Sokol v. Secretary of Health and Human Services

In the United States Court of Federal Claims

OFFICE OF SPECIAL MASTERS

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

EDWARD A. SOKOL, *

* No. 16-1631V

* Special Master Christian J. Moran

Petitioner, *

v. *

* Filed: January 9, 2020

SECRETARY OF HEALTH *

AND HUMAN SERVICES, * flu vaccine, stroke, subarachnoid

* hemorrhage (SAH)

Respondent. *

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

Jeffrey A. Golvash, Brenna, Robins & Daley, P.C., Pittsburgh, PA, for petitioner;

Voris E. Johnson, Jr., United States Dep’t of Justice, Washington, DC, for

respondent.

DECISION DENYING ENTITLEMENT1

Edward A. Sokol received a dose of the influenza (“flu”) vaccine on January

22, 2014, and he developed problems speaking by February 2, 2014. Doctors

diagnosed him as suffering a stroke, specifically a subarachnoid hemorrhage. Mr.

Sokol contends that the vaccination caused his stroke and seeks compensation

through the National Childhood Vaccine Compensation Program. 42 U.S.C.

§ 300aa–10 through 33 (2012).

1

Because this decision contains a reasoned explanation for the action in this case, the

undersigned is required to post it on the United States Court of Federal Claims’ website in

accordance with the E-Government Act of 2002. 44 U.S.C. § 3501 note (2012) (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), the

parties have 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, the undersigned

agrees that the identified material fits within this definition, the undersigned will redact such

material before posting the decision.

To assist him, Mr. Sokol retained a neurologist, George A. Small, who wrote

two reports, exhibits 7 and 9. The Secretary disagreed with Mr. Sokol’s claim and

retained a neurologist, Steven Messé, who also wrote two reports, exhibits A and

C. Both neurologists, as well as Mr. Sokol, testified at a hearing held in

Pittsburgh, Pennsylvania, near Mr. Sokol’s hometown.

After considering this testimonial evidence and the documentary evidence,

the undersigned finds that Mr. Sokol has not met his burden of proof. This is

based on: (1) the relatively inferior qualifications of Mr. Sokol’s expert, when

compared to respondent’s expert; (2) weaknesses in Dr. Small’s asserted medical

theory; (3) failure to establish that the stroke arose in an acceptable time between

the vaccination and injury; and (4) the presence of alternative factors that could

cause a stroke. See infra Part III.

I. Events in Mr. Sokol’s Life

Mr. Sokol was born in 1956. It is likely that Mr. Sokol was born with an

aneurysm in his brain. Tr. 67 (Dr. Small), 90 (Dr. Small). An aneurysm is an

irregularity in an artery in which the artery balloons. Dorland’s Illustrated Medical

Dictionary 82 (32d ed. 2012); Tr. 65. Approximately 1-2 percent of people are

born with aneurysms in their brains. Tr. 150. There is no allegation that the 2014

flu vaccination caused Mr. Sokol’s aneurysm.

As an adult, Mr. Sokol worked as an electrician but stopped working around

2009. Tr. 35. He has not filed any medical records for the period before the

vaccination. In the hearing, Mr. Sokol explained that from about 2009 to the

vaccination date (January 22, 2014), Mr. Sokol received almost no medical

treatment. Tr. 30-31. As discussed below, the lack of treatment does not mean

that Mr. Sokol was entirely healthy. He could have been suffering from problems,

such as hypertension, that a doctor had not diagnosed due to a lack of medical care.

See Tr. 197-98.

In January 2014, Mr. Sokol decided to get a flu vaccine. The vaccination in

2014 was the second flu vaccination in Mr. Sokol’s life. Tr. 14.

As previously stated, Mr. Sokol received the flu vaccine on January 22,

2014. Because cold weather increases the risk for hypertension, the weather

around this date is relevant in considering the cause of Mr. Sokol’s stroke. The

temperature on that day in Pittsburgh ranged from a low of negative 5 degrees to a

2

high of positive 12 degrees. Exhibit 28 at 3.2 Over the next few days, the

temperature warmed, but was still cold. By January 27, 2014, the temperature

ranged from 1 degree to 43 degrees. But, on January 28, 2014, the temperature fell

to a low of negative 8 degrees and a high of 7 degrees. The temperature then

rebounded, reaching a high of 53 degrees on February 1, 2014, with a low of 31 on

that day. Exhibit 29 at 3.

Approximately four days after the vaccination, Mr. Sokol started having flu-

like symptoms. Exhibit 3 at 8; exhibit 1(a) at 70; Tr. 16. The symptoms lasted

about three days, ending by January 30, 2014. Exhibit 3 at 8; Tr. 16; see also Tr.

