Tr. 7. She opted not to take medications, 

and remained without any significant issues related to her MS until about 2007, when she was hit 

by a car while working as school crossing guard. Tr. 8. Six months later, she developed symptoms 

of MS with facial and tongue numbness. Tr. 8, 21. She took Copaxone for about two years until it 

caused her to develop hives. Tr. 9, 24. Avonex made her sick as well. Tr. 9, 24. Infusions of 

solumedrol “cleared it up.” Tr. 8, 24-25. She may have had additional steroid infusions thereafter. 

Tr. 8. She also developed episodes of shingles, which were treated with Valtrex. She continues to 

have repeated “break outs” of shingles and left leg weakness during her menstrual cycle. Tr. 22. 

The following winter, petitioner began “feeling achy.” Dr. Faches referred her to Dr. Bai, 

a rheumatologist. Tr. 8. Dr. Bai diagnosed her with fibromyalgia and prescribed medication. Tr. 

8. She stopped taking the medications in the spring and was able to work and live her life normally. 

Tr. 9. Petitioner did not recall seeing Dr. Bai again until after the tetanus shot. Tr. 26. She did not 

follow up with Dr. Bai regularly. She went only if she had a problem with her fibromyalgia. Tr. 

26. Petitioner stated she would report all of her health-related issues to Dr. Faches. Tr. 27. 

Petitioner smoked for 30 years; she tried to quit in July 2010 and gained 30 pounds. Tr. 28, 

30. She was able to quit for a few years, but returned to smoking again. Tr. 29. She has gained 50 

pounds in total since 2010. Tr. 29-30.

Petitioner was questioned about her visit with Dr. Faches a month prior to the Tdap 

vaccination, on March 4, 2011, which documented complaints of “a lot of fibromyalgia pain,” 

“problems sleeping due to pain,” and Dr. Gan’s prescribing Lyrica, but petitioner refusing it and 

requesting Lexapro instead.39 Tr. 30; Pet. Ex. 6 at 83. Petitioner denied having any pain or 

problems sleeping the month before the tetanus shot. She did not recall seeing Dr. Faches on that 

date. Tr. 30-31. 

Petitioner testified that she tripped in her house and a staple went under the nail bed of her 

toe. Tr. 9, 33. The next day, April 1, 2011, she saw Dr. Faches and informed her that she was 

taking Lexapro, Valtrex, Xanax, and Provigil,40 which helped with clarity and was prescribed by 

Dr. Gan. Tr. 33; Pet. Ex. 6 at 82. Petitioner did not recall having a sore throat or advising Dr. 

 

37 Petitioner never filed an affidavit with her petition. The statute and the rules require the documentation 

supporting the claim be filed with the petition. 42 U.S.C.A. § 300aa-11(c); RCFC, Appendix B, Vaccine 

Rule 2. The Vaccine Rules specifically state that “if the required medical records are not submitted, the 

petitioner must include an affidavit detailing the efforts made to obtain such records and the reasons for 

their unavailability. If petitioner’s claim does not rely on medical records alone but is also based in any part 

on the observations or testimony of any person, the petitioner should include the substance of each person’s 

proposed testimony in a detailed affidavit(s) supporting all elements of the allegations made in the petition.”

RCFC, Appendix B, Vaccine Rule 2(c)(2)(B)(i)-(ii).

38 Petitioner did not supply any medical records pertaining to this initial visit. However, the record is replete 

with references to petitioner’s MS diagnosis. See, e.g., Pet. Ex. 3 at 22; Pet. Ex. 5 at 3; Pet. Ex. 9 at 76.

39 There is no record of petitioner seeing Dr. Gan during this timeframe.

40 There are no records from Dr. Gan of this prescription. 
18

Faches that she was exposed to strep, or had a stomach virus the week before, as reflected in her 

record. Tr. 34. She did recall receiving Tdap vaccine, but did not recall in which arm. She did not 

recall receiving any information about the vaccine or being told to contact the doctor’s office if 

she had any adverse effects. Tr. 35-36. Petitioner confirmed that she had tetanus vaccines in the 

past. Tr. 34. 

According to petitioner, she awoke the next day with flu-like symptoms, was unable to get 

off her couch, and felt like “somebody beat [her].” Tr. 10. Her arm hurt where she received the 

vaccine, but she could not remember which arm. She felt feverish, but did not take her temperature. 

She did not recall having a sore throat. Her “primary concern was the muscular pain.” Tr. 36. She 

did not call Dr. Faches about her symptoms, but she did cancel a hair appointment scheduled for 

that day. Tr. 37.

Petitioner recalled going to see Dr. Bai two weeks later on April 18, 2011, because she was 

having muscle pain. She confirmed that Dr. Bai was the first doctor she saw after the tetanus shot. 

Tr. 10, 37-38. She told Dr. Bai that she had muscular and joint pain in her arms, hips, and legs, 

trouble getting up and lifting her arms following receipt of a tetanus shot. Tr. 10-11, 38. Petitioner 

could not remember if Dr. Bai did a fibromyalgia examination. She told Dr. Bai that she felt 

different, that her symptoms did not feel like fibromyalgia pain. Tr. 11, 39; 48-49. Celebrex and 

Lyrica were prescribed; petitioner could not recall if she had been on those medications before. 

Tr. 40; Pet. Ex. 3 at 10.

Petitioner was questioned about Dr. Bai’s record for April 26, 2011, which noted

“significant improvement since restarted meds.” Pet. Ex. 3 at 9. Petitioner did not recall getting 

better in the weeks that followed, but if Dr. Bai’s records said that she did, she must have appeared 

to get better. Tr. 40. “I could have had a good day and then that’s what [Dr. Bai] wrote.” Tr. 44.

She stated, within a month or two of receiving the Tdap vaccine, “I went downhill to the point 

where I couldn’t roll over in bed. I couldn’t get up.” Tr. 10. “I ended up getting worse and seeking 

another opinion....Definitely by sometime in June and then going into July...So it was definitely 

in that June to July where this was not working for me anymore.” She added “I was always 

symptomatic. It always felt like it was, you know, there. Maybe some days were better than others, 

but past June it started getting consistent and worse.” Tr. 40-41. When questioned about the 

accuracy of Dr. Bai’s record regarding improvement once on medications for fibromyalgia,

petitioner responded “I don’t remember. I don’t remember. I only remember the end result was 

that getting worse.” Tr. 45. 

Petitioner was questioned about her visit with Dr. Bai on June 30, 2011, which documented

complaints of stiffness in her lower extremities for the first time. Tr. 43. Petitioner stated that she 

had lower back problems, stiffness and difficulty getting up prior to that appointment, but Dr. Bai 

must not have written it down. Tr. 43. She stated the pain may not have been there; it may have 

developed later.41 Tr. 43, 48. Petitioner was questioned about the change in her condition between 

April and June of 2011. She admitted that the medication Dr. Bai prescribed did help her, but “then 

 

41 This statement was contrary to her prior testimony that, after the vaccine, her “primary concern was pain,” 

and that she complained to Dr. Bai of pain. Tr. 10, 36-38.
19

it got worse. Whatever she had me on was not working anymore, which is why I went back.” Tr. 

47-48. She explained,

...I felt like I was getting worse where I couldn’t, like, get out of bed, get off the 

toilet. It was getting increasingly more difficult for me to get up. It would take me 

like two hours in the morning in my office to just, like, get my body moving...In 

my opinion, it was going on all along. But it got significantly worse in June and 

into July. It was a progression. I don’t know—I don’t remember—I only remember 

the bad. Not the good.

Tr. 46. 

Petitioner stated after the medications stopped working, she went to Dr. Toma for a second 

opinion. Tr. 11, 41. He prescribed steroids, and “[t]he minute I took the steroids, I felt like a new 

person,” but as soon as the steroids were tapered, her symptoms returned. Tr. 11-12, 41-42. 

Petitioner agreed that she had taken steroids for her MS several times since 2008, and that she 

always felt better while on prednisone. Tr. 54-57. 

Petitioner stated that she went to her neurologist, Dr. Gan, on July 13, 2011, and he “didn’t 

know what to do with me. He had no idea.” Tr. 12. Petitioner stated she told all of the doctors that 

her symptoms began after the tetanus vaccine. Tr. 12. 

According to petitioner, she did not see a doctor again until she saw Dr. Faches on 

December 8, 2011. She claimed that she was unable to see Dr. Faches, because Dr. Faches moved 

her offices.42 Tr. 12, 49-50. At that visit, she told Dr. Faches that she did not want to go back to 

Dr. Bai or Dr. Toma because they did not believe her or have any theory about what was wrong 

with her. Dr. Faches referred her to Dr. Grewal. Tr. 12. According to petitioner, she self-medicated 

with steroids until she could get in to see Dr. Grewal.43 Tr. 12. She could not recall which doctor 

first suggested PMR to her. Tr. 62.

Petitioner saw Dr. Grewal in January of 2012; he took her off steroids in order to do a 

muscle biopsy, and then she went back on steroids. 

44 Tr. 12-13. She started IVIG treatments in 

June of 2013. Tr. 13. Now she takes multiple medications in addition to IVIG to treat her weight 

gain and high blood pressure. Tr. 13.

 

42 Dr. Faches’ record shows that there was an appointment in September of 2011, but the reason was not 

documented. Pet. Ex. 6 at 30. 

43 There is no record of who prescribed the steroids that petitioner was taking at that time, or of the dosage 

that petitioner was taking. Dr. Grewal’s record does not include a prescription for steroids until March 

2012. 

