Personality neuroscience and psychopathology: should we start with biology and look for neural-level factors?

Abstract

“Personality is an abstraction used to explain consistency and coherency in an individual’s pattern of affects, cognitions, desires and behaviors [ABCDs]” (Revelle, 2007, p. 37). But personality research currently provides more a taxonomy of patterns than theories of fundamental causes. Psychiatric disorders can be viewed as involving extremes of personality but are diagnosed via symptom patterns not biological causes. Such surface-level taxonomic description is necessary for science, but consistent predictive explanation requires causal theory. Personality constructs, and especially their clinical extremes, should predict variation in ABCD patterns, with parsimony requiring the lowest effective causal level of explanation. But, even biologically inspired personality theories currently use an intuitive language-based approach for scale development that lacks biological anchors. I argue that teleonomic “purpose” explains the organisation and outputs of conserved brain emotion systems, where high activation is adaptive in specific situations but is otherwise maladaptive. Simple modulators of whole-system sensitivity evolved because the requisite adaptive level can vary across people and time. Sensitivity to a modulator is an abstract predictive personality factor that operates at the neural level but provides a causal explanation of both coherence and occasional apparent incoherence in ABCD variation. Neuromodulators impact all levels of the “personality hierarchy” from metatraits to aspects: stability appears altered by serotonergic drugs, neuroticism by ketamine and trait anxiety by simple anxiolytic drugs. Here, the tools of psychiatry transfer to personality research and imply both interaction between levels and oblique factor mappings to ABCD. On this view, much psychopathology reflects extremes of neural-level personality factors, and we can view much pharmacotherapy as temporarily altering personality. So, particularly for personality factors linked to basic emotions and their disorders, I think we should start with evolutionary biology and look directly at conserved neural-level modulators for our explanatory personality constructs and only invoke higher order, emergent, explanations when neural-level explanation fails.

Neuropsychological Theory as a Basis for Clinical Translation of Animal Models of Neuropsychiatric Disorder

“…This fits both previous doubts about the current categories and the recent move to a trait perspective on psychopathology (Kotov et al, 2021 ; Michelini et al, 2021 ; DeYoung et al, 2022 ). It also fits the nosological mapping of the neuropsychological theory (Gray and McNaughton, 2000 ; McNaughton and Corr, 2004 ; McNaughton, 2020 ) summarized in Figure 1C . The first important feature of this nosology is that theta is a modulator across the range of conflict control structures, with its strongest effects in the middle of the hierarchy (see shading in figure).…”

“…Goal attraction, goal repulsion, and goal inhibition (activated by conflict between goals) are each controlled by systems in which modules are organized hierarchically in relation to motivational distance (from contacting to distant) and neural location (caudal to rostral). Conservation of modulatory control during phylogeny (McNaughton, 2020 ) means that hormonal compounds, e.g., benzodiazepine receptor ligands, and neuromodulators, e.g., serotonin, can target all the modules of a specific system (as with benzodiazepines and goal inhibition; yellow highlight) or all the modules of several systems (as with serotonin). Note that in the case of serotonin (most obviously via specific serotonin reuptake inhibitors), its effects (indicated by the gradation of the purple shading) appear to be to shift control from lower to higher levels of the systems (Carver et al, 2008 ) rather than to increase or decrease activity across an entire system.…”

“…There is also the capacity for more localized dysfunction and pharmacological specificity, as with obsession (orange highlight) and panic (red highlight). Figure and legend based on (McNaughton et al, 2016 ; Silva and McNaughton, 2019 ; McNaughton, 2020 ) with permission of the author. a, anterior; b, basal; c, central; d, dorsal; ext, external; int, internal; l, lateral; m, medial; p, posterior v, ventral; BNST, bed nucleus of the stria terminalis; SAD, Social Anxiety Disorder; OCD, obsessive compulsive disorder; OFC, orbitofrontal cortex; PAG, periaqueductal gray; θ, these compounds affect the system as a whole by reducing theta rhythmic input.…”

Connecting quantitatively derived personality–psychopathology models and neuroscience

“…Given the different strengths and weaknesses of various individual analytic approaches used in the literature, these articles highlight the power of triangulating evidence from multiple neuroscience and quantitative methods for uncovering the neurobiological bases of the personality-psychopathology continuum. Two review articles complement the breaths of the topics and methods covered by the empirical studies and provide useful recommendations for future research in this field (McNaughton, 2020;Shane et al, 2021).…”

Non-human contributions to personality neuroscience – from fish through primates. An introduction to the special issue

“…If a change in state is adaptive, trait sensitivity must also depend on adaptive value (Blanchard & Blanchard, 1989). The long-term trait control of emotions and its linkage to neurological and psychiatric illness (Greene et al, 2020;McNaughton, 2020) make nonhuman models of emotional behaviour a valuable platform to study the conserved fundamental states and traits contributing to human emotions. According to Darwin, comparative work is less "liable to confound conventional or artificial gestures and expressions with those which are innate or universal" (Darwin, 1872, p. 50).…”