-1- 

### STATE OF MICHIGAN

COURT OF APPEALS

ALEXANDER FIGURSKI, minor, by his conservator, HOWARD LINDEN,

Plaintiff-Appellant, UNPUBLISHED March 5, 2015

v No. 318115 Livingston Circuit Court TRINITY HEALTH-MICHIGAN, d/b/a/ SAINT JOSEPH MERCY LIVINGSTON HOSPITAL, WILLIAM BRADFIELD, M.D., and CATHERINE McCAULEY HEALTH SERVICES CORPORATION, a/k/a SAINT JOSEPH MEDICINE FACULTY ASSOCIATES, a/k/a SAINT JOSEPH MERCY PRIMARY CARE, LC No. 11-026466-NH

Defendants-Appellees.

ALEXANDER FIGURSKI, minor, by his conservator, HOWARD LINDEN,

Plaintiff-Appellee,

v No. 319086 Livingston Circuit Court TRINITY HEALTH-MICHIGAN, d/b/a/ SAINT JOSEPH MERCY LIVINGSTON HOSPITAL, WILLIAM BRADFIELD, M.D., and CATHERINE McCAULEY HEALTH SERVICES CORPORATION, a/k/a SAINT JOSEPH MEDICINE FACULTY ASSOCIATES, a/k/a SAINT JOSEPH MERCY PRIMARY CARE, LC No. 11-026466-NH

Defendants-Appellees.

Before: S AAD , P.J., and O WENS and K. F. K ELLY , JJ.

P ER C URIAM

.-2- In this obstetrical medical m alpractice action, plaintiff Alex ander Figurski alleges that he sustained a hypoxic-ischemic injury and left middle cerebral arterial ischemic stroke (or PAIS) during labor and delivery. 1

In Docket No. 318115, this Court gr anted plaintiff’s applicati on for leave to appeal an August 21, 2013 order of Livingston Circuit Judge Theresa M. Br ennan, 2 which granted defendants’ motion in limine to exclude plaintiff’s causation e xpert concerning claims of perinatal malpractice and gran ting partial summary disposition as to those claims. 3 In that case, we hold that the trial court exceeded its role as gatekeeper an d, instead, acted as the ultimate trier of fact. Because there was suffi cient reliable scientific data in support of plaintiff’s expert’s opinion, we reverse and remand f or further proceedings.

In Docket No. 319086, this Court granted defendants’ applicati on for leave to appeal an August 7, 2013 order of Judge Brennan denying their motion in l imine to exclude plaintiff’s economic expert. 4 In that case, we hold that the trial court properly exercised its gatekeeping function and affirm the order de nying defendants’ motion in lim ine.

I. BASIC FACTS

Mary Figurski was admitted to the hospital with ruptured membr anes at approximately 11:30 p.m. on March 7, 2008. She had a lengthy labor – 29 hour s – augmented by the drug Pitocin, beginning at 4:55 a.m. on March 8 th . The baby failed to descend after two hours of pushing. Mary had developed chorioamnionitis (placental infect ion) and the doctors noticed the presence of meconium, which was an indication that the baby had a bowel movement in utero. The labor was terminated with a caesarian section at 4:45 a.m. on March 9, 2008. Records revealed “delivery of a healthy baby boy who weighed 9 lbs 13 o z.” However, plaintiff began to show signs of seizing shortly after his birth and a CT scan per formed on March 10 th revealed an acute left middle cerebral arter y ischemic stroke, which was “d ays to hours old.”

Plaintiff’s complaint was filed on December 28, 2011. The com plaint alleged that “[t]he baby was at risk for, and did develop, brain injury from trauma tic head compression and regional cerebral ischemia caused by failure to descend, macrosomia (lar ge baby), excessive contractions in the presence of failure of descent as augmented with Pitocin , hypoxia-ischmeia (regional cerebral and/or systemic) caused by uteroplacental insufficienc y and by cord compression and head compression.” The complaint alleged that defendants were negligent in administering

1 Plaintiff also alleges that the injuries were caused by neglig ence after the delivery, but those injuries are not at i ssue in these appeals.

2 Judge Brennan is a district c ourt judge, sitting by assignmentin the circuit court.

3 Figurski v Trinity Health-Michigan, unpublished order of the Court of Appeals, entered April 8, 2014 (Docket No. 318115).

4 Figurski v Trinity Health-Michigan, unpublished order of the Court of Appeals, entered April 8, 2014 (Docket No. 319086).-3- Pitocin, in failing to properly respond to fetal heart rate changes, and in failing to perform a timely c-section.

Plaintiff attached numerous affidavits of merit regarding brea ch of the standard of care for the various professionals i nvolved, including that of Dr. C arolyn Crawford. Crawford opined that a number of factors led to plaintiff’s injuries, including : mother in first time labor (primagravida), chorioamnionitis, prolonged rupture of membrane s, prolonged second stage of labor, large child for the size of the mother’s pelvis, fetal h eart rate abnormalities, and birth trauma augmented by the use of Pitocin.

Defendants filed a motion to prevent plaintiff from pursuing a claim of global hypoxic ischemic injury secondary to tra uma from the use of Pitocin and the forces of l abor. Citing MCR 2.116(C)(10), MRE 702, and MCL 600.2955, defendants argued thatplaintiff should not be able to pursue the claim where plaintiff had only been diagnosed with a left middle cerebral artery stroke; there was no hypoxic-ischemic injury other than the str oke. Defendant further argued that there was no scientific bas is to support Crawford’s opinio n that the alleged hypoxicischemic injuries were caused by the mechanical trauma from Pit ocin and the forces of labor and noted that this same theory of injury was rejected in Craig v Oakwoood Hosp , 471 Mich 67; 684 NW2d 296 (2004). Defendants argued that because there was no a dmissible expert testimony on proximate cause, plaintiff’s claims regarding global hypoxic-is chemic injury should be dismissed.

Defendants filed a concurrent motion in limine or for summary disposition, seeking to preclude plaintiff from claiming that intrapartum care and treatment caused the left middle cerebral artery ischemic stroke. Defendants made many of the s ame arguments set forth in their motion to prevent plaintiff from pursuing a claim of global hyp oxic ischemic injury, but this particular motion specifically a ddressed the perinatal arterial ischemic stroke – an injury that is not contested. While defendant s acknowledged that certain risk factors for PAIS had been identified, the cause of the stroke continued to be unknown. Defendants argued that the medical literature upon which Crawford r elied did not provide a reliabl e scientific basis for her ultimate opinion. Even if risk factors could show causation, the litera ture provided that ischemic stroke occurs in only 1 of every 200 live births with three or more kn own risk factors present, as opposed to 1 in 5,000. Defendants urged that because there was no admissible expert testimony on proximate cause, plaintiff’s claims regarding the left middl e cerebral artery stroke injury should be dismissed.

Plaintiff filed a combined response to both motions including as an exhibit, Crawford’s May 4, 2013 affidavit wherein Crawford restates her opinion abo ut the mechanism of plaintiff’s injuries. Attached to her affida vit were 51 exhibits that Craw ford utilized in reaching her opinion. 5

5 Plaintiff also included as exhi bits, the affidavit and support ing papers for another expert – Dr. Barry S. Schifrin. However, Judge Brennan permitted plaintiff to present only one expert at the Daubert hearing and plaintiff chose to present Crawford.-4- Crawford averred that “the scientific literature establishes t hat the mechanism of trauma/head compression is injur ious to the brain during partur ition (labor/delivery) and more specifically that trauma/head compression can cause ischemic st roke.” She concluded that defendants’ negligence caused the stroke and that “[t]he PAIS w ould not have occurred but for the Defendants negligently allowing multiple known risk factors for PAIS to continue unabated and unresolved during such a prolonged and difficult labor” inc luding “primagravida, chorioamnionitis, prolonged labor, prolonged second stage, and FHR [fetal heart rate] abnormalities.”

Crawford also averred that defendants’ conduct resulted in a g lobal hypoxic-ischemic injury:

I have reviewed the scientific literature. There is a sound sc ientific basis for the opinion that excessive cephalic pressure will and does cause is chemic injury in the fashion described herein. I have seen and/or reviewed in t he literature a number of cases where this etio logy is the reasonable and probable cause of injury. In my opinion, these for ces were to a reasonable degre e of medical probability the cause of Alexander Figurski’s traumatic/ischemi c/hypoxic brain damage at birth.

A hearing on defendants’ motions took place on June 13, 2013. Both defense counsel and plaintiff’s counsel made long and impassioned arguments reg arding the admissibility of Crawford’s testimony and whether more than one injury existed. The trial court indicated it would render its opinion at a late r date. However, rather thanissuing an opinion on the issue, the trial court entered an order indicating that, even after a sear ching inquiry of the articles presented, it was unable to determine whether plaintiff’s experts should be able to testify as to causation. The order provided:

When reviewing the medical lite rature supplied by the Plaintif f, the Court was cognizant of the opinion of P laintiff’s causation experts. The Court understands that the Plaintiff’s causation experts opine that “ . . .excessive compression of the fetal head caused by uterine tachysystole, h yperstimulation, uterine hypertonicity, prolonged labor, prolonged rupture of me mbranes and relative cephalopelv ic disproportion . . .”

The searching inquiry does not allow this Court to conclude th at the Plaintiff’s causation experts’ o pinions meet the requirements o f MRE 702 and MCL 600.2955. A Daubert [ 6 ] hearing is necessary to dete rmine if the opinions of Plaintiff’s expert witnesses rega rding proximate causation for Plaintiff’s left middle cerebral artery stroke and global hypoxic-ischemic injur y satisfies the requirements of MRE 702 and MCL 600.2955. Because the opinions of

6 Daubert v Merrell Dow Pharm, Inc , 509 US 579; 113 S Ct 2786; 125 L Ed 2d 469 (1993).-5- Plaintiff’s causation experts do not differ, it is only necessa ry for one of Plaintiff’s causation experts to testify at the Daubert hearing. The Plaintiff may select which doctor will testify.

After the Daubert hearing, where Dr. Crawford was the only witness to testify, th e trial court issued an opinion and orde r granting defendants’ motions in limine and for partial summary disposition. The trial court concluded that the basis for plaintiff’s expert’s opinions had not been subjected to scientific testing or peer review, an d that there was no evidence that her theory of causation was generally accepted within the relev ant medical community. The trial court found that Crawford did not present a reliable basis for her opinion, and there was no evidence her opinion had been relied on outside the context of litigation. Based on the exclusion of the expert testimony, the court found that there was no supp ort for plaintiff’s perinatal claims, and it granted partial summary disposition as to those claims.

At the same time that the part ies battled over plaintiff’s cau sation experts, defendants also filed a motion in limine to preclude plaintiff’s economics expe rt, Dr. Anthony Gamboa, from testifying. Defendants argued that Gamboa’s opinion was based on “junk science” and contrary to MRE 702 and MCL 600.2955. Defendants claimed that Gamboa, w ho did not have a degree in economics, was not qualifie d to offer an opinion. They argu ed that because he lacked a proper understanding of basic economic pr inciples, his methodologies w ere flawed and were unreliable.

The issue was debated at a June 13, 2013 hearing. The trial c ourt issued a written opinion and order on August 7, 2013 , denying defendants’ motionin limine to exclude plaintiff’s economic expert.

II. STANDARDS OF REVIEW

[A] court of appeals is to appl y an abuse-of-discretion standa rd when it reviews a trial court’s decision to admit or exclude expert tes timony. That standard applies as much to the trial court’s decisions about h ow to determine reliability as to its ultimate conclusion. Otherwise, the tria l judge would lack the discretionary authority needed both to avoid unnecessary “relia bility” proceedings in ordinary cases where the reliability of an expert’s methods is properly taken for granted, and to require appropriate proceedings in the less usu al or more complex cases where cause for questioning the expert’s reliability aris es. [ Kumho Tire Co, Ltd v Carmichael , 526 US 137, 152; 119 S Ct 1167, 1176; 143 L Ed 2d 238 (1999) (internal quotation ma rks and citation omitted).]

However, our Court has recently explained:

We review for an abuse of discretion a circuit court’s evident iary rulings. When our inquiry concerns whether the trial court correctly app lied a rule of evidence, our review is de novo. Thus, we apply de novo review in assessing whether the trial court performed its gatekeeping role in confo rmity with the legal principles articulated in Gilbert v DaimlerChrysler Corp , 470 Mich 749; 685 NW2d 391 (2004), in which our Supreme Court adopted the Daubert framework. If the trial court correctly execu ted its gatekeeping role, we review its ultimate-6- decision to admit or exclude scientific evidence for an abuse o f discretion. When a trial court excludes evidence based on an erroneous interpret ation or application of law, it necessarily abuses its discretion. [ Elher v Misra , ___ Mich App ___; ___ NW2d ___ (Docket No. 316478, issued December 2, 2014) slip op, p 7 (internal citations and footnote omitted).]

III. GENERAL REVIEW OF THE L AW ON EXPERT TESTIMONY

In order to establish a cause of action for medical malpractic e, a plaintiff must establish four elements: ( 1) the appropriate standard of c are governing the defendant’s conduct at the time of the purported negligence, (2 ) that the defendant breached that standard of care, (3) that the plaintiff was inju red, and (4) that the plaintiff’s injuries were the pr oximate result of the defendant ’s breach of the applicable standard of care. [ Craig , 471 Mich at 86.]

Proximate cause involves both the “cause in fact” and the “lega l cause.” Skinner v Square D Co
, 445 Mich 153, 162-63; 516 NW2d 475 (1994). The first requires a showing that “but for” defendants’ action, plaintiff w ould not have been injured where as the latter focuses on foreseeability and whether a defendant should be held legally r esponsible for such consequences. Id. “A plaintiff must adequately est ablish cause in fact in order for legal cause or ‘proximate cause’ to become a relevant issue.” Id.

There is no question that plaintiff suffered a perinatal arter ial ischemic stroke, or PAIS. What is at issue is the connection between plaintiff’s injury and defendants’ conduct, both “but for” and “proximate” causation. “[A] plaintiff’s prima facie c ase of medical malpractice must draw a causal connection between the defendant’s breach of the applicable standard of care and the plaintiff’s injuries.” Craig , 471 Mich at 90. Crawford opine s that “excessive compression of the fetal head caused by uterine tachysystole, hyperstimulation , uterine hypertonicity, prolonged labor, prolonged rupture of membr anes, and relative cephalopelv ic disproportion” caused the stroke. Defendants counter that there is nothing in the medica l literature to support such a position and that the cause of PAIS remains largely unknown. W hile plaintiff contends that he also suffered a global hypoxic ischemic injury, defendants counter that no such injury was detected by plaintiff’s treati ng physicians. These issues are clearly beyond the realm of the average lay person.

MRE 702 provides:

If the court determines that sc ientific, technical, or other s pecialized knowledge will assist the trier of fact to understand the evide nce or to determine a fact in issue, a witness qualified as an expert by knowledge, s kill, experience, training, or education may testify thereto in the form of an op inion or otherwise if (1) the testimony is based on sufficient facts or data, (2) the testimony is the product of reliable principles and methods, and (3) the witness has applied the principles and methods reliabl y to the facts of the case.

“The admission of expert testimony requires that (1) the witnes s be an expert, (2) there are facts in evidence that require or are subject to examination and anal ysis by a competen t expert, and (3)-7- the knowledge is in a particular area that belongs more to an e xpert than to the common man.” Surman v Surman , 277 Mich App 287, 308; 745 NW2d 802 (2007). The so-called “t rilogy of restrictions on expert testimony” includes a searching inquiry into “qualification, reliability, and fit.” Elher , slip op, p 8. Defendants do not question Crawford’s qualific ations, but they take issue with reliability and fit. As the party offering the evid ence, plaintiff bore the burden of persuading the trial court that the expert’s opinion is based o n a recognized field and methodology. Craig , 471 Mich at 80.