44 It appears that petitioner was off steroids from January through March 2012 when Dr. Grewal prescribed 

them again; she continued working during that time. See Pet. Ex. 9 at 83 (Dr. Przybylski noted on January 

18, 2012, “She had been taken off of steroids, and Dr. Grewal did not want to resume them until after a 

biopsy specimen was obtained.”); Pet. Ex. 4 at 6 (Dr. Grewal noted on March 5, 2012, that petitioner had 

“been restarted on prednisone.”). 
20

I asked petitioner to describe the differences in her symptoms from an MS flare, a 

fibromyalgia flare, and those she experienced in April 2011. She responded that an MS flare 

presents as facial paralysis and feeling drunk, like “jelly,” with her whole body feeling like it is on 

Novocain. Tr. 58. A fibromyalgia attack is muscle aches, fatigue, and a burning sensation when 

someone touches her skin. Tr. 15, 58-60. The muscle pain after the vaccination felt like somebody 

had beaten her, or she lifted weights and “overdid it.” Tr. 14-15, 58-60. It was movement 

restriction, with pain in her shoulder, lower back, and upper thighs. Tr. 14. Although petitioner 

received the Tdap vaccine in her left arm, she described joint pain in her hand, especially her right 

thumb, as well as her ankles and knees, with stiffness on both sides of her body. Tr. 14-15, 59. 

Petitioner claims since the vaccination, she has not had any fibromyalgia flares, only MS flares. 

Tr. 60-61.45 

Petitioner stated that prior to April of 2011, other than when she had MS attacks, she was 

a single working mom. She took care of her house, worked as a crossing guard for an elementary 

school, and worked for an insurance company doing audits as well as reviewing other auditors’ 

work. Tr. 16-17. She used to work up to eight cases in a day; now, she works one or two days a 

week, two or three cases. Tr. 18-19. Before the vaccination, she painted, hung wallpaper, mowed 

the lawn, and cared for her pool. Tr. 17. She now knows her limitations and has to make 

accommodations; she cannot walk too far or overdo it, or she will be unable to do anything for 

days. Tr. 15. Stairs are hard for her, and she cannot walk freely; she has to hold onto something. 

Tr. 11, 20. Cold weather bothers her as well. Tr. 18. Petitioner continues to treat only with Dr. 

Faches and Dr. Grewal. Tr. 41.

III. The Experts

A. Petitioner’s Treating Physician and Expert, Dr. Raji Grewal 

Dr. Grewal specializes in neurology at LifeCare Physicians of Hamilton in New Jersey. 

Pet. Ex. 12 at 1. He is a staff neurologist at the Neuroscience Institute of Saint Francis Medical 

Center and a Professor of Neuroscience at the School of Graduate Medical Education at Seton Hall 

University. Id. Dr. Grewal received his medical degree in 1982 from the University of Alberta at 

Edmonton in Alberta, Canada. Id. He completed residencies in internal medicine, biochemistry, 

and neurology. Id. at 2. In his current practice, Dr. Grewal provides second opinions on 

neuromuscular cases, as well as for patients with unclear diagnoses. Tr. 65. Because of this, he 

tends to get undiagnosed patients who are not always clearly neuromuscular cases. Tr. 65. Prior to 

2010, Dr. Grewal saw 40 to 50 patients a week; now he sees 30 to 35, with a mixture of new 

patients and follow-ups. Tr. 66. Dr. Grewal does not treat patients with PMR. Tr. 117-18. Dr. 

Grewal has not authored or coauthored any peer-reviewed publications on vaccines, ASIA, PMR, 

fibromyalgia, or inflammatory myositis. Tr. 118-19. He has never submitted a case report that a 

neuromuscular condition for a patient he treated may have been caused by a vaccine. Tr. 119. He 

has not been involved in immunology research, or taught immunology. Tr. 119. 

 

45 This is confusing since Dr. Grewal noted that steroids would work on MS but have no effect on 

fibromyalgia. Tr. 105. 
21

B. Respondent’s Expert, Dr. Mehrdad Matloubian

Dr. Matloubian is an Associate Adjunct Professor at the University of California at San 

Francisco School of Medicine. Resp. Ex. T at 2. Dr. Matloubian received his bachelor’s degree in 

biochemistry, Ph.D., and medical degree from UCLA. Id. at 1. He completed his residency in 

internal medicine and a fellowship in rheumatology. Id. Dr. Matloubian is an immunologist and 

board certified rheumatologist who actively evaluates and treats patients with complex 

autoimmune diseases, including rheumatoid arthritis, lupus, mixed connective tissue disease, 

PMR, different types of inflammatory myositis, and vasculitis. Tr. 189; Resp. Ex. A at 1. He sees 

patients who have been referred by general practice physicians for evaluation as well as those who 

have been referred by rheumatologists for second and third opinions. Tr. 189-90. Often, his 

patients either are not responding to treatment, have complex autoimmune diseases affecting many 

organs, or do not fit into one disease category. Tr. 190-91. Dr. Matloubian also has a Ph.D. in 

microbiology and immunology with an emphasis in virology. Tr. 209. His post-doctoral training 

focused on how lymphocytes, or white blood cells, travel from different tissues and different 

organs, and immune responses to acute and chronic viral infections focusing on both innate and 

adaptive immune responses. Tr. 275-76. Therefore, he is familiar with the mechanics of 

immunology and how the immune system responds to various antigens. Tr. 276. He has published 

several articles on immunology, particularly on lymphocyte trafficking, in peer-reviewed journals. 

Tr. 276; see also Resp. Ex. T at 10-13 (listing Dr. Matloubian’s articles published in peer-reviewed 

journals). His other research interests include autoimmune disease, interferons, plasmacytoid 

dendritic cells, antibody responses in chronic viral infection, chemokines, and chronic 

inflammation. Resp. Ex. T at 2.

IV. Findings of Fact

A. Legal Standard Regarding Fact Finding

The process for making determinations in Vaccine Program cases regarding factual issues, 

such as the timing of onset of petitioner’s alleged injury, begins with analyzing the medical 

records, which are required to be filed with the petition. 42 U.S.C. § 300aa-11(c)(2). Medical

records created contemporaneously with the events they describe are presumed to be accurate and 

“complete” such that they present all relevant information on a patient’s health problems. Cucuras 

v. Sec’y of Health & Human Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993); Doe/70 v. Sec’y of 

Health & Human Servs., 95 Fed. Cl. 598, 608 (2010) (“Given the inconsistencies between 

petitioner’s testimony and his contemporaneous medical records, the special master’s decision to 

rely on petitioner’s medical records was rational and consistent with applicable law.”). This

presumption is based on the linked proposition that (i) sick people visit medical professionals; (ii) 

sick people honestly report their health problems to those professionals; and (iii) medical 

professionals record what they are told or observe when examining their patients in an accurate 

manner, so that they are aware of enough relevant facts to make appropriate treatment decisions. 

Sanchez v. Sec’y of Health & Human Servs., No. 11-685V, 2013 WL 1880825, at *2 (Fed. Cl. 

Spec. Mstr. Apr. 10, 2013); Cucuras v. Sec’y of Health & Human Servs., 26 Cl. Ct. 537, 543 

(1992), aff’d, 993 F.2d. 1525 (Fed. Cir. 1993)(“[I]t strains reason to conclude that petitioners 

would fail to accurately report the onset of their daughter’s symptoms. It is equally unlikely that 

pediatric neurologists, who are trained in taking medical histories concerning the onset of 
22

neurologically significant symptoms, would consistently but erroneously report the onset of 

seizures a week after they in fact occurred.”). 

Where medical records are clear, consistent, and complete, they should be afforded 

substantial weight. Lowrie v. Sec’y of Health & Human Servs., No. 03-1585V, 2005 WL 6117475,

at *20 (Fed. Cl. Spec. Mstr. Dec. 12, 2005). Indeed, contemporaneous medical records are 

generally found to be deserving of greater evidentiary weight than oral testimony—particularly 

where such testimony conflicts with the record evidence. Cucuras, 993 F.2d at 1528; see also 

Murphy v. Sec’y of Health and Human Servs., 23 Cl. Ct. 726, 733 (1991), aff’d per curiam, 968 

F.2d 1226 (Fed. Cir. 1992) cert. den’d; Murphy v. Sullivan, 506 U.S. 974 (1992) (citing United 

States v. United States Gypsum Co., 333 U.S. 364, 396 (1947) (“It has generally been held that 

oral testimony which is in conflict with contemporaneous documents is entitled to little evidentiary 

weight.”)). In making contemporaneous reports, the declarant’s motivation for accurate explication 

of symptoms is more immediate, as opposed to testimony offered after the events in question, 

which is considered inherently less reliable. Reusser v. Sec’y of Health & Human Servs., 28 Fed. 

Cl. 516, 523 (1993). 

Despite the weight afforded medical records, special masters are not bound rigidly by those 

records in determining onset of a petitioner’s symptoms. Vallenzuela v. Sec’y of Health & Human 

Servs., No. 90-1002V, 1991 WL 182241, at *3 (Fed. Cl. Spec. Mstr. Aug. 30, 1991); see also Eng 

v. Sec’y of Health & Human Servs., No. 90-1754V, 1994 WL 67704, at *3 (Fed. Cl. Spec. Mstr. 

Feb. 18, 1994) (explaining that §13(b)(2) “must be construed so as to give effect also to §13(b)(1) 

which directs the special master or court to consider the medical records [reports, diagnosis, 

conclusions, medical judgment, test reports, etc.] but does not require the special master or court 

to be bound by them.”) (emphasis in original). There are situations in which compelling oral 

testimony may be more persuasive than written records—for instance, in cases where records are 

deemed to be incomplete or inaccurate.46 Campbell v. Sec’y of Health & Human Servs., 69 Fed. 

Cl. 775, 779 (2006)(“like any norm based upon common sense and experience, this rule should 

not be treated as an absolute and must yield where the factual predicates for its application are 

weak or lacking.”); Lowrie, 2005 WL 6117475, at *19 (“Written records which are, themselves, 

inconsistent, should be accorded less deference than those which are internally consistent.”)

(quoting Murphy, 23 Cl. Ct. at 733 (1991). However, when such testimony is used to overcome 

the presumption of accuracy afforded to contemporaneous medical records, it must be “consistent, 

clear, cogent, and compelling.” Sanchez, 2013 WL 1880825, at *3 (citing Blutstein v. Sec’y of 

Health & Human Servs., No. 90-2808V, 1998 WL 408611, at *5 (Fed. Cl. Spec. Mstr. June 30, 

1998)). A determination regarding a witness’s credibility is needed when determining the weight 

that such testimony should be afforded. Andreu v. Sec’y of Health & Human Servs., 569 F.3d 1367, 

1379 (Fed. Cir. 2009); Bradley v. Sec’y of Health & Human Servs., 991 F.2d 1570, 1575 (Fed. Cir. 

