Our brain has an approach-avoidance system that encourages us to seek out experiences that evoke pleasurable emotions and to avoid those that evoke painful or frightening ones. In this chapter we explore what studies of animals have taught us about how the brain regulates the emotion of fear, and we look at the nature of human anxiety disorders, particularly post-traumatic stress disorder, which is an extreme reaction of fear. By studying these disorders, scientists are learning where emotions arise in the brain and how they control our behavior. We learn about novel ways in which scientists are using drug therapy and psychotherapy to help treat people with anxiety disorders.
Because emotions are a powerful force in any decision we make, from the simplest to the most complex, this chapter touches on important biological aspects of how we reach decisions, including moral decisions. We see how damage to regions of the brain that regulate emotion damps down our emotions and adversely affects our ability to make choices, and we see how deficits in the brain regions that control emotional processing and moral decision making can lead to psychopathic behavior.
THE BIOLOGY OF EMOTION
The first person to consider the biology of emotion was Charles Darwin. In the course of his work on evolution, Darwin came to understand that emotions are mental states shared by all people in all cultures. He was particularly interested in children because he believed that they express emotions in a pure and powerful form. Since they are seldom able to suppress their feelings or fake an expression, he considered them ideal subjects for studying the importance of emotion (fig. 8.1). In his 1872 book, The Expression of the Emotions in Man and Animals, Darwin also carried out the first comparative study of emotion across species. He showed that unconscious aspects of emotion are present in animals as well as people and noted that these unconscious aspects have been extremely well conserved throughout evolution.
We are all familiar with emotions such as fear, joy, envy, anger, and excitement. To some extent these emotions are automatic: the brain systems that carry them out operate without our being aware of them. At the same time, we experience feelings of which we are fully aware, so that we are capable of describing ourselves as scared or angry or grumpy, surprised or happy. The study of emotions and moods helps reveal the porous boundaries between unconscious and conscious mental processes, documenting the ways in which these seemingly distinct kinds of cognition are constantly interacting. We first encountered the divide between unconscious and conscious processing in the brain when we explored creativity, in chapter 6, and we will return to it again when we discuss the unconscious, in chapter 11.
All of our emotions have two components. The first begins unconsciously and manifests itself as an outward expression; the second is a subjective, internal expression. The great American psychologist William James described these two components in an 1884 essay entitled “What Is an Emotion?” James had a profound insight: not only does the brain communicate with the body, but, equally important, the body communicates with the brain.
Figure 8.1. Darwin studied emotion in children because they display emotions in their purest form.
James proposed that our conscious experience of emotion takes place only after the body’s physiological response, that the brain responds to the body. He argued that when we encounter a potentially dangerous situation, such as a bear in our path, we do not consciously evaluate the danger and then feel afraid. Instead, we respond instinctively and unconsciously to the sight of the bear by running away from it and only later experience fear. In other words, we process emotion first from the bottom up—with a sensory stimulus that causes our heart rate and respiration to spike, leading us to flee—and only then from the top down—using cognition to explain the physiological changes that have taken place in our body. James noted that “without the bodily states following on the perception, the latter would be purely cognitive in form, pale, colorless, destitute of emotional warmth.”1
The second component of emotion is the subjective, internal experience of emotion, the conscious awareness of how we feel. In this book, we follow the lead of Antonio Damasio, director of the Brain and Creativity Institute at the University of Southern California, and restrict the word “emotion” to the observable, unconscious behavioral component and use “feeling” to refer to the subjective experience of emotion.
THE ANATOMY OF EMOTION
Emotions can be classified along two axes: valence and intensity. Valence has to do with the nature of an emotion, with how bad or good something makes us feel on a spectrum from avoidance to approach (fig. 8.2). Intensity refers to the strength of the emotion, the degree of arousal it evokes (fig. 8.3). We can actually map most emotions onto these two axes. Such a map doesn’t capture the entire essence of a particular emotion, but it does present it in a way that is useful when matching facial expressions to the brain systems that produce them.
Figure 8.2. The valence of emotion, from avoidance to approach
Figure 8.3. The intensity spectrum of happiness
Many structures in the brain are involved in emotion, but four of them are particularly important: the hypothalamus, which is the executor of emotion; the amygdala, which orchestrates emotion; the striatum, which comes into play when we form habits, including addictions; and the prefrontal cortex, which evaluates whether a particular emotional response is appropriate to the situation at hand (fig. 8.4). The prefrontal cortex interacts with, and in part controls, the amygdala and striatum.
Figure 8.4. The hypothalamus, amygdala, striatum, and prefrontal cortex are the four main structures in the brain involved in emotion.