“MRE 702 requires the trial court to ensure that each aspect o f an expert witness’s proffered testimony—including the data underlying the expert’s theories and the methodology by which the expert draws conclusion s from that data—is reliable.” Gilbert v DaimlerChrysler Corp , 470 Mich 749, 779; 685 NW2d 391 (2004), citing Daubert . Our Supreme Court has held:

This gatekeeper role applies to all stages of expert analysis. MRE 702 mandates a searching inquiry, not just of the data underlying e xpert testimony, but also of the manner in which the e xpert interprets and extrapola tes from those data. Thus, it is insufficient for th e proponent of expert opinion me rely to show that the opinion rests on data viewed as legitimate in the context of a particular area of expertise (such as medicine). The proponent must also show tha t any opinion based on those data expresses conclusions reached through relia ble principles and methodology.

Careful vetting of all aspects of expert testimony is especial ly important when an expert provides testimony about causation. [ Gilbert , 470 Mich at 782 (footnote omitted).]

In Daubert , the petitioners were minors who had suffered serious birth de fects. Along with their parents, the petiti oners sued respondent, a pharmace utical company, alleging that the mothers’ ingestion of Bendectin caused the birth defects. The respondent’s expert averred that he had looked at a number of published studies and none had con cluded that maternal use of Bendectin was a risk factor for birth defects. The petitioners responded with eight experts of their own, who pointed to test t ube and live animal studies linking Bendectin to malformations. The petitioners pointed to “pharmacological studies of the chem ical structure of Bendectin that purported to show similarities between the structure of the dru g and that of other substances known to cause birth defects; and the ‘reanalysis’ of previousl y published epidemiological (human statistical) studies.” The district court granted the r espondent summary judgment because the petitioners’ experts’ opinions were not generally a ccepted. The federal appeals court affirmed, citing Frye v United States , 293 F 1013, 1014; 54 App DC 46 (1923). Daubert , 509 US at 582-584.

In vacating the decision, the United States Supreme Court did away with the “general acceptance” test previously relied upon in Frye , which required that before an expert could render an opinion on novel scient ific evidence, the theory must have first gained general-8- acceptance. The Supreme Court concluded that Frye had been displaced by FRE 702. 7 Daubert, 509 US at 585-589. “That the Frye test was displaced by the Rules of Evidence does not mean, however, that the Rules themselves place no limits on the admis sibility of purportedly scientific evidence. Nor is the trial judge disabled from screening such evidence. To the contrary, under the Rules the trial judge must ensure that any and all scientif ic testimony or evidence admitted is not only relevant, but reliable.” Id. at 589.

Under FRE 702, “[t]he subject of an expert’s testimony must be ‘scientific knowledge.’ The adjective ‘scientific’ implies a grounding in the methods and procedures of science. Similarly, the word ‘knowledge’ connotes more than subjective b elief or unsupported speculation.” Id. at 589-590. The Court cautioned that:

Of course, it would be unreasonabl e to conclude that the subjec t of scientific testimony must be ‘known’ to a ce rtainty; arguably, there are n o certainties in science . . . But, in order to qualify as ‘scientific knowled ge,’ an inference or assertion must be derived by the scientific method. Proposed t estimony must be supported by appropriate validat ion—i.e., ‘good grounds,’ based on what is known. In short, the requirement that an expert’s testimony pe rtain to ‘scientific knowledge’ establishes a standar d of evidentiary reliability. [ Id. at 590.]

Moreover, the evidence must “fit” and connect to the “pertinentinquiry as a precondition to admissibility” in order to be deemed relevant. Id. at 591-592.

The Daubert Court explained that, unlike an ordinary witness, an expert was permitted to testify without any firsthand knowledge or observation and “[p] resumably, this relaxation of the usual requirement of firsthand knowledge . . . is premised on a n assumption that the expert’s opinion will have a reliable basis in the knowledge and experie nce of his discipline.” Id. at 592. As a result, trial courts are charged with making “a preliminar y assessment of whether the reasoning or methodology underlying the testimony is scientific ally valid and of whether that reasoning or methodology properly can be applied to the facts i n issue.” Id. at 592-593. In so doing, “[m]any factors will bear on the inquiry, and we do not presume to set out a definitive checklist or test.” Id. at 593. The Court then set fortha number of “general observat ions” that a trial court may consider, including: 1) whether a theory has b een tested; 2) whether the theory has been subjected to peer review and publication; 3) the poten tial rate of error; and 4) whether the theory has gained general acceptance. Id. at 593-594. But “[t]he inquiry envisioned by Rule 702 is, we emphasize, a flexible one. Its overarching subject is the scientific validity and thus the evidentiary relevance and re liability—of the principles tha t underlie a proposed submission. The focus, of course, must be solely on prin ciples and methodology, not on the conclusions that they generate .” Id. at 594-595 (footnote omitted, emphasis added).

7 FRE 702 provided: “If scientific , technical, or other special ized knowledge will assist the trier of fact to understand the evidence or to determine a fact in is sue, a witness qualified as an expert by knowledge, skill, experience, training, or education, may te stify thereto in the form of an opinion or otherwise.”-9- The Daubert Court rejected the idea that its decision would result in a “fr ee-for-all” and permit plaintiffs to present uns ound evidence to the juries:

Vigorous cross-examination, presen tation of contrary evidence, and careful instruction on the burden of proof are the traditional and appr opriate means of attacking shaky but admissible evidence. . . . These convention al devices, rather than wholesale exclusion under an uncompromising ‘general accep tance’ test, are the appropriate safeguards wher e the basis of scientific testim ony meets the standards of Rule 702. [ Id. at 596.]

The United States Supreme Court revisited Daubert six years later in Kumho Tire Co, Ltd v Carmichael , 526 US 137; 119 S Ct 1167; 143 L Ed 2d 238 (1999), when it wa s called upon to determine how Daubert applies to experts who were not scientists. Kumho was a products liability case. The plaintiff sued a tire manufacturer after a tire blew and presented an engineering expert who opined that a defect in the tire caused the accident. Id. at 141-147. The manufacturer did not challenge the expert’s qualifications, butnevertheless argued that the expert’s methodology was unreliable. Id. at 153.

The Court first concluded that “ Daubert’s general holding—setting forth the trial judge’s general ‘gatekeeping’ obligati on—applies not only to testimony based on scientific knowledge, but also to testimony based on ‘technical’ and ‘other specializ ed’ knowledge.” Id. at 141, 149. Because there are many different experts and various areas of e xpertise, the factors considered in determining whether to allow an expert to testify must be flexi ble: “we can neither rule out, nor rule in, for all cases and for all time the applicability of th e factors mentioned in Daubert , nor can we now do so for subsets of cases categorized by category o f expert or by kind of evidence. Too much depends upon the particular circumstances of the parti cular case at issue.” Id. at 150. As Daubert made clear, “its list of factors was meant to be helpful, not d efinitive.” Id. at 151. In performing its gatekeeping requirement, a trial court must “ens ure the reliability and relevancy of expert testimony. It is to make certain that an expert, whethe r basing testimony upon professional studies or personal experience, employs in the cou rtroom the same level of intellectual rigor that charact erizes the practice of an expertin the relevant field.” Id. at 152.

The Kumho Court then went on to conclude t hat the district court did not abuse its discretion when it concluded that the expert’s opinion was unre liable because it fell outside the range where experts might reasonably differ. Id. at 153. “[N]o one denies that an expert might draw a conclusion from a set of observations based on extensive and specialized experience,” but the expert’s novel method was not used by other experts in the industry despite the prevalence of testing. Id. at 156-157. Ultimately, the expert’s testimony failed the four criteria set forth in Daubert and “any other set” of reasona ble reliability criteria. Id. at 158. “In sum, Rule 702 grants the district judge the discretionary authority, reviewab le for its abuse, to determine reliability in light of the parti cular facts and circumstances of the particular case.” Id.

In response to Daubert and Kumho , Michigan’s legislature enacted MCL 600.2955, which provides:

(1) In an action for the death of a person or for injury to a person or property, a scientific opinion re ndered by an otherwise qualifi ed expert is not-10- admissible unless the court determines that the opinion is reli able and will assist the trier of fact. I n making that determi nation, the court sha ll examine the opinion and the basis for the opinion, which basis includes the facts, technique, methodology, and reasoning relied on by the expert, and shall c onsider all of the following factors:

(a) Whether the opinion and its basis have been subjected to s cientific testing and replication.

(b) Whether the opinion and its basis have been subjected to peer review publication.

(c) The existence and maintenance of generally accepted stand ards governing the application and interpretation of a methodology o r technique and whether the opinion and its basis are consistent with those standards.

(d) The known or potential erro r rate of the opinion and its basis.

(e) The degree to which the opi nion and its basis are general ly accepted within the relevant expert community. As used in this subdivis ion, “relevant expert community” means individuals who are knowledgeable in th e field of study and are gainfully employe d applying that knowledge on the free market.

(f) Whether the basis for the opinion is reliable and whether experts in that field would rely on the same basis to reach the type of op inion being proffered.

(g) Whether the opinion or methodology is relied upon by expe rts outside of the context of litigation.

(2) A novel methodology or form of scientific evidence may be admitted into evidence only if its propone nt establishes that it has ach ieved general scientific acceptanc e among impartial and disinterested experts in the field.

Our state courts have issued a number of opinions addressing the reliability of expert testimony. In Gilbert , the plaintiff sued her employe r for sexual harassment, arguin g that the harassment created a permanent change in her brain chemistry, which caused her to relapse into substance abuse and depression. Gilbert , 470 Mich at 753. She presented the expert opinion of a social worker who testified that the plaintiff would suffer an untimely and excruciating death. Id . The plaintiff’s expert was the plaintiff’s counselor and tes tified as both a fact witness and an expert witness. He testified that he received a master’s degre e in psychobiology and also received a prestigious award as an undergraduate, but neither o f these claims was true. Id. at 759-760. The Court noted that “[t]his witness not only lacked any training, education, or experience in medicine, but also testified falsely about his cr edentials. Nevertheless, plaintiff asked the jury to treat this w itness’s testimony as a ‘prognosi s,’ and to compensate plaintiff for the loss of her health an d, eventually, her life.” Id. at 753-754.-11- In a strongly-worded opinion, the Supreme Court took both the trial court and the appellate court to task for cons idering such “junk science”:

[P]roperly understood, the court’s gatekeeper role is the same under Davis–Frye and Daubert . Regardless of which test the court applies, the court may admit evidence only once it ensures, pursuant to MRE 702, that expert testimony meets that rule’s standard of reliabil ity. In other words, both test s require courts to exclude junk science; Daubert simply allows courts to consider more than just “general acceptance” in determining whether expert testimony mu st be excluded.

This gatekeeper role applies to all stages of expert analysis. MRE 702 mandates a searching inquiry, not just of the data underlying e xpert testimony, but also of the manner in which the e xpert interprets and extrapola tes from those data. Thus, it is insufficient for th e proponent of expert opinion me rely to show that the opinion rests on data viewed as legitimate in the context of a particular area of expertise (such as medicine). The proponent must also show tha t any opinion based on those data expresses conclusions reached through relia ble principles and methodology. [ Id. at 782 (internal footnotes omitted).]

Noting the particular care that must be taken to vet expert te stimony that touches on causation, the Court stated:

When a court focuses its MRE 702 inquiry on the data underlying expert opinion and neglects to evaluate the extent to which an expert extrapol ates from those data in a manner consistent with Davis 8–Frye (or now Daubert), it runs the risk of overlooking a yawning “analytical gap” between that data and th e opinion expressed by an expert. As a re sult, ostensibly legitimate dat a may serve as a Trojan horse that facilitates the surreptitious advance of junk science and spurious, unreliable opinions.” [ Id. at 783.]

The Gilbert court concluded that both the tr ial court and the Court of Appe als had failed to recognize such core gatekeeping principles. Id. at 783. The result was that a social worker who lacked any medical education, experience, training, skill o r knowledge was permitted to interpret plaintiff’s medical r ecords and offer an “opinion that he was wholly unqualified to give.” Id. at 784-785. The Court explained:

Mr. Hnat unquestionably used the content of plaintiff’s treatme nt records to render an opinion that required medical expertise. He speculat ed about plaintiff’s impending physical inability to work, testified about the type of medical complications that plaintiff w ould soon experience, predicted the cause of her death, and gave testimony concer ning plaintiff’s life expectanc y. Mr. Hnat expressed his “opinion” on physiological disease, cause of deat h, and plaintiff’s lifespan. Yet there was no evidence or showing that Mr. Hnat w as qualified by

8 People v Davis , 343 Mich 348; 72 NW2d 269 (1955).-12- training, experience, or knowledge to render such opinions or i nterpret medical records that would arguably support such a diagnosis or prognos is. There was, in other words, no evidence that Mr. Hnat was qualified to testifythat defendant’s actions concerning workplace harassment caused neurological and physiological changes in plaintiff and shortened her life. [ Id. at 787-788.]

Thus, while the witness may have been an expert in social work and substance abuse, “[i]n order for Mr. Hnat to provide an admissible opinion interpreting medi cal records for purposes other than those related to the expert ise of social workers, plaintif f bore the burden of showing that Mr. Hnat was qualified by knowledge, skill, experience, training, o r education in medicine .” Id. at 788. His qualification did not go mer ely to the weight of the evidence, but its admissibility in the first instance. Id. “Where the subject of the proffered testimony is far beyond th e scope of an individual’s expertise . . . that testimony is inadmissible und er MRE 702. In such cases, it would be inaccurate to say that the expert’s lack of expertise or exp erience merely relates to the weight of her testimony. An expert who lacks ‘knowledge’ in the field at issue cannot ‘assist the trier of fact.’” Id. 789. The Court concluded that the witness’s “prognosis” testim ony that was based on his interpretation of the plaintiff’s medical records was erron eous because the witness lacked medical training and, therefore, did not have the ability to interpret the records. Id. at 789-790. Gilbert’s primary focus was on the fact that the witness was not qualifie d to offer an opinion. The Court’s focus was on the witness’s professional qualificati ons and whether his background permitted him to offer an interpretation of those records.

That same year, the Michiga n Supreme Court decided the Craig case, which is very much in step with the case at bar, as it involved the same plaintiff ’s attorney and one of the same purported experts – Dr.Gabriel. The plaintiff in Craig suffered from cerebral palsy and mental retardation. The plaintiff argued at trial that the defendants (the hospital and treating physicians) negligently administered an ex cessive amount of Pitocin. The t rial court denied the defendants’ request to have a Davis-Frye hearing on the admissibility of the plaintiff’s causation exper t and ultimately a jury entered an aw ard for the plaintiff. The Cour t of Appeals affirmed as to liability, but ordered remittutur. Craig, 471 Mich at 70-71. Our Supreme Court reversed. Craig was decided under the Davis-Frye framework and the Supreme Court noted that, under that framework,

expert opinion based on novel scientific techniques is admissib le only if the underlying methodology is generally accepted within the scienti fic community. Thus, in determining whether th e proposed expert opinion was gr ounded in a ‘recognized’ field of scientific, technical, or other specializ ed knowledge as was required by MRE 702, a trial court was obligated to ensure that the expert opinion was based on accurate and generally accepted methodologies. [ Craig , 471 Mich at 80 (internal footnotes omitted).]

