Sometimes an anxiety reaction takes the form of a smothering, nightmarish panic in which people lose control of their behavior and, in fact, are practically unaware of what they are doing. Anyone can react with panic when a real threat looms up suddenly. Some people, however, experience panic attacks—periodic, short bouts of panic that occur suddenly, reach a peak within minutes, and gradually pass (APA, 2013).

The attacks feature at least four of the following symptoms of panic: palpitations of the heart, tingling in the hands or feet, shortness of breath, sweating, hot and cold flashes, trembling, chest pains, choking sensations, faintness, dizziness, and a feeling of unreality (APA, 2013). Small wonder that during a panic attack many people fear they will die, go crazy, or lose control.

More than one-quarter of all people have one or more panic attacks at some point in their lives (Kessler et al., 2010, 2006). Some people, however, have panic attacks repeatedly and unexpectedly and without apparent reason. They may be suffering from panic disorder. In addition to the panic attacks, people who are diagnosed with panic disorder experience dysfunctional changes in their thinking or behavior as a result of the attacks (see Table 5-9). They may, for example, worry persistently about having additional attacks, have concerns about what such attacks mean (“Am I losing my mind?”), or plan their lives around the possibility of future attacks (APA, 2013).

Around 2.4 percent of all people in the United States suffer from panic disorder in a given year; more than 5 percent develop it at some point in their lives (Kessler et al., 2012). The disorder tends to develop in late adolescence or early adulthood and is at least twice as common among women as among men. Poor people are 50 percent more likely than wealthier people to experience panic disorder (Sareen et al., 2011).

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For reasons that are not understood, the prevalence of this disorder is somewhat higher among white Americans than among minority groups in the United States (Levine et al., 2013; Woodward et al., 2012). In addition, the features of panic attacks seem to differ somewhat from group to group (Barrera et al., 2010). For example, Asian Americans appear more likely than white Americans to experience dizziness, unsteadiness, and choking, while African Americans seem less likely than white Americans to have those particular symptoms. Surveys indicate that at least one-third of those with panic disorder in the United States are currently in treatment (NIMH, 2011; Wang et al., 2005).

As you read earlier, panic disorder is often accompanied by agoraphobia, the broad phobia in which people are afraid to travel to public places where escape might be difficult should they have panic symptoms or become incapacitated. In such cases, the panic disorder typically sets the stage for the development of agoraphobia. That is, after experiencing multiple unpredictable panic attacks, a person becomes increasingly fearful of having new attacks in public places.

In the 1960s, clinicians made the surprising discovery that panic disorder was helped more by certain antidepressant drugs, drugs that are usually used to reduce the symptoms of depression, than by most of the benzodiazepine drugs, the drugs useful in treating generalized anxiety disorder (Klein, 1964; Klein & Fink, 1962). This observation led to the first biological explanations and treatments for panic disorder.

What Biological Factors Contribute to Panic Disorder?To understand the biology of panic disorder, researchers worked backward from their understanding of the antidepressant drugs that seemed to control it. They knew that these particular antidepressant drugs operate in the brain primarily by changing the activity of norepinephrine, yet another one of the neurotransmitters that carries messages between neurons. Given that the drugs were so helpful in eliminating panic attacks, researchers began to suspect that panic disorder might be caused in the first place by abnormal norepinephrine activity.

Several studies produced evidence that norepinephrine activity is indeed irregular in people who suffer from panic attacks. For example, the locus coeruleus is a brain area rich in neurons that use norepinephrine, and serves as a kind of “on-off” switch for most norephrine-using neurons throughout the brain (Hedaya, 2011). When this area is electrically stimulated in monkeys, the monkeys have a panic-like reaction, suggesting that panic reactions may be related to increases in norepinephrine activity in the locus coeruleus (Redmond, 1981, 1979, 1977). Similarly, in another line of research, scientists were able to produce panic attacks in human beings by injecting them with chemicals known to increase the activity of norepinephrine (Bourin et al., 1995; Charney et al., 1990, 1987).

