A Global Approach to Cognitive Dysfunction as a Framework for Neurodivergence
Abel Wajnerman Paz and Jorge Ignacio Fuentes
We propose a global approach to distinguishing between cognitive function and dysfunction as an appropriate framework for thinking about neurodivergence. It has been a commonplace in philosophy of psychiatry, at least since Wakefield (1992), to define mental disorders in terms of a descriptive element and an evaluative element. Usually, the descriptive element is cast in terms of the function/dysfunction contrast, and the evaluative element in terms of harm/no-harm. So we get the equation mental disorder = dysfunction + harm.
Within this framework, conditions such as autism and ADHD have often been classified as mental disorders when they are associated with significant harm or impairment. The implicit assumption seems to be that the presence of harm warrants an inference to underlying brain dysfunction. However, the notion of neurodivergence challenges the idea that departures from statistically typical brain functioning should automatically be interpreted as dysfunctional, even when they are associated with disadvantage or harm in certain contexts (Singer 1999; Armstrong 2010). Originating in the autism self-advocacy movement, the neurodiversity framework emphasizes that many forms of cognitive difference reflect natural and enduring variations in human neurobiology rather than pathological states (Singer 1999; Ortega 2009). Nevertheless, this framework seems insufficient to address a critical question: how are we to distinguish between pathological and non-pathological forms of cognitive variation?
This is precisely the question our global approach aims to address. While misclassifying a form of neurodivergence as a disorder carries clear ethical risks—such as stigma, discrimination, and overmedicalization (Chapman 2020)—it is equally problematic to deny the possibility of genuine dysfunction altogether, as many efforts for developing therapeutic tools that can improve people’s wellbeing may be partially based on this assumption. Our aim is therefore not to reject the notion of dysfunction wholesale, but to offer principled criteria for distinguishing dysfunctions from non-pathological variations in cognitive functioning. In doing so, we focus on autism and ADHD as central test cases, arguing that these conditions do not necessarily involve dysfunction, even when they are associated with harm.
The function/dysfunction distinction has been a key point of controversy in the philosophy of biology and medicine. Perhaps the most well-known approach is Boorse’s (1975) theory of health and disease. According to this view, the physiological function of a biological trait is its species-typical causal contribution to survival and reproduction. Disease is represented by the decline in function below a normal efficiency threshold, and health is the absence of any disease. This is a dispositional account of functions as opposed to an etiological one (such as Millikan’s 1995; and also Wakefield’s 1992), meaning that instead of making evolutionary history essential to functions, it grounds function attribution on the current disposition of a trait.
For reasons we cannot go into detail here, Garson and Piccinini (2014) reformulate the goal contribution account, avoiding appealing to typicality and replacing it with non-negligibility. So they define function in terms of a non-negligible contribution to survival or inclusive fitness. Conversely, dysfunction with respect to function F is defined in terms of a trait that cannot perform F in at least one appropriate situation at the rate that is appropriate.
We adapt their definition to neurocognitive functions, a special case of biological functions. Thus, the function of a neurocognitive capacity C or its underlying neural mechanism M is the performance of a process P that non-negligibly contributes to improving success in a type of task T, on those occasions in which performing T contributes to the individual’s fitness. For instance, spatial memory (C), presumably implemented by place cells located in the hippocampus (M), improves performance in tasks such as resource navigation (T), in situations such as locating food or returning safely to shelter. In these situations, this capacity improves foraging efficiency and raises the probability of escaping from danger, respectively.
Thus, we endorse the core naturalistic intuition that biological and cognitive functions are defined by their contributions to survival or success. However, we argue that in the neurocognitive domain, this framework must be expanded to accommodate forms of functional variability that do not straightforwardly amount to dysfunction, as emphasized by the neurodivergence framework. In particular, identifying dysfunction cannot rely solely on local underperformance in isolated capacities. Neurocognitive functions form an integrated and dynamic architecture: a reduction in one capacity may enable or enhance others. Whether a capacity is dysfunctional, therefore, depends on its role within the individual’s overall cognitive strategy rather than on its isolated performance profile.
This expansion also requires moving beyond an exclusively individualistic notion of fitness. Human adaptive success is deeply social, and variation in cognitive styles across individuals can enhance the adaptive potential of groups. As a result, traits that appear suboptimal at the individual level may nevertheless contribute positively to the inclusive fitness of a community. On this basis, we propose that a neurocognitive capacity is dysfunctional only if it fails to perform its function at an appropriate rate in appropriate situations, and if there exists no broader individual or collective cognitive configuration in which its reduced performance makes a non-negligible contribution to adaptive success in some range of situations.
We can illustrate this idea with autism and ADHD. Many capacities that are often reduced in autistic individuals—such as social reciprocity, pragmatic communication, joint attention, emotional decoding, and behavioral flexibility—can be understood as different manifestations of a more general limitation in global processing. Global processing involves integrating heterogeneous cues (social, perceptual, emotional) into unified, context-sensitive representations that guide rapid and flexible action. This mode of processing is particularly relevant for social cooperation, where inferring intentions depends on combining multiple weak signals, and for behavioral flexibility, where adaptive success requires tracking the overall structure of changing situations. However, reduced global integration in autistic individuals is often accompanied by enhanced local information processing, characterized by a focus on fine-grained, highly structured features and increased perceptual precision. This trade-off can support adaptive success at both individual and group levels by enabling heightened sensitivity to pattern irregularities, sustained precision in long-duration tasks, and careful monitoring of environmental variables, which can contribute to effective performance in, for instance, guarding or sentry-like roles. On our account, limitations in global processing are not dysfunctional when either contexts favoring local processing are as common as those favoring global processing, or when the adaptive demands of the latter can be met through the complementary capacities of other members of the community.
A parallel analysis applies to ADHD, which is commonly described in terms of deficits in sustained attention or inhibitory control. Stable and reliable focus clearly contributes to fitness in certain contexts, such as resource-rich but predictable environments, tasks with high switching costs, precision-sensitive activities, or social roles structured around routine and reliability. However, attentional variability can also be understood as reflecting an adaptive trade-off between exploration and exploitation. While exploitation favors persistence and delayed rewards, exploration supports rapid task switching and sensitivity to new opportunities. Because environments are variable and resource distributions uneven, neither strategy is globally optimal, and natural selection may therefore maintain cognitive variability associated with ADHD traits. Exploratory profiles are particularly advantageous under conditions of uncertainty, environmental volatility, patchy resource distribution, innovation-driven competition, or rapidly shifting social networks. From this perspective, attentional deficits are non-dysfunctional when either exploratory demands are as prevalent as exploitative ones, or when the survival of individuals or communities in exploitation-dependent contexts can be supported by the complementary attentional strategies of others.
We conclude that eurocognitive function attribution can be local, but assessing whether its degradation equals dysfunction requires a more global perspective, and that autism and ADHD seem grounded in cognitive trade-offs rather than dysfunctionality.