The Emotional Foundations of Personality

by Kenneth L Davis

  CHAPTER 18

  Affective Neuro-Personality and Psychopathology

  Once these affects are re-represented in higher MindBrain regions, they tend to remain idiographically self-centered, and much of emotional education as well as psychotherapy may need to proceed by “deconditioning” and “recontextualization” of emotional self-centeredness. That allows one to accept one’s negative feelings as one’s own, and not of others’ making.

  —Jaak Panksepp, “The Primary Process Affects in Human Development, Happiness, and Thriving”

  IN 2013, THE U.S. DEPARTMENT of Health and Human Services reported that 43.8 million adults in the United States eighteen or more years of age (18.5 percent of the population) had some form of mental illness in 2013, and a total of 15.7 million of these adults (6.7 percent of the population) had had at least one major depression episode (NSDUH: Mental Health Findings, 2013). Depression, of all the major psychiatric disorders, is associated with the highest risk of suicide, highlighting how the psychological pain of mental illness can erode the will to live and lead some people to take their own lives. Mortality data from the Centers for Disease Control and Prevention (2014) show that suicide is the tenth leading cause of death in the United States, with over forty thousand deaths by suicide in 2012, or 1.6 percent of all deaths in the United States. The details are frightening: (1) Suicide is the seventh leading cause of death for males and the fourteenth leading cause for females. (2) Although “females are more likely than males to have suicidal thoughts,” (3) “males take their own lives at nearly four times the rate of females and represent 77.9% of all suicides” (Centers for Disease Control and Prevention, 2015).

  These figures dramatize the impact of mental disorders in the general population. But what actually is mental illness? What causes these bouts of human suffering? Why do afflicted individuals have such difficulty escaping from their periods of maladaptive behavior and thought? How can we develop more effective treatments for these psychological problems? Unfortunately, the neural nature of psychological pain remains largely a mystery, at least compared to physical pain (Panksepp & Biven, 2012). However, there is a growing database highlighting how feelings of loneliness (i.e., separation distress, arising from the PANIC/Sadness system) may be foundational for the intrapsychic pain that leads to so much human suffering (Panksepp, 2016), which could be treated more easily with ultralow doses of safe opioids, such a buprenorphine and perhaps tramadol, than the medical system is willing to admit (Yovell et al., 2016).

  As discussed in Chapter 4, over one hundred years ago William McDougall tried to answer the question of what mental illness is by putting forward the thesis that abnormal behavior simply represented extreme, exaggerated arousals of our normal primary instincts. In other words, psychopathology could be placed on the same personality dimensions as more moderate expressions of personality, but with imbalanced affective instinctive reactions so pronounced they became a liability to survival rather than an asset. This would be analogous to losing the ability to regulate one’s normal body temperature and experiencing life-threatening fever or hypothermia. McDougall’s insight suggested that many mental illnesses could best be understood as special cases of imbalanced activities of our usually adaptive primary emotional urges. In short, to understand many mental illnesses, we may not require unique categories specific to mental illness. Instead, they could fruitfully be thought of as cases in which the regulation of normal emotional behaviors and feelings were excessive or inadequate or had broken down in ways that could be demonstrated neuroscientifically (for such views, see Panksepp, 2004, 2006).

  We concur with McDougall’s basic point. But until recently, neuroscience has had difficulty conceptualizing how to study the neural nature of emotional feelings in humans. Many still resist the evidence-based idea that basic emotional systems are shared homologously across all other mammals, including those like laboratory rats, in which the detailed neuroscientific work can be conducted. However, this idea has become more substantive as the neuroscience revolution has revealed more and more about how our emotional feelings arise from subcortical brain activities (Panksepp, 1998a, 2004, 2006, 2016). As we have discussed throughout this book, the mammalian subcortical primary emotional systems are foundation pillars for our personalities, and many psychopathologies arise from imbalances of such primary brain emotional systems. Both personality disorders and other psychopathologies arise when these fundamental BrainMind systems become imbalanced. In such affectively disordered states, our emotional systems can create distressing feelings (as well as excessive joy, as in mania), often accompanied with distorted and extreme thoughts and behaviors. For instance, the psychological pain that leads people to commit suicide can arise from sustained overactivity of the PANIC/Sadness system, which can lead to depression (e.g., Panksepp & Yovell, 2014; Panksepp, 2015, 2016) and can be treated by medicines that reduce the painful feelings of separation distress (Yovell et al., 2016).

