Personality Disturbances as Emergent Phenomena Reflective of Underlying Neurobehavioral Systems: Beyond Dimensional Measurement, Phenotypic Trait Descriptors, and Factor Analysis.

BACKGROUND AND OVERVIEW: The conceptualization of personality pathology, or personality disturbance, is now at a substantive crossroads. Some researchers (and clinicians) prefer a focus on the domains of personality pathology that are well-described and captured in traditional categorical diagnostic approaches that, in some instances, abut normal personality constructs. Other workers argue to move the study of personality disorder (PD) closer to personality science seeking continuous connections between PD and established dimensions of healthy-range, normal personality. Most of the latter efforts revolve around correlational and factor analytic study of phenotypic expressions of PD features and normal personality dimensions. It is notable, however, that both visions of the PD/personality interface are essentially unlinked to an understanding of shared neurobiological underpinnings (i.e., neurotransmitter-influenced neurobehavioral systems) of both personality disturbance and normal personality1. Here, we present a nontechnical, conceptual overview of our approach to this problem, advancing a neurobehavioral approach that seeks to anchor both normal personality and personality disturbance within a matrix of brain-based neurobiological systems, incorporating genetic, epigenetic, and environmental inputs. In this brief paper, we seek only to provide a necessarily cursory introduction to how we conceptualize this area and illustrate, in broad outline, our effort to characterize both personality and personality disturbance anchored in neurobehavioral systems. Our approach, which we began developing in the middle 1990s, can be juxtaposed with the more recently proposed DSM-5 Alternative Model of Personality Disorders as well as the well-established five-factor approach to PD.

A novel neurobehavioral framework of the effects of positive early postnatal experience on incentive and consummatory reward sensitivity.

Early postnatal experience has a profound influence on the development of organisms. In this integration, we provide a novel framework of the neurobehavioral pathways through which positive early postnatal experience acts to enhance adult reward sensitivity. The heterogeneity of the construct of reward and the underlying neurotransmitter systems (i.e., dopamine in incentive reward, opioids in consummatory reward, and oxytocin in orienting the reward systems to social cues) are first described as a means of organizing the discussion. Then, for each neurotransmitter system, their early postnatal ontogenesis is depicted for identifying potential sensitive periods for the effects of early experience. This is followed by the presentation of a model of the neurobehavioral foundation of two main forms of positive early postnatal experience that, with their essential components - novelty and positive tactile stimulation, facilitate the development of incentive and consummatory reward systems. Next, a detailed analysis of the major effects of positive early prewean and postwean experience on the neural and behavioral functioning of each neurotransmitter system is reviewed. The data support the neurobehavioral model presented, which theorizes that essential components of positive early experience enhance incentive and consummatory reward sensitivities through early activation of particular neural pathways. These activity-dependent effects are sustained via structural modifications of underlying neural circuitries.

Touch-induced face conditioning is mediated by genetic variation in opioid but not oxytocin receptors.

Soft touch possesses strong prosocial effects that facilitate social bonding and group cohesion in animals. Touch activates opioids (OP) and oxytocin (OXT), two neuromodulators involved in affiliative behaviors and social bonding. We examined whether touch serves as an unconditioned reward in affective conditioning of human faces, a basic process in social bonding, and whether this process is mediated by variation in mu-OP (OPRM1) and OXT (rs53576) receptor genes. Participants viewed affectively-neutral human faces, half of which were paired with a brief soft brushing on the forearm as an unconditioned stimulus (US). Paired and unpaired faces were rated for positive affective and sensory features of touch. Variation in OPRM1 but not rs53576 significantly modulated strength and development of conditioning, indicating that touch-induced mu-OP but not OXT activity provides rewarding properties of a US in conditioning. Implications for touch-induced mu-OP activity in normal and disordered conditioned social bonding are discussed.

Neurobehavioral foundation of environmental reactivity.

