The Physiological Substructure of Neuroticism - Research Paper Example

The cause, mechanisms, and manifestations of neurosis are complex and variable in nature. Neuroticism is generally related to physiologicalresponses in the brain that result in the experience of negative emotional states stemming from an inability to handle stress. The neurotic person is often socially awkward and highly self-conscious, and exhibits symptoms on a daily basis. Hans Eysenck’s explanation for neuroticism hypothesizes that neuroticism is caused by sensitivity to environmental stimulation resulting from an over reactive limbic system. This theory relies on an understanding of the mitigating role the sympathetic nervous system plays in emotional responses to various situations, and brings aspects of behavioral genetics into that understanding. In the present literature review, the contemporary knowledge surrounding neuroticism’s physiological substructure is examined. The Physiological Substructure of Neuroticism: A Review of the Literature The study of neurosis is one of immediate and substantial importance, although it is an area of examination more than two hundred years old (Averill & Nunley, 2010). The nomenclature was the invention of a late eighteenth century Scottish doctor who created it to describe what appeared to be nervous disorders despite a complete lack of evidenced neurological disorders (Averill & Nunley, 2010). Though the term itself has been phased out of clinical use (in favor of more specific diagnostic vocabulary), it remains widely used as an umbrella term describing a variety of psychological disorders (Averill & Nunley, 2010). For the purposes of this study, neurotic behavior will be defined using Eysenck’s definition, “maladaptive behavior accompanied by strong, irrelevant and persistent emotions, occurring in full awareness of the maladaptive and irrational nature of the behavior in question” (p. 343). Neuroticism is obviously a multi-faceted and complex subject, and one that bears further examination from a distinctly focused perspective. As a complex and multi-layered psychological condition, neuroticism is not easily explained by any single theoretical approach. Many theories have been posited in an attempt to describe the etiology of neuroticism, but only one theory has experimental and lab based study backing it; this is the conditioning theory that explains neuroticism as the result of autonomic responses (Eysenck, 1981). This theory allows for the perspective that the neuroticism of the mind arises from the appropriate response mechanisms of the body, and that such psychological diseases crystallize based on a predictable and detectable physiological pattern. Conditioning explains that an emotional response produces a behavior that is meant to decrease the subject’s discomfort with that emotion (Eysenck, 1981). This theory also puts physiological mechanisms—the autonomic nervous system’s reaction to emotional stimulus—at the helm of neurotic processes. Some of psychology’s greatest pioneers devoted their energies to establishing working theories on neuroticism. Alfred Adler was one such pioneer, and he went so far as to contribute detailed descriptions of neurotic symptomatology. He developed the Adlerian classification of movements in neuroticism. Adler’s description of the four movement characteristics of neuroticism provides further insight into the disorder’s many possible guises (1979). First Adler describes the movement known as “distance complex,” in which the neurotic tries to use distance to keep at a safe distance from the problem’s solution (1979). Distance complex can surface through fainting spells, intense and prolonged indecision, and hysteria (Adler, 1979). Distance complex, Adler described, was evident in the anxiety types of neuroses and in those with physical manifestations (1979). It was also evident in neurotic compulsions, since the compulsion could be used as a distancing measure. Second, Adler described the movement characteristic known as “hesitating attitude” (1979). In hesitating attitude, the subject can advance somewhat but does so only with postponement (Adler, 1979). The individual repeatedly falls back on this tendency toward procrastination, and in turn learns to rely upon it as a coping mechanism. Adler associates hesitating attitude with neuroses of insomnia and agoraphobia, since those issues can also serve to delay the subject’s ability to confront or deal with problems (1979). Third, Adler refers to the detour movement characteristic, in which the subject tries to move completely around the perimeter of the solution and into some arena that is of less significance (1979). Neuroses of a compulsive nature, such as obsessive compulsive washing, are manifestations of the detour movement characteristic (Adler, 1979). Compulsive washing would allow the subject to repeatedly and continually go around the problem and toward washing instead. The washing would maintain its status as the point of focus, and the subject could return to the