Bennet Omalu is a star of the silver screen and in the minds of conspiratorial thinkers everywhere. Actually Will Smith stood in for Omalu in the movie Concussion (2015), but Smith’s skills as an actor bring out the imaginary best in Omalu’s persona.
Chronic Traumatic Encephalopathy (CTE) is the name that Bennet Omalu, a pathologist, gave to the traumatic brain injuries resulting from repeated concussions experienced by football players. The concept is not particularly new; the condition of dementia pugilistica had been described previously in boxers. What was new with Omalu was his fervid imagination and his conspiratorial view of the world. The movie Concussion actually gives an intimation of some of the problems in Omalu’s scientific work. See, e.g., Daniel Engber, “Concussion Lies: The film about the NFL’s apparent CTE epidemic feeds the pervasive national myths about head trauma,” Slate (Dec. 21 2015); Bob Hohler, “BU rescinds award to ‘Concussion’ trailblazer,” Boston Globe (June 16, 2016).
Omalu has more dubious claims to fame. He has not cabined his unique, stylized approach to science to the subject of head trauma. Although Omalu is a pathologist, not a clinician, Omalu recently he weighed in with observations that Hillary Clinton was definitely unwell. Indeed, Bennet Omalu has now made a public nuisance of himself by floating conspiratorial theories that Hilary Clinton has been poisoned. Cindy Boren, “The man who discovered CTE thinks Hillary Clinton may have been poisoned,” Wash. Post (Sept. 12, 2016); Christine Rushton, “‘Concussion’ doctor suggests without evidence that poison a factor in Clinton’s illness,” Los Angeles Times. (Sept. 13, 2016).
In the courtroom, in civil cases, Omalu has a poor track record for scientific rigor. The United States Court of Appeals, for the Third Circuit, which can be tough and skeptical of Rule 702 expert witness exclusions, readily affirmed an exclusion of Omalu’s testimony in Pritchard v. Dow Agro Sciences, 705 F. Supp. 2d 471 (W.D. Pa. 2010), aff’d, 430 F. App’x 102, 104 (3d Cir. 2011). In Pritchard, Omalu was caught misrepresenting the statistical data from published studies in a so-called toxic tort case. Fortunately, robust gatekeeping was able to detoxify the proffered testimony.
More recently, Omalu was at it again in a case in which a welder claimed that exposure to welding and solvent fumes caused him to develop Parkinson’s disease. Brian v. Association of Independent Oil Distributors, No. 2011-3413, Westmoreland Cty. Ct. Common Pleas, Order of July 18, 2016. [cited here as Order].
James G. Brian developed Parkinson disease (PD), after 30 years of claimed exposure to welding and solvent fumes. It is America, so Brian sued Lincoln Electric and various chemical companies on his theory that his PD was caused by his welding and solvent exposures, either alone or together. Now although manganese in very high exposures can cause a distinctive movement disorder, manganism, manganese in welding fume does not cause PD in humans. Omalu was undeterred, however, and proceeded by conjecturing that welding fume interacted with solvent fumes to cause Brian’s PD.
At the outset of the case, Brian intended to present testimony of expert witnesses, Bennet Omalu, Richard A. Parent, a toxicologist, and Jordan Loyal Holtzman, a pharmacologist. Parent commenced giving a deposition, but became so uncomfortable with his own opinion that he put up a white flag at the deposition, and withdrew from the case. On sober reflection, Holtzman also withdrew from the case.
Omalu was left alone, to make the case on general and specific causation. Defendant Lincoln Electric and others moved to exclude Omalu, under Pennsylvania’s standard for admissibility of expert witness opinion testimony, which is based upon a patch-work version of Frye v. United States, 293 F. 1013 (D. C. Cir. 1923).
Invoking a quirky differential diagnosis, and an idiosyncratic reading of Sir Austin Bradford Hill’s work, Omalu defended his general and specific causation opinions. After briefing and a viva voce hearing, President Judge Richard E. McCormick ruled that Omalu had misapplied both methodologies in reaching his singular opinion. Order at 8.
Omalu did not make the matter easy for Judge McCormick. There was no question that Brian had PD. Every clinician who had examined him made the diagnosis. Knowing that PD is generally regarded as idiopathic, with no known cause, Omalu thought up a new diagnosis: chronic toxic encephalopathy.
