Davis v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

No. 14-978V

Filed: April 27, 2022

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

HARVARD DAVIS, * PUBLISHED

*

Petitioner, *

* Influenza (“Flu”) Vaccine;

v. * Guillain-Barré Syndrome (“GBS”);

* Chronic Inflammatory

* Demyelinating Polyneuropathy

SECRETARY OF HEALTH * (“CIDP”).

AND HUMAN SERVICES, *

*

Respondent. *

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

Lisa Roquemore, Esq., Law Office of Lisa A. Roquemore, Rancho Santa Margarita, CA, for

petitioner.

Adriana Teitel, Esq., U. S. Department of Justice, Washington, D.C., for respondent.

RULING ON ENTITLEMENT1

Roth, Special Master:

On October 14, 2014, Harvard Davis (“Mr. Davis” 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 influenza (“flu”) vaccination that

he received on August 19, 2013 caused him to develop Guillain-Barre Syndrome (“GBS”) and

chronic inflammatory demyelinating polyneuropathy (“CIDP”). Petition at 2, 7.

For the reasons stated herein, I find that petitioner’s evidence is sufficient to demonstrate

that the flu vaccine he received on August 19, 2013 was a substantial triggering factor for

1

This Ruling 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 Ruling will be available to anyone with

access to the internet. However, the parties may object to the Ruling’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 Ruling 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).

“probable CIDP.” Due to petitioner’s coexisting health issues, this decision also addresses

petitioner’s comorbidities and how they contribute[d] to his ongoing debility. Accordingly, I find

that petitioner is entitled to compensation for those injuries associated with his “probable CIDP”.

I. Issues to be Determined

The parties dispute the onset of petitioner’s injury following his August 19, 2013 influenza

vaccine, whether that injury is CIDP, the contribution of his comorbidities to his alleged CIDP,

and all three prongs of Althen. Pet. Prehearing Submission, ECF No. 124.

II. Factual Background

A. Procedural History

Mr. Davis filed his petition on October 14, 2014. ECF No. 1. Petitioner filed medical

records on numerous occasions: October 15, 2014, ECF Nos. 5-7; November 26, 2014, ECF No.

11; March 16, 2015, ECF No. 17-19; May 20, 2015, ECF No. 25; July 7, 2015, ECF No. 29;

August 21, 2015, ECF No. 33; November 9, 2015, ECF No. 39; September 27, 2016, ECF No. 47;

January 3, 2017, ECF No. 57; May 24, 2017, ECF No. 70; August 9, 2018, ECF No. 84; August

16, 2018, ECF No. 85; September 27, 2018, ECF No. 87; October 16, 2018, ECF No. 88;

November 23, 2018, ECF No. 89; December 4, 2018, ECF No. 91; December 20, 2018, ECF No.

92; January 24, 2019, ECF No. 93; February 19, 2019, ECF No. 98; March 12, 2019, ECF No.

111; March 19, 2019, ECF No. 117; March 21, 2019, ECF No. 120; May 9, 2019, ECF No. 132;

May 30, 2019, ECF No. 134; June 24, 2019, ECF No. 135; January 9, 2020, ECF Nos. 147-150;

and November 17, 2021, ECF No. 168.

Petitioner filed expert reports from Dr. Steinman with literature on March 30, 2017, ECF

No. 64; December 28, 2017, ECF No. 76; August 16, 2018, ECF No. 86; and September 5, 2019,

ECF No. 95. Petitioner filed medical literature on March 30, 2017, ECF No. 64; December 28,

2017, ECF No. 76; December 3, 2018, ECF No. 90; February 25, 2019, ECF No. 95; February 27,

2019, ECF No. 100; March 12, 2019, ECF Nos. 103-106; March 14, 2019, ECF No. 112;

September 5, 2019, ECF No. 115; September 11, 2019, ECF No.138; and December 16, 2019,

ECF No. 140.

Respondent filed expert reports from Dr. Chaudhry with medical literature on September

19, 2017, ECF No. 73; May 14, 2018, ECF No. 80; and February 22, 2019, ECF No. 99. Additional

medical literature was filed on March 7, 2019. ECF No. 112.

On April 15, 2015, Respondent filed a status report indicating a willingness to engage in

settlement negotiations. The matter proceeded on a settlement track for over 14 months until June

29, 2016, when petitioner filed a status report stating that the parties had reached an impasse in

negotiations. ECF Nos. 21, 44. Additional medical records and supplemental expert reports were

filed, and the matter then proceeded on a dual track of renewed settlement negotiations and

scheduling and preparing for hearing. After attempts at resolution again failed, an entitlement

hearing was set for and held on April 4 and 5, 2019 in Sacramento, CA. Despite two full days of

hearing, the matter could not be completed and resumed on October 30, 2019 in Washington, DC.

2

Additional evidence was filed after the hearing was completed in full. Post-hearing briefs

were filed by both parties on August 31, 2020, and petitioner filed a reply brief on October 15,

2020. ECF Nos. 165-167. Petitioner filed updated medical records on November 17, 2021. ECF

No. 168.

This matter is now ripe for decision.

B. Medical History

1. Petitioner’s Health Before Receiving the Influenza Vaccine

Petitioner was born on June 12, 1957. He has a complicated medical history, which includes

but is not limited to hypertension, transient ischemic stroke, hypercholesteremia,3 uncontrolled

Type 2 diabetes mellitus (“DM”) with peripheral vascular complications and diabetic neuropathy,4

dysphagia,5 benign prostatic hyperplasia,6 stress urinary incontinence, chronic neck, back and hip

pain, depression, gastroesophageal reflux disease (“GERD”), anemia, and vitamin D deficiency.

Pet. Ex. 16 at 10; Pet. Ex. 89 at 4. Petitioner underwent five spinal surgeries in 1995, 1999, 2000,

2001, and 2002 and the implantation of a spinal cord stimulator, which is reportedly no longer

functional but remains in place embedded in tissue. Surgery for its removal was recommended so

MRIs of the lumbar spine could be performed due to suspected cord compression, but petitioner

opted not to undergo the surgery. Pet. Ex. 10; Pet. Ex. 58 at 2; Pet. Ex. 60 at 3; Pet. Ex. 63 at 2-3.

More specifically, in 2009, petitioner was treated for a host of health issues, including but

not limited to chronic lower back pain;7 intramuscular lipoma8 with surgical removal;9 sudden

weakness, slurred speech, and stroke;10 numbness of the face and left leg, memory issues,

disorientation, and neurological deficits, though his EKG and head CT were negative; 11 syncope

3

Hypercholesteremia is another name for hypercholesterolemia, which is defined as “excessive cholesterol in the

blood.” Dorland’s Illustrated Medical Dictionary 876. (33rd ed. 2019) [hereinafter “Dorland’s”].

4

Neuropathy is “a functional disturbance or pathologic change in the peripheral nervous system, sometimes limited

to noninflammatory lesions as opposed to those of neuritis; the etiology may be known or unknown. Known etiologies

include complications of other diseases (such as diabetes or porphyria), or of toxicity states [ ].” Dorland’s 1250. The

peripheral nervous system is “the part of the nervous system consisting of nerves and ganglia outside the brain and

spinal cord.” Dorland’s 1832.

5

Dysphagia is “difficulty in swallowing.” Dorland’s 573.

6

Benign prostatic hyperplasia is an “age-associated enlargement of the prostate resulting from proliferation of both

glandular and stromal elements, beginning generally in fifth decade of life; it may cause urethral compression and

obstruction.” Dorland’s 882.

7

Pet. Ex. 12 at 26-30, 223-26.

8

An intramuscular lipoma is a “slow-growing infiltrating lesion composed of mature fat cells” occurring within the

muscle. Dorland’s 1049.

9

Pet. Ex. 12 at 32-35, 95-98, 167-220.

10

Id. at 239-268.

11

Id. at 41-68.

3

and transient cerebral ischemia;12 a mass in his neck;13 spondylosis of the cervical spine, 14 lower

urinary tract symptoms, and depression.15

In 2010, petitioner received treatment for numbness in his hand; 16 memory disorder and

dementia;17 depression, urinary tract retention, hypertension, vitamin D deficiency, anemia, and

dysphagia;18 gastrointestinal issues, diverticulosis,19 iron deficiency, and esophagitis;20 mental

health issues resulting in unemployment;21 and chronic low back pain.22 Petitioner received flu

and Adacel23 vaccines without event. Pet. Ex. 4 at 90-91, 94.

In 2011, petitioner was treated for hypertension, diverticulosis, lipoma, syncope, chronic

lower back pain, cervical spondylosis, urinary tract symptoms with trouble holding urine, Vitamin

D deficiency, depression, and uncontrolled Type 2 diabetes while taking Glipizide.24 Pet. Ex. 8 at

5-14. He was provided with blood glucose testing materials. Pet. Ex. 4 at 113, 119-122; Pet. Ex.

94 at 7, 40, 42. His medical records show he was unemployed and was seeking workers’

compensation at that time. Pet. Ex. 4 at 113-12; Pet. Ex. 94 at 52, 54.

No records were filed from September 2011 until June 2012, when petitioner contacted

Kaiser for a refill of Hydrocodone-Acetaminophen25 and Simvastatin,26 a statin. Pet. Ex. 94 at 59,

64. He was advised that his diabetes medications could not be refilled unless labs were done, even

if he no longer had insurance. Pet. Ex. 94 at 70. CVS Pharmacy records document refills

12

Pet. Ex. 12 at 103-09.

13

Id. at 79-84.

14

Cervical spondylosis is a “degenerative joint disease affecting the cervical vertebrae, intervertebral disks, and

surrounding ligaments and connective tissues, sometimes with pain or paresthesia radiating along the upper limbs as

a result of pressure on the nerve roots.” Dorland’s 1725.

15

Pet. Ex. 12 at 227-232.

16

Id. at 271-79.

17

Id. at 280-91.

18

Pet. Ex. 4 at 27-33; Pet. Ex. 12 at 295-302.

19

Diverticulosis is the “presence of diverticula, particularly of colonic diverticula, in the absence of inflammation.”

Dorland’s 552. Diverticula are “a circumscribed pouch or sac of variable size occurring normally or created by

herniation of the lining mucous membrane through a defect in the muscular coat of a tubular organ.” Dorland’s 552.

20

Pet. Ex. 4 at 43-48; Pet. Ex.12 at 304-311.

21

Pet. Ex. 4 at 58-67; 97-101.

22

Id. at 68-72.

23

Adacel is a tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis (Tdap) vaccine. Dorland’s 25.

24

Glipizide is an orally administered sulfonylurea compound used as a hypoglycemic in the treatment of Type 2

diabetes mellitus. Dorland’s 776.

25

Hydrocodone is “a semisynthetic opioid analgesic derived from codeine but having more powerful sedative and

analgesic effects.” Dorland’s 866. Acetaminophen is “the amide of acetic acid and p-aminophenol, having analgesic

and antipyretic effects similar to those of aspirin but only weak anti-inflammatory effects.” Dorland’s 11.

26

Simvastatin is “an antihyperlipidemic agent that is an HMG-CoA reductase inhibitor, used to lower blood lipid

levels in the treatment of hypercholesterolemia and other forms of dyslipidemia.” Dorland’s 1690.

4

throughout 2012 for Simvastatin, Hydrocodone,27 Atenolol,28 Mirtazapine,29 Vicodin,30 and

Remeron.31 Pet. Ex. 92 at 1-2; Pet. Ex. 94 at 101, 104, 109. He received a flu vaccine on October

10, 2012 without event. Pet. Ex. 92 at 2.

CVS Pharmacy records from 2013 reflect refills of Simvastatin, Atenolol, Hydrocodone,

Mirtazapine, Lisinopril,32 and Metformin33. Petitioner did not refill any medications to treat his

diabetes between December 29, 2012 and March 2013. Pet. Ex. 93 at 1-2.

On March 20, 2013, petitioner presented to Dr. Hopkins to establish care. The record

documented uncontrolled Type 2 DM, peripheral vascular complication, urinary incontinence,

chronic bac and hip pain, and GERD. Pet. Ex. 9 at 1. Dr. Hopkins noted a need for medication

change to control his comorbidities. Id. at 2-5.

Petitioner returned to Dr. Hopkins on April 24, 2013. The record documented “poorly

controlled DM and bilateral foot pain with neuropathy for which he limps around.” Pet. Ex. 9 at

6. He had anemia; gastritis34 with erosion of the upper GI tract treated with Prilosec and likely

slow blood loss; uncontrolled Type 2 diabetes with peripheral vascular complication that was

stable with neuropathy treated with Gabapentin; chronic lower back pain; hip pain; and arthritis.

Id. at 10.

2. Petitioner’s Health After Receiving the Influenza Vaccine

On August 19, 2013, petitioner received the subject flu vaccine at CVS Pharmacy. Pet. Ex.

93 at 2.

a. 2013

Petitioner presented to Dr. Hopkins on September 17, 2013, reporting body pain all over

after a flu vaccine. “He woke up with right leg pain and weakness. He has had poorly controlled

diabetes but now has joint pain and stiffness and has difficulty opening and closing his hand. He

denies a reaction prior to this of a rash or other reaction. His blood sugars are stable at home. The

27

Hydrocodone is “a semisynthetic opioid analgesic derived from codeine but having a more powerful sedative and

analgesic effect.” Dorland’s 867.

28

Atenolol is “a cardioselective β1-adrenergic blocking agent used in the treatment of hypertension and chronic angina

pectoris and the prophylaxis and treatment of myocardial infarction and cardiac arrythmias.” Dorland’s 169.

29

Mirtazapine is “an antidepressant compound unrelated to any of the classes of antidepressants; administered orally.”

Dorland’s 1152.

30

Vicodin is a “trademark for combination preparation of hydrocodone bitartrate and acetaminophen.” Dorland’s

2025. Hydrocodone bitartrate is “the bitartrate salt of hydrocodone, used as an analgesic and antitussive, administered

orally.” Dorland’s 867. Acetaminophen is “the amide of acetic acid and p-aminophenol, having analgesic and

antipyretic effects similar to those of aspirin but only weak anti-inflammatory effects.” Dorland’s 11.

31

Remeron is a “trademark for a preparation of mirtazapine.” Dorland’s 1597. Mirtazapine is “an antidepressant

compound unrelated to any of the classes of antidepressants; administered orally.” Dorland’s 1152.

32

Lisinopril is “the lysine derivative of the active form of enalapril; an angiotensin-converting enzyme inhibitor used

in the treatment of hypertension . . . congestive heart failure, and acute myocardial infarction.” Dorland’s 1052.

33

Metformin is “a biguanide antihyperglycemic agent that potentiates the action of insulin, used in the treatment of

type 2 diabetes mellitus; administered orally.” Dorland’s 1129.

34

Gastritis is “inflammation of the stomach.” Dorland’s 754.

5

flu shot was given two weeks” ago. Pet. Ex. 9 at 11. He tried ice and heat with some improvement

and used Vicodin and Tramadol. Pet. Ex. 9 at 11; Pet. Ex. 2 at 1. An examination revealed global

joint stiffness and pain with slow movements, but no inflammatory synovitis or rash. Pet. Ex. 9 at

12; Pet. Ex. 2 at 2. The assessment was acute arthritis and concern for flu vaccine reaction.

Petitioner was prescribed a steroid dose pack and Vicodin and advised to report the reaction to

CVS. Blood work for erythrocyte sedimentation rate (“ESR”)35 and complete blood count (“CBC”)

was normal. Pet. Ex. 9 at 13; Pet. Ex. 2 at 3.

Twelve days later, on September 29, 2013, petitioner presented to the emergency room at

Sutter Roseville Medical Center and came under the care of Dr. Tandon. Petitioner reported

debilitating joint pain throughout his body with generalized aches and pains starting a day after he

received a flu shot on August 19, 2013. Pet. Ex. 3 at 2. He did not feel well for two or three days

after the flu shot and was unable to go to work. His symptoms progressed and worsened gradually

over the next several weeks, causing difficulty getting out of bed, up from a chair, or off the toilet,

and he had stiff joints and achy muscles in both the upper and lower extremities, mostly in the

shoulder and the thigh. He tried over-the-counter medication, heat, and ice but did not feel better.

Id. at 8, 22-23. He had some relief from prednisone but has severe pain and muscle weakness

throughout his body. Onset was six weeks ago that worsened and is now severe. Id. at 2. He had

no loss of appetite, headache, visual disturbance, or decreased urine output. Id. at 2, 4, 8-9, 24. On

examination, he had generalized muscle pains and discomfort, especially in the proximal muscles

around the shoulders and thighs with no synovitis, joint swelling, or effusion. There were no focal

sensory or motor deficits and cranial nerves II-XII were intact. The assessment was diffuse

arthralgias, myalgias, and diffuse generalized weakness, with a history of Type 2 DM,

hypertension, and multiple other problems currently stable. Id. at 10. Dr. Tandon wrote, “It is

possible that he may have had an adverse reaction to the flu shot as his symptoms came after the

flu shot was given, and at this time, I will put flu shot in his allergy list.” Dr. Tandon noted

significant resolution of symptoms with steroids, so Solu-Medrol was ordered, and a neurological

consult was ordered due to his neuropathy. Id. at 10, 22-24.