  Yet, it is important to consider how the older subcortical areas of our brains seem able to overwhelm the more recently evolved cerebral cortex and its remarkable capacity for spoken language and reflective thinking. The reason seems straightforward: A basic tenet of affective neuroscience is that the subcortical emotion systems prevail in early development and remain foundational not only for our normal, everyday emotional feelings and personality traits but also our imbalanced adult emotional feelings.

  For a complementary perspective, the eminent neurologist Marsel Mesulam of Northwestern University’s School of Medicine explained it as follows: These subcortical systems can “rapidly shift information processing states throughout the cerebral cortex . . . [and] alter the tone, coloring, and interpretation of experience rather than its content” (2000, pp. 78–79). The mechanism mediating these old brain influences may lie in the distinction between cortical “channel” and subcortical affective “state” brain-mind functions (Mesulam, 2000). For state modulation, each cortical area receives inputs arising from subcortical brain regions, such as the vast biogenic amine systems, involving norepinephrine, serotonin, and dopamine, ascending from ancient brain stem regions along with various more specific neuropeptide systems (reviewed in Panksepp, 1993). These regions regulate not only many subcortical emotional circuits but also the entire cerebral cortex, thereby concurrently regulating both specific cognitive and more ancient affective messages. These connections determine the state of information processing rather than the content being transmitted along the point-to-point cortical channels that instantiate thoughts, through the “fine weave” of more rapidly acting local excitatory glutamate and inhibitory GABA systems of neocortex. These affect modulating “corticopetal” (Latin for cortex-seeking) biogenic amine projections to upper brain regions are not balanced by thoughtful “corticofugal” (Latin for cortex-fleeing) connections from the cerebral cortex to older regions of the brain. But without the cortex, the brain cannot “put the brakes on” extreme emotional feelings that arise from below.

  Our affective states of mind strongly influence not only what our senses and thoughts perceive but also our interpretations of the emotional importance of incoming messages. Thereby the affective tone of our thoughts can be shifted positively or negatively, giving personal meaning to our diverse cognitive experiences. To the extent that individuals are chronically biased toward experiencing excessively negative emotional states (and perceive, think, and act correspondingly), their pessimistic thoughts and behaviors become progressively problematic, leading to increasing life difficulties. The underlying brain changes that promote such problems in living (e.g., depression and anxiety) have been the focus of abundant brain and genetic research in the past half century. Such modern findings affirm William McDougall’s hypothesis that “morbidly exaggerated” emotions may instigate psychiatric as well as personality disorders. We will only touch upon a few high points, but first we focus on the close relationship of psychopathology and personality dimensions.

  THE COMMON DIMENS
IONS OF NORMAL AND DISORDERED LIVES

  Many studies have shown how normal brain affective mechanisms, taken to extremes, can promote various difficulties in living. Accordingly, many psychologists and psychiatrists have explored the relationship between personality and psychopathology. Specifically, there have been efforts to link diagnoses of mental illness to the Big Five/Five-Factor Model personality dimensions (Livesley, Schroeder, Jackson, & Jang, 1994; Krueger & Markon, 2014; Widiger, Costa, & McCrae, 2013). In one of the earlier more prominent efforts, John Livesley (Livesley et al., 1992) and Lee Anna Clark (1993) independently generated assessment tools that specify psychopathologies in terms of the dimensions of the Big Five/Five-Factor Model.

