Hendrix Ex Rel. Gp v. Evenflo Co., Inc.

                                                                    [PUBLISH]

               IN THE UNITED STATES COURT OF APPEALS
                      FOR THE ELEVENTH CIRCUIT           FILED
                       ________________________ U.S. COURT OF APPEALS
                                                         ELEVENTH CIRCUIT
                                                            JUNE 22, 2010
                                No. 09-10079
                                                             JOHN LEY
                          ________________________
                                                               CLERK

                  D. C. Docket No. 07-00133-CV-3-MCR-EMT

RHONDA HENDRIX,
Parent and Guardian of G.P.,
a minor child,

                                          Plaintiff-Counter Defendant-Appellant,

                                    versus

EVENFLO COMPANY, INC.,
a foreign corporation

                                          Defendant-Counter Claimant-Appellee,

FORT WALTON BEACH MEDICAL CENTER,
a Florida corporation,

                                                                     Defendant.

                               _____________

                  Appeal from the United States District Court
                      for the Northern District of Florida
                               _____________
                                (June 22, 2010)

Before CARNES, HULL and ANDERSON, Circuit Judges.

ANDERSON, Circuit Judge:
      Plaintiff-Appellant Rhonda Hendrix alleges that her son, G.P., sustained

traumatic brain injuries when a child restraint system manufactured by Defendant-

Appellee Evenflo Company, Inc., (“Evenflo”), malfunctioned during a minor traffic

accident. Hendrix further alleges that those brain injuries caused G.P. to develop

autism spectrum disorder (“ASD”) and a spinal cord defect known as

syringomyelia. The district court excluded testimony from two of Hendrix’s expert

witnesses that the accident caused G.P.’s ASD. The district court concluded that

the methods used by Hendrix’s experts were not sufficiently reliable under Daubert

v. Merrell Down Pharmaceuticals, Inc., 509 U.S. 579, 113 S. Ct. 2786 (1993).

Hendrix v. Evenflo Co., Inc., 255 F.R.D. 568 (N.D. Fla. 2009). The district court

then granted partial summary judgment to Evenflo on Hendrix’s compensatory

damages claim, determining that without the excluded testimony there was no

reliable evidence to support Hendrix’s theory that the accident caused G.P.’s ASD.

Hendrix voluntarily dismissed, with prejudice, her remaining damages claims and

filed a notice of appeal.

                    I. FACTS AND PROCEDURAL HISTORY

      The product at issue in this product liability case is the Evenflo Discovery

Model 212 Child Restraint System (“the CRS”) owned by Hendrix. The CRS,

which was manufactured in December 2000, consists of a plastic base that is

                                         2
secured to the vehicle’s seat by the safety belt and a padded plastic carrier. The

carrier is either locked into the base or secured directly to the vehicle’s seat with a

safety belt. The CRS meets the requirements imposed by federal regulations. See

49 C.F.R. § 571.213. When used properly, the base is positioned in a rear seat with

the carrier locked into the base so the child faces the rear of the vehicle.

       On April 17, 2002, Hendrix and her fifteen-day-old son, G.P., were involved

in a minor traffic accident (“the accident”) while traveling at a speed of 10-12 mph.

Hendrix claims that G.P. was properly strapped into the CRS, and that the CRS was

located in the rear center position of her SUV.1 Hendrix’s theory is that during the

accident the seat dislodged from its base because it had been “false-latched.” A

false-latch occurs when the mechanism that attaches the carrier to the base fails to

properly latch even though the latch makes an audible click leading the person

installing the seat to believe the seat is properly installed. Hendrix argues that

because of the false-latch the carrier separated from the base at impact and struck

the console between the SUV’s front seats.

       1
                For purposes of this appeal, we assume Hendrix’s version of the facts that the
carrier and the child were snapped into the base in the rear center position of the SUV. It is
undisputed that the base of the CRS was in the rear center seat, secured by a safety belt.
However, Evenflow’s theory is that the carrier and the child were actually positioned in the front
passenger seat of the SUV in contravention of the CRS safety instructions and in violation of
state law. Evenflow argues that, due to the incorrect positioning of the carrier, during impact the
carrier struck or was struck by the front passenger-side airbag.


                                                 3
       It is undisputed that the carrier fractured during the accident. While it is also

undisputed that G.P. suffered a closed-head injury as a result of the accident, the

parties do dispute the severity of the injury and whether G.P. suffered brain

damage. G.P.’s medical records reveal that he suffered, at the very least, a

contusion on his forehead and bleeding in his brain. G.P.’s injuries do not appear

to have caused immediate neurologic impairment, as G.P. exhibited no

developmental problems at his 2, 4, or 10-month check-ups.

       Nearly eighteen months after the accident, G.P. began to exhibit

developmental problems. When occupational therapy failed to cause improvement,

G.P. was referred to Dr. Suhrbier, a pediatric neurologist. Dr. Suhrbier

administered a neurologic evaluation to address G.P.’s severe neurodevelopmental

delay, impaired social interactions, and history of seizures.

       Approximately three years after the accident, Dr. Suhrbier diagnosed G.P.

with an asymptomatic spinal cord cyst. Hendrix argues that the cyst is a

syringomyelia, which can be caused by trauma but may not appear for several years

following the causative trauma.2

       Dr. Suhrbier diagnosed G.P. with ASD in April 2007, when G.P. was five



       2
               Evenflo suggests that, instead, the cyst is a hydromyelia resulting from a
congenital defect in G.P.’s brain.

                                                 4
years old. There is little information in the record regarding G.P.’s current

impairments related to his ASD diagnosis. A report filed in December 2007 by

Hendrix’s second medical expert, Dr. Hoffman3 , describes G.P. as completely

nonverbal, aggressive, lacking fine motor skills, and refusing or unable to use

utensils, and as suffering from delayed sleep-onset, hyperactivity (i.e., constant

motion, running away), and decreased response to pain. Based on information

provided by Hendrix and his personal examinations of G.P., Dr. Hoffman

concluded that G.P. has “autism spectrum disorder, a behaviorally defined disorder

with qualitatively impaired social interaction, qualitatively impaired

communication (not compensated by gesture), and restrictive repetitive and

stereotyped patterns of behavior, interests and activities.” Evenflo’s medical

expert, Dr. Epstein, also examined G.P. and described impairments consistent with

those described by Dr. Hoffman. The experts all agree that, as a result of his ASD,

G.P. will never be gainfully employed.

       On April 12, 2006, Hendrix filed suit against Evenflo both individually and

on behalf of G.P., claiming the defective CRS caused G.P. to sustain injuries that

ultimately led him to develop ASD and syringomyelia. Evenflo removed the case



       3
                Dr. Hoffman is a medical doctor who is board-certified in neurodevelopmental
disabilities and developmental-behavioral pediatrics.

                                               5
to the Northern District of Florida on the basis of diversity jurisdiction. The parties

then commenced discovery.

      Hendrix sought to introduce testimony by Dr. Suhrbier and Dr. Hoffman that

the injuries G.P. sustained in the accident caused him to develop ASD and

syringomyelia. Evenflo moved to exclude this testimony, citing as one basis for

exclusion the fact that there is no scientifically reliable basis for the experts’

opinions, as required by Daubert.

      The district court assessed the admissibility of Dr. Suhrbier’s testimony

based on Dr. Suhrbier’s deposition taken by Evenflo in July, 2007, and Dr.

