Bentley v. Highlands Hospital Corporation et al
MEMORANDUM OPINION & ORDER: (1) PBH, Dr. Styer, and Whitaker's motion to join in Highlands's Daubert challenge to Dr. Pardo's causation opinion, R. 478 , is GRANTED. (2) PBH, Dr. Styer, and Whitaker's motion to exclude Dr. Pardo's causation opinion, R. 444 , is DENIED. (3) PBH's motion to exclude Dr. DeLorenzo's causation opinion, R. 443 , is DENIED. (4) PBH's motion to exclude Dr. DeLorenzo and Dr. Betz's capacity opinions, R. 441 , is GRANTED IN PART and DENIED IN PART. The doctors may testify regarding the side effects of the three prescriptions medications as a general matter, but they may not testify that Bentley's medication regimen actually rendered her unfit to sign the release in February 2014. Signed by Judge Amul R. Thapar on 12/27/2016. (TDA) cc: COR
UNITED STATES DISTRICT COURT
EASTERN DISTRICT OF KENTUCKY
HIGHLANDS HOSPITAL CORP., et al.,
Civil No. 15-97-ART
*** *** *** ***
Science, like life, knows few certainties. So doctors who wish to offer expert testimony
at trial “need not be purveyors of ultimate truth in order to be allowed on the stand.” Jahn v.
Equine Servs., PSC, 233 F.3d 382, 393 (6th Cir. 2000). But before they may share their
opinions with a jury, the Court must be convinced that the doctors’ qualifications are in order
and that their testimony is relevant and reliable. Fed. R. Evid. 702. In aid of her medicalmalpractice suit, Robyn Bentley offers the testimony of several expert witnesses; among them,
Drs. Carlos Pardo-Villamizar, Robert DeLorenzo, and Christopher Betz. The defendants,
though, insist these three doctors cannot reliably opine about how a certain treatment or
particular medications might have affected Bentley. So the Court must now determine for
itself whether their testimony has a reliable foundation, reliably applied to the facts at hand.
In the early morning hours of July 29, 2013, Robyn Bentley checked into the emergency
room at Paul B. Hall Regional Medical Center (“PBH”). Bentley was nauseated, suffering
from back pain, and having difficulty urinating. Pain and a tingling sensation, too, radiated
throughout her legs, which felt sapped of their usual strength. Concerned that Bentley’s spinal
column might have been compromised, emergency physician Dr. Thomas Styer sent her for a
CT scan. But that scan showed no problems. So Dr. Styer diagnosed Bentley with acute back
pain, prescribed pain medication, and discharged her around 5:00 a.m. with instructions to
follow up with her family doctor. See R. 110 at 6–8; R. 356-2 at 7–8, 11–15.
Sadly, Bentley’s condition deteriorated rather quickly after that. By 9:30 a.m., she had
lost control of her left foot and her reflexes were severely diminished, so her family physician,
Dr. Burchett, sent her for an MRI at Highlands Regional Medical Center (“Highlands”). When
Highlands performed the scan early that afternoon, its radiologist reported no signs of trouble.
Unfortunately, there was a shadow in the images of Bentley’s spinal cord—the radiologist just
missed it. Meanwhile, Bentley’s symptoms continued unabated, the loss of motor control and
sensation ascending into to her abdomen. Troubled by Bentley’s worsening symptoms, Dr.
Burchett decided to send her to Central Baptist Hospital, a couple hours away in Lexington,
Kentucky. See R. 110 at 8–9; R. 356-2 at 15–21; R. 352-3 at 13–14; R. 356-3 at 2–6.
By the time she arrived at Central Baptist, Bentley had lost motor control in both legs.
She now felt, too, that her symptoms were moving into her diaphragm, making it harder for
her to breathe. Doctors at Central Baptist decided to run another MRI. This time, they spotted
inflammation in Bentley’s spinal cord, surmised it might be Devic’s disease,1 and started her
on intravenous steroids. By morning, Bentley’s symptoms had stopped progressing, her ease
Devic’s disease, or neuromyelitis optica, is an autoimmune disorder in which the body’s immune system attacks the
optic nerves and/or spinal cord.
See Devic’s Disease (Neuromyelitis), Cleveland Clinic,
http://my.clevelandclinic.org/health/articles/devics-disease (last visited Dec. 20, 2016).
of breath had returned, and her pain had abated. But sadly, neither steroids, plasmapheresis,
immuno-suppressants, nor months of therapy ever returned the motor control that Bentley had
already lost by the time she reached Central Baptist. She remains paralyzed from the chest
down. See R. 110 at 9; R. 356-3 at 7–12; R. 356-6 at 2–3; R. 356-7.
A little over two years later, Bentley filed suit against PBH, Dr. Styer, and Whitaker
National Corporation, the company that hired Dr. Styer out to the hospital. R. 1-2.2 Bentley
alleges that PBH and Dr. Styer negligently failed to diagnose and treat her emerging
neurological condition. According to Bentley, her range of symptoms suggested that the
culprit was not her spinal column, but her spinal cord. If Dr. Styer had recognized as much,
she says he would have ordered an MRI instead of a CT scan. And that MRI, read properly,
would have revealed her spinal cord inflammation and prompted Dr. Styer to initiate steroids
at a time when the treatment could have halted her paralysis in its tracks. See R. 110 at 6–11.
The defendants have offered several defenses to Bentley’s claims. For one, they argue
that there is no evidence that steroids are effective in combatting the type of spinal cord
inflammation from which Bentley was suffering.3 So, the defendants say, Bentley cannot
prove that PBH could have stopped the progression of her paralysis. See, e.g., R. 259 at 2.
