Regulatory focus theory (RFT) postulates two cognitive-motivational systems for personal goal pursuit: the promotion system, which is associated with ideal goals (an individual’s hopes, dreams, and aspirations), and the prevention system, which is associated with ought goals (an individual’s duties, responsibilities, and obligations). The two systems have been studied extensively in behavioral research with reference to differences between promotion and prevention goal pursuit as well as the consequences of perceived attainment versus nonattainment within each system. However, no study has examined the neural correlates of each combination of goal domain and goal attainment status. We used a rapid masked idiographic goal priming paradigm and functional magnetic resonance imaging to present individually selected promotion and prevention goals, which participants had reported previously that they were close to attaining (“match”) or far from attaining (“mismatch”). Across the four priming conditions, significant activations were observed in bilateral insula (Brodmann area (BA) 13) and visual association cortex (BA 18/19). Promotion priming discriminantly engaged left prefrontal cortex (BA 9), whereas prevention priming discriminantly engaged right prefrontal cortex (BA 8/9). Activation in response to promotion goal priming was also correlated with an individual difference measure of perceived success in promotion goal attainment. Our findings extend the construct validity of RFT by showing that the two systems postulated by RFT, under conditions of both attainment and nonattainment, have shared and distinct neural correlates that interface logically with established network models of self-regulatory cognition.

Psychiatric disorders can often be viewed as extremes of personality traits. The primary action of drugs that ameliorate these disorders may, thus, be to alter the patient’s position on a relevant trait dimension. Here, we suggest that interactions between such trait dimensions may also be important for disorder. Internalizing disorders show important differences in terms of range of activity and speed of response of medications. Established antidepressant and anxiolytic medications are slow in onset and have differing effects across different internalizing disorders. In contrast, low-dose ketamine is rapidly effective and improves symptom ratings in all internalizing disorders. To account for this, we propose a “double hit” model for internalizing disorders: generation (and maintenance) require two distinct forms of neural dysfunction to coincide. One hit, sensitive to ketamine, is disorder-general: dysfunction of a neural system linked to high levels of the personality trait of neuroticism. The other hit is disorder-specific: dysfunction of one of a set of disorder-specific neural modules, each with its own particular pattern of sensitivity to conventional drugs. Our hypothesis applies only to internalizing disorders. So, we predict that ketamine will be effective in simple phobia and (perhaps partially) in anorexia nervosa, but would make no such prediction about other disorders where neuroticism might also be important secondarily (e.g. attention deficit hyperactivity disorder and schizophrenia).

The personality traits of neuroticism, openness, and conscientiousness are relevant factors for cognitive aging outcomes. The present study examined how these traits were associated with cognitive abilities and corresponding resting-state functional connectivity (RSFC) of the default mode network (DMN) in an older and predominantly minority sample. A sample of 58 cognitively unimpaired, largely African-American, older adults (M age = 68.28 ± 8.33) completed a standard RSFC magnetic resonance imaging sequence, a Big Five measure of personality, and delayed memory, Stroop, and verbal fluency tasks. Personality trait associations of within-network connectivity of the posterior cingulate cortex (PCC), a hub of the DMN, were examined using a seed-based approach. Trait scores were regressed on cognitive performance (delayed memory for neuroticism, Stroop for conscientiousness, and verbal fluency for openness). Greater openness predicted greater verbal fluency and greater RSFC between the PCC and eight clusters, including the medial prefrontal cortex, left middle frontal gyrus, and precuneus. Greater PCC–precuneus connectivity predicted greater verbal fluency. Neuroticism and conscientiousness did not significantly predict either cognitive performance or RSFC. Although requiring replication and elaboration, the results implicate openness as a contributing factor to cognitive aging via concomitant cognitive performance and connectivity within cortical hubs of the DMN and add to the sparse literature on these variables in a diverse group of older adults.

“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.

Predictive associations were estimated between socioemotional dispositions measured at 10–17 years using the Child and Adolescent Dispositions Scale (CADS) and future individual differences in white matter microstructure measured at 22–31 years of age. Participants were 410 twins (48.3% monozygotic) selected for later neuroimaging by oversampling on risk for psychopathology from a representative sample of child and adolescent twins. Controlling for demographic covariates and total intracranial volume (TICV), each CADS disposition (negative emotionality, prosociality, and daring) rated by one of the informants (parent or youth) significantly predicted global fractional anisotropy (FA) averaged across the major white matter tracts in brain in adulthood, but did so through significant interactions with sex after false discovery rate (FDR) correction. In females, each 1 SD difference in greater parent-rated prosociality was associated with 0.43 SD greater FA (p < 0.0008). In males, each 1 SD difference in greater parent-rated daring was associated with 0.24 SD lower FA (p < 0.0008), and each 1 SD difference in greater youth-rated negative emotionality was associated with 0.18 SD greater average FA (p < 0.0040). These findings suggest that CADS dispositions are associated with FA, but associations differ by sex. Exploratory analyses suggest that FA may mediate the associations between dispositions and psychopathology in some cases. These associations over 12 years could reflect enduring brain–behavior associations in spite of transactions with the environment, but could equally reflect processes in which dispositional differences in behavior influence the development of white matter. Future longitudinal studies are needed to resolve the causal nature of these sex-moderated associations.