Suhrbier’s post-discovery affidavit prepared on September 9, 2008. In his

deposition, Dr. Suhrbier stated that “recognized causes of autism include genetic

disorders, metabolic disorders, epileptic encephalopathies, structural injuries and

malformations to the brain, as well as reasons that have not been fully elucidated.”

Dr. Suhrbier also claimed that autism had been associated with severe head injury

and stated his opinion that there was a “high probability” the accident had caused

G.P.’s ASD. When asked for scientific or medical literature relating autism

spectrum disorders and trauma, however, Dr. Suhrbier stated that he could not cite

from memory any specific articles.

      In his post-discovery affidavit, Dr. Suhrbier stated that his diagnosis of G.P.

                                            6
was based on:

      personal examinations, interaction with and observations of [G.P.],
      testing that I had performed on him, my review of some of his
      medical records, multiple interviews with his primary caregiver, my
      training, education and experience, my own base of knowledge and
      the utilization of the generally accepted medical methodology
      referred to as ‘differential diagnosis.’

Dr. Suhrbier explained that “[d]ifferential diagnosis, or differential etiology, is a

standard scientific technique of identifying the cause of a medical problem by

eliminating the likely causes until the most probable cause is isolated.” Dr.

Suhrbier further stated that in performing his differential diagnosis, he determined

that G.P. did not have the Fragile X genetic disorder, “the most common ‘known’

cause of autism,” and therefore concluded “[t]his means, based on our current

knowledge, that the cause of his autism is most likely not genetic in nature.” In

addition to the differential diagnosis method, Dr. Suhrbier also stated that he

sought a unifying mechanism to explain both G.P.’s ASD and his syringomyelia.

According to Dr. Suhrbier, it was important and “consistent with generally

accepted methodologies within the field of pediatrics–to the extent possible–to

look for unifying theories of diagnosis in an effort to explain a presentation of

symptoms.” Dr. Suhrbier stated that he was “quite familiar with the concept that

trauma is a recognized cause of autism and syringomyelia in very young patients.”



                                           7
Again, Dr. Suhrbier provided no research or literature to support this statement.

Dr. Suhrbier stated: “I concluded that the most likely cause of [G.P.]’s autism and

syringomyelia was the trauma that he sustained in that motor vehicle accident in

April of 2002. It was, and still is, my opinion that trauma was a substantial factor

in causing the disabilities that [G.P.] is experiencing today.”

       Dr. Hoffman first examined G.P. on March 22, 2006, approximately four

years after the accident. The district court assessed the admissibility of Dr.

Hoffman’s testimony based on Dr. Hoffman’s Independent Medical Evaluation &

Report prepared on December 14, 2007; a deposition taken by Evenflo on January

16, 2008; and a Supplemental Report prepared on June 18, 2008.

      In his Independent Report, Dr. Hoffman stated:

      [G.P.] has multiple neurodevelopmental impairments that will be
      handicapping lifelong. My medical opinion, to a reasonable degree of
      medical certainty, is that [G.P.’s] medical conditions and
      neurodevelopmental impairments (syringomyelia, autism, impaired
      adaptive behaviors) are related and secondary to the closed head and
      central nervous system injury he sustained in the [accident] at age 2
      weeks.

In his Supplemental Report, Dr. Hoffman presented ten points that he believes

explain how the accident caused both G.P.’s ASD and syringomyelia:

      First, that the brain, including the cerebellum, is actively developing
      during the perinatal/neonatal age that the injury occurred. Second,
      that this active brain development particularly includes developing

                                           8
      connections between the cerebellum and different regions of the
      cortex. Third, that abnormalities in the cerebellum and in the
      connections between the cerebellum and the cortex, are strongly
      linked to autism. Fourth, that the presence of syringohydromyelia
      presupposes abnormal cerebral spinal fluid pressure around the
      cerebellum at the site of the obex and foramen magnum. Fifth, that
      neither syringohydromyelia nor borderline Chiari I abnormalities
      were present when [G.P.] was age 2 weeks and were certainly not
      present in utero when the target ultrasound was performed. Sixth,
      that hydromyelia is almost always associated with hydrocephalus,
      which [G.P.] has never had, and Dr. Zimmerman’s opinion that [G.P.]
      does have hydromyelia goes against the clinical records in this case
      and against the accepted knowledge about the difference between
      hyrdomyelia and syringomyelia. Seventh, that the perinatal and
      neonatal intensive care follow-up literature does support the
      association between injury to the developing brain, including
      traumatic brain injury, and later occurrence of autism spectrum
      disorder. Eighth, that [G.P.] did experience at age 2 weeks . . .
      enough head injury to cause, among other things, a forehead bruise,
      irritability, poor feeding, reduced opening of left eye, subarachnoid
      and subdural hemorrhage, and soft tissue swelling in the
      parietooccipital region as well as likely hyperflexion neck injury.
      Ninth, that taken together (rather than in coincidental, idiopathic “we-
      don’t-know” isolation) the sequence of the injury to the brain, spinal
      cord, and surrounding tissues at that time then resulted in changes to
      CSF flow in the cervical spinal cord and around the foramen magnum
      with subsequent development of syringohydromyelia and also related
      altered and impaired subsequent development of the cerebellum and
      cerebellar connections to the cerebral cortex resulting in autism
      spectrum disorder . . . Tenth, there is no evidence in the medical
      record of any specific genetic disorder as a cause for [G.P.]’s autism.

Dr. Hoffman further stated that G.P.’s autism “is not a result of chromosome

abnormality nor of Fragile X syndrome, nor of perinatal distress or insult, nor of

neonatal illness. There is no sign or other indication of prenatal or perinatal insult

                                           9
or other apparent etiology for his autism.” Dr. Hoffman concluded: “G.P.’s autism

is a direct result of the injuries he sustained to his head and developing brain during

the motor vehicle accident.”

      In his deposition, Dr. Hoffman stated that he has never been involved in any

scientific studies on the causes of autism. When asked if he could cite any

scientific research to support his opinion that traumatic brain injury or close-head

injury causes autism, Dr. Hoffman responded:

              I haven’t pulled stuff for this report directly. I have thought
      about this before because I noted clinically, which is not what you are
      asking, that when I have done neonatal followup or seen children in
      followup from birth problems, as part of my clinical practice that
      have autistic features, wondering is there evidence in the literature
      linking brain injury or trauma to this. And so I have done some
      literature searches and there are reports, both animal models and
      persons showing this link. . . . I didn’t include that in my report, so I
      could find you some of those.
              If you ask what scientific basis, and what I was looking for was
      am I just coming up with this myself, or are there other people seeing
      this, too, and I reassured myself that other people are and it’s starting
      to show up in the literature. There is not, that I am aware of, like a
      major chapter or major article in the New England Journal saying this
      is a primary cause.

      Prior to trial, the district court granted Evenflo’s motion to exclude

testimony by Hendrix’s experts regarding the purported cause of G.P.'s ASD. The

court reasoned that the methods by which Dr. Suhrbier and Dr. Hoffman arrived at

the conclusion that the accident caused G.P.’s ASD were not sufficiently reliable

                                          10
under Daubert. The district court also ruled that it would permit the expert

testimony with regard to the cause of G.P.’s alleged syringomyelia. As a result of

these rulings, the district court granted partial summary judgment to Evenflo on

Hendrix’s compensatory damages claim for G.P.’s ASD, while allowing Hendrix’s

compensatory damages claim for syringomyelia and her punitive damages claim to

proceed to trial. Instead of proceeding to trial on her remaining claims, Hendrix

chose to voluntarily dismiss with prejudice her remaining claims and file this

appeal.

