Introduction
Panic disorder is a condition characterized by frequent panic attacks—that is, intense surges of anxiety. These attacks of anxiety often occur unexpectedly or “out of the blue”; the individual frequently is unable to identify an external trigger for them. Between attacks, the patient often ruminates about the possibility of additional attacks.
Panic attacks tend to be accompanied by a number of physical symptoms. Hyperventilation—overly rapid or deep breathing—is common, as are choking and smothering sensations, dizziness, faintness, and paresthesias—sensations of numbness and tingling, particularly in the extremities. Other common symptoms during panic attacks are sweating, trembling, nausea, abdominal distress, hot or cold flashes, accelerated heart rate, chest pain, and heart palpitations. Not surprisingly, many individuals who are having a panic attack believe that they are experiencing a heart attack.
Panic attacks are also frequently characterized by a number of psychological symptoms, of which depersonalization and derealization are among the most common. Depersonalization is marked by feelings of unreality regarding oneself or one’s body—sensations of being disconnected from oneself or of watching oneself as an outside observer. Derealization refers to feelings of unreality concerning the external world; objects or people may seem somehow strange or unfamiliar. Also common during panic attacks are fears of dying (for example, from a heart attack or stroke), losing one’s mind, or performing embarrassing behaviors (such as screaming uncontrollably).
The difficulties of many patients with panic disorder do not end here, however; many, but not all, of these patients develop an often debilitating syndrome known as agoraphobia. Agoraphobia is a fear of situations in which escape is difficult, inconvenient, or potentially embarrassing, or in which assistance might not be readily available. Specifically, what appears to occur is that many panic patients, dreading the possibility of a future attack, begin to fear and (in many cases) avoid situations that might precipitate such an attack. The situations and locations feared or avoided by agoraphobics are extremely varied, but they include public transportation, open spaces, shopping malls, supermarkets, large social gatherings, elevators, driving in heavy traffic, passing over bridges or through tunnels, standing in long lines, and sitting in crowded theaters or churches.
In mild cases, agoraphobics may experience moderate discomfort while traveling or shopping alone and may avoid those situations in only certain cases. In severe cases, agoraphobics may be unwilling to leave the house unaccompanied. The fears of an agoraphobic are generally alleviated by the presence of another individual, particularly one close to the patient, probably because this person could provide help in the event of an emergency, such as a heart attack.
The prevalence of panic disorder with agoraphobia in the general population of the United States has been estimated to be approximately 5 percent; an additional 2 percent of Americans have been estimated to have panic disorder without agoraphobia. Thus, panic disorder is relatively common, and it is perhaps the most frequent reason individuals seek outpatient psychiatric care. In addition, isolated panic attacks occur frequently among individuals in the general population. G. Ron Norton and his colleagues, for example, have found that approximately 34 percent of college students experience occasional panic attacks.
Panic disorder and agoraphobia have been reported to occur more frequently among women than men, although this difference is probably more marked for agoraphobia than for panic disorder. In addition, the prevalence of panic disorder appears to decline with age; its frequency has generally been reported to be highest among individuals under thirty and lowest among individuals over sixty-five. The course of panic disorder tends to be chronic but fluctuating. In other words, its symptoms often persist for many years, but they typically wax and wane depending on the level of life stress and other factors.
In addition, panic disorder patients appear to have elevated rates of several medical conditions. A subset of these patients, for example, has been reported to have mitral valve prolapse syndrome, a condition in which the heart’s mitral valve bulges into the atrium. Because this syndrome results in physical symptoms such as palpitations and chest pain, it may be a risk factor for panic disorder in some individuals. In addition, a subset of panic patients appear to have disturbances of the vestibular system, an apparatus in the inner ear responsible for maintaining balance. As dizziness is a common symptom of panic attacks, vestibular dysfunction may be an important precipitant of some panic attacks.
A number of psychiatric conditions are commonly found among patients with panic disorder and agoraphobia. Depression is a particularly frequent complication of both syndromes; in many cases, it probably results from the distress produced by panic attacks and the constriction of activities produced by agoraphobia. This depression may have tragic consequences; panic disorder patients have been reported to be at greatly increased risk for suicide compared with individuals in the general population. In addition, many panic disorder patients turn to alcohol or other substances to alleviate their anxiety. Also commonly associated with panic disorder is social phobia, a condition characterized by fears of the possible scrutiny or criticism of others. Like patients with panic disorder, many social phobics experience panic attacks. Nevertheless, in social phobia these attacks are almost invariably triggered by situations in which the patient is the perceived focus of others’ attention.