The trial court in Craig did not rely on any of the literature submitted by the plainti ff in response to the defendants’ moti on in limine to exclude his tes timony. “Instead of consulting plaintiff’s proffered scientific and medical literature, the co urt erroneously assigned the burden of proof under Davis-Frye to defendant – the party opposing the admission of Dr. Gabriel’s testimony – and held that defendant was not entitled to a heari ng because it failed to prove that Dr. Gabriel’s theory lacked ‘general acceptance.’” Id. at 81. The Court noted that while the-13- plaintiff produced literature that Pitocin could cause brain da mage, it did not connect to Dr. Gabriel’s causal theory that the excessive contractions caused the plaintiff’s head to be repeatedly ground against his mother’s pelvis, resulting in hea d trauma and cerebral palsy. Id. at 83.

Dr. Gabriel was unable to cit e a single study supporting his tr aumatic injury theory during a voir dire conducte d at trial. The only authori ties he offered for the proposition that excessive amount s of Pitocin may cause cerebra l palsy through the traumatic mechanism he described at trial were studies he c ited in which Pitocin caused cerebral palsy in animals when given in excessiv e amounts. These studies did not involve the “bump ing and grinding” mechanism on which Dr. Gabriel’s expert testimony relie d. In fact, Dr. Gabriel express ly distinguished the mechanism to which he attributed plaintiff’s injuries from thos e at work in the animal studies. It would appear, then, that there was little ev idence that Dr. Gabriel’s theory was “recognize d,” much less generally accepted , within pediatric neurology. [ Id. at 84.]

Dr. Gabriel could not identify what part of the mother’s anatom y against which the child’s head collided. Id. Moreover, “[a]t no point did Dr . Gabriel opine that the trauma tic and vascular mechanisms he described could cause cerebral palsy, or that tho se mechanisms might produce the asymmetrical development shown in plaintiff’s MRI. Thus, D r. Gabriel’s testimony supported plaintiff’s medical mal practice claim only if the jur y was permitted to assume, without supporting evidence, that a causal connection existed between t hese elements.” Id. at 84-85. There was, therefore, a “yawning gap between Dr. Gabriel’s test imony and the conclusions plaintiff hoped the jury would draw from it.” Id. at 85.

The Craig Court held that the trial court erred in failing to grant the d efendants’ motion for judgment notwithstanding the verdict where the plaintiff fa iled to establish causation. “Even if plaintiff had shown that defendants breached the standard of care, the jury had no basis in the record to connect this breach to the cerebral palsy, mental ret ardation, and other injuries now presented by plaintiff.” Id. at 90. The Court added that “[e]v en if we accept Dr. Gabriel’s testimony in full, a fatal flaw remains in plaintiff’s prima fa cie case: Dr. Gabriel never testified that the injuries stemming from this pounding and its accompany ing vascular effects could cause cerebral palsy, mental retardati on, or any of the other conditi ons now presented by plaintiff.” Id. at 91. The Craig Court concluded:

Dr. Gabriel began his testimony by explaining that an MRI imag e showed that plaintiff’s brain tissue had developed asymmetrically. He failed, however, to trace this asymmetric development either back to the traumatic and vascular mechanisms he described or forward to the specific neurological conditions presently displayed by plainti ff. Thus, how exactly the mechan isms he described led to cerebral palsy (as opposed to any other neurological imp airment) and how they were connected to the asymmetric brain development depicte d in plaintiff’s MRI was never explained.

It is axiomatic in logic and in science that correlation is no t causation. This adage counsels that it is error to infer that A causes B f rom the mere fact that-14- A and B occur together. Given the absence of testimony on caus ation supplied by Dr. Gabriel, the jury could ha ve found for plaintiff only if itindulged in this logical error-concluding, in eff ect, that evidence that plainti ff may have sustained a head injury, combined with evidence that plaintiff now has ce rebral palsy, leads to the conclusion that the conduct that caused plaintiff’s head injury also caused his cerebral palsy.

Such indulgence is prohibite d by our jurisprudence on causatio n. We have long required the plaintiff to show that but for the defendant’ s actions, the plaintiff’s injury would not have occurred. Where the connecti on between the defendant’s negligent conduct and the plaintiff’s injuries is e ntirely speculative, the plaintiff cannot establish a prima facie case of negligence . [ Id. at 93 (internal quotation marks and footnotes omitted).]

Three years later in Chapin v A & L Parts, Inc , 274 Mich App 122; 732 NW2d 578 (2007), our Court cautioned trial courts not to conduct “minitr ials” when deciding whether an expert can testify at trial under MRE 702 and MCL 600.2955(1). In Chapin , plaintiff was diagnosed with mesothelioma, after having spent 45 years workin g as an automobile brake mechanic. “Part of his job i nvolved grinding brake linings tha t contained chryso tile asbestos. At issue is whether plaintiffs’ expert presented scientifically re liable, and therefore legally admissible, evidence drawing a causal connection between mesoth elioma and inhalation of brake-lining dust.” Id. at 125. Writing for the majority Judge Davis noted:

[T]he trial court’s role as gate keeper does not require it to s earch for absolute truth, to admit only uncontested evidence, or to resolve genuin e scientific disputes. The fact[] that an opinion held by a properly qualif ied expert is not shared by all others in the field or that there exists some con flicting evidence supporting and opposing the opini on do[es] not necessarily rend er the opinion “unreliable.” A trial court doe s not abuse its discretion by n evertheless admitting the expert opinion, as long as the opinion is rationally derive d from a sound foundation. [ Id. at 127.]

Importantly, Judge Davis wrote:

The fact that two scientists value the available research diff erently and ascribe different significance to that research does not necess arily make either of their conclusions unreliable. Indeed, science is, at its heart , itself an ongoing search for truth, with new discoveries occurring daily, and with regular disagreements between even the most respected members of any gi ven field. A Daubert -type hearing of this kind is not a judicial search for truth . The courts are unlikely to be capable of achievi ng a degree of scientific know ledge that scientists cannot. An evidentiary hearing under MRE 702 and MCL 600.2955 is merely a threshold inquiry to ensure that the trier of fact is not calle d on to rely in whole or in part on an expert opinion that is only masquerading as scien ce. The courts are not in the business of resolving scientific disputes. The only proper role of a trial court at a Daubert hearing is to filter out expert evidence that is unreliable, not to admit only evidence that is un assailable. The inquiry is not i nto whether an-15- expert’s opinion is necessarily c orrect or universally accepted . The inquiry is into whether the opinion is rationa lly derived from a sound foundati on. [ Id. at 139 (emphasis added).]

The Court concluded that, even in the face of contrary evidence , the trial court correctly permitted the plaintiff’s expert to testify. “Although clearly not universally accepted, and although unsupported by epidemiological studies that may or maynot be flawed, [the plaintiff’s expert’s] opinion is certainly objective, rational, and based o n sound and trustwor thy scientific literature.” Id. at 140.

In Edry v Adelman , 486 Mich 634; 786 NW2d 567 (2010), the plaintiff brought an a ction against her doctor, alleging that his failure to follow-up on a bump under her arm delayed the diagnosis and treatment of breast cancer, impacting her surviva l rate. The Michigan Supreme Court affirmed the trial court’s decision to not allow plaintif f’s oncology expert to testify that the plaintiff’s chances of surviving five years would have been 95 percent if she had been diagnosed earlier and that the delay in diagnosis reduced her five-year s urvival chance to 20 percent. Id. at 636-640. The Edry Court concluded:

Here, [the plaintiff’s expert’s] testimony failed to meet the cornerstone requirements of MRE 702. Dr. Singer’s opinion was not based onreliable principles or methods; his testim ony was contradicted by both t he defendant’s oncology expert’s opinion and the published literature on the s ubject that was admitted into evidence, which even Dr. Singer acknowledged as authoritative. Moreover, no literature was admitted into evidence that support ed Dr. Singer’s testimony. Although he made genera l references to textbooks an d journals during his deposition, plaintiff failed to produce that literature, ev en after the court provided plaintiff a sufficient opportunity to do so. Plaintif f eventually provided some literature in support of Dr. Singer’s opinion in her motio n to set aside the trial court’s order, but the mat erial consisted only of printou ts from publicly accessible websites that provided general statistics about surv ival rates of breast cancer patients. The fact that m aterial is publicly available on the Internet is not, alone, an indication that it is unreliable, but these materials were not peerreviewed and did not directly s upport Dr. Singer’s testimony. Moreover, plaintiff never provided an affidavit explaining how Dr. Singer used the information from the websites to formulate his opinion or whether Dr. Singer eve r even reviewed the articles. [ Id. at 640-641 (internal footnote omitted).]

The Court emphasized that “[w]h ile peer-reviewed, published lit erature is not always a necessary or sufficient method of meeting the requirements of MRE 702, in this case the lack of supporting literature, combined with the lack of any other form of support for Dr. Singer’s opinion, renders his opinion unreliable and inadmissible under MRE 702.” Id. at 641. It was not enough for a party to “point to an expert’s experience and background to arg ue that the expert’s opinion is reliable.” Id. at 642.

Recently our Court reviewed the admissibility of expert opinio n in Elher v Misra , ___ Mich App ___; ___ NW2d ___ (Docket No. 316478, issued December 2, 2014). In Elher
, (unlike the case at bar) there was no dispute as to the injury or the mechanism of the injury. At-16- issue was whether the particular conduct (clipping both the bil e and cystic ducts during gallbladder surgery) breached the standard of care. Elher , slip op, pp 1, 7. Nevertheless, Judge Gleicher cited many of the foregoing cases and noted that, in a cting as gatekeeper, “‘[t]he standard focuses on the scientif ic validity of the expert’s met hods rather than on the correctness or soundness of the expert’s part icular proposed testimony.’” Id. at slip op, p 8, quoting People v Unger , 278 Mich App 210, 217-218; 749 NW2d 272 (2008). Judge Gleich er wrote:

We draw from Kumho and Edry several important lessons. A court screening scientific evidence mu st ensure that proposed scienti fic or technical testimony is reliable as well as r elevant. But the algorithm f or this analysis cannot be scripted in advance or applied in a vacuum. Rather, a court must determine which factors reasonably measure reliability given th e specific factual context and contours of the testimony presented. [ Id. at slip op, p 10.]

Because the focus must be on methodology and not the expert’s ultimate conclusion:

If an expert’s reasoning is based on scientific principles, kno wledge, experience and training, the testimony may fulfill the reliability standar ds even in the presence of conflicting conclusi ons predicated on precisely the same data, and an identical quantum of practical w isdom. This holds true even wh en a judge finds one side’s approach more persuasive. The clashing standard of care opinions in this case are exactly the sort that “[v]igorous cross-examinati on, presentation of contrary evidence, and careful i nstruction on the burden of pro of” is designed to resolve. [ Id. at slip op p, 14, quoting Daubert .]

Moreover, the courtroom door should not be closed on medical e xperts whose opinions are often supported by extensive relevant experience. Elher , slip op, p 18. In fact, the rule of evidence “expressly contemplates that an expert may be qualifie d on the basis of experience.” Id. Judge Gleicher concluded:

Gatekeeping courts are not empowered “to determine which of sev eral competing scientific theories has the best provenance.” Ruiz–Troche v Pepsi Cola of Puerto Rico Bottling Co , 161 F3d 77, 85 (CA 1, 1998). The test is whether the expert’ s reasoning is scientifically sound.

***

Ultimately, the gatekeeping inquiry asks whether the expert ha s reached his or her conclusions in a sound manner, and not whether the e xpert’s conclusions are correct. “Vigor ous cross-examination, presenta tion of contrary evidence, and careful instruction on the burden of proof are th e traditional and appropriate means of attacking shaky but admissible evidence.” Daubert , 590 U.S. at 597. Alternatively stated, the trial judge is “a gatek eeper, not a fact finder.” United States v Sandoval–Mendoza , 472 F3d 645, 654 (CA 9, 2006). Here, application of immaterial Daubert factors led the trial court to exclude expert testimony possessing none of the hallmarks of “junk scie nce.” “[N]o one denies that an expert might draw a conclusion from a set of obs ervations based on-17- extensive and specialized experience.” Kumho , 526 US at 156. [ Elher , slip op, pp 19-20.]

IV. PLAINTIFF’S CA USATION EXPERT

A. JUNE 13, 2013 HEARING

At the June 13, 2013 hearing on defendants’ various motions, d efense counsel explained that he filed two separate motions for each of the alleged inju ries to plaintiff – perinatal arterial ischemic stroke and hypoxic ischemic injury. He disputed that there was any evidence of the latter because no one other than plaintiff’s experts diagnosed hypoxic ischemic injury. Furthermore, counsel argued that plaintiff could not show negli gent perinatal care and treatment caused the stroke. He argued that, while there were known risk factors, there was simply no identified causal mechanism for PAIS. Defense counsel argued t hat these types of strokes could not be predicted or prevented.

Before he began his response, the trial court told plaintiff’s counsel: “I want you to be able to show me in the articles exactly where it says what caus es this, not just when it says what are the risk factors and associations.” Plaintiff’s counsel ac knowledged the Craig case and differentiated it by saying that the plaintiff in Craig failed to offer a “scin tilla” of support for Dr. Gabriel’s opinion whereas the present case had “an avalanche” o f support. Essentially, even if viewed as just risk factors, “this is an injury that can be prevented if they ’re careful.”

The parties then went to address the motion regarding plaintif f’s claim of global hypoxic ischemia injury secondary to alle ged perinatal trauma from Pito cin and the forces of labor. Defense counsel argued that no literature supported a finding that excessive uterine contractions can cause brain injury and it was the exact theory that the Craig Court rejected. Uterine activity was just a risk factor, not a cause of ischemia. Defense couns el asked “where is the science that supports that long second stages of labor with Petocin [sic] cause a brain injury?”

Plaintiff’s counsel denied that there were two separate injuri es: “This baby suffered one injury. That injury included a stroke. That injury also inclu ded lack of oxygen to both sides of the baby’s brain.” P laintiff’s counsel the n indicated that the re were three injuries. The following exchange took place between plaintiff’s attorney and the court:

THE COURT: Tell me what cause d the stroke in baby Figurski.

MR. FIEGER: Ischemia. In this case, ischemia.

THE COURT: And that’s lack of blood?

MR. FIEGER: No, not lack of blood.

THE COURT: It’s slow blood.

MR. FIEGER: It’s slow, it, it’s less perfusion.-18- THE COURT: And what cau sed the slow blood?

MR. FIEGER: The forces of the P etocin [sic] being allowed to continue –

THE COURT: Okay.

MR. FIEGER: -- unabated for hours.

THE COURT: So the stroke was caused by ischemia. Ischemia is a slowing of the blood. The slowing o f the blood was the result of the Petocin [sic].

MR. FIEGER: Yes.

THE COURT: So there’s a stroke. That’s an injury. There’s i schemia, but ischemia you just said is what caused the stroke. So how i s ischemia a different injury?

MR. FIEGER: Because it affects, the stroke is in the vessel and it’s, affects a specific portion of the brain. The experts have also testified this child has injuries over differe nt parts of his brain.

THE COURT: How is ischemia different than the stroke?

MR. FIEGER: The ischemia is a lack of perfusion where they ca ll it a watershed event. That affects all the cells in the brain, not just the specific area of the brain that’s affected by the stroke.

THE COURT: So the ischemia caused an, if I hear you, an injury different than the stroke. It wa s the part of the, a factor in the stroke but it also caused another injury.