Petitioner was examined by a neurologist, Dr. Mahmood and reported onset of symptoms

including generalized aches, particularly in the lower extremities, the day after a flu vaccine. By

the end of the day or the next day, his symptoms were progressively worse, and it was difficult for

him to walk. His right shoulder was first affected, then over the next several days both shoulders

had pain, tenderness, and weakness. Steroids worked, but symptoms returned and worsened within

a few days of completion. That morning, he had problems getting out of bed and came to the

emergency room. Pet. Ex. 3 at 26. Dr. Mahmood noted significant grip strength weakness,

significant proximal muscle weakness in both upper and lower extremities, trace reflexes in his

knees and upper extremities except for the triceps, and no reflexes in his ankles. Toes were

equivocal, there was no significant dystaxia,36 and sensory exam was normal. The impression was

generalized muscle weakness, arthralgias, and myalgias with a history of hypertension, DM, and

traumatic spine injury. He believed petitioner’s symptoms were related to the flu vaccine and

35

Erythrocyte sedimentation rate (“ESR”) is a non-specific test used to detect illness associated with acute and chronic

infection, inflammation, and tissue necrosis or infarction. Mosby’s Manual of Diagnostic and Laboratory Tests 199

(Pagana eds., 6th ed. 2018) [hereinafter Mosby’s].

36

Dystaxia is “difficulty in controlling voluntary movements.” Dorland’s 576.

6

suggestive of GBS, but GBS “would not explain the muscle tenderness or soreness.” IVIG was

recommended with occasional monitoring of his breathing. Id. at 27-28.

Petitioner was also examined by Dr. Rangi for chronic anemia. He reported GERD and

intermittent but worsening difficulty with swallowing over the “past several months.” Pet. Ex. 3

at 29. The assessment was microcytic iron deficiency and chronic anemia, GERD, and dysphagia.

Additional outpatient testing was recommended. Id. at 30. A CT scan showed a subtle esophageal

stricture. Id. at 35-36.

Petitioner was discharged on October 4, 2013 with a diagnosis of GBS as a complication

of flu shot, esophageal stricture, large hiatal hernia, Cameron ulcer37 with gastric ulcers, anemia,

iron deficiency probably secondary to gastrointestinal bleed, hypertension, DM, and elevated C-

reactive protein (“CRP”)38 and ESR. Pet. Ex. 3 at 37.

Petitioner returned to the ER on October 29, 2013, with complaints of muscle and joint

aches, weakness, and difficulty walking. He had a history of “atypical GBS (associated with

myalgias/arthralgias)” following a flu vaccine. Blood testing was negative for aldolase, rheumatoid

arthritis (“RA”) quantitative,39 and antinuclear antibody (“ANA”).40 CRP and ESR were elevated

but trended down with IVIG and prednisone. Pet. Ex. 3 at 60. Examination demonstrated trace but

symmetric bilateral patellar reflexes, 4+ to 5/5 strength throughout all upper and lower extremities,

and 3+ to 4/5 strength on upper abduction of the shoulders and bilateral thigh flexion. Sensory was

intact to light touch. The assessment was proximal muscle weakness, myalgias, arthralgias,

“possible neuromuscular disorder of unknown etiology at this point,” DM Type 2, hypertension,

and iron deficiency anemia. Id. at 62. Petitioner was admitted and a lumbar puncture was ordered.

An MRI could not be done due to the implanted stimulator in his back. Id. at 63. A CT scan showed

moderate osteoarthritic degenerative changes of both hips, mild tricompartmental osteoarthritic

degenerative changes of the knees with small right and trace left joint effusion, colonic

diverticulosis, and post-surgical changes of the lumbar spine and iliac bones. Id. at 73. His head

CT was negative. Id. at 74.

Dr. Mahmood examined petitioner upon admission. Petitioner reported he was “convinced

he was completely better” when discharged three weeks ago, but then noted worsening weakness

and painful movement that progressed until two days ago, when it significantly worsened. Pet. Ex.

3 at 69. On examination, he could move all four extremities but had significant muscle weakness

and pain, as well as tenderness and soreness involving the proximal and some distal muscle groups.

Tone was largely flaccid with deep tendon reflexes barely elicitable, and toes silent bilaterally.

Sensations were intact with equal and full light touch and temperature sensation in both upper and

37

A Cameron ulcer is “a peptic ulcer with a sliding hiatal hernia; it may be accompanied by chronic bleeding or be

clinically silent.” Dorland’s 1967.

38

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. Mosby’s 165-66”).

39

Rheumatoid arthritis (“RA”) quantitative, or the RA Factor, is a test used in the diagnosis of RA that is directed

toward identification of the IgM antibodies. Mosby’s 409-410.

40

Antinuclear antibodies (“ANA”) are used to diagnose systemic lupus erythematosus and other autoimmune diseases,

including but not limited to RA, polymyositis, scleroderma, infectious mononucleosis, and myasthenia gravis.

Mosby’s 80-83.

7

lower extremities. Id. at 70. The impression was polymyositis and possible paresthesia, with a

history of DM, hypertension, and lower spine disease. Id. at 70-71. Dr. Mahmood recommended

48-72 hours of steroids. Id. at 71.

A rheumatologist, Dr. Bhat was consulted on October 30, 2013 to rule out inflammatory

polymyositis. Pet. Ex. 3 at 82. A CT scan of the lower extremities and CK and aldolase levels

were normal, so inflammatory polymyositis was less likely, and he was not toxic appearing, so it

was not serum sickness. Aseptic meningitis41 was added to the differential diagnosis. Id.

Petitioner was discharged on October 31, 2013 with a diagnosis of steroid-responsive

proximal myopathy42 of unclear etiology, recent history of GBS probably related to flu vaccine,

abnormal lumbar puncture with aseptic meningitis without typical meningitis symptoms, DM,

implanted stimulator device, and probable allergy/reaction to flu vaccine. Pet. Ex. 3 at 88.

Petitioner returned to Dr. Hopkins on November 12, 2013 and reported feeling weak and

tired, with decreased strength in his legs and hands, paresthesia, and tingling in his hands, but he

felt better on steroids. He took narcotics for chronic back pain. A muscle biopsy was being

entertained. Pet. Ex. 2 at 4. On examination, there was no edema, 4/5 strength in the lower

extremities, 3/5 grip strength, and no ataxia with fair balance. Id. at 5. Dr. Hopkins noted GBS, a

flu shot, two hospitalizations, numerous neurology and rheumatology consults, petitioner feeling

tired and lethargic with recurrent symptoms when steroids were decreased, and diabetic

neuropathy with neurologic and peripheral vascular complication that “is not part of his above

syndrome.” He needed to be on disability for at least 90 days and have assistance at home. Id. at

9-10. Petitioner filed for disability on December 5, 2013 for Guillain-Barré Syndrome. Pet. Ex.

108 at 2, 239.

On December 9, 2013, petitioner presented to Dr. Seminer for outpatient neurological care

of acute weakness and “possible GBS.” Pet. Ex. 3 at 97. Petitioner reported onset of symptoms the

day after the flu vaccine with gradual weakness over the next several weeks. He was treated with

IV Solu-Medrol, improved, and was diagnosed with “steroid-responsive myopathy.” He had not

had any steroids for two weeks and his current complaints included pain in all joints, occasional

numbness and tingling in his right foot, and inability to open a jar. He did not have dysarthria,43

diplopia,44 dysphagia, or eyelid ptosis,45 and there was no muscle atrophy46 or fasciculations.47 Id.

at 97-98. Petitioner reported a four-month history of relapsing muscle weakness with some sensory

complaints. His CPK and sedimentation rate were normal, therefore myositis was unlikely. He

may have developed demyelinating neuropathy following the flu vaccine, but current findings

41

Aseptic meningitis refers to “any of several types of mild meningitis, most of which are caused by viruses.”

Dorland’s 1117. Meningitis is inflammation of the meninges. Dorland’s 1117.

42

Myopathy is defined as “any disease of a muscle.” Dorland’s 1206.

43

Dysarthria is “a speech disorder consisting of imperfect articulation due to loss of muscular control after damage to

the central or peripheral nervous system.” Dorland’s 569.

44

Diplopia is “the perception of two images of a singular object. Dorland’s 518.

45

Ptosis is “drooping of the upper eyelid.” Dorland’s 1527.

46

Muscle atrophy is “a wasting of muscle tissue.” Dorland’s 173.

47

Fasciculation is “a small local contraction of muscles, visible through the skin, representing a spontaneous discharge

of a number of fibers innervated by a single motor nerve filament.” Dorland’s 675.

8

suggested CIDP. EMG/NCS testing of the upper and lower extremities was ordered along with an

80 mg taper of prednisone, a follow up on sugar levels, and repeat ESR and CPK testing. Id. at 99.

The next day, December 10, 2013, petitioner presented to Dr. Hopkins with complaints of

weakness, fatigue, joint pain, and leg and hand numbness as lingering effects of GBS. His pulse,

blood pressure, and blood sugars were elevated by cyclical doses of prednisone. He remained out

of work. Pet. Ex. 2 at 13. He was globally weak but non-focal, with no ataxia48 and slow but steady

gait. Sensation was intact and motor strength was 4/5. Id. at 14. He was making slow progress,

with symptom flares when coming off prednisone. His diabetic neuropathy was noted, and his

blood pressure medication was increased. Id. at 18.

b. 2014

Petitioner was admitted to Sutter Roseville on January 8, 2014 for weakness likely

secondary to steroid response, exacerbation of GBS, and neuropathy of unclear etiology. Pet. Ex.

20 at 1; Pet. Ex. 100 at 1, 3. A lumbar puncture showed no infectious etiology, but elevated protein

and glucose levels suggestive of aseptic meningitis. Pet. Ex. 20 at 2; Pet. Ex. 100 at 11. Dr.

Mahmood documented a discussion with Drs. Agaiby and Saeed about the combination of

symptoms being suggestive of “some kind of neuropathic involvement which did not follow any

significant dermatomal pattern.” Pet. Ex. 100 at 12. The lack of deep tendon reflexes and history

of association with the flu vaccine suggested the possibility of GBS, which, if true, had become

chronic and should be considered CIDP. However, petitioner’s muscle stiffness, tenderness, and

soreness were more suggestive of myositis or myopathy, and the diagnosis was clouded by

impressive steroid responsiveness. Dr. Mahmood documented continued concern about possible

spinal cord involvement and noted that radiology refused to do an MRI due to petitioner’s

implanted stimulator. The diagnosis remained elusive; the steroid responsiveness and mixed

symptoms with associated urinary incontinence made spinal cord imaging and MRI very

important. Id. at 12-13.

Petitioner was discharged on January 10, 2014 with weakness secondary to steroid

responses, proximal myopathy of unclear etiology, history of GBS complication from flu vaccine,

microcytic anemia,49 and gastritis or gastric ulcer. Pet. Ex. 100 at 8-10.

Petitioner returned to Dr. Hopkins on January 23, 2014. “He has DM and neuropathy” and

is on insulin and steroids. He had chronic back and hip pain, and worsening bladder problems with

GBS. He had increased urinary symptoms. Pet. Ex. 9 at 14. He looked pale but had no edema; his

motor strength was 5/5 with grip; lower extremities were 4/5 with right foot drag, unsteady gait

and balance. Id. at 15. Dr. Hopkins’s assessment was that he may have a GBS variant in addition

to diabetic neuropathy with neurological complications. His diabetes was uncontrolled with

peripheral vascular complications. Id. at 18.

48

Ataxia is the “failure of muscular coordination; irregularity of muscular action.” Dorland’s 168.

49

Microcytic anemia is “any anemia characterized by microcytes (erythrocytes that are smaller than normal).

Dorland’s 78. Anemia is “a reduction below normal in the concentration of erythrocytes or hemoglobin in the blood

. . . it occurs when the equilibrium is disturbed between blood loss (through bleeding or destruction) and blood

production.” Dorland’s 77.

9

On January 24, 2014, petitioner returned to Dr. Seminer reporting that his hands felt a bit

heavy. He had finished prednisone four days ago, was walking with a cane, and was slightly

unsteady with right foot drag. He was treated with IV methylprednisolone and a tapering dose of

prednisone as an outpatient. He had mild difficulty swallowing. Pet. Ex. 3 at 104. His motor tone

was normal, strength was 5+, deep tendon reflexes were absent throughout, and he could support

his weight and walk on his heels and toes. He was released to work five hours a day, standing no

more than an hour at a time. A muscle biopsy was again considered. Pet. Ex. 3 at 105.

Petitioner had his first electromyography and nerve conduction study (EMG/NCS) on

January 24, 2014, which showed a few mild neuropathic electrophysiological abnormalities with

mild prolongation of sensory and motor nerve conduction across the wrist and right median nerve

consistent with right sided carpal tunnel syndrome. There was prolongation of F-wave latencies in

the right ulnar50 and tibial nerves51, which were isolated findings of “questionable” significance.

There was no other evidence of conduction slowing or neuropathy in the upper and lower

extremities. It was concluded that, “[T]he findings do not support a clinical diagnosis of Guillain-

Barre syndrome or CIDP.” Pet. Ex. 3 at 106-07.

A psychological examination conducted by the Department of Social Services on February

12, 2014 noted normal gross motor function and able to ambulate without assistance. He reported

depression about his inability to find treatment for his condition that started in October 2013 and

has worsened since. He was stressed about being able to care for himself. Pet. Ex. 108 at 142-43.

Petitioner reported a steady work history; though not currently working, he was employed by West

Marine and had worked there for 15 years as a manager.52 He reported no problems with managers

or coworkers in the past. Id.53 He was independent in activities of daily living and reportedly spent

his days eating, sleeping, and watching TV. Id. at 144. Mental health services for his depression

were suggested. He was determined not to be disabled and was denied Social Security Disability

Benefits. Pet. Ex. 108 at 145-46, 148-49.

Petitioner returned to Dr. Seminer on February 24, 2014, complaining of worsening

weakness in the upper and lower extremities, slight difficulty swallowing, and frequent urination.

Pet. Ex. 3 at 112. Dr. Seminer wrote, “Based on patient’s symptoms and slightly abnormal

electrodiagnostic studies, I think that he probably have (sic) CIDP.” He ordered IVIG three times

per month. Id. at 113.

On March 24, 2014, Petitioner returned to Dr. Hopkins for a check-up, was noted to be in

respiratory distress with chest tightness and was transported to the hospital by ambulance and

admitted. Pet. Ex. 2 at 20, 24. He was discharged on March 27, 2014 with shortness of breath

secondary to probable CIDP; history of GBS; hypertension; Type 2 DM made worse by steroids;

history of gastric ulcer; probable thalassemia;54 and resolved acute kidney injury. Pet. Ex. 3 at 117.

50

The ulnar nerve is the nerve “pertaining to the ulna or to the medial aspect of the forearm as compared with the

lateral (radial) aspect.” Dorland’s 1968.

51

The tibial nerve is the nerve “pertaining to the tibia or to the medial aspect of the leg.” Dorland’s 1897.

52

This is inaccurate. The evidence shows petitioner last worked for West Marine in 2007. He was rehired in 2012 as

an employee, not a manager. Tr. 86-87; Pet. Ex. 101 at 22, 29-31, 41, 113.

53

Petitioner’s records document an incident with a coworker in 2010. Pet. Ex. 4 at 59.

54

Thalassemia is “a heterogenous group of hereditary hemolytic anemias that have in common a decreased rate of

synthesis of one or more hemoglobin polypeptide chains and are classified according to the chain involved.” Dorland’s

10

At his April 21, 2014 visit, Dr. Seminer noted that the EMG/NCS testing done on March

26, 2014 revealed no real prolongation or absence of F-waves in the lower extremities, with an

incidental finding of median neuropathy at the right wrist. The test was otherwise normal, as was

the repetitive stimulation testing performed. Monthly IVIG infusions were ordered for CIDP and

work accommodations of no climbing or heavy lifting recommended. Pet. Ex. 3 at 152.55

On April 28, 2014, petitioner filed for reconsideration of his Social Security disability

denial submitting other unspecified arthropathies and diabetes mellitus, with a date of disability of

October 29, 2013. Pet. Ex. 108 at 239. He was determined to be disabled as of April 2014, with

payments starting June 2014 with back payments approved for April and May. Id. at 240-41, 245.56

On May 9, 2014, petitioner presented to Dr. Knox advising that his symptoms worsened

two weeks after the March IVIG infusion and within four weeks he had difficulty moving his legs.

On the date of this visit, he was on the third day of a three-day course of IVIG and was doing

better. Pet. Ex. 5 at 4. Examination revealed normal strength, tone, sensation, and gait. Dr. Knox’s

impression was “possible CIDP” given the clinical response to IVIG and marked proximal

weakness. IVIG treatments were to continue, tapered every two weeks. Pet. Ex. 5 at 4, 6, 16. IVIG

was necessary due to risks from prednisone with petitioner’s history of stroke and DM. Id. at 6.

Genetic testing conducted on May 9, 2014 resulted in Dr. Knox documenting “CANNOT

BE ON IMURAN”, which petitioner had taken in the past. Pet. Ex. 5 at 21; Pet. Ex. 89 at 48.

Petitioner returned to Dr. Knox on June 11, 2014. His last infusion was June 6, 2014. He

reported he felt good until Sunday, when he awoke tired with difficulty getting his legs to move

and fell. His legs felt like they were dragging. Pet. Ex. 5 at 18.