120.

Mr. Sokol started to have problems talking on February 1, 2014. Exhibit 3

at 8; Tr. 17. On the next day, his daughter brought him to Passavant Hospital.

Exhibit 3 at 8; Tr. 19. After imaging studies, doctors diagnosed a stroke. See

exhibit 3 at 22; Tr. 21. During his time in Passavant Hospital, the doctors

considered giving him a flu vaccination but did not because he had received a flu

vaccine two weeks earlier. Exhibit 3 at 45 (showing doctors considered

administering the vaccine on Feb. 3, 2014).

Doctors transferred Mr. Sokol to a hospital offering higher level care,

Presbyterian University Hospital. Exhibit 1 at 153-54; Tr. 21. Doctors repeated

the imaging studies and confirmed Mr. Sokol had suffered a stroke. Exhibit 1(a) at

148-50; Tr. 22.

A stroke, according to Dr. Messé, is an “injury to the brain due to a vascular

cause.” Tr. 171. Strokes are classified into two types. The more common type

(constituting approximately 80% of all strokes) is due to blockages in blood

vessels. These strokes are known as “ischemic” strokes. Tr. 171-72.

The less common type of stroke is due to the rupture of a vessel. The

rupture can happen in vessels that are within the brain itself, known as an

intraparenchymal hemorrhagic stroke. Tr. 172. The rupture can also happen in the

area surrounding the brain, the subarachnoid space. Tr. 66, 173-74. Here, Mr.

Sokol suffered a subarachnoid hemorrhagic stroke. Exhibit 3 at 8; exhibit 1(a) at

79-80, 149; Tr. 69.

Dr. Small stated that risk factors for subarachnoid hemorrhagic strokes

include cigarette smoking and use of drugs that raise a person’s blood pressure,

2

All temperature measurements are in degrees Fahrenheit.

3

such as cocaine. Tr. 68. These factors did not contribute to Mr. Sokol’s case. Dr.

Messé added other risk factors that also did not pertain to Mr. Sokol, including

female gender, use of alcohol, and family history. Tr. 175. However, Dr. Messé

brought out other risk factors that could, as discussed below, increase Mr. Sokol’s

risk for having a stroke such as increasing age, hypertension, and cold weather. Tr.

175.

According to Dr. Messé’s estimate, about one-half of subarachnoid

hemorrhage cases occur in people with no risk factor present. Tr. 176.3

Subarachnoid hemorrhages occur approximately 50,000 times per year in the

United States. Tr. 174.

Once Mr. Sokol’s subarachnoid hemorrhage was diagnosed, a neurosurgeon,

Daniel Wecht, operated on him. The purpose of the operation was to clip the

aneurysm. Exhibit 1(b) at 220. In the report from the operation, Dr. Wecht

commented: “By the way, the dissection revealed areas of hemosiderin, strongly

suggesting that the patient’s hemorrhage was not acute, but may have been days

ago. This is consistent with the patient’s rather nebulous clinical history.” Id. at

223. Hemosiderin is a type of iron that comes from blood. See Dorland’s at 843.

This description of hemosiderin is a critical aspect of Dr. Small’s opinion that the

flu vaccination caused Mr. Sokol’s stroke because, as he states, hemosiderin

indicates “chronicity of bleeding,” suggesting that onset occurred days before the

February 1 diagnosis. Tr. 74.

After the repair of Mr. Sokol’s subarachnoid hemorrhage, he remained in

Presbyterian Hospital for approximately two weeks. See exhibit 1(a) at 15 (Feb. 2,

2014 note for Mr. Sokol’s transfer to rehabilitation). He then went to a

rehabilitation facility. See exhibit 1(a) at 11.

When Mr. Sokol was discharged from the rehabilitation facility, he was

taking two medications to lower high blood pressure, amlodipine and labetalol.

Exhibit 1(a) at 13, Tr. 281. He has continued to take these two medications.

Exhibit 15 at 3 (March 3, 2014), exhibit 11 at 6 (July 7, 2017), and exhibit 14 at 1

(April 27, 2018).

During his oral testimony, Mr. Sokol stated that his main problems were

with his voice and feeling more tense. Tr. 28.

3

Dr. Small could not estimate the percentage of subarachnoid hemorrhages associated

with some risk factor. Tr. 149-51.

