Opinion ID: 149189
Heading Depth: 3
Heading Rank: 2

Heading: Application of Standards to Dr. Hoffman's Testimony

Text: The district court determined that Dr. Hoffman's testimony regarding ASD causation was insufficiently reliable under Daubert to warrant admission of that testimony at trial. The district court identified errors in Dr. Hoffman's differential etiology analysis at both the rule in and rule out steps. Specifically, the district court determined that Dr. Hoffman fail[ed] to show how, by `scientifically valid methodology,' traumatic brain injury could ever be a possible cause of autism in anyone. Hendrix, 255 F.R.D. at 598. The court also found that Dr. Hoffman failed to compile `a comprehensive list' of all possible causes of ASD and accordingly that by failing to include all of the causes currently theorized in the medical literature in his `comprehensive list' of the possible causes of ASD, Hoffman failed to `rule out' all possible causes but one. [9] Hendrix, 255 F.R.D. at 597-98. We agree with the district court that Dr. Hoffman failed to rule in traumatic brain injury as a possible cause of ASD. Because our holding in that regard is a sufficient ground upon which the district court ruling may be affirmed, we need not address the district court's decision that Dr. Hoffman failed to rule out other known or plausible causes of ASD. Dr. Hoffman's sole support for his theory that, in general, traumatic brain injury can cause ASD came from certain medical textbooks and epidemiological studies submitted by Dr. Hoffman. The district court carefully considered all of the materials cited by Dr. Hoffman and concluded that none of these works come close to providing useful evidence of a definitive [10] causal link between traumatic head injuries and autistic disorders, [11] and none provide even marginal support for Hoffman's theory of a relationship between abnormal [cerebral spinal fluid] pressure and problems with cerebellum pressure, leading to autism. Id. at 600-01. We have carefully and exhaustively reviewed the literature cited by Dr. Hoffman and conclude that the district court's conclusion with regard to each piece of literature was reasonable. We hold that the district court reasonably concluded that none of the literature supported the reliability of Dr. Hoffman's proffered physiological process, and that none of the literature supported Dr. Hoffman's opinion that a traumatic brain injury like GP's could have caused or contributed to the development of ASD. Thus, we conclude that the district court was reasonable in determining that the literature overall does not provide the necessary support for Dr. Hoffman's opinions to render those opinions admissible under Daubert. Rather than duplicating the district court's persuasive analysis of the literature provided by Dr. Hoffman, see Hendrix 255 F.R.D. at 600-03, we will focus on those pieces of literature emphasized by Hendrix on appeal. At oral argument, Hendrix's counsel stated that the most compelling literature discussing the physiological process by which traumatic brain injury could cause autism is a chapter in a textbook edited by Evenflo's medical expert Dr. Joel Morgan. See Gerry A. Stefanatos & Wilson Q. Joe, Autistic Disorder, in Textbook of Clinical Neuropsychology, 185-260 (Joel E. Morgan & Joseph H. Ricker, eds., 2008). We read this chapter carefully and failed to discern any suggestion that brain damage resulting from post-birth traumatic brain injury can cause autism spectrum disorders. We also saw no support for Dr. Hoffman's theory that abnormal cerebral spinal fluid pressure in the cerebellum could cause ASD. The chapter states that certain learning and memory patterns found in autistic individuals have been interpreted as reflection of cerebellar pathology, but also notes that studies have shown that frontal lobe and basal ganglia are also involved in learning a memory, and that [c]onsequently, these findings could not rule out an explanation in terms of a frontal-striatal dysfunction rather than anomalies of frontal-cerebellar circuits. Id. at 202. Further on in the chapter, the authors discuss the role of the cerebellum in ASD in general, and note that histological studies of the autistic brain have consistently implicated reduction of Purkinje cells of the cerebellum. Id. at 221. They do not, however, opine as to what might cause such a reduction of those cells. While these statements provide some support for the idea that the cerebellum is linked to autism in a very general sense, they offer no reliable support for Dr. Hoffman's theory that a traumatic brain injury like the one G.P. suffered could cause or contribute to the development of ASD. We found no mention at all in the chapter of Dr. Hoffman's proposed physiological process involving abnormal cerebral spinal fluid pressure leading to ASD. Notably, although the chapter catalogues the known etiological factors involved in ASD, the section titled Etiological considerations does not mention acquired trauma in the perinatal brain. Id. at 213-17. The section discusses genetic factors at length, and then goes on to list extrinsic factors such as: viruses; the presence of other neurological conditions, such as epilepsy; birthing complications; teratogenic substances, such as cocaine; and autoimmune factors. Id. The section fails to mention traumatic brain injury, and the authors qualify even the factors they do list by noting that studies directed to examining etiologic factors in [autism] have suffered from limitations due to small sample sizes, inadequate specification of diagnostic categories, and significant heterogeneity of the autistic population. Id. at 217. Hendrix's counsel also noted as particularly persuasive an article titled Late Neurologic and Cognitive Sequelae of Inflicted Traumatic Brain Injury in Infancy. Barlow et al., Late Neurologic and Cognitive Sequelae of Inflicted Traumatic Brain Injury in Infancy, 116 Pediatrics, Aug. 2005. The article describes a variety of neurologic impairments, including many of the impairments from which G.P. suffers, found in children with inflicted traumatic brain injury (e.g., shaken baby syndrome). Id. at e174. While Hendrix criticizes the district court for discounting the article based on the distinction between inflicted (non-accidental) and accidental traumatic brain injury, the article itself supports the notion that the two types of injuries are distinct. For instance, the article notes that mortality rates for infants with inflicted traumatic brain injury are greater than those for infants whose injuries were accidental. Id. at e174. The article also self-limits its findings by pointing out the small sample size, the need for further study, and