                            II. STANDARD OF REVIEW

      We review the district court’s exclusion of expert testimony for abuse of

discretion.   Rink v. Cheminova, Inc., 400 F.3d 1286, 1291 (11th Cir. 2005). We

will defer to the district court’s ruling unless it is “manifestly erroneous.” Id.

“Because the task of evaluating the reliability of expert testimony is uniquely

entrusted to the district court . . . we give the district court ‘considerable leeway’ in

the execution of its duty.” Id. (quoting Kumho Tire Co., Ltd. v. Carmichael, 526

U.S. 137, 152, 119 S. Ct. 1167, 1176 (1999)) (internal citation omitted).

      We review the district court’s ruling on a motion for summary judgment de

novo, applying the same legal standards that bound the district court. Nat’l Fire

Insur. Co. of Hartford v. Fortine Const. Co., 320 F.3d 1260, 1267 (11th Cir. 2003).

                                           11
Motions for summary judgment should only be granted when the pleadings,

depositions, answers to interrogatories, and admissions on file, together with the

affidavits, show there is no genuine issue as to any material fact and that the

moving party is entitled to judgment as a matter of law. Fed. R. Civ. P. 56(c);

Celotex Corp. v. Catrett, 477 U.S. 317, 322, 106 S. Ct. 2548, 2552 (1986).

                                 III. DISCUSSION

      Hendrix raises several issues on appeal. First, she argues that the district

court erred in finding unreliable under Daubert the experts’ testimony that the

traumatic brain injury G.P. sustained in the accident caused him to develop ASD.

Preliminary to this argument, Hendrix objects to the district court’s focus on G.P.’s

ASD diagnosis, arguing that the court should instead have assessed the experts’

testimony as it pertains to G.P.’s individual neurologic impairments. Second,

Hendrix argues that the district court erred in excluding a portion of the opinion of

Hendrix’s expert, Gary Whitman, relating to the lack of sufficient energy-absorbing

padding on the CRS, thus eliminating one of Hendrix’s theories of defective

product. Third, Hendrix argues that the district court erred in denying her request

for discovery on a recall of Evenflo safety seats.

      Upon thorough review of the record and with the benefit of oral argument,

we conclude that the district court did not abuse its discretion in excluding the

                                          12
expert testimony of Dr. Hoffman and Dr. Suhrbier based on the insufficient

reliability of that testimony under Daubert. Because without the testimony of those

two witnesses summary judgment was proper on Hendrix’s compensatory damages

claim for G.P.’s ASD, and because Hendrix voluntarily dismissed the remainder of

her claims with prejudice, we do not reach the additional issues presented in this

appeal.4

       A.      Characterizing G.P.’s Neurologic Impairments

       As a preliminary matter, we must address Hendrix’s argument that the

district court erred by asking whether the experts had established that traumatic

brain injury could ever cause ASD. Hendrix argues that, instead, the district court

should have determined whether traumatic brain injury could ever cause one or

more of the individual neurologic deficits that led to G.P.’s ASD diagnosis. As the

experts in this case testified, ASD is a disorder that is recognized and diagnosed

based on its underlying impairments. The district court, however, did not discuss

G.P.’s underlying neurologic deficits separately. Instead, the court noted that

“[a]ccording to Hendrix, [G.P.] suffers from ASD” and then went on to analyze the



       4
              In other words, Hendrix’s second and third arguments relate solely to liability, and
Evenflo has no liability on Hendrix’s claim for damages for G.P.’s ASD. Therefore, because
Hendrix’s ASD claim is the sole claim remaining after Hendrix dismissed all other claims,
Hendrix’s second and third arguments are moot.

                                                13
experts’ testimony in terms of that ASD diagnosis generally. Hendrix, 255 F.R.D.

at 577.

       Hendrix argues that the district court was required to assess the reliability of

the expert testimony regarding causation of each of G.P.’s neurologic impairments.

Because ASD is defined by its underlying deficits and behaviors, it might be

difficult to isolate the deficits underlying G.P.’s ASD diagnosis and determine

whether traumatic brain injury could have caused each deficit individually. After a

thorough review of the record, however, we conclude that the district court was not

required to undertake that complicated task because Hendrix herself failed to fairly

present this issue to the district court.

       Hendrix’s experts both referred to G.P.’s individual deficits, but opined only

that there was a causal link between traumatic brain injury and G.P.’s ASD.

Neither expert described whether or how traumatic brain injury could cause G.P.’s

individual deficits. For example, Dr. Hoffman refers in passing to G.P.’s “multiple

neurodevelopmental impairments”; however, in describing his theory of how the

accident contributed to G.P.’s injuries, Dr. Hoffman stated the following:

       abnormalities in the cerebellum, and in the connections between the
       cerebellum and the cortex, are strongly linked to autism
       ...
       the perinatal and neonatal intensive care follow-up literature does
       support the association between injury to the developing brain,

                                            14
      including traumatic brain injury, and later occurrence of autism
      spectrum disorder
      ...
      the sequence of the injury to the brain, spinal cord, and surrounding
      tissues at that time then resulted in changes to CSF flow in the
      cervical spinal cord and around the foramen magnum with . . .
      impaired subsequent development of the cerebellum and cerebellar
      connections to the cerebral cortex resulting in autism spectrum
      disorder
      ...
      there is no evidence in the medical record of any specific genetic
      disorder as a cause for [G.P.]'s autism

Thus, Dr. Hoffman applied his elaborate causation theory explicitly and

unambiguously to G.P.’s ASD diagnosis generally and not to G.P.’s impairments

individually.

      Similarly, Dr. Suhrbier notes G.P.’s underlying impairments but refers

exclusively to “ASD” and “autism” when discussing causation. Dr. Suhrbier stated

during his deposition that he had diagnosed G.P. with autism and that there “is a

high probability given the severe nature of [G.P.]’s injury and his subsequent

development of other neurologic sequela,” that the accident had caused G.P.’s

ASD. In his affidavit, Dr. Suhrbier said he had “diagnosed [G.P.] with [a]utism

(which is on the spectrum of [a]utistic [s]pectrum [d]isorder),” and that “we can

reasonably conclude that it is more likely than not that [G.P.] suffered damage to

his brain–particularly the posterior regions–which was, in turn, a substantial factor



                                          15
in causing his autism.” Dr. Suhrbier also stated that “[t]rauma of various kinds is a

known cause for . . . autism. . . . as part of my treatment of [G.P.], I concluded that

the most likely cause of G.P.’s autism . . . was the trauma that he sustained in that

motor vehicle accident in April of 2002.”

      Not only did Hendrix’s two medical experts opine only about the cause of

GP’s ASD diagnosis taken as a whole, Hendrix’s arguments to the district court

also did not attempt to parse the causation issue with respect to any of GP’s

individual impairments. Accordingly, we cannot conclude that the district court

abused its discretion in focusing on the issue which was fairly presented to it – i.e.,

the reliability Dr. Hoffman’s and Dr. Suhrbier’s testimony that traumatic brain

injury caused G.P.’s ASD. Moreover, in her initial brief before this Court, Hendrix

did not argue that it was appropriate to focus on causation of G.P.’s neurologic

impairments separately. Therefore, we conclude that she has abandoned this

argument on appeal. We now turn to the issue of whether the district court

properly excluded testimony from Hendrix’s experts that traumatic brain injury

caused G.P.’s ASD.