Bentley also sued Highlands and its radiologist, Dr. Terry Hall, but both recently settled. See R. 477; R. 484.
Described most generally, Bentley’s suffered from a bout of “transverse myelitis,” a condition involving
inflammation of the spinal cord that is “characterized by symptoms and signs of neurologic dysfunction in motor and
sensory tracts on both sides of the spinal cord.” See What is Transverse Myelitis?, Johns Hopkins Medicine,
http://www.hopkinsmedicine.org/neurology_neurosurgery/centers_clinics/transverse_myelitis/about-tm/what-istransverse-myelitis.html (last visited Dec. 20, 2016). Transverse myelitis has many possible causes, and in Bentley’s
case, doctors initially attributed the inflammation to Devic’s disease, an autoimmune disorder. Now, though, the
parties seem to agree that Bentley’s condition was instead caused by a bout of strep throat a week earlier. As a result,
Bentley’s condition might be more precisely labeled “acute, post-infectious inflammatory myelopathy”—meaning a
form of transverse myelitis involving short-term inflammation of the spinal cord brought on by a prior infection.
Second, PBH says that Bentley previously signed a release waiving her claims against the
hospital in exchange for PBH canceling her medical bill. See, e.g., R. 257 at 1–2; R. 266 at 2.
Anticipating these defenses, Bentley has retained the services of three experts. Dr.
Carlos Pardo-Villamizar and Dr. Robert DeLorenzo, both neurologists, are prepared to testify
that PBH could have stopped (or even reversed) the progression of Bentley’s paralysis if it had
administered steroids when she still had motor control and sensation in her legs. See R. 389;
R. 238-1. Dr. DeLorenzo and Dr. Christopher Betz, meanwhile, have each opined that Bentley
was cognitively impaired when she signed PBH’s release because she was on central nervous
system (“CNS”) depressants and an opioid painkiller at the time. See R. 442-3; R. 442-2.
PBH has now moved to exclude each of these opinions pursuant to Federal Rule of
Evidence 702 and Daubert v. Merrell Dow Pharmaceuticals, Inc., 509 U.S. 579 (1993). See
R. 441; R. 443; R. 444. PBH argues that the doctors’ opinions are unreliable because there is
insufficient proof that either the steroids or Bentley’s prescription medications would have had
the effects the doctors now claim. As the party seeking to admit the doctors’ opinions at trial,
Bentley bears the burden of proving, by a preponderance of the evidence, that their testimony
is admissible. See Nelson v. Tenn. Gas Pipeline Co., 243 F.3d 244, 251 (6th Cir. 2001).
First, a housekeeping matter. Technically, no defendant remaining in this case has yet
moved to exclude Dr. Pardo’s steroid/causation testimony. Only Highlands challenged its
admissibility initially. See R. 377. But Highlands recently reached a settlement with Bentley
and notified the Court that it wished to withdraw its summary judgment and Daubert motions.
See R. 477. Upon learning of this settlement, PBH, Dr. Styer, and Whitaker moved to join in
Highlands’s Daubert challenge to Dr. Pardo. R. 478. Bentley swiftly objected. R. 481.
Bentley is correct that the defendants’ request comes rather late. The scheduling order
in this case instructed the parties to notify the Court in advance of the Pre-Motion PostDiscovery Conference of any anticipated Daubert challenges. R. 107 at 4–5. And as Bentley
notes, Highlands filed notice of its intent to challenge the causation testimony of both Dr.
Pardo and Dr. DeLorenzo, see R. 275; R. 276, but PBH mentioned only the latter, see R. 259.
Nevertheless, the defendants may join in Highlands’s motion. Dr. Pardo and Dr.
DeLorenzo’s causation opinions, and the grounds for excluding them, overlap each other. See
R. 438 at 4–5. Bentley has had a full opportunity to brief the admissibility of both. See R. 447.
And for its part, PBH has actively participated in the briefing and hearings concerning the
doctors’ shared theory that earlier steroid intervention would have minimized Bentley’s
paralysis. See, e.g., R. 374; R. 404; R. 422; R. 438; R. 443; R. 450. So Bentley has been on
notice that the defendants (including PBH) were challenging the reliability of her experts’
opinions. And with no risk of unfair surprise, economy and consistency suggest the better
course is to address the admissibility both opinions now, rather than wait until trial for the
defendants to object anew on Rule 702/Daubert grounds.
The Federal Rules of Evidence take a liberal approach toward the admissibility of
opinion testimony—including from expert witnesses. Glaser v. Thompson Med. Co., 32 F.3d
969, 971–72 (6th Cir. 1994). But that does not relieve the Court of the difficult task of drawing
“the often-elusive line between admissible opinion and inadmissible speculation.” Tamraz v.
Lincoln Elec. Co., 620 F.3d 665, 667 (6th Cir. 2010). Not all “experts” are truly expert, and
not all “expert opinions” are really worth the label. So when a party challenges another’s
expert witness, the Court assumes a gatekeeping role to ensure that the jury is not exposed to
“junk science” masquerading as expert testimony. See Daubert, 509 U.S. at 597; Best v.
Lowe’s Home Ctrs., Inc., 563 F.3d 171, 176–77 (6th Cir. 2009). Only if an expert opinion is
relevant, reliable, and rendered by a genuine expert will it be admissible at trial. See Fed. R.
Evid. 702; In re Scrap Metal Antitrust Litig., 527 F.3d 517, 529 (6th Cir. 2008).
