Tuesday 18 March 2014

What is fear? |


Introduction

All emotions have three components, behavioral, autonomic, and hormonal, which are synchronized during the emotional experience. For fear, the behavioral component consists of visible reactions of the face and body. A person’s immediate facial response to a threatening stimulus involves a widening of the eyes and either the stretching of the lips horizontally or the actual opening of the mouth. Pupils dilate, and nostrils flare. With intense threats, the muscles tremble. Breathing rate increases, the skin pales, and sweating occurs. Frightened individuals usually throw their arms up and flinch away from the fearful stimulus. The hair often stands up on their bodies, particularly on the arms and head, in a process called piloerection. Urination or defecation may occur. Frightened individuals often emit inarticulate cries that seem almost reflexive. Depending on the closeness of the threatening stimulus and how long the experience lasts, these reactions may be followed by hiding, fleeing, or, if individuals find themselves trapped, fighting in desperate and uncontrolled panic. In rare cases, individuals can die while experiencing intense fear, usually because of cardiac arrhythmias. The fear response, in general, is often called the fight-or-flight response.









Charles Darwin argued in The Expression of the Emotions in Man and Animals (1872) that the physical expression of fear and the other emotions in humans was innate and had evolved from the way earlier animal species demonstrated similar emotions. As evidence, he argued that the facial expressions for various emotions were nearly identical in humans from all cultures and that similar physical responses and facial expressions occurred in most mammalian species. Later research has supported Darwin’s hypothesis, suggesting that the behavioral expression of emotions is largely inherited. This does not mean that innate emotional tendencies cannot be modified through experience and practice. Most people recognize the behaviors associated with emotions such as fear, and many can fake them to a greater or lesser extent.


Many of the behavioral effects of fear, such as sweating and piloerection, are controlled by activation of the autonomic nervous system, which contains the sympathetic and parasympathetic branches, and is part of the peripheral nervous system. The autonomic system also produces internal reactions to fear. Heart rate and blood pressure increase. Blood flow increases to the muscles, while simultaneously decreasing to internal organs such as the stomach and intestines. The saliva glands reduce their output, and the mouth becomes dry. At the same time, stress hormones are released in the body. These include epinephrine, often called adrenaline, and cortisol, a type of natural steroid. Epinephrine increases glucose metabolism to make energy available to the body’s cells and increases blood flow to the muscles. Cortisol promotes energy availability, increases blood flow, and increases alertness. It promotes blood clotting and healing should an injury occur.




Learned Fears

Fear is an innate response of most complex nervous systems and was considered by John B. Watson, the founder of behaviorism, to be one of the three basic emotions, along with rage and love. Innately, fear is first activated in an organism by exposure to painful stimuli or such experiences as loud noises or heights. However, fear can be associated with specific objects or situations through learning. Watson and Rosalie Rayner, Watson’s graduate assistant, illustrated this in a 1920 study known as the Little Albert study. The researchers exposed an eleven-month-old infant known as Albert B. to a white rat and a loud noise simultaneously. Albert quickly developed a fear of the rat, which illustrates classical conditioning. It is often said that Albert developed a phobia of white rats. Certainly, Albert developed a conditioned emotional reaction (CER), a learned emotional response to an object or situation. Phobias are believed to be examples of CERs.


Interestingly, conditioned fears develop more easily to some stimuli than to others. For example, fear of spiders and snakes is much more common than fear of automobiles or guns, even though deaths from guns and automobile accidents are more frequent in the modern world than deaths from spider or snake bites. Many researchers believe this is evidence of an evolutionary preparedness in learned fears. Cars and guns did not exist during the early evolution of the human species, but human ancestors had much to fear from snakes and other animals and from such experiences as falling from a high place or being caught in the open. The common dangers facing early humankind may have shaped humans genetically so that the species is more prone to some fears than others.




Neural Integration of Emotional Components

The primary brain structure for controlling and integrating the three components of emotion is the amygdala, an almond-shaped collection (nucleus) of neurons in the brain’s limbic system. The amygdala contains a dozen subregions and is often called the amygdaloid complex. It is involved in both processing emotions and learning about emotional situations, especially for fear and anger. Several amygdaloid areas process fear. For example, the physical brain changes that accompany classically conditioned CERs appear to occur in the amygdala’s lateral nucleus. However, the primary amygdaloid structure involved in fear is the central nucleus, which gets direct input from the lateral nucleus and is particularly responsive to aversive stimuli. Stimulation of the central nucleus in animals with drugs or electrical current triggers all three components of the fight-or-flight response. Creating a lesion in the central nucleus in animals abolishes learned fear responses; the animal becomes calmer when handled and shows lower levels of stress-related hormones. Isolation of the central nucleus by severing its inputs produces the same effects. The central nucleus directs fear responses by activating brain structures that manage heart rate, blood pressure, hormone release, and other emotional reactions.


