Galeno v. Secretary of Health and Human Services

Opinion

In the United States Court of Federal Claims OFFICE OF SPECIAL MASTERS Filed: July 9, 2026

* * * * * * * * * * * * * * * MARIE GALENO, *

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Petitioner, * No. 21-824V

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v. * Special Master Young

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SECRETARY OF HEALTH * AND HUMAN SERVICES, *

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Respondent. * * * * * * * * * * * * * * * * Laura Levenberg, Muller Brazil, Dresher, PA, for Petitioner. Tyler King, U.S. Department of Justice, Washington, DC, for Respondent.

DECISION ON ENTITLEMENT 1

On January 29, 2021, Maria Galeno (“Petitioner”) filed a petition for compensation in the National Vaccine Injury Compensation Program (“the Program”). 2 Pet., ECF No. 1. Petitioner alleged that she suffered from “small fiber neuropathy [(“SFN”) 3] resulting from the adverse effects of the influenza [(“flu”)] vaccination [she] received on February 7, 2018.” Id.

A careful analysis and weighing of all the evidence and testimony presented in this case in accordance with the applicable legal standards 4 reveals that Petitioner has failed to provide

1 Because this Decision contains a reasoned explanation for the action taken in this case, it must be made publicly accessible and will be posted on the United States Court of Federal Claims’ website, and/or at https://www.govinfo.gov/app/collection/uscourts/national/cofc, in accordance with the E-Government Act of 2002. 44 U.S.C. § 3501 note (2018) (Federal Management and Promotion of Electronic Government Services). This means the Decision will be available to anyone with access to the internet. In accordance with Vaccine Rule 18(b), Petitioner has 14 days to identify and move to redact medical or other information, the disclosure of which would constitute an unwarranted invasion of privacy. If, upon review, I agree that the identified material fits within this definition, I will redact such material from public access. 2 National Childhood Vaccine Injury Act of 1986, Pub L. No. 99-660, 100 Stat. 3755 (“the Vaccine Act” or “Act”). Hereinafter, for ease of citation, all “§” references to the Vaccine Act will be to the pertinent subparagraph of 42 U.S.C. § 300aa (2018). 3 SFN is “a type of neuropathy in which only the small sensory cutaneous nerves are affected.” Small Fiber Neuropathy, DORLAND’S MED. DICTIONARY ONLINE, https://www.dorlandsonline.com/dorland/ definition?id=137479 (hereinafter, “DORLAND’S”). 4 While I have reviewed all of the information filed in this case, only those filings and records that are most relevant to the decision will be discussed. Moriarty v. Sec’y of Health & Hum. Servs., 844 F.3d 1322, 1328 (Fed. Cir. 2016) (“We generally presume that a special master considered the relevant record

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preponderant evidence that her flu vaccine caused her to suffer from SFN. Accordingly, Petitioner is not entitled to an award of compensation.

I. Procedural History

On January 29, 2021, Petitioner filed her petition and medical records. Pet., Pet’r’s Exs. 1– 12, ECF No. 1. She later filed a statement of completion on February 22, 2021. ECF No. 7. Petitioner filed additional medical records on August 2, 2021. Pet’r’s Exs. 13–15, ECF No. 13. Respondent filed his Rule 4(c) Report, opposing compensation, on January 4, 2022. Resp’t’s Rep., ECF No. 16.

Petitioner filed an expert report from John Hixson, M.D., along with his curriculum vitae (“CV”) and supporting medical literature on October 3, 2022. Pet’r’s Exs. 16–28, ECF No. 20. Respondent filed responsive expert reports from Brian Callaghan, M.D., and Robert Fujinami, Ph.D., along with their CVs and supporting medical literature on January 31, 2023. Resp’t’s Exs. A–D (Resp’t’s Ex. A, Tabs 1–2, Resp’t’s Ex. C, Tabs 1–6), ECF No. 22. On September 19, 2023, Petitioner filed an expert report and CV from Omid Akbari, Ph.D., and supporting medical literature. Pet’r’s Exs. 29–75, ECF No. 23. Respondent filed a responsive report and medical literature from Dr. Fujinami on February 14, 2024. Resp’t’s Ex. E (Tabs 1–11), ECF No. 25. Petitioner filed a responsive report from Dr. Akbari and medical literature on May 13, 2024. Pet’r’s Exs. 76–103, ECF No. 26. Respondent filed a final supplemental report from Dr. Fujinami on July 22, 2024. Resp’t’s Ex. F, ECF No. 28.

On September 30, 2024, Petitioner filed a motion for a ruling on the record. Pet’r’s Mot., ECF No. 31. Respondent filed his response on November 13, 2024, and Petitioner filed her reply on December 12, 2024. Resp’t’s Response, ECF No. 33; Pet’r’s Reply, ECF No. 35.

This matter is now ripe for consideration.

II. Factual Background 5

On February 7, 2018, Petitioner received the subject flu vaccine at a CVS Pharmacy. Pet’r’s Ex. 1 at 7. Two days later, on February 9, 2018, Petitioner presented to an urgent care facility with complaints of body aches, arm pain, tingling in her fingers, chest heaviness, difficulty sleeping, and a low-grade fever of 99º Fahrenheit following her receipt of the flu vaccine. Pet’r’s Ex. 4 at 10. She reported that the symptoms began the day prior, on February 8, 2018. Id. Dr. Raffi Zohrabian performed a rapid flu test, which was negative, and listed “immune reaction to the [flu] vaccine” as Petitioner’s diagnosis. Id. at 11. Petitioner was discharged with instructions to take Tylenol and rest for two days. Id.

evidence even though he does not explicitly reference such evidence in his decision.”) (citation omitted); see also Paterek v. Sec’y of Health & Hum. Servs., 527 F. App’x 875, 884 (Fed. Cir. 2013) (“Finding certain information not relevant does not lead to—and likely undermines—the conclusion that it was not considered.”). 5 Petitioner did not file an affidavit in this case.

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The next day, February 10, 2018, Petitioner presented to the North Shore University Hospital emergency department (“NSUH ED”) with complaints of right arm pain, swelling, and numbness since her flu shot. Pet’r’s Ex. 5 at 26–27. Petitioner reported experiencing “myalgias/chest pressure” and pain radiating down her right arm that was worse with neck movement, as well as tingling throughout her entire body. Id. at 36. She was also noted to have a history of multiple cervical disc herniations. Id. Her providing nurse observed that Petitioner’s flu vaccine injection site was “bruised, swollen, and tender.” Id. at 27. Petitioner’s physical examination produced a positive spurling test and positive trapezius trigger points to her trapezius, scapula, and deltoid. Id. at 37. Her neurological examination produced no focal neurological deficits and showed normal strength and intact sensation. Id. The attending physician, Dr. Stephen Strasberg, opined that Petitioner’s symptoms were “possibly related to [a] reaction to [the] vaccine,” but that it was “likely radicular pain from [the] neck with cervical herniations,” and discharged her home. Id. at 38.

Petitioner presented for a neurological consultation with neurologist Slavina Gardella on February 12, 2018. Pet’r’s Ex. 6 at 3. Petitioner reported experiencing numbness and tingling in her right arm following her receipt of the flu vaccine, which progressed to involve her left arm, tips of her fingers, both feet, and pain and weakness in all four extremities. Id. On examination, Dr. Gardella noted Petitioner had fully preserved strength and +2 deep tendon reflexes (“DTRs”), though her “[s]ensory exam[ination was] somewhat scattered” and not consistent with any anatomical or neurological distribution. Id. Dr. Gardella’s differential diagnosis included “post vaccine demyelinating process involving either the central or peripheral nervous system [(“PNS”)].” Id. at 4. Dr. Gardella ordered magnetic resonance imaging (“MRI”) of Petitioner’s brain and cervical spine, testing for brain auditory evoked response (“BAER”) and visual evoked response (“VER”), and an electromyogram (“EMG”) and nerve conduction study (“NCS”) to further investigate her symptoms. Id. Petitioner’s brain MRI, BAER, VER, and EMG/NCS were all normal. Id. at 5–20. Petitioner’s spinal MRI showed mild degenerative disc changes, mild disc bulging, facet and unconvertebral joint hypertrophy, and no focal cervical cord lesion. Id. at 21.

On March 8, 2018, Petitioner presented to neurologist Anthony Geraci for a consultation.

Pet’r’s Ex. 12 at 10. In her history Petitioner reported that she began to experience pain in her arm the day after receiving the flu vaccine, which later developed into tingling the night of February 8, 2018. Id. She currently was experiencing tingling in her arms and hands, but not forearms, and occasionally in her abdomen. Id. She also reported weakness in her hands and legs and pain in her lower back and shoulders. Id. On examination, Dr. Geraci observed Petitioner retained full strength in all extremities and that her sensations for light touch, vibration, and proprioception were intact. Id. at 11. Dr. Geraci opined that Petitioner’s symptoms were “not due to any serious neurological condition,” but noted she may have a mild sensory neuropathy that would continue to improve. Id. He offered to repeat Petitioner’s EMG if her symptoms did not improve in six weeks. Id.

Petitioner underwent additional EMG testing on May 31, 2018, with neurologist Vivian Chin. Pet’r’s Ex. 7 at 43. Her physical examination prior to testing showed intact senses, normal strength, and +2 reflexes. Id. Her EMG found no evidence of a large fiber neuropathy, focal mononeuropathy, 6 or myopathy, 7 though it did present findings suggestive of chronic right cervical

6 A mononeuropathy is “a disease affecting a single nerve.” Mononeuropathy, DORLAND’S.

7 Myopathy is “any disease of a muscle.” Myopathy, DORLAND’S.

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and lumbar radiculopathy. 8 Id. The technician noted that the techniques used could not assess the presence of a SFN. Id.

Petitioner presented to rheumatologist Bruce Stein on September 27, 2018, for complaints of joint pain. Pet’r’s Ex. 10 at 4. She reported experiencing joint pain, migratory joint pain, and joint stiffness in all four extremities, which began “months ago” after her February 2018 flu vaccine. Id. Dr. Stein did not observe any signs of inflammation during Petitioner’s examination. Id. at 4–5. His assessment was fibromyalgia 9 and noted Petitioner had a positive depression screening. Id. at 5. He recommended further labs to investigate and noted that Petitioner was scheduled to undergo a nerve biopsy. Id.

Petitioner completed an epidermal nerve fiber biopsy of her right thigh and ankle on October 3, 2018. Pet’r’s Ex. 7 at 98. Both biopsies revealed “significantly low epidermal nerve fiber density.” Id. at 99. Petitioner followed up with Dr. Chin to discuss the results of her biopsy on October 24, 2018. Pet’r’s Ex. 11 at 10. Dr. Chin explained that Petitioner’s biopsy confirmed a diagnosis of SFN and that her labs were unrevealing for an etiology. Id. Petitioner reported that she continued to experience numbness, paresthesias, 10 temperature dysregulation, and throbbing headaches. Id. Dr. Chin noted that Petitioner’s SFN was “idiopathic for now,” ordered additional bloodwork, and recommended Petitioner start Cymbalta for treatment. Id. at 11.

On November 29, 2018, Petitioner presented to neurologist Stephen Roth for a consultation. Pet’r’s Ex. 7 at 29. In her history Petitioner reported a one-day onset of numbness and tingling following her flu vaccination. Id. “Since that time, she has had intermittent shooting pains in her legs and arms bilaterally,” as well as intermittent numbness throughout her body. Id. Petitioner’s physical and neurological examinations were normal. Id. at 30–31. Dr. Roth’s assessment confirmed Petitioner’s SFN from her nerve biopsy, but noted that that Petitioner suffered from a “[c]onstellation of symptoms[,] including widespread pain, paresthesias, dry eyes/mouth, dizziness, rash, fatigue, weakness, photosensitivity, headaches, and tachycardia since receiving the flu shot,” which he stated did not conform with a unifying diagnosis. Id. at 31–32. Dr. Roth ordered MRI scans of Petitioner’s brain, cervical spine, and thoracic spine, and recommended Petitioner present for an evaluation with the rheumatology department. Id. Petitioner’s spinal MRIs revealed minor degenerative changes and her brain MRI was normal. Id. at 47–51.

Petitioner followed up with Dr. Roth on January 15, 2019, and reported new onset pain behind her eyes, in addition to her other symptoms. Pet’r’s Ex. 7 at 25. In his assessment, Dr. Roth noted that due to Petitioner’s constellation of symptoms there was “some consideration given to a post-vaccination inflammatory reaction similar to Guillain-Barré Syndrome [(“GBS”) 11].” Id. at

8 Radiculopathy is a “disease of the nerve roots, such as from inflammation or impingement by a tumor or a bony spur.” Radiculopathy, DORLAND’S. 9 Fibromyalgia is “pain and stiffness in the muscles and joints that either is diffuse or has multiple trigger points.” Fibromyalgia, DORLAND’S. 10 Paresthesia is “an abnormal touch sensation, such as burning, prickling, or formication, often in the absence of an external stimulus.” Paresthesia, DORLAND’S. 11 GBS is a “rapidly progressive ascending motor neuron paralysis of unknown etiology, frequently seen after an enteric or respiratory infection.” Guillain-Barré Syndrome, DORLAND’S.

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27. However, he opined that it was “[u]nclear” whether Petitioner’s SFN was the result of this “possible post[-]inflammatory reaction.” Id. He referred Petitioner to rheumatology and neuroophthalmology , prescribed 300 mg of gabapentin twice daily, and ordered magnetic resonance angiography (“MRA”) of Petitioner’s brain to rule out vasculitis. 12 Id. at 27–28. Her brain MRA, completed on March 8, 2019, was unremarkable. Id. at 41.

Petitioner returned to Dr. Roth on June 19, 2019, and reported “no significant changes with respect to her condition.” Pet’r’s Ex. 7 at 13. Her prior reported symptoms of numbness, tingling, and chest discomfort continued, and she reported experiencing a new onset of dizziness. Id. Dr. Roth’s overall assessment of Petitioner remained the same, with the addition of “[a]nisocoria,[13] possibly secondary to [her SFN].” Id. at 15. Dr. Roth recommended Petitioner begin establishing care with a neuromuscular specialist to see whether she needed further specialized testing and instructed her to return in two months. Id. at 15–16.

Petitioner presented to neurologist Shanna Peterson on July 16, 2019, for “evaluation of [SFN] with possible associated autonomic symptoms.” Pet’r’s Ex. 15 at 6. Petitioner reported that two days after receiving the flu vaccine she began to experience tingling in both feet, which progressed up her legs and later developed into her arms and hands. Id. Petitioner also reported a recent onset of dizziness. Id. Dr. Peterson reviewed Petitioner’s prior medical records, to include her EMG and skin biopsy results, and concluded she suffered from an “[i]diopathic [SFN].” Id. at 8. She also opined that Petitioner’s recent dizziness may be a “possible component of orthostatic intolerance[] and dehydration.” Id. Petitioner was referred for autonomic testing and advised to drink more water. Id. at 9.

On August 15, 2019, Petitioner returned to Dr. Roth for a follow-up. Pet’r’s Ex. 7 at 9.

Petitioner reported that since her last visit she was evaluated by Dr. Peterson, who she stated was evaluating her for postural orthostatic tachycardia syndrome (“POTS”). 14 Id. She reported no new symptoms and no changes in her current symptoms. Id. Dr. Roth recommended Petitioner return in three months. Id. at 11.