When confronted with the other clincians’ diagnoses, Omalu did not dispute the diagnosis of PD. Instead, he attempted to evade the logical implications of the diagnosis of idiopathic PD by continually trying to change the terminology to suit his goals. Judge McCormick saw through Omalu’s semantic evasions, which bolstered the case for excluding him at trial.
Madness to His Method
In scrutinizing Omalu’s opinions, Judge McCormick found more madness than method. Omalu claimed that he randomly selected studies to rely upon, and he failed to explain the strengths and weaknesses of the cited studies when he formed his opinion.
Despite his claim to have randomly selected studies, Omalu remarkably managed to ignore epidemiologic studies that were contrary to his causal conclusions. Order at 9. Indeed, Omalu missed more than half the published studies on welding and PD. Not surprisingly, Omalu did not record his literature search; nor could explain, in deposition or at the court hearing, his inclusionary or exclusionary criteria for pertinent studies. Id. at 10. When confronted about his “interaction” opinions concerning welding and solvent fumes, Omalu cited several studies, none of which measured or assessed combined exposures. Some of the papers flatly contradicted Omalu’s naked assertions. Id. at 9.
Judge McCormick rejected Omalu’s distorted invocation of the Bradford Hill factors to support a causal association when no association had yet been found. The court quoted from the explanation provided by Prof. James A. Mortimer, the defense neuroepidemiologist, at the Frye hearing:
“First, the Bradford Hill criteria should not be applied until you have ruled out a chance association, which [Omalu] did not do. In fact, as I will point out, carefully done epidemiologic studies will show there is no increased risk of Parkinson’s disease with exposure to welding fume and/or solvents, therefore the application of these criteria is inappropriate.”
Order at 11, citing to and quoting from Frye Hearing at 318 (Oct. 14, 2015).
When cornered, Omalu asserted that he never claimed that Mr. Brian’s PD was caused by welding or solvents; rather his contention was simply that occupational exposures had created a “substantial increased risk” of PD. Id. at 14. Risk creation, however, is not causation; and Omalu had not even shown unquantified evidence of increased risk before Brian developed PD. The court found that Omalu had not used any appropriate methodology with respect to general causation. Id. at 14.
Undaunted, Omalu further compromised his credibility by claiming that Bradford Hill’s factors allowed him to establish specific causation, even in the absence of general causation. Id. at 12. Omalu suggested that he had performed a differential diagnosis, even though he is not a clinician, and as a pathologist had not evaluated any brain tissue. Id. at 10. The court deftly saw through these ruses. Id. at 11.
Judge McCormick’s conclusion should be a precautionary lesson to future courts that must gatekeep Omalu’s opinions, or Omalu-like opinions:
“In conclusion, we agree with the Defendants that while Dr. Omalu’s stated methodology in this case is generally accepted in the medical and scientific community, Dr. Omalu failed to properly apply it. He misused and demonstrated a lack of understanding of the Bradford Hill criteria and the Schaumburg criteria when he attempted to employ these methodologies to conduct a differential diagnosis or differential etiology analysis.”
Id. at 16. Gatekeeping is sometimes viewed as more difficult in Frye jurisdictions, but the exclusion of Omalu shows that it can be achieved when expert witnesses deviate materially from scientifically standard methodology.
 See Bennet I. Omalu, Steven DeKosky, Ryan Minster, M. Ilyas Kamboh, Ronald Hamilton, Cyril H. Wecht, “Chronic Traumatic Encephalopathy in a National Football League Player, Part I,” 57 Neurosurgery 128 (2005); Bennet I. Omalu, Steven DeKosky, Ronald Hamilton, Ryan Minster, M. Ilyas Kamboh, Abdulrezak Shakir, and Cyril H. Wecht, “Chronic Traumatic Encephalopathy in a National Football League Player, Part II,” 59 Neurosurgery 1086 (2006).
 See, e.g., Marianne van der Mark, Roel Vermeulen, Peter C.G. Nijssen, Wim M. Mulleners, Antonetta M.G. Sas, Teus van Laar, Anke Huss, and Hans Kromhout, “Occupational exposure to solvents, metals and welding fumes and risk of Parkinson’s disease,” 21 Parkinsonism Relat Disord. 635 (2015); James Mortimer, Amy Borenstein & Laurene Nelson, Associations of Welding and Manganese Exposure with Parkinson’s Disease: Review and Meta-Analysis, 79 Neurology 1174 (2012); Joseph Jankovic, “Searching for a relationship between manganese and welding and Parkinson’s disease,” 64 Neurology 2012 (2005).