4

II. Standards for Adjudication

A petitioner is required to establish his case by a preponderance of the

evidence. 42 U.S.C. § 300aa–13(1)(a). The preponderance of the evidence

standard requires a “trier of fact to believe that the existence of a fact is more

probable than its nonexistence before [he] may find in favor of the party who has

the burden to persuade the judge of the fact’s existence.” Moberly v. Sec’y of

Health & Human Servs., 592 F.3d 1315, 1322 n.2 (Fed. Cir. 2010) (citations

omitted). Proof of medical certainty is not required. Bunting v. Sec’y of Health &

Human Servs., 931 F.2d 867, 873 (Fed. Cir. 1991).

Distinguishing between “preponderant evidence” and “medical certainty” is

important because a special master should not impose an evidentiary burden that is

too high. Andreu v. Sec’y of Health & Human Servs., 569 F.3d 1367, 1379-80

(Fed. Cir. 2009) (reversing special master’s decision that petitioners were not

entitled to compensation); see also Lampe v. Sec’y of Health & Human Servs., 219

F.3d 1357 (Fed. Cir. 2000); Hodges v. Sec’y of Health & Human Servs., 9 F.3d

958, 961 (Fed. Cir. 1993) (disagreeing with dissenting judge’s contention that the

special master confused preponderance of the evidence with medical certainty).

Petitioners bear a burden “to show by preponderant evidence that the

vaccination brought about [the vaccinee’s] injury by providing: (1) a medical

theory causally connecting the vaccination and the injury; (2) a logical sequence of

cause and effect showing that the vaccination was the reason for the injury; and (3)

a showing of a proximate temporal relationship between vaccination and injury.”

Althen v. Sec’y of Health & Human Servs., 418 F.3d 1274, 1278 (Fed. Cir. 2005).

III. Analysis

Here, Mr. Sokol has failed to advance a persuasive case for several reasons.

First, as a foundational matter, the expert whom Mr. Sokol retained, Dr. Small, has

less expertise than the expert the Secretary retained, Dr. Messé. Second, the theory

that Dr. Small offers has flaws that tend to reduce the persuasive value of Dr.

Small’s opinion. Third, Mr. Sokol has not established that his stroke occurred

within the time predicted by the theory Dr. Small proposed. Fourth, the presence

of alternative causes decreases the likelihood that that the flu vaccination was

causal. These are developed below.

5

A. In the field of stroke, Dr. Messé’s qualifications are superior to

Dr. Small’s qualifications.

Special masters may consider the relative expertise of testifying experts

when weighing the value of their opinions. See Depena v. Sec’y of Health &

Human Servs., No. 13-675V, 2017 WL 1075101 (Fed. Cl. Spec. Mstr. Feb. 22,

2017), mot. for rev. denied, 133 Fed. Cl. 535, 547-48 (2017), aff’d without op.,

730 Fed. App’x 938 (Fed. Cir. 2018); Copenhaver v. Sec’y of Health & Human

Servs., No. 13-1002V, 2016 WL 3456436 (Fed. Cl. Spec. Mstr. May 31, 2016),

mot. for rev. denied, 129 Fed. Cl. 176 (2016); Bowman v. Sec’y of Health &

Human Servs., No. 13-807V, 2014 WL 3486773, at *7 (Fed. Cl. Spec. Mstr. June

17, 2014). In this case, Dr. Messé has more expertise in stroke and presented with

a more persuasive demeanor than Dr. Small.

Dr. Small. At the basic level, Dr. Small graduated from Jefferson Medical

College in 1988, and became board-certified in psychiatry and neurology in 1993.

Dr. Small obtained a specific board certification in electrodiagnostic medicine in

1994. Exhibit 10 (curriculum vitae) at 3; Tr. 43. These qualifications make him

competent to express the opinions he expressed.

Within the field of neurology, Dr. Small has focused his practice on treating

patients with myasthenia gravis, which is considered an autoimmune disease. Tr.

49. His knowledge about myasthenia gravis gives him some knowledge of

immunology (Tr. 141), but he is not an immunologist. Tr. 107.

There are some limitations in Dr. Small’s background. He has limited

exposure to epidemiology. Tr. 140. He does not act as a peer reviewer for medical

journals. Tr. 107.

Dr. Small’s presentation while testifying was not as strong as it could have

been. He seemed unfamiliar with or unprepared to discuss the important articles.

See Tr. 81, 86. He did not always answer questions directly. See Tr. 127

(epidemiology), 157 (clinical experience with patients who received the flu

vaccine), 281 (Mr. Sokol’s pre-existing hypertension).

Dr. Messé. Dr. Messé graduated from medical school, the University of

Michigan in 1998. Like Dr. Small, Dr. Messé became board-certified in psychiatry

and neurology (2003). However, their paths diverge as Dr. Messé has obtained a

sub-specialization in vascular neurology. Exhibit B (curriculum vitae) at 1-2.

