Jacqueline Anne Sullivan

This paper offers a critique of an account of explanatory integration that claims that explanations of cognitive capacities by functional analyses and mechanistic explanations can be seamlessly integrated. It is shown that achieving such explanatory integration requires that the terms designating cognitive capacities in the two forms of explanation are stable but that experimental practice in the mind-brain sciences currently is not directed at achieving such stability. A positive proposal for changing experimental practice so as to promote such stability is put forward and its implications for explanatory integration are briefly considered.

This chapter has two aims. The first aim is to compare and contrast three different conceptual-explanatory models for thinking about mental illness with an eye towards identifying the assumptions upon which each model is based, and exploring the model’s advantages and limitations in clinical contexts. Major Depressive Disorder is used as an example to illustrate these points. The second aim is to address the question of what conceptual-theoretical framework for thinking about mental illness is most likely to facilitate the discovery of causes and treatments of mental illness in research contexts. To this end, the National Institute of Mental Health’s Research Domain Criteria (RDoC) Project is briefly considered.

In this volume, leading philosophers of psychiatry examine psychiatric classification systems, including the Diagnostic and Statistical Manual of Mental Disorders, asking whether current systems are sufficient for effective diagnosis, treatment, and research. Doing so, they take up the question of whether mental disorders are natural kinds, grounded in something in the outside world. Psychiatric categories based on natural kinds should group phenomena in such a way that they are subject to the same type of causal explanations and respond similarly to the same type of causal interventions. When these categories do not evince such groupings, there is reason to revise existing classifications. The contributors all question current psychiatric classifications systems and the assumptions on which they are based. They differ, however, as to why and to what extent the categories are inadequate and how to address the problem. Topics discussed include taxometric methods for identifying natural kinds, the error and bias inherent in DSM categories, and the complexities involved in classifying such specific mental disorders as "oppositional defiance disorder" and pathological gambling. -/- Contributors George Graham, Nick Haslam, Allan Horwitz, Harold Kincaid, Dominic Murphy, Jeffrey Poland, Nancy Nyquist Potter, Don Ross, Dan Stein, Jacqueline Sullivan, Serife Tekin, Peter Zachar.

Neuroscience is a laboratory-based science that spans multiple levels of analysis from molecular genetics to behavior. At every level of analysis experiments are designed in order to answer empirical questions about phenomena of interest. Understanding the nature and structure of experimentation in neuroscience is fundamental for assessing the quality of the evidence produced by such experiments and the kinds of claims that are warranted by the data. This article provides a general conceptual framework for thinking about evidence and experimentation in neuroscience with a particular focus on two research areas: cognitive neuroscience and cognitive neurobiology.

In this chapter, I argue that scientific practice in the neurosciences of cognition is not conducive to the discovery of natural kinds of cognitive capacities. The “neurosciences of cognition” include cognitive neuroscience and cognitive neurobiology, two research areas that aim to understand how the brain gives rise to cognition and behavior. Some philosophers of neuroscience have claimed that explanatory progress in these research areas ultimately will result in the discovery of the underlying mechanisms of cognitive capacities. Once such mechanistic understanding is achieved, cognitive capacities purportedly will be relegated into natural kind categories that correspond to real divisions in the causal structure of the world. I provide reasons here, however, in support of the claim that the neurosciences of cognition currently are not on a trajectory for discovering natural kinds. As I explain, this has to do with how mechanistic explanations of cognitive capacities are developed. Mechanistic explanations and the kinds they explain are abstract representational byproducts of the conceptual, experimental and integrative practices of neuroscientists. If these practices are not coordinated towards developing mechanistic explanations that mirror the causal structure of the world, then natural kinds of cognitive capacities will not be discovered. I provide reasons to think that such coordination is currently lacking in the neurosciences of cognition and indicate where changes in these practices appropriate to the natural kinds ideal would be required if achieving this ideal is indeed the goal. However, I suggest that an evaluation of current practices in these research areas is suggestive that discovering natural kinds of cognitive capacities is not the goal.

Biomedical science has been remarkably successful in explaining illness by categorizing diseases and then by identifying localizable lesions such as a virus and neoplasm in the body that cause those diseases. Not surprisingly, researchers have aspired to apply this powerful paradigm to addiction. So, for example, in a review of the neuroscience of addiction literature, Hyman and Malenka (2001, p. 695) acknowledge a general consensus among addiction researchers that “[a]ddiction can appropriately be considered as a chronic medical illness.” Like other diseases, “Once addiction has taken hold, it tends to follow a chronic course.” (Koob and La Moal 2006, p. ?). Working from this perspective, much effort has gone into characterizing the symptomology of addiction and the brain changes that underlie them. Evidence for involvement of dopamine transmission changes in the ventral tegmental area (VTA) and nucleus accumbens (NAc) have received the greatest attention. Kauer and Malenka (2007, p. 844) put it well: “drugs of abuse can co-opt synaptic plasticity mechanisms in brain circuits involved in reinforcement and reward processing”. Our goal in this chapter to provide an explicit description of the assumptions of medical models, the different forms they may take, and the challenges they face in providing explanations with solid evidence of addiction. <br>.