MR. FIEGER: Yes. Exactly.

THE COURT: And what was it?

***

MR. FIEGER: He’s got g lobal brain damage.

***

THE COURT: So that’s two things: stroke, ischemia which caus ed brain damage. What the third?

MR. FIEGER: Hypoxia.

THE COURT: Hypoxia is a lack of oxygen.-19- MR. FIEGER: That’s, that’s lack of oxygen, right, as opposed to perfusion.

THE COURT: And the lack of oxygen was caused by what?

MR. FIEGER: The Petocin [sic].

Defense counsel acknowledged th at plaintiff claimed the same m echanism caused both injuries (the disputed global hypoxic ischemia and the undisput ed stroke) and his response was that neither injury could have been caused by the squeezing of the child’s brain. He argued that 1) there was no way of knowing wh at caused the stroke, and 2) there was no evidence of any injury other than the stroke; no one had diagnosed plaintiff wi th global hypoxic ischemia. Defense counsel explained his position:

Mr. Fieger’s experts, he has cited the Heuser article. He said excessive uterine contractions can lead to changes in the fetal heart rate, dimin ished placental perfusion. My motion doesn’t address that. If his experts wan t to come in and say that excessive Petocin [sic] caused a decrease in placental perfusion in this case, my motion didn’t address that. What my motion addresses is Plaintiff’s experts coming in here and saying excessive uterine activity caused squeezing of the head which caused a decrease in perfusion pressure, which l ed to a global hypoxic ischemia, which caused the child’s injury. . . .Your Ho nor, I’m not disputing that excessive uterine contractions can cause a probl em with placental perfusion. What I am disputing and what my motion concerns is it doesn’t cause head compression sufficient to cause a brain inju ry to a child.

B. DAUBERT HEARING

Dr. Crawford testified that for the past 40 years she speciali zed in neonatal perinatal medicine, or the care of sick ne wborns. She was board certifie d in pediatrics in 1976 and neonatal perinatal medicine in 1977. Crawford had been practic ing part-time at Our Lady of Lourdes Medical Center in Camde n, New Jersey, since 1999. It w as a level three institution with a high risk perinatal center. Her practice involved “the under standing of the problems during pregnancy, labor, and delivery th at impact on the fetus and newborn because that’s the history of my patient.” Part of her specialty was the diagnosis and treatment of newborns injured prior to, during, or after birth. Her oth er work included directing medi cal teams to provide care at medical clinics around the world. She routinely taught in Guat emala, Cuba and the United States. She also wrote a number of articles and chapters in me dical textbooks. During crossexamination, Crawford acknowledged that she was not a pediatric neurologist. A pediatric neurologist – Dr. Woodhouse – had diagnosed plaintiff with a st roke in this case.

For the case at bar, Crawford reviewed plaintiff’s medical rec ords, which included prenatal records, neonatal postnatal records, and pediatric rec ords. In so doing, she formed an opinion that plaintiff suffered a hypoxic ischemic injury. She explained that “hypoxia” was low oxygen “particularly to the tissues. It often includes hypoxem ia which is low oxygen in the blood. Ischemia refers to a decrease in the flow of blood cont aining oxygen to the tissues.” There was also a perinatal arterial ischemic stroke. She expla ined that “Arterial means it-20- involves an artery. And ischemic means it involves a disruptio n or decrease in the amount of blood flow through the particular artery, in this case the left middle cerebral artery which is a main branch off of the carotid that supplies a large portion of the cortex of the baby.” It was not uncommon to find hypoxia ischemia in infants who suffered a per inatal arterial ischemic stroke.

A stroke could be either “wet,” meaning a ruptured aneurism, o r “dry,” meaning that the blood did not flow properly becau se of increased intracranial p ressure. As to the latter, Crawford explained:

Personally, I’ve had experience with using blood pressure cuffs applied to children at the area of the bipar ietal diameter where the blood pressure cuff is pumped up to exceed systolic pressure. And my experience with doing that was with children who were receiving chemotherapy and we were tryin g to minimize the effect of the chemotherapy on the brain when they were bein g treated for things like leukemia. So it was a very effective mechanism. T he literature also supports the efficacy, the effectiveness of applying a blood pr essure cuff around the, uh, biperietal diameter of f etal animals, in particular sh eep. And when the blood pressure cuff is inflated to 100, 150, 200 millimeters, y ou can get an isoelectric line for the EEG on the fetal animal. And you can get decrease in the flow of blood to the cortex of t he brain, which is about 95% of the flow of the blood to the cortex gets disrupted when you have increased intr acranial pressure during that type of experiment and study, where as the flow to the brain stem is actually increased. So that, those type of animal experiments and my familiarity with using the blood pressure cuff to decrease cerebral blood flow has been part of the basis for my opinion that when you have prolonged intense uterine contractions that you ge t an increase in the intracranial press ure that, or you get an increase in pressure on the head that may be such that the babycannot increase its blood pressure to maintain circulation. So it can do it to a c ertain point, but there’s a point of failure when the increased pressure on the h ead, particularly in the biparietal 9 diameter area which is where the middle cerebral artery is . . . and that’s what, uh, leads to disr uption of blood flow. [Emphasis added.]

Crawford testified that plaintiff did not just suffer a stroke , but also had diffused encephalopathy on the right side of his brain, which was abnorm al brain function as manifested with changes in tone, seizures, and posturing. He also had apn ea, which was the cessation of breathing. Plaintiff had several diffusely (not localized) abn ormal EEG’s. He had “multiple indications of having sustained a widespread brain injury.” Pl aintiff not only suffered a “left middle cerebral artery infarct” (stroke) but also a “diffuse hy poxia ischemia to the brain,” meaning all over the brain.

Crawford explained that moldi ng can lead to distortion of the head and blood vessels. In this case, plaintiff demonstrated significant molding and caput (swelling of the scalp edema fluid) as a result of trying to get the head through the pelvis . “And the reason the middle

9 In the record, the term is spell ed “biperietal” and “biparieta l.”-21- cerebrals are affected is that the area of maximum impact of th e pressure and forces is around where you have the largest head c ircumference on the skill.”

Crawford believed that misuse of the drug Pitocin increased th e natural forces of labor by causing too many contractions:

The use of Pitocin to the point where it resulted in too many contractions in a given period of time, something called tachysystole, resul ts in increased intrauterine pressure. There w as an IUPC utilized. That’s an intrauterine pressure catheter. So the pressure within the uterus could be accuratel y measured. And it was set and calibrated to have a baseline of 20 millimeters. B ut during the labor, because of the increased number of contractions and the increas ed intensity of the contractions, the pressure withi n the uterus did not come down to resting levels on many occasions and in fact, was as high as 40 or double the nor mal amount.

***

The impact of that, of too frequent contractions and pressure that is increased is that the blood doesn’t come through the uterus to the placenta when the uterus is contracting and is strongly contracting and is fr equently contracting, that results in interruption of blood flow and oxygen through t he uterus to the placenta and to the baby. And the end result of that is you ha ve a decrease in blood flow coming to the baby. So you have an ischemic compone nt from that type of abnormal condition. You also have a hypoxic component because the blood carries the oxygen. As a result of not getting enough ox ygen, the baby starts to use up its reserves and can become hypoxic and acidot ic if this problem, if this condition continues.

The excessive contractions can als o result in physical trauma w here the head is essentially used as a “battering ram,” especially when the pelvis has not been p roven to accommodate a particular sized baby and especially in first -time labor, which is usually longer and more intense.

At this point, the trial court interrupted the testimony and a sked why it was being presented with Crawford’s actual opinion instead of hearing evi dence that the medical literature supported the opinion. The court stated: “Essentially I am lo oking for something in the literature that says it caused, it can cause, not that it may, not that it could, not that there’s a possibility. That’s w hat I’m looking for.”

Plaintiff’s counsel then asked Crawford to review the package insert for Oxytocin, which warned that strong hypertonic or prolonged tectonic contraction s could result in deceleration of heart rate and fetal hypoxia. Fetal hypoxia as a result of exc essive uterine contractions was “a well understood phenomenon.” Crawford testified that Pitocin w as a high risk drug and the package insert specifically war ns that if given inappropriately can cause hypoxia. This was wellknown and every hospital that Crawford ever worked at had “Pito cin policy,” setting forth how the drug should be administered to avoid tachysystole and fetal distress. Crawford acknowledged that the insert did not necessarily mention stroke as the specific result of misuse, but did refer to hypoxia, which was a mechanism by which a stro ke can occur.-22- Crawford testified that a numb er of factors came into play in this case:

[T]he membranes were ruptured f or 29 hours before the baby was born. So the amount of amniotic fluid that the baby was in was very diminish ed. So the cord, the umbilical cord is not buffered, buffeted by the usual prese nce of amniotic fluid. So when the uterus contracts, there’s pressure on the c ord. And that pressure can lead to variable decelerations of the fetal heart. And there were numerous variable decelerations p resent. The impact of too fre quent and too strong uterine contractions also led to what’s called utero pla cental insufficiency in that there was a decrease in the amount of oxygen and blood flow going to the baby which results in hypoxia and ischemia. And as the uterus is being intensely affected by Pitocin and there are too frequent and too intense contractions, the baby’s head is being compressed.

Therefore, three factors were at play: the cord, the function o f the placenta and “the compressive effect of the uterine contrac tions on the baby itself.” She ex plained:

First of all, when you have a c ontraction, uterin e contractions are looked upon as the apnea of the unborn. The placenta acts as the baby’s lungs delivering oxygen to the baby. When there’s [sic] contractions that are too freq uent and too intense, there is a decrease in the amount of oxygen and blood flow that comes through the placenta because the uterus is being so constricted by the contractions. So the baby gets, has decreased oxygen, decreased blood flow. And tha t’s hypoxia and ischemia. And when the cord ge ts compressed and you get variab le decelerations, the heart rate goes down and there’s a decrease in blood flow a nd oxygenation being delivered to the baby because of compression of the cord. And then finally, when you have in the first stage of labor the, the uterus is co ntracting around the fetus and in particular, the head because the head is the leadi ng so-called battering ram that’s coming through to g et through to the birth canal. When you get into the second stage, then the compression on the baby’s head is fr om the bones of the pelvis. And when the baby’s head is large, the biparietal diameter is large, the baby’s head gets jammed and doesn’t progress. Then every contr action impacts on the baby’s skull and impacts on the pressure that’s being ex erted on the baby’s skull to the point where it increases to the point where, where it exceeds cerebral profusion pressure and you get disruption of blood flow in the brain, thus result in a stroke. [H II, pp 38-39.]

Crawford cited Kumar & Paes, Contralateral Cerebral In farction Following Vacuum Extraction , 21 Am J of Perinatology 15-17 (2 004) to support her conclusio n that mechanical birth trauma has long been associated with intracranial stroke due to the skull being subject to abnormal forces, especially when there is a history of difficul t labor. Crawford insisted that it was well recognized that subjectin g a baby’s skull to abnormal pressures can cause arterial stroke; it was not junk science. Upon questioning by the court , Crawford acknowledged that the Kumar article dealt with a vacuum extraction. The authors conc luded that mechanical birth trauma is a direct cause of intracranial arterial injury that c an then subsequently lead to stroke, including the natural forces of labor. Specifically: “‘In the absence of identifiable cause, the infarction may be considered due to the skull being subjected t o abnormal forces during the-23- birthing process especially when there’s a difficult labor.’” Crawford explained that force did not necessarily mean instrumentation like forceps or vacuum; it included the force of labor itself intensified with Pitocin.

When defense counsel was questioning Crawford regarding the me aning of the Kumar article, the trial court interj ected: “Just a minute. I know he disagrees with you and you disagree with him. And I have to decide who is right . . . . I’m going to tell you, I, I wrote all over this. This was a vacuum extraction and that’s not what happened with baby Figurski. So that’s really kind of where I’m at on this artic le.” The following exchange took place regarding the article:

THE COURT: This is a case report involving a vacuum extractio n. So when I read this, I take it in its entirety from the beginning to the end. I’m told it’s a vacuum extraction. So that’s what mechanical birth trauma [][means] to me. You tell me where in this article it describes mechanical birthtrauma as anything other than a vacuum extraction?

THE WITNESS: The next paragraph, the next sentence where it s ays the trauma, mechanical birth trauma, they say, has been recognized as a direct cause of intracranial arterial injury leading to ischemic or hemorrha gic stroke in the newborn. The trauma could result from the process of natural b irth or from assisted instrumentation with forceps or [vacuum]. So the auth ors are laying out the three types of mechanical birth trauma that can affect a ba by and lead to –

THE COURT: I just –

THE WITNESS: --stroke.

THE COURT: It says from th e natural birth process.

THE WITNESS: Yes. That’s without –

THE COURT: That’s one.

THE WITNESS: Yes, that’s without instruments.

THE COURT: Or wait a minute. You said three.

THE WITNESS: Right. Vacuum, forceps, and the natural forces of labor were the three.

THE COURT: I don’t know where you get three.

MR. FIEGER: It says it in t he last sentence, your Honor.

THE COURT: Mr. Fieger, don’t even. No.

MR. FIEGER: The las t sentence says it.-24- THE COURT: No. Mr. Fieger, you’re not to testify. You, and you don’t get to help your witness. I’m trying to understand. It says the trauma could result from the process of natural birth – to me, that’s one – or from assisted instrumentation with for ceps or – [vacuum] . . .

***

THE COURT: So in other words, how I take this is it could hap pen naturally. It could happen t o, God help us, any baby; not the Doctor’s fault.

MR. FIEGER: Judge, is that what we’re doing here?

THE COURT: Oh for heaven’s sakes. Okay. Five minutes becaus e you are not going to interrupt. Five minutes.

Crawford cited Amiel-Tison, Cerebral Damage in Full-Term New-Born, Aetiological Factors, Neonatal Status and Long-Term Follow-Up , 14 Biol Neonat 234-250 (1969), which concluded that inappropriate use of Pitocin caused problems in newborns, especially in babies who got stuck mid-pelvis (dystoci a). The article also looked t o fetal distress and the evidence of meconium stained amniotic fluid, which happened with plaintiff as well. Crawford explained that the purpose of the article was to describe the affected in fants. The author w as “looking at all affected infants and trying to describe the full spectrum of fi ndings in that group. The controls would be all normal newborns. S o the control group is perhaps unstated, but known.” Although Crawford’s affidavit says that too many contractions increase i ntracranial pressure and decrease in profusion of the brain, the article did not make that exact statement. Crawford testified that the Amiel-Tison article “sets the stage for the mechanism for i ntrapartum cerebral damage due to iatrogenic uterine hyperstimulation.”

Defense counsel pressed that a lthough the article suggested an injury, it did not “say if it’s a decrease in the blood flow and oxygen through the placen ta or whether or not it’s an increase in intracranial pressure that causes a slowdown in cer ebral profusion pressure.” When defense counsel emphasized that the article only implied that i njury may result, plaintiff’s counsel objected:

MR. FIEGER: Judge, objection. What are we doing here? What, where is it supposed to say that 100% o f the time it will? I thought we’re here, they don’t have a defense here in terms of this. This is not a legi timate Daubert hearing. This is something that they think they can get away [ sic] and there’s birth trauma. And this type of injury is so accepted in medici ne that it’s beyond belief that this is being questioned.