Petitioner returned to Dr. Roth on October 15, 2019, with complaints of new onset right arm and shoulder pain for two weeks. Pet’r’s Ex. 7 at 5. Petitioner reported the pain would radiate from the right side of her neck into her shoulder and arm, and reported associated weakness with the pain. Id. Dr. Roth assessed her new symptoms to be cervical radiculopathy versus peripheral nerve entrapment and recommended an MRI and EMG to investigate. Id. at 7. Petitioner’s MRI of her cervical spine was completed on October 23, 2019, and showed no changes since her prior MRI in December 2018. Id. at 38. Petitioner’s EMG was completed on November 18, 2019, and revealed evidence of a mild cervical radiculopathy. Id. at 33.

12 Vasculitis is the “inflammation of a blood or lymph vessel.” Vasculitis, DORLAND’S. 13 Anisocoria is “inequality in diameter of the pupils.” Anisocoria, DORLAND’S. 14 POTS is “a group of symptoms . . . that sometimes occur when a person assumes an upright position, including tachycardia, tremulousness, lightheadedness, sweating, and hyperventilation.” Postural Orthostatic Tachycardia Syndrome, DORLAND’S.

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Petitioner followed up with Dr. Roth again on November 12, 2019, and reported improvement of her right arm pain. Pet’r’s Ex. 7 at 1. Dr. Roth recommended Petitioner begin physical therapy and instructed her to return again in three months. Id.

On September 4, 2020, Petitioner presented to urologist Toby Handler for urinary incontinence. Pet’r’s Ex. 9 at 22. Petitioner reported her symptoms as “gradual and . . . occurring for years.” Id. Petitioner also stated that “following her flu vaccine[] she was left with a[n] autonomic nerve neuropathy which affected her urination.” Id. Petitioner later underwent autonomic nerve testing on April 9, 2021, at Mount Sinai Hospital, which found reduced sweat volume in the proximal and distal leg and worsened baseline hypertension in an upright position suggestive of a hyperadrenergic state. Pet’r’s Ex. 14 at 2. Neurologist Bridget Mueller opined that Petitioner’s reduced sweat response “may indicate a patchy small fiber autonomic neuropathy,” but also noted it could also be “an anti-cholinergic side effect of amitriptyline.” Id.

No other relevant medical records were filed.

III. Applicable Legal Standards

To receive compensation under the Vaccine Act, a petitioner must demonstrate either that:

(1) the petitioner suffered a “Table injury” by receiving a covered vaccine and subsequently developing a listed injury within the timeframe prescribed by the Vaccine Injury Table set forth at 42 U.S.C. § 300aa-14, as amended by 42 C.F.R. § 100.3; or (2) that petitioner suffered an “off- Table injury,” one not listed on the Table, as a result of his receiving a covered vaccine. See 42 U.S.C. §§ 300aa-11(c)(1)(C); Moberly v. Sec’y of Health & Hum. Servs., 592 F.3d 1315, 1321 (Fed. Cir. 2010); Capizzano v. Sec’y of Health & Hum. Servs., 440 F.3d 1317, 1319-20 (Fed. Cir. 2006). Petitioner does not allege a Table injury in this case. Thus, she must prove that her injury was caused-in-fact by a Table vaccine.

To establish causation-in-fact, a petitioner must demonstrate by a preponderance of the evidence that the vaccine was the cause of the injury. 42 U.S.C. § 300aa-13(a)(1)(A). A petitioner is required to prove 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 1321–22 (quoting Shyface v. Sec’y of Health & Hum. Servs., 165 F.3d 1344, 1352–53 (Fed. Cir. 1999)).

In the seminal case of Althen v. Sec’y of the Dept. of Health & Hum. Servs, the Federal Circuit set forth a three-pronged test used to determine whether a petitioner has established a causal link between a vaccine and the claimed injury. See 418 F.3d at 1278–79. The Althen test requires petitioners to set forth: “(1) a medical theory causally connecting the vaccination and the injury; (2) a logical sequence of cause and effect showing that the vaccination was the reason for the injury; and (3) a showing of a proximate temporal relationship between vaccination and injury.” Id. at 1278. To establish entitlement to compensation under the Program, a petitioner is required to establish each of the three prongs of Althen by a preponderance of the evidence. See id.

Under the first prong of Althen, a petitioner must offer a scientific or medical theory that answers in the affirmative the question: “can the vaccine[] at issue cause the type of injury alleged?” See Pafford v. Sec’y of Health & Hum. Servs., No. 01-0165V, 2004 WL 1717359, at *4

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(Fed. Cl. Spec. Mstr. July 16, 2004), mot. for rev. den’d, 64 Fed. Cl. 19 (2005), aff’d, 451 F.3d 1352 (Fed. Cir. 2006). To satisfy this prong, a petitioner’s theory must be based on a “sound and reliable medical or scientific explanation.” Knudsen v. Sec’y of Health & Hum. Servs., 35 F.3d 543, 548 (Fed. Cir. 1994). Such theory must only be “legally probable, not medically or scientifically certain.” Id. at 548–49. Petitioners are not required to identify “specific biological mechanisms” to establish causation, nor are they required to present “epidemiologic studies, rechallenge[] the presence of pathological markers or genetic disposition, or general acceptance in the scientific or medical communities.” Capizzano, 440 F.3d at 1325 (quoting Althen, 418 F.3d at 1280). Scientific and “objective confirmation” of the medical theory with additional medical documentation is unnecessary. Althen, 418 F.3d at 1278–81; see also Moberly, 592 F.3d at 1322. However, as the Federal Circuit has made clear, “simply identifying a ‘plausible’ theory of causation is insufficient for a petitioner to meet her burden of proof.” LaLonde v. Sec’y of Health & Hum. Servs., 746 F.3d 1334, 1339 (Fed. Cir. 2014) (citing Moberly, 592 F.3d at 1322). Indeed, the Federal Circuit has “consistently rejected theories that the vaccine only ‘likely caused’ the injury and reiterated that a ‘plausible’ or ‘possible’ causal theory does not satisfy the standard.” Boatmon v. Sec’y of Health & Hum. Servs., 941 F.3d 1351, 1360 (Fed. Cir. 2019) (citing Moberly, 592 F.3d at 1322; LaLonde, 746 F.3d at 1339). Rather, “[a] petitioner must provide a reputable medical or scientific explanation that pertains specifically to the petitioner’s case.” Moberly, 592 F.3d at 1322. In general, “the statutory standard of preponderance of the evidence requires a petitioner to demonstrate that the vaccine more likely than not caused the condition alleged.” LaLonde, 746 F.3d at 1339.

Furthermore, establishing a sound and reliable medical theory connecting the vaccine to the injury often requires a petitioner to present expert testimony in support of her claim. Lampe v. Sec’y of Health & Hum. Servs., 219 F.3d 1357, 1361 (Fed. Cir. 2000). The Supreme Court’s opinion in Daubert v. Merrell Dow Pharmaceuticals, Inc. requires that courts determine the reliability of an expert opinion before it may be considered as evidence. 509 U.S. 579 (1993). However, in the Vaccine Program, the Daubert factors are used in the weighing of the reliability of scientific evidence proffered. Davis v. Sec’y of Health & Hum. Servs., 94 Fed. Cl. 53, 66–67 (2010) (“[U]niquely in this Circuit, the Daubert factors have been employed also as an acceptable evidentiary-gauging tool with respect to the persuasiveness of expert testimony already admitted.”); see also Cedillo v. Sec’y of health & Hum. Servs., 617 F.3d 1328, 1339 (Fed. Cir. 2010) (citing Terran v. Sec’y of Health & Hum. Servs., 195 F.3d 1302, 1316 (Fed. Cir. 1999)). Under Daubert, the

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

Terran, 195 F.3d at 1316 n.2 (citing Daubert, 509 U.S. at 592–95).

The Daubert factors are “meant to be helpful, not definitive.” Kumho Tire Co. v.

Carmichael, 526 U.S. 137, 151 (1999). The factors do not “constitute a ‘definitive checklist or

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test’” and may be applied differently depending on the facts of a particular case. Id. at 150 (quoting Daubert, 509 U.S. at 593).

“In short, the requirement that an expert’s testimony pertain to ‘scientific knowledge’

establish a standard of evidentiary reliability.” Daubert, 509 U.S. at 590 (citation omitted). Thus, for Vaccine Act claims, a “special master is entitled to require some indicia of reliability to support the assertion of the expert witness.” Moberly, 592 F.3d at 1324. Nothing requires the acceptance of an expert’s conclusion “connected to existing data only by the ipse dixit of the expert,” especially if “there is simply too great an analytical gap between the data and the opinion proffered.” Synder v. Sec’y of Health & Hum. Servs., 88 Fed. Cl. 706, 743 (2009) (quoting Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997)); see also D’Tiole v. Sec’y of Health & Hum. Servs., No. 15-085V, 2016 WL 7664475, at *24 (Fed. Cl. Spec. Mstr. Nov. 28, 2016) (stating that the Vaccine Act “require[s] a chain of reliable propositions supporting [a] petitioner’s theory”).

Under the second prong of Althen, a petitioner must prove that the vaccine actually did cause the alleged injury in a particular case. See Pafford, 2004 WL 1717359, at *4; Althen, 418 F.3d at 1279. The second Althen prong requires proof of a logical sequence of cause and effect, usually supported by facts derived from a petitioner’s medical records. Althen, 418 F.3d at 1278; Capizzano, 440 F.3d at 1326; Grant v. Sec’y of Health & Hum. Servs., 956 F.2d 1144, 1148 (Fed. Cir. 1992). A petitioner does not meet this obligation by showing only a temporal association between the vaccination and the injury; instead, the petitioner “must explain how and why the injury occurred.” Pafford, 2004 WL 1717359, at *4 (emphasis in original). The special master in Pafford noted petitioners “must prove [] both that her vaccinations were a substantial factor in causing the illness . . . and that the harm would not have occurred in the absence of the vaccination.” 2004 WL 1717359, at *4 (citing Shyface, 165 F.3d at 1352). A reputable medical or scientific explanation must support this logical sequence of cause and effect. Hodges v. Sec’y of Health & Hum. Servs., 9 F.3d 958, 961 (Fed. Cir. 1993) (citation omitted). Nevertheless, “[r]equiring epidemiologic studies . . . or general acceptance in the scientific or medical communities . . . impermissibly raises a claimant’s burden under the Vaccine Act and hinders the system created by Congress . . . .” Capizzano, 440 F.3d at 1325–26. “[C]lose calls regarding causation are resolved in favor of injured claimants.” Althen 418 F.3d at 1280.

In Program cases, contemporaneous medical records and the opinions of treating physicians are favored. Capizzano, 440 F.3d at 1326 (citing Althen, 418 F.3d at 1280). Indeed, when reviewing the record, a special master must consider the opinions of treating physicians. Capizzano, 440 F.3d at 1326. This is because “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.’” Id. In addition, “[m]edical records, in general, warrant consideration as trustworthy evidence. The records contain information supplied to or by health professionals to facilitate diagnosis and treatment of medical conditions. With proper treatment hanging in the balance, accuracy has an extra premium. These records are also generally contemporaneous to the medical events.” Cucuras, 993 F.2d at 1528. However, there is no “presumption that medical records are accurate and complete as to all of the patient’s physical conditions.” Kirby, 997 F.3d at 1383 (finding that a special master must consider the context of a medical encounter before concluding that it constitutes evidence regarding the absence of a condition). While a special master must consider these opinions and records, they are not “binding

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on the special master or court.” § 300aa-13(b)(1). Rather, when “evaluating the weight to be afforded to any such . . . [evidence], the special master . . . shall consider the entire record . . . .” Id.

In determining the accuracy and completeness of medical records, special masters will consider various explanations for inconsistencies between contemporaneously created medical records and later given testimony. The Court of Federal Claims has identified four such explanations for explaining inconsistencies: (1) a person’s failure to recount to the medical professional everything that happened during the relevant time period; (2) the medical professional’s failure to document everything reported to her or him; (3) a person’s faulty recollection of the events when presenting with testimony; or (4) a person’s purposeful recounting of symptoms that did not exist. LaLonde v. Sec’y of health & Hum. Servs., 110 Fed. Cl. 184, 203 (2013), aff’d, 746 F.3d 1334 (Fed. Cir. 2014).

To satisfy the third Althen prong, a petitioner must establish a “proximate temporal relationship” between the vaccination and the alleged injury. Althen, 418 F.3d at 1281. This “requires preponderant proof that the onset of symptoms occurred within a timeframe for which, given the medical understanding of the disorder’s etiology, it is medically acceptable to finger causation-in-fact.” de Bazan v. Sec’y of health & Hum. Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008). Typically, “a petitioner’s failure to satisfy the proximate temporal relationship prong is due to the fact that onset was too late after the administration of a vaccine for the vaccine to be the cause.” Id. However, “cases in which onset is too soon” also fail this prong; “in either case, the temporal relationship is not such that it is medically acceptable to conclude that the vaccination and the injury are causally linked.” Id.; see also Locane v. Sec’y of Health & Hum. Servs., 685 F.3d 1375, 1381 (Fed. Cir. 2012) (“[If] the illness was present before the vaccine was administered, logically, the vaccine could not have caused the illness.”).

Although a temporal association alone is insufficient to establish causation, under the third prong of Althen, a petitioner must show that the timing of the injury fits with the causal theory. See Althen, 418 F.3d at 1278. The special master cannot infer causation from temporal proximity alone. See Thibaudeau v. Sec’y of health & Hum. Servs., 24 Cl. Ct. 400, 403–04 (1991); see also Grant, 956 F.2d at 1148 (“[T]he inoculation is not the cause of every event that occurs within the ten[-]day period . . . [w]ithout more, this proximate temporal relationship will not support a finding of causation.” (quoting Hasler v. United States, 718 F.2d 202, 205 (6th Cir. 1983))).

A petitioner who satisfies all three prongs of the Althen test has established a prima facie showing of causation. Hammitt v. Sec’y of health & Hum. Servs., 98 Fed. Cl. 719, 726 (2011). A petitioner who demonstrates by a preponderance of the evidence that she suffered an injury caused by vaccination is entitled to compensation unless the respondent can demonstrate by a preponderance of the evidence that the injury was caused by factors unrelated to the vaccination. See Althen, 418 F.3d at 1278; Knudsen, 35 F.3d at 547. In such a case, the government must not merely prove the existence of an alternative cause, but that such an alternative actually caused the injury. Kundsen, 35 F.3d at 549. Consequently, when and if the petitioner establishes a prima facie case, the burden the shifts to the government to prove that an alternative cause, unrelated to the administration of the vaccine, was the “sole substantial factor” in causing the alleged injury. See de Bazan, 539 F.3d at 1354; see also Hammitt, 98 Fed. Cl. at 726 (explaining that respondent’s burden is to show that the “factor unrelated” was the “sole substantial factor” in causing the injury).

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Additionally, a factor unrelated “may not include ‘any idiopathic, unexplained, unknown, hypothetical, or undocumentable cause, factor, injury, illness or condition.’” § 300aa-13(a)(2); see also Doe v. Sec’y of Health & Hum. Servs., 601 F.3d 1349 (Fed. Cir. 2010) (stating that an idiopathic diagnosis cannot be a “factor unrelated,” as it is idiopathic).