Vascular neurology is the field “concerned with the diagnosis and treatment of

6

cerebrovascular conditions, such as stroke syndrome.” Dorland’s at 1226; accord

Tr. 170.

Dr. Messé’s patient population is almost exclusively patients who have

suffered strokes. Tr. 169. He teaches other medical professionals about stroke and

has written articles about stroke that peer-reviewed journals have published. He

was invited to join the Executive Committee of the Stroke Section of the American

Academy of Neurology. Tr. 245; exhibit B at 2. Likewise, within the American

Heart Association, he was a member of the stroke oversight committee. Exhibit B

at 2. In 2011, the American Academy of Neurology awarded him the Michael S.

Pessin Stroke Leadership award. Exhibit B at 2; Tr. 245.

As with Dr. Small, Dr. Messé has no special expertise in immunology. Tr.

192, 246. But, unlike Dr. Small, Dr. Messé studied epidemiology and received a

certificate for his education. Tr. 246. He also reviews articles for journals. Tr.

170, 245.

Dr. Messé’s strong background in stroke may have contributed to his

credible presentation while testifying. Dr. Messé was knowledgeable about the

topics on which he opined. He conceded weaknesses in studies on which he was

relying. He seemed to express his opinions with care to be accurate.

In short, on this topic (stroke), Dr. Messé was a much better witness than Dr.

Small. In describing Dr. Messé as “better,” the undersigned does not want to

communicate that Dr. Small was “bad.” Dr. Small did reasonably well. But, Dr.

Small could not bring the same degree of expertise on the specific subject of

strokes as Dr. Messé.4 Thus, the undersigned often credits Dr. Messé’s opinions in

this decision.

B. Dr. Small’s theory for how a flu vaccine can cause a subarachnoid

hemorrhage has weaknesses.

One element of a petitioner’s case is to present “a medical theory causally

connecting the vaccination and the injury.” Althen, 418 F.3d at 1278. This theory

must be sound and reliable. Boatmon v. Sec’y of Health & Human Servs., 941

F.3d 1351, 1360 (Fed. Cir. 2019).

4

If the injured person suffered from myasthenia gravis, then Dr. Small would be more

qualified than Dr. Messé. However, this point is purely hypothetical as Dr. Messé stated that he

restricts his testimony to cases involving strokes. Tr. 238.

7

Dr. Small has presented a theory based upon cytokines. In essence, the

vaccination causes the body to produce cytokines, cytokines cause inflammation,

and inflammation causes the aneurysm to rupture. Petitioner’s brief aptly

summarizes the theory:

in the context of a congenital or preexisting arterial

aneurysm, the body’s release of these proinflammatory

mediators, such as tumor necrosis factor-a, affects

arteries by causing their muscular layers to either dilate

or contract, changing arterial wall tension in both normal

cerebral arteries and those housing aneurysms, which by

definition are already weakened structures, and thus

vulnerable to rupture by reason of the inflammatory

response.

Pet’r’s Preh’g Br., filed Jan. 16, 2019, at 6. To support his theory, Dr. Small

primarily relied upon an article whose lead author is Daan Backes, exhibit 13.5

This theory suffers from various deficiencies as outlined below.

1. Dr. Small did not establish that inflammation causes stroke. As Dr.

Messé acknowledged, inflammation is associated with stroke. However, whether

the inflammation causes a stroke or whether a stroke causes inflammation is not

clear. Tr. 203. Dr. Small, on cross-examination, agreed that inflammation can be

the evidence of an injury, not the cause of the injury. Tr. 115 (discussing exhibit

18 (Tulamo) at 1).

2. The theory is too generalized. In pointing to inflammation as the

cause of an aneurysm rupture, Dr. Small opens the possibility that anything that

causes inflammation could cause stroke. Tr. 102, 107, 130. As discussed below,

cold weather and hypertension are also risk factors for stroke. While the theory

that inflammation contributes to stroke could be valid, Dr. Small has not

adequately distinguished flu vaccine from any other potential cause for

inflammation.

3. Backes may have reached an inappropriate conclusion regarding flu

infection. This group of researchers investigated whether “the increased incidence

of aneurysmal subarachnoid hemorrhage in winter is related to temperature or

increased incidence of influenza.” Exhibit 13 (Backes) at 737. The foundation for

5

The complete bibliographical information about the articles cited is found in the

appendix.

