Gelardi v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS Filed: August 11, 2026

************************* PATRICIA HUGHES GELARDI, * personal representative of * PUBLISHED ESTATE OF STEFANO GELARDI, *

*

Petitioner, * No. 18-1396V

* v. * Special Master Nora Beth Dorsey

* SECRETARY OF HEALTH * Dismissal; Influenza (“Flu”) Vaccine; AND HUMAN SERVICES, * Cerebellar Ataxia.

* Respondent. *

* ************************* Maximillian J. Muller, Muller Brazil, LLP, Dresher, PA, for Petitioner.

Sarah Christina Duncan, U.S. Department of Justice, Washington, DC, for Respondent.

DECISION 1

On September 13, 2018, Stefano Gelardi (“Mr. Gelardi”) filed a petition for compensation under the National Vaccine Injury Compensation Program (“Vaccine Act” or “the Program”), 42 U.S.C. § 300aa-10 et seq. (2018). 2 Petitioner alleged Mr. Gelardi suffered from chronic inflammatory demyelinating polyneuropathy (“CIDP”) as a result of an influenza (“flu”) vaccination administered on October 11, 2015. Petition at Preamble (ECF No. 1). Respondent argued against compensation, stating “this case is not appropriate for compensation under the terms of the [Vaccine] Act.” Respondent’s Supplemental Report (“Resp. Supp. Rept.”) at 2 (ECF No. 33).

During this matter’s pendency, on September 6, 2025, Mr. Gelardi passed away 3 and Patricia Hughes Gelardi (“Petitioner”) was appointed as the personal representative of Mr. Gelardi’s estate and the case caption was changed accordingly. Pet. Exs. 208-09; Order dated Nov. 3, 2025 (ECF No. 143). Additionally, Mr. Gelardi’s diagnosis was ultimately determined to be cerebellar ataxia, not CIDP. Joint Pre-Hearing Submission (“Joint Sub.”), filed May 6, 2025, at 1 (ECF No. 116).

After carefully analyzing and weighing the evidence presented in this case in accordance with the applicable legal standards, 4 the undersigned finds that Petitioner has failed to provide preponderant evidence that the flu vaccination caused Mr. Gelardi’s cerebellar ataxia. Thus, Petitioner has failed to satisfy her burden of proof under Althen v. Secretary of Health & Human Services, 418 F.3d 1274, 1280 (Fed. Cir. 2005). Accordingly, Petitioner is not entitled to compensation and the petition must be dismissed.

I. ISSUES TO BE DECIDED

The parties stipulate that Mr. Gelardi received the flu vaccine on October 11, 2015 and that his diagnosis was cerebellar ataxia. Joint Sub. at 1.

They dispute the onset of Mr. Gelardi’s cerebellar ataxia. 5 Joint Sub. at 1. Further, the parties dispute whether Petitioner has satisfied all three Althen prongs required to establish entitlement to causation. Id. at 2. More specifically, they dispute “(1) whether the [flu] vaccine can cause cerebellar ataxia; (2) whether [P]etitioner’s cerebellar ataxia was caused by receipt of the [flu] vaccination at issue, and; (3) whether the time between [P]etitioner’s vaccination and the onset of symptoms would be considered ‘medically acceptable to infer causation-in-fact.’” Id. II. BACKGROUND

A. Procedural History Mr. Gelardi filed his petition on September 13, 2018, along with medical records 6 and an affidavit. Petition; Pet. Exs. 1-10. Respondent filed a Rule 4(c) report on May 31, 2019, but was unable to provide Respondent’s position as medical personnel at the Division of Injury Compensation Programs (“DICP”) at the Department of Health and Human Services had not yet reviewed this case. Resp. Rept. at 1 (ECF No. 12). This case was reassigned to the undersigned in October 2019. Notice of Reassignment dated Oct. 3, 2019 (ECF No. 20).

Petitioner filed an expert report from Dr. Maria Fangchun Chen on November 5, 2019. Pet. Ex. 17. Respondent filed an expert report from Dr. Vinay Chaudhry on March 6, 2020. Resp. Ex. A. Thereafter, in May 2020, an amended Rule 4(c) Report, arguing against compensation, was filed by Respondent. Resp. Supp. Rept. at 1-2.

Petitioner filed a supplemental expert report from Dr. Chen in July 2020 and Respondent filed a supplemental expert report from Dr. Chaudhry in September 2020. Pet. Ex. 20; Resp. Ex. C.

The undersigned held a Rule 5 conference on December 3, 2020. Rule 5 Order dated Dec. 3, 2020 (ECF No. 41). Petitioner was directed to obtain expert reports addressing the diagnosis and causation of cerebellar ataxia. Id. at 2. From May 2021 to February 2025, Petitioner filed expert reports from Dr. Chen, Dr. David M. Simpson, and Dr. Omid Akbari and Respondent filed expert reports from Dr. Amanda L. Piquet and Dr. Stephen C. Jameson. Pet. Exs. 24, 34, 67, 93, 141-42, 169, 182; Resp. Exs. D, F-G, I-K.

An entitlement hearing was scheduled for October 2024, but was continued due to various scheduling conflicts. Order Granting Continuance dated Sept. 5, 2024 (ECF No. 104). Thereafter, the parties agreed to submit the case for a ruling on the record. Joint Status Rept., filed Oct. 7, 2024 (ECF No. 105).

Petitioner filed a motion for a ruling on the record on May 8, 2025. Pet. Brief in Support of Entitlement to Damages (“Pet. Br.”), filed May 8, 2025 (ECF No. 129). Respondent filed his response on July 29, 2025, and Petitioner filed a reply on September 29, 2025. Resp. Response to Pet. Motion for Ruling on the Record (“Resp. Response”), filed July 29, 2025 (ECF No. 132); Pet. Reply Br. in Support of Entitlement to Damages (“Pet. Reply Br.”), filed Sept. 29, 2025 (ECF No. 136).

Subsequently, the parties were asked to revisit the possibility of settlement. Order dated Aug. 19, 2025 (ECF No. 133). On December 2, 2025, Respondent indicated he was not amenable to settlement discussions and requested the Court adjudicate entitlement. Resp. Status Rept., filed Dec. 2, 2025 (ECF No. 144).

This matter is now ripe for adjudication.

B. Factual History 7

1. Pre-Vaccination Medical Records Prior to Mr. Gelardi’s flu vaccination on October 11, 2015, his medical history was significant for diabetes, hypercholesterolemia, erectile dysfunction, Prostate-Specific Antigen (“PSA”) elevation, and hearing loss. Pet. Ex. 11 at 3-4, 8; Pet. Ex. 2 at 6-7, 19.

In records from 2014, Mr. Gelardi’s diabetes 8 was noted to be diagnosed in 2011. See, e.g., Pet. Ex. 2 at 6, 9, 11, 14, 17. Petitioner reported his diabetes began “years ago.” See, e.g., id. at 9, 11, 14, 17. On February 17, 2014, his physician, Dr. Richard A. DeLucia, Jr., increased the daily dose of Mr. Gelardi’s diabetes medication, Metformin hydrochloride (“HCL”) (“Metformin”) 9 extended release (“ER”) tablets. Id. at 10.

On April 2, 2014, 18 months prior to the vaccination at issue in this case, Mr. Gelardi’s hemoglobin A1c (“A1c”) 10 was elevated at 6.9 (range < 5.7), he remained on Metformin, and the following month (May 2014) his diabetes was noted to be under “[e]xcellent control.” Pet. Ex. 2 at 11-12. In September 2014, Mr. Gelardi’s A1c was 6.7 and he remained on Metformin. Id. at 14-15. His diabetes was noted to be “[i]mproved, closer to goal.” Id. at 15. Mr. Gelardi received a high-dose flu vaccine on September 17, 2014, with no reported adverse effects. Id. at 16.

On March 25, 2015, Mr. Gelardi’s A1c was noted to have been 7.5 earlier that month (March 4), which was considered “too high.” Pet. Ex. 2 at 17-18. Dr. DeLucia increased his Metformin to 500 mg two tablets per day. Id. at 19.

Mr. Gelardi had a follow-up appointment with Dr. DeLucia on June 24, 2015 for his diabetes and requested a medication change as his fasting blood sugars were elevated, running between 250-300. 11 Pet. Ex. 2 at 21. His A1c earlier that month (June 12) was 9.8. Id. at 22. Dr. DeLucia noted that Mr. Gelardi’s levels were “very high lately with no change in lifestyle.” Id. at 23. Mr. Gelardi’s medication was changed to Pioglitazone HCL-Metformin (“Pioglitazone”) 12 ER tablet 15-1000 mg, two tablets once daily. Id.

On August 7, 2015, two months prior to vaccination, Mr. Gelardi’s A1c was 12.3. Pet. Ex. 2 at 134-35. He saw Dr. DeLucia on August 12 and reported that his fasting blood sugars “were running > 150.” Id. at 27. Overall, Mr. Gelardi’s diabetes was “worsening.” Id. Mr. Gelardi also reported decreased activity and urinary problems. Id. Dr. DeLucia’s assessment included diabetes with “very high [levels] lately with no change in lifestyle,” as well as “[i]nsulin deficient.” Id. at 28. Dr. DeLucia was concerned about “rapid change” and “[e]xtreme increase in uncontrolled sugars with polydipsia/polyuria and fatigue.” Id. Dr. DeLucia referred to Mr. Gelardi to an endocrinologist Aleksandra Kraeher, M.D., for a visit that day due to the need for insulin. Id.

The same day, August 12, Mr. Gelardi saw Dr. Kraeher for a diabetes consultation. Pet. Ex. 19 at 37. Dr. Kraeher noted that in 2014, 13 Mr. Gelardi was diagnosed with type 2 diabetes, which he had treated with metformin and exercise. Id. Mr. Gelardi complained of polyuria, polydipsia, some fatigue, and blood glucose levels of 300 before breakfast and dinner. Id. Lower extremity neurological examination revealed vibratory sensation was decreased in the left foot, lateral aspect. Id. at 38. Dr. Kraeher’s assessment was “diabetes mellitus . . . , type II or unspecified type, . . . worsening [eight] month[s] ago.” Id. She prescribed insulin, specifically Toujeo SoloStar Solution Pen-injector (“Toujeo”), 300 units/mL, 30 units subcutaneous injection every morning, and Pioglitazone, 15-850 MG two tablets per day. Id.

The next day, August 13, 2015, Mr. Gelardi had a follow-up visit with Dr. Kraeher to adjust his insulin; Dr. Kraeher increased his Toujeo to 40 units every morning. Pet. Ex. 19 at 34- 35.

The following week, on August 17, 2015, Mr. Gelardi followed up with Dr. Kraeher. Pet. Ex. 19 at 31. He reported his blood glucose levels were 200-250 before breakfast, 151-160 before lunch, 225-250 before dinner, and 240-250 before bedtime. Id. In addition to the previously prescribed medications, Dr. Kraeher started insulin NovoLog Flexpen Solution Pen- injector (“NovoLog”), 14 100 units/mL on a sliding scale (7-20 units before meals if blood glucose > 200 and at sleep if blood glucose above 200. Id. at 32. Additionally, Dr. Kraeher added Victoza Solution Pen-injector (“Victoza”), 15 18 mg/3 ML, 0.6 mg once daily for one week then 1.2 mg daily. Id.

On September 4, 2015, Mr. Gelardi returned to see Dr. Kraeher and reported persistent polyuria and polydipsia. Pet. Ex. 19 at 28. Blood glucose levels were 150 before breakfast, 200 before lunch, 150 before dinner, and 105-200 before bedtime. Id. Dr. Kraeher decreased Toujeo to 16 units each morning, decreased Pioglitazone to one tablet a day, stopped NovoLog, started Victoza 18 mg/3 mL, 0.6 mg for two days, and started Metformin 500 mg, two tablets every evening. Id. at 29.

Less than month prior to vaccination, on September 21, 2015, Mr. Gelardi’s A1c was elevated at 10.7. Pet. Ex. 19 at 26, 40. On September 25, 2015, Mr. Gelardi returned to Dr. Kraeher with ongoing polyuria and polydipsia. Id. at 24. Blood glucose was 183 fasting. Id. A neurologic examination revealed decreased vibratory sensation in the left foot, lateral aspect. Id. at 26. Dr. Kraeher’s impression was diabetes mellitus; Petitioner was “doing better” but “[V]ictoza dizziness” was noted. Id. Dr. Kraeher adjusted Petitioner’s medication; Toujeo was increased to 26 units every morning, Pioglitazone and Metformin were continued, NovoLog and Victoza were discontinued, and Invokana 16 100 mg tablets once per day was started. Id. at 26- 27.

2. Vaccination and Post-Vaccination Medical Records On October 11, 2015, at 71 years of age, Mr. Gelardi received a seasonal flu vaccination. Pet. Ex. 11 at 3-4, 8.

Mr. Gelardi returned to see Dr. Kraeher on October 23, 2015, still reporting polyuria and polydipsia, with some intermittent lightheadedness. Pet. Ex. 19 at 21. Assessment was “worsening [off] Victoza and more lightheaded, restart Victoza, stop [I]nvokana . . . if continues being lightheaded[,] cardiac eval[uation].” Id. at 22. Dr. Kraeher increased Toujeo to 32 units every morning, continued Pioglitazone, increased NovoLog, and restarted Victoza. Id.

On October 26, 2015, Mr. Gelardi followed up with Dr. Kraeher. Pet. Ex. 19 at 18. He no longer had polyuria or polydipsia, but reported continued intermittent lightheadedness. Id. Assessment noted his diabetes was “better” and Dr. Kraeher again recommended a cardiac evaluation if his lightheadedness continued. Id. at 19. Mr. Gelardi’s medications remained the same except his NovoLog was decreased and Invokana was discontinued. Id.

On November 24, 2015, more than six weeks after vaccination, Mr. Gelardi presented to Dr. DeLucia complaining of dizziness. Pet. Ex. 2 at 30. Dr. DeLucia indicated the cause of the dizziness was unclear, but noted Mr. Gelardi was able to perform his usual daily activities. Id. at 31.

The following day, November 25, 2015, Mr. Gelardi had a diabetes follow-up with Dr. Kraeher. Pet. Ex. 19 at 15. He reported continued intermittent lightheadedness. Id. He had an A1c of 8. Id. Assessment noted “dizziness [was] not due to diabetes.” Id. at 16. Mr. Gelardi’s morning dose of Toujeo was increased to 36 units daily, NovoLog was decreased, Victoza was increased, and other medications were unchanged. Id.

On December 1, 2015, Mr. Gelardi returned to Dr. DeLucia with continuing and worsening dizziness. Pet. Ex. 2 at 32. Dr. DeLucia noted that Mr. Gelardi’s symptoms might be medication related but ordered a magnetic resonance imaging (“MRI”) because of neurological symptoms. Id. at 33. Neurological examination was normal including “cerebellar function.” Id. The brain MRI the following day revealed “mild cortical atrophy;” “periventricular white matter disease which, in this age group, likely represent[ed] . . . small vessel ischemic changes;” and “mild chronic bilateral maxillary sinusitis.” Pet. Ex. 6 at 16 (emphasis omitted).

Mr. Gelardi returned to see Dr. Kraeher on December 16, 2015 for his diabetes. Pet. Ex. 19 at 12. He again reported continued intermittent lightheadedness. Id. Dr. Kraeher’s assessment was that his diabetes was “worsening bec[ause] [he] stopped [V]ictoza [and] then [T]oujeo.” Id. at 13. He was ordered to continue Toujeo, restart Victoza, increase NovoLog, and continue his other diabetes medications. Id.

On January 5, 2016, Mr. Gelardi’s A1c was 8.6. Pet. Ex. 19 at 9, 40.

On January 6, 2016, Mr. Gelardi presented to neurologist Michelle Dompenciel, M.D., for balance issues and dizziness/vertigo for the previous two months. Pet. Ex. 3 at 1. Dr. Dompenciel noted that Mr. Gelardi’s diabetes was not controlled. Id. On examination, Mr. Gelardi had normal strength in bilateral extremities, no ataxia, 17 and a cautious gait. Id. at 3. Neurological sensory examination showed “[b]lunted to pin-prick, light touch, and vibration . . . in the distal lower extremities.” Id. “Swaying to Romberg” 18 was also noted. Id. Impression was “[d]izziness and giddiness,” “[g]ait instability ? [peripheral neuropathy] related,” “[d]isturbance of skin sensation” to be evaluated further with electromyography (“EMG”), uncontrolled type 2 diabetes, hyperlipidemia, and “[p]ersonality changes per wife” which “correlated with the time that his [diabetes mellitus] has not been controlled.” Id. at 1, 3.

On January 7, 2016, Mr. Gelardi returned for a diabetes check-up. Pet. Ex. 19 at 9. Dr. Kraeher noted that Mr. Gelardi’s nausea was resolved after stopping Victoza. Id. Her assessment was “[t]ype 2 diabetes mellitus without complications . . . worsening off of Victoza bec[ause] of nause[a].” Id. at 10. Medication for diabetes was adjusted by adding Glipizide. Id. The records show that Mr. Gelardi was on Toujeo insulin 42 units every morning. Id.

Mr. Gelardi saw Dr. Kraeher on January 20, 2016 and reported abdominal pain, lightheadedness, and vomiting. Pet. Ex. 19 at 6. Assessment included nausea with vomiting “unspecified” and he was instructed to go to the emergency department (“ED”) if he vomited again. Id. at 7. She noted that “possibly vomiting and vertigo [we]re associated.” Id.

Mr. Gelardi presented to the ED the next day, January 21, with complaints of chronic spinning and dizziness with vomiting beginning three weeks earlier. Pet. Ex. 4 at 117. An abdominal computed tomography (“CT”) showed diverticulosis and mild improvement of a previously identified acute diverticulitis in the hepatic flexure. Id. at 120. Diagnosis was vomiting and diverticulitis, and Mr. Gelardi was discharged with prescriptions for Flagyl and ondansetron. Id. at 118, 120.

On January 26, 2016, Mr. Gelardi saw Nurse Practitioner Amanda Cording in Dr. DeLucia’s office for worsening dizziness as well as vomiting and two falls the previous day. Pet. Ex. 2 at 35. He further reported that he had not taken the antibiotics prescribed at the ED. Id.

The following day, January 27, 2016, Mr. Gelardi saw ears, nose, and throat (“ENT”) physician John Li, M.D., regarding dizziness for the past three months. Pet. Ex. 5 at 23. History of past illness indicated the “dizziness developed gradually.” Id. End-gaze nystagmus of the right and left eyes was observed on examination. Id. at 24. Regarding dizziness, Dr. Li stated that “[b]ased upon the patient’s history and cognitive symptoms[,] I have concerns about a central issue.” Id. Dr. Li also noted that there “may be a component of positional vertigo and an inner ear dysfunction.” Id.