***

THE COURT: You have said that to me so many times. . . . Th is is my response. I can’t even count on two hands now how many times y ou’ve said that in writing, here, in chambers. You have, I don’t know, I guess in some ways tried to make it sound like this is the most ignorant thing that I’m doing; that what a fool who could fall for the defense’s argument. I find it some what insulting. I’m-25- trying to do my job. And you wanted me to rely on an Oakland C ounty Circuit Judge’s opinion. That’s not help ful. We’re going to keep goin g. And stop saying that this is accepted all over the place, all over the country in courts all over the country because you haven’t show n me that. And defense has nev er argued that it has to be 100% certainty. I certainly didn’t say that in my op inion setting this hearing. And I asked her what may meant. . . . I don’t want to hear you say that again. We’re going to finish this.

After a break, defense counsel continued to question Crawford about the Amiel-Tison article. The article described seizures as a reflection of bra in injury, but did not mention stroke. It discussed necrosis and death of the brain, however, which we re not uncommon in stroke. Crawford stressed that the article was from the 1960’s before there was advanced imaging. Upon questioning from the trial c ourt, Crawford explained that the article set the stage for finding that too many contractions cause an unsafe increase in intracranial pressure, but acknowledged that the article did not specifically say that:

THE COURT: Are you acknowledging that that’s not what the Tis on article says? I want to make sure my notes aren’t wrong. I’m not asking you what she’s saying in the article. I’m asking specifically are you acknowledging that’s not what the Tison article says?

THE WITNESS: I’m saying I should have had, as I said before, I should have had another footnote there which would be the Cushing.

THE COURT: Boy, you’re like some lawyers.

THE WITNESS: Excuse me?

THE COURT: Not wanting to answer the question. Is that what her article says?

THE WITNESS: No.

Crawford further explained tha t “Cushing’s response” is a prote ctive mechanism for when there was an increase in the intracranial pressure. The natural resp onse was to increase the blood pressure in the brain to maintain cerebral profusion. However, it works up to a point and if it fails then ischemic injury results.

Crawford also cited Towner & Ciotti, Operative Vaginal Deliver y: A Cause of Birth Injury or Is It? , 50 Clinical Obstetrics & Gyn, 563-581 (2007), which dealt wit h a vacuum extraction. Crawford explained th at the point of the article w as that when excessive forces are used, there can be excessive molding (adjustment of the bones o f the skull) and injury may result. When the baby is “stuc k,” especially a big baby in an unproven pelvis, and doctors simply increase the number and frequency of contractions, “it w ill get you nowhere.” Generally the scalp will reveal evidence of dystocia and trauma – bruisin g, swelling, and indentation. Crawford explained that “what Towner is telling us is look, the se babies have probably been in trouble and having head compression and problems before you eve n applied the vacuum or the forceps.” Although Towner’s article involved forceps and vacuu ms, “Towner’s point is very-26- often the damage is already ther e.” Crawford explained that gl obal hypoxic injury is not caused only by forceps or vacuums. During cross-examination, Crawford acknowledged that the article was a “medical analysis” where the authors looked at various re ported cases, which were primarily instrumented deliveries. Such operative vaginal deli veries would mean either forceps or vacuum. The article did not mention stroke, but mentioned c erebral palsy. The article did not state that fetal injuries that were associated with vaginal del ivery could be explained by the use of force to overcome cepha lopelvic disproportion.

Crawford referenced Volpe, Neurology of the Newborn (5 thEd) Saunders Elsevier (2008). Volpe was the chairman of pediatric neurology at Bosto n Children’s Hospital. Volpe referred to a number of factors that increase the baby’s chance s of having a stroke, including fetal distress, prolonged labor, prolonged rupture of the membr anes, infection, low amniotic fluid, and first time labor. The following exchange took place between plaintiff’s attorney and Crawford regarding the Volpe text wherein Volpe set forth a num ber of risk factors for perinatal arterial ischemic stroke:

BY MR. FIEGER:

Q . Does risk factor mean a cau se in your opinion, Doctor?

A . The clustering of multiple risk factors gives you a high, a high risk situation for the development of stroke. In other words, the m ore risk factors that you have, the more likely it is tha t those risk factors were th e cause of the stroke.

***

For example, perinatal arterial ischemic stroke is uncommon, v ery uncommon in normal spontaneous vaginal deliveries or cesarean s ections prior to labor. So the PAIS incidents with emergency [] cesarean sectio ns and with evidence of meconium, evidence for fetal distress, uh, non-reas suring fetal strips, prolonged seconds stage, prolonged labor, dystocia, all of that put together indicates that those are the, when those factors are present, t hose are the causative factors for the stroke in the ch ild. The more of those factors you have, the more likely it is that that’s the, that those are the causes for the child’s stroke.

The texts did not discuss asphyxia, although fetal heart rate a bnormalities and prolonged second stage of labor were li nked with asphyxia.

Crawford cited Lee et al, Maternal and Infant Characterist ics Associated With Perinatal Arterial Stroke in the Infant , 293 J Am Med Ass’n 723-729 (2005). The article did not test whether head compression caused PAIS; rather, it was a retrospe ctive controlled study. The article concluded that fetal h eart rate abnormalities were no l onger independently associated with perinatal arterial stroke. ButCrawford pointed out that 46 pe rcent of infants with stroke had fetal heart rate abnormalities compared with 14% that had no su ch abnormality, so fetal heart rate was still statistically significant. The article did not conclude that use of Pitocin was a risk factor for stroke, though Crawford opined that it was only the inappropriate use of Pitocin that was problematic. Crawford testified that “Oxytocin is widely u sed and most of the time it’s used properly. So it wouldn’t be surprising that you wouldn’t see an effect. It’s only when you have-27- improper use of the Pitocin that you get the increased pressure and increased compression.” Ultimately, Lee concluded that it was impossible to know the ca usal pathway to perinatal stroke. However, with three or more ris k factors, the odds of stroke wa s 1 in 200.

Crawford testified that, obviously, there could be no controll ed studies on injuring children; instead, they had to rely on animal studies. There w as no way to subject women in labor to excessive Pitocin to s ee what the result would be.

Crawford referenced articles that tested the effect of blood f low on fetal sheep. Harris et al., Cerebral and Peripheral Circulatory Responses to Intracranial Hype rtension in Fetal Sheep
, 64 Circulation Research 991-1000 (1989); Harris et al., Efficacy of the Cushing Response in Maintaining Cerebral Blood Flow in Premature and Near-Term Fetal Sheep, 43 Pediatric Research 50-56 (1998); O’Brien et al, Effect of Cephalic Pressure on Fetal Cerebral Blood Flow , 1 Am J Perinatology 223-226 (1984). Crawford explained that the articles revealed that “when you compress the head as the head is [] experiencing the impact of uterine contractions or being, acting as a battering ram coming through the pelvis, it can lead to or does lead to, and they determined that it leads to increased intracranial pressure and decreased cerebral profusion pressure” leading to “ischemic insult.”

The Harris article explained that intracranial pressure result ed in the body shunting blood away from non-vital organs in orde r to increase blood flow to t he brain. Crawford acknowledged that the article indicated tha t the Cushing’s resp onse was generally effective.

The O’Brien article was a study on the fetal lambs to observe the effect of pressure on the head. The following exchange took place:

THE COURT: . . . Thi s study, its conclusion wasn’t that this pressure and the change in the, on the head r esulted in a change in the bloo d such that ischemic hypoxia or stroke occurred.

THE WITNESS: Not the point of the study. The point of the study is to show, was to show that increased pressure on the head causes a decrease in cerebral profusion. You have to take the next step –

THE COURT: And cerebral profusion is?

THE WITNESS: Is the difference between, cerebral profusion pr essure is the difference between the incre ased pressure that’s applied ex ternally and the baby’s main arterial pressure. So the Cushing effect is one wh ereby the baby increases its blood pressure t o overcome this pressure –

THE COURT: Pressure on the brain. Right, I get that.

THE WITNESS: -- external pressure. Okay.

THE COURT: And your point is –-28- THE WITNESS: And the baby can do that up to a certain point. And then as this pressure gets more and more, the baby can’t respon d. It can’t increase its blood pressure any more. And what –

THE COURT: That’s not, that’s not what 14 goes to. Really, the only point.

THE WITNESS: Well –

THE COURT: It doesn’t, the article doesn’t go so far as to sa y exactly at what point this Cushing effect doesn’t work anymore and there’s going to be a stroke. That’s all I’m trying to get at with 14.

THE WITNESS: Okay, you, what it says is that you interrupt, t his kind of pressure can interrupt and does interrupt cerebral blood flow. Now if you do it long enough, which is not what they wanted to do – they just wa nted to show that

– THE COURT: No, please don’t –

THE WITNESS: -- this is an effect –

THE COURT: -- tell me you think if you do it long enough it’s going to happen. All I’m trying to figure out is 14. It, it never conc ludes if you do it long enough there’s going to be a stroke.

THE WITNESS: You have to go to –

THE COURT: All right, no. No.

THE WITNESS: -- other ar ticles. You have to build –

THE COURT: Dr. Crawford, please. I’m just trying to understand each article.

Defense counsel questioned Crawford on Sorbe et al., Some Important Factors in the Molding of the Fetal Head During V aginal Delivery – A Photographic Study , 21 Int’l J Gyn & Obstetrics 205-212 (1983), which dealt with molding. The article conclude d that neither the frequency of the contractions nor the length of stage 1 labor w ere of importance. However, Crawford believed a prolonged second stage of labor – which was three and a half hours in this case – was very significant. The article did not specifically state that increased molding causes stroke; instead the focus of the article was the mechanical for ces of labor leading to compression of the head. While molding can occur with natural labor, Crawf ord testified that “if you increase the number of contractions and have tachysystole and increased intrauterine pressure, you can have even greater mechanical forces of labor.”

Crawford discussed Lapeer et al., Fetal Head Molding: Finite Element Analysis of Fetal Skull Subjected to Uterine Pressu res During the First Stage of Labor , 34 J Biomechanics 1125--29- 1133 (2001), and how the size of the baby, first time birth, an d use of Oxytocin are factors that increase the risk of molding, which may result in stroke. The following exchange took place regarding the article and the effect of molding on an infant:

THE COURT: [Excessive molding may be a] causative factor, butit says may and that’s what I’m struggling with. Will is different to me than may.

THE WITNESS: Well medicine i s not always 100%. In other word s –

THE COURT: I’m not –

THE WITNESS: -- if you have a f ever and I give you an aspirin – THE COURT: Trust me, I’m not, stop. Stop. I’m not looking f or 100%, okay? Not 100%. I get that. Help me understand what this art icle is saying when it says may.

THE WITNESS: I think what they’r e trying to say is that moldi ng may be helpful to get the baby’s head through, but if you have obstruc tion, if you have dystocia and you get, uh, so much force and compression on the head that you get significant molding. That is not just molding, that’s signific ant molding. And that is not a good thing. Some babies may not be affected, but if you have a baby that has an intracranial injury where you’ve had that degree of molding which implies excessive forces, particularly during the first stage w here the uterus is compressing the head, that’s a cause.

MR. FIEGER: Are you through, your Honor?

THE COURT: Yes.

BY MR. FIEGER:

Q . Doctor, in medicine is there anything 100%?

A . Not, not that often.

Q . Are there people who smoke that don’t get lung cancer?

A . Yes.

Q . Does that mean smoking isn’t –

THE COURT: Don’t waste my tim e with that, Mr. Fieger.

MR. FIEGER: Well your H onor, you asked the question.

THE COURT: I said I ’m not asking for 100%.

BY MR. FIEGER:-30- Q . When medicine says may, does that mean in some instances if you subject a baby to those forces of labor, you can cause brain in jury?

A . Yes.

Q . Okay. Are there some babies who it may not affect?

A . Yes.

Q . But does that mean that since it can happen sometimes, it ma y happen sometimes and sometimes that it may not, that it’s okay to do i t?

A . The risk is that you will injure the baby.

Crawford acknowledged that the L apeer article was actually publ ished by an engine ering journal. The article concluded that exces sive head molding may result incranial birth injur ies, but did not attempt to answer whether the same forces that caused fetal hea d molding caused stroke. Its focus was on the first stage of l abor when the uterus was the “ deforming agent.”

Crawford testified as Clancy et al, Focal Motor Seizures Heralding Stroke in Full-Term Neonates , 1390 Am J Diseases in Children 601-606 (1985), which discussed strokes in full term babies. A seizure may be a sign of an infant having had a stro ke. Plaintiff had a seizure after birth. The article says that hypoxi a and ischemia can cause stroke.

Crawford rejected the notion that there was no recognition tha t hypoxia ischemic injury can cause stroke—”My knowledge is there’s ample evidence that s ays that it is. It’s not the only cause of a stroke, but it certainly is a well recognized cause of strokes . . . it certainly is a known causative factor.” Crawford pointed to Govaert et al., Diagnosis of Perinatal Stroke II: Mechanisms and Clinical Phenotypes , 98 Acta Pediatrics 1720-1726 (2 009) and Chabrier et al., Obstetrical and Neonatal Characte ristics Vary with Birthwei ght in a Cohort of 100 Term Newborns with Symptomatic and Arterial Ischemic Stroke , 14 J Eur Paediatric Neurol Soc’y 206- 213 (2010), for the notion that the bruising, swelling and mold ing of plaintiff’s head indicated trauma, which was a risk factor. The trial court asked – “I’m trying to understand what the trauma is.” The following exchange took place:

THE COURT: Wait just a minute. Wait a minute. Is there anyw here in here that I can understand what the trauma was that, that says was a cause of the perinatal stroke. That’s all I wanted to know. And if there i sn’t there isn’t.

THE WITNESS: I think the main, the point they made is the obv ious stroke related to those kind of traumatic insults [vacuum and f orceps] was not

common.
Crawford explained that excessive uterine contractions was simp ly another form of trauma that the baby’s head could experien ce. “So forceps, vacuum, excessi ve contractions impacting on the baby’s head is another form of trauma. You don’t need forceps. You don’t need vacuum extraction to have trauma to a baby’s head during labor.” Like wise, hyperstimulated labor is a force of labor or “mechanical trauma.”-31- Crawford acknowledged that the G ovaert article was largely obs ervational with no controls and therefore, no way t o see what caused the strokes. The article did not define trauma. Crawford explained that the Cha brier article explored the diffe rent mechanisms for stroke in big and small babies. There was no control group, but Crawford bel ieved that the risk factors were the same regardless of how the data was collected. Additionall y, not all strokes were immediately diagnosed. If a newborn demonstrated signs of stro ke, imaging was likely done quickly, whereas if there was a stroke in a different part of the brain, it may take months to see the effects. The article did not specifically say that increas ed intracranial pressure leads to decreased cerebral profusion a nd stroke, but Crawford noted tha t birth trauma and acute asphyxia are more common in big babies. Crawford believed that the arti cle stood for the position that “bigger babies have more strokes because they get stuck. They have the prolonged compression of their head.”

Crawford pointed to Filipiek et al, Focal Cerebral Infarction in the Newborn: A Distinct Entity , 3 Pediatric Neurol 141-147 (1987), which acknowledged that bi rth trauma was a cause of cerebral artery infarction eve n though it was not present in th e patient for that particular case.

Crawford explained that Hamid et al., Perinatal Arterial Ischemic Stroke: An Update with Literature Review , 58 J Pak Med Ass’n 395-399 (2008), also pointed to the factors contributing to stroke, includi ng: assisted deliveries, cesarean section, birth asphyxia, and intrapartum trauma. Crawford believed that the “more factors y ou have, the more likely it is that you’ll have a stroke due to those factors.” In this case, ther e was “excess uterine contractions, the effects of Pitocin leading to excessive molding and prolong ed and ongoing compression of the fetal head.” Crawford admitted the article was a literatur e review, not a sc ientific study. It referenced the Chalmers article regarding risk factors, but did not specifically conclude that increased intracranial pressure led to a decrease in cerebral p rofusion and a stroke. (H II, pp 226-228.)