8

the study was a set of databases from Holland. For the combined effects of

influenza epidemics and decrease in temperature, the authors found an adjusted

incidence daily ratio of 1.021 with a 95% confidence interval of 0.98–1.064. Id. at

4 (table 1). The authors concluded: “Influenza epidemics and cold temperatures

are associated with an increased risk of SAH.” Id. at 743.

Dr. Messé criticized this conclusion. In his view, because the confidence

interval includes values less than 1.0, the authors should not have found an

increased risk. Tr. 186, 205-06. When the value is 1.0, one factor does not alter

the risk of the other. See Tr. 181-82.

Here, although Dr. Messé may technically be correct, the confidence interval

barely dips below 1. Thus, it seems, at least at the preponderance of the evidence

standard, that this criticism is less significant than the distinction between a flu

infection and a flu vaccination.

4. Backes studied flu infections and Dr. Small did not explain how to

extrapolate from a flu infection to a flu vaccination. The bigger problem with

Backes in trying to determine whether flu vaccination can cause subarachnoid

hemorrhages is that Backes studied flu infections, not flu vaccinations. Tr. 79.

The authors linked flu infection to subarachnoid hemorrhages through

inflammation: “A growing body of evidence points to a key role of inflammation

in the process of aneurysm rupture. Infection with the influenza virus causes an

innate immune response that releases proinflammatory mediators, which lead to

symptoms within 2 days.” Exhibit 13 (Backes) at 741.

However, the infection with a flu virus prompts a much greater response

from the immune system than a flu vaccination. Tr. 101, 108, 119 (discussing

exhibit 19 (Hayden)), 223 (discussing exhibit A3 (Smeeth)). Dr. Small appears to

have assumed that the inflammation associated with a vaccination could be as

detrimental as the inflammation associated with an infection. But, he did not

justify this assumption. This gap is especially telling because of the

epidemiological studies that are discussed next.

5. The epidemiological studies on flu vaccination do not show an

increased risk for strokes. Dr. Messé presented three epidemiologic studies that

investigated whether people who received the flu vaccine suffered strokes at an

increased incidence. Exhibits A1 (Grau), A2 (Siriwardena), A3 (Smeeth); see also

Tr. 177-85. They did not find any increased risk, and sometimes found that people

who received the flu vaccine suffered fewer strokes (suggesting that the flu vaccine

9

was actually protective). Dr. Small did not dispute the findings in the

epidemiology. Tr. 99, 128.

These studies are not perfect. For example, the studies looked at both

ischemic and hemorrhagic strokes. The Grau study finds that flu vaccine is

protective against stroke with data suggesting that the flu infection would be

associated with approximately 62 percent of all strokes, a rate that the authors

describe as “implausibly high.” Exhibit A1 (Grau) at 1505. But, these flaws do

not diminish the overall point that epidemiology does not support Dr. Small’s

theory that the flu vaccine causes subarachnoid hemorrhages. Petitioners and their

experts bear the burden in the first instance to present a persuasive medical theory

explaining how the vaccine can cause an injury. Even if the epidemiologic

evidence were excluded, Mr. Sokol would still be required to produce some indicia

that Dr. Small’s opinion is reliable and persuasive. See Moberly, 592 F.3d at 1324.

For the reasons outlined above, Dr. Small’s theory suffers from several

weaknesses that ultimately render the theory unreliable for the purposes of

establishing a causal connection.6

C. Dr. Small did not establish that Mr. Sokol’s SAH originated in an

appropriate time after the flu vaccination.

If the cytokine-based theory were accepted, then Mr. Sokol would still be

required to establish “a proximate temporal relationship between vaccination and

injury.” Althen, 418 F.3d at 1278. The timing prong actually contains two parts.

A petitioner must show the “timeframe for which it is medically acceptable to infer

causation” and the onset of the disease occurred in this period. Shapiro v. Secʼy of

Health & Human Servs., 101 Fed. Cl. 532, 542-43 (2011), recons. denied after

remand on other grounds, 105 Fed. Cl. 353 (2012), aff’d without op., 503 F. App’x

952 (Fed. Cir. 2013). While Dr. Small persuasively defined the medically

6

In other cases, petitioners have advanced cytokine-based theories with mixed success.

See Copenhaver v. Sec’y of Health & Human Servs., No. 13-1002V, 2016 WL 3456436, at *1

(Fed. Cl. Spec. Mstr. May 31, 2016), mot. for rev. denied, 129 Fed. Cl. 176 (2016); Simmons v.

Sec’y of Health & Human Servs., No. 11-216V, 2015 WL 6778563, at *4 (Fed. Cl. Spec. Mstr.