 

46 In determining the accuracy and completeness of medical records, the Court of Federal Claims has listed 

four possible explanations for inconsistencies between contemporaneously created medical records and 

later testimony: (1) a person’s failure to recount to the medical professional everything that happened during 

the relevant time period; (2) the medical professional’s failure to document everything reported to her or 

him; (3) a person’s faulty recollection of the events when presenting testimony; or (4) a person’s purposeful 

recounting of symptoms that did not exist. La Londe v. Sec’y of Health & Human Servs., 110 Fed Cl. 184, 

203-04 (2013), aff’d, 746 F.3d 1334 (Fed. Cir. 2014). 
23

1993). The special master must then determine whether to afford greater weight to 

contemporaneous medical records or testimony given at hearing. This decision must in turn be 

supported by evidence that it was the result of a rational determination. Burns by Burns v. Sec’y of 

Health & Human Servs., 3 F.3d 415, 417 (Fed. Cir. 1993). Ultimately, “the record as a whole” 

must be considered. 42 U.S.C. § 300aa-13(a).

B. Petitioner Alleges that She Suffers from PMR Caused by the Tdap Vaccine 

In his reports and records, Dr. Grewal’s diagnosis varied between PMR, PMR-like, 

myositis, inflammatory myositis and a hybrid autoimmune complex with features of both PMR 

and myositis. Dr. Matloubian disagreed, and submitted that petitioner has PMR, not myositis.

Inflammatory myositis is a heterogeneous group of disorders classified into several 

subtypes, including dermatomyositis and polymyositis. Resp. Ex. Q47 at 2. Dermatomyositis is an 

autoimmune disease which mainly affects muscle and skin, typically characterized by muscle 

weakness, elevated muscle enzymes, and skin lesions. Pet. Ex. 2248 at 1. Dermatomyositis is

thought to be caused by hyperactivation and dysregulation of the adaptive immune system, with 

both humoral and cellular components, although recent studies have highlighted the activation of 

the innate immune system as an important pathological hallmark of dermatomyositis. Id. at 1, 3; 

see also Pet. Ex. 2349 (summarizing evidence supporting the involvement of the innate immune 

system in the pathogenesis of juvenile dermatomyositis).50 Polymyositis presents with proximal 

symmetric weakness in adults. Resp. Ex. Q at 4. Polymyositis is a diagnosis of exclusion, which 

requires other causes to be ruled out before the diagnosis can be made. Id. In diagnosing 

polymyositis, several factors are considered, including timing of disease progression, pattern of 

muscle involvement, level of muscle enzymes, results of EMGs and muscle biopsies, and presence 

of certain autoantibodies. Id. at 5.

 

47 Marinos C. Dalakas, Inflammatory Muscle Diseases, 372 N ENGL J MED 18: 1734-47 (2015), filed as 

“Resp. Ex. Q.” 

48 Thorsten Hornung et al., Innate Immune-Response Mechanisms in Dermatomyositis: An Update on 

Pathogenesis, Diagnosis and Treatment, 74 DRUGS 981-98 (2014), filed as “Pet. Ex. 22.”

49 Sahil Khanna et al., Immunopathogenesis of Juvenile Dermatomyositis, 41 MUSCLE NERVE 5: 581-92 

(2010), filed as “Pet. Ex. 23.”

50 Dr. Grewal cited an additional article discussing polymyositis and dermatomyositis, which petitioner 

filed as Pet. Ex. 24; however, petitioner filed only the first page of the article. The remainder of the article 

is missing. See Kanneboyina Nagaraju, Polymyositis and Dermatomyositis: Pathophysiology, 37 RHEUM 

DIS CLIN N AM 159-71 (2011), filed as “Pet. Ex. 24.”
24

PMR is an inflammatory syndrome characterized by aching and morning stiffness in the 

shoulder and pelvic girdle. Pet. Ex. 1351 at 1; Pet. Ex. 1852 at 1. Because there are no specific 

diagnostic tests or pathologic findings determinative for PMR, it is defined by its clinical features:

(1) aching and morning stiffness which lasts for half an hour or longer in the shoulder, neck, and/or 

hip girdle, (2) ongoing for one month or longer, (3) in a person 50 years or older, and (4) whose 

bloodwork shows systemic inflammation, such as an elevated ESR. Id. Some definitions also 

include a rapid response to small doses of prednisone. Pet. Ex. 18 at 1.

PMR patients are typically in good health prior to onset and more than half initially present 

with low-grade fever, weight loss, and malaise. Pet. Ex. 18 at 7. “Arthralgias and myalgias may 

develop abruptly or evolve insidiously over weeks or months.” Id. Most patients experience onset 

of pain in the shoulder girdle first; others first experience pain in the hip or neck. The pain may 

start on one side, but usually becomes bilateral within weeks. Id. Patients often experience pain at 

night which wakes them up. Id. PMR can be isolated or related to giant cell arteritis (“GCA”). Pet. 

Ex. 13 at 1. However, “[t]he presence of another specific disease other than GCA, such as 

rheumatoid arthritis (“RA”), chronic infection, polymyositis, or malignancy excludes the diagnosis 

of PMR.” Pet. Ex. 18 at 1. 

In his reports, Dr. Grewal distinguished PMR and inflammatory myositis, explaining that 

myositis is autoimmune, characterized by elevated CPK and aldolase, with abnormal EMGs and 

muscle biopsies. Pet. Ex. 11 at 4. In PMR, muscle biopsies are often negative or nonspecific, as 

in petitioner’s case.53 Id. Dr. Grewal cautioned, “You have to be very confident that that’s what 

you are treating because the treatment can be long and prolonged and involve potentially toxic 

medication such as steroids.” Tr. 69-71; Pet. Ex. 11 at 3; Pet. Ex. 21 at 2. 

Dr. Grewal wrote that his diagnosis has never been definitive, except for, perhaps, PMR, 

but stated that it was not unusual for patients with diagnostically challenging cases to be treated 

“empirically,” without certainty of a given diagnosis. Pet. Ex. 21 at 2. If the treatment for a 

particular condition, or combination/hybrid of conditions is effective, it makes for a better basis 

for diagnosis. Id. Dr. Grewal opined petitioner had a complex disease process which does not allow 

for simple categorization; it is a “hybrid autoimmune complex with features of both conditions.” 

Id. at 2-3.

 

51 Alessandra Soriano et al., Polymyalgia rheumatica in 2011, 26 BEST PRACT RES CLIN RHEUMATOL, 91-

104 (2012), filed as “Pet. Ex. 13.”

52 David B. Hellmann, Giant Cell Arteritis, Polymyalgia Rheumatica, and Takayasu’s Arteritis, in

KELLEY’S TEXTBOOK OF RHEUMATOLOGY at 1461-80 (Elsevier 8th ed. 2009), filed as “Pet. Ex. 18.”

53 Dr. Grewal cited an article that was not filed into the record as “Medicine (Kaunas) 2003: 39(5): 489-

93.” Pet. Ex. 11 at 4. A Google search indicated that this citation refers to a case report entitled “A rare case 

of differential diagnosis of myopathy,” published in 2003 in Medicina, a peer reviewed journal of the 

Lithuanian University of Health Sciences. See “Medicina – Open Access Journal” 

http://www.mdpi.com/journal/medicina ; see also “A rare case of differential diagnosis of myopathy,” M. 

Pileckyte, PubMed, https://www.ncbi.nlm.nih.gov/pubmed/12794374
25

At hearing, however, Dr. Grewal stated when he first met petitioner, seven months after 

her vaccination, she did not have symptoms of myositis. Her tests results were either normal or 

negative. Tr. 141-42,145-46, 171. He wrote in his initial report petitioner’s “clinical features best 

fit with a ‘polymyalgia rheumatica like’ condition rather than an inflammatory myositis....” Pet. 

Ex. 11 at 4. He admitted his “thinking has always been really kind of confused with it,” because 

her symptoms did not fit solely with PMR or myositis. Tr. 148. He further admitted that the mild 

abnormalities on the EMG suggested a myositis component, but was not diagnostic of myositis. 

Tr. 145, 148. But he was thinking autoimmune process, so “even though the muscle biopsy was 

not conclusive, it didn’t support the diagnosis of myositis, I thought on the basis of an autoimmune 

process, perhaps she could benefit from [IVIG].” Tr. 103. He prescribed IVIG as a way of 

minimizing the potential side effects of prednisone and preventing MS attacks. He later admitted

that IVIG is not used as a sparing agent for steroids. Tr. 102-04, 150-51; Pet. Ex. 4 at 6.

Dr. Grewal stated since he began treating petitioner, his diagnosis has “sort of been the 

same. It’s a history of MS and this neurological disorder/myositis which is responding to the 

combination of prednisone and IVIG.” Tr. 107-08. He wrote in his report that steroids would only

alleviate the symptoms of PMR, not myositis, and IVIG would not work on PMR; he corrected 

this statement at hearing, conceding he was wrong – steroids are also effective on myositis. Pet. 

Ex. 21 at 2; Tr. 136, 148-49. Dr. Grewal explained that once petitioner was on both prednisone 

and IVIG, attempts to reduce either resulted in recurrence of symptoms; therefore, he concluded

she had a combination of PMR and myositis, evidenced by her response to both treatments and 

inability to be weaned from either. Tr. 107-08; Pet. Ex. 21 at 2 (“multiple attempts have been made 

to decrease...both the IVIG and steroids.... [W]hen either of these medications has been reduced, 

the patient’s symptoms returned....”)(emphasis in original). Dr. Grewal admitted that his only 

basis for diagnosing petitioner with myositis was her response to IVIG and his inability to wean 

her from it without an increase in symptoms. Tr. 146. 