IV. Discussion

Both parties submitted several written reports from multiple experts throughout the course of this litigation, addressing various components of Petitioner’s burden pursuant to Althen. These reports do not always follow an easily discernible progression of the Althen prongs from general causation through Petitioner’s specific symptom onset. Moreover, sections of Petitioner’s reports sometimes digress to assert tangential arguments. This makes it prohibitively difficult to provide a comprehensive and cohesive account of Dr. Akbari’s asserted causation theory in a designated section of this Decision. Therefore, this discussion section will incorporate Drs. Hixson’s and Akbari’s assertions and conclusions related to vaccine causation; rebuttal arguments from Respondent’s experts, Dr. Callaghan and Dr. Fujinami; and an analysis of the credibility and persuasiveness of the respective arguments based on the identified supporting evidence. Although all of Petitioner’s arguments have been reviewed and considered in the context of any filed supporting evidence, this decision will not explicitly discuss every assertion and every piece of literature. Moriarty, 844 F.3d at 1328 (“We generally presume that a special master considered the relevant record evidence even though he does not explicitly reference such evidence in his decision.”) (citation omitted); see also Paterek, 527 F. App’x at 884 (“Finding certain information not relevant does not lead to—and likely undermines—the conclusion that it was not considered.”).

A. General Causation

Under Althen prong one, Petitioner must set forth a medical theory explaining how the received vaccine could have caused or sustained injury. Andreu v. Sec’y of Health & Hum. Servs., 569 F.3d 1367, 1375 (Fed. Cir. 2009); 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.3c 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”), aff’d 475 F. App’x 765 (Fed. Cir. 2012). Petitioner relies exclusively 15 on the reports of Omid Akbari, Ph.D., 16 (with his referenced and filed medical literature) to articulate her causation theory. See Pet’r’s Exs. 29, 76. If Petitioner relies upon a medical opinion to support her theory, the basis for the opinion and the reliability of that basis

Although both of Petitioner’s experts filed reports that addressed Althen prong one, Petitioner 15

confirmed to Chambers that she is only relying on the reports of Dr. Akbari to support her Althen prong one argument. See Informal Comm., docketed May 12, 2026. 16 Dr. Akbari currently serves as a Professor of Immunology and Professor of Medicine at the Keck School of Medicine at the University of Southern California. Pet’r’s Ex. 29 at 2. He received his Ph.D. in Cellular and Molecular Immunology at the National Institute for Medical Research in the United Kingdom and completed a post-doctoral fellowship at Stanford University. Pet’r’s Ex. 30 at 1. Dr. Akbari has published over 120 articles across several peer-reviewed journals, many of which relate directly to the field of immunology. Pet’r’s Ex. 29 at 2.

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must be considered in the determination of how much weight to afford the offered opinion. See Broekelschen v. Sec’y of Health & Hum. Servs., 618 F.3d 1339, 1347 (Fed. Cir. 2010) (“The special master’s decision oftentimes is based on the credibility of the experts and the relative persuasiveness of their competing theories”); Perriera 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 (Ct. Cl. 1980))). Importantly, as the Federal Circuit has made clear, “simply identifying a ‘plausible’ theory of causation is insufficient for a petitioner to meet her burden of proof.” LaLonde, 746 F.3d at 1339. Instead, Petitioner must show it was more likely than not that the vaccine caused the condition alleged. Id. Dr. Akbari summarized his causation theory as “the idea that the induction of inflammasome,[17] coupled with molecular mimicry, serves as the mechanism through which an immune-stimulated response to the flu vaccination could lead to” the development of Petitioner’s SFN. Pet’r’s Ex. 29 at 26.

Noting that little is known “how the vaccine activates the immune system,” Dr. Akbari explained that “[i]mmunization with a vaccine, such as flu, causes a local inflammatory reaction that is mediated by cells of the innate immune system.” Pet’r’s Ex. 29 at 26. Two functions of the innate immune system are to recruit other immune cells via the release of cytokines and to activate the adaptive immune response through dendritic cells. Id. “Once activated, a dendritic cell will migrate to the lymph nodes and interact with B and T cells that recognize the presented antigen.” Id.

1. The Role of Th17 T Helper Cells

T cells, according to Dr. Akbari, “are differentiated by antigenic stimulation into different effector subsets call T helper (Th) cells, and are characterized by their production of specific cytokines and effector functions.” Pet’r’s Ex. 29 at 7–8. Dr. Akbari relied on Kebir et al. 18 to assert that “Th1 cells have been reported to be elevated in patients and have a pathogenic role in various neuropathy.” Id. (citing Pet’r’s Ex. 32). He further asserted that Th17 cells “secrete interleukin-17 [(“IL-17”)], a molecule that is well known to induce inflammation,” and tumor necrosis factor (“TNF”)-ɑ “which have pro-inflammatory functions, suggest[ing them] as [] important factor[s] in immune-pathogenesis of demyelination and [n]euro-inflammation.” Id. at 8 (citing Pet’r’s Ex. 37). 19 Dr. Akbari argued that “[e]merging research” found that patients with demyelination have increased levels of Th17.” Id. (citing Pet’r’s Ex. 36). 20 However, none of the articles Dr. Akbari cited seem to support these propositions.

17 Inflammasome is “a complex of cryopyrin, caspase-1, and other proteins, found in the phagocytic cells and related to the body’s system of innate immunity.” Inflammasome, DORLAND’S. 18 Hania Kebir et al., Preferential Recruitment of Interferon-y-Expressing Th17 Cells in Multiple Sclerosis, 66 ANNALS NEUROLOGY 390 (2009). 19 F. Jadidi-Niaragh & A. Mirshafiey, Th17 Cell, the New Player of Neuroinflammatory Process in Multiple Sclerosis, 74 SCANDINAVIAN J. IMMUNOLOGY 1 (2011). 20 Marinos C. Dalakas, Future Perspectives in Target-Specific Immunotherapies of Myasthenia Gravis, 8 THERAPY ADVANCED NEUROLOGIC DISORDERS 316 (2015).

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First, Dr. Akbari significantly mischaracterized the Kebir et al. study. With this article, the authors “sought to evaluate the frequency of [interferon 21 (“IFN”)]-expressing Th17 lymphocytes in [multiple sclerosis (“MS”)] and [experimental autoimmune encephalitis (“EAE”)], and study their recruitment into the central nervous system (CNS).” Pet’r’s Ex. 32 at 1. The article did not specifically examine Th1 and whether its elevation was present across multiple neuropathies. In fact, the article cast doubt on the pathogenic ability of T cells and their cytokines, acknowledging that “the precise role of the Th17 effector cytokine IL-17 in the initiation of EAE and MS remains controversial.” Id. Further, to the extent the authors identified a pathogenic role of Th cells, they were able to tie the increased cell counts to the specific symptoms of MS and the presence of lesions throughout the CNS. Id. at 12. The authors did not assert that an elevated presence of any Th cells are associated with neuropathies generally. Notably, in Dr. Akbari’s supplemental report, he indirectly acknowledged this point, stating “[d]espite the usefulness of animal models, it is crucial to acknowledge the absence of an animal model for SFN. EAE closely mirrors MS, with shared aspects in immune cell responses, but does not accurately represent SFN.” Pet’r’s Ex. 76 at 13 (emphasis added). Given Dr. Akbari’s own admission that EAE and MS are not diseases that can accurately be compared to SFN, his reliance on articles discussing the pathogenesis of EAE and MS to demonstrate the pathology of SFN following flu vaccination is less persuasive without an explained commonality.

The second article, Zambrano-Zaragoza et al., 22 noted an association between increased Th17 and certain autoimmune diseases, but again the only neuropathic disease included in this list was MS. Pet’r’s Ex. 35 at 1. Also, the article did not link Th17 to demyelination generally. See id. Another article cited to illustrate the significance of Th17 was Dalakas. Pet’r’s Ex. 36 at 1. This study looked at potential immunosuppressant therapies to treat myasthenia gravis, “an autoimmune disease caused by [] antibodies against acetylcholine receptors.” Id. The author opined that Th17 should be targeted with suppressant therapies due to its increased presence in patients suffering from the disease. Id. However, the article is wholly focused on myasthenia gravis, which involves antibodies targeting the neuromuscular junction and not the myelin sheath. Id. Indeed, it is not characterized as demyelinating disease.

Dr. Akbari also cited to Niaragh & Mirshafiey, another article that examined Th17’s role in the neuroinflammatory process of MS. See Pet’r’s Ex. 37 at 1. The authors noted that Th17’s role in secreting cytokines (including, but not limited to, IL-17) and TNF-ɑ “suggest it as an important factor in immunopathogenesis of MS, because the main feature of MS pathophysiology is the neuroinflammatory reaction.” Id. They argued this occurred via Th17’s transmission through the blood-brain-barrier (“BBB”), “an early and central event in MS pathogenesis.” Id. Here, Dr. Akbari took an article focused on the specific kinetic effects Th17 has in the disease progression of MS and applied this process broadly to all demyelination and neuro-inflammation without supporting that extrapolation. This article also highlighted the difference in Th cells and their different effects throughout the body, specifying that “neuroinflammation in the brain is mainly

21 Interferon is defined as “glycoproteins that exert virus-nonspecific but host-specific antiviral activity by inducing the transcription of cellular genes coding for antiviral proteins that selectively inhibit the synthesis of viral RNA and proteins. Interferons also have immunoregulatory functions (inhibition of B cell activation and antibody production enhancement of T cell activity . . . .” Interferon, DORLAND’S. 22 José Francisco Zambrano-Zaragoza et al., Th17 Cells in Autoimmune and Infectious Diseases, 2014 INT’L J. INFLAMMATION 1 (2014).

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mediated through the function of Th17” cells compared to spinal inflammation mediated by Th1 cells. Id. at 9.

Dr. Akbari next argued that Th17 cells “play an important role in patients with fiber neuropathy” specifically. Pet’r’s Ex. 29 at 19. He stated that “patients with neuropathy and demyelination have increased levels of Th17 cells” and that “it was shown that production of Th17 promote astrocytes to cause a variety of neuropathy including [SFN].” Id. at 20 (citing Pet’r’s Ex. 56). 23 Dr. Akbari also asserted that studies had linked higher levels of Th17 cells to the development of SFN. Id. (citing Pet’r’s Ex. 57). 24 However, neither of these referenced articles support Dr. Akbari’s claims.

The first article cited by Dr. Akbari, Sun et al., analyzes IL-17 as a potential source of neuropathic pain following a peripheral nerve injury. Pet’r’s Ex. 56 at 1. The authors focused on the presence of IL-17 in the spinal cord as a potential mediator of peripheral nerve pain and did so via ligation of the spinal cord to measure pain responses in the peripheral nerves. Id. at 2. The study noted that the cells in the spinal cord differed across species (Th17 in rats and Th1 in mice) and found that “IL-17 may contribute to neuropathic pain by promoting the proliferation of astrocytes and secretion of proinflammatory cytokines in spinal nerve ligation-induced neuropathic pain.” Id.at 1. They cautioned that the actual “tissue specific mechanism” of IL-17 remains unclear. Id. at 5–6. However, the authors did not study SFN and did not opine on any role IL-17 may play in the pathogenesis of SFN.

The second article cited by Dr. Akbari, Ryabkova et al., focused on the pathogenesis of fibromyalgia, and examined the roles that autoimmunity, neuroinflammation, SFN, and adverse events following human papilloma virus (“HPV”) vaccination played in its development. Pet’r’s Ex. 57 at 1. The article did not link SFN to the development of Th17 cells or vaccination. More importantly, the overall credibility of the article is cast into question given its reliance on a theory known as “autoimmune/inflammatory syndrome induced by adjuvants (“ASIA”).” Id. at 2. Specifically, the authors use the ASIA theory to link fibromyalgia to “vaccination, silicone breast implants, [and] mineral oil injection.” Id. ASIA was presented regularly in the Program for many years without success, and to date, it has been consistently rejected as a valid theory connecting vaccines to injury. See D’Angiolini v. Sec’y of Health & Hum. Servs., 122 Fed. Cl. 86, 101 (affirming the special master’s rejection of the theory as “still developing and incomplete), aff’d 645 Fed. Appx. 1002 (Fed. Cir. 2016); Garner v. Sec’y of Health & Hum. Servs., No. 15- 0063V, 2017 WL 1713184, at *15 (Fed. Cl. Spec. Mstr. Mar. 24, 2017); Johnson v. Sec’y of Health & Hum. Servs., No. 10-0578V, 2016 WL 4917548, at *8–9 (Fed. Cl. Spec. Mstr. Aug. 18, 2016) (describing this theory as overbroad, generalized, and vague and finding this expansive theory logically unpersuasive); Rowan v. Sec’y of Health & Hum. Servs., No. 10-0272V, 2014 WL 7465661, at *12 (Fed. Cl. Spec. Mstr. Dec. 8, 2014). Thus, Dr. Akbari’s assertion that higher levels of Th17 cells have been linked to SFN is not supported by the referenced and filed literature.

23 Caixia Sun et al., IL-17 Contributed to the Neuropathic Pain Following Peripheral Nerve Injury by Promoting Astrocyte Proliferation and Secretion of Proinflammatory Cytokines, 15 MOLECULAR MED. REPS. 89 (2017). 24 Varvara A. Ryabkova et al., Neuroimmunology: What Role for Autoimmunity, Neuroinflammation, and Small Fiber Neuropathy in Fibromyalgia, Chronic Fatigue Syndrome, and Adverse Events After Human Papillomavirus Vaccination?, 20 INT’L J. MOLECULAR SCI. 5164 (2019).

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Respondent’s expert, Dr. Robert Fujinami, Ph.D., 25 took issue with this discussion of Th17 cells, noting that “[m]uch of what [Dr. Akbari] presents is in the context of experimentally induced demyelinating disease. SFN is not generally considered to be a demyelinating disease.” Resp’t’s Ex. E at 4. In response, Dr. Akbari argued that

numerous studies have provided compelling evidence supporting the association between [flu] vaccine and Th17 induction. Subsequent to the inflammasome activation and IL-1 release, a cascade of events unfolds, leading to the differentiation of Th17 cells. These cells, armed with the potential to cause SFN and contribute to pathological processes, underscore the significance of comprehending the intricate immunological responses triggered by the flu vaccine.

Pet’r’s Ex. 76 at 9. Dr. Akbari did not explain the “cascade of events” that led to the differentiation of Th17 cells, nor did he explain how Th17 cells were “armed with the potential to cause SFN.” Id. He argued two articles “shed[] light on the nuanced dynamics of Th17 responses in the context of [flu] vaccination,” however, these articles were not filed. Id. He concluded that based on the findings of these articles, “[i]t became apparent that Th17 cells which are involved in the pathogenesis of many autoimmune diseases, secrete [IL-17], a molecule that is well known to induce inflammation.” Id. at 10 (citing Pet’r’s Ex. 35). As discussed, the citied articles he relied on in his initial report do not provide inferences that can reasonably be integrated to link Th17 production to SFN pathogenesis. While Dr. Akbari noted that Zambrano-Zaragoza et al. highlighted several different autoimmune conditions that implicate Th17 cells, SFN is not listed; and, the only neurological condition implicated is MS. See Pet’r’s Ex. 35 at 4–6. Dr. Akbari nonetheless concluded that “in specific individuals, [] the presence of Th17 cells, coupled with impaired Tregs or a dysregulated immune response, can lead to undesired outcomes such as SFN.” Id. In response, Dr. Fujinami noted that Dr. Akbari did “not present any supporting information from the medical records showing that the Petitioner mounted a dysregulated immune response during her lifetime.” Resp’t’s Ex. F at 1. Indeed, no evidence was provided by Dr. Akbari to this point, making his arguments speculative.