Mr. Gelardi followed up with neurologist Dr. Dompenciel on January 28, 2016. Pet. Ex. 3 at 9. Dr. Dompenciel reviewed the head CT and noted there was “no evidence of acute intracranial abnormality.” Id. at 10 (emphasis omitted). Impression included “[d]izziness and giddiness/[v]ertigo,” “[g]ait instability ? [peripheral neuropathy] related,” “[d]isturbance of skin sensation – evaluated further with EMG,” “[h]yperlipidemia,” “[p]ersonality changes per wife,” and “[c]ortical atrophy/[p]eriventricular white matter disease small vessel.” Id. at 11. Dr. Dompenciel prescribed aspirin, Klonopin for vertigo, and Antivert for nausea and vertigo. Id. at 12.

On February 2, 2016, a second brain MRI was done which showed mild-to-moderate cerebral atrophy; mild chronic white matter microangiopathy; and no acute ischemia, hemorrhage, or mass. Pet. Ex. 6 at 13. Mr. Gelardi also had unremarkable magnetic resonance angiography (“MRA”) of the brain and intracranial circulation (circle of Willis). Id. at 14.

On February 10, 2016, Mr. Gelardi had MR angiography of the carotid arteries, which was abnormal and revealed focal high-grade stenosis of the proximal left internal carotid artery, at least 50% to 60% stenosis at the origin and left internal carotid artery, and focal 50% to 70% stenosis at the origin of the right subclavian artery. Pet. Ex. 6 at 11-12. 19

A February 15, 2016 EMG/nerve conduction study (“NCS”) revealed mild motor demyelinating peripheral neuropathy without conduction block and no signs of sensory nerve involvement or radiculopathy. Pet. Ex. 3 at 7-8.

On February 18, 2016, Mr. Gelardi presented to the ER with complaints of double vision. Pet. Ex. 3 at 16-17. A CT angiography (“CTA”) of Mr. Gelardi’s head and neck showed a left carotid plaque with 70% stenosis, and Mr. Gelardi was admitted for further evaluation and treatment. Id. at 17-18. A vascular surgeon felt that Mr. Gelardi’s left carotid stenosis was asymptomatic and did not require surgical intervention. Id. at 16. Mr. Gelardi’s neurological examination remained stable throughout the admission, and his symptoms were thought to be secondary to ischemic cranial neuropathy in the setting of multiple vascular risks. Pet. Ex. 15 at 7. He was discharged on February 20, 2016, with diagnoses of cranial neuropathy and lightheadedness. Id.

Mr. Gelardi had an extended left common and left internal carotid endarterectomy surgery with extended pericardial patch angioplasty on March 4, 2016. Pet. Ex. 7 at 440. He was discharged the following day. Id.

On March 16, 2016, Mr. Gelardi followed up with Dr. Li for dizziness. Pet. Ex. 5 at 26. An audiology evaluation and testing revealed normal to moderately severe sensorineural hearing loss in both ears. Id. at 21. Dr. Li’s impression was bilateral sensorineural hearing loss, dizziness and giddiness, and benign paroxysmal positional vertigo (“BPPV”). 20 Id. at 27-28. Mr. Gelardi reported he had been improving since his March 4 surgery, and Dr. Li noted that he suspected Mr. Gelardi’s carotid artery was the primary problem. Id. at 28.

On March 25, 2016, an orbital MRI showed intact and symmetric orbits and periorbital contents; no retro-orbital mass; no coronal contrast enhancement; and mild mucosal thickening of the ethmoid air cells and maxillary sinuses. Pet. Ex. 6 at 10.

Mr. Gelardi followed up with Dr. Dompenciel on March 30, 2016 and reported left-sided blurry vision, right leg weakness, dizziness, and poor balance. Pet. Ex. 3 at 24. Mr. Gelardi’s wife reported some behavioral changes, such as acting inappropriately, which Mr. Gelardi denied. Id. Dr. Dompenciel recommended continuation of daily aspirin and a neuropsychological evaluation. Id. at 30.

On April 6, 2016, Mr. Gelardi returned to Dr. Li and reported he was getting better each day and overall his dizziness was improving. Pet. Ex. 5 at 29. Dr. Li performed canalith repositioning maneuvers 21 and instructed Mr. Gelardi to avoid leaning forward past 45 degrees to avoid reflux of particles. Id. at 29-30. Mr. Gelardi had canalith repositioning maneuvers again on April 20, 2016. Id. at 31-32.

Between April 7 and May 20, 2016, Mr. Gelardi attended 14 physical therapy (“PT”) sessions for persistent dizziness, blurry vision, and an unsteady gait. Pet. Ex. 4 at 28-61.

On May 20, 2016, Mr. Gelardi’s A1c was 9.0. Pet. Ex. 3 at 35.

On June 6, 2016, Mr. Gelardi followed up with Dr. Dompenciel and reported significant improvement after PT and vestibular rehabilitation. Pet. Ex. 3 at 34. Dr. Dompenciel recommended continuation of aspirin. Id. at 40.

On August 23, 2016, Mr. Gelardi presented to neurologist Dr. Roy Hamilton at the Penn Memory Center due to dizziness, impaired gait, and memory loss. Pet. Ex. 8 at 4. Mr. Gelardi’s wife reported a history of balance problems over the course of ten days after a trip to Hawaii the previous year, with later development of left eye visual blurring and double vision, which had since resolved. Id. Mr. Gelardi reported having problems with remembering names and he was sometimes confused about future plans. Id. The neurological examination was notable for diminished proprioception and vibration sense in the toes and unsteadiness when standing with the feet together and eyes closed. Id. at 5. Mr. Gelardi could not perform tandem gait without assistance, and his mental status examination was notable for a mild deficit of delayed recall. Id. Dr. Hamilton was not sure whether Mr. Gelardi’s various complaints could be tied to a single diagnosis. Id. He further noted that Mr. Gelardi’s cognitive issues did not rise to a level of interfering with his daily function, so he was best characterized as having amnestic mild cognitive impairment (“MCI”). Id. “[T]here [was] little direct evidence to point to a specific []etiology.” Id. Dr. Hamilton noted that Mr. Gelardi had signs of length-dependent neuropathy, “which could be accounted for by his poorly controlled diabetes, which in turn could explain at least some of his [] issues with balance and gait.” Id.

On September 20, 2016, Mr. Gelardi followed up with Dr. Hamilton, whose impression remained amnestic MCI (immediate recall/encoding). Pet. Ex. 8 at 9-11. Dr. Hamilton noted that the etiology of Mr. Gelardi’s deficits and the relationship between his mild deficits and his complaints of unsteady gait were still unclear. Id. at 11. Dr. Hamilton noted the possibility that Mr. Gelardi’s deficits were indicators of an insipid neurodegenerative condition and recommended a lumbar puncture. Id. Dr. Hamilton also referred Mr. Gelardi to PT for gait issues. Id.

On September 30, 2016, Mr. Gelardi followed up with Dr. Dompenciel and reported continued issues with gait, balance, and dizziness. Pet. Ex. 3 at 44. Mr. Gelardi denied numbness or tingling and reported that when his symptoms began the year before, he had recently returned from Hawaii and wondered whether he got an infection on the trip. Id. Dr. Dompenciel’s impression was dizziness and giddiness/vertigo, “likely peripheral etiology;” gait instability/imbalance “likely multifactorial;” hyperlipidemia/diabetes/hypertension management per PCP, noting uncontrol diabetes; cortical atrophy/periventricular small-vessel white matter disease; mild motor demyelinating peripheral neuropathy without conduction block or signs of sensory nerve involvement; resolved diplopia, “possibly ischemic partial cranial neuropathy;” left internal carotid artery stenosis 70% status-post endarterectomy; and mild cognitive impairment. Id. at 50. Dr. Dompenciel recommended repeating the EMG. Id.

On October 3, 2016, Mr. Gelardi received another flu vaccine. Pet. Ex. 2 at 45. No adverse effects were noted.

EMG done October 11, 2016 of the right upper and lower extremities was similar to the February 15, 2016 study and revealed a “mild motor peripheral neuropathy affecting the lower limb with demyelinating features without motor conduction block.” Pet. Ex. 3 at 55. Unlike the previous EMG, Mr. Gelardi now had mild sensory involvement and a very mild right ulnar sensory neuropathy. Id.

On October 31, 2016, Mr. Gelardi obtained a lumbar puncture, which revealed elevated proteins and glucose in the cerebrospinal fluid (“CSF”). Pet. Ex. 8 at 30-33.

Petitioner followed up with Dr. Dompenciel on November 11, 2026. Pet. Ex. 3 at 56. Mr. Gelardi’s elevated protein and glucose were noted as well as the findings of his recent EMG in October 2016. Id. at 56-57. Labs were ordered and the possibility of intravenous immunoglobulin (“IVIG”) was discussed. Id. at 62.

Notes from a December 22, 2016 phone call between Dr. Dompenciel and Mr. Gelardi and his wife indicated that Mr. Gelardi recent testing was discussed. Pet. Ex. 3 at 71. Dr. Dompenciel diagnosed Mr. Gelardi with CIDP and prescribed five days of IVIG. Id. Mr. Gelardi returned to Dr. Dompenciel on February 2, 2017 and reported he felt much better after IVIG. Id. Mr. Gelardi was to continue IVIG infusions every four weeks. Id. at 80.

On March 16, 2017, Mr. Gelardi followed up with Dr. Dompenciel and reported doing much better with IVIG, but requested an increase in frequency of infusions. Pet. Ex. 3 at 85. IVIG infusions every three weeks was ordered. Id. at 93. On April 7, 2017, Dr. Dompenciel noted that Mr. Gelardi was receiving IVIG every three weeks with mild improvement. Id. at 98. Dr. Dompenciel recommended a repeat neuropsychological evaluation in May 2017. Id. at 107.

A cervical spine MRI was performed on April 20, 2017. Pet. Ex. 6 at 9. The MRI showed mild/minimal degenerative disc changes with central disc herniation/protrusion from C3- 7, a small annular tear slightly impinging the ventral cord at C3-4, foraminal stenosis at C3-4, C5-6, and C6-7, and no spinal cord lesion. Id. 22 That same day, Petitioner also obtained another brain MRI that revealed no significant changes from the February 2016 MRI. Id. at 8.

On April 28, 2017, Mr. Gelardi reported feeling about 70% improved to Dr. Dompenciel during a follow-up visit. Pet. Ex. 3 at 113.

Mr. Gelardi attended eleven PT sessions in May 2017 for gait instability. Pet. Ex. 7 at 251. He had been resistant to walking with an assistive device and was now getting more comfortable using a single trekking pole. Id. On May 24, 2017, Mr. Gelardi returned to Dr. Dompenciel and still felt about 70% improved, but reported fatigue. Pet. Ex. 3 at 127. Dr. Dompenciel recommended testing Mr. Gelardi’s vitamin D level. Id. at 136.

On June 16, 2017, Mr. Gelardi followed up with Dr. Dompenciel and reported 75% improvement. Pet. Ex. 3 at 141. Mr. Gelardi had begun Prozac at the suggestion of his physical therapist but felt that it worsened his dizziness and wanted to try a different medication. Id. Prozac was discontinued, and Lexapro was started. Id. at 150.

On June 22, 2017, Mr. Gelardi’s A1c was 10.0. Pet. Ex. 2 at 104.

On June 26, 2017, Mr. Gelardi returned to Dr. Hamilton for an ongoing cognition evaluation. Pet. Ex. 8. at 13. Dr. Hamilton’s impression remained MCI, and he added that “apparently [Mr. Gelardi] also has CIDP.” Id. at 15. He encouraged Mr. Gelardi to remain physically, intellectually, and socially active. Id.

Throughout the remainder of 2017 and the beginning of 2018, Mr. Gelardi continued to follow up with Dr. Dompenciel. See generally Pet. Ex. 3. On September 7, 2017, Mr. Gelardi reported that he felt stable and improved on IVIG. Id. at 170. On October 25, 2017, Mr. Gelardi again reported feeling stable, but his wife disagreed. Id. at 184. He had no falls and no longer used a walker or cane, but he still stumbled when he walked. Id. His diabetes remained uncontrolled and his hemoglobin A1c went up to 10.4. Id. On November 11, 2017, his A1c was 9.9. Pet. Ex. 2 at 100. On December 1, 2017, Mr. Gelardi reported not feeling well. Pet. Ex. 3 at 199. His wife indicated that his behavior had changed and was inappropriate at times. Id. Dr. Dompenciel noted that Mr. Gelardi needed to control his diabetes. Id. On December 15, 2017, a brain MRI revealed no significant changes since the April 2017 MRI. Pet. Ex. 6 at 6. 23 On January 25, 2018, Mr. Gelardi saw Dr. Dompenciel and reported that he had stopped all his medications because of nausea. Pet. Ex. 3 at 218. His diabetes remained uncontrolled. Id. He was still receiving IVIG every three weeks. Id. at 218, 228.

On February 6, 2018, Mr. Gelardi returned to Dr. DeLucia’s office. Pet. Ex. 2 at 57. GBS with a diagnosis in December 2016 at the Cleveland Clinic was noted under past medical history. Id. at 58. Under treatment, it was further noted that Mr. Gelardi “[s]uspects due to flu vax, declines in future.” Id. at 59. He remained on a number of medications for his diabetes. Id.

On March 2, 2018, Mr. Gelardi saw an ENT for sudden dizziness. Pet. Ex. 5 at 37. On examination, there was no evidence of BPPV, and the doctor suspected that Mr. Gelardi’s symptoms could be multifactorial, “consisting of an inner ear weakness, a possible cardiovascular component[,] and a possible neurological component.” Id. at 38.

On March 7, 2018, Mr. Gelardi began PT for gait instability, functional endurance, and functional strength. Pet. Ex. 7 at 226.

On March 20, 2018, Mr. Gelardi’s A1c was 10.9. Pet. Ex. 2 at 81.

In April 2018, Mr. Gelardi had an abnormal stress test and was taken to the ED for cardiac catheterization. Pet. Ex. 7 at 152. He was found to be in acute renal failure and was admitted for further monitoring. Id. Mr. Gelardi had a stent placed and was discharged to a skilled nursing facility on May 2, 2018. Id. at 1.

At a follow-up appointment with Dr. Dompenciel on June 28, 2018, Mr. Gelardi was still receiving IVIG every three weeks and his diabetes continued to be uncontrolled. Pet. Ex. 10 at 1, 11.

On July 2, 2018, A1c was elevated at 10.2. Pet. Ex. 23 at 15. 24 Mr. Gelardi was admitted to the hospital November 14, 2018 due to reduced urine output in his Foley catheter with blood clots noted three weeks after transurethral resection of the prostate (“TURP”). Pet. Ex. 14 at 11. His Foley catheter was changed in the ED, and he was found to have severe hematuria. Id. He was referred to PT upon his discharge on November 21, 2018 for new-onset decreased strength, functional mobility, and ability to walk and balance. Id. His prior medical history included “GBS [status post] flu shot.” Id. Upon admission to a skilled nursing facility (“SNF”), a new diagnosis of Parkinson’s disease, for which he was taking Carbidopa, was noted. Id. at 26. At discharge in December, he was using a rolling walker and was modified independent with activities of daily living. Id. at 35, 187.

On March 25, 2019, three-and-one-half years after the subject flu vaccination, Mr. Gelardi presented to neurologist Mark Stafford, M.D. Pet. Ex. 16 at 20. Dr. Stafford documented a very comprehensive history of present illness. 25 Id. He noted that Mr. Gelardi received the flu vaccination before leaving to go on vacation in Hawaii. Id. Mr. Gelardi was initially doing well, but towards the end of his vacation, he started becoming nauseated and had an episode of loose stools and bowel incontinence. Id. After his gastrointestinal symptoms abated, he began experiencing dizziness and unsteadiness. Id. Dr. Stafford also noted that Mr. Gelardi had a history of poorly controlled type 2 diabetes. Id. For the past several months, Mr. Gelardi had been using a walker, had developed a mild slurring of his speech, and occasionally had “word searching difficulties.” Id. Dr. Stafford commented that Mr. Gelardi’s demyelinating EMG findings “could be accounted for by his diabetes.” Id. at 24. Dr. Stafford further explained that “[d]iabetics typically have elevated spinal fluid protein and levels of greater than 100 are typically use[d] to help distinguish CIDP from diabetic demyelinating peripheral neuropathy.” Id. Mr. Gelardi’s initial CSF protein was 91. Id.

Dr. Stafford’s neurological examination revealed that Mr. Gelardi had intact vibratory sensation, position sense, and reflexes, but remained mildly to moderately ataxic, “which one would not expect with CIDP related ataxia.” Pet. Ex. 16 at 24. Dr. Stafford’s assessment was “[s]ubacute ataxia with onset in October 2015 that [wa]s of an uncertain mechanism.” Id. Dr. Stafford explained that Mr. Gelardi’s clinical findings suggested the “possibility of a primary cerebellar disorder accounting for his ataxia.” Id. He further noted that the “fairly subacute” onset of symptoms in 2015 “raises the possibility of an autoimmune or paraneoplastic cerebellar disorder.” Id. Dr. Stafford asked Mr. Gelardi to defer IVIG until he had additional testing. Id. at 25.

On April 29, 2019, Mr. Gelardi returned to Dr. Stafford, who had reviewed the results of extensive testing. Pet. Ex. 16 at 14. Mr. Gelardi’s anti-glutamic acid decarboxylase (“GAD”) 65 antibodies, 26 tested on April 1, were markedly elevated at 250 and anti-neuronal antibodies were negative. Id. Dr. Stafford’s assessment remained “[s]ubacute ataxia with onset in October 2015 that is of an uncertain mechanism.” Id. at 18. Dr. Stafford noted that Mr. Gelardi’s positive anti- GAD antibody level might be related to IVIG, as his last IVIG infusion (March 15, 2019) was approximately two weeks prior to testing (April 1, 2019). Id. Dr. Stafford ordered repeat anti- GAD antibody testing now that Mr. Gelardi had been off IVIG for six weeks and a CT scan of his chest, abdomen, and pelvis. Id. Repeat anti-GAD65 antibody testing on May 1, 2019 remained positive at greater than 250 after Mr. Gelardi had been off IVIG for six weeks. Id. at 30.

On July 3, 2019, Mr. Gelardi returned to see Dr. Stafford. Pet. Ex. 16 at 9. Mr. Gelardi’s speech, walking, and leg numbness were unchanged. Id. He reported that his right leg had always been weaker and tended to drag. Id. Dr. Stafford’s assessment was “[s]ubacute ataxia with onset in October 2015 that [was] possibly related to an autoimmune cerebellar ataxia.” Id. at 12. Dr. Stafford added that Mr. Gelardi’s “previous [CSF] protein elevations in the setting of his diabetes were not convincing for CIDP.” Id. Mr. Gelardi had resumed IVIG, 27 and his walking had improved since his last evaluation. Id. Dr. Stafford referred Mr. Gelardi for PT. Id.