In this case, expertise is hardly an issue. In fact, the defendants concede that Drs. Pardo,
DeLorenzo, and Betz are qualified to offer their respective opinions. See R. 377 at 8; 374 at
7. And it is easy to see why. If anyone is in a position to discuss the cause and treatment of
Bentley’s condition, it is Dr. Pardo, a renowned neurologist and the head of Johns Hopkins’s
Transverse Myelitis Center. See R. 388-3. Dr. Betz is a registered pharmacist and a doctor
and professor of pharmacology. See R. 392-1. And remarkably, Dr. DeLorenzo has expertise
spanning both fields: he has a medical degree as well as a neuropharmacology Ph.D., and he
is a tenured professor of both neurology and pharmacology at Virginia Commonwealth
University. See R. 383-1; R. 438 at 2. All three doctors, meanwhile, have extensive clinical
experience treating spinal cord disorders (in the case of Drs. Pardo and DeLorenzo) and
monitoring prescription drug interactions (in the case of Drs. DeLorenzo and Betz).
The doctors’ opinions will also help the jury “understand the evidence or determine a
fact in issue.” Fed. R. Evid. 702(a). Dr. Pardo and Dr. DeLorenzo’s testimony regarding the
palliative effects of steroids on spinal cord inflammation is a key link in Bentley’s claim that
the defendants contributed to her paralysis. And Bentley will rely heavily on Dr. DeLorenzo
and Dr. Betz when she argues that her medication significantly impaired her cognitive function
at the time she signed PBH’s release in February 2014. If true, the release likely has no legal
effect and thus cannot bar Bentley’s suit. The doctors’ opinions are thus central to Bentley’s
affirmative and rebuttal cases. Not only that, but how these medications interact with the body
and combat or cause certain symptoms is a technical subject outside the ordinary understanding
of a lay juror. So, a bit of expert testimony on the subject will do the jury some good.
That leaves reliability. To be reliable within the meaning of Rule 702, expert testimony
must be grounded in “scientific knowledge.” Daubert, 509 U.S. at 589–90. In other words, a
witness may testify in the form of an expert opinion only if his testimony is “ground[ed] in the
methods and procedures of science,” and more than just “subjective belief or unsupported
speculation.” Id. at 590. But the subject of an expert’s testimony does not have to be “‘known’
to a certainty”—“arguably, there are no certainties in science.” Id. Instead, an expert may
testify as to an “inference” he has drawn provided it is “derived by the scientific method”—
i.e. “supported by appropriate validation” or “‘good grounds,’ based on what is known.” Id.
The reliability inquiry is flexible one. See id. at 594–95. The Supreme Court has
provided a list of questions to aid district courts when assessing the reliability of expert
testimony under Rule 702, including whether the expert’s theory has been tested, peerreviewed, or generally accepted. See id. at 591–95; Glaser, 32 F.3d at 972. But that list is not
exhaustive, nor any one factor dispositive. In re Scrap Metal, 527 F.3d at 528–29. District
courts are permitted “considerable leeway in deciding in a particular case how to go about
determining whether particular expert testimony is reliable.” Kumho Tire Co. v. Carmichael,
526 U.S. 137, 152 (1999). The goal is simply to ensure that a witness’s expert testimony has
a “reliable basis in the knowledge and experience of [his] discipline.” Jahn, 233 F.3d at 388;
see also Rosen v. Ciba-Geigy Corp., 78 F.3d 316, 318 (7th Cir. 1996) (“[A] district judge asked
to admit scientific evidence must determine whether the evidence is genuinely scientific, as
distinct from being unscientific speculation offered by a genuine scientist.”).
Whether Drs. Pardo and DeLorenzo can reliably opine that steroids improve outcomes
for patients like Bentley is a point of contention. Both sides (and their experts) agree that
Bentley’s inflammation came with a recommended treatment: the high-dose intravenous
corticosteroids administered by Central Baptist. See R. 450 at 2; R. 404 at 3 (explaining that
PBH does not dispute that “the administration of steroids [is] the standard of care for transverse
myelitis patients”). But, PBH says, doctors administer steroids to transverse myelitis patients
not in the knowledge that they will work, but in the hope that they might. R. 450 at 2; R. 451
at 2. According to PBH, steroids are, for lack of a better option, the “first treatment offered to
hasten recovery, reduce disease activity, and restore neurological function.” R. 450-3 at 4–5.
But there is an “absence of evidence” that they actually work. Id. As a result, PBH says, Drs.
Pardo and DeLorenzo can only offer the type of “useful but untested hypothesis” that the law
“generally treat[s] as inadmissible speculation.” Tamraz, 620 F.3d at 677.
Despite PBH’s protests, Dr. Pardo and Dr. DeLorenzo’s steroid opinions are not mere
conjecture. Rather, both doctors’ testimony represents an informed inference that each has
drawn by applying three types of knowledge to Bentley’s case. Consider each in turn.
First, the doctors begin with several general (and generally accepted) propositions.