Dr. Akbari also asserted that “the number and effector function of Tregs was associated with severity and clinical manifestation of fiber neuropathy.” Pet’r’s Ex. 29 at 21 (citing Pet’r’s Ex. 60). 26 The article referenced by Dr. Akbari, Duffy et al., examined the role of Tregs in different neuropathic disease pathologies, including GBS, chronic inflammatory demyelinating polyneuropathy (“CIDP”), neuropathic pain, CNS injuries, Alzheimer’s disease, ALS, Parkinson’s disease, and MS. See generally Pet’r’s Ex. 60. However, the article did not discuss the role of

25 Dr. Fujinami currently serves as a Professor of Pathology and Adjunct Professor in the Neurology Department at the University of Utah School of Medicine. Resp’t’s Ex. D at 1. He received his Ph.D. in Immunology-Microbiology from Northwestern University. Id. Dr. Fujinami has written several articles related to the fields of immunology, autoimmune diseases, and vaccines, and has served on several national panels for the National Institute of Health. Resp’t’s Ex. C at 2. Dr. Fujinami is not a physician and thus contained his opinions to the “immunological mechanisms/theories proposed by the Petitioner’s expert.” Id. 26 Samuel S. Duffy et al., The Role of Regulatory T Cells in Nervous System Pathologies, 96 J. NEUROSCIENCE RSCH. 951 (2018).

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Tregs in the pathogenesis of SFN. Moreover, Dr. Akbari provided no explanation as to why Tregs would be a factor in the pathogenesis of SFN other than his general reference to Tregs playing a role in the pathogenesis of other neuropathic diseases.

In his supplemental report, Dr. Akbari expanded on this argument in the context of Tregs and their effect on the immune system response. Pet’r’s Ex. 76 at 11. Citing to Schlöder et al., 27 he explained that immune balance is determined by the ratio of Tregs to T effector cells. Id. (citing Pet’r’s Ex. 86). According to Dr. Akbari, pro-inflammatory cytokines “such as IL-1 . . . can impose constraints on the expansion and effector function of Tregs, leading to an imbalance . . . this imbalance may result in an excess of . . . Th1 and Th17–both implicated in neurological disease such as SFN and autoimmunity.” Id. (citing Pet’r’s Ex. 86). However, this statement is problematic for several reasons. First, as is discussed throughout this opinion, Dr. Akbari failed to provide persuasive evidence linking Th1 or Th17 to the development of SFN. Second, Schlöder et al. did not discuss IL-1 as a cytokine that creates an effect on Tregs or their effector cells. Rather, the authors discuss IL-2, IL-4, IL-6, IL-7, IL-10, IL-13, IL-15, IL-17, IL-18, IL-33, and IL-35 as the various cytokines that have either positive or negative influences on the Treg to T effector cell balance. See generally Pet’r’s Ex. 86. IL-1 is mentioned only once in the article to distinguish receptor types I and II “as two specific surface markers that distinguish activated Foxp3 Treg from activation Foxp3 non-Treg after ex vivo expansion.” Id. at 10. The authors do not implicate IL-1 as a contributor to the Treg-T effector cell balance within the immune system, nor do they attribute it to the development of autoimmune disease or SFN.

2. Cytokines and the Development of SFN

Next, Dr. Akbari turned to the development of the cytokine IL-17, which he appeared to conflate with inflammasome while arguing that it played a role in the development of SFN. Pet’r’s Ex. 29 at 18–19. He argued that IL-1, IL-6, and TNF-ɑ “contribute to a variety of manifestations in demyelinating disease, [and] play an important role in the induction of Th17 cells.” Id. at 18. He then argued that “several reports suggest that patients with peripheral demyelination had a higher proportion of Th17 cells compared to controls,” and cited Mei et al. Id. (citing Pet’r’s Ex. 52). 28 This article recorded the levels of inflammatory cytokines present in the CSF of patients with CIDP and vasculitic neuropathy (“VN”). Pet’r’s Ex. 52 at 1. The authors found an increase of IL-17 and IL-8 in patients with CIDP and an increase of IL-6, IL-8, and IL-10 in patients with VN. Id. The authors noted that there was a “unique role[] for IL-17 in CIDP” as being “related to the severity of inflammation in the spinal roots.” Id. at 8. The authors also posited that IL-6 and IL-8 could contribute to the inflammation present in CIDP due to their associations with other autoimmune inflammatory diseases such as rheumatoid arthritis, systemic lupus erythematosus, ulcerative colitis, Crohn’s disease, and psoriasis. Id. at 8–9. However, they did not attribute the presence of increased IL-17, IL-6, or IL-8 to other neuropathies or to demyelination generally, instead attributing it specifically to inflammation of the spinal roots in CIDP patients. Id.

27 Janine Schlöder et al., Boosting Regulatory T Cell Function for the Treatment of Autoimmune Disease – That’s Only Half the Battle!, 13 FRONTIERS IMMUNOLOGY 973813 (2022). 28 Feng-June Mei et al., Th1 Shift in CIDP Versus Th2 Shift in Vasculitic Neuropathy in CSF, 228 J. NEUROLOGICAL SCI. 75 (2005).

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Dr. Akbari further asserted that higher levels of IL-17 were found in patients after receiving the flu vaccine. Pet’r’s Ex. 29 at 18 (citing Pet’r’s Exs. 53, 54). 29 However, this was not supported by the medical literature he cited. First, Bermejo-Martin et al. was a study focusing on Th1 and Th17 responses to severe pandemic flu infection, not vaccination. Pet’r’s Ex. 53 at 1. Further, the authors of this study found elevated Th17 “exclusively [] in hospitalized patients,” and not in milder cases more consistent with an immune response resulting from vaccination (versus infection). 30 Id. at 2. A second article, Lin et al., did not find IL-17 to be increased following flu vaccination. Pet’r’s Ex. 54 at 6. The study, which focused on Th17 cytokines and vaccine immunity, found that “vaccination with DNA constructs encoding [flu] virus hemagglutinin [] and IL-23 maintained cellular responses over longer periods of time [] and cleared more virus when challenged with [flu] virus than [hemagglutinin] alone.” Id. at 7. The study did not examine or find the increased presence of any cytokines following flu vaccination.

Continuing to focus on Th17-produced cytokines, Dr. Akbari stated that “[IL-17] and [TNF-ɑ], which have proinflammatory functions, suggest it is an important factor in immune- pathogenesis of demyelination.” Pet’r’s Ex. 29 at 19 (citing Pet’r’s Ex. 37). However, the article he cited, Jadidi-Niaragh & Mirshafiey, examined the role of Th17 in the neuroinflammatory process of MS. Pet’r’s Ex. 37 at 1. In fact, Dr. Akbari’s above-quoted statement overextends the authors’ statement from the abstract of the article, which reads as follows:

Th17-produced cytokine profile including [IL-17], IL-6, IL-21, IL-22, IL-23, and [TNF-ɑ], which have proinflammatory functions, suggests it as an important factor in the immuno-pathogenesis of MS, because the main feature of MS pathophysiology is the neuroinflammatory reaction. The [BBB] disruption is an early and central event in MS pathogenesis. Autoreactive Th17 cells can migrate through the BBB by the production of cytokines such as IL-17 and IL-22, which disrupt tight junction proteins in the [CNS] endothelial cells.

Id. (emphasis added). The article did not discuss Th17 or IL-17 as playing a role in the demyelination process of MS or any other demyelinating disease, nor did it extrapolate the role of IL-17 to other neuropathies generally. Dr. Fujinami took this critique further by noting that “SFN

29 Jesus F. Bermejo-Martin et al., Th1 and Th17 Hypercytokinemia as Early Host Response Signature in Severe Pandemic Influenza, 13 CRITICAL CARE 201 (2009); Yinyao Lin et al., Th17 Cytokines and Vaccine-Induced Immunity, 32 SEMINAL IMMUNOPATHOLOGY 79 (2010). 30 It is notable that this is not the first time Dr. Akbari has been critiqued by a special master for this interpretation of Bermejo-Martin et al. Indeed, several prior cases have observed that Dr. Akbari misrepresents this piece of literature in the same manner as in this case when applying his general theory of inflammasome molecular mimicry to other injuries. See Powell v. Sec’y of Health & Hum. Servs., No. 20-1726V, 2025 WL 3443590, at *32 (Fed. Cl. Spec. Mstr. Oct. 8, 2025) (noting that “Dr. Akbari did not describe the limitations of the study”); Williams v. Sec’y of Health & Hum. Servs., No. 19-1269V, 2024 WL 5040482, at *23 (Fed. Cl. Spec. Mstr. Nov. 13, 2024) (“The article does not discuss vaccination, and Dr. Akbari does not show that the flu vaccination is comparable to the H1N1 infection so as to make the results of the study applicable here.” (emphasis in original)); Nieves v. Sec’y of Health & Hum. Servs., No. 18-1602V, 2023 WL 3580148, at *25 (Fed. Cl. Spec. Mstr. May 22, 2023) (“Bermejo-Martin arguably undercuts the conclusion that the T helper cells highlighted by Dr. Akbari are necessarily pathogenic (while not supportive of the contention that vaccination stimulates them in the first place).” (emphasis in original)).

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is generally not considered to be a demyelinating disease,” and thus most of the arguments made by Dr. Akbari with respect to the demyelination process are inapplicable. Resp’t’s Ex. E at 4 (citing Resp’t’s Ex. E, Tab 8). 31 The article cited by Dr. Fujinami, Raasing et al., explained that while “[t]he exact pathophysiology of isolated SFN is unknown[,] . . . since demyelinating processes do not soley affect small nerve fibers, it is unlikely that this would be the underlying pathogenesis.” Resp’t’s Ex. E, Tab 8 at 2.

In his supplemental report, Dr. Akbari argued that Dr. Fujinami “overlooked an important aspect of [SFN]: the role of lightly myelinated small fibers.” Pet’r’s Ex. 76 at 17. Dr. Akbari stated that SFN was “principally characterized” by damage to small myelinated fibers, which he stated was supported in “many publications and even discussed in [a] recent publication.” Id. at 17–18 (citing Pet’r’s Ex 94). 32 However, the article cited by Dr. Akbari, Lauria et al., is a review of the methods for diagnosing SFN, and focused on skin punch and sweat gland biopsies. See Pet’r’s Ex. 94. The article did not mention demyelination as a “principal” factor in the pathogenesis of SFN, or even as a potential diagnostic criteria. Despite this, Dr. Akbari asserted that Dr. Fujinami’s argument “is not just incorrect but also indicative of a profound misunderstanding of the disorder’s pathology.” Pet’r’s Ex. 76 at 18.

3. Molecular Mimicry and Bystander Activation

Molecular mimicry was identified as the primary mechanism for Petitioner’s SFN. Dr.

Akbari relied on Ang et al., 33 an article reviewing GBS pathogenesis as a case of molecular mimicry, and identified four mechanisms by which molecular mimicry could occur: (1) “sharing of identical amnio acid sequences and homologous but non-identical amino acid sequences,” (2) “the recognition of non-homologous peptide sequences by a single [B cell receptor] or [T cell receptor,]” (3) a single T cell recognizing “different peptides in the context of different human leukocyte antigen [] molecules,” and (4) “that immunological receptors recognise (sic) structural similarity in complex molecular structures and their binding preferences are not necessarily based on biochemical classification.” Pet’r’s Ex. 29 at 11 (citing Pet’r’s Ex. 39 at 2). The article noted that in the case of non-homologous peptide sequences, a single T cell receptor could recognize thousands to billions of peptides. Pet’r’s Ex. 39 at 2. Dr. Akbari suggested that “given the promiscuity of T cell receptors, research now indicates that cross-reactive antibodies or T cells is a common phenomenon,” and argued that “the induction of autoimmune disease by autoantigens” may be better attributed to “how the host controls such cross-recognition.” Pet’r’s Ex. 29 at 11.

a. Molecular Mimicry

Next, Dr. Akbari stated the following:

31 Lisette R.M. Raasing et al., Current View of Diagnosing Small Fiber Neuropathy, 8 J. NEUROMUSCULAR DISEASES 185 (2021). 32 G. Lauria et al., European Federation of Neurological Societies/Peripheral Nerve Society Guideline on the Use of Skin Biopsy in the Diagnosis of Small Fiber Neuropathy. Report of a Joint Task Force of the European Federation of Neurological Societies and the Peripheral Nerve Society, 17 EUR. J. NEUROLOGY 903 (2010). 33 C. Wim Ang et al., The Guillain-Barré Syndrome: A True Case of Molecular Mimicry, 25 TRENDS IMMUNOLOGY 61 (2004).

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The research in the field of autoimmunity and flu vaccination, indeed suggest that components of the [flu] vaccine [Petitioner] received contained [flu] virus peptides able to trigger or stimulate/polarize autoreactive T cells to proteins and complex sugar associated with the structure present in the nervous system. The immune response elicited to gangliosides mainly targets sugars on the vaccine, which are also a component of the myelin sheath. Regarding the protein parts, the hemagglutinin from the [flu] has a sequence that contains “YVKQSTLKL.” [] A recent study suggests that the cross-reactivity of a CD4+T-cell clone specific for the immunodominant [flu] virus hemagglutinin peptide (bold sequence above) derived from a patient with demyelinating disease including [MS]. [] Furthermore, in another study by Harvard Medical School, a panel of 129 peptides that matched the molecular mimicry motif was tested on seven specific T cell clones from patients with demyelinating disease. Seven viral and one bacterial peptide efficiently activated three of these clones. [ T]hese results suggest that the [flu] vaccine that [Petitioner] received contains a protein that is able to stimulate and differentiate established autoreactive T cells further and contribute to the severity of demyelinating disease.

Pet’r’s Ex. 29 at 21 (citing Pet’r’s Exs. 63, 64) (emphasis added). 34 Again, Dr. Akbari did not provide a citation to support his statement that viral peptides from the flu vaccine can “trigger or stimulate/polarize autoreactive T cells to proteins and complex sugar associated with the structure present in the nervous system.” Id. Additionally, the article cited by Dr. Akbari referencing the YVKQSTLKL peptide was in reference to the pathogenesis of MS, not SFN, and Dr. Akbari again failed to draw a connection between the two, instead relying on his assertion that SFN is a demyelinating disease. See Pet’r’s Ex. 63 at 1. This article also explicitly stated that the cross- reactivity of T cell receptors “likely assures protection against many more than the originally stimulating viral variant.” Id. at 7. The other article cited by Dr. Akbari, Wucherpfennig & Strominger, discussed the activation of human T cell clones “specific for myelin basic protein,” and also focused on the pathogenesis of MS. Pet’r’s Ex. 64 at 1. Once again, Dr. Akbari failed to explain how the pathogenesis of a demyelinating disease of the CNS can be extrapolated to the pathogenesis of a non-demyelinating disease of the PNS.