On August 19, 2019, Mr. Gelardi saw endocrinologist Dr. Gary M. Pepper for his diabetes. Pet. Ex. 23 at 2. His most recent A1c values were reported as 10.7, 11.2, 10.2, and 10.5. Id. At times when Mr. Gelardi checked his blood glucose, it was running 200-350. Id. Family history was significant for a father with diabetes and mother with lupus. Id. Mr. Gelardi medications included Metformin, Lantus SoloStar (“Lantus”) insulin 70 units at bedtime, NovoLog insulin 26 units three times a day before meals along with a sliding scale. Id. Dr. Pepper’s assessment was Type 2 diabetes with diabetic kidney complication and poor compliance. Id. at 3. Dr. Pepper increased Lantus insulin to 70 units every morning, and continued Metformin and NovoLog. Id.

In January 2020, Dr. Stafford noted that Mr. Gelardi was not interested in trying rituximab 28 for his cerebellar ataxia. Pet. Ex. 62 at 17. Mr. Gelardi was using a walker, and his speech was mildly slurred. Id. His “most bothersome symptom” was urinary incontinence, and he reported not knowing that he was actively urinating. Id. Mr. Gelardi consulted a urologist, and a cystoscopy showed a large nodule at the bladder neck and residual prostate tissue. Pet. Ex. 21 at 30-33. Mr. Gelardi had a repeat TURP with removal of the nodule in July. Id. Mr. Gelardi developed Staphylococcus and yeast urinary tract infections and continued to have frequent urination and incontinence with high post-void residuals that were possibly from irritation due to infection or neurogenic bladder. Id. at 5, 11, 15. These symptoms resolved with Myrbetriq for overactive bladder. Id. at 9. In August 2020, Dr. Stafford noted that Mr. Gelardi’s wife reported he had experienced a “steady decline” after the TURP, and he had been admitted to inpatient rehabilitation. Pet. Ex. 62 at 12. But Mr. Gelardi’s ability to stand and walk had improved significantly since his discharge from the facility several weeks earlier. Id. Mr. Gelardi reported “feeling down.” Id.

In January 2021, Dr. Stafford noted that Mr. Gelardi had short-term memory loss, which was “probably [] still in the category of mild cognitive impairment,” despite his mental status score raising the possibility of early dementia. Pet. Ex. 62 at 10. Dr. Stafford prescribed Aricept, an Alzheimer’s medication. Id.

In August 2021, Mr. Gelardi was hospitalized for leg weakness after not receiving IVIG for several months; he was no longer seeing Dr. Stafford. Pet. Ex. 64 at 88. Mr. Gelardi reported significant improvement after one dose of IVIG (4/5 strength in all extremities) and was discharged to a skilled nursing facility after five days of IVIG. Id. at 126, 130-31; see Pet. Ex. 66. In September 2021, Mr. Gelardi was again hospitalized with progressive lower extremity weakness and received another five-day course of IVIG. Pet. Ex. 64 at 285, 290-93, 297-98.

From October to December 2021, Mr. Gelardi saw a new neurologist three times. Pet. Ex. 63 at 2-13. History taken at the first visit noted that Mr. Gelardi had previously seen Dr. Stafford, and that “elevated CSF proteins as per Dr. Stafford’s notes have been attributed to his [diabetes mellites].” Id. at 10. Mr. Gelardi was noted to have a “presumptive diagnosis of subacute autoimmune [cerebellar] ataxia onset in 10/15” and a “prior [history] of GBS from a flu shot in 2015.” 29 Id. In October, the neurologist diagnosed him with recurrent GBS and Parkinson’s disease, and prescribed a trial of Sinemet. 30 Id. at 12. A repeat EMG/NCS on November 1 showed “moderate symmetric, ongoing axonal sensorimotor polyneuropathy.” Id. at 16. In November, Mr. Gelardi reported improvement on Sinemet and was also prescribed Carbidopa. Id. at 6, 8.

From April 2022 through October 2023, Mr. Gelardi saw another neurologist, Arif Dalvi, M.D., four times, primarily for Parkinsonism. Pet. Ex. 166 at 10-33. At the first encounter, Mr. Gelardi was noted to have GBS with “previous successful IVIG treatment,” CIDP, and “a rapidly declining gait disorder in which he [was] now mostly wheelchair bound.” Id. at 30-31. Dr. Dalvi started Mr. Gelardi on Artane 31 for atypical Parkinsonism and recommended that he continue seeing his other neurologist and resume IVIG for GBS/CIDP. Id. at 32.

Updated records were filed but were not reviewed or discussed by the experts and do not inform the undersigned as to the issues in dispute here, so they are not summarized.

Mr. Gelardi passed away September 6, 2025. Pet. Ex. 208 at 1. Cause of death was chronic kidney disease and type 2 diabetes mellitus. Id. Other significant contributing conditions included atherosclerotic cardiovascular disease and Parkinson’s disease. Id.

C. Expert Reports

1. Petitioner’s Expert, Dr. Maria Fangchun Chen, M.D., Ph.D. 32

a. Background and Qualifications

Dr. Chen is a board-certified neurologist. Pet. Ex. 17 at 1; Pet. Ex. 18A at 1. She received her M.D. and Ph.D. from the University of Pennsylvania School of Medicine, where she also completed her medical internship and neurology residency. Pet. Ex. 18A at 1. Since 2013, she has worked as an assistant professor of clinical neurology at Penn Presbyterian Medical Center. Id. “In [her] medical practice, [she] see[s] over 2000 patients in [her] outpatient clinic at Penn Medicine. [She] also see[s] over 200 inpatients a year at the Penn Presbyterian Hospital of Penn Medicine.” Pet. Ex. 17 at 1. Throughout her career, Dr. Chen “ha[s] seen over 100 patients . . . with some form of demyelinating peripheral neuropathy.” Id. Dr. Chen has published literature regarding the mechanisms that describe how HIV injures the nervous system but has not published anything specific to cerebellar ataxia. Id.; Pet. Ex. 18A at 2.

b. Opinions In her third expert report, Dr. Chen addressed the question of whether Mr. Gelardi had cerebellar ataxia. She explained that in adults, “the predominant cause” of cerebellar ataxia is “paraneoplastic or auto-immune as in GAD65 associated cerebellar ataxia.” Pet. Ex. 24 at 2. In support of her opinion, Dr. Chen cited a paper by Joubert et al., 33 which explained that anti- GAD65 antibodies are a “hallmark of type 1 diabetes” and have also been associated with cerebellar ataxia, mostly affecting women in their 60s. Pet. Ex. 33 at 11. Onset is “insidious or subacute” and tends to progress over time. Id. This condition may occur in those with autoimmune conditions such as type 1 diabetes. Id. The illness has a “poor prognosis.” Id.

i. Althen Prong One

Regarding cerebellar ataxia, Dr. Chen explained that it has been “attributed to infections and vaccinations” in children, most commonly with the varicella vaccination, although cases have been reported after the flu vaccination. Pet. Ex. 24 at 1. Dr. Chen opined that cerebellar ataxia is rare, and like other rare adverse conditions associated with vaccinations, “causation cannot be proven.” Id. Given that cerebellar ataxia occurs following infections like chicken pox (varicella), Dr. Chen suggested that vaccination may trigger an immune response like that which occurs after infection. Id. The proposed mechanism, molecular mimicry, occurs when viral antigens trigger an immune response to similar host self-antigens. Id.

Dr. Chen identified one case report of acute cerebellitis 34 after flu vaccination. Park et al. 35 described a case report of acute cerebellitis that occurred three weeks after a flu vaccination. Pet. Ex. 30 at 1. The patient’s motor and sensory examinations were normal, but he had significant dysmetria 36 and dysdiadochokinesia, 37 particularly in the left upper and lower extremities as well as severe gait ataxia. Id. Imaging studies showed cerebellar asymmetry and hypoperfusion of the right cerebellum. Id. at 1-2. After two months, the patient “completely recovered.” Id. at 2. There is no indication that the patient had GAD65 antibodies. See id. at 1- 2. The authors “were not able to determine the definite etiology” in their case, but noted the temporal association with vaccination. Id. at 3. Because the case report described cerebellitis, the patient returned to baseline at two months, and GAD65 antibodies were not identified, the facts of this case are dissimilar from those here.

Lastly, Dr. Chen noted that “the association [of] anti-GAD antibodies subsequent to vaccination does not appear to be reported in the academic literature.” Pet. Ex. 24 at 1. Regardless, Dr. Chen concluded that “it is plausible that the [flu] vaccination may have caused cerebellar ataxia as an alternative diagnosis to consider for Mr. Gelardi.” Id. at 2.

2. Petitioner’s Expert, Dr. David M. Simpson, M.D. 38

a. Background and Qualifications Dr. Simpson is a Neurology Professor and the Director of the Neuromuscular Division and Clinical Neurophysiology Laboratories at the Icahn School of Medicine at Mount Sinai Hospital, where he has worked as an Attending Neurologist since 1984. Pet. Ex. 34 at 1. After receiving his M.D. from SUNY at Buffalo School of Medicine in 1979, he completed an internal medicine internship at University Hospitals of Cleveland, Case Western Reserve in Ohio, a neurology residency at Cornell University Medical Center in New York, and a clinical neurophysiology fellowship at Massachusetts General Hospital. Pet. Ex. 197 at 1. He is board certified in neurology, with subspecialty certifications in clinical neurophysiology and neuromuscular medicine, and electrodiagnostic medicine. Id. He is a member of various professional societies and has extensively published, presented, and lectured on central and peripheral neurological disorders. Id. at 3, 24-101; Pet. Ex. 34 at 1. Dr. Simpson’s “specialty areas in neurology include neuro-infectious disease, neuromuscular disorders, and clinical use of botulinum toxin.” Pet. Ex. 34 at 1. It does not appear that he has published or lectured on cerebellar ataxia. See Pet. Ex. 197 at 24-101.

b. Opinions Dr. Simpson agreed with Mr. Gelardi’s diagnosis of autoimmune cerebellar ataxia syndrome, “likely caused [due] to anti-GAD65 antibody.” Pet. Ex. 34 at 5. He further opined that “Mr. Geraldi’s cerebellar ataxia syndrome [was] causally related to his [flu] vaccine.” Id.

i. Althen Prong One

Dr. Simpson offered four “[s]pecific potential mechanisms” by which the vaccine’s “antigenic effects result in an abnormal immunologic response,” including molecular mimicry, neurotoxic effect, immune complex formation, and loss of self-tolerance. Pet. Ex. 34 at 5; Pet. Ex. 67 at 7.

Regarding molecular mimicry, Dr. Simpson defined it as a concept that “suggests that epitopes of a virus or vaccine[] results in development of immune antibodies and/or T cells that could cross-react with epitopes on myelin or axonal glycoproteins of nerves, leading to neuronal damage.” Pet. Ex. 34 at 5. He noted that it is an established mechanism for autoimmune conditions, including GBS, especially in the context of Campylobacter jejuni infection. Id. at 6; Pet. Ex. 67 at 7. 39 He explained that cerebellar ataxia has been reported after viral illnesses such as enteroviruses, herpes, HIV, and rabies. Pet. Ex. 34 at 6. Dr. Simpson stated that flu infections have also been associated with cerebellar ataxia syndromes in children and adults, although in adults “parainfectious and paraneoplastic etiologies are more common” causes. Id.

The other three mechanisms offered by Dr. Simpson were also defined. He defined neurotoxic effects as “[a] vaccine virus or vaccine proteins might directly damage the membranes of myelin or axons.” Pet. Ex. 34 at 5. Dr. Simpson did not otherwise discuss this mechanism.

Immune complex formation was defined by Dr. Simpson as “[t]he vaccine elicits an antibody response with resultant production of immune complexes that produce a vasculitis type syndrome.” Pet. Ex. 34 at 5. Dr. Simpson did not discuss this mechanism.

The last mechanism offered by Dr. Simpson was loss of tolerance, which he defined as an “alteration of immunoregulatory mechanisms.” Pet. Ex. 34 at 5. He did not further discuss or explain what he meant by this statement.

Dr. Simpson explained that anti-GAD65 antibody associated cerebellar ataxia is a “well- recognized syndrome” characterized by “a more insidious onset.” Pet. Ex. 34 at 6. He acknowledged that the pathogenesis of this illness is “unclear.” Id. Dr. Simpson stated that “[t]he pathophysiological mechanisms underlying anti-GAD65 antibody associated cerebellar ataxia are unknown.” Id. Although the mechanisms are not known, Dr. Simpson stated that “[i]t has been suggested that the anti-GAD65 antibody may play a direct role in its pathogenesis.” Id. at 7.

Several articles cited by Dr. Simpson discuss cerebellar ataxia and GAD65 antibodies. Honnorat et al. 40 explained that GAD is a nervous system enzyme that converts glutamate to γ- aminobutyric acid (“GABA”). 41 Pet. Ex. 36 at 1. The enzyme is also found in pancreatic cells, where it has been identified as an “essential autoantigen” critical to the development of type 1 (insulin-dependent) diabetes mellitus. Id. Anti-GAD autoantibodies are found in approximately 80% of patients who are newly diagnosed with insulin-dependent diabetes, and these autoantibodies can be detected years before onset of clinical disease. Id. Honnorat et al. identified 14 patients who had cerebellar ataxia and GAD antibodies. Id.

Research by Manto et al. 42 suggested that GAD65 antibodies “are directly involved in the pathogenesis” of cerebellar ataxia and stiff person syndrome. 43 Pet. Ex. 37 at 12. “While the exact function of GAD65 in the synaptic release of GABA remains unclear, [their] data strongly indicate[d] that GAD65 plays a major role in this process.” Id. at 10. Munoz-Lopetegi et al. 44 stated that “[t]he role of GAD65 antibodies in neuroinflammation is debatable and still unknown. An obvious theory would be that antibodies block GAD65, interfering with GABA synthesis and impairing the inhibitory GABAergic [(GABA-related)] circuits. This would result in a hyperexcitability state of the CNS.” Pet. Ex. 38 at 10-11.

Although Dr. Simpson cited the above medical literature, he did not incorporate the suggested theories related to the role of GAD65 antibodies in his proposed theory of vaccine causation. Instead, Dr. Simpson discussed the general theory of molecular mimicry, suggesting it “has been proposed” to trigger cerebellar ataxia. Pet. Ex. 34 at 6. He cited Yonee et al., 45 who described the case of a 12-year-old female who developed acute cerebellar ataxia with acute onset 12 days after receipt of the human papillomavirus (“HPV”) 16/18 adjuvanted vaccine. Pet. Ex. 50 at 1-2. She tested negative for antiganglioside antibodies; she was not tested for GAD antibodies. Id. at 2. The authors noted that molecular mimicry had been proposed as a causal mechanism for acute cerebellar ataxia and that the HPV 16/18 vaccine contained a “major capsid L1 protein” with a sequence similar to human molecules, including neuronal antigens. Id. at 3. They recommended further research to determine the pathological mechanism. Id. The child in Yonee et al. did not receive the flu vaccine. 46 See id. at 1-3. Further, Dr. Simpson has not proposed that the flu vaccine contains the proteins found in the HPV vaccine suggested to have sequence similarity with human molecules.

Dr. Simpson conceded that the question of whether “viral immunization” plays a role “in the pathogenesis” of cerebellar ataxia “is unclear.” Pet. Ex. 34 at 7. He cited Svensson et al., 47 who reported that the H1N1 vaccination campaign in Sweden, along with the H1N1 pandemic, had “subtle effects” on children and young adults who had been diagnosed with insulin- dependent (type 1) diabetes. Pet. Ex. 59 at 9. The study addressed two questions. Id. The first question was whether H1N1 infection or vaccination “triggered [pancreas] islet autoantibodies resulting in an immediate or rapid onset of diabetes.” Id. The data did not provide an answer to this question. Id. The second question was whether H1N1 infection or vaccination accelerated the development of diabetes in children who were islet autoantibody-positive. 48 Id. Due to seasonal variance in GAD antibodies, this question was also difficult to answer. Id. at 9-10. Although the data did not allow for answers to these questions, the authors stated that they could not exclude that vaccination “may have delayed the clinical onset [of insulin-dependent type 1 diabetes] in young high-risk children but induced an earlier diagnosis in others.” Id. at 10. The Svensson et al. study did not address cerebellar ataxia, GAD65 antibodies, or the association of GAD65 antibodies with cerebellar ataxia.

In his third report, Dr. Simpson also discussed the difficulty of detecting rare adverse effects associated with vaccines. Pet. Ex. 141 at 8.

Dr. Simpson also disagreed with Respondent’s expert’s (Dr. Piquet’s) contention that there is a lack of evidence to support causation here. Pet. Ex. 141 at 9. In response, Dr. Simpson again cited to Svensson et al., stating that the authors “inferred that [the H1N1] infection or vaccination triggered islet autoantibodies resulting in an immediate or rapid onset of diabetes. The authors noted that the increase of [GAD antibodies] during vaccination may indicate an accelerated disease process.” Id. (citing Pet. Ex. 59). These findings, however, were relative to diabetes; Svensson et al. did not study cerebellar ataxia. See Pet. Ex. 59. Moreover, the authors’ findings were not expressed to a probable likelihood as they concluded that “it cannot be excluded that the vaccine affected clinical onset of type 1 diabetes.” Id. at 1.

ii. Althen Prongs Two and Three

Dr. Simpson explained that Mr. Gelardi was asymptomatic prior to vaccination, had vacationed in Hawaii and was able to play golf weekly, and developed onset of neurological symptoms (dizziness, poor balance, and subjective weakness) three weeks after vaccination. Pet. Ex. 34 at 7. Ultimately, Mr. Gelardi was diagnosed with cerebellar ataxia syndrome associated with GAD65 antibody. Id. Following treatment, Dr. Simpson opined that Mr. Gelardi improved, supporting the notion that his condition was autoimmune in nature. Id. at 8.

Further, Dr. Simpson opined that onset of Mr. Gelardi’s symptoms began within an appropriate time frame after vaccination, that cerebellar ataxia is associated with GAD65 antibodies, and that medical literature supports a conclusion that his condition was “related to vaccination.” Pet. Ex. 34 at 8. Additionally, Dr. Simpson asserted that there was no alternative cause for Mr. Gelardi’s illness. Id. Dr. Simpson concluded that “beyond a reasonable degree of medical certainly[,] [] it is more likely than not” that the flu vaccination was “causally related” to Mr. Gelardi’s development of cerebellar ataxia syndrome. Id.; Pet. Ex. 67 at 10; Pet. Ex. 141 at 10.