compulsion as many times as needed to successfully avoid the uncomfortable problem. Finally, Adler describes the fourth movement characteristic of “narrowed path of approach” (1979, p. 94). This movement occurs when the subject neglects to give himself up to achieving the problem’s solution and instead only takes up an aspect of the problem (Adler, 1979). In Adler’s description, the portion of the problem usually selected for this task is not the most pertinent part, meaning that the most pertinent part is the one left behind (1979). The Adlerian movement characteristics provide a unique lens through which we can view the various manifestations of neuroticism. These earlier contributions to the description of neurosis continue to be relevant to its study even now. Determining relationships between physiological mechanisms and neuroticism can occur on broader or more general levels, and certainly there are studies to represent both ends of the spectrum. There are even specific neurotic symptoms that have been described as resulting from the autonomic nervous system’s functioning (Vogel et al., 2011). One example of this is dissociation, in which the subject experiences a separation between areas of awareness including memory, identity, and environmental perception (Vogel et al., 2011). Dissociation and its manifestations are generally thought to be evidence of defense mechanisms on the part of the autonomic nervous system, intended to reduce the harmful impact of a traumatic or otherwise undesirable experience (Vogel et al., 2011). By providing psychological distance, dissociation allows the mind to retreat into a scenario alternate to the real one, separating the subject from the perception of threatened security. While there is obviously a link between physiological functioning and neuroses, studies have also determined that a link exists between physiological processes of adolescence and social anxiety (Roberson-Nay and Brown, 2011). As Roberson-Nay and Brown describe, adolescence is a time when neurological structures grow and change rapidly so that independent thought and advanced cognitive abilities can be developed (2011). However, this intensified period of growth and development can also make the brain more vulnerable to disruptive agitation that can emerge as neuroses such as social anxiety disorder (Roberson-Nay and Brown, 2011). In this way, a developmental predisposition to anxiety may exist solely based on the brain’s healthy and normal pattern of growth. Indeed, physiological responses to perceived trauma are often examined with regard to neuroticism, and it is also notable that these responses are inextricably linked to the autonomic nervous system’s fight-or-flight response. Many traumatic experiences having the gravity to produce psychological distress have been identified, including childhood abuse or sexual abuse, neglect, witnessing natural or man-made disaster, witnessing another person dying or having their life threatened, fearing one’s own death or having one’s life threatened, and the experience of war (Bacciagaluppi, 2011). Of course, individual variations and personality characteristics play a role in the determination of which trauma-exposed individual will develop neuroticism in response and which will not. Based on the extant literature, trauma studies are one area of psychological inquiry in which the physiological mechanisms underlying resulting dysfunction are at least partially established. In the case of posttraumatic stress disorder, it seems obvious that the autonomic nervous system is impaired in such a way that it triggers the fight-or-flight response under inappropriate circumstances, at inappropriate times, and in response to stimuli that do not warrant such a level of reaction (Jovanovic et al., 2010). Furthermore, brain imagery studies have detected abnormal brain activity in the amygdala of PTSD brains, further implicating a physiological element in this type of neuroticism (Jovanovic et al., 2010). The brain seems to become confused in the wake of traumatic exposure, firing fear-driven responses even when no matching stimulus is present. Based on these findings, it seems that contemporary technological advances will continue playing a role in the further delineation of the physiological substructure of neuroticism. Recent Studies Exposing the Physiological Substructure of Neuroticism Considering the sheer number of neurotic disorders that could be considered for this study, it was determined that narrowing down the focus to one category or condition was ideal. In this way, more detailed study and analysis can be achieved. One disorder that has received renewed attention in recent years is posttraumatic stress disorder. Given the availability of a variety of recent research studies on PTSD, the disorder seemed an obvious choice. The peer-reviewed journal articles selected for review were identified through a search using the terms “physiological” and “posttraumatic.” The search was also limited to studies no older than ten years. All