We say the amygdala “orchestrates” emotion because it links the unconscious and conscious aspects of an emotional experience. When the amygdala receives sensory signals from the areas concerned with vision, hearing, and touch, it generates responses that are relayed onward, largely by the hypothalamus and other structures in the brain that control our automatic physiological responses. When we laugh or cry—when we experience any emotion—it is because these brain structures are responding to the amygdala and acting on its instructions. The amygdala is also connected to the prefrontal cortex, which regulates the feeling state, the conscious aspects of emotion, and its influence on cognition.
It goes without saying that our emotions need to be regulated. Aristotle argued that the proper regulation of the emotions was a defining feature of wisdom. “Anyone can become angry—that is easy,” he wrote in The Nicomachean Ethics. “But to be angry with the right person and to the right degree and at the right time and for the right purpose, and in the right way—that is not within everybody’s power and is not easy.”2
FEAR
Like every other emotion, fear has both an unconscious and a conscious component. The physical aspects of our emotional response to a fearful stimulus—accelerating heart rate and respiration and opening sweat glands in the skin—are mediated by the autonomic nervous system, and they take place below the level of consciousness. As we have seen, James argued that our bodily response to fear comes first and triggers our conscious feeling. Thus, without the body there would be no fear. This insight set the agenda for the study of fear.
Scientists have a very good understanding of the neural circuitry of fear. It begins with the amygdala, which orchestrates all emotion but seems to be particularly sensitive to fear. A scary stimulus arrives at the amygdala, activates a representation of danger, and triggers the body’s fear response. These are automatic, hardwired physiological and behavioral responses.
Next in the circuit is the insular cortex, a small island of neurons lying deep within the frontal and parietal lobes that translates bodily emotion into conscious awareness. It assesses bodily responses, such as degree of pain, and monitors what is going on in the viscera and the muscles, assiduously tracking our heart rate and the activity of our sweat glands. The later discovery of the insular cortex provided biological confirmation of James’s idea that our bodily response to fear precedes our awareness of fear.
Finally, a second region of the prefrontal cortex, the dorsal prefrontal cortex, is actually the point at which our conscious mind—our volition, or will—can impose itself on the way emotion is being carried out.
Our reaction to fear is an adaptive response, one that helps us survive. It is a program of actions sometimes referred to as the “fight, flight, or freeze” response. These actions include musculoskeletal changes (the facial muscles assume a mask of fear), changes in posture (a sudden startled movement, followed by rigidity), increases in heart rate and respiration, contraction of the stomach and intestinal muscles, and secretion of stress hormones such as cortisol. All of these changes in the body take place in concert, and they send signals to the brain.
Two things about fear are important here. First, the senses send signals to the amygdala, which recruits additional areas of the brain. We know this because brain imaging gives us a precise portrait of what is happening as this primal response unfolds. Second, the changes in our body, in concert with the insular cortex, make us aware of the feeling. We feel scared because the brain has noticed the changes unfolding within our body. That is why we get ready to run before we know why we are running.
THE CLASSICAL CONDITIONING OF FEAR
Until the end of the nineteenth century, the only approaches to the mysteries of the human mind were introspection, philosophical inquiries, and the insights of writers. Darwin changed all that when he argued that human behavior evolved from our animal ancestors. This argument gave rise to the idea that experimental animals could be used as models to study human behavior.
The first person to explore this idea systematically was Ivan Pavlov, who had won the Nobel Prize in Physiology or Medicine in 1904 for his study of gastric secretion. As we saw in chapter 5, Pavlov taught dogs to associate two stimuli—a neutral stimulus (such as the sound of a bell) that predicts a reward (or punishment) and a positive (or negative) reinforcing stimulus. These experiments showed that the brain is able to recognize and make use of a stimulus to predict an event (the arrival of food) and to generate a behavior (salivation) in response.
Pavlov used this finding not only to study positive reinforcement, the anticipation of something pleasurable, but also to study negative reinforcement, the consequences of fear. He did this by pairing a neutral stimulus (the sound of a bell) with an electric shock. Not surprisingly, applying an electric shock to the feet of a dog causes the animal to manifest intense fear. We cannot say what the dog is feeling—we have no way of asking it—but we can observe the dog’s behavior, its expression of fear.
Joseph LeDoux, a neuroscientist at New York University, adapted Pavlov’s strategy to rats and mice.3 He put an animal in a small chamber and sounded a tone. The animal simply ignored the tone. Then, instead of sounding a tone, LeDoux shocked the animal. This time, it responded by jumping and flinching. Finally, LeDoux sounded the tone just before he administered a shock. The animal soon associated the tone with the shock—that is, it learned that the tone predicted the shock. The next time the animal heard the tone, whether the next day, two weeks later, or a year later, it responded with the classic fear response: it froze in its cage, and its blood pressure and heart rate skyrocketed.
The fear response results from the association of the tone and the shock. As we have seen, all sensory information related to emotion travels into the brain via the amygdala. A sound, for example, goes first to the auditory thalamus; from there it is relayed directly to the amygdala and indirectly to the auditory cortex (fig. 8.5). In other words, a sound reaches the amygdala and activates the fear response before it reaches the auditory cortex. The direct pathway to the amygdala is quick, but the information it carries is not very precise. That is why the sound of a car backfiring frightens us—until we realize what the sound is.