Dr. Grewal agreed that steroid response can be nonspecific, adding that steroids can mask 

symptoms of a variety of serious conditions, including rheumatoid arthritis, cancer, infection, and 

rotator cuff problems. Tr. 152. I asked Dr. Grewal how he knew that it was not one of her other 

co-morbidities that got worse when he reduced her medications. He responded that the IVIG was 

controlling her MS. Tr. 152. 

Dr. Matloubian disagreed with Dr. Grewal’s diagnosis of inflammatory myositis. He 

explained that myositis is inflammation of the muscle; it can be caused by rare viral or bacterial 

infections, but more often, the cause is unknown. Tr. 200. “Dermatomyositis and polymyositis are 

two major types of inflammatory myopathies that affect the proximal muscles of the upper and 

lower extremities in a symmetric fashion. They are considered systemic autoimmune diseases 

since more than 80% of those affected have some type of auto-antibodies, such as ANA in addition 

to involvement of other organs, such as skin and lung.” Resp. Ex. A at 4; Resp. Ex. C at 2.

54 The 

classic presenting complaint of myositis is the insidious onset of muscle weakness. Resp. Ex. A at 

4. Muscle pain is generally mild and stiffness is unusual. Id. Clinical signs of inflammatory 

myositis are elevated liver and muscle enzymes, including CK, aldolase, AST, and ALT. Tr. 200-

01. Additionally, both dermatomyositis and polymyositis typically show inflammatory cellular 

 

54 M. Zong and I. Lundberg, Pathogenesis, Classification and Treatment of Inflammatory Myopathies, 7 

NAT REV RHEUMATOL 297-306 (2011), filed as “Resp. Ex. C.”
26

infiltrate, also known as lymphocytes, on muscle biopsy. Resp. Ex. A at 4; Tr. 209. “Inflammatory 

markers such as ESR are often normal even in patients with active disease.” Resp. Ex. A at 4. Up 

to 10% of patients may have a normal EMG, but special MRI studies may show muscle 

inflammation and edema. Id. Inflammatory autoimmune myositis kills muscle cells, which is why 

people present with weakness over time. Tr. 220. Dr. Matloubian clarified that patients with 

myositis experience “true weakness,” not weakness resulting from pain. Tr. 200, 204. Myositis 

does not have a rapid response to prednisone, but takes months of treatment for strength to return. 

Tr. 219-20, 224. 

Dr. Matloubian pointed out that petitioner’s objective testing did not show any of the 

characteristics typical of myositis which Dr. Grewal recognized when he initially wrote, “[H]er 

clinical features best fit with a polymyalgia rheumatica like condition rather than an inflammatory 

myositis.” Resp. Ex. A at 5; Pet. Ex. 11 at 4. Specifically, petitioner’s blood tests, EMG/NCS, and 

muscle biopsy did not show elevated muscle enzymes, autoantibodies, inflammatory cellular 

infiltrate, muscle damage, or electrophysiological changes associated with inflammatory myositis. 

Resp. Ex. A at 4-5. Further, petitioner had a “miraculous” recovery with prednisone; patients with 

myositis take months to fully recover. Tr. 219-20, 224. Dr. Matloubian pointed out that there was 

no complaint of muscle weakness by petitioner, only stiffness, at her medical appointments in 

December of 2011 and January of 2012. Tr. 226; Pet. Ex. 6 at 24-25, 27. Based on petitioner’s 

objective test results and lack of weakness, the key symptom of myositis, Dr. Matloubian 

concluded petitioner had PMR, not myositis. Tr. 219-20, 226. 

 

I asked Dr. Matloubian why IVIG was working if petitioner did not have myositis. He 

explained, every time petitioner receives an IVIG treatment, she receives solumedrol, a form of 

methylprednisolone, which is a high-dose steroid, just prior to the IVIG.

55 Tr. 231-32. Therefore, 

it is impossible to tell what effect the IVIG has on petitioner due to the amount of prednisone 

equivalent she receives at each treatment. Tr. 231-33; Pet. Ex. 9 at 15. When the IVIG is stopped, 

the solumedrol is also stopped. The pain petitioner experiences when the IVIG treatments are 

stopped may be due to the sudden cessation of solumedrol infusions, not the lack of IVIG. Tr. 231-

32. 

Dr. Matloubian concluded that petitioner does not meet the criteria for myositis and has no 

objective testing to support a diagnosis of myositis. Furthermore, it is not the IVIG controlling 

petitioner’s symptoms, but rather the blast of steroids she receives prior to the IVIG, adding that 

everyone has an increase in symptoms following reduction of steroids and it takes about a week 

for the pain to resolve. Tr. 218-19. 

The experts agree that petitioner has PMR. Pet. Ex. 11 at 4; Resp. Ex. A at 6. There was 

no objective proof submitted to support that petitioner suffers from inflammatory myositis, which 

petitioner’s expert conceded. 

 

55 Dr. Matloubian explained that 4 mg of methylprednisolone is equivalent to 5 mg of prednisone. At every 

IVIG treatment, petitioner would receive 125 mg of solumedrol (methylprednisolone). Pet. Ex. 9 at 15. 

Therefore, she was actually receiving 150 mg of prednisone. Tr. 231-32.
27

C. When Did Petitioner’s PMR Develop?

The experts agreed that petitioner developed PMR. They also agreed there is no known 

cause of PMR. Tr. 153, 213-16; Pet. Ex. 11 at 3; Resp. Ex. A at 5. They initially disagreed on when 

petitioner’s PMR began. 

Petitioner alleges that the onset of her PMR was the day after the vaccination or within two 

weeks after the vaccination. Tr. 282. In his reports, Dr. Grewal distinguished petitioner’s 

“symptoms of pain and discomfort that worsened after receiving the vaccine” from her

fibromyalgia symptoms, but did not suggest a specific date of onset. Pet. Ex. 11 at 4. At hearing, 

Dr. Grewal conceded that he did not know when petitioner’s PMR began. Tr. 141. Dr. Matloubian 

opined that the onset of petitioner’s PMR was June 2011. Tr. 222-23, 233.

In his report, Dr. Grewal opined that petitioner may have had fibromyalgia prior to the

receipt of the Tdap, but after the vaccination, her pain, discomfort, and clinical features best fit 

with a polymyalgia rheumatica like condition. Pet. Ex. 11 at 4. At hearing, Dr. Grewal attempted 

to parse out petitioner’s complaints of arm stiffness and joint pain from the remainder of the

complaints she made to Dr. Bai on April 18, 2011, concluding that those specific complaints were 

symptoms of PMR, not fibromyalgia or MS. Tr. 85-86; see also Pet. Ex. 3 at 11. However, he 

could not explain her significant improvement after restarting her fibromyalgia medications,

Celebrex and Lyrica, when he had previously testified that those medications would not work on 

PMR. Tr. 87, 138-39; Pet. Ex. 3 at 8-9. He conceded if petitioner had PMR at that time, he would 

not expect her to have improvement on Celebrex and Lyrica. Tr. 89. 

Dr. Grewal never addressed onset in his reports, other than to say petitioner developed 

PMR/myositis like symptoms after her tetanus vaccination in April 2011. Pet. Ex. 10 at 1; Pet. Ex. 

11 at 4; Pet. Ex. 21 at 4. He agreed at hearing that there was a significant difference in petitioner’s 

clinical presentation in April and June 2011. Tr. 139-40, 169. He was asked if the onset of PMR 

could have been in June. He responded, “You just don’t know.” Tr. 141. When presented with Dr. 

Faches’ record of December 2011, which documented petitioner’s report of not feeling well since 

July, and being asked if June was a more likely onset date for petitioner’s PMR, he stated “I’m 

guessing yes, but I don’t know.” Tr. 170. Dr. Grewal admitted that he did not know when 

petitioner’s PMR and/or myositis began. Tr. 170, 173-74.

Dr. Matloubian described the onset of PMR as abrupt; most people initially attribute it to 

having engaged in some physical activity. Resp. Ex. A at 5. Though described as muscle pain and 

stiffness, it is thought to be a disease of the joints underlying these muscle groups due to occasional 

signs of arthritis on physical exam. Id. Bursitis and synovitis are typical of PMR and can be found 

via MRI or ultrasound. Id. Because the PMR population is over 50, many patients have preexisting 

conditions like osteoporosis, fibromyalgia, or other musculoskeletal problems which muddle the 

diagnosis. Tr. 199; Resp. Ex. A at 5 (PMR “occurs quite commonly...after the age of 50...ranging 

from 10-100 cases per 100,000 people”). 

Dr. Matloubian described fibromyalgia as a non-inflammatory and non-autoimmune 

syndrome of unclear etiology characterized by diffuse musculoskeletal pain and other symptoms. 

Resp. Ex. A at 5. Like PMR, fibromyalgia is a diagnosis of exclusion. Id. Patients with 
28

fibromyalgia have a lower pain threshold and are more sensitive to pain, which is why medication 

that targets the neurological pathways are used to treat fibromyalgia. Tr. 218.56

According to Dr. Matloubian, petitioner’s PMR diagnosis and treatment were complicated 

by her fibromyalgia. Further, there was an absence of objective data to firmly establish the onset 

of her PMR relative to her vaccination. Resp. Ex. A at 4. Bilateral shoulder ultrasound or MRI is 

particularly important in treating someone who suffers from other diseases, like the petitioner, to 

distinguish between those diseases and PMR. Tr. 235-36, 262-64. MRIs were not ordered. 

Dr. Matloubian discussed petitioner’s prior history of myalgias and muscle pain, and her 

description of full body soreness and feeling as though she had been beaten the day after the 

vaccination, stating that those complaints were more indicative of fibromyalgia than PMR. Tr. 

270-71. Dr. Matloubian qualified that he could only go by the medical record, but suggested that 

petitioner’s symptoms the day after the vaccination could have also been part of the viral illness 

she reported to Dr. Faches the day before. Tr. 273. 