that the study lacked a control group. Id. at e184. In fact, the authors mention that previous similar studies used children with an accidental traumatic brain injury as control subjects against which to compare those subjects with inflicted injuries. Id. Moreover, although one patient in the study developed autism spectrum disorder, the authors note that the ASD patient may have had significant exposure to alcohol in utero. Id. at e183. The district court identified these shortcomings and noted that significantly, nothing in the study purports to show or explain the physiological process by which brain injury produces autism. Hendrix, 255 F.R.D. at 601. The court therefore concluded that this study was insufficient to support Dr. Hoffman's assertion that the literature supports his theory of causation or even a general causal link between accidental traumatic brain injury and ASD. We cannot say that this determination was an abuse of discretion. We found the most direct statement supporting the theory that traumatic brain injury can cause ASD in a textbook submitted by Dr. Hoffman that was not brought to our attention on appeal. That textbook states: Considerable precedent for deleterious effects of various perinatal insults on organizational events is provided by studies with experimental animals. Initial studies of later cortical neuronal development in undamaged areas adjacent to ischemic cortical injury in human infants show dendritic aberrations that could contribute importantly to subsequent cognitive deficits and epilepsy. It is a clinical truism that some children affected by one or more perinatal insults may exhibit neurological sequalae that are more severe than might be predicted from the extent of injury recognized by the usual brain imaging or neuropathological techniques. Volpe, Human Brain Development in Neurology of the Newborn at 82. In other words, this textbook provides some support for the idea that even minor injuries sustained by newborn brains can result in more severe neurologic impairments than one would expect from the initial extent of the injury. The textbook does not, however, link such injuries to ASD, or provide any support for Dr. Hoffman's theory of ASD causation involving abnormal cerebral spinal fluid pressure. We are satisfied that the district court did not abuse its discretion in concluding, based on the literature Dr. Hoffman himself provided, that there is no reliable support for Dr. Hoffman's assertion that perinatal and neonatal intensive care follow-up literature does support the association between injury to the developing brain, including traumatic brain injury, and later occurrence of autism spectrum disorder. [12] Because Dr. Hoffman offers no other scientifically reliable basis for his opinion, his testimony is the type of speculation, conjecture, or inference that we have cautioned district courts not to admit. Rider, 295 F.3d at 1202. Hendrix attempts to sidestep the deficiencies in the medical literature by focusing on Dr. Hoffman's experience and training. Merely demonstrating that an expert has experience, however, does not automatically render every opinion and statement by that expert reliable. As an Advisory Committee Note on Federal Rule of Evidence 702 states: If the witness is relying solely or primarily on experience, then the witness must explain how that experience leads to the conclusion reached, why that experience is a sufficient basis for the opinion, and how that experience is reliably applied to the facts. The trial court's gatekeeping function requires more than simply taking the expert's word for it. Committee Notes on Rules2000 Amendment (quoting Daubert v. Merrell Dow Pharms., Inc., 43 F.3d 1311, 1319 (9th Cir.1995)). Taking the expert's word for it is precisely what Hendrix suggests the district court should have done in this case; however, we have previously recognized that `[n]othing in either Daubert or the Federal Rules of Evidence requires a district court to admit opinion evidence that is connected to existing data only by the ipse dixit of the expert.' See McClain, 401 F.3d at 1244 (quoting Joiner, 522 U.S. at 146, 118 S.Ct. at 519 (1997)). Dr. Hoffman has not provided a reliable basis, derived by the scientific method, for concluding that traumatic brain injury can cause ASD. We decline to conclude that the district court abused its discretion in failing to admit Dr. Hoffman's testimony based on his experience alone. Because the medical literature adduced by Hendrix supports neither Dr. Hoffman's theory of causation involving abnormal cerebral spinal fluid pressure nor his ultimate opinion that a traumatic brain injury like G.P.'s can cause autism, and because Dr. Hoffman offers no other scientifically reliable basis for his opinion, [13] we hold that the district court did not abuse its discretion in concluding that Hendrix failed to establish general causation to support Dr. Hoffman's opinion. That is, Hendrix has failed reliably to rule in traumatic brain injuries like G.P.'s as a plausible cause of autism. Because this is a sufficient basis on which to affirm the district court's ruling excluding Dr. Hoffman's testimony, we need not address the district court's decision that Dr. Hoffman also failed to rule out other possible causes. The district court held: Hoffman's claim that he ruled out genetics as a potential cause of [G.P.'s] ASD based on [G.P.'s] normal Fragile X tests ignores the possibility of other genetic conditions as a cause. Given the plethora of genetic theories for autism, ruling out Fragile X as a possible cause of [G.P.'s] ASD far from eliminates all genetic causes of his ASD, let alone the other multitude of factors that have been linked to autism or ASD. Hendrix, 255 F.R.D. at 598 (footnotes omitted). The medical literature indicates that there are a dizzying array of other factors that have been mentioned as possible causes, including as many as 90 gene mutations that could play a role in the development of autism. See Frank Polleaux & Gean M. Lauder, Toward a Developmental Neurobiology of Autism, 10 Mental Retardation and Dev. Disabilities Research Rev. 303, 309, 310-12 (2004). Dr. Hoffman conceded in his deposition testimony that, unless one of the genetic chromosome anomalies that is known to cause autism is identified, medical science simply does not know what causes autism. Obviously, in such a situation, the task of ruling out other plausible causes is extremely complex. In light of our decision that Dr. Hoffman failed to reliably rule in his theory of ASD causation, we need not in this case venture into the quagmire of attempting to define the parameters of a reliable process of ruling out other possible causes of autism.