Dr. Akbari also stated that “there is another peptide to the major protein in the myelin sheath known as myelin basic protein in the [flu] A vaccines. The amino acid sequence of the hemagglutinin is” FYKNLI. Pet’r’s Ex. 29 at 22. He compared this to the myelin basic protein peptide sequence of FFKNIV, which he noted had three differences, and called it an “undeniable example of a molecular mimicry with [flu] A strains appeared in vaccine that [Petitioner] received.” Id. Dr. Akbari then cited to articles explaining that a homology of five peptides in a sequence of 12 was sufficient to induce molecular mimicry, however, he did not explain how this applied to a homology of three peptides in a sequence of six, nor did he explain how he identified

34 Silva Markovic-Plese et al., High Level of Cross-Reactivity in Influenza Virus Hemagglutinin-Specific CD4+ T-Cell Response: Implications for the Initiation of Autoimmune Response in Multiple Sclerosis, 169 J. NEUROIMMUNOLOGY 31 (2005); Kai W. Wucherpfenning & Jack L. Strominger, Molecular Mimicry in T Cell-Mediated Autoimmunity: Viral Peptides Activate Human T Cell Clones Specific for Myelin Basic Protein, 80 CELL 695 (1995).

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either the hemagglutinin peptide or the myelin basic protein peptide. See id. (citing Pet’r’s Exs. 65, 66). 35 Further, Dr. Akbari did not explain why a myelin basic protein, which comprises the myelin sheath, would be involved in the pathogenesis of SFN, which affects axonal nerves. Dr. Akbari also argued that “structural homology is just as important as sequence homology” in inducing molecular mimicry, and provided the following explanation:

Alterations or mutations in amino acids, which thereby confer an altered confirmation or 3D structure of the receptor, are known to also change the receptors’ ability to recognize foreign antigen and to bind to incorrect peptides. The idea that there are significant portions of the protein peptide sequence that will show similarity to a putative microbial antigen is no longer a widely held belief in understanding how molecular mimicry can occur.

Id. Dr. Akbari provided no citations for his assertions and did not identify any potential structural compatibility between a portion of the flu vaccine and the axons affected by SFN. Id. Dr. Akbari continued by stating that “[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 [major histocompatibility complex (“MHC”)] molecules.” Id. at 22–23 (citing Pet’r’s Ex. 40, 67). 36 However, the articles cited by Dr. Akbari again do not support his arguments. First, Mycko et al. contains zero discussion of molecular mimicry or MHC molecules, as it is an article analyzing microarray gene expression profiling of chronic lesions in MS. See Pet’r’s Ex. 40. The other article cited by Dr. Akbari, Kohm et al., does discuss MHC molecules in the context of molecular mimicry, but does so specifically in the setting of the pathogenesis of MS. Pet’r’s Ex. 67 at 1. The article explained that “support for infection-induced molecular mimicry stems from the correlation between [MHC] II haplotype [human leukocyte antigen (“HLA”)]-DR2 usage and susceptibility to MS. . . . [o]ne potential explanation could be that this particular MHC molecule can present an infectious-agent-encoded peptide epitope in a conformation that resembles that of myelin peptides.” Id. The article continued with a discussion of MHC molecule cross-reaction to myelin basic protein, but Dr. Akbari failed to explain how this cross-reaction is at all relevant to the case of SFN, a disease that is not defined by demyelination.

Dr. Fujinami also took issue with this section of Dr. Akbari’s report, explaining that Dr.

Akbari’s theory relied on “the T cell receptor . . . recogniz[ing] [] a cross-reactive peptide from the hemagglutinin contained in the [flu] vaccine and also recogniz[ing] some undefined protein found on the peripheral nerve neuron/axon in the context of MHC/HLA class II molecules.” 37 Resp’t’s Ex. E at 5. However, “[t]he flaw in Dr. Akbari’s theory of Th17 cells being effector cells is that these T helper cells would need to recognize MHC/HLA class II with the cross-reacting stretch of amino acids/peptides being present on specific peripheral nerve neurons. The current scientific

35 Kai W. Wucherpfennig et al., Recognition of the Immunodominant Myelin Basic Protein Peptide by Autoantibodies and HLA-DR2-Restricted T Cell Clones From Multiple Sclerosis Patients, 100 J. CLINICAL INVESTIGATION 1114 (1997); Anand M. Gautam et al., A Viral Peptide With Limited Homology to a Self Peptide Can Induce Clinical Signs of Experimental Autoimmune Encephalomyelitis, 161 J. IMMUNOLOGY 60 (1998). 36 Adam P. Kohm et al., Mimicking the Way to Autoimmunity: An Evolving Theory of Sequence and Structural Homology, 11 TRENDS MICROBIOLOGY 101 (2003). 37 MHC is the animal model equivalent to HLA, which is expressed in humans. See Resp’t’s Ex. E at 5.

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data suggest that MHC/HLA class II molecules are not expressed on/in neurons.” Id. (citing Resp’t’s Ex. E, Tabs 8, 9). 38 Indeed, in a study conducted by Redwine et al., the authors examined the presence of MHC molecules in mice after inducing demyelination, and found MHC class II molecules did not present on neurons, astrocytes, or endothelial cells. Resp’t’s Ex. E, Tab 9 at 3– 4. The only location where the authors identified the presence of MHC class II cells during demyelination was on “microglia/macrophage lineage cells expressing CD11b.” Id. at 4. The authors thus concluded that “[m]icroglia . . . are the only cell type capable of presenting antigen to both CD8+ and CD4+ T cells.” Id. at 5. Thus, Dr. Fujinami concluded that “Dr. Akbari’s theory of T helper cell involvement in neuronal destruction through molecular mimicry[] has significant issues if the T helper cells . . . cannot recognize the putative cross-reacting peptide/MHC/HLA class II complex on the surface of peripheral neurons/axons involved in SFN.” Resp’t’s Ex. E at 5. Dr. Fujinami provided the following graphic to explain his point:

Id. at 6. He explained that “[t]he antigen presenting cell in Dr. Akbari’s theory would be on the neuron and the CD4 T cell would be the Th17 cell in his report. The Ag [] would be the putative neuronal peptide that cross-reacts with [flu] hemagglutinin.” Id. at 5 (emphasis added). However, “[n]eurons do not have HLA/MHC class II molecules on their surface to be able to present the putative neuronal peptide that is part of his theory. Neurons lack the ability to present peptides to the Th17 cells.” Id.

In response, Dr. Akbari further explained the immune system response following vaccination and cited two articles which showed increased levels of inflammasome and IL-1

38 Jeffrey M. Redwine et al., In Vivo Expression of Major Histocompatibility Complex Molecules on Oligodendrocytes and Neurons During Viral Infection, 156 AM. J. PATHOLOGY 1219 (2001).

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following vaccination. Pet’r’s Ex. 76 at 5–6 (citing Pet’r’s Exs. 83, 84). 39 He summarized the results of these studies:

1) antigen-presenting cells, including macrophages and monocytes, play a crucial role in vaccination and play an active role in fast response within the first few days; 2) vaccines, including flu vaccination, induce inflammasome activation, as evidenced by the production of the IL-1 superfamily[; and] 3) [p]atients are heterogenous and a new clustering of patients help us to understand the response and possible adverse effects to vaccines.

Id. at 6–7. Dr. Akbari then concluded that “[t]he three points presented unequivocally debunk Dr[.] Fujinami’s statements, ignoring heterogeneity of human subject.” Id. at 7. Heterogeneity, according to Dr. Akbari, results in different responses to vaccines, and thus could possibly result in SFN following flu vaccination based on his theory. Id.

Consequently, the section and basic figure of MHC and TCR in the [graphic] presented by Dr. Fujinami[] might serve as an introductory example suitable for medical students and those new to the field of immunology. However, in numerous instances, we observe more rapid responses due to several factors. . . . These include the activation of the inflammasome, followed by lymphocyte mimicry, repeated exposure to flu vaccine with many overlap antigens each year and the involvement of immunoregulatory pathways among many others, including impairment of regulatory pathways and [Tregs].

Id. Dr. Akbari further stated that it was a “myopic perspective” to claim sequence homology was the only factor involved in the development of autoimmune disease following vaccination. Id. at 17. In addition to this and sequence homology, Dr. Akbari appeared to invoke a theory of rechallenge with the following explanation:

In immunology, the necessity of a second (or possibly third or multiple) signal to induce a pathogenic disease is often crucial. These requirements also elucidate how molecular mimicry can contribute to both immune tolerance and immune autoreactivity. Scientific theories are neither inherently false nor true; they consistently reside somewhere in between. Some theories exhibit greater credibility and acceptance than others, prompting the use of qualifiers such as “more likely than not” or being based on a “preponderance of evidence.[”]

Id. Dr. Akbari’s responses do not at all address the actual argument made by Dr. Fujinami, which is that the HLA/MHC molecules Dr. Akbari relies on to support his theory of molecular mimicry are not present on the neurons damaged by SFN. Instead, Dr. Akbari appears to relate this to an argument about the timing of the disease following vaccination, with general references towards

39 Slim Fourati et al., Pan-Vaccine Analysis Reveals Innate Immune Endotypes Predictive of Antibody Responses to Vaccination, 23 NATURE IMMUNOLOGY 1777 (2022); Thomas Hagan et al., Transcriptional Atlas of the Human Immune Response to 13 Vaccines Reveals a Common Predictor of Vaccine-Induced Antibody Responses, 23 NATURE IMMUNOLOGY 1788 (2022).

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adverse effects following other vaccines and generalized inflammation following flu vaccination, and generalized statements regarding molecular mimicry that appear unconnected to Dr. Fujinami’s actual critique. This is wholly insufficient on its own to provide a connection between the flu vaccine and SFN, and even more so given that Dr. Akbari failed to explain how his theory of molecular mimicry would apply given the lack of HLA/MHC molecules present on the damaged neurons.

b. Bystander Activation

Dr. Akbari also appeared to invoke the theory of bystander activation as a potential mechanism facilitating molecular mimicry. Pet’r’s Ex. 29 at 11. “Because memory T cells readily respond to cytokines, bystander memory T cells to an unrelated antigen can be transiently activated during an infection or immunization process.” Id. (citing Pet’r’s Ex. 41). 40 However, Dr. Akbari did not explain how bystander activation could facilitate molecular mimicry, nor did he mention the concept again in his reports. Furthermore, this assertion is confounded by the article he cited in support, Fujinami et al., which highlighted bystander activation as an entirely separate process from molecular mimicry in the pathogenesis of autoimmune diseases. Pet’r’s Ex. 41 at 2. Fujinami et al. provided the following explanation of the mechanism:

Virus infections lead to significant activation of [antigen-presenting cells (“APCs”)] such as dendritic cells. These activated APCs could potentially activate preprimed autoreactive T cells, which can then initiate autoimmune disease. . . . [V]irus-specific T cells migrate to areas of virus infection/antigen . . . T cells recognize these infected cells and release cytotoxic granules resulting in the killing or death of the infected cells. Under these circumstances the dying cells, the CD8+ T cells and [macrophages] within the inflammatory focus release cytokines . . . which can lead to bystander killing of the uninfected neighboring cells. This results in additional immunopathology at sites of infection.

Id. The article stated that “[m]olecular mimicry, bystander activation, and viral persistence . . . are three mechanisms that can initiate immunoreactivity leading to autoimmune disease.” Id. at 1. Notably, the authors focused on virus-induced autoimmune disease, declaring “[v]iruses have been shown to be one of the environmental factors that are capable of precipitating autoimmune disease;” however, there was no such assertion about vaccines. Id. at 12. Indeed, “[t]he data suggest that viruses that have molecular mimicry with self-proteins may be used as vaccines to prevent autoimmune disease later in life. Id. at 7.

4. The Flu Vaccine’s Stimulation of Autoreactive T Cells

Dr. Akbari next argued that the flu vaccine was capable of causing inflammatory diseases generally and stated that a “literature search from 1979 to 2013 revealed [] 71 documented cases

40 Robert S. Fujinami et al., Molecular Mimicry, Bystander Activation, or Viral Persistence: Infections and Autoimmune Disease, 19 CLINICAL MICROBIOLOGY REVS. 80 (2006).

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of inflammatory diseases after vaccination.” Pet’r’s Ex. 29 at 21 (citing Pet’r’s Ex. 62). 41 He stated that the “most commonly reported vaccination that was associated with neuropathy and demyelinating diseases [was] vaccination against [flu] viruses.” Id. However, Dr. Akbari’s reliance on this article is quite problematic. First, as explained above, SFN is not a demyelinating disease. Thus, the applicability of any demyelination process to its pathogenesis is questionable. Second, the article, Karussis & Petrou, relied on “[t]he pathogenic role of adjuvants in the induction of autoimmune syndromes, [as] has been highlighted by Yehuda Shoenfeld who introduced the term ASIA syndrome.” Pet’r’s Ex. 62 at 7. As explained above, this theory of causation has been found to be wholly without merit in the Program and casts overall doubt on the credibility of the article. However, even assuming the baseline case reports relied upon in the article are credible, none of the reports listed SFN as being associated with any vaccine. See id. at 5.

5. Inflammasome and Its Role in SFN Following Flu Vaccination

To explain the “mechanism of action by which flu vaccine induce[s SFN], particularly in [one to two] days after vaccination,” Dr. Akbari cited to Crooke et al. 42 Pet’r’s Ex. 29 at 7 (citing Pet’r’s Ex. 47). Crooke et al. was a study designed to test the hypothesis “that age-related dysfunction of inflammasome may be associated with poor [flu]-vaccine response among older adults.” Pet’r’s Ex. 47 at 1. The authors defined inflammasome as “a class of multimeric complexes comprised of NOD-like receptors [] that are responsible for the enzymatic processing and maturation of certain innate cytokines.” Id. at 2. They further noted “studies have found recognition of [flu] A by the inflammasome complex to be essential for establishing protective adaptive immunity.” Id. More specifically,

Activation of the inflammasome occurs upon recognition of intracellular pathogens or other cellular stressors through two distinct signaling events. In the case of [flu], recognition of viral RNA by [toll-like receptor (“TLR”)] 7 results in the [] expression of inflammatory cytokine proforms [] while the [flu] virus M2 protein or the PB1-F2 polymerase stimulate activation of the NLRP3 . . . inflammasome complex . . . . Activation of the inflammasome complex leads to increased caspase- 1 activity, the processing of inflammatory cytokines into their bioactive forms, and the ultimate release of inflammatory mediators via pyroptosis. 43

Id. The study went on to explain that in older adults, “[s]ignificant decreases in IL-6, TNF-ɑ, IL- 12p40, and IFN-ɑ production have been observed following [TLR] stimulation in myeloid dendritic cells . . . identifying strong associations between dysregulated TLR function and [flu] antibody response.” Id. Thus, given that the authors found inflammasome to generate a protective effect against flu in animal models, they wished to determine that same effect on humans via

41 Dimitrios Karussis & Panayiota Petrou, The Spectrum of Post-Vaccination Inflammatory CNS Demyelinating Syndromes, 13 AUTOIMMUNITY REVS. 215 (2014). 42 Stephen N. Crooke et al., Inflammasome Activity in Response to Influenza Vaccination Is Maintained in Monocyte-Derived Peripheral Blood Macrophages in Older Adults, 2 FRONTIERS AGING 719103 (2021). 43 Pyroptosis is a “type of programmed cell death associated with infection by intracellular pathogens. It is characterized by INFLAMMASOME formation; activation of CASPASE 1; and CYTOKINES mediated inflammation.” Pryoptosis, NAT’L INST. OF HEALTH, NAT’L LIBRARY OF MED. https://www.ncbi.nlm.nih.gov/mesh/? term=pyroptosis.