Inflammation is a byproduct of the immune system’s attempt to combat harmful stimuli.4 It is
a sign, in other words, of the body’s attempt to defend itself. Sometimes, though, the immune
system takes aim at the wrong target, mistaking the body’s own cells for foreign dangers and
See generally What is Inflammation?, U.S. Nat’l Library of Medicine:
https://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0072482/ (last visited Dec. 20, 2016).
attacking healthy body tissue as a result. That is what happened in Bentley’s case. The parties
agree that Bentley was suffering from post-infectious inflammatory myelopathy. See R. 3514 at 2; R. 447 at 5. A recent bout of strep throat had tricked Bentley’s immune system into
attacking nerve cells in her spinal cord. The resulting inflammation climbed up both sides of
her lower spinal cord, destroying the myelin sheathing on her nerve cell fibers, and disrupting
communication between her spinal cord and the remainder of her central nervous system.5
Doctors, meanwhile, have long turned to corticosteroids to treat a host of inflammatory
conditions. Corticosteroids like methylprednisolone—which Central Baptist used to treat
Bentley—mimic the effects of cortisol, a natural anti-inflammatory hormone produced by the
adrenal glands.6 These cortisol-like chemicals suppress the body’s immune response on
multiple fronts, inhibiting the production of pro-inflammatory chemicals and disrupting the
operation of the body’s white blood cells.7 And it is these same properties that have led doctors
to use corticosteroids to treat spinal cord inflammation in transverse myelitis patients.8
See generally Transverse Myelitis Fact Sheet, Nat’l Institute of Neurological Disorders and Stroke,
visited Dec. 20, 2016) (explaining that, in transverse myelitis patients, “[a]ttacks of inflammation can damage or
destroy myelin, the fatty insulating substance that covers nerve cell fibers” resulting in “nervous system scars that
interrupt communications between the nerves in the spinal cord and the rest of the body”).
See, e.g., Steroids, The Johns Hopkins Lupus Center, https://www.hopkinslupus.org/lupus-treatment/lupusmedications/steroids/ (last visited Dec. 20, 2016).
See, e.g., Peter J. Barnes, How Corticosteroids Control Inflammation: Quintiles Prize Lectures 2005, British J.
Pharmacol., 148(3), 245-254 (June 2006); Livertox: Corticosteroids, U.S. Nat’l Library of Medicine,
https://livertox.nih.gov/Corticosteroids (last visited Dec. 20, 2016); Corticosteroids, Cleveland Clinic,
http://myclevelandclinic.org/health/articles/corticosteroids (last visited Dec. 20, 2016).
See, e.g., Amer Awad & Olaf Stüve, Idiopathic Transverse Myelitis and Neuromyelitis Optica: Clinical Profiles,
Pathophysiology and Therapeutic Choices, Current Neuropharmacology, 9(3), at 419 (Sept. 2011) (“The rationale of
using steroids in [transverse myelitis] is based on its numerous effects on the immune system leading to a global
immunosuppression. Some of these effects include but not limited to: inhibition of lymphocyte proliferation and
differentiation, redistribution of lymphocytes, alteration of lymphokine function of especially tumor necrosis factor
(TNF), IL-1 and IL-2, and inhibition of macrophage function, in particular antigen presentation and processing.”);
Transverse Myelitis Fact Sheet, supra (“Physicians often prescribe anti-inflammatory corticosteroid therapy soon after
the diagnosis is made in order to decrease inflammation and hopefully improve the chances and speed of neurological
According to Dr. Pardo and Dr. DeLorenzo, the idea that steroids would benefit patients
like Bentley is thus simply an application of a generally accepted treatment to a particular
manifestation of the condition it treats. Steroids combat inflammation by suppressing the
body’s immune response. Inflammation is responsible for the loss of neurological function in
patients with inflammatory myelopathies. Ergo, steroids are capable of counteracting the
neurological decline in transverse myelitis patients. If administered, too, before the immune
system has pushed nerve fibers beyond the point of no return, steroids can preserve what
function remains and provide cover for the body to rebuild the damaged myelin.9 See generally
R. 434 at 7–10 (Dr. DeLorenzo); R. 440 at 16–19 (Dr. Pardo). A “causal chain” that the
defendants even concede is plausible—and perhaps even right. R. 451 at 2.
Dr. Pardo and Dr. DeLorenzo find further support for this syllogism in a second source
of knowledge: the evolving literature on inflammatory conditions of the central nervous
system. That literature is far more supportive of Dr. Pardo and Dr. DeLorenzo’s opinions than
the defendants let on. See R. 447 at 11–14, 25–26. For instance, studies published in 2004
and 2006 suggested that “high-dose steroids improved time to ambulation and ultimate motor
recovery” in transverse myelitis patients,10 and that steroids can be “somewhat effective if
recovery. Although no clinical trials have investigated whether corticosteroids alter the course of transverse myelitis,
these drugs often are prescribed to reduce immune system activity because of the suspected autoimmune mechanisms
involved in the disorder.”).
See generally Monika Bradl & Hans Lassman, Oligodendrocytes: Biology and Pathology, Acta Neuropathol, vol.
119, at 46–47 (2010), https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2799635/pdf/401_2009_Article_601.pdf
(discussing remyelination or “the restoration of new myelin sheaths to demyelinated axons”).
Chitra Krishnan et al., Demyelinating Disorders: Update on Transverse Myelitis, 6 Current Neurology and
Neuroscience Reports, no. 3, 236, 238 (2006).
given in the acute phase.”11 A recent peer-reviewed article concluded with a high degree of
statistical confidence that earlier onboarding of steroids correlated with improved neurological
outcomes among juvenile transverse myelitis patients in an Indian hospital.12 And finally,
several other studies have shown that the palliative effects of corticosteroids extend to other
demyelinating conditions of the central nervous system: reducing inflammatory lesions in
patients suffering from multiple sclerosis13 and fighting exacerbations of neuromyelitis
optica.14 At the end of the day, then, several observational studies—of patients with transverse
myelitis or other inflammatory disorders of the spinal cord—suggest that earlier steroid
intervention does in fact improve neurological outcomes in patients with inflammatory
conditions of the spinal cord.
Importantly, this pattern has also borne out in the doctors’ practices. This brings us to
the third pillar on which the doctors rest their opinions: clinical experience. See Messick v.