Sensitivity to environmental context has been of interest for many years, but the nature of individual differences in environmental sensitivity has become of particular focus over the past 2 decades. What is particularly uncertain are the neural variables and processes that mediate the effects of environment on developmental outcomes. Accordingly, we provide a neurobehavioral foundation of reactivity to the environment in several steps. First, the different patterns of environmental sensitivity are defined to identify the significant factors involved in the manifestation of these patterns. Second, we focus on neurobiological reactivity as the construct underlying variation in sensitivity to the environment by (a) providing an organizing threshold model of elicitation of neurobiology by environmental context; and (b) integrating the literature on 2 sets of neuromodulators in terms of each modulator's (a) contribution to neural and behavioral reactivity to stimulation, and (b) relation to emotional-motivational systems (dopamine, opiates and oxytocin, corticotropin-releasing hormone) or the general modulation of those systems (serotonin, norepinephrine, and GABA). Discussion concludes with (a) a comprehensive neurobehavioral framework of environmental reactivity based on a combinatorial model of a supertrait, (b) methodological implications of the model, and (c) a developmental perspective on environmental reactivity.

Social traits modulate attention to affiliative cues.

Neurobehavioral models of personality suggest that the salience assigned to particular classes of stimuli vary as a function of traits that reflect both the activity of neurobiological encoding and relevant social experience. In turn, this joint influence modulates the extent that salience influences attentional processes, and hence learning about and responding to those stimuli. Applying this model to the domain of social valuation, we assessed the differential effects on attentional guidance by affiliative cues of (i) a higher-order temperament trait (Social Closeness), and (ii) attachment style in a sample of 57 women. Attention to affiliative pictures paired with either incentive or neutral pictures was assessed using camera eye-tracking. Trait social closeness and attachment avoidance interacted to modulate fixation frequency on affiliative but not on incentive pictures, suggesting that both traits influence the salience assigned to affiliative cues specifically.

On the nature of extraversion: variation in conditioned contextual activation of dopamine-facilitated affective, cognitive, and motor processes.

Research supports an association between extraversion and dopamine (DA) functioning. DA facilitates incentive motivation and the conditioning and incentive encoding of contexts that predict reward. Therefore, we assessed whether extraversion is related to the efficacy of acquiring conditioned contextual facilitation of three processes that are dependent on DA: motor velocity, positive affect, and visuospatial working memory. We exposed high and low extraverts to three days of association of drug reward (methylphenidate, MP) with a particular laboratory context (Paired group), a test day of conditioning, and three days of extinction in the same laboratory. A Placebo group and an Unpaired group (that had MP in a different laboratory context) served as controls. Conditioned contextual facilitation was assessed by (i) presenting video clips that varied in their pairing with drug and laboratory context and in inherent incentive value, and (ii) measuring increases from day 1 to Test day on the three processes above. Results showed acquisition of conditioned contextual facilitation across all measures to video clips that had been paired with drug and laboratory context in the Paired high extraverts, but no conditioning in the Paired low extraverts (nor in either of the control groups). Increases in the Paired high extraverts were correlated across the three measures. Also, conditioned facilitation was evident on the first day of extinction in Paired high extraverts, despite the absence of the unconditioned effects of MP. By the last day of extinction, responding returned to day 1 levels. The findings suggest that extraversion is associated with variation in the acquisition of contexts that predict reward. Over time, this variation may lead to differences in the breadth of networks of conditioned contexts. Thus, individual differences in extraversion may be maintained by activation of differentially encoded central representations of incentive contexts that predict reward.

Modeling borderline personality disorder based on the neurobehavioral foundation of major personality traits.

Borderline personality disorder (BPD) is an exceedingly complex behavioral phenomenon that is in need of conceptual clarification within a larger model of personality disorders (PDs). The association of personality traits to BPD is discussed initially as a means of introducing a dimensional personality approach to understanding BPD. While this model suggests that PDs emerge at the extremes of personality dimensions, attempts to demonstrate such an association have been empirically disappointing and conceptually unilluminating. Therefore, in this article, we attempt to extend such models by outlining the neurobehavioral systems that underlie major personality traits, and highlight the evidence that they are subject to experience-dependent modification that can be enduring through effects on genetic expression, mainly through processes known as epigenetics. It is through such processes that risk for personality disorder may be modified by experience at any point in development, but perhaps especially during early critical periods of development. We conclude by presenting a multidimensional model of PDs, in general, and BPD, in particular, that relies on the concepts developed earlier in the article. Our goal is to provide a guide for novel clinical conceptualization and assessment of PDs, as well as research on their psychobiological nature and pharmacological treatment.