Petitioner presented to Dr. Hopkins on June 19, 2014 reporting exacerbation of CIDP. He

was using a cane and complained of fatigue, weakness, falling, and feeling depressed. Pet. Ex. 2

at 25; Pet. Ex. 9 at 19. He appeared tired on examination, with symmetrical weakness and unsteady

gait but without tremor or ataxia. Pet. Ex. 2 at 26; Pet. Ex. 9 at 20. The assessment was CIDP.

Petitioner was directed to restart steroids, Levemir for diabetes, and continue his other

medications. His hypertension was stable; CIDP was the primary issue. Pet. Ex. 2 at 30.

On July 9, 2014, petitioner returned to Dr. Knox, who noted that while intravenous Solu-

Medrol (IVSM) worked better than IVIG, petitioner’s blood sugar was uncontrolled on it. Pet. Ex.

5 at 34. Petitioner followed up with Dr. Knox again on July 17, 2014. Id. at 40. He had no clear

weakness but had slight foot drop with walking. He was released to work 20 hours per week. Id.

at 43. Petitioner received IVIG infusions through August 1, 2014. Pet. Ex. 3 at 154-219.

1878. Hemolytic anemias are “any of a group of acute or chronic anemias characterized by excessive hemolysis and

impaired erythropoiesis.” Dorland’s 78.

55

It is unclear from the records whether petitioner was working at this time since he had been awarded disability.

56

Petitioner was ultimately awarded Medicare Part A (hospital insurance) and Part B (medical insurance) beginning

in April 2016. Pet. Ex. 108 at 248; Pet. Ex. 109.

11

On August 25, 2014, at an appointment with Dr. Hopkins, petitioner reported working 20

hours a week. His weakness was stable. He was taking Levemir,57 Metformin, Cellcept,58 and

Solu-Medrol, which affected his DM. He had fatigue, lethargy, GI upset, and weakness. Pet. Ex.

2 at 32; Pet. Ex. 9 at 26. Dr. Hopkins’s assessment was CIDP; chronic but stable back pain; diabetic

neuropathy with neurologic complication, stable with mixed presentation given his primary

neurologic disorder; hypertension; and diabetes. Pet. Ex. 2 at 40; Pet. Ex. 9 at 34.

Petitioner returned to Dr. Knox on September 9, 2014. He was receiving IVIG infusions

on Mondays and Thursdays but felt weak by the weekend. Pet. Ex. 5 at 55. He wanted IVSM three

times per week because he began feeling weakness after three days. Pet. Ex. 13 at 296. He saw Dr.

Knox again on November 3, 2014. He was receiving infusions three times per week and felt “great

and functional.” He was stronger but still using a cane. His blood sugar was high. Id. at 306, 309.

Petitioner returned to Dr. Knox on November 18, 2014, still feeling great with his strength back to

normal. Blood sugar level was still high. Id. at 311.

Another EMG/NCS study was performed on November 18, 2014 and was no different

when compared to the March 26, 2014 study. Pet. Ex. 13 at 198-201, 315; Pet. Ex. 3 at 104-08.

Dr. Knox wrote “interesting that the ncs never showed demyelinating ????” Pet. Ex. 13 at 315.

Petitioner was on full disability at this time. Id. at 316.

On November 25, 2014, petitioner was sent by the infusion center to the ER for two days

of neck swelling and difficulty swallowing. Pet. Ex. 13 at 345. A small hiatal hernia and mild

multilevel cervical spondylosis were noted. Id. at 349.

After an examination on December 11, 2014, Dr. Knox documented that petitioner was

using a cane but had no power loss. Pet. Ex. 13 at 320. His blood sugar level was 500 and

unsustainable. Id. at 321.

c. 2015

On January 13, 2015, Dr. Knox noted a recent ER visit for cellulitis of the left leg on

December 27, 2014. Petitioner needed help to stand, had slight weakness, and no reflexes. He was

directed to secure and see a new PCP before February since Dr. Hopkins no longer accepted his

insurance. Pet. Ex. 13 at 321-26.

At a visit to Dr. Knox on February 12, 2015, petitioner complained of weakness. He was

unable to get subcutaneous methotrexate, so he was using pills and taking folic acid. Petitioner

reported his blood sugar was less than 200 now that he was off steroids. He claimed to be getting

weaker, falling, and having difficulty chewing. Pet. Ex. 20 at 5. Dr. Knox again advised he needed

a PCP for diabetes control. Id. at 5, 10.

57

Levemir is a “trademark for a preparation of insulin detemir.” Dorland’s 1018. Insulin detemir is “a long-acting

insulin analogue in which the threonine at position 30 of the B insulin chain is omitted, and a 14-carbon fatty acid

chain is attached to the amino acid at position 29; administered subcutaneously in the treatment of diabetes mellitus.”

Dorland’s 934.

58

Cellcept is a “trademark for preparations of mycophenolate mofetil.” Dorland’s 320. Mycophenolate mofetil is an

immunosuppressive agent. Dorland’s 1199.

12

On February 16, 2015, petitioner presented to a new PCP, Dr. Belsky. Pet. Ex. 20 at 10-

12. Dr. Belsky’s assessment was uncontrolled Type 2 DM with peripheral vascular complication;

hypertension well-controlled on Lisinopril and Atenolol; high cholesterol controlled on statins;

history of transient ischemic attack and stroke; CIDP followed by neurology; and anemia followed

by hematology. He also had suspected thalassemia for which he received IV iron infusion. Id. at

14.59 On March 13, 2015, Dr. Belsky documented that Medi-Cal no longer covered freelance

glucometers and petitioner had not tested his sugar since he ran out of strips on March 6, 2015. Id.

at 15. On March 16, 2015, petitioner presented for diabetes education and insulin management.

Steroid use elevated his blood sugar to the 500s. Id. at 18-19.

On March 18, 2015, petitioner returned to Dr. Knox, who documented that petitioner was

self-prescribing 20 mg of prednisone four times per day for the past month and a half. Pet. Ex. 20

at 19. The impression was still CIDP, though the clinical diagnosis was “concerning.” He was to

resume IV steroids at 1 mg once per week. Pet. Ex. 20 at 25.

On March 20, 2015, petitioner returned to Dr. Belsky frustrated by the uncertainty of his

diagnosis. Dr. Belsky ordered IV steroid infusions but cautioned petitioner against taking the 80

mg of oral steroids daily that he was self-prescribing. Pet. Ex. 20 at 26.

On May 1, 2015, petitioner saw Dr. Ambriz for an eye examination and was cautioned to

control his blood sugar to avoid diabetic eye complications and the risk of blindness. Id. at 31.

On May 20, 2015, petitioner returned to Dr. Knox with difficulty swallowing and choking

on food, losing his voice, and water coming through his nose and mouth when drinking. He

continued to self-prescribe 80 mg of prednisone per day. Pet. Ex. 20 at 32.

At the time of his June 24, 2015 visit with Dr. Knox, petitioner had received IVIG/Solu-

Medrol, felt great with “some power back,” and could stand, walk, talk, and breathe. Dr. Knox

wrote, “The question has always been the diagnosis…” An examination showed “slight weakness

infraspinatus. Slight weakness of hip flexion. The rest of the power is strong.” Pet. Ex. 20 at 46.

A NCS of the right upper and lower limb on that date were comparable to those performed on

March 26, 2014. Repetitive stimulation testing showed no decremental responses. The impression

was “possible primary muscle disorder. Normal CPK argues against a muscle disorder affecting

the muscles themselves and thus I suspect we may be dealing with an inflammatory response

muscle disorder such as seen in sarcoid.” Dr. Knox noted a need for a muscle biopsy, a second

opinion, a referral to neurosurgery, and continuing intervention with steroids, with more directed

therapies “once we have a better sense of what is going on.” Id. at 47. In a July 1, 2015 addendum,

Dr. Knox wrote that a muscle biopsy should be done on the left. Petitioner cannot have an MRI

because he claims the spinal stimulator cannot be removed. Id. at 48.

At his July 17, 2015 visit, Dr. Knox noted petitioner had an infusion three days prior and

was feeling better but still had problems swallowing at times. A muscle biopsy was scheduled for

August 3, 2015.60 Pet. Ex. 20 at 48. He saw Dr. Belsky for a right wrist injury from a fall five days

later and reported struggling with lower leg weakness. Pet. Ex. 16 at 2.

59

No records associated with iron infusions were filed.

60

The scheduled muscle biopsy was ultimately cancelled due to loss of insurance. Pet. Ex. 18 at 1.

13

Petitioner was examined by Dr. Carroll on August 26, 2015 for microcytic anemia with

iron deficiency that did not respond to iron supplementation, due to malabsorption and alpha

thalassemia trait. He was to be treated with intravenous iron Dextran quarterly as needed to keep

his ferritin greater than 100. Pet. Ex. 20 at 61.

Petitioner returned to Dr. Knox on October 1, 2015 and reported feeling better, swallowing

better, walking great, and being better able to stand up from a chair, with no heaviness and barely

any numbness in his hands. Pet. Ex. 18 at 1. Dr. Knox wrote, “Possible myopathy but with

numbness places this into the cidp or similar Could be myelopathy but has no spasticity Responsive

to steroids Not (sic) sign abnormal emg Needs muscle biopsy The muscle biopsy should be done

on the left, repeat the left iliopsoas.” Id. at 7.

Petitioner was admitted to the hospital overnight on December 8, 2015 for chest pain,

shortness of breath, and possible loss of consciousness during an IVIG infusion. Pet. Ex. 20 at 79.

Cardiac testing was negative. Id. at 197, 206-07.

d. 2016

At a January 26, 2016 visit, Dr. Knox wrote “it would be nice ot (sic) confirm cidp need

another ncs and then muscle biopsy.” He was okay with continuing IVIG for now. Pet. Ex. 20 at

102. At his March 18, 2016 visit, petitioner reported feeling great and “back to me again.” Dr.

Knox noted petitioner mixes power with sensory loss when he speaks, which is “hard to separate

out.” Id. at 103.

On March 25, 2016, Dr. Belsky discussed petitioner’s elevated creatinine and kidney injury

with unclear etiology, possibly related to infusions. Pet. Ex. 20 at 110. On April 1, 2016, Dr. Belsky

stopped Metformin and Lisinopril and ordered urinalysis and a renal ultrasound. Id. at 116. Dr.

Belsky saw him regularly over the next several months for ongoing kidney issues. See Pet. Ex. 20.

On August 11, 2016, Medicare denied petitioner’s IVIG (Privigen) treatments for failure

to meet authorization requirements, which include EMG findings of two of the three criteria:

reduced conduction velocity of 2 or more motor nerves; prolonged distal latency of 2 or more

motor nerves; prolonged F-wave latencies of 2 or more motor nerves or the absence of F-waves.

Pet. Ex. 24 at 1. An appeal was filed and on October 7, 2016, petitioner’s Privigen was approved

from August 10, 2016 through January 7, 2017. Pet. Ex. 24 at 20; Pet. Ex. 98 at 2.

At an August 18, 2016 visit, petitioner reported feeling great receiving weekly IVIG

infusions and prednisone. Pet. Ex. 20 at 147. Dr. Knox’s impression was lower extremity weakness

responsive to IVIG and prednisone and “[p]robable CIDP,” but the only supportive evidence was

prolonged F-waves/H reflexes. Another lumbar puncture “was not worth it.” Id. at 148. He

prescribed 150 mg of Imuran a day with hopes of weaning him from IV medications. Id. Petitioner

continued to receive IVIG through the end of 2016. See Pet. Ex. 22.

On December 21, 2016, Dr. Belsky wrote a letter on petitioner’s behalf stating that he had

CIDP and would benefit from an increase to the 16 hours of daily skilled home care he was

receiving. Pet. Ex. 23.

14

e. 2017

On January 30, 2017, Dr. Knox wrote “Inflammatory NM (neuromuscular) disease Likely

CIDP Confirmed by clear clinical presene (sic) of response to IVIG But testing limited Cannot get

mri Is (sic) spine LP-OK EMG – prolonged F-waves. But with numbness places this into the cidp

or similar Maybe - with immune modulators will improve.” Pet. Ex. 89 at 9.

On February 3, 2017, Dr. Belsky again advised petitioner about his self-prescribing of 80

mg a day of corticosteroids in addition to what his physicians prescribed. He strongly encouraged

petitioner to stop, as it complicated the management of his comorbidities. Pet. Ex. 89 at 11-12. Dr.

Belsky noted that Dr. Knox had reduced petitioner’s Solu-Medrol dose by half. Id. at 11.

On March 27, 2017, petitioner presented to Dr. McMullen for diabetes follow up. He was

not tracking his sugars or how much insulin he was taking but advised he took between 20 and 40

units of Humalog61 before meals, though it was unclear how he decided how much to take. Pet.

Ex. 89 at 16-17. He had a caretaker during the day. Id. at 17.

By June 30, 2017, petitioner’s IVIG infusions had stopped, and his sugar levels were better.

He felt his overall strength was stable, but he continued to struggle with walking long distances

and used a cane or ski poles to do so. Pet. Ex. 89 at 40.

On July 13, 2017, petitioner presented to the ER with worsening weakness, pain, leg

swelling, numbness and a history of CIDP. He reported having no IVIG treatment since May 23,

2017. Pet. Ex. 89 at 218. An ultrasound for deep vein thrombosis was negative. Id. at 225. His

symptoms were consistent with cellulitis, and he was prescribed Bactrim. Id. at 223.

Petitioner returned to the ER on July 28, 2017 with leg redness and swelling after finishing

the antibiotics with no relief. He reported receiving IVIG for three years for CIDP which was

discontinued 47 days ago. Pet. Ex. 89 at 237. Dr. Lapin noted bilateral lower extremity swelling

and erythema with possible elements of cellulitis. Due to his DM, petitioner was prescribed

Zosyn62 and Vancomycin63 and an echocardiogram was ordered to rule out heart failure. There

was no compartment syndrome or compromised renal function. His international normalized ratio

(“INR”)64 was 1 with lower extremity bruising, and some capillary fragility secondary to trauma.

Neurology was consulted due to progressive weakness since his last treatment in May. Id. at 248.

He was discharged on August 1, 2017. The discharge summary documented DM and cellulitis of

61

Humalog is a “trademark for preparations of insulin lispro.” Dorland’s 863. Insulin lispro is “a rapid-acting insulin

analogue in which the lysine and proline residues at positions at 28 and 29 on the insulin B chain are reversed;

administered subcutaneously in treatment of diabetes mellitus.” Dorland’s 934.

62

Zosyn is a “trademark for combination preparations of piperacillin sodium and tazobactam sodium.” Dorland’s

2065. Piperacillin sodium is “the sodium salt of piperacillin, used in the treatment of infections caused by susceptible

organisms and in intra-abdominal surgery for the prevention of infection; administered intramuscularly or

intravenously.” Dorland’s 1428. Tazobactam sodium is “the sodium salt of tazobactam, used in combination with

piperacillin sodium to broaden its spectrum of activity against beta-lactamase producing organisms.” Dorland’s 1845.

63

Vancomycin is “an antibiotic . . . which is highly effective against cocci, especially staphylococci, and other gram-

positive bacteria.” Dorland’s 1993.

64

International normalized ratio (“INR”), also known as prothrombin time (“PT”), is used to evaluate the adequacy

of the extrinsic system and common pathway in the clotting mechanism. It measures the clotting ability of factors I

(fibrinogen), II (prothrombin), V, VII, and X (ie, the extrinsic system and common pathway). Mosby’s 391-93.

15

the left lower extremity. He received one IVIG treatment and was prescribed three days of Keflex

for cellulitis, which was nearly resolved on discharge. Id. at 275-79.65

On August 7, 2017, petitioner presented to Dr. McMullen. He reported he had not received

IVIG since May but had been hospitalized for IV antibiotics for cellulitis. His legs were still

swollen, and his arms and feet felt heavy and numb. He changed his insulin dose on his own and

was not having excessive urination or thirst. Pet. Ex. 89 at 52. Petitioner also presented to Dr.

Carroll on the same day for anemia responding well to iron supplementation, but it appeared he

had a malabsorption problem and GI bleeding with thalassemia trait. Dr. Carroll advised continued

iron dextran66 supplementation to keep his ferritin greater than 100. The record noted that his CIDP

was IVIG, steroid, and Imuran refractory. Rituximab,67 which was off label, was suggested. Id. at

58.

On August 9, 2017 Dr. Knox referred petitioner to Dr. Katz for a second opinion on CIDP

and whether Rituximab should be used. Pet. Ex. 89 at 295.

Petitioner presented to Dr. Katz on August 15, 2017 with a four-year history of “CIDP”

which started with his legs and arms getting heavier, then his finger started feeling fat and numb.

He could not hold himself up, get up and down a ladder, would “trip over himself”, and fell several

times. His current symptoms included heaviness, neck muscle pain, head drop, tiring easily when

walking, truncal weakness, a numb/dumb feeling in his hands, and jolts down his legs which come

and go based on his treatment cycle. He received IVIG twice a week for the past two years and

said, “he has had two cardiac arrests from IVIG in the past.” He has DM and blames his current

DM on prednisone. Pet. Ex. 85 at 1; Pet. Ex. 89 at 299. Dr. Katz found no evidence of CIDP, which

upset petitioner. Pet. Ex. 85 at 4. Dr. Katz referenced multiple normal NCS studies, the presence

of reflexes, and weakness of “breakaway type.” Id. The CSF protein level on lumbar puncture was

explained by IVIG just before testing. Nothing in his history fit GBS and nothing in the chart

supported progression. Dr. Katz further noted petitioner has not had any clear recurrence in three

months without IVIG and questioned why petitioner could not walk and was in a wheelchair. Pet.