Crawford testified that Cheong et al., Neonatal Arterial Ischem ic Stroke: Obstetric Issues , 14 Seminars Fetal & Neonatology Med 267-271 (2009), indicated that chorioamnionitis and prolonged rupture of the membranes were risk factors for pe rinatal ischemic stroke and “widely associated with cerebra l palsy.” Crawford acknowledged that the Cheong article did not specifically relate intracranial pressure to decreased cerebral blood flow and stroke, but she explained that it talked of overdosing with Pitocin, leading to prolonged tachysystole, which can cut off a baby’s oxygen. It was not a controlled study, but a review article looking at the obstetric factors in neonatal arterial ischemic stroke. It con cluded that although perinatal risk factors have been identified, the “ideology” of stroke remained unclear and further studies were needed. While the article did not list increased intracranial pressure as a risk of stroke, Crawford opined that it could be implied. M econium was not independentl y associated as a risk factor.

In concluding direct examinati on, plaintiff’s counsel asked:

Q . So a doctor such as yourself, if you see a, a, look at a med ical record such as in this case and look at Alexander Figurski’s course of labor and see the following: one, he has chorioamnionitis; two, a prolonged rupt ure of membranes; three, a prolonged second stage [of labor]; four, fetal distres s; five, emergency c--32- section and has a diagnosis of perinatal arterial ischemic stro ke at birth, what does a physician do to make diagnos is [] in the real world?

A . You gather information from the history and the physical, th e laboratory tests, the neuroradi ological imaging tests and put i t all together and make a diagnosis.

Q . And when you put all of that toge ther here, what was your co nclusion?

A . He had PAIS from, from an abnormal labor that was involved w ith excessive use of Pitocin and head compression . . .

Crawford explained that while not one particular individual article supported her theory, a combination of the articles and the information extracted the refrom supported her ultimate opinion.

Defense counsel asked Crawford to “forget about strokes” and p oint to literature that supported her opinion that increas ed intracranial pressure caus es a decrease in cerebral profusion pressure, leading to global hypoxic ischemic injury or diffuse hypoxic ischemic injury. Crawford cited the Harris article, for the notion that compress ion of the fetal head during normal labor may produce transient cerebral ischemia or decreased cere bral blood flow. None of the fetal sheep showed evidence of cerebral ischemia, but Crawford pointed out that the article demonstrated that “intracranial pressure will increase or can i ncrease more than the fetal arterial pressure. And this leads to cerebral or brain ischemia.” Esse ntially, the Cushing method would fail because the external pressure was too great. Although the study was not conducted to determine whether increased cranial pressure would increase fet al arterial pressure and produce ischemia, the author references studies to that effect. And al though none of the sheep suffered ischemia, “[t]heir study was just to show that in a short perio d of time you can get an interruption of cerebral blood flow with incr eased external pressure on the head.”

Defense counsel then presented Crawford with Raju et. al, Ischemic Perinatal Stroke: Summary of a Workshop Sponsored by the Nati onal Institute of Child Health and Human Development and the National Institute of Neurological Disorders and Stroke , 120 Pediatrics 609-616 (2007), which concluded that “there are no reliable pre dictors of ischemic perinatal stroke on which to base preventi on or treatment strategies.” B ut Crawford pointed out that the author also concluded that perinatal stroke is usually multifac torial. Crawford believed that politics caused the artic le to conclude as it did.

C. TRIAL COURT’S OPINION

After taking the matter under advisement, the trial court issu ed a lengthy opinion and order on August 21, 2013. The court noted that defendants did not dispute Dr. Crawford’s qualifications or whether expert testimony would assist the tri er of fact. Rather, defendants challenged the scientific basis underlying plaintiff’s causatio n theory.

The trial court first undertook a review of the literature in support of plaintiff’s causation theory as it pertained to the alleged hypoxic-ischemic injury.-33- The court found that Dr. Crawford relied on the FDA-approved p ackage insert for Pitocin, warning that overdosag e could result in hyperstimulati on of the uterus leading to fetal hypoxia, and that management of an overdose consists of immedia te discontinuation of Pitocin. The trial court noted that

while the package insert certain ly states that fetal hypoxia may result from a Pitocin overdose and associated uterine hyperactivity, it does not indicate the mechanism by which such an injury may occur. In particular, it fails to lead to the conclusion that the hyperstimulation caused by the use of Pitoc in will lead to increased intracranial pressure, decreased cerebral perfusion p ressure and a hypoxic-ischemic injury. Consequently, without more, one canno t rationally extrapolate Plaintiff’s causati on theory from the warnings cont ained on the insert.

The court found that although it is indisputable that a baby’s head can be likened to a battering ram, the literature cited by Dr. Crawford did not sup port a conclusion that hypoxicischemic injury of perinatal arterial ischemic stroke will occu r as a result of that mechanism.

The trial court rejected Crawf ord’s reliance on the Deaver, Etiological Factors in Cerebral Palsy , 28 Bull NY Acad Med 532-536 (1952), because it was an observa tion review and concluded that trauma, especially when a child was large an d the pelvis was small, could cause injury. The article did not describe the mechanism of any injury. The trial court noted that “[a]lthough the [sic] Dr. Crawford has made reference to cephal opelvic disproportion, she referenced it only as [a] factor contributing to the mechanism of injury (increased intracranial pressure) and not as the mechan ism of injury or trauma on its o wn.”

The trial court rejected Crawfor d’s use of the Towner article because it was an observatory review and not a scientific study. It did not deal with the causal mechanism alleged in this case, but only with operative vaginal deliveries. “Thi s article does little to support Plaintiff’s causation theory.”

The trial court also rejected the Harris articles as well as C ushing, Concerning a Definitive Regulatory Mechanism of the Vasomotor Centre Which Controls Blood Pressure During Cerebral Compression , 12 Bull Johns Hopkins Hosp 290-292 (1901); and Paton et al., Harvey Cushing and the Regulation of Blood Pre ssure in Giraffe, Rat and Man: Introducing “Cushing’s Mechanism” , 94 Exper Physiology 11-17 (2009), noting the “significant gap ” between the scientific findings in those articles and Crawford’ s conclusions. As an example, the trial court pointed to Crawfor d’s acknowledgement during cross- examination that the Cushing response was highly effective in sustaining cerebral blood flow . Additionally, the purpose of the study was the evaluation of the Cushing response in fetal sheep . The trial court noted that “[o]verall, the articles/studies [] lend essentially nothing to Dr. Crawford’s conclusion/opinion that Cushing response may be ove rcome, opening the door for bra in damage.”

The trial court rejected the O’Brien article for Crawford’s pr oposition that simulated uterine contractions in fetal sh eep reduced cerebral perfusion. By Crawford’s admission, none of the sheep suffered hypoxic-ischemic injury. The study indicate d that redistribution of cerebral blood flow was unclear. “Conseque ntly, without more, the O’Bri en study/article fails to draw the causal link asserted in the Plaintiff’s theory that forces of labor can lead to increased-34- intracranial pressure and a subs equent decrease in cerebral bra in perfusion pressure resulting in a stoke or hypoxic-ischemic injury.”

The trial court noted that while the Sorbe and Lapeer studies of molding showed that Pitocin-induced labors were more likely to result in molding, t hey did not conclude that excessive head molding could resu lt in injuries such as hypoxia , ischemia, or stroke.

The trial court also rejected the Sato article and Schwarcz et al., Pressure Exerted By Uterine Contractions on the Head of the Hu man Fetus During Labor in Perinatal Factors Affecting Human Development , in Pan Am Hearlth Org, Sci Pub No 185 (1969), pp115-126, because the articles addressed pressures exerted on the fetal h ead during uterine transactions, but they did not conclude that such forces were likely to cause hyp oxic-ischemic injuries. The trial court noted that the latter Sch warcz article only indicated “po ssible” damage to the brain and that further study was necessary.

The court noted that s eparate from Dr. Crawford’s affidavit, p laintiff submitted additional articles: Hayes et al., A Case-Control Study of Hypoxic-I schemic Encepholopathy in Newborn Infants at > 36 Gestation , 208 Am J Obstetrics & Gyn (2013); and Heuser et al., Tachysystole in Term Labor: Incidence Risk Factors, Ou tcomes, and Effect on Fetal Heart Tracings, 209 Am J Obstetrics and Gyn 1-6 (2013. The trial court noted that whil e Hayes and Heuser found that excessively frequent uterine con tractions was a risk factor ass ociated with hypoxic ischemic encephalopathy, and use of Pitoci n was a strong predictor of ex cessively frequent uterine contractions during labor (or t achysystole), the articles did n ot link those contractions with hypoxic-ischemic injury.

Turning to the causation theory regarding perinatal arterial i schemic stroke (PAIS), the court found that Dr. Crawford and the cited articles only ident ified a number of risk factors associated with PAIS, and mad e no findings that would support p laintiff’s theory of causation.

The trial court rejected the Clancy article because although i t noted “that the etiology of stroke in three of the infants was intrapartum hypoxia-ischemia , it makes no finding or description as to the mechanism causing the hypoxia-ischemia or how global/diffuse cerebral injury could cause a focal injury.”

The trial court also rejected the Kumar article for the propos ition that natural childbirth could cause stroke as a result of the skull being subjected to abnormal forces. The use of a vacuum extraction was abnormal force and the st udy indicated th at doctors should only implicate vacuum application “as a cause of stroke when they have ruled o ut other potential causes.” Likewise, the trial court rejected Roessmann et al., Thrombosis of the Middle Cerebral Artery Associated with Birth Trauma , 30 Neurology 889-892 (1980), because it involved forceps (p 2 1 n 11).

The trial court rejected the G ovaert article because “[a]lthou gh the article identifies ‘asphyxia’ as a cause of arteria l ischemic stroke, it says noth ing as to the mechanism causing the underlying asphyxia.” Likewise, the trial court rejected Ment et al., Perinatal Cerebral Infarction , 16 Annals Neurol559-568 (1984), because “although cereb ral infarction was noted to-35- be attributable to perinatal as phyxia, it makes no findings in relation to Plaintiff’s causal mechanism.”

The trial court rejected the C habrier article because althoughthe article concluded that “increased size is a risk factor associated with stroke, the article makes no mention of increased compression of the fetal head or hyp oxic-ischemic injury caused by such pressure.”

The trial court rejected the remaining articles and texts – in cluding, Lee, Volpe, Cheong, because “they either 1) do not address, relate or study the Pla intiff’s causation theory or 2) they identify only risk factors associ ated with PAIS rather than anytype of determined cause.”

The court found that plaintiff failed to specifically address the factors enumerated in MCL 600.2955(1).

Subsection (1)(a): The basis of plaintiff’s experts’ opinions had not been subject to scientific testing. “Instead, at most, the studies presented b y the Plaintiff, when taken as a whole, stand for a belief that a logical assumption can be made that e xcessive uterine contractions could possibly increase intracranial pressure to a point and for a le ngth of time which one could assume would potentially cause brain damage. However, an ‘assumption’ is not the equivalent to an actual cause and effect link.”

Subsection (1)(b): The opinion was not subject to peer review . None of the articles discuss plaintiff’s causal mechanism.

Subsections (1)(c) and (d): The literature did not establish a methodology or technique for testing or supporting the pro ffered opinion. “The inability to assess the Plaintiff’s experts’ opinion against generally accepted standards applicable to meth odology or technique as well as a potential error rate further militate against the reliability o f the opinion itself.”

Subsections (1)(e): There was no evidence that the theory pre sented was generally accepted within the relevant medical community. Instead, the l iterature demonstrates that the “theory needs or warrants more study.”

Subsection (1)(f): The trial court wrote:

[I]t is clear the Plaintiff’s expe rts have not presented a reli able basis for their opinions. Rather, the Plainti ff has relied on nothing more tha n the ipse dixit of the plaintiff’s experts. In particul ar, as repeatedly noted in the Court’s review of the literature, the articles and studi es presented by the Plaintiff either completely fail to stand for the proposition they were cited for or their findi ngs and discussion stop considerably short of the conclusion for which they were c ited. Therefore, the gap between the data and the expert’s opinion is only bridg ed by the expert’s
own statements.

Subsection (1)(g): Plaintiff’s e xperts did not present a reli able basis for their opinions, and there was no evidence thei r opinions had been relied on out side the context of litigation.-36- The court found that plaintiff failed to meet his burden of de monstrating that his experts’ causation opinions were reliable:

Because the Plaintiff has failed to carry his burden to demons trate that the opinion of his causation experts are reliable, this Court must exclude the testimony. In making this finding this Court is absolutely cog nizant that its function is not to seek truth, weigh evidence or assess credibi lity. The Court fully recognizes that fulfilling its gatekeeper role under MRE 702 an d MCL 600.2955 does not require it to hold a minitrial on causation or to dete rmine what causal theory is definitely present in any given case. However, under MCL 600.2955 and MRE 702, it is incumbent on this Court to ens ure that the P laintiff’s expert causation testimony meets the baseline threshold inquiry and th at the opinion underlying the testimony is rationally derived from a sound foundation. That being said, because the literature and scientific evidence reli ed on by the Plaintiff fails to actually stand for the conclusions that Plaintiff’s experts purportedly draw from it, this Court finds that the gap between Dr. Crawford’s t estimony/opinion and the scientific/medical evidence and literature from which s he extrapolates it is too great. This gap not only makes the opinion unreliable it a lso indicates that it is irrelevant (not probative of a fact at issue) and will not a ssist the trier of fact to understand the evidence.

D. ANALYSIS

The trial court’s opinion perha ps would have been appropriate had the trial court been sitting as the trier of fact. H owever, the trial court went we ll beyond her gatekeeping function and, instead of determining whether Crawford could offer an opinion on causation, the trial court actually resolved the issue of causation. No doubt the trial court was encourag ed by defendants, who were also functioning under an erroneous view of plaintiff’ s burden and the trial court’s gatekeeping function. In one of its motions in limine, defenda nts wrote that “a plaintiff has the burden of proof as to proximate causation and must present subs tantial evidence that excludes other hypotheses with a fair am ount of certainty.” That burdendoes not exist at the Daubert hearing; instead, plaintiff’s burden at the Daubert hearing was to show that Crawford was qualified to render an opinion on causation and that her opinio n was reliable and relevant. Such an inquiry must focus on principles and methodology, not the conclusions they generate .” Daubert, 509 US at 594-595 (emphasis added

. ) The trial court failed to heed Chapin’s admonishment that, as gatekeeper , the trial court’s analysis mu st not hinge on discovering absolute truth or resolving genuine scientific disputes. Chapin , 274 Mich App at 139. Although the trial court repeatedly stated that it was aware of its role to not seek absolute truth behind the science, the record reveals that it simply failed to heed its o wn warning. The trial court undertook an examination of plaint iff’s literature in an attemp t to search for the “truth.”

Particularly glaring is the trial court’s failure to refer to Crawford’s Daubert testimony in its opinion and order. Crawford e xplained that n o single artic le supported her theory, but that the sum of all the articles supported her conclusion that injudicio us use of Pitocin, compounded by-37- the other factors at birth, resulted in compression of plaintif f’s head and lack of blood flow to the brain, or ischemia. 10 The trial court also completely ignored that Crawford’s opini on was based, not only on the literature provide d, but on her own extensive p rofessional experience.