Novartis Pharm. Corp., 747 F.3d 1193, 1198 (9th Cir. 2014) (“Medicine partakes of art as well
as science, and there is nothing wrong with a doctor relying on extensive clinical
Between them, Drs. Pardo and DeLorenzo have treated, reviewed, or
consulted on hundreds of cases of transverse myelitis, generally, and inflammatory
See R. 440 at 14–15; R. 434 at 18.
They report that those
Chitra Krishnan et al., Transverse Myelitis: Pathogenesis, Diagnosis, and Treatment, 9 Frontiers in Bioscience,
1483, 1492 (2004).
See Renu Suthar et al., Acute Transverse Myelitis in Childhood: A Single Centre Experience from North India, 20
J. European Pediatric Neurology Soc’y, no. 3, 352 (May 2016).
See, e.g., Florian Then Bergh et al., Monthly Intravenous Methylprednisolone in Relapsing-Remitting Multiple
Sclerosis—Reduction of Enhancing Lesions, T2 Lesion Volume and Plasma Prolactin Concentrations, BMC
Neurology, 6:19 at 6 (May 2016).
See, e.g., Kleiter, I. et al., Neuromyelitis Optica: Evaluation of 871 Attacks and 1,153 Treatment Courses, Annals
of Neurology, 79:2, 206–17, at 207 (2016).
experiences have shown the power of steroids to combat neurological decline in patients
suffering from acute inflammatory myelopathies. Specifically, they have discovered that
patients treated with IV corticosteroids while they still have motor control and/or sensation
overwhelmingly have fair or good outcomes. At the least, the steroids halt the loss of
neurological function, and in many cases they reverse the deficits all together. And the faster
the patient is treated the more function left to preserve. Because if a patient still has motor
control or sensory function when doctors administer steroids, then the corresponding nerves
have not yet been fully destroyed. See R. 434 at 10, 17, 26; R. 440 at 17–18, 33–38.15
With that knowledge in hand, Drs. Pardo and DeLorenzo examined Bentley and
reviewed both her medical records and her deposition testimony. See R. 389 at 1; R. 238-1 at
1. They noted that Bentley was still able to walk with assistance when she left PBH on the
morning of July 29. See R. 440 at 36; R. 356-2 at 15. In fact, it was not until Bentley visited
her family doctor four hours later that she first lost control of an appendage (her left foot). See
R. 440 at 49; R. 356-2 at 15–16. So Drs. Pardo and DeLorenzo surmised that Bentley still had
substantial neurological function in her lower extremities when she left PBH—meaning
steroids might have done her some good. Crucially, too, once Central Baptist administered
steroids, the upward progression of Bentley’s paralysis apparently stopped and her shortness
of breath ceased.16 See R. 440 at 94; R. 434 at 26–27; R. 356-3 at 11. So the doctors found
The defendants make much of the idea that neither doctor can reliably determine when Bentley’s inflammation has
resulted in permanent cell death, which the defendants suggest marks the moment of no return for neurological
function. See, e.g., R. 443 at 8–9. However, this criticism does not appear to undermine the reliability of the doctors’
opinions. After all, the doctors’ testimony appears to define the “therapeutic window” not based on cell death
(something they cannot reliably determine) but based on outward signals of motor control and sensory perception.
And either way, because Bentley still had both when she left PBH, presumably her nerve cells were still hanging on.
The defendants argue that the doctors have misread Bentley’s medical records, see, e.g., R. 443 at 7–8, but this type
of factual dispute is best left for the jury. See, e.g., In re Scrap Metal, 527 F.3d at 530.
indications in the record that steroids actually did help Bentley—even if they came too late to
save much of her neurological function. Finally, there was an explanation for this success in
Bentley’s lab work from July 30, 2013: her spinal fluid held a high concentration of
lymphocytes, white blood cells particularly susceptible to steroid therapy. See R. 447 at 14.
Drs. Pardo and DeLorenzo have thus laid a foundation for each step they have taken
from the general proposition with which they began (steroids combat inflammation) to the
specific inference with which they end (steroids would have helped Bentley if given earlier).
True, that steroids have anti-inflammatory properties is not, standing alone, enough to justify
the doctors in concluding that steroids would have helped Bentley in this case. But Drs. Pardo
and DeLorenzo offer more than that. They have explained both the physiological process by
which steroids combat inflammation, and why patients who have sensation or motor control
when steroids are administered are likely to at least retain that function. They have pointed to
scientific literature that, though not definitive, supports the general principle that steroids
improve neurological outcomes for inflammatory myelopathy patients. They thoroughly
reviewed Bentley’s medical records, assessing her symptomology to determine that she still
had significant function in all extremities when she left PBH. And perhaps most importantly,
they have found support that steroids actually worked in this case.
Rule 702 permits experts to draw conclusions “from a set of observations based on
extensive and specialized experience.” Kumho Tire, 526 U.S. at 156. The experts need only
explain how they have reliably applied their experience to the facts at hand. See Thomas v.
City of Chattanooga, 398 F.3d 426, 432 (6th Cir. 2005). Under the circumstances, Drs. Pardo
and DeLorenzo have done at least that much, so their steroid opinions are sufficiently reliable
to be admitted at trial. See, e.g., Jahn, 233 F.3d at 391 (holding doctors’ methodology was
reliable where they drew conclusions based on clinical indicia in the patient’s incomplete
medical records); Heller v. Shaw Indus., Inc., 167 F.3d 146, 155 (3d Cir. 1999) (“[E]xperience
with hundreds of patients, discussions with peers, attendance at conferences and seminars . . .
are tools of the trade, and should suffice for the making of a differential diagnosis even in those
cases in which peer-reviewed studies do not exist to confirm the diagnosis[.]”).