3. Petitioner’s Expert, Dr. Omid Akbari, Ph.D. 49 a. Background and Qualifications

Dr. Akbari is a Professor of Immunology at the University of Southern California, Keck School of Medicine. Pet. Ex. 93 at 2; Pet. Ex. 196 at 2. He received a Ph.D. in cellular and molecular immunology at the National Institute for Medical Research in London, United Kingdom. Pet. Ex. 196 at 1. Thereafter, he completed a postdoctoral fellowship at Stanford University. Id. Dr. Akbari’s research focuses on “analysis of cytokines and inflammation with the focus specifically on dysregulated immune responses” as well as “the role of immune tolerance and how immune cells induce autoimmune and allergic diseases.” Pet. Ex. 93 at 2; see also Pet. Ex. 196 at 6-11. His laboratory research includes multiple studies regarding how a vaccination “can result in an appropriate or dysregulated immune response and inflammation.” Pet. Ex. 93 at 3; see also Pet. Ex. 196 at 6-11. Dr. Akbari serves as an associate editor and reviewer on several journals. Pet. Ex. 93 at 2; Pet. Ex. 196 at 5-6. He has authored or co- authored over 100 publications. Pet. Ex. 196 at 15-33.

b. Opinions

i. Althen Prong One

Dr. Akbari opined that “by a preponderance of scientific evidence, had it not been for the flu vaccination, Mr. Gelardi would not have developed autoimmune cerebellar ataxia[] and neuropathy.” Pet. Ex. 93 at 17. He offered “molecular mimicry[50] as a credible medical theory causally linking the flu vaccination” to Mr. Gelardi’s illness. Id. at 1. He also offered mechanisms “involving inflammasome activation . . . and the suppression of regulatory T cells [(“Tregs”)], particularly in immune-privileged sites like the cerebellum.” Pet. Ex. 182 at 10.

Dr. Akbari provided an overview of autoimmune cerebellar ataxia or “Immune-Mediated Cerebellar Ataxias (IMCAs),” noting the diverse types, including gluten, postinfectious, paraneoplastic (cancer), opsoclonus myoclonus syndrome, primary autoimmune form, and the condition here, anti-GAD antibody ataxia. Pet. Ex. 93 at 6. Several autoantibodies that target cerebellar neurons have been identified in immune-mediated cerebellar ataxias, starting with an autoantibody found in a patient with ovarian cancer, and extending to other types of cancers. Id. at 6-7.

According to Dr. Akbari, the significance of anti-GAD65 antibodies is debated, with some scientists arguing they do not have any pathogenic role and others disagreeing. Pet. Ex. 93 at 7. Mitoma et al. stated that “[a]ccumulating evidence indicates that GAD 65 [antibodies] impair cerebellar GABAergic synapses, leading to clinical manifestations of [cerebellar ataxias].” Pet. Ex. 96 at 2. Recent studies show that GAD65 antibodies “play a pathogenic role” in the development of cerebellar ataxias and that GAD65 antibodies “elicit a decrease in GABA release at cerebellar synapses” as well as functional deficits in cerebellar motor control. Id. at 10. This process is followed by events that lead to cerebellar atrophy. Id.; see also Pet. Ex. 98 at 1 (“These studies provide substantial evidence of the pathogenesis of anti-GAD65 [antibodies] in [cerebellar ataxia].”).

Although he cited literature about GAD65 cerebellar ataxia, Dr. Akbari did not offer a theory specific to this form of cerebellar ataxia. Instead, after providing a brief overview of cerebellar ataxia in general and citing several articles that specifically discuss anti-GAD65 antibodies, Dr. Akbari discussed theories related to cerebellar ataxia generally, not anti-GAD65 antibody cerebellar ataxia.

The first concept discussed by Dr. Akbari related to the role of IL-17 in cerebella ataxia. Pet. Ex. 93 at 7-9; Pet. Ex. 142 at 4-6. He stated that a subset of T helper cells, “Th17 cells secrete interleukin-17 [(‘IL-17’)], a molecule . . . known to induce inflammation” and “involved in the pathogenesis of many autoimmune diseases.” Pet. Ex. 93 at 7. He asserted these conditions include demyelinating illnesses and that studies have shown Th17 cells play a role in causing “a disease with ataxic gait” in animals. Id. at 8. He opined that the flu vaccination increases levels of IL-17 and Th17 cells. Id. The articles 51 cited by Dr. Akbari for the proposition that the flu vaccine increases IL-17 and Th17 cells and that these cells contribute to the pathogenesis of GAD65 antibody cerebellar ataxia do not, however, provide such support.

Zambrano-Zaragoza et al. 52 described Th17 cells in autoimmune diseases, including multiple sclerosis, rheumatoid arthritis, psoriasis, brain glioma, Hashimoto’s thyroiditis, atherosclerosis, type 1 diabetes, spondyloarthropathies, systemic lupus, and others. Pet. Ex. 99 at 4-7. Th17 cells were not generally described as independent inducers of disease.; instead, the authors suggested Th17 cells played a role in the disease process. See id. For example, Th-17 cytokines were found in glioma tissues, “suggesting” they played a role in the development or progression of tumors in brain gliomas. Id. at 4. Cerebellar ataxias were not discussed.

Rodrigues Dos Passos et al. 53 described Th17 pathways in multiple sclerosis and neuromyelitis optica spectrum disorders, noting Th17 cells can pass the blood brain barrier and induce inflammation in the CNS; however, the findings are not specific to cerebellar ataxia. See Pet. Ex. 102. Levraut et al. 54 described IL-17 concentrations in CSF in autoimmune encephalitis patients, specifically those with autoimmune limbic encephalitis, 55 and how the results can be used to assess disease severity for treatment purposes. See Pet. Ex. 104. The authors suggested that CSF Th17 cells play a role in the pathogenesis of this form of encephalitis. Id. at 6. The paper does not address Th17 levels following vaccination.

After citing studies and papers describing IL-17 and Th17 in autoimmune disease processes, Dr. Akbari opined that the flu vaccine increases levels of IL-17 and Th17. Pet. Ex. 93 at 8. Lin et al. 56 reported that “Th17 cells have evolved to mediate protective immunity against a variety of pathogens,” including viral infections. Pet. Ex. 107 at 5. This conclusion is inapposite to Dr. Akbari’s assertion that IL-17 and Th17 cells induced by the flu vaccination induce autoimmune disease.

Next, Dr. Akbari asserted that “many studies demonstrate[] that [the] flu vaccine is capable of causing autoimmune ataxia,” however, he cited only one case report, by Saito and Yanagisawa, from 1989, about a child who developed ataxia eight days after receiving a flu vaccination. Pet. Ex. 93 at 9 (citing Pet. Ex. 54). The child’s symptoms resolved within four months, but she had a recurrence of symptoms 33 months later (not associated with vaccination), after which she had “marked cerebellar atrophy.” Pet. Ex. 54 at 1. The etiology and pathogenesis of the child’s acute cerebellar ataxia were not determined. Id. In his second and fourth expert reports, Dr. Akbari noted a case report of a child with acute cerebellar ataxia following a flu infection, not vaccination. Pet. Ex. 142 at 5; Pet. Ex. 182 at 6. This case report does not appear to be filed.

Moving to molecular mimicry, Dr. Akbari proffered several protein homologies he suggested may be relevant. The first homology is between a protein sequence in hemagglutinin 57 in the flu virus (yvkqstlkl) with protein sequences found in multiple sclerosis patients. Pet. Ex. 93 at 9 (citing Pet. Ex. 115). 58 Based on this paper by Markovic-Plese et al., Dr. Akbari suggested that the flu vaccine given to Mr. Gelardi contained a protein that stimulated and differentiated “established autoreactive T cells” and contributed to the “severity of demyelinating disease.” 59 Pet. Ex. 93 at 9-10. He did not provide literature or any other foundational evidence to suggest that the pathogenesis of GAD65 cerebellar ataxia is like that of multiple sclerosis.

The next protein sequence homology offered by Dr. Akbari was another sequence found in hemagglutinin (fyknli) and a similar sequence in the human myelin sheath (ffkniv). Pet. Ex. 93 at 10. Although not identical, Dr. Akbari explained that the sequences share five amino acids in common which is sufficient to “induce and differentiate autoreactive T cells [] and cause severe injury in animal models.” Id.

Next, Dr. Akbari’s explained that “a single T cell can recognize different peptides in the context of different human leukocyte antigen (HLA) molecules.” 60 Pet. Ex. 93 at 11. He stated, “[i]t is now thought that human autoimmune disease most likely involves cross recognition of foreign and self-peptides being presented in the context of several MHC molecules.” Id.

In offering these examples of molecular mimicry and homology, Dr. Akbari did not reference medical literature or other evidence that identified examples of potential homology between the flu virus or vaccination relevant to anti-GAD65 antibody cerebellar ataxia.

After his discussion of molecular mimicry, Dr. Akbari turned his attention to the subject of Tregs in the “induction and maintenance of peripheral tolerance.” Pet. Ex. 93 at 11. He discussed T effector cells (“Teffs”) and the importance of balance between Tregs and Teffs to maintain immune homeostasis. Id. at 11-12. Dr. Akbari expanded on this topic in his second report, relying on Li et al. 61 Pet. Ex. 142 at 6-10 (citing Pet. Ex. 157). Dr. Akbari concluded that the findings by Li et al. provided insights into the relationship between autoimmunity and exposure to microorganisms, including vaccines, and discussed the role of these T cells in controlling autoimmunity. Id. at 8. Of note, Li et al. did not discuss vaccines.

Dr. Akbari suggested that in some individuals, “such as Mr. Gelardi,” the flu vaccine can stimulate pathogenic Teff cells to induce ataxia due to impaired Tregs. Pet. Ex. 142 at 9. He cited Moise et al., 62 stating they showed “depletion of Tregs in vivo result[s] in increased flu vaccination responses in mice.” Pet. Ex. 142 at 9 (citing Pet. Ex. 158). Further, Dr. Akbari asserted that many groups have shown that after flu vaccination, “Treg-depleted mice . . . exhibit[] a very robust T cell response associated with severe adverse effects.” Id. A review of the study by Moise et al., however, does not stand for the proposition that the flu vaccine induces ataxia due to pathogenic Teffs or impaired Tregs. The purpose of the study was to design a vaccine protective against avian flu H7N9 through immune engineering to “harness preexisting [flu] T cell immunity to increase CD4+ T cells that are needed for protective antibody development.” Pet. Ex. 158 at 2. While very technical, the study does not relate to the flu vaccination that was administered here or cerebellar ataxia.

Another study cited by Dr. Akbari was offered to show that Tregs are “associated with severity and clinical manifestation of cerebellar ataxia.” Pet. Ex. 142 at 10 (citing Pet. Ex. 160). 63 Jiang et al. injected neurotoxin 3-acetylpyridine (“3-AP”) 64 into animals “to induce cerebellar ataxia” so that researchers could assess behavior and motor coordination and the effects on neuronal cells and neurotransmitters. Pet. Ex. 160 at 1. There is no evidence to suggest that flu vaccine at issue here contained the neurotoxin 3-AP.

Lastly, as related to Tregs, Dr. Akbari cited Glatigny et al., 65 a study about experimental autoimmune encephalomyelitis or EAE (used to study multiple sclerosis), and the function of Tregs to mediate the illness and ability to enter the CNS. Pet. Ex. 142 at 10 (citing Pet. Ex. 161). It is not clear how the study relates to the flu vaccine or how the flu vaccine can cause cerebellar ataxia.

The next mechanism offered by Dr. Akbari involves the role of inflammasome and Th17 cells in the “induction of neurodegenerative disease.” Pet. Ex. 93 at 13-14. During this section of his report, he discussed adjuvants, 66 like alum, 67 and toxins. See id. There is no evidence that the flu vaccination at issue here contained an adjuvant, alum, or toxin.

In his second report and fourth reports, Dr. Akbari expanded his discussion of inflammasomes and offered references that discussed these subjects in the absence of adjuvants. Pet. Ex. 142 at 2-3; Pet. Ex. 182 at 7. Dr. Akbari stated that “activation of the inflammasome by flu vaccine can further potentiate development of pathogenic Th17 cells that play an important role in neuropathy and directly correlate to severity of the disease.” Pet. Ex. 142 at 12. It was difficult to ascertain how Dr. Akbari’s additional explanation of inflammasomes was relevant to flu vaccine causation here.

A general discussion of host susceptibility, immune intolerance due to environmental and genetic factors are included in Dr. Akbari’s report, but these discussions do not address how the flu vaccine can cause the type of cerebellar ataxia here. See Pet. Ex. 93 at 14-16. Lastly, Dr. Akbari generally addresses host susceptibility and neuropathy in diabetic patients. Id. at 16-17; Pet. Ex. 142 at 11.

In his third report, Dr. Akbari responds to Respondent’s expert reports by Dr. Piquet and Dr. Jameson. See Pet. Ex. 169. Dr. Akbari again provided a general discussion of inflammasome activation, inflammasome and its effect on Tregs, the balance between Teffs and Tregs, and mitigation of autoimmunity by Tregs. Id. at 2-4; see also Pet. Ex. 182 at 7-9. It is not clear how the references shed light on the question of how the flu vaccine can cause cerebellar ataxia.

Dr. Akbari asserted that Dr. Jameson offered a “myopic assessment of the disease pathogenesis, particularly in relation to the role of Tregs,” and that this “constitute[d] an attempt to mislead the court” and is an “erroneous contention.” Pet. Ex. 169 at 5. Dr. Akbari reiterated his opinion that there are “many studies [that] support the notion that induction of inflammasome along with Th17 polarization occur after administration of [the] [flu] vaccine, and these immune responses are capable of causing demyelination.” Id. at 7.

Further, Dr. Akbari addressed the difficulties in providing proof of vaccine causation, the limitations of using animal models, and the challenges to investigating rare diseases after vaccination. See Pet. Ex. 169 at 8-12.

In several of his reports, Dr. Akbari referenced case reports of flu infections and cerebellitis. See, e.g., Pet. Ex. 182 at 5-6. Hayase and Tobita 68 described a case of cerebellitis after a flu infection, where CSF fluid showed flu B by polymerase chain reaction (“PCR”) testing. Pet. Ex. 185. Sfeir and Najem 69 described a 37-year-old female who was diagnosed with cerebellitis after a flu infection. Pet. Ex. 190 at 1. The patient developed an onset of acute ataxia and slurred speech following a four-day illness of fever, fatigue, headache, cough, vomiting, and reduced oral intake. Id. Testing (nasopharyngeal swab) revealed positive flu A (H1N1) infection. Id. at 2. Treatment with an antiviral resulted in improvement, and the patient recovered within two months. Id. The authors noted that the mechanisms of cerebellitis include direct infection of the CNS or delayed autoimmune demyelination, although in the reported case, the mechanism was likely direct infection. Id. A literature review revealed eight cases of flu cerebellitis, seven following flu-like infections and one after a respiratory illness. Id. Dr. Akbari stated that the study “raise[d] the possibility that components of the [flu] vaccine . . . may play a role in triggering autoimmune responses.” Pet. Ex. 182 at 5. Here, Dr. Akbari uses the word possibility, which is insufficient to establish causation. 70

Dr. Akbari cited a paper from Blackmore et al. 71 showing that autoimmune-prone mice that were given intranasal inoculations of the flu infection could develop an upper respiratory illness that could cause EAE in the mice. Pet. Ex. 191 at 1-2. Dr. Akbari stated that the study “raise[d] the possibility that components of the [flu] vaccine . . . might similarly induce immune mediated responses in susceptible individuals.” Pet. Ex. 182 at 6. Again, Dr. Akbari uses the word possibility. 72

After offering case reports and papers related to flu infection, Dr. Akbari referenced cases of ataxia associated with vaccination. Connolly et al. 73 reported a study of 73 children treated for acute cerebellar ataxia at St. Louis Children’s Hospital over a period of 23 years. Pet. Ex. 183 at 1. Of the 73 children, two cases occurred after vaccination, one for smallpox and one for measles. Id. at 2, 2 tbl. 1. The majority of cases occurred after infectious illnesses, including chickenpox (varicella) or other viral illnesses. Id. at 1-2, 2 tbl.1. The flu virus was not specifically identified. See id. Fifty-three of the 60 children who had follow up information completely recovered, including the two who had received vaccinations. Id. at 3-4, 4 tbl. 3. Antibodies were not studied and brain imaging (when performed) was normal except in one child. Id. at 3.

Other case reports referenced by Dr. Akbari involved other vaccines including HPV, hepatitis B, and varicella. Pet. Ex. 182 at 3-4.

The only flu vaccination case in an adult cited by Dr. Akbari was Park et al., also cited by Dr. Chen, and described acute cerebellitis in a 66-year-old male with onset three weeks after a flu vaccination. Pet. Ex. 30 at 1. Brain CT showed “markedly cerebellar asymmetry, suggesting hypoperfusion in the right cerebellum.” Id. at 1-2. The patient reached a clinical recovery in two months, and his cerebellar asymmetry resolved and was not seen in a repeat CT study four months later. Id. at 2. The authors stated that the “pathogenic mechanisms remain uncertain,” however, they suggested direct infection or autoimmune demyelination processes. Id. Although they were unable to determine the cause in their patient, the authors noted the temporal association was suggestive of vaccine causation. Id. at 3. They further confirmed that their case was the first report of acute cerebellitis occurring after a flu vaccination in an adult. Id.

In citing these case reports, Dr. Akbari acknowledged that “cerebellitis and cerebellar ataxia are distinct conditions,” 74 although he opined that they likely arise from “similar immunological mechanisms.” Pet. Ex. 182 at 10. He did not explain the basis for his opinion. Further, Dr. Akbari did not explain the similarities or differences between cerebellitis and cerebellar ataxia, or provide a basis to extrapolate the mechanisms from one to the other in the context of vaccination.

ii. Althen Prongs Two and Three

In his third expert report, Dr. Akbari responded to Respondent’s expert Dr. Piquet’s opinion related to whether Mr. Gelardi’s diabetes caused his neuropathy (diabetic neuropathy). Pet. Ex. 169 at 13-16. Dr. Akbari described the mechanisms which cause impairment of peripheral nerves in diabetics and opined that nerve function deteriorates over a long period of time due to the prolonged effect of elevated blood sugar on nerves. Id. at 13. In contrast, he explained that ataxia due to autoimmune cerebellar ataxia has a “more rapid onset, [] over days to a few weeks,” and is caused by immune system attack on the cerebellum, the part of the brain that controls coordination and balance. Id. at 14. Additionally, diabetic neuropathy is usually characterized by a “‘stocking and glove’ distribution . . . affecting the feet and hands first and progressing towards the body’s center,” whereas autoimmune cerebellar ataxia is a “lack of coordination of muscle movements” resulting from the immune attack on the brain. Id. Lastly, Dr. Akbari noted that diabetic neuropathy is chronic, but autoimmune cerebellar ataxia is usually acute and may require hospitalization and immunosuppressant therapy. Id. at 14-15. Overall, “even though they may share a few similar symptoms,” there are “pertinent clinical differences.” Id. at 14.