While the Daubert hearing was underway, the partie s referred to an Oakland Circui t Court case that dealt with similar causation theories. That ca se – VanSlembrouck v Halperin
, unpublished opinion of the Court of Appeals, issued October 28, 2014 (Docket No. 309680) – was decided while this appeal was pending. While an unpublishe d opinion of this Court lacks precedential value, the analysis therein is germane, helpful, i nstructive, and persuasive for the case at bar and we adopt its reasoning as our own. MCR 7.215(C )(1); Paris Meadows, LLC, v Kentwood , 287 Mich App 136, 145 n 3; 783 NW2d 133 (2010).

The child in VanSlembrouck had a host of neurological problems. The plaintiffs’ experts opined that birth trauma caused the child’s disabilities, while the defendants maintained that the child suffered from a genetic abnormality. The plaintiffs’ exp erts acknowledged that the child’s brain never fully developed, but urged that she would not have suffered significant deficits absent birth trauma. VanSlembrouck , slip op, pp 1-2. There was no debating that the child’s birth was traumatic. While her h ead spontaneously delivered, h er shoulders became stuck and doctors had to perform maneuvers to deliver her. She weighed 1 0.5 and had an Apgar score of one. She was limp, blue and unrespo nsive and had a fractured c ollarbone. Id. at slip op, p 2.

Like the case at bar:

Plaintiffs’ experts posited th at Pitocin-induced hyperstimulati on of Kimberly VanSlembrouck’s uterus, combined with Markell’s large size, com pressed Markell’s head during the last hour of Kimberly’s labor. Accor ding to their theory, head compression resulted in cerebral ischemia (lack of adequate blood flow to the cerebrum), bleeding into the brain itself, and perm anent brain damage attributable to the trauma. [ Id. at slip op, p 2.]

The trial court c onducted a four-day Daubert hearing on defendants’ motion in limine to prevent the experts from offering such a theory of causation. The tria l court found the plaintiffs’ experts were qualified and their opinions w ere scientific ally reliable. Ultimately, a jury found in favor of the plaintiffs. Id. at slip op, p 3.

On appeal, this Court looked at the evidence presented by the plaintiffs at the Daubert hearing. Like in the case at bar , the plaintiffs offered Dr. C rawford, Dr. Yitzchak Frank, Dr. Gabriel, and Dr. Barry Schifrin. Id. at slip op, pp 9-10.

Crawford testified that it was well known that trauma may occu r when a baby’s head acts as “a battering ram” against the mother’s pelvis and that the t rauma may be manifested as a brain bleed. This was especially t rue in large infants.

10 Even if there was no global in jury, the uncontested fact remai ns that plaintiff suffered a perinatal arterial ischemic stroke.-38- In her opinion, Markell’s brain injury was attributable to “[l] ack of oxygen and lack of blood flow.” She elaborat ed: “This baby was banged thro ugh the pelvis for a long period of time. The uterus was stimulated to contract ex cessively” by Pitocin. “[W]here you have so frequent contractions that you do n’t provide oxygenated blood to the baby’s brain ... [y]ou cause increased pressure, the blood can’t profuse the brain.” [ Id. at slip op, p 10.]

When confronted with the incongruence of her theory with the AC OG Task Force on Neonatal Encephalopathy and Cerebral Pals y, Crawford rejected the report and found that it was the medical community’s self-serv ing attempt to cut down on lawsuit s. Id. at slip op, p 11.

Dr. Gabriel similarly testified that the child’s brain injury occurred as a result of lack of blood supply, or “ischemic abnormality to the brain.” This was brought about by pressure on the child’s skull during labor a nd delivery. He explained:

“by virtue of reduced blood flow to the brain because the high pressure, the abnormal, the non-physiological [pressure] on the skull plates, what we call the calvari[um], during the delivery process increases the pressure in the brain which in turn reduces the ability of th e arteries to supply the brainwith blood. The artery pressure has to fight against the increased pressure in the bra in. As a consequence blood flow diminishes and the cerebral blood flow diminishes to a point where ischemia can occur. It can occur global or [diffused] or focal or regional or multifocal.” [ Id. at slip op, p 12.]

Like in the case at bar, Gabriel supported this theory with ref erence to Volpe, Neurology of the Newborn . Finding the actual passage in the text helpful for review, t his Court bolded the text from Volpe: “‘ when intracranial pressure increases, cerebral perfusion pressu re decreases; if intracranial pressure increases markedly, cerebral perfusion pressure declines below the lower limit of autoregulation and CBF [cerebral blood flow] may be impaired severely .’” Id. at slip op, p 13.

Dr. Schifrin testified that ischemia resulted in a decrease of blood flow, depriving the brain of oxygen.

Maximum oxygen exchange between baby and mother occurs when th e uterus is not contracting. “Th e greater the amount of uterine activity ... the greater the interference of oxygen availability.” When the uterus contracts, Dr. Schifrin testified, the baby raises its b lood pressure “slightly to over come the rise in pressure in the uterus,” thereby maintaining adequate blood flo w to the brain. Usually, this mechanism allows a baby to preserve enough blood flow during contractions to protect the brain from injury. But the baby’s ability to autoregulate flow in this manner may be overwhelmed “if the pre ssure is so high either because of the duration of the contractions” or when the “added effects of pushing” increase the amplitude of the contractions. Ischemia occurs when the duration or intensity of the uter ine contractions overcomes the baby’s ability to raise its blood pressure to comp ensate for the pressure being e xerted by the uterus.-39- In such circumstances, the baby may suffer an ischemic (rather than an hypoxic) injury. [ Id. at slip op, p 14.]

As in the case at bar, the electronic fetal monitor strip indic ated that the uterine activity was excessive “due to the adm inistration of Pitocin.” Id.

Unlike the case at bar, the defendant in VanSlembrouck offered a number of their own experts in an effort to challeng e the plaintiffs’ causation the ory. Id. at slip op, pp 14-15.

In affirming the trial court’s decision to allow the plaintiff s to present their causation theory, this Court first noted:

that the following § 2955 factors are not germane to this case: “(a) Whether the opinion and its basis have been s ubjected to scientific testing and replication,” and “(d) The known or potential error rate of the opinion and its b asis.” Defendants do not explain how plaintiffs’ theories of fetal head compressi on could be subjected to scientific testing and replication in human childr en or evaluated regarding an “error rate.” Nevertheless, several medical articles submitted by plaintiffs describe scientific studies involving fetal sheep. These studies lend support to plaintiffs ’ causation theory . [ Id. at slip op, p 22 (emphasis added).]

The Court then looked to the two factors in subsection 2955 whi ch require the trial court to examine the scientific literature, particularly (b) which asks whether the opinion has been subject to peer review, and (g) whether the opinion has been relied upo n by experts outside of litigation. The Court noted the volume of literature supplied in the case. Id. at slip op, p 22. Many of these same articles and treatises wer e presented in the case at bar:

Multiple peer-reviewed articles supplied to Judge Nichols lent credence to plaintiffs’ experts’ causation theory. Specifically, several articles and textbook excerpts substantiated that a traumatic birth process can cause fetal head compression, which in turn may resu lt in brain bleeds and permanent neurological injury. Dr. Crawford’s thesis that in the presence of cephalopelvic disproportion the fetal head acts as a “battering ram” against the maternal pelvis emanates from a 2007 article published in a peer-reviewed obste trical journal. This article corroborates that brain bleeding may result from h ead trauma:

Virtually all significant fetal head and neck injuries that are associated with vaginal (both spontaneous and operative) delivery can be e xplained by the use of force to overcom e cephalopelvic disproportion. Cephalopelvic disproportion is a relative term as each specific maternal fetal pair is unique; unique fet al size and positioning in the maternal pelvis and unique pelvis size and shape. As the fetal head descends in to the pelvis, it can be likened to a battering ram taking the brunt o f the pelvic resistance leading to molding to allow passage. Molding of the fetal cranium eventually can overcome the disproportion, but potentia lly at a cost. Excessive molding leads to distortion of the relatively f ixed-40- tentorium and falx structures and subsequent tearing leading to subdural hemorrhages....

The scalp is the fetal defense to the resistance of the birth c anal tissues, both soft tissue and the bony pelvis. With significant resistan ce and repetitive pushing against this resistance, shear forces can be generated leading to scalp trauma and cephalohematomas. [Towner and Ciott i, Operative Vaginal Delivery: A Cause of Birth Injury Or Is It? , 50 Clinical Obstetrics & Gynecology 563, 571 (2007).][ 11 ]

A peer-reviewed medical journal article published in 1983 simil arly explains that “[t]he mechanical forces of labor subject the infant’s head to considerable compression, shearing, and molding. Intrapartum and neonatal de ath can occur from mechanical trauma to the brain during birth.” Sorbe & Dahl gren, Some Important Factors in the Molding of th e Fetal Head During Vaginal Delivery—A Photographic Study , 21 Int’l J Gynaecology & Obstetrics 205 (1983).[ 12 ]

***

The Volpe textbook also supports that mechanical trauma can damage a fetus’s brain:

In this discussion, ... “perinatal trauma” refers to those adve rse effects on the fetus during labor or delivery and in the neonatal period t hat are caused primarily by mechanical factors . Thus specifically excluded are the disturbances of labor and delive ry that lead principally to hyp oxicischemic brain injury.... (Never theless, overlap between mechan ical trauma and the occurrence of hypoxic-ischemic cerebral injury is important to recognize because perinatal mechanical insults mayresult in primarily hypoxic-ischemic cerebral injury, probably secondary to disturbances of placental or cerebral blood flow.) [Volpe, Neurology of the Newborn at 813 (italics in original, bold added).][ 13 ]

In a 1952 article, the author s pecifically identifies “trauma due to cephalopelvic disproportion” as a cause of cerebral palsy, elab orating:

Most of the traumatic causes of brain injury at birth may be co nsidered as physiologic. Just being born is a difficult hurdle to pass. In the birth process, the baby uses its head for a battering ram propelled b y strong uterine contractions. When the child’s head is large and the pe lvis small,

11 Exhibit 9 to Crawford’s affidavit in this case.

12 Exhibit 15 to Crawford’s affidavit in this case.

13 Exhibits 28 and 30 to Crawford’s affidavit in this case.-41- the natural safeguards which allow the skull to conform to the shape of the birth canal may be insufficient to protect the brain from injur y. [Deaver, Etiological Factors in Cerebral Palsy , 28 The Bulletin: NY Acad Med 532, 536 (1952).][ 14 ]

***

These articles generally validate that cephalopelvic disproport ion and difficult, traumatic delivery can cause fetal distress, compression of the fetal skull, brain bleeds, and neurologic injury satisfying MCL 600.2955(b) and (g ). [ VanSlembrouck , slip op, pp 22-24 (some emphasis in original).]

The Court noted that the articles were primarily written by phy sicians other than the testifying experts. Id. at slip op, pp 24-25 n 17.

The remaining factors -- subsections § 2955(e) and (f) – dealtwith whether the proffered theory was generally accepted. “Although defendants’ experts c laimed that plaintiffs’ causation theories had been debunked or were no longer accepted as scient ifically valid, defendants produced no literature supporting this argument. Given that pl aintiffs’ literature submissions corresponded to their causation th eory, Judge Nichols did not a buse his discretion in finding the data ‘legitimate.’” Id. at slip op, p 25 n 18.

In addressing the scientific reliability of the plaintiffs’ pr offered opinion under MRE 702, this Court noted that

Trial courts must carefully evaluate whether adequate data supp orts an expert’s opinion and whether the opinion qualifies as reliable in the re levant expert community. Part of this process involves consideration of alte rnate scientific explanations for a given result. . . . However, this does not mean that a trial court is empowered to decide which of two competing and adequately su pported scientific theories should prevail. [ VanSlembrouck , slip op, pp 26-27.]

The Court noted that General Electric Co v Joiner , 522 US 136, 142; 118 S Ct 512; 139 L Ed 2d 508 (1997) mandated that a trial court “close the evidentiary g ate” only when “an expert’s conclusions lack any genuine rel ationship to the science allege d to support them.” VanSlembrouck , slip op, p 27. The Court then noted how the science and fact s appeared to support both parties’ causation theories. Id. “Faced with this conflict among the experts, the trial court did not abuse its discretion by deciding to admit b oth theories, finding both supported by peer-reviewed literature and c redible expert opinion, thereb y qualifying as reliable.” Id. at 28.

The Court then rejected the defendants’ attempt to impeach the plaintiffs’ theory with evidence that Dr. Gabriel’s cau sation testimony had been deemed inadmissible as unreliable by numerous other panels of the Court. The Court noted that “ Daubert and Craig instruct that a

14 Exhibit 8 to Crawford’s affidavit in this case.-42- trial court’s admissibility decision must flow from the record created during the reliability hearing.” Id. at slip op, p 28. The Court also found unavailing the defendan ts’ attempt to use Craig as res judicata of the issue of w hether Pitocin caused birth tr auma. The Court noted that in Craig, Dr. Gabriel’s opinion lacked e videntiary support. “Unlike in Craig , the peer-reviewed literature in this case supports that head compression can caus e brain injury” and the “plaintiffs’ experts had no difficulty explai ning the head compression mecha nism.” Id. at pp 29-30.

Looking to VanSlembrouck , we adopt its reasoni ng and conclude that plaintiff in this ca se presented sufficient scientifically reliable data to advance it s causation theory. While defendants maintain that there is no known cause of PAIS and that further study is needed, they do not dispute, however, that there are many identified factors that are found in PAIS cases. And while it is plaintiff’s burden to show that the experts’ opinions are sound, it is notable that defendants failed to offer their own expert at the Daubert hearing to debunk Crawford’s theory. Even if plaintiff’s theory can be deemed “shaky,” “[v]igorous cross-examination, presentation of contrary evidence, and careful i nstruction on the burden of pro of are the traditional and appropriate means of attacking sh aky but admissible evidence. . . . These conventional devices, rather than wholesale exclusion under an uncompromising ‘genera l acceptance’ test, are the appropriate safeguards where the basis of scientific testimony meets the standards of Rule 702.” Daubert, 509 US at 596. Again, Chapin cautions:

An evidentiary hearing under MRE 702 and MCL 600.2955 is merelya threshold inquiry to ensure that the trier of fact is not called on to re ly in whole or in part on an expert opinion that is only masquerading as science. The co urts are not in the business of resolving scientific disputes. The only proper rol e of a trial court at a Daubert hearing is to filter out expert evidence that is unreli able, not to admit only evidence that is unassailable. T he inquiry is not into whether an expert’s opinion is necessarily correct or universally accepted. The inquiry is into whether the opinion is rationally derived from a sound foundation. [ Chapin 274 Mich App at 139.]

The trial court, in exceeding her role as gatekeeper, attempted to find absolute truth in the literature. Instead, the matte r should have been presented to the trier of fact.

V. PLAINTIFF’S DAMAGES EXPERT

Defendants argue that the trial court abused its discretion wh en it determined that Gamboa could offer an opinion as t o plaintiff’s damages when he did not have sufficient knowledge, education, training, or experience in the field of e conomics. Because he lacked such basic knowledge, defendants clai m that his methodology was unre liable. We disagree.