The defendants base much of their opposition to Dr. Pardo and Dr. Lorenzo on the
argument that their steroid-intervention testimony is not supported by sufficient scientific
literature. The American Academy of Neurology (“AAN”), PBH notes, concluded in 2011
that there “is insufficient evidence to determine the utility of corticosteroids in alleviating
[transverse myelitis] attacks.” R. 450-3 at 4. Indeed, the defendants point out, no study has
conclusively established that early steroid treatments reduce neurological deficits in cases like
Bentley’s. See R. 443 at 5–7; R. 444 at 5–9. On this much, the defendants are right. No
double-blind or epidemiological study has firmly proven that steroids are effective in treating
acute inflammatory myelopathy. And the type of retrospective studies that might fill the gap
are only now underway—including some under Dr. Pardo’s supervision. See R. 440 at 88.
Nevertheless, the defendants’ protests are overblown. For starters, a medical expert
does not need to cite published studies for his opinion to be reliable within the meaning of
Rule 702. See, e.g., Dickerson v. Cardiac & Thoracic Surgery of E. Tenn., P.C., 388 F.3d 976,
980 (6th Cir. 2004). Submission of a medical theory “to the scrutiny of the scientific
community” is no doubt “a component of ‘good science.’” Daubert, 509 U.S. at 593. But
some propositions are simply “too particular, too new, or of too limited interest to be
published.” Id. So experts may sometimes testify that some act caused a patient’s medical
harm—even if no published literature has yet reached that same conclusion. See, e.g., Best,
563 F.3d at 180–81. And the same is true when the causation is flipped and an expert wants
to testify that some act might have prevented a patient’s medical harm.
Dr. Pardo and Dr. DeLorenzo, of course, have cited literature that supports their
testimony. As discussed, there have been an array of small (and peer-reviewed) studies that
suggest both that steroids improve neurological outcomes in patients with spinal cord
inflammation and that faster treatment is correlated with better medical outcomes. Even the
AAN acknowledges as much—referring to this simply as “Class IV” evidence, i.e. evidence
other than from controlled trials, including “consensus or expert opinion.” See R. 443-2 at 4
(“Only Class IV evidence exists concerning the utility of steroids.”).17 What’s more, Drs.
Pardo and DeLorenzo have explained why those early studies were so tentative in their
conclusions: Until recently, researchers failed to differentiate between various forms of
transverse myelitis, only some of which involve inflammation and so are treatable by steroids.
See, e.g., R. 440 at 13; R. 434 at 6. Sure, at the end of the day none of these studies definitively
answer the steroid-intervention question on which the two doctors will opine. But Rule 702
“does not require anything approaching absolute certainty” in an expert’s opinion. Tamraz,
620 F.3d at 671. And given that the doctors were neither required to cite studies nor reach
their conclusions with absolute certainty, it would seem more than a bit incongruous to fault
them for drawing support from studies that “suggest” their clinical observations are correct.
The defendants also argue that Dr. Pardo and Dr. DeLorenzo cannot extrapolate from
these various studies. For example, because they involved different neurological disorders (for
The AAN defines “Class IV” evidence in an appendix to its evidence based guidelines, which is available at
example, multiple sclerosis or neuromyelitis optica) or a different class of patients (children).
See R. 443 at 5–6; R. 444 at 6–8. But Drs. Pardo and DeLorenzo have explained that the
inflammatory process is the same across these cases: The disorder provokes the immune
system into attacking nerve cells throughout the spinal cord, causing inflammation that
damages nerve tissue and short circuits neural signals. Steroids counteract that inflammatory
process in several ways, including by inhibiting the production and operation of certain white
See R. 434 at 6–9, 13–14; R. 440 at 17–18. And introduced early enough,
steroids can accomplish that task before the immune system pushes those nerve cells beyond
the point of repair. Under the circumstances, Dr. Pardo and Dr. DeLorenzo may reliably
extrapolate from these studies to Bentley’s analogous condition, especially when the studies
merely confirm what their clinical practice has already borne out. See, e.g., Kennedy v.
Collagen Corp., 161 F.3d 1226, 1230 (9th Cir. 1998); R. 409-3 at 7 (“UpToDate Article”)
(“Even without placebo-controlled trials evaluating glucocorticoids specifically in TM, there
is good evidence that intravenous glucocorticoids are effective in acute inflammatory central
nervous system diseases like TM, such as multiple sclerosis.”).
Nor do the defendants’ remaining arguments undermine the reliability of the doctors’
opinions. Dr. DeLorenzo did not, as PBH off-handedly suggests, form his opinion solely for
purposes of this case, see R. 443 at 10—he has been treating transverse myelitis patients for
years. Nor is this a case where the extant scientific literature contradicts the experts’ testimony.
Contra Tamraz, 620 F.3d at 670–71; Conde v. Velsicol Chem. Corp., 24 F.3d 809, 813–14 (6th
See Awad & Stüve, supra, at 419 (“The rationale of using steroids in TM is based on its numerous effects on the
immune system leading to a global immunosuppression. Some of these effects include but are not limited to:
inhibition of lymphocyte proliferation and differentiation, redistribution, of lymphocytes, alteration of lymphokine
function of especially tumor necrosis factor (TNF), IL-1 and IL-2, and inhibition of macrophage function, in particular
antigen presentation and processing.”).
