The Emotional Foundations of Personality

by Kenneth L Davis

  CHAPTER 14

  The Earlier History of Biological Theories of Personality

  Hans Eysenck, Jeffrey Gray, and Robert Cloninger

  We are what we feel and perceive.

  If we are angry, we are the anger.

  If we are in love, we are the love.

  If we look at a snowy mountain peak, we are the mountain.

  While dreaming, we are the dream.

  —Thich Nhat Hanh, Silence: The Power of Quiet in a World Full of Noise

  FEW OF THE PERSONALITY THEORIES we have reviewed so far and compared to our affective neuroscience theory of personality have delved deeply into brain sources of personality variability. Some have offered speculations, but few have attempted to integrate neuroscientific thinking into their theories. In this chapter we briefly review the work of three eminent scientists who made serious efforts to not just name and describe personality traits but to consider the possible underlying neural substrates of human personality differences. We highlight the work of Hans Eysenck, who spent most of his career as professor of psychology at the Institute of Psychiatry, King’s College London, and his most eminent colleague and student, Jeffrey Gray, who added the first modern neuroscientific dimensions to emotion theorizing, and conclude with the seminal work of Robert Cloninger at Washington University in St. Louis, who focused on possible neurochemical substrates of human personality. As we share the revolutionary flavor of their work, we also contrast their seminal contributions to our affective neuroscience approach.

  HANS EYSENCK

  Hans Eysenck (1916–1997) was born in Germany during the First World War and emigrated to England after refusing to join the German military during the tragic events leading to the Second World War. He received his Ph.D. in psychology in 1940 from the University College London and, as fate would have it, began his career in a WWII British emergency hospital treating psychiatric casualties. He was an early advocate of diagnosing psychiatric patients using psychological dimensions rather than distinct categories based on symptom states—a battle he fought with the psychiatric powers on the European side of the Atlantic. So, it is not surprising that much of his career focused on delineating psychological characteristics, which he surmised were foundational for human personality.

  His approach was similar to Raymond Cattell’s (see Chapter 12) in that he utilized factor analysis, which was increasingly popular at the time. However, he deviated from Cattell by shifting his emphasis from factor-analytically identified “traits” (Cattell’s source traits) to higher-order superfactors derived from the lower-order traits (Eysenck, 1990). Eysenck called these higher-order factors “types” and over his career identified three, Extraversion, Neuroticism, and Psychoticism, which had considerable impact on psychiatric theorizing.

  Eysenck also differed from Cattell in his source of theoretical ideas. While Cattell used many Freudian concepts, Eysenck was influenced by Pavlov. In his 1957 book The Dynamics of Anxiety and Hysteria, Eysenck offered Pavlov’s idea of “excitation versus inhibition” in the nervous system as the basis of Introversion versus Extraversion, with introverts being characterized by more excitatory neural processes and more sensitive to sensory overload than extraverts. As the basis of his Neuroticism, Eysenck adopted Pavlov’s idea of nervous system “mobility,” which was the ability of the nervous system to give one impulse priority over another. In other words, Eysenck was the first to robustly link personality theorizing to the emerging neuroscientific revolution that embraced the systematic experimental study of behavior.

  In 1967 Eysenck amended his theory, adding his third personality dimension, Psychoticism-Socialization, reporting that higher levels of testosterone were associated with lower levels of socialization and higher psychoticism. He also slightly adjusted his definitions of Extraversion and Neuroticism by suggesting that the ascending reticular activation system controlled the cortical arousal characteristic of Introversion-Extroversion differences, and that the emerging limbic system concept along with the sympathetic nervous system accounted for how human personalities were influenced by an underlying Neuroticism-Stability dimension. He also reported twin studies that further convinced him that biological causes played an important part in personality.

  Eysenck may be most easily summarized as an early variant of the Big Five model discussed in Chapter 12. At his higher-order level, he accepted the Big Five Extraversion and Neuroticism dimensions. However, he argued that his Psychoticism dimension was a combination of the Big Five Agreeableness and Conscientiousness factors. He did not include the fifth Big Five factor, Openness to Experience, because he regarded it as a cognitive rather than a personality dimension. He later published the Eysenck Personality Questionnaire (Eysenck & Eysenck, 1975), which focused on empirically measuring his three psychiatrically focused personality dimensions: Extraversion, Neuroticism, and Psychoticism.