Ex. 85 at 4; Pet. Ex. 89 at 302. Dr. Katz ordered another EMG but did not expect to see any

difference and deferred to Dr. Knox. Pet. Ex. 85 at 4; Pet. Ex. 89 at 302. Dr. Katz advised that

petitioner did not have CIDP. Pet. Ex. 89 at 72. Dr. Knox then changed his impression to

inflammatory or pseudo-neurological disease, referred petitioner to rheumatology, and stopped

petitioner’s medication, which angered petitioner. Id at 79-80.

At his October 4, 2017 visit with Dr. Carroll, petitioner expressed anger at Dr. Katz’s

opinion that he had arthritis rather than CIDP. He had a marked increase in pain and disability

since IVIG stopped. Petitioner had not seen the rheumatologist and or been compliant with iron

infusions. Pet. Ex. 89 at 83.

65

Records from this hospitalization are contained in Pet. Ex. 88 as well.

66

Iron dextran is “a sterile colloidal solution of ferric hydroxide, FE(OH) 3, complexed with partially hydrolyzed low

molecular weight dextran, in water for injection; administered intravenously or intramuscularly as a hematinic.”

Dorland’s 949.

67

Rituximab is “a chimeric murine/human monoclonal antibody that binds the CD 20 antigen; used as an

antineoplastic in the treatment of CD 20-positive, B-cell non-Hodgkin lymphoma; administered intravenously.”

Dorland’s 1624.

16

Petitioner then presented to the ER on October 14, 2017, reporting a history of CIDP with

a “flare-up” of heaviness, weakness, and numbness. His last IVIG infusion was in August because

his CIDP diagnosis was questioned by a specialist at UCSF. Pet. Ex. 89 at 316-17. He was admitted

for neurological consult with Dr. Byrd, who noted that petitioner’s IVIG had been stopped by two

neurologists who ruled out CIDP, but petitioner refused to accept this and presented to the ER for

treatment. Dr. Byrd refused to order IVIG and suggested physical therapy, but petitioner left

against medical advice. Id. at 323, 335.

At his visit with Dr. Belsky on October 24, 2017, petitioner said he presented to the ER in

hopes of receiving IVIG but left when they would not provide it. He had increasing weakness in

his arms and legs over the past two months; his hands felt numb, and he was wearing diapers, so

he did not have to get up as much. He used a walker or cane at home but spent most of the day on

the couch because he was too tired and weak to walk. He had help during the day. Pet. Ex. 89 at

86.

On October 30, 2017, petitioner saw Dr. Scalapino, a rheumatologist. Pet. Ex. 89 at 87. His

assessment was peripheral neuropathic pain with poor balance:

It is not clear to me whether he has CIDP, CIDP related to diabetes, or some other

peripheral neuropathy that involves sensory over motor and is associated with rather severe

paresthesias, loss of position and vibratory sensation and distal loss of strength, especially

hands. It looks as though his electrophysiologic testing was only lukewarm support for the

diagnosis. Against [CIDP] is the fact that his reflexes seem intact but in favor of CIDP is

the fact that he has clearly responded temporarily to IVIG and steroids.

Pet. Ex. 89 at 94. He further noted diabetic peripheral neuropathy associated with Type 2 diabetes

that is approaching good control, but there is no expectation for the neuropathy to normalize at this

point. Absorption problems may be contributing to neurologic symptoms, though it was doubtful

given the chronology of problems following vaccination. He was vitamin D deficient with bad

degenerative joint disease of the hip contributing to his difficulty getting up and down from a chair,

etc., but it does not seem to give him any pain. Id. at 94-95.

On November 7, 2017, petitioner presented to Dr. McMullen complaining of numbness

and pain in his arms and legs. Dr. McMullen wrote that his diagnosis of CIDP was now

questionable; he no longer received infusions but was self-medicating with 20 mg of prednisone

three times per day. He declined to have diabetic education sent to his home. Pet. Ex. 89 at 95.

On November 17, 2017, petitioner presented to the ER following a fall that morning

injuring his back. He was unable to stand, had a history of leg weakness, hit his head on the wall

when he fell, and had numbness through his body all the time. Pet. Ex. 89 at 353. Lower extremity

swelling and rash was noted, and he was prescribed Norco68 for pain. Id. at 358.

On December 6, 2017, petitioner returned to Dr. Belsky with right hip pain and acute right-

sided low back pain from a fall. Dr. Belsky noted it was likely a contusion, but he was at increased

risk for fracture due to ongoing corticosteroid use which he had been warned to stop many times.

68

Norco is a “trademark for combination preparations of hydrocodone bitartrate and acetaminophen.” Dorland’s 1272.

17

Pet. Ex. 89 at 100. Petitioner reported spending his days watching TV but enjoys getting out,

looking at real estate, and spending time on a friend’s boat. He was taking 600 mg of Gabapentin

at bedtime. Id. at 101. A friend planned to move in to assist him with activities of daily living. Id.

at 102. He was prescribed Tramadol69 and referred to orthopedics. Id. at 104. X-rays of the right

hip showed severe degenerative changes; x-rays of the lumbar spine showed multilevel

degenerative changes. Id. at 151-52.

Another EMG/NCS on December 20, 2017 showed no changes. Pet. Ex. 89 at 180-84.

f. 2018

On February 13, 2018 petitioner presented to the ER with wrist pain from a fall. Pet. Ex.

89 at 378. X-rays of his wrist, hand, and shoulder showed no fractures and venous doppler of the

left extremity showed no deep venous thrombosis. Id. at 384, 386.

Petitioner presented to Dr. Latov in New York City on March 8, 2018, complaining of

weakness and difficulty walking. Pet. Ex. 58 at 1. He reported generalized weakness three weeks

after the flu vaccine in August 2013 for which he was hospitalized and treated with IVIG for CIDP.

He reported multiple relapses. IVIG and steroid treatment was discontinued six months ago. He

was on Methotrexate in 2015 and Imuran in 2016, both without benefit. His creatinine was

elevated, EMG/NCS studies were normal, but he remained weak, using bilateral walking canes.

Pet. Ex. 58 at 1-2; Pet. Ex. 63. Another EMG/NCS was ordered.

Petitioner presented to Dr. Belsky for right hip pain in March 2018 and received a cortisone

injection. Pet. Ex. 60 at 2. X-rays showed advanced degenerative changes in the right hip, and he

underwent hip surgery on May 7, 2018. Pet. Ex. 60 at 6-7, 15; Pet. Ex. 71; Pet. Ex. 59 at 21. During

his hospitalization, he was noted to be neurovascularly intact, with limited range of motion of the

right leg secondary to right hip surgery. He had normal reflexes. Pet. Ex. 71 at 23.70

At a visit with Dr. McMullen on April 6, 2018, Dr. McMullen wrote, “Hx of: neuropathy

? CIPD versus DM.” Pet. Ex. 60 at 8.

At a follow up with Dr. Belsky on May 23, 2018, it was noted that petitioner was in a

rehabilitation facility, working with a physical therapist three times per week, and taking Percocet.

Pet. Ex. 60 at 26. He reported seeing Dr. Latov. Pet. Ex. 60 at 26-27; Pet. Ex. 64.

The EMG/NCS study ordered by Dr. Latov performed on June 21, 2018 was read as

abnormal with evidence of chronic generalized sensorimotor polyneuropathy with demyelinating

features. Median neuropathy of the right carpal tunnel was noted, most likely as part of the

underlying disease process. Pet. Ex. 58 at 6.

69

Tramadol is “an opioid analgesic used for the treatment of moderate to moderately severe pain following surgical

procedures and oral surgery; administered orally.” Dorland’s 1920.

70

Records of the complete hospital stay are contained in Pet. Ex. 82. Records of this hospitalization are also included

in Pet. Ex. 88.

18

On July 19, 2018, petitioner was hospitalized for a “CIDP flare.” Pet. Ex. 59 at 1. He had

not received IVIG for six months. Id. at 19. He reported that testing at Weill Cornell showed

generalized sensorimotor polyneuropathy with demyelinating features, but he was advised he

needed to be treated in his home state of California. He received five days of IVIG and was

discharged feeling much better. Pet. Ex. 59 at 2.

Petitioner presented to Dr. Belsky for a Medicare Annual Wellness visit on August 6, 2018.

Pet. Ex. 106 at 614. Dr. Belsky documented idiopathic peripheral neuropathy with generalized

weakness, no longer on corticosteroids, followed by neurology; uncontrolled Type 2 diabetes

mellitus with long-term insulin use followed by an endocrinology; anxiety and depression treated

with Zoloft;71 anemia with thalassemia trait and malabsorption due to GI bleed. Weight loss was

discussed. Id. at 614-15.72

Petitioner returned to Dr. Knox on August 10, 2018. His hip replacement and visit to

Cornell were noted and that he was told he has CIDP. He reported receiving five days of IVIG in

July 2018. On that day he complained of “firing” in his arms and hands, vibrating feelings,

numbness in his fingers, and urgent need to urinate. Pet. Ex. 99 at 1. Neurological examination

was normal. “Ankle and knee reflexes are trace but present. Brachioradialis biceps and triceps are

1+. Maybe a slight 5 weakness of right toe curling, maybe slight difficulties pinprick sensation in

the top of the right toe, vibration 7 seconds”. Id. at 5. Weak fingers with hand numbness. It “must

be something else” if not CIDP. Most commonly, it would be something associated with the neck,

but an EMG showed only carpal tunnel syndrome. Petitioner was referred to orthopedics for carpal

tunnel surgery. Dr. Knox again documented that the lower back stimulator needed to be removed

so an MRI could be done of his lumbar spine. Petitioner demonstrated “give way weakness,”73

and the need for petitioner’s records from Cornell. Id. at 10.

On September 21, 2018, petitioner presented to another neurologist, Dr. Xiong at UC

Davis. Pet. Ex. 65 at 13. He reported a history of weakness and numbness in all extremities since

a 2013 flu shot. He received the shot and felt like he was getting a cold, then his arm and hand

were painful. The next day his hip joints hurt and a few days later he felt weak in the feet. About

3 weeks later he could not get up from the toilet and had difficulty raising his arm overhead; he

felt pins and needles in his hands and his toes and legs were tingling. He went to the hospital, was

diagnosed with GBS, treated with IVIG, and was back to normal. Then, 47 days later, he had

similar symptoms and was treated with IV steroids. About 30 days after that, his feet and hands

felt numb, and he had difficulty breathing. He received IVIG for five days and improved. He was

diagnosed with CIDP and received high dose steroids for a year. He received IVIG for one to two

years until it was stopped over 8 months ago. He felt worse without it. He had a right hip

replacement in May 2018 and was hospitalized in July 2018 for weakness and numbness, received

five days of IVIG, and felt 60 percent better, but started to decline a month later. He took

Methotrexate and Imuran for a time in 2015 and 2016 without benefit. He saw Dr. Latov in March

71

Zoloft is a brand name for preparations of sertraline hydrochloride. Dorland’s 2061. Sertraline hydrochloride is a

“selective serotonin reuptake inhibitor, used to treat depressive, obsessive-compulsive, and panic disorders;

administered orally. Dorland’s 1671.

72

This record makes no reference to petitioner using any supportive aids to walk.

73

While give way or giveaway weakness is often attributed to a patient who is not fully cooperating, is hysterical,

malingering, or has conversion disorder, Dr. Chaudhry indicated that it can also be a result of pain or issues with

balance. Tr. 210-11, 386.

19

2018, who recommended IVIG again, but Dr. Knox and Dr. Katz disagreed. Id. Dr. Xiong’s

impression was sensorimotor neuropathy with unclear underlying etiology. He noted that diabetes

could contribute partially to his neuropathy, but it would be unusual for it to fluctuate. After

reviewing the records, Dr. Xiong’s working diagnosis was CIDP, but he stated it would be

challenging to resume IVIG given his renal insufficiency while on IVIG. Id. at 20.

Dr. Latov wrote an addendum to his March record on September 26, 2018, “EMG and NCS

on 6/21/18 showed changes consistent with a demyelinating polyneuropathy. Impression/Plan: He

has a demyelinating polyneuropathy, probable chronic inflammatory demyelinating

polyneuropathy (CIDP), although other causes of demyelinating polyneuropathy including MAG

neuropathy, POEMS syndrome, or CMT1 should also be considered.” Pet. Ex. 63 at 4.

Another EMG/NCS study ordered by Dr. Xiong and done at UC Davis on November 14,

2018 showed abnormal findings consistent with moderate motor and sensory peripheral

neuropathy with both demyelinating and axonal features and superimposed carpal tunnel

syndrome. Pet. Ex. 65 at 25.

Petitioner returned to Dr. Xiong on November 16, 2018 and was noted to be weaker. He

wanted to know if he could start IVIG or Rituximab. Pet. Ex. 65 at 26. Dr. Xiong ordered IVIG

with follow up in three months. Pet. Ex. 65 at 33-34.

g. 2019

Additional records were filed after the hearing, including records from physical therapy to

improve mobility and make petitioner more independent with activities of daily living. Pet. Ex. 81

at 6. The physical therapy assessment included signs and symptoms suggestive of general

weakness in all extremities but worse proximally, with significant static and dynamic balance

deficits and significant sensation loss in all extremities. Id. at 27.

At a visit on February 8, 2019, Dr. Xiong noted “poor effort in exam” but normal muscle

tone and bulk at his neck and appendages without fasciculations. He had mild action tremors in

the right hand, but “FTN (Finger to Nose) intact bilaterally.” He displayed difficulty rising and

swing upon standing. Pet. Ex. 107 at 5. Dr. Xiong commented that the testing done at Cornell, Dr.

Latov was significantly different from all the testing performed since 2013. There was sensory

level loss below the neck, distal more than proximal weakness, and elements of poor effort. He

had decreased/absent ankle reflexes with “otherwise preserved DTR (Deep Tendon Reflexes).” Id.

at 9-10. “Diabetes could contribute to his peripheral neuropathy and possible

inflammatory/immune-mediated etiology cannot (sic) completely rule out at this time. It is unusual

for diabetic neuropathy to have significant fluctuation of symptoms and signs.” Id. His slightly

elevated IgA level in September 2018 could be related to IVIG treatment in July 2018. “Repeated

EMG showed both demyelinating and axonal loss features, but it did not meet the EFNS

electrophysiological criteria of CIDP.” Hospital records show elevated CSF protein in 2013 and

2014, “but he was dx with diabetes before 2013. Therefore, CSF protein elevation could be

partially related to diabetes and IVIG infusions at that time.” He reported wetting himself, which

raised concern of possible myelopathy. Petitioner refused MRIs of the brain and cervical spine to

20

rule out a possible CNS lesion. He refused repeat lumbar puncture and CSF studies and requested

a second opinion with a neuromuscular specialist. Id.

On November 14, 2019, petitioner presented to Dr. Lin, a neurologist, for “unclear

neuropathy diagnosis and DM that presents for second opinion on neuropathy.” Pet. Ex. 107 at 11.

Dr. Lin appears to have taken the history from Dr. Xiong’s records, as it is identical. Petitioner

thought he was seeing a neuromuscular specialist, not another neurologist. Petitioner reported his

weakness had worsened, he was not on any immunomodulating treatment and was not receiving

IVIG, PLEX, or Rituximab, but thought it would be therapeutic. He acknowledged the diagnostic

uncertainty but felt IVIG was beneficial. He claimed it was discontinued due to complications with

his kidney function, which was now back to normal, though his file did not confirm that. Petitioner

reported a willingness to receive IVIG again, even it meant potential complications. Pet. Ex. 7 at

13. Dr. Lin’s examination showed minor decrease in muscle strength, intact reflexes except at the

Achilles, no ankle clonus, decreased sensation to pinprick from around C5 and below bilaterally,

decreased vibration sensation at the thumbs, and absent sensation at B/L hallux. Finger to nose

was without dysmetria or tremor B/L; heel to shin was without dysmetria B/L; rapid alternating

movement was without dysdiadochokinesia B/L; and Romberg test was negative. Pet. Ex. 107 at

15. Dr. Lin’s impression was neuropathy of unclear etiology, possibly with some contribution from

diabetic neuropathy. Petitioner was referred to a neuromuscular disorders clinic and directed to

discuss the possibility of restarting IVIG with them. Id. at 18.

Petitioner received an email thereafter that UC Davis did not have a specialist in CIDP, but

Dr. Belsky could refer him to Stanford or UCSF. Pet. Ex. 107 at 20.

h. 2020

Updated medical records from 2020 and 2021 were filed on November 17, 2021. These

records were not certified, and Petitioner’s Exhibit 112 was printed from the website

“myhealthonline.sutterhealth.org”.

Petitioner was seen by Dr. Carroll on November 18, 2020 for chronic iron

deficiency/anemia. His diagnoses included CIDP, DM, hypertension, and iron deficiency. Pet. Ex.