Gray’s theory of personality postulates that fear and anxiety are distinct emotional systems with only the latter being sensitive to anxiolytic drugs. His work was mainly based on animal research, and translational studies validating his theory are scarce. Previous work in humans showed an influence of the benzodiazepine lorazepam on both systems, however, dependent on dosage (1 and 2 mg) and personality differences in negative emotionality. The present study aims to replicate these findings, and in addition tests the drug threshold effect by introducing a lower dosage of 0.5 mg lorazepam. Fifty healthy adults (23 males, agemean 22.40, SD ± 3.68) participated in an experimental threat-avoidance paradigm designed to dissociate risk assessment intensity (RAI, reflecting anxiety) and flight intensity (FI, reflecting fear) and completed two self-report questionnaires assessing facets of negative emotionality (Spielberger State Trait Anxiety Inventory and Fear Survey Schedule). In a randomized placebo-controlled within-subjects design, 0.5 and 1 mg of lorazepam were applied per os. Saccadic peak velocity was assessed by means of eye-tracking in order to control for sedating drug effects. Results showed the expected and specific anxiolytic effect of lorazepam on RAI, however, only in the 0.5 mg condition. FI was not influenced by lorazepam, and previous findings of interaction effects of lorazepam with self-reported negative emotionality could not be corroborated. Overall, this study demonstrates anxiolytic effects of lorazepam in dosages ≤1 mg in the absence of a drug effect on fear using a translational behavioural task. However, a putative moderating role of personality on defensive behaviour has to be clarified in future research.

Dopamine (DA) is known to be involved in various aspects of reward processing and goal-directed behavior. The present preregistered study aims at directly accessing the causal influence of DA activity on reward motivation in humans, while also accounting for trait extraversion. Therefore, we examined the effect of a single dose of the DA D2 receptor antagonist sulpiride (200 mg) on effort allocation in a modified version of the Effort-Expenditure for Reward Task (EEfRT). Based on its presumably DA increasing action, we expected the low dose of sulpiride to increase participants’ willingness to allocate effort during the modified EEfRT relative to placebo, especially in trials with low probability of reward attainment. Further, we expected a moderating effect of trait extraversion on the effects of sulpiride. Two hundred and three healthy male participants were tested in a randomized, double-blind between-subjects design. Contrary to our expectations, sulpiride reduced the average number of clicks within the modified EEfRT and did not interact with reward attributes, suggesting a more global and not reward-specific effect of sulpiride. Furthermore, trait extraversion did not moderate the effect of sulpiride. Our results provide initial support for the validity of the modified version of the EEfRT, suggesting a possible inhibiting effect of a low dose of sulpiride on approach motivation regardless of trait extraversion. However, given the mixed pattern of findings and the possible confounding role of motoric abilities, further studies examining these effects are clearly warranted.

There is an expanding literature on the theoretical and empirical connections between personality and psychopathology, and their shared neurobiological correlates. Recent cybernetic theories of personality and psychopathology, as well as affective neuroscience theory, provide grounding for understanding neurobiological–personality–psychopathology (NPP) associations. With the emergence of large sample datasets (e.g., Human Connectome Project) advanced quantitative modeling can be used to rigorously test dynamic statistical representations of NPP connections. Also, research suggests that these connections are influenced by sex, and large samples provide the opportunity to examine how NPP associations might be moderated by sex. The current study used a large sample from the Duke Neurogenetics Study (DNS) to examine how amygdala activation to facial expressions was linked with self-report of personality traits and clinical interviews of internalizing and externalizing symptoms of psychopathology. Structural equation modeling results revealed direct associations of amygdala activation with personality trait expression, as well as indirect associations (though personality) with symptoms of psychopathology. Moreover, the NPP links were moderated by sex. The current results are in line with research that identifies a broader role played by the amygdala in personality and provide potential insights for continued research in personality neuroscience and recent theories on the neurobiology of personality.