Dr. Matloubian acknowledged petitioner’s testimony that she complained of joint pain and 

stiffness to Dr. Bai on April 18, 2011, stating that the stiffness in the morning could have been a 

complaint of PMR. But Dr. Matloubian explained many diseases have the same symptoms; just 

because she complained of morning stiffness in April did not mean that she had PMR at that time. 

Tr. 269. He also noted that the records document “Musculoskeletal: Intact,” “well appearing,” 

“antalgic with cane,”57 no muscle weakness, and full range of motion all joints.58 Tr. 280; Pet. Ex. 

3 at 10. More importantly, her symptoms improved with Celebrex and Lyrica, which would not 

happen if it were PMR; PMR responds only to prednisone. Tr. 267-68; Pet. Ex. 6 at 10-11. Then 

in June, petitioner presented with confusing complaints of pain in her hands, wrists, elbows, 

shoulders, hips, knees, lower back, and leg muscles. Only the complaints of shoulder and hip 

stiffness with difficulty getting up from a chair were consistent with PMR. Tr. 222-23; Pet. Ex. 3 

at 7; Pet. Ex. 5 at 3; Resp. Ex. A at 5-6. 

Dr. Matloubian concluded that, because petitioner’s symptoms in April and May responded 

to her medication for fibromyalgia, and PMR would not respond to those medications, those 

symptoms were more likely related to her fibromyalgia. Tr. 221. He opined that the onset of PMR 

was more likely in June, when petitioner first reported pain and stiffness in her hips and shoulders. 

Tr. 222-23, 233.

 

56 Fibromyalgia will respond to steroids, but steroids are not the standard of care for fibromyalgia. Tr. 216.

57 Petitioner used a cane due to her broken toe. Pet. Ex. 6 at 82. 

58 During the hearing, I pointed out that Dr. Bai’s records seem to be two pages for each visit, front and 

back, but the visits on April 26, 2011, and May 9, 2011 do not have the back page filed. Petitioner’s counsel 

was asked to look into the possibility of incomplete records. Tr. 281. No additional records were filed, nor 

was any response from counsel filed regarding these records. 
29

Petitioner’s testimony supports an onset date of June 2011. According to petitioner the 

medication Dr. Bai prescribed in April had worked, but “then it got worse...which is why I went 

back.” “...I felt like I was getting worse.... [I]t was getting increasingly more difficult for me to 

get up.... [I]t got significantly worse in June and into July.” Tr. 45-46, 47-48, 40-41, 44; Pet. Ex. 

3 at 9. 

Furthermore, one month prior to her receipt of Tdap vaccine, petitioner presented to Dr. 

Faches with complaints of “a lot of fibromyalgia pain” and “problems sleeping due to pain.” Pet. 

Ex. 6 at 83. These symptoms are consistent with those she presented to Dr. Bai with on April 18, 

2011. Pet. Ex. 3 at 11. 

Based on the medical records and testimony, I find that the onset of petitioner’s PMR was 

in June 2011. 

V. Causation and Analysis

A. Legal Standard Regarding Causation

The Vaccine Act provides two avenues for petitioners to receive compensation. First, a 

petitioner may demonstrate a “Table” injury—i.e., an injury listed on the Vaccine Injury Table 

that occurred within the provided time period. 42 U.S.C. § 300aa-11(c)(1)(C)(i). “In such a case, 

causation is presumed.” Capizzano v. Sec’y of Health & Human Servs., 440 F.3d 1317, 1320 (Fed. 

Cir. 2006); see § 13(a)(1)(B). Second, where the alleged injury is not listed on the Vaccine Injury 

Table, a petitioner may demonstrate an “off-Table” injury, which requires that the petitioner 

“prove by a preponderance of the evidence that the vaccine at issue caused the injury.” Capizzano, 

440 F.3d at 1320; see § 11(c)(1)(C)(ii). A petitioner need not show that the vaccination was the 

sole cause, or even the predominant cause, of the alleged injury; showing that the vaccination was 

a “substantial factor” and a “but for” cause of the injury is sufficient for recovery. Pafford v. Sec’y 

of Health & Human Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006); Shyface v. Sec’y of Health & 

Human Servs., 165 F.3d 1344, 1352 (Fed. Cir. 1999).59 Petitioners are not required “to eliminate 

alternative causes as part of establishing [their] prima facie case.” Doe v. Sec’y of Health & Human 

Servs., 601 F.3d 1349, 1357-58 (Fed. Cir. 2010); see Walther v. Sec’y of Health & Human Servs., 

485 F.3d 1146, 1152 (Fed. Cir. 2007) (holding that a “petitioner does not bear the burden of 

eliminating alternative independent potential causes”). Once a petitioner has proven causation by 

preponderant evidence, “the burden then shifts to the respondent to show by a preponderance of 

the evidence that the injury is due to factors unrelated to the administration of the vaccine.” 

Deribeaux ex rel. Deribeaux v. Sec’y of Health & Human Servs., 717 F.3d 1363, 1367 (Fed. Cir. 

2013) (citing 42 U.S.C. § 300aa-13(a)(1)(B)).

To prove causation, petitioners must satisfy the three-pronged test established in Althen v. 

Sec’y of Health & Human Servs., 418 F.3d 1274 (Fed. Cir. 2005). Althen requires that petitioners 

show by preponderant evidence that a vaccination petitioner received caused his or her injury “by 

providing: (1) a medical theory causally connecting the vaccination and the injury; (2) a logical 

 

59 The Vaccine Act also requires petitioners to show by preponderant evidence that the “residual effects or 

complications” of the alleged vaccine-related injury lasted for more than six months. § 11(c)(1)(D)(i). It is 

undisputed that this six-month requirement is satisfied in this case.
30

sequence of cause and effect showing that the vaccination was the reason for the injury; and (3) a 

showing of a proximate temporal relationship between vaccination and injury.” Id. at 1278. 

Together, these prongs 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.’” Stone v. Sec’y of Health & Human Servs., 

676 F.3d 1373, 1379 (Fed. Cir. 2012) (quoting Shyface, 165 F.3d at 1352-53). Causation is 

determined on a case-by-case basis, with “no hard and fast per se scientific or medical rules.” 

Knudsen v. Sec’y of Health & Human Servs., 35 F.3d 543, 548 (Fed. Cir. 1994). Petitioners are not 

required to identify “specific biological mechanisms” to establish causation, nor are they required 

to present “epidemiologic studies, rechallenge, the presence of pathological markers or genetic 

disposition, or general acceptance in the scientific or medical communities.” Capizzano, 440 F.3d 

at 1325 (quoting Althen, 418 F.3d at 1280). “[C]lose calls regarding causation are resolved in favor 

of injured claimants.” Althen, 418 F.3d at 1280.

Each of the Althen prongs requires a different showing. Under the first Althen prong,

petitioner must provide a “reputable medical theory” demonstrating that the vaccine received can 

cause the type of injury alleged. Pafford, 451 F.3d at 1355-56 (citation omitted). To satisfy this 

prong, petitioner’s “theory of causation must be supported by a ‘reputable medical or scientific 

explanation.’” Andreu, 569 F.3d at 1379 (quoting Althen, 418 F.3d at 1278). This theory need only 

be “legally probable, not medically or scientifically certain.” Id. at 1380 (emphasis omitted) 

(quoting Knudsen, 35 F.3d at 548). Nevertheless, “petitioners [must] proffer trustworthy testimony 

from experts who can find support for their theories in medical literature.” LaLonde, 746 F.3d at

1341. 

The second Althen prong requires proof of a “logical sequence of cause and effect.” 

Capizzano, 440 F.3d at 1326 (quoting Althen, 418 F.3d at 1278). Even if the vaccination can cause 

the injury, petitioner must show “that it did so in [this] particular case.” Hodges v. Sec’y of Health 

& Human Servs., 9 F.3d 958, 962 n.4 (Fed. Cir. 1993) (citation omitted). “A reputable medical or 

scientific explanation must support this logical sequence of cause and effect,” id. at 961 (citation 

omitted), and “treating physicians are likely to be in the best position to determine whether a 

logical sequence of cause and effect show[s] that the vaccination was the reason for the injury,” 

Paluck v. Sec’y of Health & Human Servs., 786 F.3d 1373, 1385 (Fed. Cir. 2015) (quoting Andreu, 

569 F.3d at 1375). 

However, medical records and/or statements of a treating physician’s view do not per se 

bind the special master to adopt the conclusions of such an individual, even if they must be 

considered and carefully evaluated. Section 12(b)(1)(providing that “[a]ny such diagnosis, 

conclusion, judgment, test result, report or summary shall not be binding on the special master or 

court.”); Snyder v. Sec’y of Health & Human Servs., 88 Fed. Cl. 706, 746 n.67 (2009)(“there is 

nothing...that mandates that the testimony of a treating physician is sacrosanct—that it must be 

accepted in its entirety and cannot be rebutted”). As with expert testimony offered to establish a 

theory of causation, the opinions or diagnoses of treating physicians are only as trustworthy as the 

reasonableness of their suppositions or bases. The views of treating physicians should also be 

weighed against other, contrary evidence also present in the record – including conflicting opinions 

among such individuals. Hibbard v. Sec’y of Health & Human Servs., (100 Fed. Cl. 742, 749 

(2011) (determining it is not arbitrary or capricious for a special master to weigh competing 

treating physicians’ conclusions against each other), aff’d. 698 F.3d 1355 (Fed. Cir. 2012); Caves 
31

v. Sec’y of Health & Human Servs., 100 Fed. Cl. 119, 136 (2011), aff’d, 463 Fed. Appx. 932 (Fed. 

Cir. 2012); Veryzer v. Sec’y of Health & Human Servs., No. 06-522V, 2011 WL 1935813, at *17 

(Fed. Cl. Spec. Mstr. Apr. 229, 2011), mot. for review den’d, 100 Fed. Cl. 344 (Sept. 29, 2011), 

aff’d, 475 Fed. Appx. 765 (Fed. Cir. 2012).

