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undermine the legitimacy of workers’ experiences. Scientific uncertainty around the cause of symptoms stood in vivid contrast to the persistence with which office employees asserted the authority of their experiences.
Sick building syndrome revealed the inability of science—in this case, toxicological models—to adequately represent the complex relationships between office workers and their environment.
Following the lessons of sick building syndrome, it is important to critically interrogate the material processes making CTE both an embod- ied experience and an elusive object of scientific knowledge-making. The production of uncertainty around CTE grows out of the assumption that more precise research will eventually reveal the “truth” about whether repetitive brain trauma causes CTE pathology and symptoms. Such an assurance, however, ignores how the brain supports, complicates, and resists the production of knowledge in ways contingent on specific mate- rial processes, which may or may not be perceptible via dominant neuro- scientific practices. There is no guarantee that brain processes will neatly coincide with scientific paradigms (such as dose-response curves or threshold limit values3) that expect bodies to react predictably and con- sistently to harm. The inherent challenge in conceptualizing CTE lies in the recognition that neural matter itself often refuses to be fully knowable or predictable (Pitts-Taylor 2016).
In this way, the major dilemma emerging from my analysis so far is that the context of uncertainty in which we come to know (and not know) CTE did not emerge from a cosmic void and is not manufactured out of thin air. While actively structured by human actors invested one way or another in the outcome of neuroscientific findings, uncertainty around CTE still comes from somewhere. The brain is not a blank slate on which scientists can project uncertainty about CTE to suit their interests;
nor do objective neuroscientific practices discover matter and processes that are “already there,” passively waiting to be captured by the scientific gaze (Pitts-Taylor 2016). Uncertainty emerges through the active struc- turing of what is known and knowable, but also through the brain’s mate- rial complexity that resists coherence or standardization.
CTE is, therefore, a phenomenon encapsulating the intersections of the discursive and the material: on the one hand, scientists shape “what CTE is” by establishing diagnostic criteria and applying neuroscientific
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techniques; on the other hand, brain matter has the capacity to continu- ally transform and shape experiences in ways defying neuroscientific clas- sification. Like sick building syndrome, CTE is defined by the tensions between how imperfect systems of scientific knowledge can inscribe meaning onto the body and the unpredictable, unrelenting materiality of human experience. These tensions are illustrated through defining char- acteristics of CTE that both support and resist uncertainty: latency, imperceptibility, and multiplicity.
Latency and Imperceptibility
If CTE materializes as a progressive condition, this means that associated neurodegenerative processes occur gradually with symptoms typically presenting years or decades after exposure to brain trauma (Montenigro et al. 2014). Such a conception requires that CTE, both in its neuro- pathological development and in its diagnosis, takes time. There is con- siderable lag between exposure to injury and emergence of symptoms, but also between the onset of lived symptoms and postmortem diagno- ses. The temporal dimensions of CTE reflect what Murphy (2013) calls the politics of latency. In medicine, latency can be conceived as a period of incubation through which illness and disease gradually materialize in the body and become perceptible over time. Yet latency is not a guaran- tee: any potential state of being can emerge, remain unrealized, or escape scientific classification. As such, latency induces a crucial gap in knowledge- making practices that influence neuroscientific conceptions of CTE. The temporal variability with which CTE materializes in the brain and potentially impacts athletes’ everyday experience complicates the creation of reliable timescales of cause and effect. The inability for neuroscience to detect or measure abnormal production of tau protein in real time facilitates uncertainty regarding the temporal relationships between injury exposure, symptoms, and pathology onset.
The production of uncertainty around CTE is similarly enabled by domains of imperceptibility. Imperceptibility and uncertainty are related phenomena; that which lies outside the boundaries of perceptibility can be represented as non-existent or uncertain. CTE exemplifies important
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distinctions between what material relationships might exist within and between bodies and what can be perceived via technoscientific practice.
The condition’s proposed link to asymptomatic, subconcussive brain impacts by definition constitutes a domain of imperceptibility. These impacts are not substantial enough to induce acute symptoms, but some studies suggest that they might contribute to cumulative neurophysiolog- ical damage associated with CTE (Montenigro et al. 2017; Tagge et al.
2018). If subconcussive impacts are linked to the gradual development of CTE, then the material consequences of these injuries are initially imper- ceptible and lie latent until they reemerge years later as perceivable symp- toms and/or brain pathology.
Multiplicity
Scientific debates about CTE causality often revolve around multiplicity, specifically in determining why some athletes exposed to repetitive brain trauma develop CTE, while others do not or do not experience symp- toms. As Montenigro et al. (2015) write, “while head trauma is a neces- sary variable for developing CTE, it is not sufficient. That is, not everyone who experiences repetitive impacts will get the disease” (p. 314). This supposition is substantiated by reports of athletes with documented neu- rocognitive decline who were not diagnosed with CTE postmortem (e.g.
Hazrati et al. 2013). Thus, a key aspect of contemporary CTE research involves determining how exposure to repetitive brain trauma combines with other variables to induce the neuropathological changes associated with the condition. The scientific literature on CTE identifies genetic predispositions, preexisting psychiatric conditions, drug and alcohol abuse, and sleep disturbances, as potential factors that might prompt or intensify the production of abnormal tau in some people and not others (McCrory et al. 2017; Montenigro et al. 2015; Solomon 2018).
The potential influence of contemporaneous variables has, predictably, been a focal point of neuroscientific arguments highlighting the perceived tenuousness of causal links between repetitive brain trauma and CTE. Isolating the influence of factors that contribute to CTE onset is a difficult task for scientists, exacerbated by the latency and imperceptibility
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of the condition’s defining characteristics. There are numerous complicat- ing factors beyond repetitive brain impacts that can be alluded to as
“unknowns” in neuroscientific theorizing around why CTE materializes in the brains and lives of some athletes and not others. These unknowns emerge through the material complexity of the brain, but also the neuro- scientific emphasis on parsing the effects of brain trauma within the vast array of human experiences that shape, and are shaped by, the brain.
Multiplicity, then, like latency and imperceptibility, serves as a renewable resource in the production of uncertainty around CTE.