  Although Eysenck’s reliance on factor analysis places his thinking in more of a top-down than a bottom-up category, he consistently emphasized the importance of psychological science linking his thinking to neuroscientific foundations of personality. In a paper debating how many basic human personality factors actually existed, Eysenck cited the “need for a nomological or theoretical network to accompany and be part of any model. Only thus can we avoid the problems of subjectivity and the possibilities of misinterpretations attaching to the conceptualization and naming of factors” (1992, p. 670). Further on he wrote, “We need to anchor our dimensions of personality in something more concrete than the morass of factor analysis, and biology supplies us with the necessary tools” (p. 672). Had he considered affective neuroscience perspectives and the dramatic emotional consequences of deep brain stimulation, he likely would have further modified his ideas about the biological bases of personality, a step that was taken by his most illustrious student.

  JEFFREY GRAY

  Jeffrey Alan Gray (1934–2004) was born in London. He did not begin his studies in psychology, receiving his first university degree in modern languages before beginning graduate studies. He was also trained in Russian during his British national military service and translated the work of Russian psychologist Boris Teplov into English for Eysenck while working as his graduate student.

  In contrast to Eysenck, Gray began with a more bottom-up perspective. He completed his dissertation on emotional behavior in animals, and much of his life’s research dealt with diverse physiological influences on learning behavior in rats. He believed that the “reinforcement contingencies” encountered by animals created emotions (see Gray, 1990), a view that was countered by the suggestion that shifts in emotional and other affective feelings constituted the construct of “reinforcement” (Panksepp, 1990b). From his perspective, and building upon Eysenck’s seminal thoughts, he postulated that the brain has a basic Behavioral Activation System and a countervailing Behavioral Inhibition Systems.

  Figure 14.1. Geometrical factor alignment of Gray’s behavioral activation system (BAS) and behavioral inhibition system (BIS).

  While he built on Eysenck’s factorial studies of neuroticism and extraversion, Gray argued that a geometric shift in Eysenck’s model was needed to properly account for the two major personality dimensions Gray proposed: a behavioral inhibition system (BIS) that gave rise to anxiety and a behavioral approach system (BAS) that engendered impulsivity (see Figure 14.1). Gray contended the BIS and BAS constructs did not line up directly with Eysenck’s extraversion and neuroticism dimensions. Gray’s anxiety dimension fell between high neuroticism and low extraversion but inclined more toward neuroticism. Likewise, impulsivity aligned between high extraversion and high neuroticism, inclining more toward extraversion, as illustrated in Figure 14.1 (Gray, 1970; Corr, Pickering, & Gray, 1997). Gray argued that extraversion and neuroticism were derived from impulsivity and anxiety, which were their fundamental neurophysiological bases. In 1994, Carver and White gave a boost to research into Gray’s theory by constructing personality scales to measure his hypothesized BAS
and BIS systems.

  In laying out his theory, Gray also deviated from classical learning theory by asserting that there was not just a single reinforcement mechanism but two: BAS reflected sensitivity to rewards, and BIS, sensitivity to punishments. However, from an affective neuroscience perspective there are many distinct reward and punishment systems: positively and negatively valenced affects manifest by the primary emotions that are closely related to personality, but there are also the homeostatic affects such as HUNGER that have been so widely utilized in rat learning research. Indeed, these powerful brain-based emotional command systems can also be thought of as evolved learning systems that facilitate ongoing adaptation to our specific environments. In other words, the shifting tides of many positive and negative affective systems constituted what behaviorists had become accustomed to calling “reinforcement” processes in the brain (Panksepp, 1990b), and to understand the affective foundations of personality one has to focus on more affective systems than just the BAS and BIS.