      B.     Exclusion of Expert Testimony on Causal Link Between Traumatic
             Brain Injury and ASD

      1.     Legal Standards for Admitting Scientific Evidence of Causation


                                           16
      Hendrix seeks to admit expert testimony that the traumatic brain injury G.P.

sustained in the accident caused his ASD. Because this is a diversity case, we

apply Florida’s substantive law regarding a plaintiff’s burden of proof on

causation. McLeod v. Am. Motors Corp., 723 F.2d 830, 832 (11th Cir. 1984).

Under Florida law, Hendrix may recover damages upon showing that the trauma

was a “substantial factor” causing G.P.’s ASD. Gross v. Lyons, 763 So.2d 276, 279

(Fla. 2000); Hart v. Stern, 824 So.2d 927, 929-30 (Fla. 5th DCA 2002). A

purported cause is a substantial factor if it operates in combination with another

cause, such as the negligent act of another or the plaintiff’s pre-existing physical

condition, to cause an injury. Gross, 763 So.2d at 279; Hart, 824 So.2d at 929-30.

      Although the standards for finding causation are governed by Florida law,

we apply federal law to determine whether the expert testimony proffered to prove

causation is sufficiently reliable to submit it to the jury. Flury v. Daimler Chrysler

Corp., 427 F.3d 939, 944 (11th Cir. 2005) (noting that in diversity cases, the

Federal Rules of Evidence govern the admissibility of evidence in federal court).

The Federal Rules of Evidence provide:

      If scientific . . . knowledge will assist the trier of fact to understand
      the evidence or to determine a fact in issue, a witness qualified as an
      expert by knowledge, skill, experience, training, or education, may
      testify thereto in the form of an opinion or otherwise, if (1) the
      testimony is based upon sufficient facts or data, (2) the testimony is

                                          17
      the product of reliable principles and methods, and (3) the witness has
      applied the principles and methods reliably to the facts of the case.

Fed. R. Evid. 702. “Unlike an ordinary witness . . . an expert is permitted wide

latitude to offer opinions, including those that are not based on firsthand

knowledge or observation.” Daubert, 509 U.S. at 592, 113 S. Ct. at 2796. “[T]his

relaxation of the usual requirement of firsthand knowledge . . . is premised on an

assumption that the expert’s opinion will have a reliable basis in the knowledge

and experience of his discipline.” Id. A trial court assessing the reliability of an

expert’s evidence must therefore perform a “gatekeeping” function by conducting

“a preliminary assessment of whether the reasoning or methodology underlying the

testimony is scientifically valid and of whether that reasoning or methodology

properly can be applied to the facts in issue.” Id. at 592-93, 113 S. Ct. at 2796. We

have offered district courts the following general guidance in determining whether

to admit scientific evidence under Daubert:

      Given time, information, and resources, courts may only admit the
      state of science as it is. Courts are cautioned not to admit speculation,
      conjecture, or inference that cannot be supported by sound scientific
      principles. “The courtroom is not the place for scientific guesswork,
      even of the inspired sort. Law lags science; it does not lead it.”

Rider v. Sandoz Pharms. Corp., 295 F.3d 1194, 1202 (11th Cir. 2002) (quoting

Rosen v. Ciba-Geigy Corp., 78 F.3d 316, 319 (7th Cir. 1996)).



                                          18
      This circuit requires trial courts acting as gatekeepers to engage in a

“rigorous three-part inquiry” assessing whether:

      (1) the expert is qualified to testify competently regarding the matters
      he intends to address; (2) the methodology by which the expert
      reaches his conclusions is sufficiently reliable as determined by the
      sort of inquiry mandated in Daubert; and (3) the testimony assists the
      trier of fact, through the application of scientific, technical, or
      specialized expertise, to understand the evidence or to determine a
      fact in issue.

United States v. Frazier, 387 F.3d 1244, 1260. The proponent of the expert

testimony bears the burden of showing, by a preponderance of the evidence, that

the testimony satisfies each prong. See Boca Raton Cmty. Hosp., Inc. v. Tenet

Health Care, 582 F.3d 1227, 1232 (11th Cir. 2009). Here, the parties raise no

issues regarding the first and third prongs. Therefore, our analysis will focus on

whether the district court abused its discretion in excluding the expert testimony of

Dr. Hoffman and Dr. Suhrbier upon finding that the testimony was not sufficiently

reliable under Daubert.

      The Daubert Court described several factors trial judges may use to assess

the reliability of proffered scientific testimony, including: (1) whether the theory

or technique “can be (and has been) tested,” (2) “whether the theory or technique

has been subjected to peer review and publication,” (3) “in the case of a particular

scientific technique, . . . the known or potential rate of error,” and (4) whether the

                                           19
theory or technique is generally accepted by the relevant scientific community.

Daubert, 509 U.S. at 592-94, 2786 S. Ct. at 2796-97; see also Rink, 400 F.3d at

1292 (discussing these factors in the context of assessing an expert’s particular

scientific technique). This list, however, is not exhaustive, and district courts

“have substantial discretion in deciding how to test an expert’s reliability.” Rink,

400 F.3d at 1292.

       In addition, the Supreme Court has noted that, in the context of this analysis,

“conclusions and methodology are not entirely distinct from one another.” General

Elec. Co. v. Joiner, 522 U.S. 136, 146, 118 S. Ct. 512, 519 (1997). Although

experts “commonly extrapolate from existing data . . . nothing in either Daubert or

the Federal Rules of Evidence requires a district court to admit opinion evidence

that is connected to existing data only by the ipse dixit of the expert.” Id. Rather,

the trial court is free to “conclude that there is simply too great an analytical gap

between the data and the opinion proffered.” Id.

       Hendrix’s experts rely primarily on the differential etiology method5 to link

       5
                Although the parties and other cases often refer to this method as “differential
diagnosis,” throughout the opinion we will use the more precise term “differential etiology.” See
McClain v. Metabolife Int’l, Inc., 401 F.3d 1233, 1252 (11th Cir. 2005) (describing differential
diagnosis and noting that “[t]he more precise but rarely used term is differential etiology”).
Differential diagnosis is “the determination of which of two or more diseases with similar
symptoms is the one from which the patient is suffering, by a systematic comparison and
contrasting of the clinical findings.” STEDMAN’S MEDICAL DICTIONARY, 428 (25th ed.
1990). Etiology refers to the “science and study of the causes of disease and their mode of

                                               20
G.P.’s traumatic brain injury to his ASD diagnosis. Differential etiology is a

medical process of elimination whereby the possible causes of a condition are

considered and ruled out one-by-one, leaving only one cause remaining. See supra

n.5. Hendrix argues that the experts’ opinions were reliable because differential

etiology is a well-recognized scientific method that has been accepted by many

courts as a valid basis for expert testimony. See, e.g., Best v. Lowe’s Home

Centers, Inc., 563 F.3d 171, 178-84 (6th Cir. 2009); McClain, 401 F.3d at 1252-

53; Clausen v. M/V New Carissa, 339 F.3d 1049, 1057 (9th Cir. 2003). We have

previously noted that, when applied under circumstances that ensure reliability, the

differential etiology method can provide a valid basis for medical causation

opinions. See McClain, 401 F.3d at 1252. Here, the reliability of the method must

be judged by considering the reasonableness of applying the differential etiology

approach to the facts of this case and the validity of the experts’ particular method

of analyzing the data and drawing conclusions therefrom. See Kumho Tires, 526

U.S. at 153-54, 119 S. Ct. at 1177 (“[T]he specific issue before the court was not

the reasonableness in general of a tire expert's use of a visual and tactile inspection




operation.” Id. at 542 (emphasis added). It is undisputed that G.P. has been diagnosed with
ASD; it is the cause of his condition that is at issue. Therefore, the relevant methodology used in
this case is differential etiology, i.e., the process of determining which of two or more causes is
responsible for the patient’s symptoms.