Dr. Akbari reiterated the results of Mr. Gelardi’s MRI, MRA, and EMG/NCS from February 2016. Pet. Ex. 169 at 15. He opined Mr. Gelardi’s February 2016 MRI “was very clear and distinct with symptoms associated with [Type 2 diabetes],” including cerebral atrophy, chronic white matter micro angiopathy, atherosclerosis and/or stenosis of the carotid arteries and subclavian artery. Id. And he emphasized the finding of “demyelinating peripheral neuropathy,” which he argued is linked to Mr. Gelardi’s ataxia and thus, “[i]t is essential to recognize [] all references to demyelinating disease hold relevance to this case.” Id. at 14-15. Dr. Akbari did not expand on this statement or otherwise explain how peripheral neuropathy is related to cerebellar ataxia.

Regarding a temporal association, Dr. Akbari opined that the time frame between vaccination and the development of Mr. Gelardi’s neuropathy was consistent with “what is known about the timing of neuropathy resulting from vaccinations.” Pet. Ex. 93 at 17. This opinion indicates that Dr. Akbari believed that peripheral neuropathy was the presenting symptom or initial manifestation of Mr. Gelardi’s cerebellar ataxia.

In contrast, Dr. Simpson, Petitioner’s expert neurologist, tied onset of Mr. Gelardi’s cerebellar ataxia to complaints of “dizziness, poor balance, and weakness.” Pet. Ex. 34 at 2. Respondent’s expert neurologist Dr. Chaudhry stated that “[g]ait ataxia is the most common clinical presentation.” Resp. Ex. A at 14.

Here, it appears that Dr. Akbari conflates “neuropathy” with “ataxia.” However, neuropathy and ataxia are two different medical terms with distinct definitions. Neuropathy is “a functional disturbance or pathologic change in the peripheral nervous system,” while ataxia involves the CNS and is the “failure of muscular coordination.” Neuropathy, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/dorland/definition?id=33813 (last visited July 20, 2026); Ataxia, Dorland’s Med. Dictionary Online, https://www.dorlandsonline.com/ dorland/definition?id=4630 (last visited July 20, 2026); Pet. Ex. 199 at 1. This distinction is important since the expert neurologists and the medical literature state that cerebellar ataxia does not present with neuropathy, but instead presents with dizziness, poor balance, weakness, and gait ataxia. See, e.g., Pet. Ex. 96 at 1 (“[C]erebellar ataxias [] [are] a group of disorders characterized by motor incoordination and impaired cognitive operations”); Pet. Ex. 199 at 2 (“[Acute cerebellar ataxia] is usually characterized by hypotonia, gait disorders, speech abnormalities, dysmetria, nystagmus[,] and intention tremor.”).

Dr. Akbari reported that there “were 146 cases of ataxia reported after vaccination in the United States from 1990 to 2010,” and “very relevant to this case, the onset of [a]taxia was within [six] weeks after vaccination in 105 cases.” 75 Pet. Ex. 93 at 17. Here, Dr. Akbari references ataxia, not neuropathy. But he does not distinguish ataxia due to other causes from ataxia associated with GAD65 autoimmune cerebellar ataxia. See Pet. Ex. 199 at 1 (“Ataxia can be considered a non-specific sign of various disorder that may involve different levels of the [CNS], resulting in impaired movements, coordination[,] and balance.”).

4. Respondent’s Expert, Dr. Vinay Chaudhry, M.D. 76

a. Background and Qualifications Dr. Chaudhry is board certified in neurology, neuromuscular diseases, electrodiagnostic medicine, and clinical neurophysiology. Resp. Ex. A at 1. He specializes in the field of neuromuscular diseases, including the management of peripheral neuropathies, and electrodiagnostic studies. Id. He received his M.B. and B.S. in India and then completed an internship and various residencies and fellowships from 1980 to 1989. Resp. Ex. B at 1-2. Thereafter, he began teaching neurology courses at Johns Hopkins University School of Medicine. Id. at 3. Dr. Chaudhry has an active clinical practice where he sees over 2,000 patients per year, with most related to peripheral nerve diseases. Resp. Ex. A at 1. He has authored or co-authored over 200 publications. Resp. Ex. B at 3-21. “[He] [is] considered an expert in evaluation and treatment of patients with peripheral neuropathies including . . . [GBS] and [CIDP].” Resp. Ex. A at 1.

b. Opinions Dr. Chaudhry opined that Mr. Gelardi’s diagnosis was cerebellar ataxia associated GAD65 antibodies, 77 “one of the best-characterized cerebellar syndromes” known to be caused by an autoimmune mechanism. Resp. Ex. A at 14. “Cerebellar ataxia accounts for 28% of neurological presentation of patients with GAD antibodies.” Id. (citing Resp. Ex. A, Tab 16; 78 Resp. Ex. A, Tab 17). 79 Diabetes mellitus is “often associated” with this condition; more than 50% of patients who had GAD antibody cerebellar ataxia also have diabetes. Id. (citing Resp. Ex. A, Tab 16; Resp. Ex. A, Tab 17). Dr. Chaudhry concluded that Mr. Gelardi had the “typical symptoms, signs, CSF findings, antibody findings, [] response to treatment[,] balance problems, vertigo, insulin-requiring diabetes, diplopia [(double vision)], transient leg weakness, oligoclonal bands . . . , high titers of [GAD antibodies] . . . , and improvement with IVIG.” Id.

A study by Kumar and Subhakumari, 80 cited by Dr. Chaudhry, examined the role of GAD antibodies and latent autoimmune diabetes in adults. Resp. Ex. A, Tab 15. Diagnostic criteria for latent autoimmune diabetes in adults include age of 30 years of greater, positive results for at least one of four pancreatic antibodies (one of which is GAD65 antibodies), 81 and no treatment with insulin in the first six months after diagnosis. Id. at 1-2. Latent autoimmune diabetes in adults shares characteristics of both type 1 diabetes and type 2 diabetes, 82 but is “considered [] a distinct form of diabetes that lies somewhere between type 1 and type 2 diabetes and therefore has [] been denominated as type 1.5 diabetes.” Id. at 1. The study group was comprised of 297 people with a diagnosis of type 2 diabetes (made within the past three years), ages 30 to 70, and an initial period of six months after diagnosis with no insulin therapy. Id. at 1-2. The goal of the study was to determine how many diagnosed with type 2 diabetes met the criteria for latent autoimmune diabetes in adults. Id. Of the 297 people diagnosed with type 2 diabetes, 45 (15.2%) met the criteria for latent autoimmune diabetes in adults. Id. at 3. Among the 45 latent autoimmune diabetes in adults subjects, all had at least one antibody, 37 of 45 (82.2%) were positive for anti-GAD antibodies, and 13 of 45 (28.9%) were positive for anti-IA2 antibodies. Id. Anti-GAD antibodies were found to be “strong[] predictors of insulin requirement.” Id. at 5.

Dr. Chaudhry explained that about 80% of GAD-antibody cerebellar ataxia patients have “concomitant organ specific autoimmune disorders,” including diabetes, which “usually precede the onset of ataxia by several years.” Resp. Ex. C at 2 (quoting Resp. Ex. C, Tab 5 at 3). 83 The clinical course is characterized by a subacute presentation that occurs over weeks to months. Resp. Ex. C, Tab 5 at 3. Brain MRIs often show “progressive atrophy of the cerebellum.” Id.

Regarding causation, Dr. Chaudhry opined that the flu vaccination administered to Mr. Gelardi in 2015 “did not play a causative role in the cerebellar ataxia associated with uncontrolled diabetes.” Resp. Ex. A at 20; see also Resp. Ex. C at 10 (“The flu vaccine did not cause his neurological condition.”). Instead, Dr. Chaudhry opined that Mr. Gelardi “had autoimmune ataxia likely caused by the anti-GAD 65 antibodies.” Resp. Ex. C at 10.

In support, Dr. Chaudhry cited Ariño et al., 84 who noted that although the pathogenic role of GAD65 antibodies is not clear, they may play a role in processes that result in “neurochemical and neurophysiological abnormalities” that affect “the function of Purkinje cells” 85 and ultimately result in death of these cells. Resp. Ex. A, Tab 10 at 6. He also cited Graus et al., who noted that although “[t]he pathogenesis of . . . cerebellar ataxia associated with GAD antibodies remains unknown[,] . . . mechanisms [] involv[ing] cytotoxic T cells, either alone or in combination with autoantibodies, cannot be dismissed.” Resp. Ex. C, Tab 5 at 11.

5. Respondent’s Expert, Dr. Amanda L. Piquet, M.D. 86 a. Background and Qualifications

Dr. Piquet is “a board certified neurologist with subspecialty training in autoimmune neurology and neuroimmunology.” Resp. Ex. D at 1. She obtained her M.D. from Pennsylvania State College of Medicine, after which she completed an internal medicine internship and neurology residency at Brigham & Women’s Hospital/Massachusetts General Hospital and an autoimmune neurology/neuroimmunology fellowship at University of Utah Healthcare. Resp. Ex. L at 1. She has taught in the neurology at the University of Utah and University of Colorado since 2017. Id.

Dr. Piquet “ha[s] extensive clinical experience with GAD65 autoimmune neurological disorders.” Resp. Ex. F at 1. Dr. Piquet is “regularly involved in the care of patients with various neuroimmunological conditions including . . . [GAD65] antibody-mediated disorders.” Resp. Ex. D at 1. She has “diagnosed and managed several patients with GAD65 antibody neurological disease including phenotypes with stiff person spectrum disorder [] [and] cerebellar ataxia.” Id. She has also published on the subject of autoimmune neurological disorders, including autoimmune cerebellar ataxia and stiff person syndrome. Id.; see, e.g., Resp. Exs. D, Tabs 1-2; Resp. Ex. F, Tab 1; Pet. Ex. 95. And she is a member of the Stiff Person Syndrome Research Foundation and other relevant committees. Resp. Ex. L at 2.

b. Opinions Dr. Piquet agreed that Mr. Gelardi had “autoimmune ataxia syndrome likely caused by anti-GAD65 antibody.” 87 Resp. Ex. D at 3. She opined “[t]he most likely cause is GAD65 antibody syndrome,” but noted that Mr. Gelardi did not undergo comprehensive testing for coexisting antibodies and his CSF was not tested for GAD65 antibodies. Id. Regardless of the lack of comprehensive testing, Dr. Piquet opined that Mr. Gelardi’s clinical course is consistent with “autoimmune cerebellar ataxia and/or stiff person syndrome spectrum disorder [] with a cerebellar phenotype.” Id.

In a study authored by Dr. Piquet, she defined stiff person syndrome as a “rare neurological disorder characterized by progressive muscle stiffness and painful spasms.” Resp. Ex. D, Tab 2 at 2. 88 GAD65 antibodies are associated with the illness. Id. In the study of 17 patients with GAD65 antibodies reported by Dr. Piquet, eight had “significant cerebellar and/or [P]arkinsonian signs.” Id.

i. Althen Prong One

Dr. Piquet agreed that “the pathophysiology of GAD65 autoimmunity remains elusive.” Resp. Ex. F at 5. She explained that “GAD65 autoimmune disease . . . is well known to be a chronic, progressive autoimmune neurological disorder.” Resp. Ex. D at 3. She cited Rakocevic et al., 89 who studied a large cohort of patients with stiff person syndrome (a GAD autoimmune disease) who had follow up at eight years. Id. at 3-4 (citing Resp. Ex. D, Tab 4). The authors found it to be “a progressive disease leading to physical disability over time.” Resp. Ex. D, Tab 4 at 1. Most of the patients lost their ability to walk independently regardless of treatment. Id.

Rakocevic et al. confirmed that the illness has an autoimmune basis due to the presence of anti-GAD antibodies in the blood and CSF, glycine receptor antibodies in some patients, and an association with other autoimmune diseases including type 1 diabetes. Resp. Ex. D, Tab 4 at 6. However, the authors maintained “[t]he pathogenic potential of anti-GAD antibodies remain[ed] unsettled.” Id. Although the presence of GAD antibodies in CSF suggested “possibl[e] in-situ action of antibodies within the CNS, [] it is unclear what drives their CNS persistence.” Id.

Dr. Piquet explained that there is “very little published data” to support any “correlation between GAD65 autoimmune disease and vaccination.” Resp. Ex. D at 5. She noted that while the two case reports cited by Petitioner’s experts showed a temporal association, neither involved GAD65 antibody disease. Id. (citing Pet. Exs. 54, 185).

Regarding the opinions of Dr. Simpson, and his proposed mechanisms of molecular mimicry, neurotoxic effect, immune complex formation, and loss of self-tolerance, Dr. Piquet opined that although these concepts are “outlined and defined” by Dr. Simpson in his report, “no evidence [was] provided to support [] causation.” Resp. Ex. D at 3. Further, Dr. Piquet stated that Dr. Simpson’s example of GBS associated with Campylobacter jejuni is not relevant to the condition and facts here. Id. “There [was] no clear proposed mechanism of molecular mimicry between [flu] and GAD65 in [his] report.” Id.

Moreover, Dr. Piquet opined that molecular mimicry has not been identified as a relevant causal mechanism for either a flu infection or flu vaccination and GAD65 disease. Resp. Ex. D at 5. There have been “[n]o studies [that] have sufficiently identified cross-reactivity between [flu] (infection or vaccination) and GAD65 epitopes.” Id. She specifically disagreed with Dr. Simpson’s reliance on the study by Svensson et al. to support the theory of molecular mimicry and she detailed numerous issues with the study and its application here. 90 Resp. Ex. F at 3-4 (citing Pet. Ex. 59). She noted that the Svensson et al. findings were specific to the Pandemrix vaccination for H1N1 and in the setting of Type 1 diabetic children. Id. at 4 (quoiting Resp. Ex. D at 8). Additionally, Svensson et al. “did not measure the specific epitope of GAD65 antibodies” and “only mention GAD antibodies,” thus, the authors “do[] not clarify the details of the antibody assay in the methods section.” Id. Dr. Piquet concluded that the vaccines and illness here was not studied or described. Id.

Dr. Piquet also reviewed the articles cited by Dr. Simpson and explained why they did not support vaccine causation. 91 See Resp. Ex. D at 5-8. As explained by Dr. Piquet, generally the medical articles cited by Dr. Simpson did not relate to GAD65 cerebellar ataxia, and thus, are not on point with the facts and circumstances here. See id.

Next, Dr. Piquet responded to Dr. Akbari’s opinions related to the role of IL-17 to the illness here. Resp. Ex. F at 5. Dr. Piquet opined that because GAD65 autoimmune cerebellar ataxia is not thought to be a demyelinating disease, it is not appropriate to compare it to other demyelinating illnesses (like Dr. Akbari did). Id. Dr. Piquet also opined that IL-17 is not known to play a role in GAD65 autoimmune cerebellar ataxia. Id. In Levraut et al., the authors studied IL-17 in non-NMDAR autoimmune encephalitis, and none of the patients had GAD65 antibodies. Id. (citing Pet. Ex. 104). Dr. Piquet explained that GAD65 patients were “intentional excluded from this study.” Id. Thus, she concludes that it is “impossible” to use the study to draw any relevant conclusions. Id.

Dr. Piquet concluded that there is “no data to suggest a causal relationship between influenza (infection or vaccination) and GAD65 autoimmune neurological disease.” Pet. Ex. F At 6.

ii. Althen Prongs Two and Three

Dr. Piquet opined it “is more likely than not that the [flu] vaccine did not cause Mr. Gelardi’s autoimmune cerebellar ataxia.” Resp. Ex. D at 8.

First, she opined that Mr. Gelardi’s illness began prior to vaccination but “was subclinical prior to his [flu] vaccine.” Resp. Ex. D at 8. The illness is “well known to have co-existing autoimmunity with diabetes” and is a “chronic, progressive autoimmune neurological disorder.” Id. at 3. Dr. Piquet cited Rakocevic et al., who examined patients with stiff person syndrome (a GAD autoimmune disease), some of which had a cerebellar phenotype, and noted that the disease begins in a subtle fashion before progressing, although in older patients (over 50 years of age at onset), disability develops sooner. Resp. Ex. D, Tab 4 at 6. The condition is associated with other autoimmune conditions such as diabetes and thyroiditis. Id. Due to the clinical course, the illness is challenging to diagnose with an average time from onset to diagnosis of five years (range: 1 to 19 years). Id. at 2.

To illustrate her opinion that Mr. Gelardi had subclinical GAD65 antibody autoimmune cerebellar ataxia prior to vaccination, she summarized relevant points in his clinical course. 92 Dr. Piquet explained that Mr. Gelardi’s diabetes was well controlled in 2014 (A1c ranged from 6.7 to 6.9); however, in 2015, Mr. Gelardi’s A1c increased and his diabetes was more difficult to control, with values of 9.8 on June 24 and 12.3 on August 7. Resp. Ex. D at 4. Dr. Piquet opined that this pattern of increase is “highly suspicious for the onset of [Mr. Gelardi’s] autoimmunity beginning the summer of 2015 prior to vaccination on [October 11, 2015].” Id. According to Dr. Piquet, this prodromal syndrome characterized by elevated A1c prior to onset of neurological illness is not uncommon in patients with GAD65. Id. She explained that a history of type 1 diabetes occurs in approximately half of these patients and “it usually precedes neurological manifestations.” Id. (quoting Resp. Ex. D, Tab 5 at 6 (“A personal history of [Type 1 diabetes mellitus] is present in about half of cases . . . and it usually precedes neurological manifestations.”)).

Thus, Dr. Piquet concluded that “Mr. Gelardi showed signs of GAD65 autoimmunity” prior to his vaccination on October 11, 2015, “with an abrupt worsening of diabetes that became harder to control.” Resp. Ex. D at 8.