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vaccine-activation. Id. Overall, the study concluded that inflammasome activation was not impaired in older adults 28 days after vaccination, and that “an alternative mechanism unaffected by age is responsible for stimulating inflammasome activation following flu vaccination. Id. at 8– 9. The authors also noted that “inflammasome has been implicated as a critical component for protective immunity against [flu] in several animal studies,” though similar studies had not been conducted in humans. Id. at 9. Dr. Akbari thus used this article as support of the proposition that the flu vaccine can trigger the development of inflammasome. Pet’r’s Ex. 29 at 16.

Dr. Fujinami, took issue with this section of Dr. Akbari’s report, providing the following critique:

Somehow, stimulation by the [flu] hemagglutinin in the [flu] vaccine of macrophages/monocytes first leads to inflammasome activation; then second leads to inflammation; then third leads to damage and/or death of particular neurons or dying back of axons within the PNS, and it is only these small axonal fibers that are damaged. I am at a loss as to how this could happen, let alone within two days after vaccination.

Resp’t’s Ex. E at 4. He argued that Dr. Akbari did not explain how the flu vaccine “disseminated specifically to the tissue resident macrophages that may or may not be in close approximation with the small nerve fibers that control pain and then killed/damaged only those axons.” Id. Dr. Fujinami explained that Dr. Akbari had not presented any evidence to support the presence of these macrophages in close proximity to the peripheral nerve axons damaged by SFN, or “why these specific tissue macrophages . . . have inflammasome activation that could lead to a significant dying back of neurons/axons at these particular sites within the body.” Id. Dr. Fujinami also critiqued Dr. Akbari’s reliance on TNF-ɑ as a cytokine associated with neuropathies, as these macrophages are “found in the [CNS], not the PNS,” and that such an association is “not supported by documentation from the scientific literature.” Id.

In Dr. Akbari’s supplemental report, he acknowledged that there were no studies linking SFN to flu vaccination but nonetheless asserted that his “hypothesis” remained valid. Pet’r’s Ex. 76 at 2–3. In support, Dr. Akbari cited to Christian et al., 44 which measured local and systemic inflammatory reactions following flu vaccination. Id. at 2 (citing Pet’r’s Ex. 79). Dr. Akbari claimed the article supported “the notion that subjective reports of local and systemic reactions such as IL-1b following vaccination correspond with biological indicators of inflammatory status and adverse effects.” Id. at 3. However, the authors did not discuss IL-1b. Instead, the authors noted that those who had local-site arm soreness one day after vaccination had increases in pro inflammatory cytokines, TNF-ɑ and macrophage migration inhibitory factor, and those with systemic reactions (such as headache, muscle aches, malaise, fatigue, and fever) had “marginally higher IL-6 at baseline compared to those with no systemic symptoms.” Pet’r’s Ex. 79 at 7. The authors concluded that these subjective symptoms “correspond with inflammatory responses following [flu] vaccination.” Id. Using this article as support, Dr. Akbari stated that “cytokines are produced at the site of vaccination in response to the flu vaccine and often bind to IL-1 receptors and initiate an immune response and induce a cascade of events.” Pet’r’s Ex. 76 at 2. Dr. Akbari

44 Lisa M. Christian et al., Proinflammatory Cytokine Responses Correspond With Subjective Side Effects After Influenza Virus Vaccination, 33 VACCINE 3360 (2015).

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did not explain what this “cascade of events” entailed but nonetheless asserted that “[t]he results of these studies overall support the notion that the inflammasome and subsequent production of IL-1b get sufficiently triggered by the flu vaccination.” Id. at 3 (citing Pet’r’s Ex. 80 at 3 (finding that IL-1b is elevated after live-attenuated flu vaccination and flu infection)). 45

Dr. Akbari next explained that similar to other immune responses, inflammasome “should be regulated and is only upregulated for the first few days.” Pet’r’s Ex. 76 at 3. However, he then added that “[a]s a matter of fact, in many individuals, this immune regulation is simply impaired. This was discussed in a recent publication.” Id. No citation was given for this assertion. Man & Kanneganti, 46 which Dr. Akbari later used to explain the regulatory pathways of inflammasome, also addressed the regulatory mechanisms of inflammasome, but the authors did not conclude that many individuals suffer from an impaired immune system. See Pet’r’s Ex. 81.

Dr. Akbari then asserted that “[i]f a biological system (including humans) experiences impairment in these regulatory mechanisms, the inflammasome can cause pathology after immunization.” Pet’r’s Ex. 76 at 3. Dr. Akbari cited to Won et al., 47 to assert that a “dysregulated inflammasome response (and high levels of IL-1 and IL-18)” was associated with “many adverse effects after vaccination including . . . myopericarditis.” Id. at 4 (citing Pet’r’s Ex. 82). However, this statement is not supported by the article. Rather, Won et al. examined the biological mechanisms of myopericarditis following COVID-19 vaccination and found IL-18 and NLRP3 inflammasome to be contributors to its pathogenesis. Pet’r’s Ex. 82 at 6. The article did not provide any other examples of a dysregulated inflammasome response following vaccination, nor did the article examine any vaccine other than the COVID-19 mRNA vaccine. Later in his supplemental report, Dr. Akbari argued that inflammasome had been linked to neuroinflammation and the development of “various neurological diseases, including Alzheimer’s, Parkinson’s, and [MS].” Pet’r’s Ex. 76 at 8. No citations were provided for this assertion, and Dr. Akbari’s prior cited articles do not support this proposition.

Dr. Akbari conceded that “[t]he connection between vaccine-induced inflammasome activation and the development of SFN necessitates further investigation.” Pet’r’s Ex. 76 at 4. He argued that “[t]he studies that Dr. Fujinami presented, which suggest no association between the two, lack a sufficient number of subjects to fully comprehend the underlying mechanisms and the potential implications for vaccine safety and efficacy.” Id. at 4. Dr. Akbari concluded by asserting that “current evidence supports a significant association between vaccine-induced inflammasome activation and the subsequent induction of sterile inflammatory responses, such as SFN.” Id. at 5.

45 Weichun Tang et al., Post-Vaccination Serum Cytokines Levels Correlate With Breakthrough Influenza Infections, 13 SCI. REPS. 1174 (2023). 46 Si Ming Man & Thirumala-Devi Kanneganti, Regulation of Inflammasome Activation, 265 IMMUNOLOGICAL REVS. 6 (2015). 47 Taejoon Won et al., Increased Interleukin 18-Dependent Immune Responses Are Associated With Myopericarditis After COVID-19 mRNA Vaccination, 13 FRONTIERS IMMUNOLOGY 851620 (2022).

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6. The Flu Vaccine’s Association with SFN

Dr. Akbari’s next section of his reports purported to show an association between the flu vaccine and the development of SFN. Pet’r’s Ex. 29 at 23. First, he cited to Kreẞ et al., 48 which found increased levels of “IL-6, IL-8, and TNF gene expressions” in patients with SFN. Id. (citing Pet’r’s Ex. 69 at 8). Dr. Akbari then cited to Zheng et al., 49 which he stated, “provided mechanistic and diagnostic information and reported higher levels of IL-6, IL-17, and TNF in patients with [SFN].” Id. at 23–24 (citing Pet’r’s Ex. 70). However, the study did not address SFN; instead, it focused on the correlation between inflammatory cytokines, negative emotions, and the onset of diabetic peripheral neuropathy in the setting of type 2 diabetes. Pet’r’s Ex. 70 at 1.

Turning specifically to the flu vaccine, Dr. Akbari cited a case report he claimed “show[ed ]that flu vaccine[] is capable of causing [SFN].” Pet’r’s Ex. 29 at 24 (citing Pet’r’s Ex. 71).50 However, the case report cited by Dr. Akbari did not involve a case of SFN—it was a report of “biopsy proven vasculitis, presenting as mononeuritis multiplex, following [flu] vaccination.” Pet’r’s Ex. 71 at 4. Dr. Fujinami also critiqued Dr. Akbari’s statement, explaining that “vasculitis neuropathy is a large fiber neuropathy,” not a SFN. Resp’t’s Ex. E at 7.

Dr. Akbari then stated that other vaccines, such as rabies, varicella, Lyme disease, and COVID-19 had been reported to cause SFN, as “all these vaccines similar to flu vaccine induce inflammasome, however due to the robust regulatory mechanism, the side effects are generally rare.” Pet’r’s Ex. 29 at 24. Dr. Akbari then appeared to change the cytokines underlying the focus of his theory, arguing that the “induction of inflammasome (IL-1 and IL-6) along with T cell stimulation, after administration of vaccine such as flu vaccine, is able to trigger pathogenic T cells and cause [SFN].” Id. He also made general comments regarding the importance of genetic and environmental factors in the development of autoimmune diseases, but did not identify any such factors present in Petitioner and did not provide citations to support most of his arguments to this point. Id. at 24–25.

Dr. Fujinami’s final critique of Dr. Akbari’s theory was that he relied on an assumption that immunizations would generate the same level of immune response as an active infection. Resp’t’s Ex. E at 6. Citing again to Raasing et al., Dr. Fujinami explained that the incidence rate of SFN is approximately 12 per 100,000 individuals, whereas GBS is one to two cases per 100,000 individuals. Id. (citing Resp’t’s Ex. E, Tabs 1, 8). 51 “Since the number of individuals are similar to GBS, a demonstrable increase in SFN following [flu] infection and/or vaccination would be noted in the population, as is the case for GBS.” Id. at 7. Fujinami stated that HIV, Lyme, and Hepatitis C infections have all been associated with SFN, but not the flu virus. Id. (citing Resp’t’s

48 Luisa Kreẞ et al., Cytokine Expression Profiles in White Blood Cells of Patients with Small Fiber Neuropathy, 24 BMC NEUROSCIENCE 1 (2023). 49 Ya-Hong Zheng et al., A Cross-Sectional Study on the Correlation Between Inflammatory Cytokines, Negative Emotions, and Onset of Peripheral Neuropathy in Type 2 Diabetes, 16 NEUROPSYCHIATRIC DISEASE & TREATMENT 2881 (2020). 50 J. Hull et al., Severe Vasculitic Neuropathy Following Influenza Vaccination, 75 J. NEUROLOGY NEUROSCIENCE PSYCHIATRY 1504 (2004). 51 Katharina M. Busl et al., Guidelines for Neuroprognostication in Adults with Guillain-Barré Syndrome, 38 NEUROCRITICAL CARE 564 (2023).

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Ex. E, Tab 8). He noted that the authors in Raasing et al. also noted the possibility of vaccine- induced SFN and cited to case studies done by Souayah et al. 52 and Kafaie et al., 53 though neither implicated the flu vaccine as a potential cause. Resp’t’s Ex. E, Tab 8 at 2 (citing Resp’t’s Ex. E, Tabs 10 (case reports identifying SFN after rabies, varicella, and Lyme disease vaccines), 6 (a single case report of SFN after HPV vaccination). Notably, the authors in Kafaie et al. identified a petition in the Program at the time of their report that alleged the flu vaccine caused a petitioner to develop SFN; however, they noted that the “petition alone cannot be used to assess relationship between vaccination and SFN. At this time, there is no conclusive evidence to suggest the association between [flu] vaccine and SFN.” Resp’t’s Ex. E, Tab 6 at 2.

To further emphasize this point, Dr. Fujinami cited to Croxford et al., 54 a study which induced CNS autoimmune disease via flu infection in mice. See Resp’t’s Ex. E, Tab 2. The authors engineered a “nonpathogenic neurotropic Theiler’s murine encephalomyelitis virus variant” to “encode a mimic peptide from protease IV of [flu virus], sharing [six] of 13 [amino acids] with the dominant encephalitogenic proteolipid protein [epitope].” Id. at 1. The authors found that infection of this variant “induced a rapid-onset, nonprogressive paralytic disease,” while immunized mice “did not develop disease, associated with the failure to induce activation of PLP-specific CD4+ Th1 cells.” Id. Mice that were previously infected and then immunized developed an even more severe form of disease. Id. at 2. The authors concluded that such an example of molecular mimicry would “require[] both the presence of the mimic sequence and the persistent stimulation of innate immune system by the pathogen.” Id. Relying on these findings, Dr. Fujinami argued that “infection is very different than vaccination in the induction of autoimmune neuroinflammatory disease. . . . The examples Dr. Akbari provide[d] are of microbes inducing autoimmune disease and not vaccinations.” Resp’t’s Ex. E at 7 (emphasis in original). Dr. Fujinami went on to state that “in the span of 34 years, only 15 case reports [CNS disease following flu vaccination] are highlighted by Dr. Akbari,” none of which [are] related to SFN. Id.

In response, Dr. Akbari argued that “noteworthy similarities and shared mechanisms” exist between vaccination and natural infection, such as the possibility for molecular mimicry and that “vaccines aim[] to simulate a comparable experience for the immune system without inducing pathology.” Pet’r’s Ex. 76 at 16.

Dr. Akbari also devoted a section of his supplemental report to identifying the “common”

aspects “in all the aforementioned cases of vaccination-induced SFN.” Pet’r’s Ex. 76 at 21.

All the evidence points to common denominators, including the induction of the inflammasome, activation of innate cells alongside T cell activation by vaccines. These factors can initiate immune responses, leading to the destruction of myelin in myelinated small fibers and directly affecting the function of unmyelinated small fibers, thus causing SFN.

52 Nizar Souayah et al., Small Fiber Neuropathy Following Vaccination for Rabies, Varicella, or Lyme Disease, 27 VACCINE 7322 (2009). 53 Jafar Kafaie et al., Small Fiber Neuropathy Following Vaccination, 18 J. CLINICAL NEUROMUSCULAR DISEASE 37 (2016). 54 J. Ludovic Croxford et al., Viral Delivery of an Epitope From Haemophilus Influenzae Induces Central Nervous System Autoimmune Disease by Molecular Mimicry, 174 J. IMMUNOLOGY 907 (2005).

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Furthermore, the activation of the inflammasome, a crucial component of the innate immune system, is consistently observed in various instances of vaccination- induced SFN. This activation sets off a cascade of inflammatory responses that disrupt the delicate balance within the nervous system, contributing to the development of SFN.

Moreover, the impact on both myelinated and unmyelinated small fibers underscores the complexity of SFN development following vaccination. Myelin destruction in myelinated fibers disrupts signal transmission, while direct effects on unmyelinated fibers can impair sensory and autonomic functions collectively contributing to the manifestation of SFN.

In summary, vaccination-induced SFN shares common underlying mechanisms, including inflammasome activation, innate and T cell-mediated immune response, and damage to both myelinated and unmyelinated nerve fibers. Understanding these shared factors is essential for further research and the development of preventative strategies to mitigate the risk of SFN associated with vaccination.

Id. In a similar pattern to the rest of Dr. Akbari’s reports, no citations were provided for these assertions, and his prior-referenced literature does not contain scientific support for his arguments.