                                                21
to determine whether overdeflection had caused the tire's tread to separate from its

steel-belted carcass. Rather, it was the reasonableness of using such an approach,

along with Carlson's particular method of analyzing the data thereby obtained, to

draw a conclusion regarding the particular matter to which the expert testimony

was directly relevant.”) (emphasis in original); see also Quiet Tech. DC-8 v. Hurel-

Dubois UK LTD., 326 F.3d 1333, 1343 (11th Cir. 2003).

      A reliable differential etiology analysis is performed in two steps. First, the

expert must compile a “comprehensive list of hypotheses that might explain the set

of salient clinical findings under consideration. . . . The issue at this point in the

process is which of the competing causes are generally capable of causing the

patient’s symptoms.” McClain, 401 F.3d at 1253 (quoting Clausen v. M/V NEW

CARISSA, 339 F.3d 1049, 1057-58 (9th Cir. 2003)). Second, the expert must

eliminate all causes but one. See McCullock v. H.B. Fuller Co., 61 F.3d 1038,

1044 (2d Cir. 1995).

      With regard to the first step, the district court must ensure that, for each

possible cause the expert “rules in” at the first stage of the analysis, the expert’s

opinion on general causation is “derived from scientifically valid methodology.”

Hollander v. Sandoz Pharm. Corp., 289 F.3d 1193, 1211 (10th Cir. 2002) (quoting

Siharath v. Sandoz Pharms. Corp., 131 F. Supp. 2d 1347, 1362-63 (N.D. Ga.

                                           22
2001)). This is because “a fundamental assumption underlying [differential

etiology] is that the final, suspected ‘cause’ . . . must actually be capable of causing

the injury.” McClain, 401 F.3d at 1253. Thus, the experts’ purported use of the

differential etiology method “will not overcome a fundamental failure to lay the

scientific groundwork” for the theory that traumatic brain injury can, in general,

cause autism. See McClain, 401 F.3d at 1252 (“This approach, however, will not

usually overcome the fundamental failure of laying a scientific groundwork for the

general toxicity of the drug and that it can cause the harm a plaintiff suffered.”).

       Some specific principles arise in the context of establishing general

causation in cases dealing with medical injuries. In McClain, we distinguished

cases in which the medical community generally recognizes that a certain chemical

can cause the injury the plaintiff alleges from those in which the medical

community has not reached such a consensus. 401 F.3d at 1239.6 We stated that in

       6
                Hendrix attempts to distinguish this case from McClain on the grounds that ours
is an “ordinary trauma” case whereas McClain is a toxic tort case. Although we are not dealing
with a toxic tort, which is “[a] civil wrong arising from exposure to a toxic substance, such as
asbestos, radiation, or hazardous waste,” Black’s Law Dictionary (8th ed. 2004), we are dealing
with a medical injury allegedly arising from use of a defective product. In McClain, as in our
case, the court was required to analyze expert medical opinions regarding the cause of an injury;
thus, the relevant inquiry was similar. See McClain, 401 F.3d at 1236 (holding that the district
court erroneously admitted expert testimony that a weight-loss supplement caused the plaintiff’s
medical problems). Because Hendrix has provided no reason to distinguish between the
causation evidence in McClain and the instant case for the purposes of the Daubert analysis, we
conclude that the principles articulated in McClain with regard to admitting expert medical
testimony on the cause of an injury may properly guide our reliability inquiry on the causation
issue.

                                                23
the second category of cases, the district court must apply the Daubert analysis not

only to the expert’s methodology for figuring out whether the chemical caused the

plaintiff’s specific injury, but also to the question of whether the drug or chemical

can, in general, cause the harm plaintiff alleges. Id. Thus, the district court must

assess the reliability of the expert’s opinion on general, as well as specific,

causation. Id.

       Hendrix does not contend that the medical community generally recognizes

traumatic brain injury as a cause of autism. Therefore, the district court was correct

to apply the Daubert analysis to the question of whether traumatic brain injury can,

in general, cause autism.7 We afford the district court substantial discretion to

decide how to test the reliability of the general causation evidence presented by Dr.

Hoffman and Dr. Suhrbier. Rink, 400 F.3d at 1292.

       In reviewing the district court’s reliability determination, we note that we

       7
                 Hendrix argues that Florida’s “substantial factor” test absolves her of establishing
general causation between traumatic brain injury and autism. This argument appears to be based
on a misunderstanding that the “substantial factor” test means that a substantial likelihood of
causation is sufficient to impose liability. That is not the case. Florida law’s “substantial factor”
requirement is best understood to mean that Hendrix could recover if a jury found that G.P.’s
injuries were a partial or contributing cause of his ASD. The district court did not exclude the
expert testimony on the basis that it did not show that the injury was the only cause of G.P.’s
ASD; rather, the district court found that there was no scientifically reliable evidence that such
brain injuries, in general, could ever cause autism. Even the “substantial factor” test requires the
plaintiff to show a causal link based on reliable evidence between a purported cause and the
alleged injury, as the district court required. Gross, 763 So.2d at 279-80. The district court’s
failure to explicitly articulate Florida’s causation standard was neither prejudicial nor an abuse of
discretion.

                                                 24
have previously identified some of the scientifically valid methods for establishing

general causation. For instance, we will admit expert opinions pursuant to Daubert

that are supported by epidemiological studies,8 provided the expert explains how

the findings of those studies may be reliably connected to the facts of the particular

case. Rider, 295 F.3d at 1198 (noting that, although they are not mandatory,

“epidemiological studies may be powerful evidence of causation”); see also, Norris

v. Baxter Healthcare Corp., 397 F.3d 878, 882 (10th Cir. 2005) (“[E]pidemiology

is the best evidence of general causation in a toxic tort case.”). An expert’s opinion

will likely also survive Daubert if the expert describes the physiological process,

derived by the scientific method, by which a particular cause leads to the

development of a given disease or syndrome. McClain, 401 F.3d at 1253 (“The

underlying predicates of any cause-and-effect medical testimony are that medical

science understands the physiological process by which a particular disease or

syndrome develops and knows what factors cause the process to occur.”) (quoting

Black v. Food Lion, Inc., 171 F.3d 308, 314 (5th Cir. 1999)); see also Daubert, 509

U.S. at 590, 113 S. Ct. at 2795 (noting that in order to qualify as “scientific

       8
               “Epidemiology is the ‘study of the distribution and determinants of health-related
states and events in populations and the application of this study to control of health problems.’”
In re TMI Litigation, 193 F.3d 613, 660 n.81 (3d Cir. 1999) (quoting Federal Judicial Center,
Reference Manual on Scientific Evidence 174 (1994)).



                                                 25
knowledge” for the purposes of Fed. R. Evid. 702, “an inference or assertion must

be derived by the scientific method”).

      Courts have also identified other methods that, when used alone, are unable

to provide scientifically valid proof of general causation. For instance, in McClain,

we explained that the “post hoc ergo propter hoc fallacy assumes causality from

temporal sequence. . . . It is called a fallacy because it makes an assumption based

on the false inference that a temporal relationship proves a causal relationship.”