Petitioner’s expert neurologist, Dr. Simpson, disagreed with Dr. Piquet’s opinion that Mr. Gelardi developed his illness prior to vaccination, and he argued that prior to vaccination, Mr. Gelardi had been playing golf up to five days a week. Pet. Ex. 141 at 9. However, Dr. Piquet noted that while the “exact date of onset is difficult to discern,” there was “no objective evidence of a cerebellar syndrome documented until February [2016],” when Mr. Gelardi developed symptoms of diplopia. Resp. Ex. F at 2; see also Resp. Ex. D at 2. Dr. Piquet stated there was “objective evidence based on laboratory work up of poorly controlled diabetes prior to vaccination which is consistent with GAD65 autoimmunity including latent autoimmune diabetes in adults.” Resp. Ex. F at 2 (emphasis omitted). Dr. Piquet maintained that type 1 diabetes is seen in approximately half of these cases and “it usually precedes neurological manifestations.” Id. at 3 (quoting Resp. Ex. D, Tab 5 at 6). Dr. Piquet noted that Mr. Gelardi’s A1c was 6.7 and 6.9 in 2014 but abruptly increased to 9.8 in June 2015, and then 12.3 on August 7, 2015. Id. She concluded that this abrupt elevation is “highly suspicious for the onset of his autoimmunity beginning the summer of 2015, prior to [] vaccination.” Id. Therefore, she opined that Mr. Gelardi’s autoimmune disease, “more likely than not began well prior to his [October 11, 2015] vaccination, and that the neurological manifestations . . . may not have become apparent until February 2016.” Id.

Secondly, Dr. Piquet disagreed that examples of GBS post-flu vaccine with an onset of three to 42 days reflects an appropriate time interval to use here since GBS is a “different neurological syndrome with different pathophysiology” and the conditions do not share a common causal mechanism. Resp. Ex. F at 2.

In conclusion, Dr. Piquet opined that it is “more likely than not that the [flu] vaccine did not cause Mr. Gelardi’s GAD65 autoimmune cerebellar ataxia.” Resp. Ex. F at 6.

6. Respondent’s Expert, Stephen C. Jameson, Ph.D. 93

a. Background and Qualifications Dr. Jameson is an immunologist with a focus on “the immune system and its response to vaccines and infections.” Resp. Ex. G at 1. More specifically, “[his] research focus has been on application of animal models to study the cellular immune responses against pathogens and vaccines, and the impact of these responses on protective immunity, immunopathology and autoimmunity.” Id. at 2. He obtained his Ph.D. at the University of Cambridge in English, which was followed by postdoctoral training at Scripps Research Institute and at the University of Washington. Id. at 1; Resp. Ex. M at 1. He has been a professor in the Center for Immunology, Masonic Cancer Center and Department of Laboratory Medicine and Pathology, at the University of Minnesota Medical School since 1995. Resp. Ex. G at 2; Resp. Ex. M at 1. Dr. Jameson has almost 200 publications “nearly on all aspects of immunology and the immune response to pathogens.” Resp. Ex. G at 2; Resp. Ex. M at 13-29.

Since Dr. Jameson is not a medical doctor, he limited his opinions to immunology and Althen prong one—whether the flu vaccine can cause GAD65 autoimmune cerebellar ataxia. Resp. Ex. G at 2. At the outset, he identified two points where there was agreement between the parties’ experts: (1) that Mr. Gelardi had an “autoimmune cerebellar ataxia, associated with . . . GAD65, and did not have [CIDP] and (2) that the “mild demyelination noted for Mr. Gelardi [was] consistent with neuropathy arising from his long-term battle with diabetes.” 94 Id.

b. Opinions Dr. Jameson opined that “more likely than not[,] [] the [flu] vaccine did not cause Mr. Gelardi’s GAD65 autoimmune cerebellar ataxia.” Resp. Ex. G at 12 (emphasis omitted).

Dr. Jameson explained that although the pathogenesis of GAD65 autoimmune cerebellar ataxia is not completely known, “it is thought to involve antibodies to GAD65 interfering with release of GABA-containing synaptic vesicles.” Resp. Ex. G at 3. He stressed that “autoimmune cerebellar ataxia is not a demyelinating disease.” Id.

In responding to Dr. Akbari’s expert opinions, Dr. Jameson observed that “Dr. Akbari raise[d] many ideas about how immune responses may cause various forms [of] neuropathology” but opined “it is critical to determine a) whether these studies and hypotheses are pertinent to Mr. Gelardi’s GAD65 autoimmune cerebellar ataxia, and b) the likelihood that Mr. Gelardi’s autoimmune cerebella ataxia was provoked by the [flu] vaccine he received on [October 11, 2015]”. Resp. Ex. G at 3-4.

Regarding the first question, whether Dr. Akbari’s opinions and the studies he cites are relevant to autoimmune cerebellar ataxia, Dr. Jameson noted that mechanisms related to demyelinating illnesses are not relevant to GAD65 autoimmune cerebellar ataxia. Resp. Ex. G at 4. Dr. Jameson stated that extrapolation of mechanisms relevant to demyelinating conditions ignores the specificity characteristic of the adaptive immune system. Id. “T cells and the antibodies produced by B cells exhibit high degrees of specificity.” Id. (emphasis omitted). For example, studies showing whether vaccines can induce autoimmune responses that cause demyelination by targeting myelin basic protein or other parts of the myelin sheath are designed to be “very narrow” and they have a “precise focus.” Id. at 4-5. These studies “cannot be coopted into a hypothesis” related to the pathogenesis of a different autoimmune neurological disease, where there are “different targets of immune attack.” Id. at 5. Dr. Jameson stated that “Dr. Akbari did not provide any clinical or pre-clinical research studies indicating that [flu] or [flu] vaccines induce T cell responses or antibodies against GAD65 . . . and it is not clear . . . that such studies exist.” Id.

The concept of specificity characteristic to the adaptive immune system is “an essential point,” illustrated by the Blackmore et al. paper which was relied on by Dr. Akbari. Resp. Ex. J at 5 (citing Pet. Ex. 191). Dr. Jameson explained that Blackmore et al. did not show that flu- specific T cells caused encephalomyelitis; instead, the data indicated that the pathogenic cells “were not [flu] specific.” 95 Id. (emphasis omitted). Thus, the study is not relevant. Id.

Turning to the second question, whether there is evidence that the flu vaccine can cause autoimmune cerebellar ataxia, Dr. Jameson responded to Dr. Akbari’s proposed associations between the immune system “that are involved in the responses to [flu] vaccine and [] also involved in CNS autoimmune diseases.” Resp. Ex. G at 5. Dr. Jameson agreed that immune responses to vaccines and autoimmune conditions involve interactions between T cells (including Th17 and Treg cells noted by Dr. Akbari) and B cells (which produce antibodies). Id. He also agreed that immune responses involve inflammatory processes, including inflammasome activation. Id. But Dr. Jameson explained that that fact that these processes occur, does not mean that they are linked to each other. Id. at 5-6.

For example, although Dr. Akbari argued that IL-17 and Th17 responses occur in reaction to flu infection or vaccination, this was in the context of EAE and multiple sclerosis, different autoimmune diseases. Resp. Ex. G at 6. Although Dr. Jameson agreed that Th17 cells can play a role in “some autoimmune diseases,” Dr. Akbari failed to explain that Th17 responses are also “a normal and critical way that our bodies deal with certain pathogens,” including bacterial and fungal infections. Id. Further, deficiencies in Th17 cells can contribute to uncontrolled infections. Id. Dr. Jameson explained that Th17 cells are “important for normal homeostasis of the intestines, as well as other mucosal tissues.” Id. In other words, the fact that vaccines provoke Th17 responses does not allow one to “predict[] autoimmune pathogenesis as a likely outcome.” Id. Further, Dr. Jameson disagreed that flu vaccines cause “a strong Th17 response.” Resp. Ex. J at 3.

Further, seasonal flu vaccines, and specifically the vaccination at issue here, have not been shown to induce pathological Th17 responses. Resp. Ex. G at 7. Dr. Jameson observed that the studies cited by Dr. Akbari used “novel vaccines” designed for the express purpose of “driving development of Th17 cells.” Id. Therefore, the studies do not support Dr. Akbari’s assertions as it relates to the flu vaccination. Id.; see also Resp. Ex. K at 2-3.

Moreover, Dr. Jameson opined that there is no evidence that Th17 responses are involved in autoimmune cerebellar ataxia. Resp. Ex. G at 7. The one reference cited by Dr. Akbari in support of IL-17/Th17 cells and ataxia relate to a different illness, non-NMDA-receptor autoimmune encephalitis. Id. (citing Pet. Ex. 104). Again, these differences do not allow extrapolation of findings to the present case. Id.

Moving to Dr. Akbari’s opinions related to the role of Tregs, Dr. Jameson raised the same concerns noted above, beginning with the lack of specificity. Resp. Ex. G at 7. He explained that Tregs “typically restrain immune responses.” Id. T effector cells, or Teffs, are cells that “actively drive immune responses.” Id. While vaccinations may affect the Treg/Teff balance, specificity is important: “During an immune response against a pathogen, such as [flu], it is critical that Teff specific for [flu] increase in numbers and[] transiently outnumber Treg specific for the same antigen.” Id. (emphasis omitted). Dr. Jameson stated that imbalances “do[] not inevitably lead to autoimmunity,” especially because the Teff response is focused on the pathogen. Id.

Dr. Jameson offered additional reasons why the studies cited by Dr. Akbari for his theory based on Treg/Teff imbalances are not germane. See Resp. Ex. G at 8. For example, some related to demyelinating diseases, and cerebellar ataxia is not a demyelinating illness, or otherwise did not specifically address cerebellar ataxia. Id.

In his expert report, Dr. Akbari stated that “the role of Treg/Teff after immunization with flu and also the role of Tregs in controlling unwanted immune response such as autoimmune cerebellar ataxiad are well established.” Pet. Ex. 93 at 12. Dr. Jameson disagreed with this statement. Resp. Ex. G at 8. Dr. Jameson opined that Dr. Akbari offered no evidence that there are changes in the Treg/Teff balance due to vaccination or that such changes are related to those that occur during the autoimmune disease at issue here. Id. Second, the studies cited by Dr. Akbari do not relate to the pathogenesis of autoimmune cerebellar ataxia. Id.

Dr. Jameson also took issue with Dr. Akbari’s statement that “in some individuals such as Mr. Gelardi, after vaccination, based on preponderance of evidence, pathogenic Teff cells are able to induce ataxia and this is simply due to impaired Tregs.” Resp. Ex. J at 3 (quoting Pet. Ex. 142 at 9). Dr. Jameson explained that “the specificity of T cells dictates their responses, [and] without evidence that Teff cells responding to the vaccine cross-react with antigens expressed in the brain, the frequency of [Tregs] is beside the point.” Id.; see also Resp. Ex. K at 2-3.

As for Dr. Akbari’s discussion of inflammasome, Dr. Jameson agreed that inflammasome activation is important “in normal immunity against infections” and “critical for protective immunity against pathogens.” Resp. Ex. G at 9 (emphasis omitted). Dr. Jameson observed, however, that Dr. Akbari failed to provide references to support the statement that “many studies support the notion that induction of inflammasome [] along with T cell stimulation, after administration of [the flu] vaccine, is able to trigger pathogenic T cells and cause encephalitis.” Id. (quoting Pet. Ex. 93 at 14). Again, Dr. Jameson explained that while inflammasome activation is involved in immune responses to infections and vaccinations, this is no evidence that these responses cause pathology. Id. Further, Dr. Jameson opined Dr. Akbari failed to provide evidence that inflammasome activation is associated with GAD65 autoimmune cerebellar ataxia. Id.

In other words, relative to Dr. Akbari’s inflammasome hypothesis, Dr. Jameson stated that whether the flu vaccination activates the inflammasome is not at issue, instead, “the point of contention is whether such immune responses toward [the flu] vaccination are likely to be a cause of subsequent autoimmune cerebral ataxia.” Resp. Ex. J at 2 (emphasis omitted).

Next, Dr. Jameson turned to the two case studies cited by Dr. Akbari to support his statement that “many studies demonstrated that [the] flu vaccine is capable of causing autoimmune ataxia.” Pet. Ex. 93 at 9. Dr. Jameson stated that neither case report related to a patient with GAD65 antibodies, a key fact here. Resp. Ex. G at 10. Further, Dr. Jameson questioned the diagnosis in one case based on the opinions of Dr. Piquet. Id. (citing Resp. Ex. F at 6 (opining the woman had a demyelinating syndrome similar to acute disseminated encephalomyelopathy, which is not the same as GAD65 autoimmune cerebellar ataxia)). The second case involved a five year old, and the authors were cautious about attributing causation to vaccination, stating that the pathogenesis of ataxia “remained to be clarified.” Id. (quoting Pet. Ex. 54 at 7-8). Dr. Jameson did not find one case report sufficient to demonstrate causation. Id.

Regarding the study cited by Dr. Akbari reporting 146 cases of ataxia after vaccination, Dr. Jameson noted that there was no mention of the flu vaccination. 96 Resp. Ex. G at 11. Because the flu vaccination was not mentioned, Dr. Jameson opined that the study lacked relevance here. Id.

In addition to responding to Dr. Akbari’s opinions, Dr. Jameson also provided opinions about Dr. Simpson’s reports, particularly about Dr. Simpson opinions related to Svensson et al. Resp. Ex. G at 11-12 (citing Pet. Ex. 59). Dr. Simpson opined that Svensson et al. showed that flu vaccination “triggered [pancreas] islet autoantibodies resulting in an immediate or rapid onset of diabetes.” Pet. Ex. 67 at 9. Dr. Jameson disagreed with Dr. Simpson’s characterization of the study, noting that there was no increase in the number of new diabetics during the flu vaccination campaign, and this fact argued against the notion that the vaccine increased the incidence of autoimmune diabetes. Resp. Ex. G at 11. Instead, Dr. Jameson suggested that Svensson et al. showed that the flu vaccine raised levels of “pre-existing GAD specific antibodies” during vaccination, and after vaccination these antibodies decreased. Id. (emphasis omitted) (citing Pet. Ex. 59 at 6). This finding of a transient increase in detectable GAD antibodies is consistent with existing studies showing that vaccination can “provoke a transient burst of antibody production by B cells” that have been produced due to prior immune responses. Id. at 11-12.

In conclusion, Dr. Jameson explained that although Dr. Akbari and Dr. Simpson offer various theories and cite studies about an alleged association between immune responses against vaccinations and CNS autoimmune diseases, these opinions and arguments are not specific and thus not relevant to GAD65 autoimmune cerebellar ataxia. Resp. Ex. G at 12. Further, Dr. Jameson opined that Dr. Akbari’s supplemental reports describe immune system processes involved in response to infections and vaccines, as well as those involved in autoimmune responses, which are not in dispute and are not relevant to the question of whether the flu vaccine can cause autoimmune cerebellar ataxia. Resp. Ex. J at 6. Due to the lack of evidence to show that the flu vaccine can cause GAD65 autoimmune cerebellar ataxia, Dr. Jameson concluded that “more likely than not[,] [the flu] vaccine did not cause Mr. Gelardi’s GAD65 autoimmune cerebellar ataxia.” Resp. Ex. G at 12; Resp. Ex. J at 6.

III. DISCUSSION

A. Standards for Adjudication The Vaccine Act was established to compensate vaccine-related injuries and deaths. § 10(a). “Congress designed the Vaccine Program to supplement the state law civil tort system as a simple, fair and expeditious means for compensating vaccine-related injured persons. The Program was established to award ‘vaccine-injured persons quickly, easily, and with certainty and generosity.’” Rooks v. Sec’y of Health & Hum. Servs., 35 Fed. Cl. 1, 7 (1996) (quoting H.R. Rep. No. 908 at 3, reprinted in 1986 U.S.C.C.A.N. at 6287, 6344).

Petitioner’s burden of proof is by a preponderance of the evidence. § 13(a)(1). The preponderance standard requires a petitioner to demonstrate that it is more likely than not that the vaccine at issue caused the injury. Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1322 n.2 (Fed. Cir. 2010). Proof of medical certainty is not required. Bunting v. Sec’y of Health & Hum. Servs., 931 F.2d 867, 873 (Fed. Cir. 1991). Petitioner need not make a specific type of evidentiary showing, i.e., “epidemiologic studies, rechallenge, the presence of pathological markers or genetic predisposition, or general acceptance in the scientific or medical communities to establish a logical sequence of cause and effect.” Capizzano v. Sec’y of Health & Hum. Servs., 440 F.3d 1317, 1325 (Fed. Cir. 2006). Instead, Petitioner may satisfy her burden by presenting circumstantial evidence and reliable medical opinions. Id. at 1325-26.

In particular, Petitioner must prove that the vaccine was “not only [the] but-for cause of the injury but also a substantial factor in bringing about the injury.” Moberly, 592 F.3d at 1321 (quoting Shyface v. Sec’y of Health & Hum. Servs., 165 F.3d 1344, 1352-53 (Fed. Cir. 1999)); see also Pafford v. Sec’y of Health & Hum. Servs., 451 F.3d 1352, 1355 (Fed. Cir. 2006). The received vaccine, however, need not be the predominant cause of the injury. Shyface, 165 F.3d at 1351. A petitioner who satisfies this burden is entitled to compensation unless Respondent can prove, by a preponderance of the evidence, that the vaccinee’s injury is “due to factors unrelated to the administration of the vaccine.” § 13(a)(1)(B). However, if a petitioner fails to establish a prima facie case, the burden does not shift. Bradley v. Sec’y of Health & Hum. Servs., 991 F.2d 1570, 1575 (Fed. Cir. 1993).

“Regardless of whether the burden ever shifts to the [R]espondent, the special master may consider the evidence presented by the [R]espondent in determining whether the [P]etitioner has established a prima facie case.” Flores v. Sec’y of Health & Hum. Servs., 115 Fed. Cl. 157, 162-63 (2014); see also Stone v. Sec’y of Health & Hum. Servs., 676 F.3d 1373, 1379 (Fed. Cir. 2012) (“[E]vidence of other possible sources of injury can be relevant not only to the ‘factors unrelated’ defense, but also to whether a prima facie showing has been made that the vaccine was a substantial factor in causing the injury in question.”); de Bazan v. Sec’y of Health & Hum. Servs., 539 F.3d 1347, 1353 (Fed. Cir. 2008) (“The government, like any defendant, is permitted to offer evidence to demonstrate the inadequacy of the [P]etitioner’s evidence on a requisite element of the [P]etitioner’s case-in-chief.”); Pafford, 451 F.3d at 1358-59 (“[T]he presence of multiple potential causative agents makes it difficult to attribute ‘but for’ causation to the vaccination. . . . [T]he Special Master properly introduced the presence of the other unrelated contemporaneous events as just as likely to have been the triggering event as the vaccinations.”).