Studies of the human amygdala generally report similar results to those seen in animals. Stimulation of the human amygdala in patients undergoing evaluation for brain surgery causes the emotion of fear. Lesions of the amygdala, as can occur with injuries or when damaged tissue is removed, make it harder for people to acquire CERs, and they are less likely to remember strongly emotional events. Studies have shown that activity increases in the amygdala when people perceive negative events, such as seeing a film about an automobile accident, or even while hearing threatening words such as slaughter or mutilate. Amygdala damage impairs people’s ability to recognize facial expressions of fear and to recognize “scary” music, even while recognition of happy or sad music is unaffected.




Feeling and Cognition in Emotion

In experiencing emotions such as fear, more occurs than just physical responses of the body and hormonal system. There are subjective feelings and thought processes (cognitions) accompanying the emotion. The relationship between the physical responses, the feelings, and the cognitions has posed problems for psychologists because subjective phenomena are difficult to measure in humans and almost impossible to study in animals. One early theory that tried to explain the relationship between the physical and feeling aspects was theJames-Lange theory. William James and Carl Lange, two psychologists working independently in the late 1800s, each concluded that the physical responses of emotions, such as the increased heart rate and dry mouth of fear, occur immediately after perception of a stimulus, and these physical responses cause the subjective feeling. Research generally supports the James-Lange theory for fear. Patients with spinal cord injuries that prevent brain recognition of the body’s autonomic response to a fearful (or angry) stimulus often report less intense emotional feelings. Also, merely simulating the facial expressions of emotions activates elements of the autonomic nervous system and can produce some feeling aspects of emotion. Still other evidence suggests that cognitions, in particular, can also influence physiological states, such as those activated during fear. A strange noise in the house late at night triggers the fight-or-flight system, but the emotion immediately dissipates when the cat is identified as the cause.


A useful way to examine emotions is to consider primary versus secondary emotions. Fear is a primary emotion. It is an evolved and adaptive physiological response that occurs automatically in response to particular sensory stimulations such as loud sounds. The fear response produces a cascade of bodily reactions that help individuals deal with immediate threats. The amygdala is intimately involved in this process. Conscious awareness of the emotion either occurs parallel to the physiological response or follows it. Secondary emotions are more complex and generally begin in higher levels of the brain, particularly the prefrontal cortex, which is involved in planning and organizing behaviors. Secondary emotions, such as anxiety and shame, are acquired through learned experience and involve complex cognitions. However, they also activate the amygdala and the physiological mechanisms of emotion.


Consider
anxiety, a secondary emotion related to fear. Anxiety is more about an expectation of threat than about immediate danger. It arises primarily from learned experiences and cognitive evaluations of a situation. For example, someone who drinks too much at a wedding and has a bad experience may develop anxiety when invited to another wedding. The anxiety is based on a cognitive expectation of what could go wrong. The anxiety activates some autonomic and hormonal elements of the fear response, although to a lesser degree than an actual threatening stimulus. If this mild anxiety helps the person avoid further bad experiences at weddings, perhaps by not drinking, then the anxiety has been adaptive and will eventually disappear. Unfortunately, while genuinely fearful situations usually arise and then terminate quickly, learned anxieties can become chronic and produce long-term activation of the fight-or-flight response. This results in the physically damaging effects of long-term stress. As an example, long-term activation of the amygdala’s central nucleus can produce gastric ulcers in animals and probably has similar effects in humans. As negative physical effects are occurring, anxious people also experience negative moods, agitated thoughts, and a sense of losing control. Although they may not have immediate urges to physically hide or flee, they try to escape mentally by avoiding the anxiety-provoking situation or by distracting themselves from the negative thoughts. Thus, the normally adaptive mechanisms of the fear response become tied to maladaptive anxiety, which may develop into anxiety disorders such as phobia or panic disorder.




Bibliography


Blanchard, Robert J., et al., eds. Handbook of Anxiety and Fear. Oxford: Academic, 2011. Digital file.



Butcher, James N., Susan Mineka, and Jill M. Hooley. “Panic, Anxiety, and Their Disorders.” Abnormal Psychology. 13th ed. Boston: Allyn, 2006. Print.



Carlson, Neil R. “Emotion.” Physiology of Behavior. 9th ed. Boston: Allyn, 2007. Print.



Freeman, Daniel, and Jason Freeman. Anxiety: A Very Short Introduction. Oxford: Oxford UP, 2012. Print.



Johnson, Steven. “Emotions and the Brain: Fear.” Discover Magazine 1 Mar. 2003. Print.



Laird, James D. Feelings: The Perception of Self. New York: Oxford UP, 2007. Print.



LeDoux, Joseph. The Emotional Brain. New York: Simon, 1998. Print.



Plamper, Jan, and Benjamin Lazier, eds. Fear: Across the Disciplines. Pittsburgh: U of Pittsburgh P, 2012. Print.



Watson, J. B., and R. Rayner. “Conditioned Emotional Reactions.” Journal of Experimental Psychology 3 (1920): 1–14. Print.



Zillmer, Eric A., Mary V. Spiers, and William Culbertson. “Higher Functional Systems.” Principles of Neuropsychology. 2nd ed. Belmont: Wadsworth, 2007. Print.

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