These findings strongly tied norepinephrine and the locus coeruleus to panic attacks. However, research conducted in recent years suggests that the root of panic attacks is probably more complicated than a single neurotransmitter or a single brain area. It turns out that panic reactions are produced in part by a brain circuit consisting of areas such as the amygdala, hippocampus, ventromedial nucleus of the hypothalamus, central gray matter, and locus coeruleus (Henn, 2013; Etkin, 2010; Ninan & Dunlop, 2005) (see Figure 5-5). When a person confronts a frightening object or situation, the amygdala is stimulated. In turn, the amygdala stimulates the other brain areas in the circuit, temporarily setting into motion an “alarm and escape” response (increased heart rate, respiration, blood pressure, and the like) that is very similar to a panic reaction (Gray & McNaughton, 1996). Most of today’s researchers believe that this brain circuit—including the neurotransmitters at work throughout the circuit—probably functions improperly in people who experience panic disorder (Henn, 2013; Bremner & Charney, 2010; Burijon, 2007).

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Note that the brain circuit responsible for panic reactions appears to be different from the one responsible for broad and worry-dominated anxiety reactions—the circuit that was discussed on page 141. Although some of the brain areas and neurotransmitters in the two circuits obviously overlap—particularly the amygdala, which seems to be at the center of each circuit—the finding that the panic brain circuit and the anxiety brain circuit are different has further convinced many researchers that panic disorder is biologically different from generalized anxiety disorder and, for that matter, from other kinds of anxiety disorders.

Why might some people have abnormalities in norepinephrine activity, locus coeruleus functioning, and other parts of the panic brain circuit? One possibility is that a predisposition to develop such abnormalities is inherited (Buttenschøn et al., 2011; Burijon, 2007; Torgersen, 1990, 1983). Once again, if a genetic factor is at work, close relatives should have higher rates of panic disorder than more distant relatives. Studies do find that among identical twins (twins who share all of their genes), if one twin has panic disorder, the other twin has the same disorder in as many as 31 percent of cases (Tsuang et al., 2004). Among fraternal twins (who share only some of their genes), if one twin has panic disorder, the other twin has the same disorder in only 11 percent of cases (Kendler et al., 1995, 1993).

Drug TherapiesAs you have just read, researchers discovered in 1962 that certain antidepressant drugs could prevent panic attacks or reduce their frequency. Since the time of this surprising finding, studies across the world have repeatedly confirmed the initial observation (Bandelow & Baldwin, 2010; Stein et al., 2010).

It appears that all antidepressant drugs that restore proper activity of norepinephrine in the locus coeruleus and other parts of the panic brain circuit are able to help prevent or reduce panic symptoms (Pollack, 2005; Redmond, 1985). Such drugs bring at least some improvement to 80 percent of patients who have panic disorder, and the improvement can last indefinitely, as long as the drugs are continued. In recent years alprazolam (Xanax) and other powerful benzodiazepine drugs have also proved effective in the treatment of panic disorder (NIMH, 2013; Bandelow & Baldwin, 2010; Stein et al., 2010). Apparently, the benzodiazepines help individuals with this disorder by indirectly affecting the activity of norepinephrine throughout the brain. Clinicians also have found the same antidepressant drugs and powerful benzodiazepines to be helpful in cases of panic disorder accompanied by agoraphobia.

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Cognitive theorists have come to recognize that biological factors are only part of the cause of panic attacks. In their view, full panic reactions are experienced only by people who further misinterpret the physiological events that are taking place within their bodies. Cognitive treatments are aimed at correcting such misinterpretations.