Cir. 1994). More importantly, though, while other courts have occasionally rejected generic
medical testimony that “earlier treatment is better,” those cases share flaws not present in this
one: Drs. Pardo and DeLorenzo have reliably explained the mechanism by which steroids
work, why earlier intervention is crucial in inflammatory myelopathies, and why they believe
Bentley could have benefitted from it. Contra McDowell v. Brown, 392 F.3d 1283, 1299–
1301 (11th Cir. 2004); Jones v. Pramstaller, 874 F. Supp. 2d 713, 724–25 (W.D. Mich. 2012);
Tomlinson v. Collins, No. 2:09-cv-0125, 2010 WL 4317030 (S.D. Ohio Oct. 25, 2010).
None of this is to say that Dr. Pardo and Dr. DeLorenzo are correct. Perhaps the jury
will view their opinions skeptically. But whether their conclusions are accurate is not for the
Court to decide. See Daubert, 509 U.S. at 594–95. At this stage, the question is simply
whether their testimony is “the product of reliable principles and methods” applied reliably to
the facts of this case. Fed. R. Evid. 702(c)-(d). In other words, do the doctors have “good
grounds” for concluding that it was more likely than not that PBH could have minimized
Bentley’s paralysis by starting her on IV corticosteroids earlier on July 29? See Pride v. BIC
Corp., 218 F.3d 566, 577 (6th Cir. 2000) (quoting Daubert, 509 U.S. at 590).
The answer to those questions is yes. The doctors began with a generally accepted
principle: Steroids combat inflammation and reduce tissue damage by suppressing the body’s
immune response. From there they journey to a specific conclusion:
Steroids could have
minimized the inflammatory damage to Bentley’s spinal cord. But the doctors do not simply
leap from A to Z. They connect their specific inference to the general premise through their
clinical experience, their knowledge of the physiological processes of inflammation, and
analogies to related disorders (and the studies about them). And perhaps most important of
all, the doctors point out that their theory finds support in the facts of this very case: Bentley’s
symptoms stopped progressing after Central Baptist administered IV steroids. Under the
circumstances, Drs. Pardo and DeLorenzo have exhibited the degree of intellectual rigor
expected of someone in their field. See, e.g., Kennedy, 161 F.3d at 1229–30. And any
remaining concerns regarding their methodology or conclusions can be handled through
vigorous cross examination. See Daubert, 509 U.S. at 596; Best, 563 F.3d at 180.
Along with pharmacologist Dr. Christopher Betz, Dr. DeLorenzo has also opined that
Bentley lacked the mental capacity necessary to make independent business or legal decisions
when she signed PBH’s liability release in February 2014. See R. 442-2; 442-3. Drs. Betz and
DeLorenzo attribute Bentley’s impaired state to the “synergistic effects” of three medications
that she began taking after a February 11 surgery. R. 442 at 9 (discussing the doctors’ reports).
According to the doctors, two of those medications were CNS depressants (gabapentin and
lamotrigine), which inhibit the transmission of neural signals and have sedative effects. See
id. at 9–11. A third (hydrocodone) was an opioid that blocks pain receptors in the brain and
can cause “clouding of consciousness, drowsiness, mental deficiency, sedation, and stupor.”
See id. at 11. Drs. Betz and DeLorenzo have testified that, in their clinical experience, these
medications can cause “mental fogginess and fatigue” when used in combination. See id. at
12 (citing R. 432 at 19–20); see also R. 434 at 111–12. And between Bentley’s dosage and
her testimony that her memory of this period is significantly impaired, the doctors conclude
that Bentley’s three-drug regimen must in fact have impaired her cognitive function.
As support, Drs. Betz and DeLorenzo cite entries in two databases used by pharmacists.
The Lexi-Drugs database entries for gabapentin and lamotrigine, they note, both warn that
these drugs may enhance the CNS-depressant effect of hydrocodone. See R. 442-6 at 9;
R. 442-8 at 13. And a Lexicomp Interaction Analysis for hydrocodone and CNS depressants
recommends that doctors start patients “with a 20% to 30% lower hydrocodone dose when
using [it] with any other depressant.” R. 442-11 at 2. The reason? “This warning is due to
the potential for additive or synergistic CNS depression, leading to an increased risk of adverse
effects such as respiratory depression, hypotension, excessive sedation, and coma.” Id.
Surveying the whole, half of the doctors’ testimony appears admissible: Dr. Betz and
Dr. DeLorenzo can reliably testify regarding the possible side effects of these medications.
Both have extensive experience in pharmacology—Dr. DeLorenzo has forty-one years as a
neuropharmacologist under his belt, see R. 442-3 at 1, and Dr. Betz has spent years managing
and monitoring medication regimens in a clinical setting, see R. 432 at 4–5. Both doctors have
also grounded their account of the side effects in their experience, in an assessment of
Bentley’s medical records, and in industry warnings regarding these medications. See R. 4422; R. 442-3. From this foundation, the doctors can reliably say that these medications,
individually or in tandem, can sometimes impair cognitive function. See, e.g., Best, 563 F.3d
at 180–81; Jahn, 233 F.3d at 391–92; Dickerson, 388 F.3d at 980–81.
Go beyond this opinion, though, and the ice grows too thin to support the doctors’
testimony. Dr. Betz and Dr. DeLorenzo also want to testify that the medications had such an
effect on Bentley. The doctors’ journey to this conclusion takes them down the following path:
(1) In their experience, and according to warnings accompanying these medications, these
drugs can impair cognitive function. (2) Bentley reports impaired memory of the period when
she was taking them. (3) Therefore the drugs must have impaired her cognitive function.
Standing alone, though, this reasoning is more logical fallacy than scientific knowledge.