 

The third Althen prong requires that petitioner establish a “proximate temporal 

relationship” between the vaccination and the alleged injury. Althen, 418 F.3d at 1281. This 

“requires preponderant proof that the onset of symptoms occurred within a timeframe for which, 

given the medical understanding of the disorder’s etiology, it is medically acceptable to infer 

causation-in-fact.” De Bazan v. Sec’y of Health & Human Servs., 539 F.3d 1347, 1352 (Fed. Cir. 

2008). Typically, “a petitioner’s failure to satisfy the proximate temporal relationship prong is due 

to the fact that onset was too late after the administration of a vaccine for the vaccine to be the 

cause.” Id. However, “cases in which onset is too soon” also fail this prong; “in either case, the 

temporal relationship is not such that it is medically acceptable to conclude that the vaccination 

and the injury are causally linked.” Id.; see also Locane v. Sec’y of Health & Human Servs., 685 

F.3d 1375, 1381 (Fed. Cir. 2012) (“[If] the illness was present before the vaccine was administered, 

logically, the vaccine could not have caused the illness.”).

Finally, although this decision discusses many but not all of the literature in detail which 

was submitted by the parties, the undersigned reviewed and considered all of the medical records 

and literature submitted in this matter. See Moriarty ex rel. Moriarty v. Sec’y of Health & Human 

Servs., 844 F.3d 1322, 1328 (Fed. Cir. 2016) (“We generally presume that a special master 

considered the relevant record evidence even though [s]he does not explicitly reference such 

evidence in h[er] decision.”); Simanski v. Sec’y of Health & Human Servs., 115 Fed. Cl. 407, 436 

(2014) (“[A] Special Master is ‘not required to discuss every piece of evidence or testimony in her 

decision.’” (citation omitted)), aff’d, 601 F. App’x 982 (Fed. Cir. 2015).

 

B. The Expert Reports and Testimony

Establishing a sound and reliable medical theory often requires a petitioner to present 

expert testimony in support of his claim. Lampe v. Sec’y of Health & Human Servs., 219 F.3d 

1357, 1361 (Fed. Cir. 2000). Vaccine Program expert testimony is usually evaluated according to 

the factors for analyzing scientific reliability set forth in Daubert v. Merrell Dow Pharm., Inc., 509 

U.S. 579, 594-96 (1991).60 Cedillo v. Sec’y of Health & Human Servs., 617 F.3d 1328, 1339 (Fed. 

Cir. 2010) (citing Terran v. Sec’y of Health & Human Servs., 195 F.3d. 1302, 1316 (Fed. Cir. 

1999)). 

The Daubert factors are usually employed by judges in the performance of their evidentiary 

gatekeeper roles to exclude evidence that is unreliable and/or could confuse the jury. In Vaccine 

Program cases, by contrast, these factors are used in the weighing of the reliability of scientific 

evidence proffered. Davis v. Sec’y of Health & Human Servs., 94 Fed. Cl. 53, 66-67 

 

60 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.” Terran, 195 F.3d at 1316 n.2 (citing Daubert, 509 U.S. at 592-95). 
32

(2010)(“uniquely in this Circuit, the Daubert factors have been employed also as an acceptable 

evidentiary-gauging tool with respect to persuasiveness of expert testimony already admitted”). 

The flexible use of the Daubert factors to evaluate the persuasiveness of expert testimony has 

routinely been upheld. See, e.g., Snyder, 88 Fed. Cl. at 742-45. In this case, as in numerous other 

Vaccine Program cases, Daubert has not been employed to determine what evidence should be 

admitted, but rather to determine whether expert testimony offered is reliable and/or persuasive. 

Where both sides offer expert testimony, a special master’s decision may be “based on the 

credibility of the experts and the relative persuasiveness of their competing theories.” 

Broekelschen v. Sec’y of Health & Human Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010)(citing 

Lampe, 219 F.3d at 1362). However, nothing requires the acceptance of an expert’s conclusion, 

“connected to existing data only by the ipse dixit of the expert,” especially if “there is simply too 

great an analytical gap between the data and the opinion proffered.” Snyder, 88 Fed. Cl. at 743 

(quoting Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997)); see also Isaac v. Sec’y of Health & 

Human Servs., No. 08-601V, 2012 WL 3609993, at *17 (Fed. Cl. Spec. Mstr. July 30, 2012), mot. 

for review den’d, 108 Fed. Cl. 743 (2013), aff’d, 540 F. App’x. 999 (Fed. Cir. 2013) (citing Cedillo, 

617 F.3d at 1339). Weighing the relative persuasiveness of competing expert testimony, based on 

a particular expert’s credibility, is part of the overall reliability analysis to which special masters 

must subject expert testimony in Vaccine Program cases. Moberly v. Sec’y of Health & Human 

Servs., 592 F.3d 1315, 1325-26 (Fed. Cir. 2010) (“[a]ssessments as to the reliability of expert 

testimony often turn on credibility determinations”); see also Porter v. Sec’y of Health & Human 

Servs., 663 F.3d 1242, 1250 (Fed. Cir. 2011) (“this court has unambiguously explained that special 

masters are expected to consider the credibility of expert witnesses in evaluating petitions for 

compensation under the Vaccine Act.”). 

Application of the Althen prongs reveals evidentiary deficiencies in petitioner’s claim: (1) 

petitioner failed to offer a persuasive or reliable medical theory; (2) the theory provided is not 

applicable to the facts of petitioner’s case; and (3) petitioner has not established a medically 

acceptable timeframe in which her symptoms could have begun or developed. 

1. Petitioner Has Failed to Articulate a Plausible Medical Theory Causally 

Connecting Tdap Vaccine to PMR and/or Myositis.

To satisfy Althen Prong I, petitioner must present a “sound and reliable medical or scientific 

explanation” causally connecting the vaccine to her alleged injuries. Knudsen, 35 F.3d at 548. 

Petitioner’s causation theory has several deficiencies. 

In his reports, Dr. Grewal relied on ASIA theory, stating that it “is a well known and studied 

reaction to vaccine adjuvants.” Pet. Ex. 11 at 3. However, Dr. Grewal did not explain how the

aluminum adjuvant in the Tdap vaccine is capable of causing or triggering PMR and/or myositis. 

ASIA theory, or “Autoimmune Syndrome Induced by Adjuvants,” groups together “a range 

of emerging autoimmune diseases with possible adjuvant-associated causes.” Resp. Ex. H61 at 1. 

 

61 David Hawkes et al., Revisiting adverse reactions to vaccines: A critical appraisal of Autoimmune 

Syndrome Induced by Adjuvants (ASIA), 59 J AUTOIMMUN 77-84 (2015), filed as “Resp. Ex. H.”
33

To qualify for a diagnosis of ASIA, a person must have been exposed to an external stimuli such 

as an infection, vaccine, or adjuvant, prior to experiencing clinical manifestations which typically 

include muscle weakness, joint pain, chronic fatigue, and/or neurological symptoms, particularly 

those associated with demyelination. Id. at 2. Suggested “minor criteria” for ASIA include the 

presence of autoantibodies against the suspected stimulus, specific HLA markers, or development 

of an autoimmune disease such as MS. Id.

In setting forth his theory, Dr. Grewal compared PMR and myositis to GCA and 

dermatomyositis, stating that all four of these diseases involve inflammation thought to be induced 

or triggered by a combination of genetic and environmental factors. Dr. Grewal posited that the 

Tdap vaccine can act as an environmental factor capable of triggering an inflammatory disease in 

a genetically predisposed person. Pet. Ex. 21 at 3. Dr. Grewal did not focus on the Tdap vaccine 

or ASIA theory itself, but rather addressed the immune system’s role in both PMR and myositis,

submitting literature which elaborated on the immunological points of both diseases. Dr. Grewal 

described the role of interferons (“IFNs”) in GCA and dermatomyositis appearing to suggest that 

aluminum adjuvants could induce interferon production, causing or triggering PMR and/or 

myositis, like interferons trigger GCA and dermatomyositis. However, despite the literature 

offered by Dr. Grewal, none supported this theory, but rather distinguished PMR from GCA, and 

myositis from dermatomyositis. See Pet. Ex. 22 at 3 (“[S]everal potential autoantigens of DM are 

IFN regulated and therefore enhanced under inflammatory conditions...”); Pet. Ex. 23 at 7 (“Type 

I IFNs contribute to the pathogenesis of autoimmune diseases, including [juvenile 

dermatomyositis]”); Pet. Ex. 3362 at 4 (“...interferon [gamma] seems to play a specific pivotal role 

in...the pathogenesis of GCA...The absence of interferon [gamma] expression in...samples from 

patients with isolated PMR suggests that its production may be crucial to the development of 

GCA”)(emphasis added); Pet. Ex. 18 at 3-4 (interferon gamma is “abundantly expressed” in GCA 

but absent from PMR)(emphasis added). The literature provided by Dr. Grewal contained 

extensive information on the symptomatology, diagnosis, mechanics, and immunological 

processes of PMR and myositis. See generally Pet. Ex. 34-37. The literature did not identify any 

known causes or triggers of PMR or myositis, and none of the articles suggested that aluminum 

adjuvants could induce interferon production. Dr. Grewal testified that his theory was based on 

literature he read about aluminum, then conceded that he did not provide copies of any of that 

literature in this case. Tr. 155; Pet. Ex. 11 at 3. He further conceded that none of the articles filed 

suggested that aluminum adjuvants induce interferon production. Tr. 164. 

At hearing, Dr. Grewal was unable to articulate what ASIA or “ASIA-like” theory was. 

When asked to explain how aluminum triggers an autoimmune condition, Dr. Grewal responded 

that there was “something within the vaccine itself....Perhaps it’s the aluminum.” “[T]he body 

produces antibodies against that particular—what’s in the vaccine. And then there’s some crossreactivity between some other components of the body which results in the second autoimmune 

disease in this particular case.” Tr. 112-13. Dr. Grewal suggested that there was a difference 

between exposure to aluminum via injection and exposure to aluminum through typical 

environmental sources such as air or food. Tr. 112-13. He provided nothing further. 