Oct. 30, 2015); Godfrey v. Sec’y of Health & Human Servs., No. 10-565V, 2015 WL 10710961,

at *3 (Fed. Cl. Spec. Mstr. Oct. 27, 2015), mot. for rev. denied, slip op. (Fed. Cl. April 29, 2016);

Koehn v. Sec’y of Health & Human Servs., No. 11-355V, 2013 WL 3214877, at *1 (Fed. Cl.

Spec. Mstr. May 30, 2013), mot. for rev. denied, 113 Fed. Cl. 757 (2013), aff’d, 773 F.3d 1239

(Fed. Cir. 2014).

10

acceptable interval, preponderant evidence does not establish that Mr. Sokol’s

SAH arose in the relevant period.

1. The medically acceptable timeframe for a cytokine-driven

response may extend to four days as Dr. Small postulated.

The medically acceptable timeframe depends, at least in part, on the theory

being offered. Langland v. Sec’y of Health & Human Servs., 109 Fed. Cl. 421,

443 (2013); Garner v. Sec’y of Health & Human Servs., No. 15-063V, 2017 WL

171384, at *15-16 (Fed. Cl. Spec. Mstr. Mar. 24, 2017). In other words, “the

‘etiology’ of the disorder determines the appropriate temporal relationship.”

Veryzer v. Sec’y of Health & Human Servs., 100 Fed. Cl. 344, 356 (2011) (citing

Bazan v. Sec’y of Health & Human Servs., 539 F.3d 1347, 1352 (Fed. Cir. 2008)),

aff’d, 475 Fed. App’x 765 (Fed. Cir. 2012). Here, as discussed above, Dr. Small

has proposed a theory based upon cytokines.

While vaccinations do lead to an increase in cytokines as part of the

expected and normal response of the immune system, the increase typically

resolves within approximately six days. The strongest support for this statement is

a study in which researchers infected 20 volunteers with an influenza virus and

measured cytokine levels for eight days. The cytokine levels returned to normal by

day 6. Exhibit 19 (Hayden) at 646 (figure 5).

Other evidence suggests that the expansion in cytokines lasts for 48 hours,

but these reports hold limited value. For example, Lanza and colleagues measured

cytokine levels 48 hours after an influenza vaccination and found an increase.

Exhibit 12 (Lanza); see also Tr. 87-88, 110, 124, 192, 207. Lanza did not study

cytokines more than 48 hours later. Dr. Small stated that, while the study reflected

an elevation of cytokines 48 hours after vaccination, this does not necessarily

indicate that the inflammatory response completely ceases at this point. Tr. 160-61

(“[T]hat doesn’t mean the inflammatory response is gone, it would mean that that

particular inflammatory marker dropped, though.”). Backes, the study of influenza

infection and strokes, stated that an “[i]nfection with influenza virus causes an

innate immune response that releases proinflammatory mediators, which lead to

symptoms within 2 days.” Exhibit 13 (Backes) at 741; see also Tr. 82.

Although there are issues with establishing onset, discussed below,

petitioner’s presentation of the Hayden article, coupled with respondent’s lack of

rebuttal with respect to its findings, show that Dr. Small’s proposed timeframe is

acceptable. Dr. Small opined that “immune inflammatory response to vaccination

would typically manifest and persist 1-4 days post-vaccination,” and that Mr.

11

Sokol manifested symptoms 4 days after vaccination. Exhibit 16 at 3. While this

is outside the 48-hour range found in the Lanza study, this is within the 6-day

range found in the Hayden study. This grounding in the findings of the Hayden

study make this proposition more than mere speculation. See Koehn v. Sec’y of

Health & Human Servs., 773 F.3d 1239, 1244-45 (Fed. Cir. 2014) (ruling that the

special master was not arbitrary and capricious in finding that the onset of a

condition months after vaccination was not consistent with a theory based on

cytokines).

2. Dr. Small did not persuasively establish that Mr. Sokol’s SAH

developed within the relevant time.

To complete the proof on prong 3, Mr. Sokol must present preponderant

evidence that his SAH started within the time the cytokine-based theory predicts.

This task is challenging as the experts could offer little guidance about when Mr.

Sokol’s aneurysm ruptured. Dr. Messé was direct in saying that he did not know

when the aneurysm ruptured. Tr. 194. When asked twice about the first symptom

of Mr. Sokol’s SAH, Dr. Small answered inconsistently. He identified both the

flu-like symptoms and Mr. Sokol’s language problem as the first symptom at

different points. Tr. 120, 122. These events occurred on different days, with the

flu-like symptoms lasting from January 26, 2014, to January 30, 2014 (four to

eight days after the January 22, 2014 vaccination) and the speech problems starting

on February 1, 2014 (10 days after vaccination). The flu-like symptoms resolved

before Mr. Sokol started having language problems. Tr. 120.