Posttraumatic stress disorder (PTSD) is often complicated by the after-effects of mild traumatic brain injury (mTBI). The mixture of brain conditions results in abnormal affective and cognitive functioning, as well as maladaptive behavior. To better understand how brain activity explains cognitive and emotional processes in these conditions, we used an emotional N-back task and functional magnetic resonance imaging (fMRI) to study neural responses in US military veterans after deployments to Iraq and Afghanistan. Additionally, we sought to examine whether hierarchical dimensional models of maladaptive personality could account for the relationship between combat-related brain conditions and fMRI responses under cognitive and affective challenge. FMRI data, measures of PTSD symptomatology (PTSS), blast-induced mTBI (bmTBI) severity, and maladaptive personality (MMPI-2-RF) were gathered from 93 veterans. Brain regions central to emotion regulation were selected for analysis, and consisted of bilateral amygdala, bilateral dorsolateral prefrontal (dlPFC), and ventromedial prefrontal/subgenual anterior cingulate (vmPFC-sgACC). Cognitive load increased activity in dlPFC and reduced activity in emotional responding brain regions. However, individuals with greater PTSS showed blunted deactivations in bilateral amygdala and vmPFC-sgACC, and weaker responses in right dlPFC. Additionally, we found that elevated emotional/internalizing dysfunction (EID), specifically low positive emotionality (RC2), accounted for PTSS-related changes in bilateral amygdala under increased cognitive load. Findings suggest that PTSS might result in amygdala and vmPFC-sgACC activity resistant to moderation by cognitive demands, reflecting emotion dysregulation despite a need to marshal cognitive resources. Anhedonia may be an important target for interventions that improve the affective and cognitive functioning of individuals with PTSD.

Brain laterality refers to the asymmetric location of functional elements within the bilateral brain of animals and humans. Thus far, five lateralized functions have been recognized in humans: handedness, language ability, spatial skills, facial recognition, and emotion recognition. Recently, a sixth asymmetric functional element bearing on personality has been discovered. It is the larger side of the split bilateral anterior cingulate cortex (ACC). This appears to be the final output element of the executive system of which, by logic, there can be only one. Which side is somewhat larger varies among the general population in a seemingly idiosyncratic manner, yet with a genetic basis because true-breeding lineages exist. Here, hemisity is binary measure where a person is inherently born either right brain or left brain oriented. This is determined by nine statistically robust sets of four biophysical tests, none of which depend upon personality, and five behavioral questionnaires. Crucially these hemisity methods have been validated by the Magnetic Resonance Imaging (MRI)-based discovery that the larger side of the ACC is on the same side as one’s hemisity, making MRI the primary standard for hemisity determination (r = 0.96). There are at least 30 measurable differences in individual characteristics and behaviors between those persons whose hemsity is on the right compared to those with it on the left. The hemisity of 2929 individuals was determined by these methods. Large groups included 1428 junior and senior high schools students both in Hawaii and Utah. There were somewhat comparable numbers present for both types of hemisity. Hemisity of individuals was found stable from infancy to old age. There was no relation between hemisity and handedness. Larger corpus callosum (CC) size of male or female subjects was larger in right brainer that in left brainers. Twin studies demonstrate that CC size is inherited. Thirty-eight percent of individuals of both sexes were right brain oriented, while 62% of individuals of both sexes were left brain oriented. In pairings, there were more than twice as many couples with opposite hemisity. Of these couples, the right brain male and females were dominant. Reproductive outcomes of these were “Like father like son, Like mother like daughter.”

A growing body of research supports the value of a multimodal assessment approach, drawing on measures from different response modalities, for clarifying how core biobehavioral processes relate to various clinical problems and dimensions of psychopathology. Using data for 507 healthy adults, the current study was undertaken to integrate self-report and neurophysiological (brain potential) measures as a step toward a multimodal measurement model for the trait of affiliative capacity (AFF) – a biobehavioral construct relevant to adaptive and maladaptive social-interpersonal functioning. Individuals low in AFF exhibit a lack of interpersonal connectedness, deficient empathy, and an exploitative-aggressive social style that may be expressed transdiagnostically in antagonistic externalizing or distress psychopathology. Specific aims were to (1) integrate trait scale and brain potential indicators into a multimodal measure of AFF and (2) evaluate associations of this multimodal measure with criterion variables of different types. Results demonstrated (1) success in creating a multimodal measure of AFF from self-report and neural indicators, (2) effectiveness of this measure in predicting both clinical-diagnostic and neurophysiological criterion variables, and (3) transdiagnostic utility of the multimodal measure at both specific-disorder and broad symptom-dimension levels. Our findings further illustrate the value of psychoneurometric operationalizations of biobehavioral trait dimensions as referents for clarifying transdiagnostic relationships between biological systems variables and empirically defined dimensions of psychopathology.