 

62 Miguel A. Gonzalez-Gay et al., Giant Cell Arteritis and Polymyalgia Rheumatica: Pathophysiology and 

Management, 23 DRUGS AGING 8: 627-49 (2006), filed as “Pet. Ex. 33.”
34

Dr. Grewal appeared to be similarly out of his depth when discussing Tdap vaccine. He 

could name the main antigenic components – tetanus, diphtheria, and pertussis toxoids – but was 

unaware of whether or how any of these antigens could trigger the development of PMR or 

myositis. Tr. 162-63.

Dr. Grewal ultimately admitted that there was no scientific basis to support a connection 

between Tdap vaccine and PMR or myositis. Tr. 166. When I asked Dr. Grewal to articulate his 

theory in this case, he responded: 

...there’s nothing else that I can pinpoint when I go back in the history. And I take 

her at face value. She got the vaccine and she started to become symptomatic and 

got much worse. The thing continued to get worse as time went on. And the only 

response, the only medication she responded to were the steroids, suggesting it’s 

autoimmune.

Tr. 167. 

Dr. Matloubian stated that, while Tdap vaccine contains 0.33 mg of aluminum, it is slowly 

absorbed over time and insufficient to cause aluminum toxicity. Tr. 241; Resp. Ex. A at 8; see also

Resp. Ex. L63 at 4-5 (discussing the rate of absorption of aluminum adjuvant delivered by 

intramuscular injection). None of the components of the Tdap vaccine, including aluminum, is

associated with PMR or myositis. Tr. 238-39. 

Dr. Matloubian voiced several criticisms of ASIA theory, most significantly that a recent 

critical analysis of 27 studies on ASIA reached the conclusion that “there is currently a lack of 

reproducible evidence for any consistent relationship between [aluminum] adjuvant and 

autoimmune conditions.” Resp. Ex. A at 6, citing Resp. Ex. H at 1. Dr. Matloubian explained that 

the criteria for ASIA theory do not specify a temporal relationship between the stimulus and the 

clinical manifestations; therefore, ASIA could apply to any person who has been exposed to a 

stimulus and develops an autoimmune condition even if there are years between stimulus and 

condition. Tr. 240; Resp. Ex. H at 2. It is also too broad in its classification of possible autoimmune 

diseases. For example, Dr. Matloubian explained, MS, inflammatory myositis, and PMR are 

“entirely different diseases,” but ASIA theory lumps them all together in an “artificial category,” 

despite differences in their mechanisms and underlying pathologies. Tr. 240. Due to the variety of 

diseases encompassed by ASIA theory, the theory is too broad to be reproduced scientifically and 

therefore cannot be tested. Tr. 240.

Dr. Grewal agreed with many of Dr. Matloubian’s criticisms of ASIA theory, including 

that the theory is so broad as to apply to any person who has ever been exposed to an adjuvant and 

later developed an autoimmune condition, even if the condition occurred years after the stimulus. 

Tr. 159. He further agreed that ASIA theory is controversial and uniformly unaccepted by both 

immunologists and rheumatologists. Tr. 159. Yet, he still maintained that ASIA could apply to a 

 

63 R. Mitkus et al., Updated aluminum pharmacokinetics following infant exposures through diet and 

vaccination, 29 VACCINE 9538-43 (2011), filed as “Resp. Ex. L.”
35

unique situation, like petitioner, and that as a neuromuscular doctor, he is “in tune to patients 

having vaccine-related events.”64 Tr. 115. He provided no explanation for this statement. 

Dr. Grewal and Dr. Matloubian agreed that there are no known causes or triggers for PMR 

and myositis. Tr. 153-54, 237. The only known environmental risk factors for myositis are statins 

and UV exposure. Tr. 154. Dr. Matloubian opined that a temporal connection between Tdap 

vaccine and an autoimmune disease alone is insufficient as many of these diseases take years to 

develop before they are clinically apparent. Tr. 237.

In assessing the reliability and credibility of an expert’s opinion, I must consider whether 

the expert offering the opinion is testifying within his training or expertise. Walton v. Sec’y of 

Health & Human Servs., No. 04-503V, 2007 WL 1467307, at *17-18 (Fed. Cl. Spec. Mstr. Apr.

30, 2007) (otolaryngologist not well suited to testify about disciplines other than her own 

specialty). In recognizing the liberality with which evidence offered in Vaccine Program cases is 

treated, I read and evaluated all of the testimony of the experts offered and all of the literature filed 

in this case, and gave appropriate weight to whether certain testimony is beyond a particular 

expert’s purview. See, e.g., King v. Sec’y of Health & Human Servs., No 03-584V, 2010 WL 

892296, at *78-79 (Fed. Cl. Spec. Mstr. Mar. 12, 2010) (finding petitioner’s expert far less 

qualified to offer opinion on general causation issues pertaining to autism than specific issues 

pertaining to the petitioner’s actual medical history, given the nature of the expert’s 

qualifications.). To that end, by his own admission, Dr. Grewal specializes in neurology and treats 

chronic inflammatory demyelinating polyneuropathy, Guillain-Barré Syndrome, myositis, and 

myasthenia gravis, all of which are autoimmune nerve diseases. Tr. 117. He does not treat PMR,

nor is PMR a neurological disorder. He would refer someone with PMR to a rheumatologist. Tr. 

117-18. He also does not treat patients with fibromyalgia. Tr. 118. Dr. Grewal admitted that he 

has never seen a case like petitioner’s before. Tr. 66. In contrast, Dr. Matloubian is a 

rheumatologist who routinely treats patients with PMR, fibromyalgia, and myositis. Resp. Ex. A 

at 1. While Dr. Grewal’s testimony was clearly outside of his area of expertise, Dr. Matloubian’s 

opinions were grounded in literature and relevant experience. 

Furthermore, ASIA theory has been proffered several times in the Vaccine Program and 

repeatedly rejected. See, e.g., Rowan v Sec’y of Health & Human Servs., No. 10-272V, 2014 WL 

7465661, at *12 (Fed. Cl. Spec. Mstr. Dec. 8, 2014) mot. for review den’d, 2015 WL 3562409 

(Fed. Cl. May 18, 2015) (denying entitlement to petitioner who claimed the aluminum adjuvant in 

the HPV vaccine caused her headaches, migraines, and chronic fatigue syndrome). No special 

masters have ever found ASIA or ASIA-like theories to be persuasive. See, e.g., Rowan, 2014 WL 

7465661, at *6-7 (“ASIA is not a proven theory....[T]he data only ‘suggest the possibility of 

accelerated autoimmunity/inflammation following vaccination,’” and “precisely how adjuvants 

cause autoimmune illness ‘is not always known’”); see also Bushnell v. Sec’y of Health & Human 

Servs., No. 02-1648V, 2015 WL 4099824, at *8 (Fed. Cl. Spec. Mstr. June 12, 2015) (denying 

compensation in a case that alleged that an aluminum adjuvant exacerbated a mitochondrial 

disorder and precipitated autism); Harris v. Sec’y of Health & Human Servs., No. 10-332V, 2014 

WL 3159377, at *16 (Fed. Cl. Spec. Mstr. June 10, 2014) (noting that aluminum adjuvants are 

 

64 He did not state whether he has had any patients other than the petitioner who have reported adverse 

events following vaccination.
36

considered to be safe and have been used for nearly a century); D’Angiolini v. Sec’y of Health & 

Human Servs., No. 99-578V, 2014 WL 1678145, at *60 (Fed. Cl. Spec. Mstr. Mar. 27, 2014), mot. 

for review den’d, 122 Fed. Cl. 86 (2015), aff’d, 645 F. App’x. 1002 (Fed. Cir. 2016)(noting that 

ASIA “is not generally accepted in the medical community and its diagnostic criteria do not 

differentiate between healthy and ill people”).

Dr. Grewal’s conclusory statements do not constitute a “sound and reliable” theory for how

Tdap vaccine could cause PMR or myositis. Additionally, he failed to provide any corroborating 

evidence or reliable scientific studies to support his theory that Tdap or aluminum could cause 

PMR or myositis. Furthermore, despite his reliance on ASIA theory, he appeared to have only 

passing familiarity with it, as evidenced by his inability to articulate the theory. Dr. Grewal did 

not provide evidence or a plausible theory of causation in this case. 

Petitioner has not put forth opinions, case studies, or medical literature presenting a 

plausible medical theory by which Tdap vaccine could cause or trigger PMR and/or myositis. 

Alone, Dr. Grewal’s belief that Tdap vaccine caused petitioner to develop PMR and/or myositis is 

insufficient to support causation. See Langland v. Sec’y of Health & Human Servs., 109 Fed. Cl. 

421, 438 (2013)(quoting Langland ex rel M.L. v. Sec’y of Health & Human Servs., No. 07-36V, 

2011 WL 386985, at *24 (Fed. Cl. Spec. Mstr. Feb. 4, 2011)) (“...a treating doctor’s opinion that 

a vaccination caused a particular injury ‘cannot substitute for the explanation of a plausible theory 

as to how a given vaccine can cause the alleged injury.’ In other words, in the absence of a theory 

showing a vaccine could cause a particular injury, a doctor’s belief that it did will not prove 

causation....”) (emphasis in original).

Accordingly, petitioner has not satisfied Prong I. 

2. Petitioner Has Failed to Demonstrate a Logical Sequence of Cause and Effect 

Connecting Tdap Vaccine to Her Development of PMR and/or Myositis. 

Even if petitioner had been able to sustain her burden of causation under Prong I, that Tdap 

vaccine can cause PMR and/or myositis, she could not sustain her burden under Prong II to show 

that it did so in this case. 

According to Dr. Grewal, when a person is exposed to some antigen, whether via ingestion 

or infection, there is some kind of reaction from the body. Tr. 71-72. A person with a preexisting 

autoimmune condition like MS, lupus, or arthritis, has a propensity for autoimmunity. Tr. 72.

Because petitioner already had MS, she had a propensity for autoimmune reactions. Tr. 115.