Neurogenetic and experiential processes underlying major personality traits: implications for modelling personality disorders.

Abstract The association of personality traits to personality disorders (PDs) is assumed by many to fit a dimensional model, where PDs emerge at the extremes of personality dimensions. Nevertheless, attempts to demonstrate such an association have been empirically disappointing and conceptually unilluminating. In this article we attempt to extend such models by outlining the neurobehavioural systems that underlie major personality traits, and highlight the evidence that they are subject to experience-dependent modification that can be enduring through effects on genetic expression, mainly through processes known as epigenetics. It is through such processes that risk for personality disorder may be modified by experience at any point in development, but perhaps especially during early critical periods of development. We conclude by presenting a novel multidimensional model of PDs that relies on the concepts developed earlier in the article. Our goal is to provide a guide for research on the psychobiological nature and pharmacological treatment of PDs.

Genetic, environmental, and epigenetic factors in the development of personality disturbance.

A dimensional model of personality disturbance is presented that is defined by extreme values on interacting subsets of seven major personality traits. Being at the extreme has marked effects on the threshold for eliciting those traits under stimulus conditions: that is, the extent to which the environment affects the neurobiological functioning underlying the traits. To explore the nature of development of extreme values on these traits, each trait is discussed in terms of three major issues: (a) the neurobiological variables associated with the trait, (b) individual variation in this neurobiology as a function of genetic polymorphisms, and (c) the effects of environmental adversity on these neurobiological variables through the action of epigenetic processes. It is noted that gene-environment interaction appears to be dependent on two main factors: (a) both genetic and environmental variables appear to have the most profound and enduring effects when they exert their effects during early postnatal periods, times when the forebrain is undergoing exuberant experience-expectant dendritic and axonal growth; and (b) environmental effects on neurobiology are strongly modified by individual differences in "traitlike" functioning of neurobiological variables. A model of the nature of the interaction between environmental and neurobiological variables in the development of personality disturbance is presented.

A neurobehavioral model of affiliative bonding: implications for conceptualizing a human trait of affiliation.

Because little is known about the human trait of affiliation, we provide a novel neurobehavioral model of affiliative bonding. Discussion is organized around processes of reward and memory formation that occur during approach and consummatory phases of affiliation. Appetitive and consummatory reward processes are mediated independently by the activity of the ventral tegmental area (VTA) dopamine (DA)-nucleus accumbens shell (NAS) pathway and the central corticolimbic projections of the u-opiate system of the medial basal arcuate nucleus, respectively, although these two projection systems functionally interact across time. We next explicate the manner in which DA and glutamate interact in both the VTA and NAS to form incentive-encoded contextual memory ensembles that are predictive of reward derived from affiliative objects. Affiliative stimuli, in particular, are incorporated within contextual ensembles predictive of affiliative reward via: (a) the binding of affiliative stimuli in the rostral circuit of the medial extended amygdala and subsequent transmission to the NAS shell; (b) affiliative stimulus-induced opiate potentiation of DA processes in the VTA and NAS; and (c) permissive or facilitatory effects of gonadal steroids, oxytocin (in interaction with DA), and vasopressin on (i) sensory, perceptual, and attentional processing of affiliative stimuli and (ii) formation of social memories. Among these various processes, we propose that the capacity to experience affiliative reward via opiate functioning has a disproportionate weight in determining individual differences in affiliation. We delineate sources of these individual differences, and provide the first human data that support an association between opiate functioning and variation in trait affiliation.

The orbitofrontal cortex in methamphetamine addiction: involvement in fear.

We used Tellegen's Multidimensional Personality Questionnaire (MPQ) harm avoidance (fear) scale and the constraint superfactor as personality measures of inhibitory control and examined their association with glucose metabolism in the orbitofrontal gyrus at rest in 14 recently abstinent methamphetamine-dependent subjects and 22 comparison subjects. Higher MPQ scores were associated with higher relative orbitofrontal gyrus metabolism in the methamphetamine-dependent subjects. There was a tendency towards a negative association for the comparison subjects (test of coincidence of regression lines for the two subject groups: F = 3.3, df = 2,32; = 0.051). These results suggest that the role of the orbitofrontal cortex in inhibitory control can be manifested in stable personality predispositions and further implicate this region in the core characteristics of drug addiction.