Callous-unemotional (CU) traits are early-emerging personality features characterized by deficits in empathy, concern for others, and remorse following social transgressions. One of the interpersonal deficits most consistently associated with CU traits is impaired behavioral and neurophysiological responsiveness to fearful facial expressions. However, the facial expression paradigms traditionally employed in neuroimaging are often ambiguous with respect to the nature of threat (i.e., is the perceiver the threat, or is something else in the environment?). In the present study, 30 adolescents with varying CU traits viewed fearful facial expressions cued to three different contexts (“afraid for you,” “afraid of you,” “afraid for self”) while undergoing functional magnetic resonance imaging (fMRI). Univariate analyses found that mean right amygdala activity during the “afraid for self” context was negatively associated with CU traits. With the goal of disentangling idiosyncratic stimulus-driven neural responses, we employed intersubject representational similarity analysis to link intersubject similarities in multivoxel neural response patterns to contextualized fearful expressions with differential intersubject models of CU traits. Among low-CU adolescents, neural response patterns while viewing fearful faces were most consistently similar early in the visual processing stream and among regions implicated in affective responding, but were more idiosyncratic as emotional face information moved up the cortical processing hierarchy. By contrast, high-CU adolescents’ neural response patterns consistently aligned along the entire cortical hierarchy (but diverged among low-CU youths). Observed patterns varied across contexts, suggesting that interpretations of fearful expressions depend to an extent on neural response patterns and are further shaped by levels of CU traits.

Quantitative models of psychopathology (i.e., HiTOP) propose that personality and psychopathology are intertwined, such that the various processes that characterize personality traits may be useful in describing and predicting manifestations of psychopathology. In the current study, we used data from the Human Connectome Project (N = 1050) to investigate neural activation following receipt of a reward during an fMRI task as one shared mechanism that may be related to the personality trait Extraversion (specifically its sub-component Agentic Extraversion) and internalizing psychopathology. We also conducted exploratory analyses on the links between neural activation following reward receipt and the other Five-Factor Model personality traits, as well as separate analyses by gender. No significant relations (p < .005) were observed between any personality trait or index of psychopathology and neural activation following reward receipt, and most effect sizes were null to very small in nature (i.e., r < |.05|). We conclude by discussing the appropriate interpretation of these null findings, and provide suggestions for future research that spans psychological and neurobiological levels of analysis.

Personality has been correlated with differences in cytokine expression, an indicator of peripheral inflammation; however, the associations between personality and central markers of inflammation have never been investigated in vivo in humans. Microglia are the resident macrophages of the central nervous system, and the first responders to tissue damage and brain insult. Microglial activation is associated with elevated expression of translocator protein 18kDa (TSPO), which can be imaged with positron emission tomography (PET) to quantify immune activation in the human brain. This study aimed to investigate the association between personality and TSPO expression across the psychosis spectrum. A total of 61 high-resolution [18F]FEPPA PET scans were conducted in 28 individuals at clinical high risk (CHR) for psychosis, 19 First-Episode Psychosis (FEP), and 14 healthy volunteers (HVs), and analyzed using a two-tissue compartment model and plasma input function to obtain a total volume of distribution (VT) as an index of brain TSPO expression (controlling for the rs6971 TSPO polymorphism). Personality was assessed using the Revised NEO Personality Inventory (NEO-PI-R). We found TSPO expression to be specifically associated with neuroticism. A positive association between TSPO expression and neuroticism was found in HVs, in contrast to a nonsignificant, negative association in CHR and significant negative association in FEP. The TSPO-associated neuroticism trait indicates an unexplored connection between neuroimmune activation and personality that varies across the psychosis spectrum.

Psychophysiological measures have become increasingly accessible to researchers and many have properties that indicate their use as individual difference indicators. For example, the error-related negativity (ERN), an event-related potential (ERP) thought to reflect error-monitoring processes, has been related to individual differences, such as Neuroticism and Conscientiousness traits. Although various tasks have been used to elicit the ERN, only a few studies have investigated its variability across tasks when examining the relations between the ERN and personality traits. In this project, we examined the relations of the ERN elicited from four variants of the Flanker task (Arrow, Social, Unpleasant, and Pleasant) that were created to maximize the differences in their relevance to personality traits. A sample of 93 participants with a history of treatment for psychopathology completed the four tasks as well as self-report measures of the general and maladaptive five-factor model (FFM) traits. Confirmatory factor analyses (CFAs) of ERN amplitudes indicated that three of the four tasks (Arrow, Social, and Unpleasant) were unidimensional. Another set of CFAs indicated that a general factor underlies the ERN elicited from all tasks as well as unique task-specific variances. The correlations of estimated latent ERN scores and personality traits did not reflect the hypothesized correlation patterns. Variability across tasks and the hierarchical model of the ERN may aid in understanding psychopathology dimensions and in informing future endeavors integrating the psychophysiological methods into the study of personality. Recommendations for future research on psychophysiological indicators as individual differences are discussed.