of the selected studies provide further details on the physiological mechanisms beneath the manifestation of neuroticism identified as posttraumatic stress disorder. Numerous studies directly examined the link between physiology and neuroses, with sensitivity to pre-trauma exposure measures and post-trauma exposure measures. In Gutner et al.’s 2010 study of physiologic predictors of PTSD, heart rate and skin conductance responses were measured in a sample of women who had been assaulted within one month of the study. The measurements received at this initial assessment were later compared to those at a later assessment, three months out (Gutner et al., 2010). The environment in which the study’s subjects were placed was highly controlled for sound and temperature quality, and the subjects heart rate and skin conductance were measured at five samples per second (Gutner et al., 2010). The participants were measured while they were alone, then during neutral interviewing, during their description of the traumatic experience, and then again during a phase of recovery (Gutner et al., 2010). The participants had to speak about the trauma they’d experienced for five minutes during that portion of the study. Gutner et al.’s study sought especially to clarify whether the physiological responses related to heart rate would occur specifically in relation to the subject’s discussion of traumatic material, or if the responses would linger even after that part of the discussion had ended, making them part of a more global physiological response (2010). By comparing their data to existing data from other studies, the authors were able to draw some conclusions. First, they found that if a person has a high rate of physiological reactivity (as evidenced by heart rate tests) to their own speech about trauma at one month, they will be more likely to experience other symptoms such as numbing and re-experiencing at three months (Gutner et al., 2010). This means that the subjects who had the most elevated physiological response to trauma reminders in the short term were at a greater risk for extended and magnified posttraumatic stress symptoms (Gutner et al., 2010). The specific populations these studies examine add to their unique results. Like Gutner et al., Schmahl, Elzinga, and Bremner (2002) also examine the physiological substructures of neuroses in their study of adult women with a history of childhood abuse. Again, heart rate was measured; in this case, subjects’ blood pressure was also recorded (Schmahl et al., 2002). As the authors describe, “trauma may result in long-term changes in stress-response neurobiological systems” (Schmahl et al., 2002, p. 272). For their study, the participants’ blood pressure and heart rate were measured before participants were exposed to audio scripts relaying details of abuse and abandonment (Schmahl et al., 2002). Then, blood pressure and heart rate were again measured after listening to these scripts for some time (Schmahl et al., 2002). One of the participants, who had severe symptoms of posttraumatic stress disorder, showed a high degree of reactivity based on the measurements (Schmahl et al., 2002). Another participant had no diagnosis of PTSD, although she had been abused as a child too. This participant didn’t show any unusual physiological response (Schmahl et al., 2002). Notably, this study also revealed that individuals who exhibit dissociative symptoms in the time directly following exposure to trauma are likely to show decreases in physiological responses within the two weeks following the traumatic experience (Schmahl et al., 2002). Indeed, posttraumatic stress disorder is a type of neuroticism that expresses its physiological substructure in a variety of ways. According to the reporting of Gill et al., even the immune system plays a role in PTSD (2009). Furthermore, the immune system’s role in regulating various bodily functions means that its impairment will affect the body on numerous levels (Gill et al., 2009). The mechanism thought to be at play in this complicated relationship involves cortisol; trauma has an activating effect on several areas of the brain and also causes the brain to release cortisol (Gill et al., 2009). Too much cortisol in the blood has a deleterious effect on the immune system and can cause inflammation and other immune responses (Gill et al., 2009). As the study concludes, there is also evidence of a relationship between inflammatory hormones and behavior, further demonstrating the physiological substructures of neuroses (Gill et al., 2009). Kirsch, Wilhelm, and Goldbeck’s study of psychophysiological traits in PTSD is focused specifically on the physiological underpinnings of the disease in children and adolescents (2011). According to Kirsch et al., physiological changes as a result of trauma exposure have usually been focused on autonomic nervous system and immune system effects instead of structural or central nervous system effects (2011). Their study further describes the multiple physiological symptoms at work in