  From Gray’s learning theory perspective, the reward and punishment systems were each unidimensional. Yet, each of seven primary emotional-adaptation systems of affective neuroscience may possess different conditioning parameters in the brain, with additional, distinct homeostatic affects (e.g., HUNGER or THIRST, etc.) and sensory affects (various pains and pleasures). However, only the emotional affects are major contributors to personality development, even as they share many of the general brain chemistries for learning, such as glutamate and gamma-aminobutyric acid (GABA). For example, the SEEKING system is more of a general anticipatory reward system, whereas the CARE system may be more of a maternal-social reward system. The PLAY system may be a social emotional system that is especially robust during childhood, with some neurochemistries that are distinct from CARE and LUST. In addition, the PANIC/Sadness system may have acquired addictive-like qualities (being very strongly modulated by brain opioids), which would make its extinction patterns different from those of the FEAR system. As each of these primary emotions are thought to have evolved for distinct survival issues, serving different purposes at different times in our ancestral past, it is likely their learning parameters were evolutionarily adjusted to meet unique survival needs as well. Moreover, the development of the Affective Neuroscience Personality Scales was motivated by the need for personality psychologists to measure each of the distinct primary emotions that are most closely related to personality and psychopathology and to provide an assessment of their relative strengths and weaknesses in an individual’s life. Although both Eysenck and Gray emphasized the need for personality studies to focus on brain issues, a sufficient analysis of core mammalian affects was not evident in either Eysenck’s or Gray’s theorizing.

  In 2000, Gray and McNaughton published a revision of Gray’s theory. In the revised reward sensitivity theory, the BAS remained largely unchanged. However, the BIS assumed responsibility for goal conflict resolution and became a “risk assessment” system: “the ‘increased attention’ output of the behavioural inhibition system” (p. 20). While the BIS once accounted for all punishment, in the revised theory it retained only its anxiety function, which was distinct from fear. Yet, BIS anxiety also included “separation anxiety” (p. 91), which was considered a childhood phenomenon and was not given any special status as in the affective neuroscience PANIC/Sadness system. Specifically, in the modified BIS, anxiety was generated by neural processing not only in the septal-hippocampal circuitry but also in the cingulate and prefrontal cortices. A proposed new brain system, the fight-flight-fear system, dealt with all defensive behavior, including fear. So, one of the more controversial positions taken by Gray and McNaughton (2000) was that fear and anxiety represented different brain systems and what we would call PANIC/Sadness was included with BIS anxiety. From our perspective, the natural emotional systems of mammalian brains were not adequately integrated into the revisions of the BAS and BIS.

  Joseph LeDoux (1994) has shown that the amygdala is clearly linked to both fear and anxiety. Further, while the hippocampus provides cognitive-spatial information related to fear conditioning, it is not needed for the threat-evoked affective experiences of anxiety or fear. Others have also found that deep brain stimulation in the periaqueductal gray can generate alertness (corresponding to risk assessment and increased anxious attention), freezing, or fleeing in animal models, depending on the strength of the electrical current (Vianna, Landeira-Fernandez, & Brandão, 2001). This also applies to humans. For instance, Dean Mobbs and colleagues published a brain imaging study in humans that simulated a predator attack (Mobbs et al., 2007). They described a single “forebrain-midbrain network, which includes the vmPFC (ventromedial prefrontal cortex) at the lowest level of threat and interacts with the midbrain PAG (periaqueductal gray) as the threat level increases” (p. 1082)—meaning as predator threat is imminent, as opposed to far away, and dread increases (discussed in more detail in Chapter 16). All this is consistent with Panksepp’s observations that anticipatory anxiety and raw fear are all part of the same ancient FEAR circuit. Thus, in contrast to Gray’s theory, it seems likely that “anxiety” and “risk assessment” in potentially dangerous situations are tapping into the same emotional FEAR circuit that is activated when survival is imminently in jeopardy.

  Perhaps when one has worked with deep brain stimulation à la Walter Hess and Jaak Panksepp, it is easier to conceptualize the foundational emotional systems embedded in the subcortical brain than when starting from a learning theory perspective. Furthermore, why not study the behavioral, biological, and psychological mechanisms of each affective brain system separately, rather than lumping all “rewards” together into a single BAS and all “punishments” together into a single BIS or FFFS? That would better allow us to consider specific and general “sensitivities” in each emotional or homeostatic affect system and further refine our definition of mammalian affective space—our genetically endowed sensitivities as well as life-span changes in sensitivities derived from addictive or traumatic experiences.