Dr. Grewal’s PMR-like/myositis-like diagnosis rested solely on petitioner’s positive 

response to a combination of IVIG and steroids. Petitioner’s response to the treatment “provides 

[a] very strong kind of empirical proof that this is an autoimmune process.” Tr. 148-51, 113-14; 

Pet. Ex. 21 at 2. He then concluded, “[S]he has a complex disease process which does not allow 

simple categorization. My diagnosis is that she has features of PMR and myositis, both of which 

are autoimmune.” Pet. Ex. 21 at 2. He stated that epidemiology is not helpful in determining 

petitioner’s diagnosis because her condition is not straightforward, but “whatever is going on with 

her is autoimmune. Autoimmune/inflammatory.” Tr. 114-15. He then theorized that the aluminum 
37

in Tdap vaccine caused an autoimmune reaction. Tr. 112. Dr. Grewal supported his theory by 

discussing interferon activity as a potential cause of GCA and dermatomyositis. Pet. Ex. 21 at 3. 

Petitioner does not have dermatomyositis or GCA. At hearing, he conceded that there was no 

literature to support that aluminum adjuvants induce interferon production. Tr. 164. He also agreed 

that petitioner had taken Avonex, an interferon, in the past, but did not develop myositis or PMR. 

Tr. 164. He further acknowledged that the Shoenfeld article he relied on for the ASIA theory 

requires the detection of HLA on muscle biopsy to support an ASIA-provoked autoimmunity. 

HLA was not detected on petitioner’s muscle biopsy; her muscle biopsy was essentially normal.

Tr. 171-72.

Dr. Grewal concluded that petitioner developed PMR or “PMR-like disease” as a direct 

result of the tetanus vaccine, based on the development and worsening of clinical features after the 

vaccination, the mechanism he described as related to vaccine adjuvant, the dramatic clinical 

response to prednisone, and the presence of an elevated CRP. Pet. Ex. 11 at 4. Dr. Grewal’s opinion 

hinged on his belief that petitioner developed an autoimmune condition, not present prior to the 

vaccination, but present after, establishing cause and effect based on temporal relationship. Tr. 

166-67; Pet. Ex. 4 at 17; Pet. Ex. 7 at 20; Pet. Ex. 21 at 4. “In determining a cause, one must 

consider immune insults occurring at or near the time the disease process began. In [petitioner’s] 

case, it was the tetanus shot.” Pet. Ex. 21 at 4. At hearing, he stated, “[I]t’s been my feeling since 

I first started to take care of her that if she had not received that vaccine, I doubt that she would 

have developed this problem. But I don’t know that.” Tr. 174; see also Tr. 97 (“... [I]n April she 

got the vaccine, something happened and she got worse.”). He agreed that, despite petitioner’s 

supposed propensity for autoimmune disease, she would not automatically develop an autoimmune 

disease in response to a vaccine. “...[S]he had this vaccine before and didn’t get any symptoms. I 

think a lot of this is sort of hit and miss and bad luck on the part of the patient.” Tr. 115. 

It is the law of the Vaccine Program that evidence of the development of a disease and/or 

injury temporally following a vaccination is insufficient on its own to establish causation. Grant 

v. Sec’y of Health & Human Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992). Merely identifying the 

vaccine as causal because of its existence as a known, pre-onset occurrence is insufficient to 

establish causation without corroborative record proof demonstrating the “logical sequence of 

cause and effect” required. Id. A wide variety of indirect and circumstantial evidence can support 

that determination, whether in the form of test results or witness testimony.

Here, the evidence is lacking. Dr. Grewal testified honestly and without hesitation. He was 

respectful and pleasant with the Court. He had no trouble responding to any of the questions asked 

of him. However, his opinions simply lacked the foundation necessary to show that petitioner’s 

Tdap vaccination caused her to develop PMR, other than his personal belief that petitioner did not 

have it before, but developed it after, and therefore it was caused by the vaccine. Dr. Grewal’s 

conclusions were not enough to demonstrate a “logical sequence of cause and effect” connecting 

petitioner’s receipt of Tdap vaccine to her development of PMR and/or myositis.

Dr. Matloubian’s opinions were more persuasive and grounded in science rather than 

personal belief. According to Dr. Matloubian whether petitioner has PMR, myositis, or both, 

neither is related to her tetanus vaccination. He explained that, for vaccine-induced immune 

complexes to lead to organ damage, a large amount of antigen is necessary to form these 
38

complexes. This may theoretically occur with a live, attenuated vaccine, where there is viral 

replication, but the amount of antigen in Tdap vaccine is comparatively low. Resp. Ex. A at 7. 

Additionally, petitioner did not display signs of immune complexes, like high complement levels 

or positive autoantibodies. She tested negative for autoantibodies like rheumatoid factor, 

cryoglobulins, and ANA. Id. Therefore, petitioner’s PMR was not due to formation of immune 

complexes as a result of Tdap vaccine. Id.

Dr. Matloubian disagreed with Dr. Grewal’s contention that petitioner’s MS made her more 

susceptible to autoimmune disease from vaccines. Tr. 244-45. Studies have shown that, in patients 

with preexisting autoimmune diseases, vaccines do not exacerbate existing autoimmune diseases 

and do not cause new autoimmune diseases. Tr. 245. The American College of Rheumatology 

guidelines recommend that patients with rheumatoid arthritis receive influenza vaccine. Tr. 245; 

Resp. Ex. M.65 It was notable that Tdap vaccine did not elicit aggravation of petitioner’s MS. 

I also do not find persuasive Dr. Grewal’s conclusory statement that petitioner was more 

susceptible to autoimmune attack due to her pre-existing MS. Dr. Grewal provided no proof of 

such susceptibility other than circular reasoning that because petitioner developed PMR at some 

point after receipt of the Tdap vaccination and did not have it before, but she had MS before, she 

was somehow more susceptible to autoimmunity from Tdap vaccine, which he agreed did not 

trigger her MS, but triggered PMR. 

 

The experts agreed, and the literature supports, that PMR is an idiopathic disease with no 

known cause. Tr. 153; Resp. Ex. A at 5. The experts further agreed that there is no known 

component in Tdap vaccine that has been linked to PMR. Tr. 166, 239. Given the above, the 

evidence best supports the conclusion that petitioner’s PMR was idiopathic in origin, as opposed 

to vaccine caused. Accordingly, petitioner has failed to sustain her burden under Prong II. 

3. Petitioner Has Failed to Show an Appropriate Temporal Relationship Between 

Her Receipt of Tdap Vaccine and Her Development of PMR and/or Myositis. 

Having already determined that onset in this matter was in June 2011, over two months 

after receipt of Tdap vaccine, to satisfy her burden on the third Althen prong, petitioner needed to 

demonstrate an appropriate timeframe for the development of PMR following Tdap vaccine. 

However, since petitioner cannot show Tdap vaccine could cause PMR and/or myositis, petitioner 

cannot show what a reasonable timeframe for the onset of PMR and/or myositis following Tdap

vaccine would be. Langland, 109 Fed. Cl. at 443 (“[T]o satisfy the ‘proximate temporal 

relationship’ prong of the Althen test, petitioners must demonstrate, by a preponderance of the 

evidence, that the onset of symptoms occurred within a time frame for which it is medically 

acceptable to infer causation-in-fact....With no reputable theory as to how the vaccination could 

cause the injury, this exercise is not possible.”) (citing De Bazan, 539 F.3d at 1352). 

Dr. Grewal did not provide any explanation for how Tdap vaccine could cause PMR, 

myositis, or a combination of the two diseases, or how it could do so within one day, two weeks, 

or two months of the vaccination. Rather, he repeatedly insisted that because petitioner developed 

 

65 Johanna Westra et al., Vaccination of patients with autoimmune inflammatory rheumatic disease, 11 NAT 

REV RHEUMATOL 3: 135-45 (2015), filed as “Resp. Ex. M.”
39

PMR and/or myositis after receiving Tdap vaccine, the vaccine was the cause of the disease. 

However, a temporal correlation alone is not enough to establish vaccine causation. LaLonde, 746 

F.3d at 1341.

Dr. Matloubian concluded that temporal association without biological plausibility is not 

enough. ASIA theory is controversial and not accepted by most immunologists and 

rheumatologists. Resp. Ex. A at 8. In response to petitioner’s testimony that she woke up the 

morning after the vaccination and felt like she had been beaten, Dr. Matloubian gave an example 

of post-infectious reactive arthritis, to describe the time it takes for autoimmune reaction, noting

“it takes about one to three weeks after immunization to get [post-infectious reactive arthritis] 

because it takes about that time for T-cells and B-cells to get activated.” Tr. 282-83. Based on that 

timeframe, if Dr. Grewal’s theory were correct that environmental events such as infection or 

vaccine can trigger PMR, then it was more likely that her gastrointestinal virus the week prior to

her vaccination were the cause. Resp. Ex. A at 8.

Petitioner failed to present evidence to support a temporal relationship between her Tdap 

vaccination on April 1, 2011 and the onset of her symptoms in June 2011. Accordingly, petitioner 

has failed to present preponderant evidence to support Prong III. 

VI. Conclusion

When petitioners fail to carry their burden, the Secretary is not required to present an 

alternate explanation for the vaccinee's condition. De Bazan, 539 F.3d at 1352. The petitioner in 

this matter has failed to put forth a prima facie showing of causation; therefore, respondent is not 

required to demonstrate that a “factor unrelated” was the sole cause of petitioner’s condition. 

While petitioner suffers greatly from a host of debilitating and chronic conditions, a 

situation that is sad and for which I am greatly sympathetic, she has not put forth preponderant 

evidence that Tdap vaccine that she received on April 1, 2011, caused her to develop PMR and/or 

myositis. She has not demonstrated entitlement to compensation. Her petition is therefore 

dismissed.

In the absence of a timely filed motion for review (see Appendix B to the Rules of the 

Court), the Clerk shall enter judgment in accordance with this decision.66

IT IS SO ORDERED. 

 

s/ Mindy Michaels Roth

 Mindy Michaels Roth

Special Master

 

66 Pursuant to Vaccine Rule 11 (a), if a motion for review is not filed within 30 days after the filing of the 

special master’s decision, the clerk will enter judgment immediately.