McClain, 401 F.3d at 1243. Thus, a mere temporal relationship between an event

and a patient’s disease or symptoms does not allow an expert to place that event on

a list of possible causes of the disease or symptoms. Case studies and clinical

experience, used alone and not merely to bolster other evidence, are also

insufficient to show general causation. See Rider, 295 F.3d at 1199 (“Although a

court may rely on anecdotal evidence such as case reports . . . courts must consider

that case reports are merely accounts of medical events. They reflect only reported

data, not scientific methodology.”) (internal citation omitted); see also Norris, 397

F.3d at 887 (“We cannot allow the jury to speculate based on an expert’s opinion

which relies only on clinical experience in the absence of showing a consistent,

statistically significant association between breast implants and systemic disease.”).

                                          26
       In the second step of the differential etiology analysis, the expert must

eliminate all causes but one. See McCullock, 61 F.3d at 1044. While the first step

focuses on general causation, in the second step the expert applies the facts of the

patient’s case to the list created in the first step in order to form an opinion about

the actual cause of the patient’s symptoms, i.e., to determine specific causation. In

Clausen, the Ninth Circuit stated that an “expert must provide reasons for rejecting

alternative hypotheses using scientific methods and procedures and the elimination

of those hypotheses must be founded on more than subjective beliefs or

unsupported speculation.” 339 F.3d at 1058 (internal quotation omitted). Thus,

“[a] district court is justified in excluding evidence if an expert ‘utterly fails . . . to

offer an explanation for why the proffered alternative cause’ was ruled out.” Id.

(quoting Cooper v. Smith & Nephew, Inc., 259 F.3d 194, 202 (4th Cir. 2001)).

       With these principles in mind, we now review the district court’s

determination that the experts’ testimony in this case was unreliable under

Daubert.

2.     Application of Standards to Dr. Hoffman’s Testimony

       The district court determined that Dr. Hoffman’s testimony regarding ASD

causation was insufficiently reliable under Daubert to warrant admission of that

                                             27
testimony at trial. The district court identified errors in Dr. Hoffman’s differential

etiology analysis at both the “rule in” and “rule out” steps. Specifically, the district

court determined that Dr. Hoffman “fail[ed] to show how, by ‘scientifically valid

methodology,’ traumatic brain injury could ever be a possible cause of autism in

anyone.” Hendrix, 255 F.R.D. at 598. The court also found that Dr. Hoffman

“failed to compile ‘a comprehensive list’ of all possible causes of ASD” and

accordingly that “by failing to include all of the causes currently theorized in the

medical literature in his ‘comprehensive list’ of the possible causes of ASD,

Hoffman failed to ‘rule out’ all possible causes but one.”9 Hendrix, 255 F.R.D. at



       9
                 Although the district court stated that the expert must make a list of “all possible
causes for the condition,” Hendrix, 255 F.R.D. at 597, we note that McClain and Clausen merely
require the list to be “comprehensive.” See McClain, 401 F.3d at 1253; Clausen, 339 F.3d at
1057-58. As the Supreme Court stated in Daubert, “it would be unreasonable to conclude that
the subject of scientific testimony must be ‘known’ to a certainty; arguably, there are no
certainties in science.” 509 U.S. at 590, 113 S. Ct. at 1795 (quoting Brief for Nicolaas
Bloembergen et al. as Amici Curiae 9). Requiring experts to compile a list of all possible causes
of a patient’s symptoms violates this principle. Thus, we think an expert performing a
differential etiology need only compile a comprehensive list of known causes in order to
adequately complete the first step of the differential etiology method. We do not, however,
believe the district court’s misstatement of the first step of the differential etiology method led to
any error in the court’s overall analysis, in part because the court determined that Dr. Hoffman
did not even take into account all possible causes cited in the literature that Dr. Hoffman himself
presented. Moreover, because we affirm the judgment of the district court only on the basis of its
“ruling in” decision, even if there was error in its “ruling out” decision, our holding would not be
affected. Therefore, the district court did not abuse its discretion in finding that Dr. Hoffman’s
list of ASD causes was not comprehensive.

                                                  28
597-98. We agree with the district court that Dr. Hoffman failed to “rule in”

traumatic brain injury as a possible cause of ASD. Because our holding in that

regard is a sufficient ground upon which the district court ruling may be affirmed,

we need not address the district court’s decision that Dr. Hoffman failed to rule out

other known or plausible causes of ASD.

       Dr. Hoffman’s sole support for his theory that, in general, traumatic brain

injury can cause ASD came from certain medical textbooks and epidemiological

studies submitted by Dr. Hoffman. The district court carefully considered all of the

materials cited by Hoffman and concluded that “none of these works come close to

providing useful evidence of a definitive10 causal link between traumatic head

injuries and autistic disorders,11 and none provide even marginal support for


       10
                 Hendrix complains about the district court’s use of the word “definitive,” again
accusing the district court of adopting an inflexible bright-line standard of certainty. For the
reasons noted in the preceding footnote, we agree that Daubert does not require certainty; it
requires only reliability. However, despite the district court’s inappropriate choice of the word
“definitive,” the context of the district court’s opinion leaves us confident that the court required
no more than reliability. As the district court said in the very same sentence, Dr. Hoffman’s cited
literature provided not even “marginal support” for his theory of causation. Our own review of
the cited literature amply confirms the lack of support.
       11
              Hendrix objects to the district court’s rationale, arguing that medical literature
proving a causal link between trauma and an illness is not a mandatory prerequisite to the
admission of opinion testimony on causation from a qualified medical doctor. In general, we do
not require medical doctors to support their expert opinions with medical literature. See Rider,
295 F.3d at 1198 ("It is well-settled that while epidemiological studies may be powerful evidence

                                                 29
Hoffman’s theory of a relationship between abnormal [cerebral spinal fluid]

pressure and problems with cerebellum pressure, leading to autism.” Id. at 600-01.

We have carefully and exhaustively reviewed the literature cited by Dr. Hoffman

and conclude that the district court’s conclusion with regard to each piece of

literature was reasonable. We hold that the district court reasonably concluded that

none of the literature supported the reliability of Dr. Hoffman’s proffered

physiological process, and that none of the literature supported Dr. Hoffman’s

opinion that a traumatic brain injury like GP’s could have caused or contributed to

the development of ASD. Thus, we conclude that the district court was reasonable



of causation, the lack thereof is not fatal to a plaintiff's case."). The proponent of such opinions,
however, retains the burden of offering some proof that the expert’s testimony on general
causation is reliable. In Rider, for example, we stated:

       In the absence of epidemiology, plaintiffs may still prove medical causation by
       other evidence. In the instant case, however, plaintiffs simply have not provided
       reliable evidence to support their conclusions. To admit the plaintiffs' evidence,
       the Court would have to make several scientifically unsupported “leaps of faith”
       in the causal chain. The Daubert rule requires more.

295 F.3d at 1202.

         Here, Dr. Hoffman chose to rely exclusively on medical literature to establish general
causation between traumatic brain injury and ASD. Therefore, the medical literature must
provide enough support for Dr. Hoffman’s general causation opinion to satisfy Daubert’s
reliability requirement. See McClain, 401 F.3d at 1239-40 (concluding that expert’s opinions on
general causation should be excluded because the expert did not “support his opinions with
sufficient data or reliable principles, as identified by the Daubert rubric . . .”).

                                                  30
in determining that the literature overall does not provide the necessary support for

Dr. Hoffman’s opinions to render those opinions admissible under Daubert.