The Cognitive Explanation: Misinterpreting Bodily SensationsCognitive theorists believe that panic-prone people may be very sensitive to certain bodily sensations; when they unexpectedly experience such sensations, they misinterpret them as signs of a medical catastrophe (Gloster et al., 2014; Clark & Beck, 2012, 2010). Rather than understanding the probable cause of their sensations as “something I ate” or “a fight with the boss,” those prone to panic grow increasingly upset about losing control, fear the worst, lose all perspective, and rapidly plunge into panic. For example, many people with panic disorder seem to “overbreathe,” or hyperventilate, in stressful situations. The abnormal breathing makes them think that they are in danger of suffocation, so they panic. They further develop the belief that these and other “dangerous” sensations may return at any time and so set themselves up for future panic attacks.

In biological challenge tests, researchers produce hyperventilation or other biological sensations by administering drugs or by instructing clinical research participants to breathe, exercise, or simply think in certain ways. As you might expect, participants with panic disorder experience greater upset during these tests than participants without the disorder, particularly when they believe that their bodily sensations are dangerous or out of control (Bunaciu et al., 2012; Masdrakis & Papakostas, 2004).

Why might some people be prone to such misinterpretations? One possibility is that panic-prone individuals generally experience, through no fault of their own, more frequent or more intense bodily sensations than other people do (Nillni et al., 2012; Nardi et al., 2001). In fact, the kinds of sensations that are most often misinterpreted in panic disorders seem to be carbon dioxide increases in the blood, shifts in blood pressure, and rises in heart rate—bodily events that are controlled in part by the locus coeruleus and other regions of the panic brain circuit. Another possibility, supported by some research, is that people prone to bodily misinterpretations have had more trauma-filled events over the course of their lives than other persons (Hawks et al., 2011).

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Whatever the precise causes of such misinterpretations may be, research suggests that panic-prone individuals generally have a high degree of what is called anxiety sensitivity; that is, they focus on their bodily sensations much of the time, are unable to assess them logically, and interpret them as potentially harmful. Studies have found that people who scored high on anxiety-sensitivity surveys are up to five times more likely than other people to develop panic disorder (Hawks et al., 2011; Maller & Reiss, 1992). Other studies have found that individuals with panic disorder typically earn higher anxiety-sensitivity scores than other persons do (Allan et al., 2014; Reinecke et al., 2011; Dattilio, 2001).

Cognitive TherapyCognitive therapists try to correct people’s misinterpretations of their bodily sensations (Craske & Barlow, 2014; Clark & Beck, 2012, 2010). The first step is to educate clients about the general nature of panic attacks, the actual causes of bodily sensations, and the tendency of clients to misinterpret their sensations. The next step is to teach clients to apply more accurate interpretations during stressful situations, thus short-circuiting the panic sequence at an early point. Therapists may also teach clients to cope better with anxiety—for example, by using relaxation and breathing techniques—and to distract themselves from their sensations, perhaps by striking up a conversation with someone.

In addition, cognitive therapists may use biological challenge procedures to induce panic sensations, so that clients can apply their new skills under watchful supervision (Gloster et al., 2014; Baker, 2011). Individuals whose attacks typically are triggered by a rapid heart rate, for example, may be told to jump up and down for several minutes or to run up a flight of stairs. They can then practice interpreting the resulting sensations appropriately, without dwelling on them.

According to research, cognitive treatments often help people with panic disorder (Craske & Barlow, 2014; Gloster et al., 2014; Elkins & Moore, 2011; Teachman, 2011). In studies across the world, around 80 percent of participants given these treatments have become free of panic, compared with only 13 percent of control participants. Cognitive therapy has proved to be at least as helpful as antidepressant drugs or alprazolam in the treatment of panic disorder, sometimes even more so (Baker, 2011; McCabe & Antony, 2005). In view of the effectiveness of both cognitive and drug treatments, many clinicians have tried combining them. It is not yet clear, however, whether this strategy is more effective than cognitive therapy alone. For individuals who display both panic disorder and agoraphobia, research suggests that it is most helpful to combine behavioral exposure techniques with cognitive treatments and/or drug therapy (Gloster et al., 2014, 2011; Arch & Craske, 2011).