Defendants filed a motion in limine to preclude Gamboa from te stifying because his opinion was based on “junk science” and contrary to MRE 702 and MCL 600.2955. Gamboa hoped to testify at trial regardi ng plaintiff’s potential educa tional attainment, potential future earnings, and current and future cost of hiring a home health a ide. Defendants however, claimed that Gamboa was not qualified to offer such an opinion. He did not have a degree in economics and thus lacked the knowledge of basic economic principles, inc luding how to calculate educational attainment or wage growth rates. Gamboa did not kno w what a “Mincer equation”-43- was, which was the most widely accepted standard in analyzing aperson’s earning potential. He practiced self-proclaimed “vocational economics,” but because h e lacked a proper understanding, defendants maintained that Gamboa’s methodologies were flawed and unreliable. Although he published and presented talks on these methods, these activitie s were limited to litigation. Gamboa’s inflated growth factor provides for a 5.2% increase in wages regardless of education. He used the same rate to calculate the future cost of medical c are by assuming the attendants will likewise experience a 5.2% growth rate in wages. To the extent that Gamboa relied upon legitimate sources, there was a “ yawning analytical gap” betwee n the data and his opinion.

The issue was debated at a June 13, 2013 hearing. The trial c ourt noted: “I don’t disagree that the argument shoul dn’t be, and I won’t let it be, about whether [the growth rate] should be 3% or 5.2%. Absolutel y not. It’s whether the opinio ns he’s given are based on reliable science and – and principles and peer review and not j ust part of litigation. I don’t care if it were 10% if it could be backed up by all of that.”

A. GAMBOA’S DEPOSITION TESTIMONY

Gamboa received a Bachelors of Science in Education, with a ma jor in History and a minor in English in 1966. A year later in 1967 Gamboa complete d a Masters Degree program in Guidance and Counseling, with an emphasis in Vocational Counsel ing. Gamboa went on to receive a Ph.D. in Guidance Counseling, with an emphasis on Voc ational Counseling, as well as Research and Statistics. He had also taken post-doctoral work. Some of it was closely related to vocational counseling. His MBA had no relation to his Ph.D., b ut was very similar in terms of research. Gamboa completed a t en-month course with an econometrician (economist with strong statistical background), which focused on the economics of disability and the development of the first work-life expectancy tab les for persons with disabilities

. Gamboa did not have a degree in economics. He acknowledged th at the American Economic Association was the main association for economists. The following exchange took placed during Gamboa’s deposition:

Q . The American Economics Associ ation defines different fields of research within economics.

Correct?

A . I believe that is correct.

Q . And one of the research areas within the field of economics is something called, “labor economics”?

A . Yes. That, I’m familiar with.

Q . Okay. The term “vocational economics”, is that a term of art for your company, or is that one of the areas or fields of research with in economics recognized by the American Economic Association?-44- A . It’s the former. Just as you have persons who identify them selves as “home economists”, I don’t believe the American Economics Assoc iation recognizes home economists or home economics as a subset of the field of labor economics or the subset of economics, per se.

But I can tell you that “vocational economics” is a term that w e began using because we felt that it really described what we we re doing.

When you look at an earning capacity loss, particularly in cas es of partial disability, it’s about 90 percent vocational and maybe 10 percent economics.

When you’re looking at a case such as this, it’s more vocation al, really, than economics.

Gamboa prepared between 200 and 300 vocational economic assess ments on an annual basis. Nearly all of the cases were litigation related. They prepared two to three Life Care Plans reduced to present day value.

Gamboa testified that in generating his report for this case h e first interviewed Mary Figurski to determine the parents’ level of education. The mother had an associate’s degree and worked as a paralegal. The father had a high school diploma an d worked as a sales consultant. Gamboa also asked about plainti ff’s particular limitations. Th e mother reported that the fouryear-old plaintiff had spastic hemiplegia and significant weakn ess in the right arm and leg. He walked with a brace around the foot and frequently fell. Plain tiff had an individualized educational program. He spoke in four to five word sentences and was in a special needs school where he received occupational therapy, speech therapy, and phy sical therapy. Plaintiff was eight to 10 months behind his peers developmentally. He was no t yet potty trained. The mother reported that she did not believe plaintiff would ever live ind ependently. Plaintiff could not dress himself and was limited in terms of daily living. After speaking with the mother and reviewing plaintiff’s medical information, Gamboa determined th at plaintiff was “catastrophically injured” and would “never live independently, and who will be dependent on others throughout the life expect ancy.” Gamboa explained that even though plaintiff was only 10 months behind his peers, that would likely change, “because what happens with youngsters who are as severely impaired as he is, they tend to grow into t he disability, which means that the older they get and the more they’re compared to their peer group, the further down the bellshaped curve they fall.”

Gamboa was asked to assess plaintiff’s earning capacity loss and to perform a present value calculation on the Life Care Plan prepared by Dr. Yarkony . Michigan was unique in defining future value and present value using a simple interestdiscount factor. Gamboa explained that he used the approach but that the legislature ma y have recently changed that law so that interest could be calcu lated in a more “conventional ma nner,” as understood in the financial community. Under new law, the deduction will be by c ompound interest and present value calculations will go down significantly. He explained th at earning capacity varies greatly depending on the use of simple interest versus compound interes t,. The conventional approach would show 2.1 to 2.8 million dollars and Michigan’s approach w ould yield 6.2 to 8.3 million.-45- Gamboa explained that he used a five-step process in making a calculation. The first step was to define a base dollar figure that reasonably represented earning capacity without any injury. He could not use actual earnings because he was dealin g with a four-year-old. Instead, he used a proxy or an approximati on of plaintiff’s earning capa city, or so-called “ human capital,” which typically involved examining the parents’ education and t he individual’s intellect and physical ability. Plaintiff’s pre-injury earning capacity was the average earnings of males with no disability who have either a h igh school diploma or an Assoc iate’s Degree. The range was $47,000 to $59,000. It was an age-earning cycle. At age 19, t he earnings would be at $19,000 or the low $20,000’s, but then those earnings would go up every ye ar, reflecting an increase in human capital as a result of education and experience. Gamboa was not familiar with the “Mencer equation.” He acknowledged that there might be other m ethods for calculating future earnings (i.e.. regressions), but he believed his method was va lid and reliable, keying in on gender, capacity to complete formal education, age, and the abs ence of disability had there been no injury. There were certainly more variables to consider, bu t Gamboa believed that generic data was the preferred method. G amboa would then take the wage and adjust it for future growth and then bring it down using the Michigan statute to reduce the present day value. Gamboa defended the use of growth f actor rate at 5.2 percent.

Step two of the analysis was the pre-injury statistical work-l ife expectancy, which varies as a function of age, gender, and education. The work-life exp ectancy range was 36.6 years for high school graduates and 37.7 y ears for an Associate’s Degree. The numbers took into account all of the variables that c ould cause an individual not to be e mployed, including, death, disability, recession, etc.

Step three would be the amount of wages somebody could earn wi th the current disability. Gamboa determined th at there was no earning capaci ty and “that this is not an individual who will ever work c ompetitively.” Gamboa was basin g this on information provided by doctors and was not coming to a medical opinion on whether p laintiff was disabled. The medical doctor had opined that plaintiff would need 24-hour car e for the rest of his life.

Step four would be to calculate i njury work-life expectancy, w hich would again be zero.

Step five was the present value calculation and, in Michigan, that involved a traditional present value calculation, a future calculation, using simple i nterest of five percent. For computing future value, the beginning cash flow had a growth fa ctor of 5.2 percent attached. So the future cash value for when plaintiff turned 19 grows from $ 47,000 to $105,000. The 5.2 percent represented the increase in wage and fringe benefits fo r 60 years. Gamboa looked to 1951 to 2011. The growth rate was not specific to inflation, w hich would have been 3.7 percent. Wages typically came in a point h igher than inflation and “wage growth is inappro priate to use. You really need to be using increa ses or growth specific to com pensation, which takes into consideration both wages and fri nge benefits.” “I’m not using a wage growth factor. I’m using a compensation growth factor and that’s 5.2 percent.” Gamboa use d the Consumer Price Index for the years 1951-2011 to predict i nflation. It was not possible to accurately forecast future inflation.

Gamboa believed that his offset method of using “what today’s dollars are” was appropriate. He assumed that the rate of growth and the discount on percentage was the same.-46- His 5.2 percent historical growth for 1951-2011 did not differe ntiate for educational levels. Gamboa did not know whether wag es had grown from 1951-2011 at the same rate for people with just high school education versus people with a Bachelor’s degree. He believed that wage growth for high school graduates has kept pace with inflation. “The basis for that is that if all workers experienced increases in compensation greater than infl ation, I see no reason why I would expect high school graduates would not have.” When askedwhether he could point to any publications that forecasted a growth rate of 5.2 percent, Gamboa responded: “I can’t think of any. That doesn’t mean it doesn’t exist. I don’t know what the forecast has been, but I certainly have not seen anything.” While there were some gover nment reports, Gamboa was not familiar with them. The earning capacity loss was in the range of 2.2 million to 2.9 million dollars.

Gamboa also calculated the present day value of the Life Care Plan. Gamboa calculated the growth rate for home healthcare workers at 3.2 percent from plaintiff’s age six to 12 and then 5.2 percent for when plaintiff was 12 to 25. One was considere d short term and the other was long term. (G Dep, pp 100-105.) He was not aware of the speci fic hourly wage in Michigan for certified nursing assistants; the Life Plan used agency data (G Dep, pp 116-117).

B. TRIAL COURT’S OPINION

After taking the matter under advisement, the trial court issu ed a written opinion and order on August 7, 2013, denying defendants’ motion in limine t o exclude plaintiff’s economic expert.

The court rejected defendants’ argument that plaintiff was req uired to obtain an expert exclusively from the field of labor economics to meet the requi rements of MRE 702 and MCL 600.2955. Dr. Gamboa’s knowledge, skill, and experience were s ufficient to meet the requirements of MRE 702. The tri al court noted that Gamboa’s m ethod had been accepted by other courts, including the Oakland Circuit Court in the VanSlembrouck case. “Of particular relevance in this case is Gamboa’s knowledge, skill and experie nce dealing with the economic aspects related to vocational issues.” The trial court also no ted that Gamboa had written a number of published artic les directly on point.

The court found that Dr. Gamboa’s opinion also met the require ments of MCL 600.2955. The court found that Gamboa’s methods were subject to decades o f research, had been subjected to peer review, and used generally accepted standards and metho ds. “The Court agrees with Plaintiff’s argument that general acceptance is but one of the factors to be considered in the analysis and that disagreement i s to be expected and encouraged .” Any known or potential error was not relevant to the inquiry. The trial court also acknowle dged that damage calculations were not necessary except in the context of litigation, so it was no wonder that Gamboa’s methodology was created for use in litigation.

The trial court concluded:

Gamboa’s education and experience provides him with specialize d knowledge pertaining to the immediate and ongoing needs of pers ons with-47- disabilities in finding and maintaining employment. His educat ion and experience enable him to assess anindividual’s loss of lifetim e earnings.

He does not have a degree in economics. A degree in economics is not a prerequisite to being qualified as an expert in the area of los s of earnings as a result of an injury. His vocational expertise qualifies him to testify as to the impact of the Plaintiff’s loss of lifetime earnings and work-li fe expectancy. His expertise involves knowledge of statistics and how disabilities impact a person’s ability to perform work and earn money. These are the skills G amboa has used for over twenty years.

The Court agrees with Gamboa that forecasting future earnings is not an exact science. Furthermore, “general acceptance” does not requ ire that 100% of the community accept this methodology. Or, that he have a degr ee in economics.

This Court is convinced that Gamboa’s methodology is sufficien tly reliable to satisfy MRE 702 and MCL 600.2955(1). While Defenda nts assert evidence as to why an individual should apply the methodologies of labor economics instead of vocational economics, it is not the Court’ s province to decide which is preferable. That is for the jury to decide. I nstead, the Court must limit its review to its gatekeeping obligations and ensure that the testimony that will be introduced to the jury will assist it in understanding the evidence or determining a fact in issue. Gilbert, supra

.

C. ANALYSIS

Unlike with Crawford where defendants conceded that she was qu alified to offer an opinion, the primary issue here is Gamboa’s qualification to of fer his expert opinion on plaintiff’s future wage loss. As previously stated, “[t]he adm ission of expert testimony requires that (1) the witness be an expert, (2) there are facts in evide nce that require or are subject to examination and analysis by a competent expert, and (3) the kno wledge is in a particular area that belongs more to an expert than to the common man.” Surman , 277 Mich App at 308. The so-called “trilogy of restrictions on expert testimony” include s a searching inquiry into “qualification, rel iability, and fit.” Elher , slip op, p 8.

Unlike with the causation expe rt, the trial court clearly unde rstood her role as gatekeeper. Gamboa was qualified as a vocational rehabilitation expert. He held a number of degrees, including a Master’s in Vocationa l Counseling and Ph.D. in an a rea that included vocational counseling and education. Gamboa also received an MBA and test ified that he liked to focus on statistics. Gamboa had been with Vocational Economics Inc. in one capacity or another since 1977. His work there n ecessarily included o ffering expert opin ions on the cost o f future care and compensation loss. He was a prol ific writer in the area of ear ning capacity loss and work-life expectancy. As the tr ial court aptly noted:

In this case, the relevant community is a broad one; one that includes any discipline that might be able to accurately and reliably offer a calculation of Plaintiff’s lost future earnings and medical costs in present d ay dollars. Neither-48- MCL 600.2955(1) nor this Court is concerned with labels used to characterize a particular field of expertise. More importantly, the Court is concerned with ensuring that the proffered testimony “will assist the trier of fact to understand the evidence or to determine a fact in issue . . .” MRE 702. Ther efore, the relevant community in this case includes both labor economics as asserte d by Defendants and vocational economics as asserted by Plaintiff. It is not i mperative that one have a degree in economics. The Court acknowledges that Dr. Ga mboa’s testimony will not be purely economic in nature. He will offer to the trier of fact his vocational expertise on the expected impact of the Plaintif f’s disability on his annual earnings and work-life expectancy.

Moreover, although defendants did not like Gamboa’s method, th ere was nothing unusual about his calculating the loss of lifetime earnings by looking to what plaintiff would have earned absent an injury, what he was capable of earning with the injury, and the present value of the difference. The trial court’s d etailed and thorough opinion cl early reveals that her goal was not to resolve whether Gamboa’s method was the correct one, but whe ther he was entitled to offer his opinion at all. In rejecting defendants’ claim that Gamboa ’s method was unreliable, the trial court noted:

Defendants are highly critical of Gamboa’s use of the 5.2% comp ensation growth factor and the method in which it was derived. Plaintiff respo nds that simply because Defendants disagreed with Gamboa’s methodology is not a basis for precluding him from testifying. Rather, their disagreements sh ould be the subject of cross examination. Plaintiff argues that the process of det ermining lost future compensation and reducing to present value dollars is nothing n ew and Defendants’ complaints do not undermine the reliability of Gamb oa’s methodology. The Court agrees with Plaintiff’s argument.

The trial court correctly concl uded that the differing methods of calculating plaintiff’s damages was best left to the ultimate trier of fact.

VI. CONCLUSION

In Docket No. 318115, we reverse the trial court’s order that granted defendants’ motion in limine to exclude plaintiffs’ causation experts from testify ing and granted partial summary disposition on plaintiff’ s perinatal claims.

In Docket No. 319086, we affirm the trial court’s order denyin g defendants’ motion in limine to exclude defendant’s da mages expert from testifying.

We remand for further proceedings not inconsistent with this o pinion. As the prevailing party, plaintiff may tax cos ts. MCR 7.219. We do not retain j urisdiction.

/s/ Henry William Saad /s/ Donald S. Owens /s/ Kirsten Frank Kelly