  More recently there have been attempts to incorporate psychometric measures of maladaptive personality elements into the DSM-V psychiatric diagnostic process. While most such efforts have failed, one partial success was the inclusion of Section III in the DSM-V, which addresses “personality disorders” in terms of the Big Five/Five-Factor Model, thereby providing specific experimental assessments to describe and classify patients. In doing this, the DSM-V retained the traditional medical model that seeks to more explicitly demarcate normality from abnormality. Accordingly, the DSM-V retained Section II of the previous version, which delineates the old diagnostic categories of personality disorders. Thus, the categorical versus factorial debate continues, with the dominant categorical diagnostic model still based on clinical authority and collective wisdom rather than emerging research evidence, which ideally, in the future, would be based on primary-process emotional inquiries.

  Table 18.1. Personality Inventory for DSM-5 personality disorder facets

  Facet Brief Definitions

  Emotional lability Exhibiting unstable emotions that are inconsistent to the event experienced.

  Anxiousness Feelings of tenseness including apprehensiveness in uncertain situations.

  Separation insecurity Dread of being socially rejected by or separated from one’s social contacts.

  Submissiveness Adapting to the interests or desires of others even when contrary to one’s own interests or desires.

  Hostility Frequent feelings of anger or irritation even in response to minor conflicts.

  Perseveration Persistence of a behavior despite that behavior not being effective.

  Withdrawal Avoiding social contacts and preferring to be alone.

  Intimacy avoidance Avoiding close or sexual relationships.

  Anhedonia Lacking the capacity to enjoy life events or take an interest in doing things.

  Depressivity Feeling hopeless and pessimistic including possible thoughts of suicide.

  Restricted affectivity Blunted reactions to normally emotionally arousing situations and remaining indifferent in such circumstances.

  Suspiciousness Expectations of being mistreated by others and questioning their loyalty or intent.

  Manipulativeness Attempting to influence or control others to achieve one’s own ends.

  Deceitfulness Dishonesty including misrepresentation and fabrication in communications to others.

  Grandiosity Feeling superior to others and entitled to special treatment.

  Attention seeking Exhibiting behavior intended to make one’s self the focus of attention.

  Callousness Lacking concern for others and lacking remorse after harming others in some way.

  Irresponsibility Disregarding commitments and obligations including carelessness with others’ property.

  Impulsivity Frequently acting spontaneously without a plan or assessing possible outcomes.

  Distractibility Having one’s attention easily distracted from a task and difficulty staying focused on a goal.

  Risk taking Engaging in risky activities regardless of the level of potential danger involved.

  Rigid perfectionism Insisting on flawless performance by self and others including the belief that there is only one correct way.

  Unusual beliefs and experiences Believing one possesses supernatural abilities and has unusual experiences that seem to include delusional elements.

  Eccentricity Exhibiting odd behavior, appearance, and speech including having strange thoughts.

  Cognitive and perceptual dysregulation Having unusual thought experiences including being detached from one’s self and the external world seeming unreal.

  Adapted from Krueger and Markon (2014).

  For those with such interests, Section III of the DSM-V does provide experimental assessments, the main one being an extensive 220-item questionnaire (Krueger, Derringer, Markon, Watson, & Skodol, 2012) that measures twenty-five statistically derived scales or facets that essentially represent the maladaptive extremes of the five-factor personality model (see Table 18.1 for the full list of facets). These facets were factor analytically summarized into five factors that very closely resemble the Big Five/Five-Factor Model. This new assessment is called the Personality Inventory for DSM-V (PID-5) and is owned and provided by the American Psychiatric Association (for a lucid discussion of this transition process and the ten-year-long political process that resulted in the American Psychiatric Association board not endorsing the personality disorder dimensional model, see Krueger and Markon 2014).