112 at 1. Dr. Carroll planned to continue with intravenous iron supplementation quarterly and keep

ferritin greater than 100. Petitioner was encouraged to see his neurologist regarding his severe

pain. His diabetes was noted as “suboptimally controlled.” Id. at 2.

i. 2021

Petitioner participated in a video visit with Dr. Lai on March 5, 2021 for an acute flare of

CIDP. Dr. Lai noted petitioner responded to IVIG previously and may need to present to the ER if

things worsen. Pet. Ex. 112 at 4.

On April 17, 2021, petitioner presented to the ER with two days of right lower leg redness

and reported infections in the same leg in the past. Pet. Ex. 112 at 6.74

74

This record appears incomplete.

21

Petitioner presented to Dr. Belsky on April 22, 2021 for a routine examination. He

complained of fatigue, weakness, and joint inflammation and was referred to rheumatology. Pet.

Ex. 112 at 11-12. On examination, he was sitting in a wheelchair in no acute distress. He was noted

as “[a]ble to stand with effort. Slow movements. Give away weakness in all muscles to upper and

lower extremities. Hands and feet all warm and symmetrically edematous.” There was no sign of

cognitive impairment. Id. at 14. Lab results for that date were negative for ANA and CCP antibody

IGG but showed elevated CRP and ESR. Id. at 27, 29, 31, 33. X-rays of his hands and feet showed

inflammation. Id. at 36-39. Dr. Belsky discussed the acute inflammatory changes in petitioner’s

hands and feet with Dr. Knox. Id. at 11.

On May 25, 2021, petitioner presented to rheumatologist Dr. Zohuri, who documented that

petitioner refused to put on a gown for the examination, expressed frustration that this was his third

rheumatologic examination, and wanted IVIG treatment. Pet. Ex. 112 at 43. Dr. Zohuri took a full

history noting there was no clear diagnosis. Id. The review of symptoms for rheumatologic process

was negative and petitioner’s biggest complaint was weakness and sensory loss. Id. at 42. Dr.

Zohuri noted that ANA and Lyme testing were negative, polymyositis was unlikely because he

had global weakness rather than proximal muscle weakness, and he had elevated IgA at one point,

probably due to IVIG treatment at the time. There was no rheumatologic etiology found to explain

his elevated ESR/CRP, but he had elevated inflammatory markers during his “GBS

diagnosis/possible CIDP/demyelinating process ‘flare’”, which was the most plausible reason for

the current elevated markers. His right hip replacement pathology showed all degenerative changes

and nothing inflammatory, supporting a lack of inflammatory arthritis. Dr. Zohuri felt the issue

was largely neurologic and his plan was to “check ANCA [antineutrophil cytoclasmic antibodies]75

and double check with neuro if a muscle biopsy will be high yield.” Pet. Ex. 112 at 43.

Petitioner was admitted to the hospital on June 21, 2021 with generalized weakness,

swelling in the bilateral extremities, joints of the shoulder, and hand, and severe pain. There was

concern for cellulitis and CIDP flare. Empiric antibiotics improved the swelling of his legs, but his

weakness persisted. Neurological consult was ordered. The neurology assessment noted “[i]t is

unclear whether pt has CIDP, and ultimately he will need to see a neuromuscular specialist again

for another opinion since there have been differing opinions among the neuromuscular

[physicians] that he has seen.” His presenting complaints were not consistent with exacerbation of

CIDP. Pet. Ex. 112 at 142-43. Neurology felt it was inflammatory arthropathy rather than a CIDP

flare and did not think IVIG would help though petitioner requested it. Prednisone was started and

his swelling and pain improved within a few days, but petitioner advised that he benefits more

from IVIG than prednisone long term. Id. at 166. He was encouraged to follow up with a

neuromuscular specialist for this issue. Id. at 167. His diabetes was poorly controlled during his

hospitalization. Id. at 154. He was discharged on June 24, 2021. Id. at 170.76

On October 4, 2021, petitioner presented to Dr. Shaoulian at the Neurology Muscular

Dystrophy and Neuropathy Institute with an eight-year history of CIDP initially diagnosed as GBS

75

Antineutrophil cytoclasmic antibody (“ANCA”) is a blood test used to assist in the diagnosis of Wegener

granulomatosis, a regional systemic vasculitis in which the small arteries of the kidneys, lungs, and upper respiratory

tract are damaged by a granulomatous inflammation. Mosby’s 79.

76

The record routinely documents petitioner’s refusal to have his leg braces brought to the hospital, adhere to a diabetic

diet, or to engage in physical therapy unless he received IVIG. Pet Ex. 112 at 105, 111, 112.

22

and treated with steroids beginning 18 days after a flu vaccine. He was diagnosed with CIDP after

a recurrence 47 days later. He presented with poor balance, a history of falls, use of a cane, walker

and a wheelchair for short and long distances, respectively. Pet. Ex. 111 at 6. The assessment after

examination was weakness in all extremities with loss of vibration sense in the distal lower and

upper extremities and decreased pain sensation in the distal lower extremities. The 2018

EMG/NCS from Cornell was read as generalized sensorimotor polyneuropathy with demyelinating

features. Labs from Sutter in 2017 and 2018 were negative for monoclonal bands and he had

multiple levels of foraminal narrowing. The diagnosis on that date was hyperesthesia; difficulty

walking, not elsewhere classified; and weakness. Id. at 7.

On November 8, 2021, petitioner returned to Dr. Shaoulian for EMG/NCS testing using a

bipolar needle. “Different muscles were tested to reflect different root and nerve distributions. The

EMG was normal.” Pet. Ex. 111 at 1. The conclusion documented “significant delayed F-waves

and decreased CMAP velocities. The study is consistent with demyelinating sensory motor

neuropathy.” Id. at 1. Dr. Shaoulian also conducted an examination on that date, noting weakness

in all extremities, with loss of vibration sense in the distal lower and upper extremities and

decreased pain sensation in the distal lower extremities. Id. at 5. Dr. Shaoulian wrote that the

EMG/NCS “is consistent with a demyelinating sensory motor neuropathy. Based on the patient’s

history, exam and workup he has CIDP.” He ordered IVIG for two months. Id.

C. Testimony of Petitioner Harvard Davis77

Petitioner appeared in a wheelchair at hearing.78 Petitioner earned an undergraduate degree

from Queens College in business management and associate degree from El Paso University in

human resource management. Tr. 5. He was in the marine business for over thirty years as a

mechanic, rigger, installation and set-up mechanic, and a master tech authorized to train people

and bring them into the business. Tr. 6. An average day in the industry includes putting the right

product in the customers’ hands based on their needs, unloading shipments, stacking, counting,

inventorying products, and interacting with customers. Tr. 6-7.

According to petitioner, he worked at a West Marine store until 2007 when he took a job

with Cope McPhetres. From 2010 until the end of 2011, he worked for Goodwill. He was then

unemployed until he returned to West Marine in March of 2012, where he was working at the time

of his vaccination in August of 2013. Tr. 86-87. Later, petitioner stated that Cope McPhetres went

bankrupt in 2008 or 2009 and he was then on unemployment until he was hired by Goodwill

Industries at the beginning of 2010. He was dismissed from employment by Goodwill in 2011 and

rehired by West Marine in 2012. Tr. 123-24. When asked, petitioner agreed that he was dismissed

77

Petitioner did not file an affidavit in support of his 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).

78

During his testimony, Dr. Chaudhry referenced petitioner using a wheelchair at hearing. Tr. 352.

23

from Goodwill in 2010 and was out of work for around 15 months until he was rehired by Marine

West in March of 2012. Tr. 125.79

Petitioner described himself as lively, “on the move”, working, and able to handle his social

life. His health was “perfect” prior to the August 19, 2013 flu vaccine. Tr. 8. He went

wakeboarding, played basketball, snowboarded, did offshore boating, and “just had lots of fun.”

Tr. 10. Petitioner agreed he had a “mini stroke” in 2010, high blood pressure, spinal surgeries after

a motor vehicle accident, and always had some pain, but could put it out of his mind. Tr. 9.

Petitioner acknowledged having diabetes and not monitoring his blood sugar levels but

controlled it by watching his weight and taking Glipizide. 80 Petitioner acknowledged that Dr. Van

sent him to a class to learn to monitor his diabetes, but he did not go due to loss of insurance and

never got the monitoring equipment. Tr. 88-92. Petitioner testified that he did not see a doctor in

2012 because he did not have insurance. Tr. 15-16. Petitioner stated CVS filled all his

prescriptions, but he did not see any physicians during the period he was uninsured. Tr. 15-19; 92.

He stated he received a flu vaccine every year and paid for the 2012 flu vaccine himself. Tr. 20.

Petitioner testified that the severity of his diabetes was due to the steroids needed following

his flu vaccine and it was Dr. Belsky who sent him to the class to learn how to control his diabetes.

“My levels were not that outrageous, Ma’am. And I didn’t have any – I didn’t have any thirst. I

didn’t have any – I had weight gain. I had gained a lot of weight, and that was one of the things

Dr. Van really counseled me about was, Mr. Davis, you need to lose weight.” Petitioner ultimately

agreed that it was Dr. Van in 2011 who told him he needed to go to class to learn to monitor his

diabetes and ordered all the equipment, but he did not go. Tr. 128-29. Petitioner stated his

endocrinologist Dr. McMullen told him in 2017 that the Solu-Medrol treatment drove his numbers

so high he could no longer control his diabetes with pill therapy. Tr. 129-131.

Petitioner stated he provided his medical history to Dr. Hopkins at his first visit on April

24, 2013. He acknowledged that the records note multiple medical problems including poorly

controlled diabetes with neuropathy and “bilateral foot pain from which he limps around.” He

disagreed that he had bilateral foot pain or that he limped around but rather had a heel callous that

caused pain and when he got rid of the callous, he felt great, was back to working, climbing ladders,

going to car shows, playing ball, and exercising on the treadmill. Tr. 10-11, 13-14. Dr. Hopkins

ran a pin over his feet and said he had neuropathy, but he did not know what neuropathy was prior

to this visit. He denied his “feet hurt that much.” Tr. 15, 96, 130-31; Pet. Ex. 9 at 6. According to

petitioner, Dr. Hopkins prescribed Gabapentin but he never filled the prescription or took it. Tr.

11. Petitioner agreed that Dr. Hopkins’s record also documented decreased sensation in his feet,

chronic lower back and hip pain, and arthritis in his back. Tr. 97-98; Pet. Ex. 9 at 7-10.

79

Petitioner could not recall when he stopped working after his August 2013 vaccination, but believed it was in 2015.

Tr. 102.

80

A June 2011 medical record shows petitioner’s diabetes to be uncontrolled with high blood sugar levels. He was

scheduled by his physician to attend a maintenance basics class and was to email blood sugar readings to his then-

PCP, Dr. Van. Petitioner acknowledged the content of the record but stated he did not go to the class because Goodwill

cut off his insurance. Pet. Ex. 4 at 116, 119.

24

Petitioner described the events following his August 19, 2013 flu vaccine. It was Monday,

his day off, and he was doing errands. He stopped at work, was told the vaccine came in and that

the company pays for it, so he got the vaccine. He finished his errands and went home. He was

doing work at home, felt “blah”, started getting stiff, and his shoulder where he got the shot started

to hurt “because the shot was on the top of his arm”. Tr. 20-21. He finished his work and laid on

the couch. He then contacted another employee to switch days off so he could stay home on

Tuesday. He laid on the couch all day Tuesday and went to bed early. He felt good on Wednesday,

went to work, and was able to function “pretty good.” Tr. 21-23.

Petitioner was asked about the history he provided at the ER, which included right leg pain

the day after the vaccination, being unable to work for three days, and worsening symptoms in the

weeks that followed. Petitioner stated that he had symptoms for weeks before he presented to the

emergency room. Tr. 23-27; Pet. Ex. 3 at 8. Petitioner then stated he did not feel well immediately

after the vaccination, but it was “different kind of symptoms” than those he experienced the day

of the car show, September 14. Tr. 27. On that day, when he awoke at 5:00 am, he had difficulty

getting out of bed because the side of his right leg was numb, and he had hip pain. He could not

walk straight or get his leg to do what he wanted it to. Tr. 27-28. His “hands were like flippers”,

he could not grip anything and had difficulty opening his car door and getting into the car. He

drove to the car show palming the steering wheel. Tr. 28-29. When he arrived, someone had to

help him open the car door and get out of the car. Tr. 30. He stated he was confronted by security,

who thought he was intoxicated because he could not walk straight. Security drove him back to

his car and he left the show around 1:30 pm. Tr. 31-32. According to petitioner, he could not

control his body, so he drove home slowly, unable to apply pressure to the gas pedal. Tr. 33.

Petitioner stated he went to work the next day but was unable to get the keys in the door,

kept dropping things, tried to run but couldn’t, couldn’t get up the ladder to get product, couldn’t

pick up coins at the cash register, and could not separate paper money. Tr. 33-36.

Petitioner testified he reported all of this to Dr. Hopkins on September 17, 2013 and has

no idea why these complaints were not in the record. Tr. 36-37. He recalled that Dr. Hopkins knew

he had arthritis in his back and asked what was different about the past few weeks. Petitioner told

him he had gotten his flu vaccine and Dr. Hopkins told him he had Guillain-Barre, a reaction to

the flu shot, and gave him a steroid pack. Tr. 36-38.

Petitioner stated the next fifteen days were “horrible” and he had a hard time functioning.

The steroid pack worked for a day or two but the “symptoms came back like a vengeance.” Tr. 37.

After he finished the steroids, he could not do anything; he could not unload boxes, raise his hands

over his head, or operate the cash register. Tr. 39-40.

Petitioner stated when he awoke on September 29, 2013, he stumbled to the bathroom, was

unable to get up from the toilet, and had to crawl into his bedroom and call his roommate for help

getting to his car. He drove to the hospital and asked someone in the parking lot to get help, and a

man took him into the emergency room in a wheelchair. Tr. 40-42.

Petitioner stated he told Dr. Mahmood that the day after the flu vaccine, he could not lift

himself up and his legs felt weak, but he did not tell him he could not walk. He felt “icky” but not

25

like the “crippling event like it was on the 14th”. Tr. 42-44. Petitioner stated he was referring to

September 14, 2013, when he told Dr. Mahmood about the shoulder pain, tenderness, weakness,

and inability to open the car door or reach overhead. Tr. 45.

When asked again later if he reported generalized aches in his lower extremities the day

after the flu vaccine that worsened in the following days to Dr. Mahmood, he responded that he

was trying to explain that he got a flu shot a few weeks prior and it was a few days after the shot

that he started feeling differently. Tr. 118-19; Pet. Ex. 3 at 26-28. He believed the hospital already

had his history. Tr. 47. When he reported joint pain, he meant his knuckles hurt when he tried to

close his hands, his shoulders hurt when he raised his hands overhead, his hips hurt, his legs were

heavy, and he could not lift them or straighten his knees. These symptoms were, “Overwhelming.

Debilitating. Nonfunctioning. Allowing me not to function or do anything. No strength.” He had

none of these symptoms before the flu vaccine. Tr. 50-51. He had no spinal pain before the

vaccination and did not take pain medication after 2010 or 2011. Tr. 51. Petitioner would only

admit that he took Vicodin and Tramadol for back pain prior to the flu vaccine when confronted

with a record from 2012. Tr. 92-95; Pet. Ex. 8 at 38-39.

Petitioner stated Dr. Mahmood told him he had GBS from the flu vaccine and had to report

it to the CDC. Dr. Mahmood did not tell him that GBS would not explain the muscle tenderness

or soreness. Tr. 42, 47, 99.

According to petitioner, he went home and back to work after five days of IVIG and some

physical therapy. Tr. 48, 51. IVIG was the “miracle drug”; he had his strength back, he could run

and do whatever he wanted. Tr. 52. About a month later, when he tried to help a customer at work,

he could not reach his arms overhead or use the ladder because his right leg was not working

correctly and his “foot just kept dropping.” Tr. 52-54. Over the next week, it accelerated and on

October 29, 2013, he got out of bed, “fell right down on my face,” and “had no legs.” Tr. 54. He

called his neighbor to take him to the hospital. Tr. 55. He told the doctor in the ER about his

symptoms, referencing the incident at the store two days prior when he could not climb a ladder.

Tr. 56-57; Pet. Ex. 3 at 69.

According to petitioner, he saw Dr. Mahmood again who ran several tests and put him on

Solu-Medrol and steroids. The spinal tap came back higher than it should be, but everything else

was normal. Tr. 58-60. Dr. Mahmood said his symptoms were unclear and he may have myopathy

that was steroid responsive. Petitioner “got lost in the science of it”. Tr. 99-100. After the Solu-

Medrol, he felt great again for 30-40 days, but then he went to Dr. Hopkins’s office because he

couldn’t breathe, and they called an ambulance. Tr. 60.

Petitioner stated Dr. Mahmood wanted an MRI of his back, which could not be done

because he had a stimulator implanted in his back since 1995. He did not recall any doctor other

than Dr. Knox saying his symptoms were related to diabetes, but he agreed he “still wasn’t

monitoring” his diabetes at that time. Tr. 61.

Petitioner stated Dr. Seminer, his neurologist, thought he had CIDP and gave him steroids.