  CLONINGER’S CONTRIBUTIONS: BRIDGING TO NEUROSCIENTIFIC FOUNDATIONS OF PERSONALITY

  C. Robert Cloninger (born 1944) is an American psychiatrist and geneticist. He attended medical school at Washington University in St. Louis and has remained with that institution throughout his career. His personality interests and theories may fit more in the clinical tradition of personality theory. With his unified biosocial theory of personality (Cloninger, 1986), Cloninger connected clinical approaches focusing on abnormal human behaviors to the temperamental characteristics found in all humans and to emerging potential linkages to animal research. In other words, like McDougall and Eysenck before him, Cloninger advanced the view that “abnormal” disorders represented extreme cases of the same personality dimensions evident in normal people at more moderate levels (Cloninger, 1987). Thus, in line with Jeffrey Gray’s work, Cloninger promoted a view that could be linked to emerging neuropsychological work in animals.

  Cloninger’s biosocial theory of personality hypothesized that there were three genetically inherited personality traits, which he would later call temperaments: Novelty Seeking, Harm Avoidance, and Reward Dependence, which could be measured with his Tridimensional Personality Questionnaire (TPQ; Cloninger, 1987). With the release of the TPQ, Cloninger included a discussion of how eight clinically diagnosed personality disorders from the DSM-III (American Psychiatric Association, 1980) could be described by his three biosocial personality scales. That is, there were eight possible combinations of high or low scores on his three TPQ scales, and he illustrated how combinations of the three biosocial personality traits potentially defined the clinical personality disorders. For example, the Antisocial personality disorder was characterized by high Novelty Seeking, low Harm Avoidance, and low Reward Dependence scores whereas the Histrionic personality disorder was described by high Novelty Seeking, low Harm Avoidance, but high Reward Dependence scores. This underscored Cloninger’s belief that the underlying structure
of normal personality traits was the same as that for clinically defined behavior disorders. In other words, maladaptive behavior could be placed on the same continua as behavior describing the general population.

  Cloninger’s Brain Systems

  Around the same time, W. John Livesley (1991) was also working on a common model to bridge the divide between the clinical and normal personality worlds (for a fuller treatment, see Chapter 18), but Cloninger went further by hypothesizing that each of his three biosocial personality dimensions reflected variations in different brain systems, which were largely based on the major monoamine neural modulators (Cloninger, 1987) dopamine, serotonin, and norepinephrine (collectively called “biogenic amines”) that were receiving massive neuroscience and behavioral/psychological experimental attention in the 1970s and 1980s. Figure 14.2 depicts the chemical structures of dopamine, norepinephrine, and serotonin, all of which are similar small molecules. All monoamines contain one amine group, which for dopamine and norepinephrine is connected to an aromatic benzene ring; serotonin has a more complex “indole” ring structure. We highlight his monoamine theory for historical reasons as current neuroscientific thinking has moved toward more complex/sophisticated views in the last three decades.

  Cloninger argued that Novelty Seeking was primarily associated with behavior-activating dopaminergic neurons, with dopaminergic neural projections from the midbrain ventral tegmental area and substantia nigra to the forebrain. The major neural modulator in the Harm Avoidance system was postulated to be serotonin. That system had its roots in the behavior-inhibiting serotonin neurons largely located in raphe nuclei, with projections to the limbic system and the prefrontal cortex. However, Cloninger also noted that benzodiazepines, with actions similar to alcohol, block such learned behavioral inhibition via gamma aminobutyric acid GABA inhibition of serotonergic neurons. Norepinephrine was the major neuromodulator that Cloninger linked with his Reward Dependence system, with major projections from midbrain locus coeruleus to much of the brain, including the neocortex. Reward Dependence functioned as a behavioral maintenance system, with norepinephrine increasing the “signal-to-noise ratio” or salience of relevant stimuli, helping them stand out from those that are less relevant (Cloninger, 1987, pp. 576–577).