      Rather than duplicating the district court’s persuasive analysis of the

literature provided by Dr. Hoffman, see Hendrix 255 F.R.D. at 600-03, we will

focus on those pieces of literature emphasized by Hendrix on appeal. At oral

argument, Hendrix’s counsel stated that the most compelling literature discussing

the physiological process by which traumatic brain injury could cause autism is a

chapter in a textbook edited by Evenflo’s medical expert Dr. Joel Morgan. See

Gerry A. Stefanatos & Wilson Q. Joe, Autistic Disorder, in Textbook of Clinical

Neuropsychology, 185-260 (Joel E. Morgan & Joseph H. Ricker, eds., 2008). We

read this chapter carefully and failed to discern any suggestion that brain damage

resulting from post-birth traumatic brain injury can cause autism spectrum

disorders. We also saw no support for Dr. Hoffman’s theory that abnormal cerebral

spinal fluid pressure in the cerebellum could cause ASD. The chapter states that

certain learning and memory patterns found in autistic individuals have been

“interpreted as reflection of cerebellar pathology,” but also notes that “studies have

shown that frontal lobe and basal ganglia are also involved” in learning a memory,

and that “[c]onsequently, these findings could not rule out an explanation in terms

                                          31
of a frontal-striatal dysfunction rather than anomalies of frontal-cerebellar circuits.”

Id. at 202. Further on in the chapter, the authors discuss the role of the cerebellum

in ASD in general, and note that “histological studies of the autistic brain have

consistently implicated reduction of Purkinje cells of the cerebellum.” Id. at 221.

They do not, however, opine as to what might cause such a reduction of those cells.

While these statements provide some support for the idea that the cerebellum is

linked to autism in a very general sense, they offer no reliable support for Dr.

Hoffman’s theory that a traumatic brain injury like the one G.P. suffered could

cause or contribute to the development of ASD. We found no mention at all in the

Chapter of Dr. Hoffman’s proposed physiological process involving abnormal

cerebral spinal fluid pressure leading to ASD.

      Notably, although the chapter catalogues the known etiological factors

involved in ASD, the section titled “Etiological considerations” does not mention

acquired trauma in the perinatal brain. Id. at 213-17. The section discusses genetic

factors at length, and then goes on to list “extrinsic factors” such as: viruses; the

presence of other neurological conditions, such as epilepsy; birthing complications;

teratogenic substances, such as cocaine; and autoimmune factors. Id. The section

fails to mention traumatic brain injury, and the authors qualify even the factors they

                                          32
do list by noting that “studies directed to examining etiologic factors in [autism]

have suffered from limitations due to small sample sizes, inadequate specification

of diagnostic categories, and significant heterogeneity of the autistic population.”

Id. at 217.

      Hendrix’s counsel also noted as particularly persuasive an article titled Late

Neurologic and Cognitive Sequelae of Inflicted Traumatic Brain Injury in Infancy.

Barlow et al., Late Neurologic and Cognitive Sequelae of Inflicted Traumatic

Brain Injury in Infancy, 116 Pediatrics, Aug. 2005. The article describes a variety

of neurologic impairments, including many of the impairments from which G.P.

suffers, found in children with inflicted traumatic brain injury (e.g., shaken baby

syndrome). Id. at e174. While Hendrix criticizes the district court for discounting

the article based on the distinction between inflicted (non-accidental) and

accidental traumatic brain injury, the article itself supports the notion that the two

types of injuries are distinct. For instance, the article notes that mortality rates for

infants with inflicted traumatic brain injury are greater than those for infants whose

injuries were accidental. Id. at e174. The article also self-limits its findings by

pointing out the small sample size, the need for further study, and that the study

lacked a control group. Id. at e184. In fact, the authors mention that previous

                                           33
similar studies used children with an accidental traumatic brain injury as control

subjects against which to compare those subjects with inflicted injuries. Id.

Moreover, although one patient in the study developed autism spectrum disorder,

the authors note that the ASD patient “may have had significant exposure to

alcohol in utero.” Id. at e183. The district court identified these shortcomings and

noted that “significantly, nothing in the study purports to show or explain the

physiological process by which brain injury produces autism.” Hendrix, 255

F.R.D. at 601. The court therefore concluded that this study was insufficient to

support Dr. Hoffman’s assertion that the literature supports his theory of causation

or even a general causal link between accidental traumatic brain injury and ASD.

We cannot say that this determination was an abuse of discretion.

      We found the most direct statement supporting the theory that traumatic

brain injury can cause ASD in a textbook submitted by Dr. Hoffman that was not

brought to our attention on appeal. That textbook states:

      Considerable precedent for deleterious effects of various perinatal
      insults on organizational events is provided by studies with
      experimental animals. Initial studies of later cortical neuronal
      development in “undamaged” areas adjacent to ischemic cortical
      injury in human infants show dendritic aberrations that could
      contribute importantly to subsequent cognitive deficits and epilepsy.
      It is a clinical truism that some children affected by one or more

                                         34
       perinatal insults may exhibit neurological sequalae that are more
       severe than might be predicted from the extent of injury recognized
       by the usual brain imaging or neuropathological techniques.

Volpe, Human Brain Development in Neurology of the Newborn at 82. In other

words, this textbook provides some support for the idea that even minor injuries

sustained by newborn brains can result in more severe neurologic impairments than

one would expect from the initial extent of the injury. The textbook does not,

however, link such injuries to ASD, or provide any support for Dr. Hoffman’s

theory of ASD causation involving abnormal cerebral spinal fluid pressure.

       We are satisfied that the district court did not abuse its discretion in

concluding, based on the literature Dr. Hoffman himself provided, that there is no

reliable support for Dr. Hoffman’s assertion that “perinatal and neonatal intensive

care follow-up literature does support the association between injury to the

developing brain, including traumatic brain injury, and later occurrence of autism

spectrum disorder.”12 Because Dr. Hoffman offers no other scientifically reliable


       12
                In addition to concluding from our own review of the medical literature that it
does not support Dr. Hoffman’s theory of causation, we also note that Dr. Hoffman himself was
quite qualified in the support he claims from the literature. In his supplemental report, he noted
that: “Thus, there is a general consensus by many in the scientific community that the etiology
for autism spectrum disorders often does include environmental factors, and some researchers
have reported specifically the association between insults to the perinatal-newborn brain and
subsequent development of autism.” In a similar vein, Dr. Hoffman testified that he had noticed

                                                35
basis for his opinion, his testimony is the type of “speculation, conjecture, or

inference” that we have cautioned district courts not to admit. Rider, 295 F.3d at

1202.

        Hendrix attempts to sidestep the deficiencies in the medical literature by

focusing on Dr. Hoffman’s experience and training. Merely demonstrating that an

expert has experience, however, does not automatically render every opinion and

statement by that expert reliable. As an Advisory Committee Note on Federal Rule

of Evidence 702 states:

        If the witness is relying solely or primarily on experience, then the
        witness must explain how that experience leads to the conclusion
        reached, why that experience is a sufficient basis for the opinion, and
        how that experience is reliably applied to the facts. The trial court's
        gatekeeping function requires more than simply “taking the expert's
        word for it.”

Committee Notes on Rules - 2000 Amendment (quoting Daubert v. Merrell Dow

Pharms., Inc., 43 F.3d 1311, 1319 (9th Cir. 1995)). “Taking the expert’s word for


in his practice that some children with early brain injuries later develop autistic features, had
wondered if others were seeing this too, and then “reassured [him]self that other people are, and
it’s starting to show up in the literature.” In other words, Dr. Hoffman refers both to his own
experience and to the literature as evidencing only a temporal relationship, or a mere correlation.
However, we held in McClain that a mere temporal relationship, itself, would not ordinarily be
sufficient to prove a causal relationship. See McClain, 401 F.3d at 1243 (“Proving a temporal
relationship between taking Metabolife and the onset of symptoms does not establish a causal
relationship.”)