B. Factual Issues A petitioner must prove, by a preponderance of the evidence, the factual circumstances surrounding her claim. § 13(a)(1)(A). To resolve factual issues, the special master must weigh the evidence presented, which may include contemporaneous medical records and testimony. See Burns v. Sec’y of Health & Hum. Servs., 3 F.3d 415, 417 (Fed. Cir. 1993) (explaining that a special master must decide what weight to give evidence including oral testimony and contemporaneous medical records). Contemporaneous medical records, “in general, warrant consideration as trustworthy evidence.” Cucuras v. Sec’y of Health & Hum. Servs., 993 F.2d 1525, 1528 (Fed. Cir. 1993). But see Kirby v. Sec’y of Health & Hum. Servs., 997 F.3d 1378, 1382 (Fed. Cir. 2021) (rejecting the presumption that “medical records are accurate and complete as to all the patient’s physical conditions”); Shapiro v. Sec’y of Health & Hum. Servs., 101 Fed. Cl. 532, 538 (2011) (“[T]he absence of a reference to a condition or circumstance is much less significant than a reference which negates the existence of the condition or circumstance.” (quoting Murphy v. Sec’y of Health & Hum. Servs., 23 Cl. Ct. 726, 733 (1991), aff’d per curiam, 968 F.2d 1226 (Fed. Cir. 1992))), recons. den’d after remand, 105 Fed. Cl. 353 (2012), aff’d mem., 503 F. App’x 952 (Fed. Cir. 2013).

There are situations in which compelling testimony may be more persuasive than written records, such as where records are deemed to be incomplete or inaccurate. Campbell v. Sec’y of Health & Hum. Servs., 69 Fed. Cl. 775, 779 (2006) (“[L]ike any norm based upon common sense and experience, this rule should not be treated as an absolute and must yield where the factual predicates for its application are weak or lacking.”); Lowrie v. Sec’y of Health & Hum. Servs., No. 03-1585V, 2005 WL 6117475, at *19 (Fed. Cl. Spec. Mstr. Dec. 12, 2005) (“[W]ritten records which are, themselves, inconsistent, should be accorded less deference than those which are internally consistent.” (quoting Murphy, 23 Cl. Ct. at 733)). Ultimately, a determination regarding a witness’s credibility is needed when determining the weight that such testimony should be afforded. Andreu v. Sec’y of Health & Hum. Servs., 569 F.3d 1367, 1379 (Fed. Cir. 2009); Bradley, 991 F.2d at 1575.

Despite the weight afforded to medical records, special masters are not rigidly bound by those records in determining onset of a petitioner’s symptoms. Valenzuela v. Sec’y of Health & Hum. Servs., No. 90-1002V, 1991 WL 182241, at *3 (Fed. Cl. Spec. Mstr. Aug. 30, 1991); see also Eng v. Sec’y of Health & Hum. Servs., No. 90-1754V, 1994 WL 67704, at *3 (Fed. Cl. Spec. Mstr. Feb. 18, 1994) (noting Section 13(b)(2) “must be construed so as to give effect also to § 13(b)(1) which directs the special master or court to consider the medical records (reports, diagnosis, conclusions, medical judgment, test reports, etc.), but does not require the special master or court to be bound by them”).

C. Causation To receive compensation through the Program, Petitioner must prove either (1) that Mr. Gelardi suffered a “Table Injury”—i.e., an injury listed on the Vaccine Injury Table— corresponding to a vaccine that he received, or (2) that Mr. Gelardi suffered an injury that was actually caused by a vaccination. See §§ 11(c)(1), 13(a)(1)(A); Capizzano, 440 F.3d at 1319-20. Petitioner must show that the vaccine was “not only a but-for cause of the injury but also a substantial factor in bringing about the injury.” Moberly, 592 F.3d at 1321 (quoting Shyface, 165 F.3d at 1352-53).

Because Petitioner does not allege Mr. Gelardi suffered a Table Injury, she must prove a vaccine he received caused his injury. To do so, Petitioner must establish, by preponderant evidence: “(1) a medical theory causally connecting the vaccination and the injury; (2) a logical sequence of cause and effect showing that the vaccination was the reason for the injury; and (3) a showing of a proximate temporal relationship between vaccination and injury.” Althen, 418 F.3d at 1278.

The causation theory must relate to the injury alleged. Petitioner must provide a sound and reliable medical or scientific explanation that pertains specifically to this case, although the explanation need only be “legally probable, not medically or scientifically certain.” Knudsen v. Sec’y of Health & Hum. Servs., 35 F.3d. 543, 548-49 (Fed. Cir. 1994). Petitioner cannot establish entitlement to compensation based solely on his assertions; rather, a vaccine claim must be supported either by medical records or by the opinion of a medical doctor. § 13(a)(1). In determining whether a petitioner is entitled to compensation, the special master shall consider all material in the record, including “any . . . conclusion, [or] medical judgment . . . which is contained in the record regarding . . . causation.” § 13(b)(1)(A). The undersigned must weigh the submitted evidence and the testimony of the parties’ proffered experts and rule in Petitioner’s favor when the evidence weighs in his favor. See Moberly, 592 F.3d at 1325-26 (“Finders of fact are entitled—indeed, expected—to make determinations as to the reliability of the evidence presented to them and, if appropriate, as to the credibility of the persons presenting that evidence.”); Althen, 418 F.3d at 1280 (noting that “close calls” are resolved in Petitioner’s favor).

Testimony that merely expresses the possibility—not the probability—is insufficient, by itself, to substantiate a claim that such an injury occurred. See Waterman v. Sec’y of Health & Hum. Servs., 123 Fed. Cl. 564, 573-74 (2015) (denying Petitioner’s motion for review and noting that a possible causal link was not sufficient to meet the preponderance standard). The Federal Circuit has made clear that the mere possibility of a link between a vaccination and a petitioner’s injury is not sufficient to satisfy the preponderance standard. Moberly, 592 F.3d at 47 1322 (emphasizing that “proof of a ‘plausible’ or ‘possible’ causal link between the vaccine and the injury” does not equate to proof of causation by a preponderance of the evidence); Boatmon v. Sec’y of Health & Hum. Servs., 941 F.3d 1351, 1359-60 (Fed. Cir. 2019). While certainty is by no means required, a possible mechanism does not rise to the level of preponderance. Moberly, 592 F.3d at 1322; see also de Bazan, 539 F.3d at 1351.

IV. ANALYSIS

A. Althen Prong One Under Althen prong one, Petitioner must set forth a medical theory explaining how the received vaccine could have caused the sustained injury. Andreu, 569 F.3d at 1375; Pafford, 451 F.3d at 1355-56. Petitioner’s theory of causation need not be medically or scientifically certain, but it must be informed by a “sound and reliable” medical or scientific explanation. Boatmon, 941 F.3d at 1359; see also Knudsen, 35 F.3d at 548; Veryzer v. Sec’y of Health & Hum. Servs., 98 Fed. Cl. 214, 223 (2011) (noting that special masters are bound by both § 13(b)(1) and Vaccine Rule 8(b)(1) to consider only evidence that is both “relevant” and “reliable”). If Petitioner relies upon a medical opinion to support her theory, the basis for the opinion and the reliability of that basis must be considered in the determination of how much weight to afford the offered opinion. See Broekelschen, 618 F.3d at 1347 (“The special master’s decision often times is based on the credibility of the experts and the relative persuasiveness of their competing theories.”); Perreira v. Sec’y of Health & Hum. Servs., 33 F.3d 1375, 1377 n.6 (Fed. Cir. 1994) (stating that an “expert opinion is no better than the soundness of the reasons supporting it” (citing Fehrs v. United States, 620 F.2d 255, 265 (Ct. Cl. 1980))).

The undersigned finds that Petitioner has failed to provide preponderant evidence of a sound and reliable mechanism whereby a flu vaccination can cause GAD65 antibody-associated cerebellar ataxia. The reasons for this finding are discussed below.

First, Petitioner’s expert Dr. Chen offered molecular mimicry as a causal theory, but this opinion was not developed. Further, Dr. Chen acknowledged that the flu vaccination has not been associated with GAD65 cerebellar ataxia in the medical literature. She provided no evidence in support of molecular mimicry relative to the flu vaccination and GAD65 cerebellar ataxia. Thus, the undersigned finds her opinions conclusory. See Kreizenbeck v. Sec’y of Health & Hum. Servs., No. 08-209V, 2018 WL 3679843, at *31 (Fed. Cl. Spec. Mstr. June 22, 2018), mot. for rev. denied, 141 Fed. Cl. 138 (2018), aff’d, 945 F.3d 1362 (Fed. Cir. 2020) (explaining when evaluating whether petitioners have carried their burden of proof, special masters consistently reject “conclusory expert statements that are not themselves backed up with reliable scientific support”).

Of note, Dr. Chen opined that in adults the predominant cause of cerebellar ataxia is autoimmune GAD65 associated cerebellar ataxia, and that GAD65 antibodies are a hallmark of type 1 diabetes which is also associated with cerebellar ataxia. This opinion is like those expressed by Respondent’s experts, Dr. Chaudhry and Dr. Piquet, and does not support vaccine causation.

Second, Petitioner’s expert, Dr. Simpson, offered four causal mechanisms: molecular mimicry, neurotoxic effect, immune complex formation, and loss of tolerance. He did not discuss or develop the last three of these theories or provide evidence in the form of medical literature or otherwise, and therefore, there is no information for the undersigned to evaluate to determine the validity of these three mechanisms. Thus, the undersigned finds no support those three theories of causation. 97

Regarding molecular mimicry, Dr. Simpson proposed that epitopes in the flu vaccine cross reacted with myelin or axonal glycoproteins of nerves, a mechanism applicable to GBS, a demyelinating illness of the peripheral nerves. However, Dr. Simpson did not offer evidence that GAD65 cerebellar ataxia was a demyelinating condition, or explain how a theory applicable to a peripheral demyelinating illness was relevant to a CNS cerebellar illness associated with GAD65 antibodies. Dr. Simpson did not identify any foundational evidence to suggest that components of the flu vaccination have been found to induce GAD65 antibodies or GAD65 cerebellar ataxia. While he cited case studies and other articles, these were not on point since they did not relate to GAD65 antibody cerebellar ataxia and/or they did not relate to the flu vaccine.

Further, Dr. Simpson acknowledged that GAD65 antibody cerebellar ataxia was a specific and distinct entity and that while its causal mechanisms are unclear, GAD65 antibodies may “play a direct role” in the cause of this illness. Pet. Ex. 34 at 7. He cited medical literature supporting the conclusion that anti-GAD65 antibodies are associated with cerebellar ataxia and stiff person syndrome. See, e.g., Pet. Ex. 38 at 1. Dr. Simpson recognized the fact that the type of cerebellar ataxia at issue here is unique and distinct, and he acknowledged that the GAD65 antibodies were relevant to disease pathogenesis. Despite that, Dr. Simpson did not offer a mechanism to explain how the flu vaccine could induce an immune process where GAD65 antibodies are involved which result in cerebellar ataxia. Respondent’s expert, Dr. Piquet, was persuasive in establishing that the current body of knowledge related to GAD65 cerebellar ataxia does not support vaccine causation.

Moving to Petitioner’s third expert, Dr. Akbari, an immunologist, the undersigned finds that he also fails to provide support for vaccine causation. Dr. Akbari explains that the significance of anti-GAD65 antibodies has been debated, with some scientists arguing that the antibodies do not play a pathogenic role and others disagreeing. However, he cited medical literature stating there is accumulating evidence that anti-GAD 65 antibodies impair GABAergic synapses which leads to the manifestations of cerebellar ataxia. See Pet. Ex. 96 at 2. Recent studies show these antibodies “play a pathogenic role” in the development of cerebellar ataxias and cause a “decrease in GABA release at cerebellar synapses” resulting in functional deficits in cerebellar motor control. Id. at 10; see also Pet. Ex. 98 at 1 (“These studies provide substantial evidence of the pathogenesis of anti-GAD65 [antibodies] in [cerebellar ataxia].”).

Although Dr. Akbari references papers and articles detailing developments in the understanding of the causes of GAD65 cerebellar ataxia, he fails to incorporate this information into his opinions so that they are relevant here. Simply put, Dr. Akbari does not provide a theory relevant to the pathogenic processes described relative to GAD65 cerebellar ataxia. After providing a brief overview of cerebellar ataxia and citing several articles that specifically discuss anti-GAD65 antibody cerebellar ataxia, Dr. Akbari advances general immune theories. The evidence he offers via case studies and other articles do not show an association between the flu vaccination and GAD65 autoimmune cerebellar ataxia.

In contrast, Respondent’s expert immunologist, Dr. Jameson, offers cogent responses to each of the general theories offered by Dr. Akbari, noting a lack of specificity and relevance. Dr. Jameson provides a point by point explanation why each idea discussed by Dr. Akbari is not supported by the evidence or is not relevant to the facts and circumstances here. An example relates to Dr. Akbari’s opinions regarding Th17 responses. While Th17 cells play a role in some autoimmune diseases, Dr. Jameson explains they are also important in the immune system response to certain infections and maintaining immune homeostasis of intestinal and mucosal tissues. Dr. Jameson effectively explains the deficiencies in Dr. Akbari’s theory about Th17 responses to the flu vaccination. Another example is where Dr. Akbari offers homology supporting molecular mimicry based on protein sequence similarity found in the flu virus infection and patients with multiple sclerosis, not cerebellar ataxia. Each theory offered by Dr. Akbari suffers from a lack of specificity or relevance.

Further, at times, Dr. Akbari offers statements that misrepresent the referenced literature. For example, when discussing his theory related to Tregs and Teffs, he states that “in some individuals such as Mr. Gelardi, after vaccination, based on preponderance of evidence, pathogenic Teff cells are able to induce ataxia and this is simply due to impaired Tregs.” Pet. Ex. 142 at 9. Dr. Jameson described this statement as a “rather astonishing intellectual leap” from the literature. Resp. Ex. J at 3. Dr. Abkari cited a paper by Moise et al. in support of this statement. Moise et al. examined a way to “harness preexisting [flu] T cell immunity” to develop a vaccine protective against avian flu infection. Pet. Ex. 158 at 2. Moise et al. did not discuss the flu vaccine given here or cerebellar ataxia.

Another misleading statement by Dr. Akbari was based on the article by Blackmore et al. Dr. Akbari stated that “[t]he authors showed the presence of viral-specific T cells in the choroid plexus and induced a temporal transcriptomic alteration in the cerebellum.” Pet. Ex. 142 at 5. Dr. Jameson explained “Blackmore et al. presented no such data, or any data to indicate that the CNS-infiltrating cells—including those associated with CNS pathology—were specific for [flu].” Resp. Ex. J at 5.

The use of misleading statements derived from medical literature is not a new issue for Dr. Abari. See, e.g., Nieves v. Sec’y of Health & Hum. Servs., No. 18-1602V, 2023 WL 2580148, at *44-45 (Fed. Cl. Spec. Mstr. Apr. 17, 2023) (“[E]vidence that vaccines might stimulate production of some immune cells, or even interact with them, does not mean that the vaccine causes the injury . . . .”); Santiago v. Sec’y of Health & Hum. Servs., No. 21-1562V, 2026 WL 2250479, at *42 (Fed. Cl. Spec. Mstr. July 8, 2026) (finding Dr. Akbari mischaracterized the literature and “failed to provide foundational evidence” to support his assertions). Dr. Akbari’s practice of offering misleading statements and conclusions based on medical articles renders his opinions less credible and persuasive.

In contrast to the expert opinions offered by Petitioner, Respondent’s experts presented clear and cogent reports explaining that the existing body of knowledge does not allow for a conclusion based on preponderant evidence that the flu vaccine can cause GAD65 cerebellar ataxia.

Further, the undersigned finds Dr. Piquet to be the most knowledgeable expert about GAD65 cerebella ataxia. She completed an autoimmune neurology/neuroimmunology fellowship, she is a member of the Stiff Person Syndrome Research Foundation and other relevant committees, and she has authored on the subject. Dr. Piquet “ha[s] extensive clinical experience with GAD65 autoimmune neurological disorders.” Resp. Ex. F at 1. And she has cared for “several patients with GAD65 antibody neurological disease including phenotypes with stiff person spectrum disorder [] [and] cerebellar ataxia.” Resp. Ex. D at 1. Dr. Piquet’s expert reports illustrate her familiarity with the illness and her opinions are supported by relevant literature.

Due to her knowledge and expertise, supportive evidence with appropriate medical literature, and the detail provided in her expert reports, the undersigned finds her opinions to be persuasive. See Koehn v. Sec’y of Health & Hum. Servs., No. 11-355V, 2013 WL 3214877, at *32 (Fed. Cl. Spec. Mstr. May 30, 2013) (“In weighing the persuasiveness of opinion testimony, special masters may consider the relative expertise of the witness.”), aff’d, 773 F.3d 1239 (Fed. Cir. 2014); see also Dwyer v. Sec’y of Health & Hum. Servs., No. 03-1202V, 2010 WL 892250, at *64 (Fed. Cl. Spec. Mstr. Mar. 12, 2010) (giving greater weight to M.D. epidemiologists’ opinions on medical issues than to Ph.D. epidemiologist’s opinion); Pafford, 451 F.3d at 1359 (affirming the special master’s rejection of expert’s testimony because he lacked proper qualifications in the specialty areas in which he testified).

Dr. Piquet effectively establishes that there is insufficient data to support an association between the flu vaccination and GAD65 autoimmune disease. She carefully distinguished the facts in the two case reports about the flu vaccine and ataxia, noting that neither case involved GAD65 antibody cerebellar ataxia. And she carefully reviewed each relevant article cited by Dr. Simpson, and explained in detail why it was not supportive of vaccine causation.

Lastly, case law is scant. There are only two Vaccine Act cases involving GAD65 antibodies. In Agarwal, Petitioners alleged their minor child sustained an injury of autoimmune limbic encephalitis (“ALE”) with associated GAD65 antibodies following tetanus-diphtheria- acellular pertussis and meningococcal vaccinations, followed three days later by fever. Agarwal ex rel. R.A. v. Sec’y of Health & Hum. Servs., No. 16-191V, 2020 WL 5651683, at *1, *3 (Fed. Cl. Spec. Mstr. Aug. 31, 2020). Seven to eight days after vaccination, she had a generalized tonic-clonic seizure, requiring EMS transport and hospitalization. Id. at *4. That same evening, the child developed status epilepticus, and was ultimately diagnosed with ALE with residual effects of intractable epilepsy and cognitive deficits. Id. at *4-*7. Petitioner’s expert asserted that the vaccines induced an inflammatory response that led to fever and seizures, that there is an overlapping mechanism of fever and inflammation in epileptogenesis, and that the causal mechanism specific to vaccine causation was a cytotoxic T-cell mediated process. Id. at *30. Respondent’s expert agreed that autoimmunity could occur in seven days. Id. at *31. The special master granted entitlement to compensation. Id. at *32. Given the different facts, a clear onset of febrile seizure following different vaccinations, a different diagnosis, and different expert opinions, the findings in Agarwal cannot be extrapolated to this case.