  In contrast, the Affective Neuroscience Personality Scales (ANPS) is a categorical assessment. It provides measures of six primary emotions, which can be useful for placing disordered lives as well as more normal personalities in affective space (which can also be conceptualized dimensionally). The PID-5 has three facets that more or less correspond to primary emotions: The ANPS RAGE/Anger, FEAR, and PANIC/Sadness scales would likely line up closely with the PID-5 Hostility, Anxiousness, and Separation Insecurity scales. However, many of the corresponding PID-5 items have a more tertiary than primary flavor. For example, one of the PID-5 Hostility items reads, “I always make sure I get back at people who wrong me.” One of the PID-5 Anxiousness items reads, “I always expect the worst to happen,” and a Separation Insecurity item reads, “I’d rather be in a bad relationship than be alone.” Most troubling from an affective neuroscience perspective is the absence of scales that closely correspond to the SEEKING, CARE, or PLAY emotional systems. For example, does a low level on the PID-5 Withdrawal scale equate to a high level of PLAY? As we discuss later in this chapter, the absence of positive emotions may be as critical to maintaining mental health as regulating the negative emotions. In sum, much work is needed to relate the primary mammalian brain emotions credibly to psychiatric symptoms, many of which undoubtedly are mixtures of primary emotions, with many others representing more tertiary expressions. The ANPS provides an explicit neuroscience-based anchoring tool that may better help us proceed systematically from primary-process affective issues to tertiary-process levels of cognitive complexity.

  ANPS DIMENSIONS OF AFFECTIVE IMBALANCE; OR, ONE WAY TO AVOID DIAGNOSTIC CONFUSION

  Here we show that the ANPS may be usefully deployed to describe and discriminate between psychiatric diagnostic categories such as type I bipolar disorder (BPD-I), type II bipolar disorder (BPD-II), and major depressive disorders. BPD-I and BPD-II are similar, but BPD-I is symptomatically more severe and perhaps more indicative of the classic manic-depression diagnosis. In BPD-II, the manic phase is less debilitating and is often seen as actually increasing personal effectiveness due to increased energy and goal-directed activity. In BPD-II, the high energy phase is thus called hypomania, which may also be characterized by increased irritability (e.g., possibly a combination of high SEEKING and RAGE/Anger).

  According to the quantitative genetic model of bipolar spectrum illness (Evans et al., 2005), the same genetic variants contribute to the development of affective temperaments such as depression, as well as psychiatric problems such as BPD, in which periods of mania and depression may occur successively. In a study of the distribution of affective personality traits in families with members having a BPD diagnosis, Savitz, Merwe, and Ramesar (2008a) found that the ANPS PANIC/Sadness scale was significant
ly higher in BPD-I–diagnosed family members than in two control groups made up of unaffected family members or family members with a DSM-IV diagnosis other than depression, such as alcoholism or generalized anxiety disorder. Consistent with the model, both the ANPS PANIC/Sadness and FEAR scores were highest for individuals diagnosed with BPD-I or BPD-II but generally lower for individuals with recurrent major depression or that had only had a single depressive episode and lowest for the two control groups. However, after controlling for self-rated depression using the Beck Depression Inventory (Beck & Steer, 1993) or mania using the Altman Self-Rating Mania Scale (Altman, Hedecker, Peterson, & Davis, 1997), only the PANIC/Sadness scale continued to differentiate significantly between groups, perhaps suggesting the relative importance of this primary emotion in these disorders.

  In a related paper, Savitz, Merwe, and Ramesar (2008b) also reported that the ANPS RAGE/Anger scale differentiated BPD-II subjects better than BPD-I subjects compared to unaffected family members. BPD-II patients, who are often characterized by an irritable mood, also had significantly higher RAGE/Anger scores than individuals with previous depressive episodes or unaffected relatives. Savitz et al. (2008b) reported in this study that Beck Depression Inventory scores were significantly correlated with higher RAGE/Anger scores and lower SEEKING and PLAY scores, a finding that supports research on the importance of promoting positive emotions (e.g., SEEKING and PLAY) in the treatment of depression (Panksepp et al., 2014; Panksepp & Yovell, 2014) (also discussed later in this chapter). Another research team (Sawaya et al., 2015) similarly reported that, compared to a control group, a group of patients who had experienced a major depressive episode showed significantly lower ANPS SEEKING and PLAY scores, as well as significantly higher RAGE/Anger, FEAR, and PANIC/Sadness scores. Thus, we continue to see that lower positive affects in addition to elevated negative affect systems are important considerations for disordered personalities.