the disease, and agrees with the other studies that show the physiological changes that occur in posttraumatic stress disorder (Kirsch et al., 2011). The authors also assert that there may be physiological characteristics in place prior to trauma exposure that could be predictive of a person’s probability of developing the disease after exposure has taken place, which may suggest a genetic component (Kirsch et al., 2011). This study is made relatively unique due to its focus on younger subjects, and as such had little in the way of similar studies to provide comparisons. Nonetheless, the results seem significant and have the potential for generalizability if replicated in similar studies. The study of Kirsch et al. was based on a search of peer-reviewed studies on physiological characteristics of trauma-exposed children up to age eighteen (2011). The studies of interest analyzed symptoms including heart rate and blood pressure, as did previously discussed studies (Kirsch et al., 2011). However, other symptoms including endocrine functions, immune system functions, and traits measured by electromyographic and electrodermal study were also included (Kirsch et al., 2011). Their research confirmed that children that went on to develop fully-blown posttraumatic stress disorder had higher heart rate immediately after exposure when compared to children that didn’t develop posttraumatic stress disorder (Kirsch et al., 2011). This study’s findings suggest that while the development of neuroses like posttraumatic stress disorder has much to do with the trauma exposure, there is also a determining element based on the individual’s physiological predisposition. This seems related to Foster and MacQueen’s statement that from the genetic perspective, neuroticism has a 50% rate of heritability (2008, p. 9). This study in addition to those previously discussed points toward the identifiable, measurable, and proven physiological substructures of posttraumatic stress disorder. Conclusion The present literature review reveals the existing evidence of neuroticism’s physiological substructure. A complex and complicated topic, neuroticism takes many shapes. One form of neuroticism that has been robustly studied is posttraumatic stress disorder. The research examined here describes posttraumatic stress disorder as a form of neuroticism with physiological underpinnings that manifest in the form of heart rate, skin conductance, blood pressure, cortisol, inflammatory, immune, respiratory, and other changes. Future research should address gaps in the study of young subjects. Further clarification of physiological traits that predispose the subject to developing posttraumatic neuroticism will also aid in understanding this complex disease process. References Adler, A. (1979). The structure of neurosis. In Ansbacher, H.L., & Ansbacher, R.R. (Eds.), Superiority and social interest (pp. 83-95). New York: Norton & Company. Averill, J.R., & Nunley, E.P. (2010). Neurosis: The dark side of emotional creativity. In D. H. Cropley, A. J. Cropley, J. C. Kaufman, & M. A. Runco (Eds.), The dark side of creativity (pp. 255-276). New York: Cambridge. Bacciagaluppi, M. (2011). The study of psychic trauma. Journal of the American Academy of Psychoanalysis and Dynamic Psychiatry, 39(3), 525-538. Eysenck, H.J. (1981). Behavior therapy and the conditioning model of neurosis. International Journal of Psychology, 16(4), 343-370. Foster, J.A., & MacQueen, G. (2008). Neurobiological factors linking personality traits and major depression. Canadian Journal of Psychiatry, 53(1), 6-13. Gill, J.M., Saligan, L., Woods, S. & Page, G. (2009). PTSD is associated with an excess of inflammatory immune activities. Perspectives in Psychiatric Care, 45(4), 262-277. Gutner, C.A., Pineles, S.L., Griffin, M.G., Bauer, M.R., Weierich, M.R., & Resick, P.A. (2010). Physiological predictors of posttraumatic stress disorder. Journal of Traumatic Stress, 23(6), 775-784. Jovanovic, T., Norrholm, S.D., Blanding, N.Q., Davis, M., Duncan, E., Bradley, B., & Ressler, K.J. (2010). Impaired fear inhibition is a biomarker of PTSD but not depression. Depression and Anxiety, 27(3), 244-251. Kirsch, V., Wilhelm, F.H., & Goldbeck, L. (2011). Psychophysiological characteristics of PTSD in children and adolescents: A review of the literature. Journal of Traumatic Stress, 24(2), 146-154. Roberson-Nay, R., & Brown, R.C. (2011). Neurodevelopmental aspects of social anxiety. In Alfano, C.A. & Beidel, D.C. (Ed.). Social anxiety in adolescents and young adults (pp. 53-71). Washington: APA. Schmahl, C.G., Elzinga, B.M., & Bremner, J.D. (2002). Individual differences in psychophysiological reactivity in adults with childhood abuse. Clinical Psychology and Psychotherapy, 9(4), 271-276. Vogel, M., Meier, J., Gronke, S., Waage, M., Schneider, W., Freyberger, H.J., & Klauer, T. (2011). Differential effects of childhood abuse and neglect: Mediation by posttraumatic distress in neurotic disorder and negative symptoms in schizophrenia? Psychiatry Research, 189(1), 121-127. Read More