The other case involving GAD65 antibodies is Althaus, which was decided by the undersigned. Althaus v. Sec’y of Health & Hum. Servs., No. 18-1868V, 2026 WL 687262, at (Fed. Cl. Spec. Mstr. Feb. 10, 2026). It involved the diagnosis of autoimmune cerebellar visual syndrome with associated GAD65 antibodies. Id. at *9, *20. Petitioner had onset of double vision/distorted vision in her left eye the day after vaccination. Id. at *23-24. She tested positive for insulinoma-associated-2 (“IA-2”) antibodies and insulin auto-antibodies (“IAA”), and was diagnosed with latent autoimmune diabetes in adults. Id. at *6, *8. Molecular mimicry was advanced as the causal theory by Petitioner. Id. at *20. Respondent’s expert, Dr. Bouffard, opined that Petitioner was positive for the “GAD65 antibody with an extremely high titer thought to be pathogenic by her neuro-ophthalmologist.” Id. at *14 (internal quotation marks omitted). Further, onset within a day of vaccination was too short to implicate molecular mimicry. Id. at *21. Compensation was denied primarily based on Althen prong three because a one-day onset was too quick to implicate the adaptive immune system and molecular mimicry. Id. at *21-28.

Thus, there is no caselaw supporting a finding that the flu vaccine can cause GAD65 cerebellar ataxia.

For all of these reasons, the undersigned finds that Petitioner has failed to offer a sound and reliable mechanism to explain how the flu vaccine can cause GAD65 cerebellar ataxia.

B. Althen Prong Two Under Althen prong two, Petitioner must prove by a preponderance of the evidence that there is a “logical sequence of cause and effect showing that the vaccination was the reason for the injury.” Capizzano, 440 F.3d at 1324 (quoting Althen, 418 F.3d at 1278). “Petitioner must show that the vaccine was the ‘but for’ cause of the harm . . . or in other words, that the vaccine was the ‘reason for the injury.’” Pafford, 451 F.3d at 1356 (internal citations omitted).

In evaluating whether this prong is satisfied, the opinions and views of the vaccinee’s treating physicians are entitled to some weight. Andreu, 569 F.3d at 1367; Capizzano, 440 F.3d at 1326 (“[M]edical records and medical opinion testimony are favored in vaccine cases, as treating physicians are likely to be in the best position to determine whether a ‘logical sequence of cause and effect show[s] that the vaccination was the reason for the injury.’” (quoting Althen, 418 F.3d at 1280)). Medical records are generally viewed as trustworthy evidence, since they are created contemporaneously with the treatment of the vaccinee. Cucuras, 993 F.2d at 1528. Petitioner need not make a specific type of evidentiary showing, i.e., “epidemiologic studies, rechallenge, the presence of pathological markers or genetic predisposition, or general acceptance in the scientific or medical communities to establish a logical sequence of cause and effect.” Capizzano, 440 F.3d at 1325. Instead, Petitioner may satisfy her burden by presenting circumstantial evidence and reliable medical opinions. Id. at 1325-26.

Since Petitioner failed to prove Althen prong one, it follows that she cannot prove Althen prong two. However, even if Petitioner had proven Althen prong one, the undersigned finds there is not preponderant evidence in the record to support a logical sequence of cause-and-effect showing the October 11, 2015 flu vaccine to be the cause of Petitioner’s cerebellar ataxia. See Althen, 418 F.3d at 1278.

In determining whether Petitioner has established a prima facia case, and as related to Althen prong two, the undersigned finds it relevant to consider “evidence of other possible sources of injury” in determining “whether a prima facie showing has been made that the vaccine was a substantial factor in causing the injury in question.” Stone, 676 F.3d at 1379. “In asserting an off-Table injury, [Petitioner] need[s] to show, by preponderant evidence, that [the] vaccination was a substantial factor” in causing the alleged vaccine injury. Winkler v. Sec’y of Health & Hum. Servs., 88 F.4th 958, 962 (Fed. Cir. 2023). Petitioner “[does] not need to show that [Mr. Gelardi] did not suffer from an infection, or that said infection did not contribute to [the alleged injury]. Nor [does] [she] have to show that the vaccination was the only cause of [Mr. Gelardi’s] [vaccine-related illness].” Id.; see also Walther v. Sec’y of Health & Hum. Servs., 485 F.3d 1146, 1149-52 (Fed. Cir. 2007) (finding a petitioner does not bear the burden of eliminating alternative independent potential causes). Thus, the undersigned considers evidence relating to the association between GAD65 antibodies and Petitioner’s alleged vaccine-related illness (cerebellar ataxia), as “[s]uch contemplation of a potential causative agent when evaluating whether or not a petitioner has established a prima facie case is in accordance with the law.” Winkler, 88 F.4th at 963; see also Flores, 115 Fed. Cl. at 162-63 (“[T]he special master may consider the evidence presented by the [R]espondent in determining whether the [P]etitioner has established a prima facie case.”).

The treating physician who made the diagnosis of cerebellar ataxia did not relate the condition to Mr. Gelardi’s flu vaccination. When Dr. Stafford initially evaluated Mr. Gelardi in March 2019, a complete history of his illness was documented, including that Mr. Gelardi had received the flu vaccination prior to the onset of dizziness. Dr. Stafford completed a diagnostic workup that included antibody testing which revealed elevated anti-GAD65 antibodies. Dr. Stafford’s diagnosis was “[s]ubacute ataxia with onset in October 2015 that is of an uncertain mechanism.” Pet. Ex. 16 at 18, 24. Dr. Stafford did not attribute Mr. Gelardi’s cerebellar ataxia to his flu vaccination.

Generally, treating physician statements are typically “favored” as treating physicians “are likely to be in the best position to determine whether a ‘logical sequence of cause and effect show[s] that the vaccination was the reason for the injury.’” Capizzano, 440 F.3d at 1326 (quoting Althen, 418 F.3d at 1280). However, no treating physician’s views bind the special master, per se; rather, their views are carefully considered and evaluated. § 13(b)(1); Snyder, 88 Fed. Cl. at 746 n.67. “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.” Welch v. Sec’y of Health & Hum. Servs., No. 18-494V, 2019 WL 3494360, at *8 (Fed. Cl. Spec. Mstr. July 2, 2019). Here, Dr. Stafford documented a complete history, including the subject flu vaccination, and did not relate Mr. Gelardi’s condition to vaccination.

Respondent’s experts opined that Mr. Gelardi’s had not only GAD65 antibody cerebellar ataxia but that he also had GAD65 antibodies associated with diabetes. Dr. Chaudhry cited Kumar and Subhakumari, who identified the criteria for establishing a diagnosis of latent autoimmune diabetes in adults. These criteria included age of 30 years or older, positive results for at least one of four pancreatic antibodies (one of which was GAD65 antibodies), and no treatment with insulin in the first six months after diagnosis. Mr. Gelardi satisfied all these criteria. Dr. Chaudhry explained that about 80% of patients with GAD-antibody ataxia have concomitant organ specific autoimmune disorders, including diabetes. Diabetes usually begins several years before the onset of ataxia. Here, Mr. Gelardi’s clinical course is consistent with GAD65 antibody-associated diabetes and cerebellar ataxia.

Dr. Piquet also explained that GAD65 cerebellar ataxia is well known to co-exist with diabetes. Dr. Piquet cited Rakocevic et al., who explain that GAD65 antibody autoimmune cerebellar ataxia is associated with other autoimmune conditions such as diabetes.

In summary, the undersigned finds that Mr. Gelardi’s treating physician did not offer support for vaccine causation of his cerebellar ataxia, and that Mr. Gelardi met the criteria for latent autoimmune diabetes in adults associated with GAD65 autoimmunity. These findings, along with the findings regarding onset described below, do not support a conclusion that there is preponderant evidence of a logical sequence of cause and effect. Therefore, the undersigned finds that Petitioner has failed to prove Althen prong two by preponderant evidence.

C. Althen Prong Three Althen prong three requires Petitioner to establish a “proximate temporal relationship” between the vaccination and the injury alleged. Althen, 418 F.3d at 1281. That term has been defined as a “medically acceptable temporal relationship.” Id. Petitioner must offer “preponderant proof that the onset of symptoms occurred within a time frame for which, given the medical understanding of the disorder’s etiology, it is medically acceptable to infer causation-in-fact.” de Bazan, 539 F.3d at 1352. The explanation for what is a medically acceptable time frame must also be consistent with the theory of how the relevant vaccine can cause the injury alleged (under Althen Prong One). Id.; Koehn v. Sec’y of Health & Hum. Servs., 773 F.3d 1239, 1243 (Fed. Cir. 2014); Shapiro, 101 Fed. Cl. at 542; see Pafford, 451 F.3d at 1358.

Since Petitioner failed to prove Althen prong one, it follows that she cannot prove Althen prong three. In addition, there are independent reasons why the undersigned finds Petitioner failed to prove Althen prong three.

Petitioner received the flu vaccine at issue on October 11, 2015.

Regarding the onset of Mr. Geraldi’s GAD65 cerebellar ataxia, Petitioner’s expert, Dr. Simpson opined that neurological symptoms of dizziness, poor balance, and subjective weakness began three weeks after vaccination, and that this onset was appropriate for an autoimmune mechanism. However, Dr. Simpson did not offer a mechanism to explain how the flu vaccine could induce GAD65 autoimmune cerebellar ataxia, and thus, he cannot prove Althen prong three.

Moreover, there are several problems with Dr. Akbari’s opinions related to onset. First, he opined that neuropathy was the initial manifestation of Mr. Gelardi’s cerebellar ataxia. He opined that the development of Mr. Gelardi’s neuropathy was consistent with what is known about the timing of neuropathy resulting from vaccination. However, Mr. Gelardi’s treating doctors attributed his neuropathy to his diabetes and not to his GAD65 cerebellar ataxia. See, e.g., Pet. Ex. 8 at 4-5 (Dr. Hamilton attributing Mr. Gelardi’s signs of length-dependent neuropathy to “his poorly controlled diabetes”); Pet. Ex. 16 at 24 (Dr. Stafford commenting that Mr. Gelardi’s demyelinating EMG findings “could be accounted for by his diabetes”).

Dr. Akbari attempts to distinguish neuropathy caused by diabetes from neuropathy due to autoimmune cerebellar ataxia. For diabetic neuropathy, Dr. Akbari opined that nerve function deteriorates over a long period of time due to the prolonged effect of elevated blood sugar on nerves. In contrast, he explained that ataxia due to autoimmune cerebellar ataxia has a more rapid onset of days to weeks. However, since Mr. Gelardi’s physicians attributed his neuropathy to diabetes, and not his GAD65 cerebellar ataxia, the undersigned finds Dr. Akbari’s opinion is inconsistent with the medical record evidence. Further, because he is not a medical doctor or clinician, and does not diagnosis or treat patients in general or like Mr. Gelardi, his opinion on symptoms related to disease presentation specific to GAD65 autoimmune cerebellar ataxia is less persuasive than that expressed by treating physicians or the expert neurologists. See Koehn, 2013 WL 3214877, at *32 (“In weighing the persuasiveness of opinion testimony, special masters may consider the relative expertise of the witness.”); Dwyer, 2010 WL 892250, at *64 (giving greater weight to M.D. epidemiologists’ opinions on medical issues than to Ph.D. epidemiologist’s opinion); Pafford, 451 F.3d at 1359 (affirming the special master’s rejection of expert’s testimony because he lacked proper qualifications in the specialty areas in which he testified).

Even if one assumed that neuropathy was related to cerebellar ataxia, onset is not clear. Mr. Gelardi had sensory abnormalities prior to vaccination. One month prior to vaccination, in September 2015, Dr. Kraeher documented that he had an abnormal sensory examination due to decreased vibratory sensation of the left foot. This was noted again on January 6, 2016 when Dr. Dompenciel documented an abnormal sensory examination, specifically “[b]lunted to pin-prick, light touch, and vibration . . . in the distal lower extremities.” Pet. Ex. 3 at 1. On January 28, 2016, Dr. Dompenciel questioned whether Mr. Gelardi had peripheral neuropathy. EMG performed on February 18, 2016 revealed mild motor demyelinating peripheral neuropathy. As noted above, both Dr. Hamilton and Dr. Stafford attributed Mr. Gelardi’s peripheral neuropathy to his diabetes. Thus, while Mr. Gelardi had abnormal sensory examinations prior to vaccination, it was not until January 2016 that peripheral neuropathy is documented and February 2016 that an EMG showed mild motor demyelinating neuropathy. Therefore, based on the medical records, sensory abnormalities began before vaccination and peripheral neuropathy was noted January 28, 2016, three months after vaccination. Dr. Akbari did not offer an onset date or time frame for the onset of Mr. Gelardi’s neuropathy, or note the medical record evidence related to sensory and/or motor neuropathy. He did not explain the relationship between onset of neuropathy after vaccination or how such onset was appropriate given his theories of causation.

Therefore, the undersigned finds that Dr. Akbari did not offer preponderant evidence to support Althen prong three.

Respondent’s expert, Dr. Chaudhry, provided opinions and medical literature related to GAD65 autoimmune diabetes. Dr. Piquet opined that Mr. Gelardi had subclinical GAD65 antibody autoimmune cerebellar ataxia prior to vaccination. Her opinion is based on the medical records showing Mr. Gelardi had a significant worsening of his diabetes in the summer of 2015. Mr. Gelardi’s diagnosis was well controlled in 2014 (A1c ranged from 6.7 to 6.9); however, in 2015, Mr. Gelardi’s A1c increased to 9.8 in June 2015 and 12.3 in August 2015. According to Dr. Piquet, the worsening of Mr. Gelardi’s diabetes in the summer of 2015 heralded the onset of his GAD65 autoimmunity. Further, Dr. Piquet noted that the prodromal syndrome characterized by elevated A1c prior to the onset of neurological illness is not noncommon in patients with GAD65. Both Dr. Chaudhry and Dr. Piquet cited medical literature to support their opinions. See, e.g., Resp. Ex. C, Tab 5 at 3 (noting about 80% of GAD-antibody cerebellar ataxia patients have “concomitant organ specific autoimmune disorders,” including diabetes, which “usually precede the onset of ataxia by several years”); Resp. Ex. D, Tab 5 at 6 (“A personal history of [Type 1 diabetes mellitus] is present in about half of cases . . . and it usually precedes neurological manifestations.”).

As described by Dr. Piquet, Mr. Gelardi’s abrupt increase in his A1c in June and August 2015 was “highly suspicious for the onset of [Mr. Gelardi’s] autoimmunity.” Resp. Ex. D at 4. Dr. Piquet concluded that Mr. Gelardi’s GAD65 autoimmunity began in the summer of 2015, prior to his October 11, 2015 vaccination, although he did not have objective evidence of cerebellar ataxia until February 2016 when he had diplopia.

The medical records show that on August 12, 2015, Dr. DeLucia documented that Mr. Gelardi’s diabetes was worsening and uncontrolled. Dr. DeLucia assessed Mr. Gelardi as insulin deficient and referred him to an endocrinologist, Dr. Kraeher, who saw Mr. Gelardi the very same day. Dr. Kraeher prescribed insulin that day, August 12. Thereafter, Mr. Gelardi’s records show that Dr. Kraeher continued to prescribe insulin for treatment of Mr. Gelardi. Thus, Mr. Gelardi met the criteria for latent autoimmune adult diabetes. Dr. Chaudhry and Dr. Piquet together provide a persuasive opinion supported by medical literature that Mr. Gelardi’s clinical course of uncontrolled diabetes heralded the onset of his autoimmunity by summer 2015, prior to vaccination.

Based on Dr. Chaudhry’s and Dr. Piquet’s opinions, supportive medical literature, and the medical records, the undersigned finds by preponderant evidence that the onset of Mr. Gelardi’s GAD65 autoimmune diabetes occurred in the summer of 2015, prior to his vaccination.

The onset of Mr. Gelardi’s GAD65 cerebellar ataxia is more difficult to determine. Dr. Simpson places onset at three weeks after vaccination. On October 23, 2015, Dr. Kraeher noted that Mr. Gelardi had some intermittent lightheadedness. More than six weeks after vaccination, on November 24, 2015, Mr. Gelardi complained of dizziness (for about one month), loss of balance, lightheadedness, and unsteadiness as documented by Dr. DeLucia. Neurological examination by Dr. DeLucia on December 1, 2015, was normal; Dr. DeLucia specifically noted that Mr. Gelardi’s “cerebellar function” was normal. Pet. Ex. 2 at 33. On January 6, 2016, Mr. Gelardi saw neurologist Dr. Dompenciel, and at that visit, he reported balance issues. However, on examination, Mr. Gelardi had normal strength in both legs and no ataxia, although he did have a cautious gait. Mr. Gelardi became ill with diverticulitis and was hospitalized on January 21, 2016. The following week, January 26, 2016, Mr. Gelardi’s dizziness was worse, and he had fallen twice. In February 2016, Mr. Gelardi was diagnosed with significant high-grade stenosis of the left internal carotid artery. On February 18, 2016, he had double vision.

Dr. Piquet opined that the onset of Mr. Geraldi’s cerebellar disease was difficult to determine because there was no objective evidence of it until he developed diplopia in February 2016. In hindsight, she agreed the symptoms Mr. Gelardi complained about on November 24, 2015, including dizziness, loss of balance, lightheadedness, and unsteadiness documented by Dr. DeLucia, may have been manifestations of his autoimmune neurological disease.

However, assuming the onset of symptoms (dizziness, loss of balance, lightheadedness, and unsteadiness) represented the onset of Mr. Geraldi’s GAD65 cerebellar ataxia, and that these symptoms began approximately three weeks after vaccination, the undersigned does not find that Petitioner has proven Althen prong three, since Petitioner has failed to prove Althen prongs one and two. That is, Petitioner failed to prove by preponderant evidence that the flu vaccine can cause GAD65 cerebellar ataxia or did cause Mr. Gelardi’s GAD65 cerebellar ataxia, and thus, cannot prove prong three by preponderant evidence.

Therefore, the undersigned finds by preponderant evidence that Mr. Gelardi’s GAD65 autoimmunity began in summer 2015 when his diabetes worsened, and he became insulin dependent, and the onset of his GAD65 cerebellar ataxia may have been characterized by dizziness, loss of balance, lightheadedness, and loss of balance, but was not caused by the flu vaccination he received on October 11, 2015.

V. CONCLUSION

The undersigned extends her sympathy to Petitioner for all of the problems that Mr. Gelardi suffered due to his neurological condition. The undersigned’s Decision, however, cannot be decided based upon sympathy, but rather on the evidence and law.

For the reasons discussed above, the undersigned finds that Petitioner has failed to establish by preponderant evidence that the flu vaccination Mr. Gelardi received caused him to develop the neurological condition at issue. Therefore, Petitioner is not entitled to compensation, and the petition must be dismissed.

In the absence of a timely filed motion for review pursuant to Vaccine Rule 23, the Clerk of Court SHALL ENTER JUDGMENT in accordance with this Decision.

IT IS SO ORDERED. s/Nora Beth Dorsey Nora Beth Dorsey Special Master