7. Petitioner’s Citations to Prior Cases

In support of her argument pursuant to Althen prong one, Petitioner cited to two of my prior decisions involving a SFN injury following flu vaccination. I granted entitlement in both of these cases, and both cases presented molecular mimicry as their theory of causation under Althen prong one. However, Petitioner provided no further context as to why these cases are relevant to her claim. As an initial matter, “[w]e are cautious to not apply a one-size-fits-all approach in every case, because the nuance matters,” particularly with respect to Althen’s first prong. Hunt v. Sec’y of Health & Hum. Servs., No. 21-1379V, 2026 WL 1601989, at *26 (Fed. Cl. Spec. Mstr. May 8, 2026). “[M]any cases alleging the same vaccine/injury cause-and-effect were done with experts that may overlap but are not the same on both sides; sharing theories that are similar but not identical; and using literature that has been at times novel, outdated, updated, or even abandoned.” Id. at *23. Thus, an examination of the specifics of each case is warranted to determine their relevance to the case at bar. As explained below, these cases are quite distinguishable from Petitioner’s, and do not support an acceptance of Dr. Akbari’s theory as presented here.

The first case, Drobbin, involved a petitioner who suffered from SFN following his receipt of a flu vaccine. Drobbin v. Sec’y of Health & Hum. Servs., No. 14-225V, 2020 WL 3799206 (Fed. Cl. Spec. Mstr. Jan. 21, 2020). The petitioner’s experts presented a theory of molecular mimicry and filed articles specifically applying this theory to the development of SFN. Id. at *16. This was supported by evidence showing the medical community had determined molecular mimicry can cause some flu-vaccine-induced peripheral neuropathies. Id. at *17. The petitioner also provided evidence of parallels between atypical axonal GBS and autoimmune SFN “to illustrate how the pathogenesis of one can instruct with the respect to the other.” Id. The Respondent’s expert, Dr.

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Donofrio, argued that “molecular mimicry can only be considered as a viable causation theory when the cross-reaction has been identified and tested to prove pathogenesis,” and offered no specific critique or contradiction contained in the petitioner’s report. Id. This standard for causation was too high for what is accepted in the Program, and given the petitioner’s otherwise unrebutted arguments that were supported by scientific evidence, I found that the petitioner had satisfied his burden pursuant to Althen prong one. Id.

The second case cited by Petitioner, E.M., also involved a petitioner who used molecular mimicry to connect her flu vaccine to the development of SFN. E.M. v. Sec’y of Health & Hum. Servs., No. 14-753V, 2021 WL 3477837 (Fed. Cl. Spec. Mstr. July 9, 2021). The petitioner’s expert, Dr. Steinman, presented a theory that her flu vaccine “triggered an autoimmune response to the alpha 3 nicotinic acetylcholine receptor via molecular mimicry,” resulting in SFN. Id. at *36. This theory relied on the notion of a recall response, allowing the immune system to develop “ample immunological memories,” which can generate a subsequent immune response up to eight years later. Id. Dr. Steinman also provided homologies between the flu vaccine and the alpha 3 nicotinic acetylcholine receptor through a BLAST search and his own filtration process, and pointed to animal studies explaining the relevance of his selected sequences. Id. at *37. The Respondent’s expert, Dr. Donofrio, did not dispute the relevance of these sequences, and instead made a broad assertion regarding the lack of epidemiologic evidence of vaccine causation. Id. at *38. Despite this, Dr. Donofrio conceded that epidemiologic studies are not the only way to establish vaccine causation via molecular mimicry. Id. Given Dr. Steinman’s persuasive arguments, backed by reliable evidence, and the lack of a specific critique by Dr. Donofrio, I found the petitioner had presented preponderant evidence to satisfy Althen prong one. Id. at *39.

The facts of the present case are markedly different. The petitioner in Drobbin relied on identifying cross-reactive components of the vaccine and PNS to explain his theory of molecular mimicry and persuasively analogized the disease to atypical axonal GBS. The petitioner in E.M. identified cross-reactive peptides between the vaccine and the alpha 3 nicotinic acetylcholine receptor and provided studies to support the relevance of those peptide sequences. Conversely, Dr. Akbari relied on the induction of inflammasome and sparsely commented on potential cross- reactive peptides that were not present on the peripheral neurons/axons affected by SFN. While all three petitioners used the same core mechanism of molecular mimicry to explain their theories, the specifics of all three theories identified differed in terms of their fundamental principles.

In addition to the core differences between the theories presented in these three cases, the petitioners in Drobbin and E.M. provided much more compelling evidence and explanations to support their theories than Dr. Akbari. The petitioner in Drobbin provided medical literature directly explaining the role molecular mimicry played in SFN; Dr. Akbari did not. The petitioner in Drobbin also filed evidence and presented persuasive arguments explaining the parallel pathogenesis of atypical axonal GBS and SFN; Dr. Akbari did not. The petitioner in E.M. explained the pathogenic relevance of the alpha 3 nicotinic acetylcholine receptor in the development of SFN; Dr. Akbari did not. And, both of the petitioners in Drobbin and E.M. also filed evidence regarding the cross-reactive peptides between the flu vaccine and PNS that would lead to the pathogenesis of SFN; Dr. Akbari did not. Further, the Respondent’s arguments in both Drobbin and E.M. amounted to a lack of epidemiologic and scientifically proven evidence to support the petitioner’s claim, a bar far too high than what has been established in the Program.

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Here, Dr. Fujinami provided several cogent and compelling critiques of Dr. Akbari’s theory, which Dr. Akbari failed to rebut.

“Special masters are neither bound by their own decision nor by cases from the Court of Federal Claims, except, of course, in the same case on remand.” Hanlon v. Sec’y of Health & Hum. Servs., 40 Fed. Cl. 625, 630 (1998). This is because in Vaccine Act cases, the nuance matters. See Hunt, 2026 WL 1601989, at *26. Molecular mimicry is often “invoked as the mechanistic ‘skeleton key’ that unlocks how an autoimmune disease process may have occurred” in Program cases. Ampofo-Addo v. Sec’y of Health & Hum. Servs., No. 21-1231V, 2025 WL 2463643, at *20 (Fed. Cl. Spec. Mstr. July 31, 2025). However, “merely chanting the magic words ‘molecular mimicry’ in a Vaccine Act case does not render a causation theory reliable, absent additional evidence specifically tying the mechanism to the injury and/or vaccine in question.” McKown v. Sec’y of Health & Hum. Servs., No. 15-145V, 2019 WL 4072113, at *50 (Fed. Cl. Spec. Mstr. July 15, 2019). Dr. Akbari’s reports lack this additional evidence. While true that I have found petitioners to be entitled to compensation when asserting similar injuries as the current Petitioner based on similar theories of causation, the fact that I have accepted two distinct theories that invoke molecular mimicry with regard to this particular vaccine and injury does not mean that I am bound to accept a third. As I explained above, Dr. Akbari’s theory does not contain the same level of reliable evidence needed to satisfy Althen’s first prong, and he failed to rebut Dr. Fujinami’s critiques to central components of his theory. Petitioner’s reliance on these prior cases is therefore misplaced.

8. Concluding Remarks for Althen Prong One

In sum, Dr. Akbari presented evidence showing a possible relationship between IL-17, Th17, and the development of MS and EAE via mechanisms other than molecular mimicry. He has also shown that various cytokines play various roles in various different forms of inflammation and autoimmune diseases. However, what he has failed to do is provide any evidence whatsoever linking SFN to the flu vaccine or explain how the literature relating to the demyelinating CNS condition, MS, relates to the pathogenesis of the non-demyelinating PNS disease, SFN. Dr. Akbari himself even admitted that MS and EAE do “not accurately represent SFN,” and it is unclear why he would rely so heavily on this literature given this contradictory argument. See Pet’r’s Ex. 76 at 13.

Furthermore, Dr. Akbari’s actual discussion of cytokines varied throughout his reports, as at different points he implicated Th17, IL-17, IL-1, and IL-6 in the development of SFN. However, none of this was supported by the literature. He also admitted in his reports that his theory would apply to almost any vaccine, and it appears to not be limited to any form of injury. Dr. Akbari relied on a theory of molecular mimicry, but only provided a peptide sequence with three out of six matches, and did not provide literature to show how this would be sufficient. Dr. Akbari also did not provide any literature to support the accuracy of these peptides, nor did he provide any search criteria he used to find these peptides, such as a BLAST search.

Dr. Akbari’s theory of molecular mimicry appears to be at odds with his theory of inflammasome, as the two peptides he purports to identify are located on the flu vaccine hemagglutinin and the myelin basic protein; if inflammasome is indeed implicated in the

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development of SFN via molecular mimicry, Dr. Akbari has failed to provide this evidence or explain how it would be implicated in its development beyond his assertions that the flu vaccine can cause inflammasome. This statement is the equivalent of stating the flu vaccine generates an immune response, and without more, such a statement is insufficient to prove vaccine causation.

Dr. Akbari also never responded to Dr. Fujinami’s central critique, which is the lack of MHC/HLA class II molecules on the neurons affected by SFN that Dr. Akbari relied on for his theory. These MHC molecules underpin Dr. Akbari’s theory of cross-reactivity; however, in order for a cross-reaction to occur, there must be something to cross-react to. Dr. Akbari failed to respond at all to this issue, instead addressing it as if it were related to the timing of symptom onset. The medical literature provided by Dr. Fujinami supports the notion that no such molecules exist on the peripheral neurons/axons, and without this, Dr. Akbari’s theory fails.

Finally, the sheer level of inaccuracy contained within Dr. Akbari’s reports greatly reduces his credibility in the eyes of the Court. Of the 45 references contained in Dr. Akbari’s report, 22 were gravely inaccurate or misrepresented. This does not include the numerous occasions Dr. Akbari made scientific conclusions without providing any form of evidence. And this is not a oneoff instance. Dr. Akbari has been warned repeatedly by other special masters due to the overall lack of cohesiveness of his reports, the frequent mischaracterization of the literature he cites, and his habit of asserting scientific conclusions without providing any supporting evidence. See e.g., Ampofo-Addo, 2025 WL 2463643, at *19 (rejecting Dr. Akbari’s theory for relying on conclusory statements, mischaracterizing medical literature, and lacking preponderant evidence); Ray v. Sec’y of Health & Hum. Servs., No. 20-321V, 2025 WL 3900631, at *22–24 (Fed. Cl. Spec. Mstr. Dec. 12, 2025) (“Petitioner and her experts mischaracterize the medical literature to support their contentions . . . Dr. Akbari mischaracterizes the findings, adversely affecting his credibility and reliability of his opinions. This critique of Dr. Akbari is not new.”) (citing Powell v. Sec’y of Health & Hum. Servs., No. 20-1726V, 2025 WL 3443590, at *32 (Fed. Cl. Spec. Mstr. Oct. 8, 2025) (“Dr. Akbari mischaracterizes the medical literature he cites which further adversely affects his credibility and the reliability of his opinions.”); Williams v. Sec’y of Health & Hum. Servs., No. 19-1269V, 2024 WL 5040482, at *43 (Fed. Cl. Spec. Mstr. Nov. 13, 2024) (rejecting Dr. Akbari’s theory because “(1) his proffered ideas about causation lack development, (2) he suggests the adoption of [a] legal standard other than preponderant evidence, and (3) he mischaracterizes the findings of medical articles.”); Nieves v. Sec’y of Health & Hum. Servs., No. 18-1602V, 2023 WL 3580148, at *44–45 (Fed. Cl. Spec. Mstr. May 22, 2023) (Dr. Akbari’s “theory amounts to a confusing, inter-related patchwork of contentions . . . . There were also several erroneous foundational contentions in Dr. Akbari’s opinion.”)); M.M. v. Sec’y of Health & Hum. Servs., No. 18-583V, 2024 WL 4164557, at *37 (Fed. Cl. Spec. Mstr. Sept. 12, 2024) (Dr. Akbari “misrepresents the literature he cites. . . . Dr. Akbari’s expert report, . . . is a meandering discussion of various topics that do not relate to how the flu vaccine can exacerbate asthma. It is difficult to understand and offers no cohesive theory that can be thoughtfully analyzed.”). 55

Dr. Akbari’s theory amounts to little more than speculation, relying on conclusory statements and misrepresentations of scientific literature to advance his theory. As has been articulated several times in the Program, a special master is not bound to “the ipse dixit of the

55 Due to this history of repeated behavior and his performance in the present case, Dr. Akbari’s fees will be addressed accordingly.

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expert,” especially if “there is simply too great an analytical gap between the data and the opinion proffered.” Snyder v. Sec’y of Health & Hum. Servs., 88 Fed. Cl. 706, 743 (2009) (quoting Gen. Elec. Co. v. Joiner, 522 U.S. 146 (1997)). I do not find Dr. Akbari’s theory to be reliable, credible, or persuasive in any manner. Accordingly, Petitioner has failed to satisfy her burden pursuant to Althen prong one.

B. Specific Causation: A Logical Sequence of Cause and Effect

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). This includes instances where an action is “a substantial factor in bringing about the harm, and that the harm would not have occurred but for that action.” Shyface, 165 F.3d at 1365 (internal citations omitted). The Federal Circuit has explained that in such cases, “while the vaccination must be a substantial factor in the [injury], it need not be the sole factor or even the predominate factor.” Pafford, 451 F.3d at 1357.

A successful argument pursuant to Althen prong two is heavily dependent on a reliable causation theory. Petitioner’s inability to meet her burden demonstrating how the flu vaccine can cause SFN effectively precludes her from being able to show that her symptoms were actually caused by the vaccine according to said theory. This hinders any meaningful discussion on prong two.

Petitioner relied on the report of John Hixson, M.D., 56 as well as the reports of Dr. Akbari to support her argument pursuant to Althen prong two. Dr. Hixson detailed Petitioner’s initial onset of symptoms, noting that Petitioner had no neurological issues prior to vaccination, experienced generalized inflammation from the vaccine in the days immediately following, and then developed SFN approximately five days after vaccination. Pet’r’s Ex. 16 at 5. He also noted that her neurologist considered this to be a “post-vaccination demyelinating process.” Id. at 6 (citing Pet’r’s Ex. 6 at 3–4). Dr. Hixson’s application of his asserted biological mechanism is summarized tersely: “[g]iven the absence of neurologic symptoms and signs prior to the vaccination in February 2018, and the abnormal findings in October 2018 consist[ent] with a small fiber nerve injury, a logical sequence of ‘cause and effect’ is established in this case.” Pet’r’s Ex. 16 at 6.

Likewise, Dr. Akbari’s discussion of the evidence that Petitioner’s SFN was vaccinecaused consisted entirely of the following:

Based on my examination of the records and the understanding of the onset of fiber neuropathy post flu vaccination, the timing of the vaccine administration and the

56 Dr. Hixson is a Professor of Clinical Neurology at the University of California, San Francisco. Pet’r’s Ex. 17 at 1. He received his M.D. from Johns Hopkins University School of Medicine, and he completed his internship and neurology residency at the University of Pennsylvania. Id. Dr. Hixson also completed an epilepsy and neurophysiology fellowship at the University of Iowa. Id. In his current position Dr. Hixson cares for neurology patients with a specialty in epilepsy. Pet’r’s Ex. 16 at 1.

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symptom development aligns with reports from various sources. This correlation substantiates the notion that fiber neuropathy was triggered by an event like the flu vaccine, establishing a logical sequence of cause and effect between [Petitioner’s] vaccination and her subsequent adverse reactions. This rapid induction of inflammasome within a short timeframe leads to robust immune response triggered by molecular mimicry, which can subsequently aggregate symptoms.