                                                 36
it” is precisely what Hendrix suggests the district court should have done in this

case; however, we have previously recognized that “‘[n]othing in either Daubert or

the Federal Rules of Evidence requires a district court to admit opinion evidence

that is connected to existing data only by the ipse dixit of the expert.’” See

McClain, 401 F.3d at 1244 (quoting Joiner, 522 U.S. at 146, 118 S. Ct. at 519

(1997)). Dr. Hoffman has not provided a reliable basis, derived by the scientific

method, for concluding that traumatic brain injury can cause ASD. We decline to

conclude that the district court abused its discretion in failing to admit Dr.

Hoffman’s testimony based on his experience alone.

       Because the medical literature adduced by Hendrix supports neither Dr.

Hoffman’s theory of causation involving abnormal cerebral spinal fluid pressure

nor his ultimate opinion that a traumatic brain injury like GP’s can cause autism,

and because Dr. Hoffman offers no other scientifically reliable basis for his

opinion,13 we hold that the district court did not abuse its discretion in concluding



       13
                For example, there is no evidence that Dr. Hoffman’s theory of causation has been
tested or subject to peer-reviewed publication. See Daubert, 509 U.S. at 593-94; 2786 S. Ct. at
2796-97. And, other than Dr. Hoffman’s own unsupported and qualified assertion of general
acceptance in the scientific community, there is no evidence that Dr. Hoffman’s theory is
generally accepted in the relevant scientific community. See McClain, 401 F.3d at 1244 (with
respect to the ipse dixit of an expert).

                                               37
that Hendrix failed to establish general causation to support Dr. Hoffman’s

opinion. That is, Hendrix has failed reliably to “rule in” traumatic brain injuries

like GP’s as a plausible cause of autism.

      Because this is a sufficient basis on which to affirm the district court’s ruling

excluding Dr. Hoffman’s testimony, we need not address the district court’s

decision that Dr. Hoffman also failed to “rule out” other possible causes. The

district court held:

      Hoffman’s claim that he ruled out genetics as a potential cause of
      [GP’s] ASD based on [GP’s] normal “Fragile X” tests ignores the
      possibility of other genetic conditions as a cause. Given the plethora
      of genetic theories for autism, “ruling out” Fragile X as a possible
      cause of [GP’s] ASD far from eliminates all genetic causes of his
      ASD, let alone the other multitude of factors that have been linked to
      autism or ASD.

Hendrix, 255 F.R.D. at 598 (footnotes omitted). The medical literature indicates

that there are a dizzying array of other factors that have been mentioned as possible

causes, including as many as 90 gene mutations that could play a role in the

development of autism. See Frank Polleaux & Gean M. Lauder, Toward a

Developmental Neurobiology of Autism, 10 Mental Retardation and Dev.

Disabilities Research Rev. 303, 309, 310-12 (2004). Dr. Hoffman conceded in his

deposition testimony that, unless one of the genetic chromosome anomalies that is

                                            38
known to cause autism is identified, medical science simply does not know what

causes autism. Obviously, in such a situation, the task of “ruling out” other

plausible causes is extremely complex. In light of our decision that Dr. Hoffman

failed to reliably “rule in” his theory of ASD causation, we need not in this case

venture into the quagmire of attempting to define the parameters of a reliable

process of “ruling out” other possible causes of autism.

      3.     Application of Standards to Dr. Suhrbier’s Testimony

      Hendrix also objects to the district court’s exclusion of Dr. Suhrbier’s

testimony. Dr. Suhrbier, G.P.’s treating physician, sought to testify as an expert

witness under Rule 702. In order to be admitted into evidence, Dr. Suhrbier’s

opinions must also be based on a scientifically reliable methodology under

Daubert. See United States v. Henderson, 409 F.3d 1293, 1299-1300 (11th Cir.

2005).

      Dr. Suhrbier purported to both perform a differential etiology and to look for

a unifying theory to explain G.P.’s ASD and syringomyelia. Like Dr. Hoffman, he

concluded that the “most likely cause of [G.P.]’s autism and syringomyelia was the

trauma that he sustained in that motor vehicle accident in April of 2002.” Unlike

Dr. Hoffman, however, Dr. Suhrbier did not even attempt to provide any evidence

                                         39
to support a general causal link between traumatic brain injury and ASD. He

presented no medical literature, described no relevant physiological process, and

provided no other support for his conclusion that traumatic brain injury can cause

autism. Based on the Daubert requirements for admitting expert testimony, we

cannot say that the district court abused its discretion in determining that there was

too great an analytical gap between Dr. Suhrbier’s evidence and conclusions

regarding G.P.’s ASD diagnosis to submit those conclusions to the jury.14

                                     IV. CONCLUSION

       Under Daubert, it is the unique role of the district court to determine whether

an expert’s opinion is sufficiently reliable to allow it to be presented to a jury.

Here, the district court concluded that Hendrix failed to present scientifically

reliable evidence that traumatic brain injury can ever cause autism. Thus, the


       14
                 Hendrix also argues that the expert testimony of Dr. Hoffman and Dr. Suhrbier is
reliable because both sought to find a “unifying mechanism” explaining both G.P.’s ASD and
syringomyelia. Both doctors came to the conclusion that the unifying mechanism was the
traumatic brain injury G.P. sustained in the accident. This argument fails for the same reason
Hendrix’s argument related to differential etiology fails. There is no evidence that is
scientifically reliable under Daubert indicating that traumatic brain injury can ever cause or
contribute to ASD. Therefore, it follows that there is no scientifically reliable evidence that
traumatic brain injury can cause or contribute to both ASD and syringomyelia. Moreover,
regardless of the rarity of either condition or the probability that both conditions would be
present in the same individual, Hendrix’s experts have provided no support for the notion that the
accident is a more likely unifying mechanism than some other common cause.

                                                40
district court excluded the experts’ theories because of a lack of reliable proof of

general causation between the alleged injury and the purported cause of that

injury.15 Upon thorough review of the record and with the benefit of oral argument,

we conclude that the district court properly executed its gatekeeper function under

Daubert, and therefore the court did not abuse its discretion in excluding the expert

testimony.

       We emphasize that we express no opinion regarding whether traumatic brain

injury sustained in the perinatal or neonatal period can ever cause or contribute to

later development of an autism spectrum disorder. Rather, as we have previously

stated: “The courtroom is not the place for scientific guesswork, even of the

inspired sort. Law lags science; it does not lead it.” Rider, 295 F.3d at 1202

(quoting Rosen, 78 F.3d at 319). We emphasize also that our conclusion, and that

of the district court, is based only on the evidence presented in this case. Given the

current state of scientific knowledge regarding the causes of autism spectrum

disorders (as it has been presented to us by the parties), we are unable to say that

the district court abused its discretion in excluding this expert testimony. Because


       15
               We can reject summarily Hendrix’s argument that the testimony of Evenflo’s
experts constituted reliable evidence of such general causation.

                                              41
without this testimony there is no genuine dispute of material fact regarding

causation of G.P.’s ASD, the district court’s grant of summary judgment on

Hendrix’s sole remaining claim was appropriate.

      Accordingly, the district court’s exclusion of expert testimony and grant of

summary judgment are

      AFFIRMED.




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