Dr. Small attempted to date the beginning of Mr. Sokol’s SAH with Dr.

Wecht’s finding of hemosiderin during the February 4, 2014 operation to clip the

aneurysm. In Dr. Small’s opinion, hemosiderin is “old blood” that existed for one

week or more before Dr. Wecht’s discovery of it during the operation. Tr. 73-74,

91, 95.

Dr. Small seemed to be stretching the usefulness of Dr. Wecht’s description.

Preliminarily, as Dr. Messé described, hemosiderin is detected through laboratory

testing and laboratory testing for hemosiderin is not readily apparent in the record.

Tr. 215-17. Thus, Dr. Wecht’s use of the term “hemosiderin” might be mistaken.

More significantly, when asked to explain how long the production of

hemosiderin takes, Dr. Small did not know. Tr. 153. In contrast, Dr. Messé

spontaneously listed the steps that take place to form hemosiderin. Tr. 194-95. In

his rebuttal testimony, Dr. Small did not disagree with the process that Dr. Messé

described. Tr. 283. Dr. Messé estimated that the production of hemosiderin takes

12

“usually a month or two . . . maybe two weeks at the very, very earliest.” Tr. 194-

95. After hemosiderin is produced, hemosiderin can last forever in the body. Tr.

162 (Dr. Small), 195 (Dr. Messé).

Given Dr. Messé’s board certification in vascular neurology, the

undersigned is inclined to credit Dr. Messé’s opinion about an aspect of the

circulatory system. If Dr. Messé’s estimate that the quickest amount of time for

hemosiderin to form (two weeks) is accurate, then the bleed occurred 14 days

before Dr. Wecht discovered the blood on February 4, 2014. This date is January

21, 2014, which is one day before the vaccination.

A bleed on January 21, 2014 is not necessarily incompatible with a problem

in speaking on February 1, 2014. There can be a lag between the bleeding and the

start of neurological symptoms. Tr. 164-65 (Dr. Small), 269-70 (Dr. Messé).

In sum, as Dr. Messé testified: “the timing here is just super difficult.” Tr.

268. Some evidence (the hemosiderin) suggests the bleeding started before the

vaccination. Other evidence (the onset of speech problems) suggests that the

timing occurred too long after the vaccination and cytokine expansion for the

cytokines to have caused the rupture. See Tr. 125 (Dr. Small acknowledging that if

the speech problems were the first manifestation of the neurologic problem, then

the vaccination is less likely to be the cause). Relatively little persuasive evidence

suggests that the aneurysm rupture happened in the time Dr. Small’s theory

predicted. Thus, Mr. Sokol has failed to meet his burden of proof for prong 3.

D. The presence of alternative risk factors for subarachnoid

hemorrhages decreases the likelihood that the flu vaccine caused

Mr. Sokol’s stroke.

Finally, the Secretary has identified two factors that place Mr. Sokol at

increased risk for a subarachnoid hemorrhage and Mr. Sokol has not persuasively

countered them. In determining whether petitioners have met their burden of

proof, special masters may consider all relevant evidence, including evidence that

something other than a vaccine may have caused the injury. Doe 11 v. Sec’y of

Health & Human Servs., 601 F.3d 1349, 1357-58 (Fed. Cir. 2010). Here, the

Secretary has put forward two potential alternative causes: hypertension and cold

weather.

Hypertension. The experts agree that hypertension can be a risk factor for

an aneurysm to rupture. For Dr. Small, see Tr. 93-95, 132-33, 158; for Dr. Messé,

see exhibit A at 4 (Dr. Messé’s report), Tr. 197.

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The more difficult issue is whether Mr. Sokol suffered from hypertension

before he was vaccinated. As mentioned earlier, Mr. Sokol did not file medical

records about his health in the years before vaccination because he did not seek

medical attention. Tr. 197. This lack of information allows Dr. Small to state that

he did not see any evidence that Mr. Sokol suffered from hypertension before the

vaccination. Tr. 94.

Once Mr. Sokol did go to the hospital, his doctors placed him on two

medicines to control his hypertension. Exhibit 1(a) at 13 (report from discharge

from rehabilitation facility).7 Mr. Sokol thereafter has continued to be prescribed

two drugs to lower his high blood pressure. Exhibit 15 at 3 (March 3, 2014);

exhibit 11 at 6 (July 7, 2017); exhibit 14 at 1 (April 27, 2018).