Pet’r’s Ex. 29 at 26. In response, Dr. Fujinami reiterated his comment that the timeline of neuroinflammation did not support a logical sequence of cause and effect. Resp’t’s Ex. C at 5.

In evaluating whether prong two 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. Curcuras, 993 F.2d at 1528. While Dr. Hixson is correct in stating that Dr. Gardella listed a potential demyelinating process from the vaccine in Petitioner’s differential diagnosis, this was her first neurological visit five days after she received the vaccine and before any kind of testing had been accomplished. Petitioner was subsequently diagnosed with SFN, and while Dr. Roth did at one point question whether this could be related to her vaccine, her other providers diagnosed Petitioner’s SFN as idiopathic, and Dr. Roth made no further treatment notes regarding a potential relationship between the vaccine and Petitioner’s SFN. See Pet’r’s Ex. 11 at 11 (Dr. Chin noting Petitioner’s SFN was “idiopathic for now” after her October 2018 biopsy); Pet’r’s Ex. 7 at 25 (Dr. Roth considering a “post-vaccination inflammatory reaction similar to [GBS]” but noting it was “unclear” whether this was the cause of Petitioner’s SFN); Pet’r’s Ex. 15 at 6 (Dr. Peterson noting Petitioner’s SFN was idiopathic).

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, 400 F.3d at 1325. Instead, Petitioner may satisfy her burden by presenting circumstantial evidence and reliable medical opinions. Id. at 1325–26. Petitioner abandoned Dr. Hixson’s causation theory asserting molecular mimicry with a five-day onset and now relies on Dr. Akbari’s theory of inflammasome induction and molecular mimicry with a one-to-two-day onset. The case study that Dr. Akbari relied on to illustrate this clinical presentation involved a patient who develop SFN following two doses of a COVID-19 vaccine. See Pet’r’s Ex. 99. In that case, Petitioner was a 57-year-old female who presented one week after her second COVID-19 vaccine dose with “subacute onset of intense burning dysesthesias in the feet, gradually spreading to the calves and . . . hands, unaccompanied by other neurological [] symptoms.” Id. at 1. The patient was treated with gabapentin, and her symptoms improved. Id. During her two-week follow- up, “she reported complete resolution of neuropathic pain,” and discontinued her treatment. Id. Examination revealed however, that “stocking-type small fiber modality loss persisted.” Id. This patient presented differently from Petitioner in all manner of ways. First, the former’s symptoms occurred following the second dose of an adjuvanted COVID-19 vaccine, while Petitioner was injected once with a nonadjuvanted, single dose, flu vaccine. The case study patient did not present

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with the initial flu-like symptoms that Petitioner experienced. Instead, the case study patient’s symptoms began with sensory distortion in her lower extremities. Id. at 1. The case study patient’s symptoms also improved within a couple of weeks, whilst Petitioner continued to experience tingling in her upper and lower extremities over eighteen months post vaccination. Pet’r’s Ex. 99 at 1; Pet’r’s Ex. 15 at 6, Ex. 7 at 9. Indeed, the differences between the case study and Petitioner’s case culminate with the authors’ conclusion that the cause of the case study patient’s symptoms was likely a hypersensitivity to the adjuvant and not molecular mimicry. Pet’r’s Ex. 99 at 1–2. Petitioner has failed to provide preponderant evidence of a logical sequence of cause and effect between her flu vaccination and her SFN.

C. Appropriate Temporal Relationship

Althen prong three requires Petitioner to establish a “proximate temporal relationship”

between the vaccination and the injury alleged. Althen, 418 F.3d at 1281. 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-infact .” de Bazan, 539 F.3d at 1352. The explanation for what is a medically acceptable time frame must also coincide 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 at 1239, 1243 (Fed. Cir. 2014); Shapiro, 101 Fed. Cl. at 542; see Pafford, 451 F.3d at 1358. A proximate relationship between a vaccine and an injury, standing alone, does not constitute preponderant evidence of vaccine causation. See, e.g., Veryzer, 100 Fed. Cl. at 356 (explaining that timing “alone will not demonstrate the requisite causal link and that [P]etitioner must posit a medical theory causally connecting the vaccine and injury”).

Petitioner relied on the reports of Dr. Akbari and Dr. Hixson to support her argument towards Althen prong three. However, the two experts presented differing arguments for the onset of Petitioner’s SFN.

1. Dr. Hixson’s Argument

Dr. Hixson opined that Petitioner’s early symptoms of “arm soreness, fatigue, and low-

grade fever” were consistent with a post-vaccination inflammatory response, but that she later developed “enduring neurologic symptoms of limb paresthesias” five days after vaccination. Pet’r’s Ex. 16 at 5–6. He asserted that these long-term symptoms “would be “consistent with the pathogenesis of an autoimmune process involving molecular mimicry following vaccination.” Id. Dr. Hixson deemed that an onset period of “one day [to] two months” would be appropriate for the development of SFN after vaccination and cited to Souayah et al. in support. Id. at 5 (citing Pet’r’s Ex. 28). As discussed above, Souayah et al. was a series of case reports discussing SFN occurring in temporal relationship to rabies, varicella, and Lyme disease vaccinations, not flu vaccination. Pet’r’s Ex. 28 at 1. This distinction is noteworthy because the article details five patients, none of which mirror Petitioner’s clinical presentation. Petitioner was vaccinated on February 7, 2018, and reported she experienced flu-like symptoms, along with arm tingling one day post vaccination; three days post vaccination, Petitioner added pain radiating from her arm and tingling throughout her entire body. For comparison, Patient One from Souayah et al. “received [the] rabies vaccine over three days within a one-week period[, and s]everal hours after

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the second injection, he developed burning paresthesias.” Id. Patient Two “developed burning and itching sensations . . . one day after a [Lyme disease] vaccination” that incompletely resolved but “then returned more intensely one year later, immediately following a second LYMErix vaccination.” Id. at 1–2. Patient Three also received two Lyme disease vaccines, developing flu- like symptoms after the first one and “severe, sharp stabbing” chest pains “approximately one week after the second injection,” administered one month later. Id. at 2. Patient Four developed headaches and neck stiffness “a few days after receiving” vaccinations for Lyme disease and hepatitis A with neuropathic symptoms developing in subsequent weeks. Id. The final patient studied by Souayah et al. developed progressive “numbness and hyperesthesias in all extremities about two months following a second [varicella zoster] vaccine.” Id. These cases, involving different vaccines and symptoms following a second vaccine dose or multiple vaccines at once, do not provide a roadmap that is consistent with Petitioner’s symptom onset: general flu-like symptoms with arm tingling one day post vaccination, followed by generalized distal paresthesias “after five days.” Pet’r’s Ex. 16 at 5–6.

Dr. Fujinami went further, arguing that five days would not be sufficient time for the flu vaccine to “induce an autoimmune response to nervous system antigens.” Resp’t’s Ex. C at 5 (citing Resp’t’s Ex. C, Tabs 3, 6). 57 He cited Wang et al. to provide an appropriate timeline for pathogenic molecular mimicry. The researchers there used a complete Fruend’s adjuvant in genetically susceptible mice to induce EAE, and that they did not see clinical signs of neuroinflammation until 10 days after immunization. Resp’t’s Ex. C, Tab 6 at 5. Although this literature cited by Dr. Fujinami does not involve SFN, Dr. Hixson’s explanation of molecular mimicry does not provide any mechanistic explanation as to why a five-day (or a one-day) onset would be appropriate for the development of SFN following flu vaccination.

2. Dr. Akbari’s Argument

Alternatively, Dr. Akbari cited to Chatziandreou et al. 58 to support the argument that inflammasome production could cause the development of SFN within one to two days. Pet’r’s Ex. 29 at 17 (citing Pet’r’s Ex. 77). 59 The authors in Chatziaandreou et al. “examine[d] the role of lymph node macrophages (“LNMs”) in the induction of the cytokine storm triggered by inactivated

57 Neal A. Halsey, The Science of Evaluation of Adverse Events Associated with Vaccination, 13 SEMINARS PEDIATRIC INFECTIOUS DISEASES 205 (2002); Xiaojie Wang et al., Diffusion Basis Spectrum Imaging Detects and Distinguishes Coexisting Subclinical Inflammation, Demyelination, and Axonal Injury in Experimental Autoimmune Encephalomyelitis Mice, 27 NMR BIOMEDICINE 843 (2014). 58 Nikolaos Chatziandreou et al., Macrophage Death Following Influenza Vaccination Initiates the Inflammatory Response that Promotes Dendritic Cell Function in the Draining Lymph Node, 18 CELL REPS. 2427 (2017). 59 Dr. Akbari did not file the Chatziandreou et al. article with his initial report. Instead, the article listed as a citation reference was Irvine et al., an article discussing timing and location in vaccines. See Pet’r’s Ex. 51. This article also does not reference any works by Chatziaandreou et al., nor does the article discuss the “[t]ime kinetics of inflammasome induction, measured by IL-1a post influenza vaccination,” that Dr. Akbari claimed. See Pet’r’s Ex. 29 at 17. Dr. Akbari asserted that the article found “IL-1a [to be] significantly elevated as early as 30 min[utes] after flu vaccination and after 90 min[utes] reaches to the high levels of approximately 300 pg/ml.” Id. at 17–18. Irvine et al. made no such claim and did not analyze inflammasome levels following vaccination. See Pet’r’s Ex. 51. Darrell J. Irvine et al., Controlling Timing and Location in Vaccines, 158 ADV. DRUG DELIVERY REVS. 91 (2020).

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[flu] virus vaccine.” Pet’r’s Ex. 77 at 2. The authors found that LNMs suffered from cell death within the first three hours after vaccination and remained absent for up to one week. Id. at 4. However, “[t]he observed death mechanism was not exclusively associated with viral antigen, as . . . numbers were also significantly reduced after vaccination with heat-inactivated Streptococcus pneumoniae.” Id. The authors noted that pro-inflammatory IL-1a cytokines began to release in as little as 30 minutes following vaccination, with a “cytokine storm” peak at 12 hours post- vaccination. Id. at 7. They did not define this process as molecular mimicry. Further, while the article focused its findings on how to better improve the “humoral response against [flu] vaccine,” it did not attribute this LNM cell death to the development of SFN or any other disease. Id. at 12. Dr. Akbari also did not explain how the death of LNMs in response to the flu vaccine was related to the death of macrophages near the nerve axons affected by SFN.

Dr. Fujinami critiqued this section of Dr. Akbari’s report, opining that one to two days after vaccination was too short a timeframe “for the differentiation, activation, proliferation, and migration to the sites of purported peripheral nerve damage and for clinical signs to occur.” Resp’t’s Ex. E at 4. He again cited to Wang et al. to explain the 10-day onset of neuroinflammation following the inducement of EAE. Id. (citing Resp’t’s Ex. C, Tab 6). Dr. Akbari contested Dr. Fujinami’s use of EAE, an animal model of MS, to compare the time kinetics of SFN. Pet’r’s Ex. 76 at 13. He also argued that different EAE models used different approaches, and that “Dr. Fujinami only talked about the oldest EAE model and expects us to compare the model utilizing strong adjuvate and self-peptide to [P]etitioner, and extend the shortcomings of the murine model to this case.” Id. Dr. Fujinami replied that he felt the comparison was appropriate given the theory presented by Dr. Akbari relied on the flu vaccine causing “clinical signs and pathological changes in the [PNS] leading to inflammatory demyelinating disease.” Resp’t’s Ex. F at 2.

Dr. Akbari devoted a separate section of his supplemental report to explaining the temporal relationship between the flu vaccine and SFN. Pet’r’s Ex. 76 at 18. He began this section with the following statement: “Temporal association does not equate to causality. Factors such as the timing of symptom onset relative to vaccination and the exclusion of other potential causes of SFN are critical in evaluating case reports and studies.” Id. In support of his argument he cited to Kafaie et al. and Souayah et al., though as previously discussed in this opinion, these case studies do not provide persuasive evidence of an appropriate timeline for molecular mimicry following flu vaccination. See Pet’r’s Ex. 76 at 19 (citing Resp’t’s Ex. E, Tabs 6, 10). Dr. Akbari also cited to a case report by Waheed et al., 60 which reported a case of SFN with symptom onset occurring one week following the second dose of a COVID-19 vaccine. Id. at 20 (citing Pet’r’s Ex. 99). Key distinctions between the case study patient and Petitioner include different vaccines that require two doses versus one dose, respectively, and the lack of any early-presenting flu-like symptoms. Dr. Akbari did not account for the differences or explain how they are similar. Furthermore, the authors of Waheed et al. denied the role of molecular mimicry in their case and stated that “the lack of significant homology between any SARS-CoV-2 genetic or linear protein structure and human linear protein structures in this study make molecular mimicry as a cause less likely.” Pet’r’s Ex. 99 at 1–2. Instead, they proposed “an immune-mediated hypersensitivity to the solvent/adjuvant.” Id. at 1. Dr. Akbari did not address this hypothesis presented by the authors and instead summarized that “[a] presumed casual association is based on the temporal relationship

60 Waqar Waheed et al., Post COVID-19 Vaccine Small Fiber Neuropathy, 64 MUSCLE & NERVE E1 (2021).

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between vaccination and symptom onset, as well as the exclusion of more common causes of [SFN] such as diabetes.” Pet’r’s Ex. 76 at 21.

Dr. Akbari acknowledged that causation could not be based on temporal association to vaccination alone; however, he proceeded to root his analysis in precisely that framework. The articles relied on by Dr. Akbari to show a temporal relationship either directly exclude molecular mimicry, acknowledge a lack of association between the flu vaccine and SFN, or relate to entirely different diseases. Further, although Dr. Fujinami’s argument rests primarily on an EAE study, I find the timing and reasoning somewhat probative given at the very least, all the experts seem to agree it is an example of pathogenic molecular mimicry. Dr. Akbari’s disregard of the EAE model as it pertains to Althen prong three is nonspecific and contradictory, as Dr. Akbari relied nearly exclusively on MS and EAE models to argue for his theory pursuant to Althen prong one.

It should be noted that while both Dr. Akbari and Dr. Hixson present causation theories born out of molecular mimicry, their theories were incompatible, especially regarding timing. Dr. Hixson characterized the immediate localized inflammation that Petitioner experienced as unrelated to her later neurological symptoms and SFN that developed five days later. Pet’r’s Ex. 16 at 5–6. Alternatively, Dr. Akbari detailed “symptoms associated with inflammasome induction and hypersensitivity in less than [two] days after vaccination . . . [that] progressed to signs consistent with [SFN] linked to vaccines.” Pet’r’s Ex. 29 at 26. To satisfy a petitioner’s burden under Althen prong three, the explanation for what is a medically acceptable time frame must also coincide with the theory of how the relevant vaccine can cause the injury alleged under Althen prong one. de Bazan, 539 F.3d at 1352. Here, the theories of Dr. Hixson and Dr. Akbari diverge beyond reconciliation, and thus I find that both experts’ arguments are insufficient to satisfy Petitioner’s burden under Althen prong three.

V. Conclusion

For the reasons discussed above, I find that Petitioner has not established by preponderant evidence that her flu vaccine administered on February 7, 2018, caused her to suffer from SFN. Therefore, Petitioner is not entitled to compensation, and I must DISMISS her claim. 61

IT IS SO ORDERED.

s/Herbrina D.S. Young Herbrina D.S. Young Special Master

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