Tr 62. He recalled an EMG that showed a little abnormality but was overall normal. IVIG was

26

started. Tr. 62-63; Pet. Ex. 3 at 113.81 When presented with the EMG results and Dr. Seminar’s

record, petitioner agreed Dr. Seminar did not think the study supported GBS or CIDP. Tr. 101;

Pet. Ex. 3 at 106-07.

Petitioner stated he saw Dr. Knox for the first time some time in 2014 when he was taken

by ambulance to the hospital after having trouble breathing. Tr. 65. Dr. Knox said he had CIDP

and did an EMG. He started him on steroids and Toradol, then Benadryl, then IVIG several weeks

later, which gave him bad headaches and he could not function at work. Tr. 66-67, 101.

Petitioner stated Dr. Knox got frustrated that the nerve conduction studies did not show

anything but told him he had CIDP, an autoimmune disease that attacks the nerves. He was giving

him IVIG to help the nerves, but he stopped it due to the headaches. Tr. 67. Petitioner agreed that

Dr. Knox’s records in June and July 2015 state, “possible primary muscle disorder” and that Dr.

Knox wanted a muscle biopsy. Tr. 103-04; Pet. Ex. 20 at 46-47. He further agreed that at his next

visit on October 1, 2015, Dr. Knox wrote “possible myopathy but with numbness places this into

the CIDP or similar; could be myelopathy, but has no spasticity?” Tr. 104; Pet. Ex. 18 at 7.

Petitioner agreed that Dr. Knox was questioning the CIDP diagnosis in 2015, “He was looking for

all types of other findings, and blood tests showed that, too.” Tr. 105.

Petitioner recounted that Dr. Knox took him to a dinner in 2016 with other doctors and

nurses to discuss his case and why his EMGs were normal. There was a slideshow and handouts,

and the discussion used his name. Tr. 68, 71-73; Pet. Ex. 91. The doctors spoke about how the

small nerves could be the problem. Dr. Muley82 told him that the nervous system is like wires;

myelin is insulation that covers the wire if there is a break somewhere and IVIG coats and rebuilds

that. Tr. 69-70. Dr. Muley told him Rituxan may be an option, as it has worked on patients with

CIDP. Tr. 70. He filed the only paperwork he received from the dinner as Pet. Ex. 91. Tr. 71-73.

He never heard anything further after the dinner and did not receive any write up about his case.

Tr. 121-22.

Petitioner stated insurance stopped his IVIG treatment in 2016 but it resumed after an

appeal via email, but he could not find the emails. Tr. 74. Dr. Knox stopped his treatment again in

2017 after an incident at the infusion center requiring hospitalization. Tr. 75.

Petitioner stated Dr. Knox sent him to Dr. Katz in San Francisco for a second opinion. Tr.

77. Dr. Katz did not perform an examination, spent the visit searching for his file and discussing

the photographs on his wall of New York, and said “You look too healthy to have CIDP”. Tr. 77-

79. Petitioner could not explain how Dr. Katz’s record reflected an examination and findings other

than to say “I don’t know. I just remember sitting there talking with him, you know. I’ve had other

exams that I – that were so much more thorough than what he gave me, and just sitting and talking

to me and then not finding my records and talking about a picture on the wall…” Tr. 105.

81

Petitioner was asked if he had any independent recollection of the events he was testifying to and admitted that he

did not but was reading from the records. He was asked to put away his notes.

82

Petitioner recalled this doctor’s name as “Mule”, but the record filed from the event, Pet. Ex. 91, lists Dr. Muley as

the speaker.

27

Petitioner testified to only seeing Dr. Knox once more after his visit with Dr. Katz because

Dr. Knox stopped his treatment, stating his problems were due to his diabetes. Petitioner told Dr.

Knox that he never needed insulin for his diabetes until he was treated with steroids, but he now

needed insulin. Dr. Knox wanted him to have surgery to remove the stimulator and for carpal

tunnel and scheduled it twice. Tr. 79-81. At that point, he lost confidence in Dr. Knox and sought

another opinion from Dr. Latov in New York City. Tr. 79-81, 105-06. Later, petitioner conceded

that he continued to see Dr. Knox in 2017 and until after he saw Dr. Latov in 2018. Tr. 107.

Updated records filed show that Dr. Knox was still listed as petitioner’s physician in 2021. Pet.

Ex. 112 at 11.

Petitioner described Dr. Latov’s examination as an hour and half to two hours long. Dr.

Latov told him he should have been on Rituxan rather than IVIG and ordered EMG testing, which

showed “sensorimotor polyneuropathy, and there was demyelination.” Tr. 82. Dr. Latov told him

he had CIDP or “Poems or something” and a treatment plan needed to be started in California. Tr.

83. Petitioner agreed he had not received IVIG for about eight months at that time. Tr. 84.

Petitioner later agreed that Dr. Latov wrote generalized weakness and sensory loss of unclear cause

after his visit and that he only saw Dr. Latov once. Tr. 107-09; Pet. Ex. 58 at 4. The addendum

written in September of 2018 was not associated with a visit. Tr. 108-09; Pet. Ex. 63. He then

stated he saw Dr. Latov twice, in March and in June, when the EMG was performed, but did not

speak to him after the EMG and never saw him again. Petitioner stated Dr. Latov did not

communicate with Dr. Knox or any other doctor in California about Rituxan; Rituxan was only

discussed between Dr. Latov and petitioner at the March visit. Tr. 109-112. Petitioner was covered

by Medicaid/Medi-Cal at that time. Tr 112-14.

Petitioner stated he saw Dr. Brown at the hospital in July 2018 and then Dr. Xiong at UC

Davis in September and November 2018. Tr. 114. He received physical therapy from October to

December 2018. Tr. 115; Pet. Ex. 63. Petitioner stated he had another EMG in the fall of 2018 and

NeuTrexin83 was suggested. Tr. 115-16; Pet. Ex. 64 at 13; Pet. Ex. 81 at 1. At the time of the

hearing, petitioner was not receiving any treatment for his neurological issues and had not had an

IVIG infusion or IV steroids since July of 2018. Tr. 116-17.

Petitioner denied that he was self-prescribing prednisone or that he was warned to stop

taking it by his doctors as reflected in his records. He claimed he only had a half a bottle from his

visit with Dr. Seminer and only took it between treatments. He had no idea where the information

in the medical record came from. Tr. 125-26.

Petitioner disagreed that his diagnosis of CIDP was uncertain. Tr. 119-120. “What I do

believe is that because my tests are irregular, the EMG, that’s what they’re basing so much of this

on”, but “they’ve continued to say CIDP”. Tr. 120. He agreed that Dr. Latov’s inclusion of other

differential diagnoses, including CIDP, would be the “right thing to possibly do if . . . you’ve only

seen me one time or two times.” Tr. 120.

Petitioner recalled that Dr. Scalapino told him it was unclear whether he had CIDP, CIDP

related to diabetes, or some other peripheral neuropathy. At that time, he had “full blown” diabetes

83

NeuTrexin is a brand name for trimetrexate, which is “a folic acid antagonist structurally related to methotrexate; it

competitively inhibits dihydrofolate reductase . . . administered intravenously as the glucuronate salt.” Dorland’s

28

with blood sugar levels of 600 due to steroids. No one ever discussed the progression of diabetic

neuropathy with him. Tr. 126-27; Pet. Ex. 89 at 94.

D. Petitioner’s Declaration

Following the hearing, petitioner filed a declaration addressing the muscle biopsies that

were ordered. Pet. Ex. 110. Petitioner declared that Dr. Knox’s “records were repetitive. In other

words, he did not recommend a biopsy on several occasions to me. Rather, he discussed it with me

a couple of times, originally, and again, after I explained that I had not obtained one due to lack of

insurance. The record in March 2016, indicated ‘but can wait for now.’” Id. at 2. Petitioner further

declared that neither Dr. Knox nor Dr. Latov ordered or recommended a muscle biopsy after he

had insurance in April 2016. Id. Petitioner listed references in the record where muscle biopsy was

documented but denied that the muscle biopsies were mentioned to him when he saw Dr. Knox

and Dr. Xiong in 2017 and 2018. Id. at 1-2. Petitioner declared he would have done it if he thought

it was vital to his health. Id. at 2.

III. The Experts

A. Petitioner’s Expert, Dr. Lawrence Steinman84

Dr. Steinman is a neurologist at Stanford University. Pet. Ex. 75. He graduated from

Dartmouth College with a degree in physics and attended Harvard Medical School, where he also

completed a fellowship in chemical neurobiology. During his residency at Stanford University

Hospital, he completed a fellowship in chemical immunology. He has been a professor at Stanford

since 1980, with appointments in neurology, neurological sciences, pediatrics, and genetics. Id.

Dr. Steinman is board certified in neurology and has published hundreds of articles on the

immunological aspects of neurologic disease. He is considered an expert on multiple sclerosis

(MS) and holds several patents for therapies used to treat MS. Dr. Steinman’s most updated CV

was filed on February 5, 2019. Pet. Ex. 75.85

84

Dr. Steinman is a brilliant doctor, who is well known to the court and has for many years testified on behalf of

petitioners in the Vaccine Program. He has however in recent years been cautioned about his conduct with the court,

counsel, and witnesses. He is once again cautioned here for digressing from his role as an expert to criticize others

particularly those who questioned the diagnosis of CIDP. Tr. 232, 238, 241. Dr. Steinman made his customary

comments that he was not an advocate for either side but simply presenting the science. Tr. 176, 242-43, 252. However,

many of his digressions were argumentative and adversarial. See D.G. v. Sec’y of Health & Hum. Servs., No. 11-577V,

2019 WL 2511769, at *189 (Fed. Cl. May 24, 2019) (criticizing Dr. Steinman’s behavior toward respondent’s expert

and noting that his conduct made him an advocate), Caredio v. Sec'y of Health & Hum. Servs., No. 17-0079V, 2021

WL 4100294, at *15 n.13 (Fed. Cl. July 30, 2021), review denied, No. 17-79V, 2021 WL 6058835 (Fed. Cl. Dec. 3,

2021) (noting that Dr. Steinman’s “various asides” greatly detracted from his credibility), Sanchez v. Sec'y of Health

& Hum. Servs., No. 11-685V, 2020 WL 5641872 at *15 (Fed. Cl. Aug. 26, 2020), review denied sub nom. Sanchez

by & through Sanchez v. Sec'y of Health & Hum. Servs., 152 Fed. Cl. 782 (2021) (citing several cases in which

“[s]pecial masters have indicated that Dr. Steinman presents as an advocate for the petitioners who retain him.”).

Notably, his demeanor was appropriate and respectful during the continuation of the hearing in the fall of 2019.

29

B. Respondent’s Expert, Dr. Vinay Chaudhry

Dr. Vinay Chaudhry received his Bachelor of Medicine and Bachelor of Surgery degrees

from All India Institute of Medical Sciences. Resp. Ex. B. He is board certified in neurology,

electrodiagnostic medicine, clinical neurophysiology, and neuromuscular medicine. Dr. Chaudhry

has served as a professor of neurology at Johns Hopkins since 2004, where he has chaired the

neurology credentials committee since 2009. He has acted as a consultant for respondent regarding

cases in the Vaccine Program since 1999. Dr. Chaudhry is a member of the editorial board for the

journal Neurologist. Dr. Chaudhry is an expert on electrodiagnostic studies as they relate to

neuromuscular diseases. He has an active clinical practice and is involved in clinical research and

teaching at the Johns Hopkins Hospital in Baltimore, MD. Id.

IV. 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).86 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

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.

86

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

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 Althen prong requires a different showing. Under the first 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

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

31

(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 much but not all the literature submitted by the

parties, the undersigned reviewed and considered all 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 by the factors

for analyzing scientific reliability set forth in Daubert v. Merrell Dow Pharm., Inc., 509 U.S. 579,

594-96 (1991).87 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 (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

87

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

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 support for petitioner’s claim: (1)

petitioner offered a persuasive or reliable medical theory; (2) the theory provided was applicable

in part to the facts of petitioner’s case; and (3) petitioner established a medically acceptable

timeframe in which his symptoms could have begun or developed.

1. Petitioner Has Articulated a Sound and Reliable Medical Theory Causally

Connecting Influenza Vaccine to CIDP.

To satisfy Althen Prong I, petitioner must present a “sound and reliable medical or scientific

explanation” causally connecting the vaccine to his alleged injuries. Knudsen, 35 F.3d at 548.

a. Dr. Steinman’s Opinions

In Dr. Steinman’s opinion, petitioner suffers from CIDP caused by the influenza vaccine

he received on August 19, 2013. He submits that the 2013/2014 influenza vaccine petitioner

received could have triggered an immune cross-reaction to myelin and axons through molecular

mimicry, leading to an immune response to antigens associated with CIDP. Pet. Ex. 25 at 16.

Additionally, he submits that there are highly relevant molecular mimics with Contactin-1 and

Neurofascin in the 2013/2014 flu vaccine component A/Victoria/361/2011. Pet. Ex. 25 at 9, 6.

Dr. Steinman submits that CIDP is the chronic version of GBS, with symmetrical sensory

loss and chronicity – it fluctuates but goes on for a long time. Tr. 142-44; Pet. Ex. 27; Pet. Ex. 28.

GBS is usually the initial diagnosis, but it becomes CIDP after a second episode. GBS “peaks and

then it peters out” with or without remaining deficit, but CIDP continues with fluctuating

33

symptoms. Tr. 144. Steroids commonly used to treat CIDP should not be prescribed for GBS and

may worsen it. Tr. 145; Pet. Ex. 27. Dr. Steinman agreed that Dr. Hopkins prescribed steroids with

good response on September 17, 2013, referring to the use of steroids as an “interesting operational

problem,” because if the first attack was CIDP and not GBS, then prednisone was not a bad idea

in retrospect. “This gets to the whole issue, people can be lumpers or splitters and say that the two

diseases are very different and point to, one is acute and one is chronic, but it has to begin sometime

in some patients. It begins with the first attack.” Tr. 560-61. Dr. Steinman referred to NINDs, a

branch of the NIH related to neurology, stating it “explicitly” states GBS and CIDP are part of the

same disease entity. Tr. 560; Pet. Ex. 27.

1. The first theory involves antiganglioside antibodies through molecular

mimicry.

Dr. Steinman has been studying molecular mimicry for a quarter century. The 2013/2014

influenza vaccine that petitioner received contained H1N1 influenza virus strains that can elicit

antiganglioside antibodies through the mechanism of molecular mimicry, which has been

associated with inflammatory neuropathy and is the same target triggered in both campylobacter

jejuni infection and CIDP. Tr. 164-66, 181-82, 258; Pet. Ex. 25 at 6, 8, 16; Pet. Ex. 42;88 Pet. Ex.

43.89 Gangliosides are sugars and the key structures associated with the pathogenesis of

inflammatory polyneuropathy. The concept of molecular mimicry involves shared structures on a

virus, bacteria, or vaccine that can trigger a cross-reactive response to self: “T cells recognize

foreign antigens when presented by HLA molecules of the immune system. In some people,

especially those who have certain HLA types, a foreign antigen may resemble an antigen produced

by the body. Such molecular mimicry provokes the T cells to attack body tissues that contain the

self-antigens.” Pet. Ex. 25 at 7-8.

Dr. Steinman provided a diagram of molecular mimicry, literature, and a description of the

components of the flu vaccine petitioner received to show how well-received the concept of

molecular mimicry is. Tr. 162-65; Pet. Ex. 25 at 5, 8; Pet. Ex. 34;90 Pet. Ex. 77;91 Pet. Ex. 83;92

Pet. Ex. 84. He relied on several articles, though none addressed CIDP, to lay the groundwork for

his opinion and “exemplify molecular mimicry and the components of the flu vaccine.” Tr. 162-

63; Pet. Ex. 34; Pet. Ex. 77; Pet. Ex. 83. He referenced a 2012 IOM report as recognizing C. jejuni

infection as the exemplification of molecular mimicry and its function. Tr. 164, 167; Pet. Ex. 42.

According to Dr. Steinman, the literature supports his hypothesis in that C. jejuni is often

present in poultry, and influenza vaccines are manufactured in chicken eggs. Therefore,

contamination by C. jejuni of the eggs used to produce the influenza vaccine could induce GBS in

88

C.W. Ang et al., Structure of Campylobacter jejuni Lipopolysaccharides Determines Antiganglioside Specificity

and Clinical Features of Guillian Barre and Miller Fisher Patients, 70 INFECTION AND IMMUNITY 1202 (2002), filed

as “Pet. Ex. 42.”

89

Y. Fukami et al., Anti-GQ1b antibody syndrome: anti-ganglioside complex reactivity determines clinical spectrum,

23 EUROPEAN J. OF NEUROLOGY 320 (2016), filed as “Pet. Ex. 43.”

90

Syed Sohail Ahmed et al., Antibodies to influenza nucleoprotein cross-react with human hypocretin receptor 2,

SCIENCE TRANSLATIONAL MED. (2015), http://stm.sciencemag.org/, filed as “Pet. Ex. 34.”

91

Jennifer M. Martinez-Thompson et al., Composite Ganglioside Antibodies and Immune Treatment Response in

MMN and MADSAM, 57 MUSCLE & NERVE 1000 (2018), filed as “Pet. Ex. 77.”