This information allows Dr. Messé to infer that Mr. Sokol’s hypertension

existed before the aneurysm rupture. Tr. 197-98. On cross-examination, Dr.

Messé testified that hypertension is “not typically something that appears out of

nowhere. It’s usually chronic and long-lasting typically if you’re requiring

multiple medications to control it.” Tr. 202. When asked on rebuttal to address

Dr. Messé’s reasoning, Dr. Small was not responsive. Tr. 282-83.

Based upon this circumstantial evidence, the undersigned finds on a more-

likely-than-not basis that Mr. Sokol probably suffered from hypertension before his

stroke. This hypertension could explain why he had a stroke.

Cold Weather. Most aneurysmal ruptures occur in cold weather. Exhibit 13

(Backes); Tr. 132, 199. As such, doctors believe that cold weather contributes to

the ruptures. Tr. 158. From the date of vaccination through Mr. Sokol’s language

difficulties, the weather in Pittsburgh was generally cold. Exhibits 28-29. Thus,

Dr. Small conceded that the cold weather could have played a role in causing Mr.

Sokol’s stroke. Tr. 152.

However, at the same time, Dr. Small maintained that the vaccination was a

“strong, significant contributor” to the stroke. Tr. 158; accord exhibit 9 at 2.

Through his attorney, Mr. Sokol advanced the argument that, assuming that Mr.

Sokol had pre-existing hypertension, Mr. Sokol had lived through periods of cold

weather with high blood pressure without having a stroke. It was only after Mr.

Sokol received the flu vaccination that his aneurysm ruptured. Thus, in Mr.

7

Mr. Sokol presented to the hospital with hypertension. However, this data point does

not necessarily suggest that his hypertension was long-standing as Mr. Sokol might have had

elevated blood pressure due to the uncertainty of not knowing what was wrong with him and the

anxiety over going to a hospital. Tr. 94.

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Sokol’s view, because the vaccination was the only new factor, this addition must

have caused the stroke. See Tr. 103, 207 (cross-examination of Dr. Messé).

Although this argument has some superficial appeal, it is ultimately not

persuasive. The argument resembles the logical fallacy post hoc, ergo propter

hoc—that because the rupture happened after the stroke, the stroke must have

caused the rupture. As Dr. Messé persuasively explained, the risk factors can

explain why Mr. Sokol suffered a stroke. Adding the vaccination is not necessary.

Tr. 236.

IV. Conclusion

Mr. Sokol started to experience neurologic symptoms of a stroke

approximately 10 days after he received a flu vaccine. Mr. Sokol was hospitalized

and required rehabilitation to gain back most, but not all, of his functioning. Mr.

Sokol’s health problems are unfortunate.

Although Mr. Sokol merits sympathy, he has not established that the flu

vaccine caused his stroke. Through an expert who lacked a specialized

background in strokes, Mr. Sokol advanced a causal theory that was flawed. The

chronology of events in Mr. Sokol’s life is not consistent with the appropriate

temporal relationship and Mr. Sokol suffered from risks factors other than the

vaccination. Therefore, he is not entitled to compensation.

The Clerk’s Office is instructed to issue judgment in accord with this

decision if a motion for review is not filed.

IT IS SO ORDERED.

s/ Christian J. Moran

Christian J. Moran

Special Master

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Appendix of Articles Cited

Daan Backes et al., Increased incidence of subarachnoid hemorrhage during cold temperatures

and influenza epidemics, 125 J. Neurosurgery 737 (2016), filed as exhibit 13.

Armin J. Grau et al., Influenza Vaccination Is Associated With a Reduced Risk of Stroke, 36

Stroke 1501 (2005), filed as exhibit A, tab 1.

Frederick G. Hayden et al., Local and Systemic Cytokine Responses during Experimental Human

Influenza A Virus Infection, 101 J. Clinical Investigation 643 (1998), filed as exhibit 19.

Gaetano A. Lanza et al., Inflammation-related effects of adjuvant influenza A vaccination on

platelet activation and cardiac autonomic function, 269 J. Internal Med. 118 (2010), filed

as exhibit 12.

A. Niroshan Siriwardena et al., Influenza and pneumococcal vaccination and risk of stroke or

transient ischaemic attack—Matched case control study, 32 Vaccine 1354 (2014), filed

as exhibit A, tab 2.

Liam Smeeth et al., Risk of Myocardial Infarction and Stroke after Acute Infection or

Vaccination, 351 New England J. Med. 2611 (2004), filed as exhibit A, tab 3.

Rika Tulamo et al., Inflammatory changes in the aneurysm wall: a review, 2 J.

Neurointerventional Surgery 120 (2010), filed as exhibit 18.

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