Simply put, Drs. Betz and DeLorenzo have not reliably connected the various links in
their chain of inferences. The doctors admit that not all patients experience the side effects
they describe—indeed, only a minority appear to. See, e.g., R. 432 at 42; see also R. 442-6 at
7 (indicating that immediate release formulations of gabapentin may cause dizziness in 1728% of patients and drowsiness in 19-21% of patients); R. 442-8 at 11 (reporting that fewer
than 10% of lamotrigine patients experience drowsiness and fatigue). Nor can Dr. Betz or Dr.
DeLorenzo predict reliably which patients will fall in that minority. What’s more, Drs. Betz
and DeLorenzo cannot say when or how often these drugs have synergistic effects. The best
they offer is the Lexicomp notation that these drugs “may” have synergistic effects, see, e.g.,
R. 442-8 at 13, since they are not aware of any study of the drugs’ interaction, see R. 432 at
45; R. 434 at 112–14. But even these warnings, the doctors admit, are just drug companies’
attempts to insulate themselves from liability through disclosures made in an abundance of
caution. See R. 441-1 at 10–11; R. 441-2 at 2; cf. McClain v. Metabolife Int’l, Inc., 401 F.3d
1233, 1248–50 (11th Cir. 2005) (rejecting an expert’s reliance on FDA recommendations
because public health guidelines took a protective “cost-benefit approach” to disclosure that is
less demanding than that required of an expert wishing to testify that a supplement actually
caused medical harm). And finally, even assuming the medications caused Bentley fatigue or
drowsiness, Dr. Betz and Dr. DeLorenzo do not explain how they know that these effects
would have been so severe as to deprive Bentley of the mental capacity necessary to exercise
independent and informed judgment. They just say they must have been. But then again, the
“‘ipse dixit of the expert’ alone is not sufficient” to make his opinion reliable. Tamraz, 620
F.3d at 671 (quoting Gen. Elec. Co. v. Joiner, 522 U.S. 136, 146 (1997)).
In the end, Drs. Betz and DeLorenzo cannot connect their general observation to the
specifics of this case. Instead, they end where they started: with the idea that the Bentley’s
prescription drug regimen must be responsible for the loss of memory she reported in her
deposition. See, e.g., R. 441-1 at 2–3. But this type of post hoc ergo propter hoc reasoning is
insufficient to render the second (case-specific) half of their opinion reliable under Rule 702.
See, e.g., Rolen v. Hansen Beverage Co., 193 F. App’x 468, 473 (6th Cir. 2006). The Court
will therefore grant PBH’s motion insofar as it seeks to exclude this particular component of
Dr. Betz and Dr. DeLorenzo’s pharmacological opinions.
Why the divergent treatment of the two sets of opinions considered today? After all,
neither is the paradigmatic example of reliability, backed by double-blind, peer-reviewed
clinical studies affirming the specific conclusions that the experts now draw. And absent such
lodestars, both are guided largely by the doctors’ clinical experience and “suggestive”
secondary literature. So one might ask whether the Court can reliably draw a line between
the two. The answer, though, is yes, because these similarities are largely superficial.
Dr. Pardo and Dr. DeLorenzo have advanced a model for predicting when patients are
capable of neurological recovery: If a patient still has motor control or sensation, then their
nerve fibers have not yet been irreparably damaged. They have seen this model play out in
clinical practice, and they applied it to the evolution of Bentley’s symptoms, noting that she
did not lose motor control of an appendage until hours after she left PBH. They also explain
the mechanics of it all, drawing on the anti-inflammatory properties of steroids and a range of
studies discussing the effectiveness of steroids in combating both transverse myelitis in
children and a range of other inflammatory neurological conditions. And lastly, the doctors
circle back to the fact that doctors appeared to have documented that steroids actually stopped
the progression of Bentley’s symptoms once they were administered at Central Baptist. Under
the circumstances, Bentley has proven by a preponderance that the doctors’ steroidintervention conclusions are reliably based in the methods and principles of their discipline—
they are not, in other words, pure conjecture or “junk science.” Dickerson, 388 F.3d at 982.
Dr. Betz and Dr. DeLorenzo’s capacity opinions, by contrast, rely not on a drug’s primary
purpose, but its side effects. Side effects only a small minority of patients suffer, and ones no
doctor actually observed in this case. The best these experts can say with confidence is that
Bentley’s medication might cause symptoms such as fatigue and drowsiness. Their clinical
experience and the drug database reports bear that much out, so they can testify reliably to this
point. But Drs. Betz and DeLorenzo cannot say why or when certain patients fall into the
small minority who actually suffer these side effects.
Or when these drugs will have
“synergistic” effects, let alone effects substantial enough to deprive someone of independent
judgment. And most importantly, they cannot reliably count Bentley among the apparent
minority of side-effect sufferers with no clinical indications other than her own self-serving
Dr. Betz and Dr. DeLorenzo therefore cannot reliably opine that Bentley’s
medications actually caused her to lack the mental capacity necessary to sign PBH’s release.
Accordingly, it is ORDERED as follows:
PBH, Dr. Styer, and Whitaker’s motion to join in Highlands’s Daubert
challenge to Dr. Pardo’s causation opinion, R. 478, is GRANTED.
PBH, Dr. Styer, and Whitaker’s motion to exclude Dr. Pardo’s causation
opinion, R. 444, is DENIED.
PBH’s motion to exclude Dr. DeLorenzo’s causation opinion, R. 443, is
PBH’s motion to exclude Dr. DeLorenzo and Dr. Betz’s capacity opinions,
R. 441, is GRANTED IN PART and DENIED IN PART. The doctors may
testify regarding the side effects of the three prescriptions medications as a
general matter, but they may not testify that Bentley’s medication regimen
actually rendered her unfit to sign the release in February 2014.
This the 27th day of December, 2016.
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