92

L. Steinman and S. Ahmed, Supplementary Materials (confidential submitted supplementary materials for Ahmed

et al., supra note 90), filed as “Pet. Ex. 83.”

34

susceptible hosts by eliciting antiganglioside antibodies after vaccination. Pet. Ex. 41 at 2.93 The

exact pathogenesis of post-campylobacter neuropathy is unknown, but molecular mimicry

between bacterial glycoconjugates and peripheral nerve gangliosides has been implicated. Cross-

reactive antibodies between C. jejuni lipopolysaccharides and gangliosides have been identified in

GBS and Miller Fisher Syndrome. Antiganglioside antibody reactivity against GM1, GM1b, and

GaINAc-GD1a is associated with pure motor GBS, and anti-GQ1b antibody reactivity has a strong

association with oculomotor symptoms and ataxia. Tr. 167-68; Pet. Ex. 42 at 1; Pet. Ex. 43.

Further, cellular immunity is suspected to be implicated due to findings of macrophages and T

CD4+ lymphocytes in nerve biopsies. The data support the hypothesis of an antigen-driven T cell

attack against nerves, even if the target of the immune response remains unclear. Tr. 167-68; Pet.

Ex. 42 at 1; Pet. Ex. 43; Pet. Ex. 51 at 1.94

Dr. Steinman relied on the Nachamkin95 study to show that mice made antiganglioside

responses, which are associated with CIDP, when the mice were injected with vaccines containing

H1N1. Tr. 167, 576; Pet. Ex. 25; Pet. Ex. 41. Dr. Steinman conceded Nachamkin was published in

2008 and used the 1976/1977, 1991/1992, and 2004/2005 swine flu vaccines to “test the

hypothesis,” not the H1N1 vaccine received here. Tr. 259-260; Pet. Ex. 41. He further agreed the

study concluded that more research was needed regarding influenza vaccine components eliciting

antiganglioside response and the role of these antibodies, if any, in vaccine association with GBS.

Tr. 260-61. He added that follow-up studies have been done, though neither he nor respondent

referenced or provided them. Tr. 261, 309-310. While he submitted that the H1N1 component was

integral to his theory on antigangliosides, he did not know if the H1N1 received by petitioner was

the same as the H1N1 used in Nachamkin, which would affect the results. He was admittedly

unprepared for the question and could not answer it. Tr. 310.

Dr. Steinman referred to the Ang96 study as “an exquisite paper” cited in the 2012 IOM

report as the best paper on molecular mimicry and how C. jejuni causes an immune response to

gangliosides resulting in GBS. Tr. 266; Pet. Ex. 42. He also relied on Fukami,97 which discusses

the nuances of gangliosides. Pet. Ex. 43. Though vaccines were not discussed, Dr. Steinman stated

the articles were submitted to show the complexity of gangliosides as fundamental to inflammatory

neuropathies. Tr. 268. He stated the Wang98 study shows that humans over the age of 60 produce

antiganglioside antibodies after flu vaccine. Tr. 576; Pet. Ex. 95.99

93

Irving Nachamkin et al., Anti-Ganglioside Antibody Induction by Swine (A/NJ/1976/H1N1) and Other Influenza

Vaccines: Insights into Vaccine-Associated Guillain-Barre Syndrome, 198 J. OF INFECTIOUS DISEASES 226 (2008),

filed as “Pet. Ex. 41.”

94

Alexandra Richard et al., Transcriptome Analysis of Peripheral Blood in Chronic Inflammatory Demyelinating

Polyradiculoneuropathy Patients Identifies TNFR1 and TLR Pathways in the IVIg Response, 95 MED. 1 (2016), filed

as “Pet. Ex. 51.”

95

Nachamkin et al., supra note 93.

96

Ang et al., supra note 88.

97

Fukami et al., supra note 89.

98

David J. Wang et al., No evidence of a link between influenza vaccines and Guillain-Barre syndrome-associated

antiganglioside antibodies, 6 INFLUENZA & OTHER RESPIRATORY VIRUSES 159 (2012), filed as “Pet. Ex. 95.”

99

Id.

35

Dr. Steinman discussed a study done at the Mayo Clinic showing subtle differences

between MMN, MADSAM,100 and CIDP, all of which are chronic inflammatory neuropathies and

show antiganglioside antibodies and responsiveness to IVIG. Tr. 168-69; Pet. Ex. 77. See also Pet.

Ex. 76;101 Pet. Ex. 78.102 He added that section 6.2 of the 2013/2014 flu vaccine package insert

contained post-marketing reports of GBS following vaccination and “more dramatically”, section

5.1 contained a warning from Sanofi and the FDA of some kind of association between GBS and

the vaccine. He admitted CIDP was not specifically addressed but stated he did his best to find

peer-reviewed literature to show that the flu vaccine can trigger an inflammatory neuropathy. Tr.

161, 577; Pet. Ex. 84 at 11.

Initially, Dr. Steinman discounted Type 2 diabetes as a cause of CIDP, relying on a case

study of an insulin-dependent patient with Type 2 diabetes and neuropathy who developed CIDP

following campylobacter infection. The campylobacter infection, not the Type 2 diabetes, was

determined to be the cause of the inflammatory demyelinating neuropathy through molecular

mimicry. Pet. Ex. 25; Tr. 155-57; Pet. Ex. 36.

2. Dr. Steinman’s other theory involves Contactin I and Neurofascin.

Dr. Steinman presented another theory that involves “highly relevant molecular mimics

with contactin-1 and neurofascin [are] contained in the flu vaccine component

A/Victoria/362/2011.” Pet. Ex. 25 at 6, 9. Unlike gangliosides, Contactin-1 and Neurofascin are

proteins with amino acid homology that “can cause neuroinflammatory disease with clinical

paralysis, when such a molecular mimic is injected into an experimental animal.” Pet. Ex. 25 at

10; Tr. 170; Pet. Ex. 78. These proteins are located on the peripheral nerve where the electrical

current jumps over the axons present on the myelin sheath. The antibodies directed against

Contactin-1 and Neurofascin are most likely the IgG4 isotype and are associated with aggressive

symptom onset, sensory ataxia, tremor, and poor response to IVIG treatment. Pet. Ex. 45 at 5.103

The reasons that Contactin-1 affects motor neurons are unknown. Tr. 170-71; Pet. Ex. 46 at 5, 8;104

Pet. Ex. 47 at 9.105

Dr. Steinman relied on Devaux106 to show that of 533 CIDP patients studied, 38 or 7 percent

were found to have anti-neurofascin 155 IgG4 antibodies, which was impressive because it is very

rare. Pet. Ex. 43; Pet. Ex. 45 at 5, 8. The group with antibodies and CIDP were younger at onset

and had ataxia, tremors, CNS demyelination, and poor response to IVIG. Tr. 275; Pet. Ex. 43 at 1;

Pet. Ex. 45 at 5, 8; see also Pet. Ex 46 at 1-2.

100

MMN stands for multifocal motor neuropathy; MADSAN stands for multifocal acquired demyelinating sensor and

motor neuropathy. See Pet. Ex. 77 at 1.

101

Juliane Klehmet et al., Analysis of anti-ganglioside antibodies by a line immunoassay in patients with chronic-

inflammatory demyelinating polyneuropathies (CIDP), 56 CLIN. CHEM. LAB. MED. 919 (2018), filed as “Pet. Ex. 76.”

102

Luis Querol et al., Antibodies against peripheral nerve antigens in chronic inflammatory demyelinating

polyradiculoneuropathy, 7 SCI. REP. 1 (2017), filed as “Pet. Ex. 78.”

103

Jérôme J. Devaux et al., Neurofascin-155 IgG4 in chronic inflammatory demyelinating polyneuropathy, 86

NEUROLOGY 800 (2016), filed as “Pet. Ex. 45.”

104

Yumako Miura et al., Contactin I IgG4 associates to chronic inflammatory demyelinating polyneuropathy with

sensory ataxia, 138 BRAIN 1484 (2015), filed as “Pet. Ex. 46.”

105

Constance Manso et al., Contactin-I IgG4 antibodies cause paranode dismantling and conduction defects, 139

BRAIN 1700 (2016), filed as “Pet. Ex. 47.”

106

Devaux et al., supra note 103.

36

Dr. Steinman conducted BLAST searches comparing A/Victoria/361/2011 in the subject

vaccine to Contactin-1 and Neurofascin to identify sequences of homology between the two

proteins and the subject vaccine. Tr. 258, 273. The BLAST search for Neurofascin found 7 out of

9 identical amino acids, while the BLAST search for Contactin-1 found 5 out of 6 identical amino

acids in one area and 5 out of 10 identical amino acids in another. Tr. 172-73. He stated that “[t]his

degree of homology can cause neuroinflammatory disease with clinical paralysis, when such a

molecular mimic is injected into an experimental animal,” citing to studies in his laboratory

showing 5 out of 12 amino acids and 4 out of 11 nonconsecutive amino acids as sufficient to trigger

experimental encephalomyelitis (EAE) in mice. Pet. Ex. 25 at 11-12, 14-15. The results from Dr.

Steinman’s lab studies imply the components of the 2013/2014 influenza vaccine can trigger

inflammatory neuropathy, or in his study, EAE, via an immune response to gangliosides,

Contactin-1, or Neurofascin, each associated with CIDP. Pet. Ex. 25 at 15; Pet. Ex. 74 at 1, supp.

ref. 2,107 supp. ref. 3.108

He agreed that the mouse studies showing that 5 out of 12 identical amino acids were

sufficient to cause paralysis did not study CIDP, but rather whether something in a virus or vaccine

that had homology with something in a protein would cause paralysis in the animal when the

system was “revved up” with an adjuvant. Tr. 172-73, 269-270. However, the finding of 5 out of

12 amino acids needed to cause paralysis was “striking.” He agreed the study used Freund

adjuvant,109 a potent adjuvant, but that was so a million mice did not have to be killed. Tr. 270. Dr.

Steinman stated, “people criticize the study,” but it was peer reviewed, which is a rigorous process

by people who don’t like him, so “you can take or leave it” and “[i]f you don’t like my analogy

with EAE or how much identity you need, if you don’t like the fact that it’s a peer-reviewed

publication, I’m not here to elevate beyond what it is.” Tr. 173-75, 271.

Dr. Steinman disagreed that two proteins could have similar segment homology by random

chance rather than clinical significance. Tr. 272-73.

Dr. Steinman conceded there is no epidemiologic evidence that flu vaccine can cause CIDP

but relies on his service to the Department of Justice in the 1980s and his testimony about whether

the swine flu vaccine triggered GBS, though it is unclear if the swine flu vaccine and GBS is an

adequate surrogate for the 2013/2014 influenza vaccine and GBS/CIDP. Tr. 154-55; Pet. Ex. 25 at

16.

Dr. Steinman remarked that Dr. Chaudhry did not challenge the molecular mimicry theory

other than to say petitioner did not have the antibodies or clinical presentation for anti-Neurofascin

or Contactin-1, which includes sensory ataxia and tremors. Dr. Steinman conceded the literature

he relied on for his theory of Contactin-1 and Neurofascin as a cause of CIDP did not look at post-

vaccination, but the best he could say is it would be the same. Tr. 182.

107

Martinez-Thompson et al., supra note 91.

108

Querol et al., supra note 102.

109

Freund adjuvant is a water-in-oil emulsion incorporating antigen, in aqueous phase into light weight paraffin oil

with the aid of emulsifying agent. “On injection, this mixture…induces strong persistent antibody formation.”

Dorland’s 32.

37

b. Dr. Chaudhry’s opinion

Dr. Chaudhry submits that the concept of H1N1 influenza vaccine eliciting antiganglioside

antibodies is controversial, but more importantly, antiganglioside antibodies have not been

generally associated with CIDP. Resp. Ex. A at 11; Resp. Ex. D at 11. Further, Dr. Chaudhry

disagrees that GBS and CIDP are a continuum of the same disease, adding that Dr. Steinman relied

on a definition of CIDP from the NIH website that is written for laypeople and does not provide

the pathogenesis, which is different for GBS and CIDP as demonstrated by responses to treatment.

However, Dr. Chaudhry deferred to Dr. Steinman’s expertise on molecular mimicry conceding he

may be correct, but today’s science does not support CIDP due to molecular mimicry. Tr. 431-32.

Dr. Chaudhry explained that not all forms of GBS or CIDP are the same and not all have

molecular mimicry. Acute motor axonal neuropathy (“AMAN”) and Miller Fisher variant are the

only forms of GBS associated with molecular mimicry. Tr. 430. CIDP has several forms, but a

“triggering agent has not been found except for in rare cases of CIDP associated with melanoma

in which the tumor cells share carbohydrates, epitopes and Schwann cells.” That is the only

molecular mimicry cause of CIDP known to date. Tr. 430-31, 433; Resp. Ex. A, Tab 2 at 2.110

Dr. Chaudhry commented on several papers submitted by Dr. Steinman discussing MMN,

MADSAM, and CIDP, stating that they are different diseases and only 10 percent have antibodies.

The gangliosides are different kinds of IgM and IgG, and IgM GN1 gangliosides are found in 60

to 70 percent of multifocal motor neuropathy patients, but they have not been noted as pathogenic.

Patients have antibodies to gangliosides in a lot of different conditions, but whether they produce

a response is not known for CIDP and their significance is currently unknown. Tr. 434.

In the Nachamkin111 study, Dr. Chaudhry pointed out that the mice developed antibodies

after receiving double or triple the dose of injection and yet did not become clinically symptomatic

or develop GBS. Yuki, who discovered the molecular mimicry hypothesis for GBS in AMAN

resulting from c. jejuni infection, was approached by the WHO to conduct a study over concern

for vaccine safety. He did not find any of the flu vaccines studied to have ganglioside antibody

response in men or in mice. Further, CIDP is not known to be caused by ganglioside antibodies,

and more importantly, Dr. Chaudhry stated petitioner did not have CIDP, so the hypothesis for

molecular mimicry is irrelevant. Tr. 438-39.

Dr. Chaudhry agreed Contactin-1 and Neurofascin can affect the axon and cause axonal

damage, but each of the only nine patients known to have had Contactin-1 and Neurofascin

antibody-induced CIDP had very abnormal EMGs. Tr. 355-56. The younger patients had sensory

ataxia with tremor, clear EMG findings, and a lack of response to IVIG. Summarily, the literature

addressing Contactin-1 and Neurofascin antibodies reported in CIDP showed objective evidence

of marked demyelination on EMG and a lack of response to IVIG. Tr. 435-36; Resp. Ex. A at 11.

Further, the literature Dr. Steinman relied on for this theory does not discuss CIDP, it discusses

EAE. Resp. Ex. A at 11.

110

Jean-Michel Vallat, Chronic inflammatory demyelinating polyradiculopathy: diagnostic and therapeutic

challenges for a treatable condition, 9 LANCET NEUROL. 402 (2010), filed as “Resp. Ex. A, Tab 2.”

111

Nachamkin et al., supra note 93.

38

Dr. Chaudhry deferred to Dr. Steinman’s knowledge of immunology and the use of BLAST

search similarities and hypotheses. However, there are no Contactin-1 or Neurofascin antibodies

causing CIDP in his own patients with CIDP, and further, CIDP presents differently than the onset

of GBS two to three weeks after infection. He asks all his patients if they had vaccines or an

infection and the CIDP patients do not provide a history of either. Tr. 435-37, 456-58.

Dr. Chaudhry agreed there were issues years ago with GBS following the swine flu

vaccine, but he has only seen one or two patients with GBS after flu vaccine in the past 30 years.

The cause and effect are still up in the air, but he accepts GBS after flu vaccine as a table injury.

Tr. 459-460. However, the same cannot be said for CIDP, as there is no data to support vaccines

causing CIDP. Tr. 460-62.

c. Analysis of Prong I

Dr. Steinman opined that CIDP is the chronic form of GBS, and petitioner developed GBS

and/or CIDP from the flu vaccine. Pet. Ex. 25; Pet. Ex. 74. His theories include molecular mimicry

involving antigangliosides and highly relevant molecular mimics with Contactin-1 and

Neurofascin that existed in the 2013/2014 flu vaccine component A/Victoria/361/2011, with

several homologies “that can cause neuroinflammatory disease with clinical paralysis, when such

a molecular mimic is injected into an experimental animal.” Pet. Ex. 25 at 6, 9, 10. He concluded

that components of the 2013/2014 influenza vaccine can trigger inflammatory neuropathy via an

immune response to gangliosides, Contactin-1, or Neurofascin, as each antigen is associated with

CIDP. Id. at 15.

Dr. Chaudhry did not disagree with the theory of molecular mimicry per se, deferring to

Dr. Steinman’s expertise, but he remarked that Contactin-1 and Neurofascin is very rare and has

only been detected in nine patients with CIDP who had distinct symptoms that do not exist in this

case. He disagreed that CIDP is the chronic form of GBS because the two diseases have different

pathogenesis and treatment, and he disagreed that there is support for molecular mimicry occurring

in CIDP, except with melanoma. Most importantly, he disagreed that GBS or CIDP was the correct

diagnosis in this case.