Figure 8.5. Diagram of the neural circuit of conditioned fear, beginning with a conditioned stimulus (CS)
How does this learning take place within the amygdala? One of the key requirements scientists have discovered is that, for a fear association to be created, stored, and consolidated in the brain, the tone and the shock must give rise to classical conditioning. Classical conditioning takes place when the tone and the shock are registered sequentially (tone closely followed by shock) by the same cells in the lateral nucleus, the first relay area of the amygdala. When that happens, the tone, which was initially ineffective in activating those cells, becomes highly effective, causing them to send information to the central nucleus of the amygdala. The central nucleus activates motor cells and thus initiates action—jumping and flinching—in response to the sound.
Because two areas of the amygdala are involved in fear, scientists have come to understand that people can develop pathological fear in two different ways. In some people, the lateral nucleus has learned to be overly sensitive to the world, responding with fear to things that others don’t even notice, such as people walking by or the sounds of a bird flying overhead. In other people, the central nucleus is overly reactive, triggering emotional responses that are disproportionate to the threat.
Research on the anatomy of the fear response—on how rodents react to a shock—has deepened our understanding of how people respond to fear. When the circuits of fear in our brain go awry, they give rise to various anxiety disorders. Imaging studies have confirmed that the amygdala is hyperactivated in people who are coping with anxiety, post-traumatic stress, and other fear-related disorders.
HUMAN ANXIETY DISORDERS
We all become anxious occasionally, especially when confronted by danger. But if we experience a chronic state of excessive worry and guilt for no discernible reason, we are suffering from a generalized anxiety disorder. These disorders frequently occur with depression. Fear-related anxiety disorders include panic attacks, phobias (such as fear of heights, animals, or public speaking), and post-traumatic stress disorder. For many years, the various anxiety disorders were considered separate syndromes, but because of their similarities, scientists now regard them as a related cluster of disorders.
Nearly one-third of all Americans will experience symptoms of an anxiety disorder at least once during their lifetime, making these disorders the most common psychiatric illnesses by far. Moreover, anxiety disorders can affect children as well as adults.
Perhaps the most widely known fear-related disorder is post-traumatic stress disorder (PTSD), which is caused by experiencing or observing life-threatening events such as physical assault or abuse, war, terrorist attack, sudden death, or natural disaster. All told, about 8 percent of the U.S. population—at least 25 million people—will experience PTSD at some point in their lifetime. More than forty thousand U.S. war veterans are known to be affected by the disorder, and thousands more cases are thought to be unreported (fig. 8.6).
Exposure to trauma affects the amygdala, which generates our response to fear, and the dorsal prefrontal cortex, which helps regulate our response to fear, but trauma is especially damaging to the hippocampus. The hippocampus, as we have seen, is critical for storing memories of people, places, and objects, but it is also important for recalling memories in response to environmental stimuli. As a result of trauma’s damage to the hippocampus, people with PTSD experience several major symptoms: they have flashbacks, or spontaneous re-experiencing of the traumatic event; they avoid sensory experiences associated with the initial event; they become emotionally numb and withdraw from others; and they are irritable, jumpy, aggressive, or have trouble sleeping. The disorder is commonly accompanied by depression and substance abuse, and can lead to suicide.
Figure 8.6. Post-traumatic stress disorder has afflicted soldiers throughout history. A marine returns after two days of battle on the beaches of the Marshall Islands in February
1944.
Most psychiatric disorders, as we have seen, involve the interaction of a genetic predisposition with an environmental trigger. Post-traumatic stress disorder is a perfect example of this interaction. Not everyone who is exposed to a traumatic stress will develop PTSD. In fact, if one hundred people were exposed to the same traumatic event, about four men and ten women would develop the disorder. (Scientists don’t know why men who experience traumatic stress are so much less likely to develop PTSD.) In addition, studies of identical twins suggest that if one twin responds to a trauma with PTSD, the other twin will also develop PTSD in response to that trauma. These findings indicate that one or more genes predispose people to the disorder, and this may also explain why PTSD so often occurs with other psychiatric disorders: they may share some of the same genes.
Another primary cause of PTSD is childhood trauma. People who have suffered trauma as children are much more likely to develop PTSD as adults because trauma affects the developing brain differently than it does the adult brain. Notably, early trauma can cause epigenetic changes, that is, molecular changes in reaction to the environment that do not alter the DNA of a gene but do affect the expression of that gene. Some of these epigenetic changes are initiated in childhood and persist into adulthood. One such change is known to occur in a gene that regulates our response to stress; this change heightens the risk of developing PTSD in response to traumatic stress in adulthood.
The Disordered Mind Page 18