The experts are credited with having extensive knowledge and experience with these

diseases and spending significant time discussing whether a causal link exists between the flu

vaccine and CIDP via theories of molecular mimicry or Contactin-1 and Neurofascin. Prior cases

in the program have addressed whether GBS and CIDP are distinct diseases or a continuum of the

same disease, referring to the two as “related” peripheral neuropathies with a number of

overlapping symptoms that “may” share a common pathogenesis. See Strong v. Sec’y of Health &

Human Servs., No. 15-1108V, 2018 WL 1125666 (Fed. Cl. Spec. Mstr. Jan. 12, 2018) (referencing

the “large and persuasive” body of evidence reliably connecting flu vaccine and GBS and noting

the common symptoms and pathogenesis of CIDP and GBS); Daily v. Sec’y of Health & Human

Servs., 2011 WL 2174535 (Fed. Cl. Spec. Mstr. May 11, 2011) (finding that a theory of CIDP

caused by molecular mimicry is plausible based on the premises that vaccination can cause GBS,

molecular mimicry can cause GBS, and there is a biological basis for similarity between GBS and

CIDP). In that regard, there is agreement that petitioner can satisfy Althen Prong I in a case like

this by relying on the theory of molecular mimicry. This decision therefore does not reach any

39

conclusions about Dr. Steinman’s theory involving Contactin-1 and/or Neurofascin, as there is

nothing in the record to suggest the presence of either Contactin-1 or Neurofascin in petitioner.

Thus, petitioner has established a medical theory causally linking the flu vaccine to GBS and CIDP

by molecular mimicry, satisfying Prong I.

2. Petitioner Has Demonstrated a Logical Sequence of Cause and Effect That the

Receipt of the Influenza Vaccine Triggered an Immune-Mediated Inflammatory

Reaction that Contributed to His Already Compromised Neurological Condition

from Various Comorbidities.

Having already determined Prong I and in order to determine Prong II, petitioner’s

diagnosis must be addressed. As a threshold matter, petitioner must first establish that he actually

suffered the injury alleged in the petition. See Broekelschen v. HHS, 618 F.3d 1339, 1346 (Fed.

Cir. 2010). As the Federal Circuit has made clear, “the statute places the burden on petitioner to

make a showing of at least one defined and recognized injury.” Lombardi v. HHS, 656 F.3d 1343,

1353 (Fed. Cir. 2011) (affirming a special master’s decision to dismiss a petition when the

petitioner could not establish that she had any of the three diagnoses alleged). “The function of a

special master is not to ‘diagnose’ vaccine-related injuries, but instead to determine based on the

record evidence as a whole and the totality of the case, whether it has been shown by a

preponderance of the evidence that a vaccine caused [petitioner’s] injury.” Lombardi, 656 F.3d at

1352-53 (internal citation omitted). Thus, where “the existence and nature of the injury itself is in

dispute, it is the special master’s duty to first determine which injury is best supported” by the

evidence. Id. at 1352 (citing Broekelschen, 618 F.3d at 1345) (emphasis added).

a. Overview of Guilain Barre Syndrome, Chronic Inflammatory Demyelinating

Polyneuropathy, Diabetes Mellitus, and Diabetes Mellitus with Neuropathy

Guillain-Barre Syndrome (“GBS”) is a disorder in which the body’s immune system

starts to destroy the myelin sheath that surrounds the axons of many peripheral nerves or the axons

themselves. Pet. Ex. 27 at 1.112 GBS presents with varying degrees of weakness or tingling

sensations in the legs and ascends symmetrically to the arms and upper body. GBS can affect

anyone at any age and usually occurs a few days or weeks after respiratory or gastrointestinal viral

infection. GBS can also be triggered by surgery, and vaccinations may increase the risk of GBS in

rare instances. Id.113 There are varying degrees of progression of the disease, and it can be life

112

Guillain-Barre Syndrome Fact Sheet, NAT’L INST. OF NEUROLOGICAL DISORDERS AND STROKE,

http://ninds nih.gov (Mar. 30, 2017, 1:07 PM), filed as “Pet. Ex. 27.”

113

In March 2017, GBS was added to the table of vaccine injuries associated with the influenza vaccine, occurring

within 3-42 days following vaccination. - the criteria for a Table GBS injury in the Act’s qualifications and aids to

interpretation (“QAI”), set forth at 42 C.F.R. § 100.3(c)(15). The QAI specify that: GBS is an acute monophasic

peripheral neuropathy that encompasses a spectrum of four clinicopathological subtypes . . . [T]he interval between

the first appearance of symptoms and the nadir of weakness is between 12 hours and 28 days. This is followed in all

subtypes by a clinical plateau with stabilization at the nadir of symptoms, or subsequent improvement without

significant relapse. Treatment related fluctuations in all subtypes of GBS can occur within 9 weeks of GBS symptom

onset and recurrence of symptoms after this time-frame would not be consistent with GBS. 42 C.F.R. §

100.3(c)(15)(i). To “qualify as any subtype of GBS, there must not be a more likely alternative diagnosis for the

weakness.” 42 C.F.R. § 100.3(c)(15)(v). In particular, the “[e]xclusionary criteria for the diagnosis of all subtypes of

GBS include the ultimate diagnosis of any of the [listed] conditions,” and the list is not exhaustive. See 42 C.F.R. §

100.3(c)(15)(vi); see also 42 U.S.C. § 300aa-13(a)(1).

40

threatening. However, most individuals have a good recovery, although some have a certain degree

of weakness. Id. Oral steroids and intravenous methylprednisolone are not beneficial in treating

GBS. Resp. Ex. C, Tab 1 at 8.114

Chronic inflammatory demyelinating polyneuropathy (“CIDP”), sometimes called

chronic relapsing polyneuropathy, is an immune-related, idiopathic, clinically heterogeneous

disorder which causes damage to the myelin sheath of the peripheral nerves. Pet. Ex. 36 at 1 115;

Pet. Ex. 28 at 1.116 It is characterized by progressive weakness and areflexia, with features of

demyelination including prolonged distal and F-wave latencies, reduced conduction velocity,

conduction block and temporal dispersion on electrophysiological testing, and inflammation and

demyelination/remyelination on nerve biopsy. Resp. Ex. A at 9. The diagnostic criteria for CIDP

are sufficiently broad to include all patients who could benefit from immunomodulatory treatment.

Pet. Ex. 68 at 1.117 Typical (sensorimotor, symmetrical, predominantly proximal weakness) and

atypical (predominantly distal weakness, focal presentations, pure sensory, pure motor, and pure

ataxia) variants are accepted to lie within the CIDP spectrum. Pet. Ex. 68 at 1; Pet. Ex. 37 at 1.118

Clinical criteria include motor or sensory dysfunction in more than one limb for more than two

months with hyporeflexia and characteristic CSF and electrodiagnostic test results. Pet. Ex. 38 at

1.119 Some CIDP subtypes exhibit differences in disease progression (relapsing or progressive),

associated clinical features (cranial involvement), concomitant disease (diabetes mellitus), and

paraclinical features (IgG or IgA monoclonal gammopathy) that further broaden the spectrum of

disease. Pet. Ex. 68 at 1.

CIDP can occur at any age and presents with symptoms of tingling or numbness starting in

the toes and fingers, weakness of the arms and legs, loss of deep tendon reflexes, fatigue, and

abnormal sensations. Pet. Ex. 28 at 1. A good response to intravenous immunoglobulin (IVIg) and

plasma exchange suggests a pathogenetic contribution of humoral factors, including

autoantibodies. Pet. Ex. 68 at 2. Some patients with CIDP have a spontaneous recovery, while

many have bouts of symptoms with partial recovery in between relapses. Some individuals are left

with residual numbness or weakness. Id. at 1.

A diagnosis of CIDP is based on clinical features, neurological examination, and

electrodiagnostic criteria including EMG and NCS, which are necessary to confirm the diagnosis.

Laboratory testing, elevated CSF protein levels with a leukocyte count of less than 10 cells/mm,

MRIs of the lumbosacral and cervical nerve roots or brachial or lumbosacral plexuses, nerve

114

Hugh J. Willison et al., Guillain-Barre syndrome, 388 LANCET 717 (2016), filed as “Resp. Ex. C, Tab 1.”

115

Yusuf A. Rajabally et al., Chronic inflammatory demyelinating polyneuropathy after Campylobacter jejuni

infection mimicking vasculitic mononeuritis multiplex in a diabetic, J. PERIPHERAL NERVOUS SYS. 98 (2004), filed as

“Pet. Ex. 36.”

116

Chronic Inflammatory Demyelinating Polyneuropathy (CIDP) Information Page, NAT’L INST. OF NEUROLOGICAL

DISORDERS AND STROKE, http://ninds nih.gov (Mar. 30, 2017, 1:27 PM), filed as “Pet. Ex. 28.”

117

Luis Querol et al., Autoantibodies in chronic inflammatory neuropathies: diagnostic and therapeutic implications,

13 NATURE REVS. NEUROLOGY 533 (2017), filed as “Pet. Ex. 68.”

118

A. Chiò et al., Comorbidity between CIDP and diabetes mellitus: only a matter of chance?, 16 EUROPEAN J. OF

NEUROLOGY 752 (2009), filed as “Pet. Ex. 37.”

119

J.M. Brostoff et al., Post-influenza vaccine chronic inflammatory demyelinating polyneuropathy, 37 AGE AND

AGING 229 (2007), filed as “Pet. Ex. 38.”

41

biopsy, and clinical improvement after immunomodulatory treatment can help rule out other

causes for neuropathy and support the diagnosis. Resp. Ex. A, Tab 5 at 2-3.120

The 2010 European Federation of Neurological Societies/Peripheral Nerve Society

(EFNS/PNS) guidelines are “globally accepted for both clinical and research purposes due to their

high sensitivity and specificity for CIDP.” Resp. Ex. A, Tab 5 at 3. “The EFNS/PNS defines CIDP

as ‘definite,’ ‘probable,’ or ‘possible,’ based on motor distal latency prolongation, reduction of

motor conduction velocity, prolongation or absence of F-waves, motor conduction block, and

distal compounds muscle action potential (CMAP) duration.” Id. Testing of multiple limbs is more

sensitive for atypical CIDP. Id.

Both GBS and CIDP are considered immune-mediated polyneuropathies associated with a

variable clinical course and outcome. “GBS patients usually reach their maximum disability within

4 weeks of onset compared to at least 2 months for CIDP.” Pet. Ex. 39 at 1.121 A June 2008 study

by questionnaire conducted on 461 members of the Dutch society of neuromuscular disorders with

GBS and CIDP focused on four areas: preceding vaccinations within 8 weeks of onset of GBS or

CIDP, family members with GBS or CIDP, occurrence of common auto-immune disease, and

persistent symptoms at a variable time point after the diagnosis. Id. at 3. Of the 323 questionnaires

returned, 23 GBS and 8 CIDP patients reported onset within 8 weeks of vaccination, most often

the flu vaccination. None of the 106 GBS patients reported recurrence after subsequent flu vaccine.

Of 24 patients with CIDP after the flu vaccine, 5 reported an increase in symptoms after one or

more vaccinations. Id. There were two patients with both GBS and CIDP. “Although the

combination of having both GBS and CIDP could be by chance, these patients support the

hypothesis that GBS and CIDP may constitute a clinical continuum or that there are common host

factors which influence susceptibility to these disorders.” Id. at 4. The study showed that

subsequent flu vaccination was safe for those who had suffered GBS or CIDP following

vaccination, but a host of biases associated with the study by questionnaire were noted. Id. at 5-6.

Petitioner submitted a case study of a 74-year-old who developed progressive right-sided

paresthesia and weakness with dysarthria, ascending weakness of upper and lower limbs, and

exertional dyspnea two days after receipt of a flu vaccine. He had a prior history of coronary artery

bypass grafting, gout, and chronic renal impairment. Pet. Ex. 38 at 1. At this time, CIDP after flu

vaccine had not been previously reported. Onset was rapid compared to the latent period of

approximately two weeks between vaccine and GBS, and the initial presentation was unusual, with

facial numbness, dysarthria with prominent symptoms of dyspnea, and unresponsiveness after the

second immunoglobulin course. Pet. Ex. 38 at 1-2. The study noted:

Viruses and viral vaccines have been proposed as putative triggers in the pathogenesis of

autoimmune disease with postulated mechanisms including antigen mimicry, triggering

self-reactive T-cell clones, and cytokine upregulation that may induce aberrant MHC class

II expression. Whilst autoimmune neurological sequelae of influenza vaccination have

120

Vera Bril et al., The dilemma of diabetes in chronic inflammatory demyelinating polyneuropathy, 30 J. DIABETES

COMPLICATIONS 1401 (2016), filed as “Resp. Ex. A, Tab 5.”

121

Krista Kuitwaard et al., Recurrences, vaccinations and long-term symptoms in GBS and CIDP, 14 J. PERIPHERAL

NERVOUS SYS. 310 (2009), filed as “Pet. Ex. 39.”

42

been described, the development of CIDP after influenza vaccination has not been

previously reported.

Pet. Ex. 38 at 1. The study reached no conclusions regarding the correlation of the gentleman’s flu

vaccine and onset of atypical CIDP other than to say that “[r]arely, individual patients may develop

certain restricted patterns of autoimmune neurological damage and physicians need to be aware of

novel presentations.” Id. at 2.

Diabetes mellitus (“DM”) affects about 9.3 percent of the general population in the United

States, but 25.9 percent of persons 65 and over. Type 2 DM accounts for more than 90 percent of

the cases and results in insulin resistance. Prevalence of Type 2 DM increases with age, elevated

body mass, and family history. Type 2 DM has a gradual onset and early symptoms may go

unnoticed. Resp. Ex. A, Tab 5 at 3. Neuropathy is somewhat common in patients with DM:

“[w]hile it is estimated that 50% of patients with DM have some form of neuropathy, more than

80% of these cases are diabetic peripheral neuropathy (DPN) – a length dependent, sensory more

than motor, axonal neuropathy.” Resp. Ex. A, Tab 5 at 4; Resp. Ex. D, Tab 3 at 7.122 Early diabetic

neuropathy manifests with distal loss of sensation in the feet and/or loss of deep tendon reflexes

in the ankles. The risk of developing diabetic neuropathy increases with duration of DM and

glycemic control. Resp. Ex. A, Tab 5 at 4.

CIDP is reported more frequently in patients with Type 2 DM and diagnosing CIDP in

these patients is more challenging due to superimposed axonal damage that can obscure EMG

findings. Further, DM can also cause elevated protein in CSF, which is part of diagnostic criteria

for CIDP. Resp. Ex. A, Tab 5 at 2, 4; Resp. Ex. D, Tab 3 at 8. According to a health insurance

administration claims database study, the prevalence of CIDP in the non-diabetic population is 6

per 100,000 people, while the prevalence of CIDP in the DM population is 54 per 100,000 people.

In addition to the concomitant axonal damage, the increased prevalence of both CIDP and DM in

the over 50 population also creates controversy in the association of the two. While patients with

CIDP and DM are both responsive to immunological treatment, more definite testing is needed to

distinguish the two conditions. Resp. Ex. A, Tab 5 at 7, 9. However, response to “immunoglobulin

therapy, although non-specific, indicates an immune basis to the neuropathy.” Pet. Ex. 36 at 4.

While the etiology of CIDP is unknown, “more than one-third of cases are associated with

other disorders,” including DM. Pet. Ex. 37 at 1. A 2001 article submitted addressing the

association between CIDP and DM suggested it “seems to be just coincidental”, but later studies

suggest otherwise. Id. at 2. The 2001 article concluded that epidemiological findings do not support

a pathogenetic correlation between DM and CIPD. However, when a patient with DM has

symptoms of peripheral neuropathy, “a thorough EP [electrophysiological] examination is

required to search for signs of demyelination, meeting the diagnostic criteria for CIDP, as some

patients with CIDP may have response to therapy, differently from those with the classic axonal

diabetic neuropathy.” Id. at 3.

In 2004, a study noted, “Recent reports suggest that CIDP could be more frequent in

diabetics.” Pet. Ex. 36 at 1. Superimposed on an axonal polyneuropathy, CIDP probably occurs

122

Gérard Said, Diabetic Neuropathy, in Handbook of Clinical Neurology 579-89 (G. Said & C. Krarup eds., 2013),

filed as “Resp. Ex. D, Tab 3.”

43

more frequently in diabetics, which itself results in various types of neuropathies. Id. Though the

exact incidence of CIDP in diabetics remains uncertain, it is probably much higher than in the

general population. Id. at 5. Only 60-70 percent of sural nerve biopsies in CIDP show typical signs

of demyelination, and though rare, diabetic neuropathies can fulfill electrophysiological criteria

for CIDP. Id at 4. The severity of symptoms, marked distal weakness, and imbalance could

represent clinical indicators of CIDP superimposed on a diabetic polyneuropathy, though the

diagnosis remains difficult in practice. Id. at 5.

b. Dr. Steinman’s Opinion

Dr. Steinman adamantly argues that petitioner has CIDP because of the “repeated use of

the word ‘CIDP’ as a diagnosis” throughout the medical records and the administration of “very

expensive medicines” like IVIG, which have serious side effects. Tr. 150. Dr. Steinman reviewed

the record “extensively,” and concluded “a lot” of doctors, specialists, and institutions diagnosed

petitioner with CIDP. Tr. 140-41. He stated petitioner’s treating physicians couched their diagnosis

in terms of “possible or probable CIDP” rather than just “CIDP” because they were not writing an

opinion for th

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