Possible Causes
A variety of models have been proposed for the causation of panic disorder and agoraphobia. Early explanations tended to focus largely or exclusively on physiological factors. In the 1960s, Donald Klein and his colleagues reported that panic disorder improved following administration of imipramine, a drug traditionally used to treat depression, whereas more sustained and long-lasting (generalized) anxiety did not. Based on this finding, Klein and his coworkers argued that panic is biologically distinct from other forms of anxiety. Although Klein’s observation was important, it should be noted that making inferences about the nature of a disorder from the treatment of that disorder is logically flawed: A condition’s treatment bears no necessary implications for its cause (for example, one would not be justified in concluding that headaches are caused by a lack of aspirin).
Nevertheless, it seems likely that physiological factors play an important role in panic disorder. Identical twins (who share all the same genes) with panic disorder are more likely than are fraternal twins (who share only half of their genes, on average) to have co-twins with panic disorder, suggesting that genetic factors play at least some role in this disorder. It is not known, however, whether these genetic factors predispose a person to panic disorder per se or to anxiety in general.
There is evidence that the locus coeruleus, a structure in the pons (which is located at the back of the brain), is overactive during panic attacks. The locus coeruleus is a major center for norepinephrine, a chemical transmitter in the nervous system that appears to play a major role in the genesis of arousal and anxiety. Finally, it has been found that many patients with panic disorder, unlike those without the condition, develop panic attacks following infusion of certain substances, such as sodium lactate and caffeine. It is possible, however, that this is simply attributable to greater arousal on the part of panic disorder patients; the infusion of these substances may provoke attacks in these patients because they are already on the verge of panicking.
Many subsequent models of the causation of panic disorder have attempted to move beyond physiological abnormalities to examine how panic disorder patients react to and construe their environment. One of the most influential of these might be termed the “fear of fear” model. According to Dianne Chambless, Alan Goldstein, and other proponents of this model, individuals who are afraid of their own anxiety are particularly prone to the development of panic disorder. During frightening experiences, this fear of fear can spiral into a panic attack.
A more recent theory of panic disorder is the cognitive model of David Clark, Aaron T. Beck, and other researchers. According to this model, panic attacks result from the catastrophic misinterpretation of unusual or unexpected bodily sensations. In other words, panic attacks may occur when a physical symptom (such as rapid heartbeat or dizziness) is misinterpreted as presaging a disastrous outcome (heart attack or stroke). Interestingly, many of the physical symptoms of anxiety, such a rapid heartbeat, can themselves be exacerbated by anxiety, as anyone who has felt his or her heart race uncontrollably while giving a speech can attest. Thus, the misinterpretation of certain physical sensations may set in motion a cycle in which these sensations progressively increase in intensity, giving rise to further misinterpretations and ultimately culminating in a panic attack. The cognitive model is also consistent with the evidence, mentioned earlier, that some panic patients have physiological abnormalities, such as mitral valve prolapse and vestibular dysfunction. These abnormalities might be chronically misinterpreted by some individuals as indicative of serious consequences, and thereby provide a repeated trigger for panic attacks.
There is good evidence that many cases of panic disorder and agoraphobia are treatable by means of either medication or psychotherapy. Imipramine, as well as several other antidepressant drugs, appears to ameliorate the symptoms of these syndromes. It is not clear, however, whether these drugs actually exert their impact on panic or whether they instead work by alleviating the depressive symptoms so common to these patients. Alleviating depressive symptoms may then provide agoraphobics with the energy and confidence needed to confront previously avoided situations.
Panic disorder and agoraphobia also are amenable to interventions involving confrontation with feared situations. For example, many panic patients improve following flooding, a technique involving prolonged and intense exposure to feared stimuli. In the case of panic disorder, patients typically are exposed, in graduated fashion, to increasingly anxiety-producing situations. Patients are encouraged to remain in the situation until their anxiety subsides.
The efficacy of flooding and related treatments for panic disorder and agoraphobia can be explained in at least two ways. One possibility is that flooding works by a process known as habituation. Habituation is a process in which physiological or psychological responses decline in intensity with repeated stimulation. For example, many parachute jumpers find that their anxiety reactions gradually decrease with each succeeding jump; habituation may be the basis of this phenomenon. A second possibility is that flooding works by means of the cognitive model. That is, prolonged exposure to feared stimuli may demonstrate to patients that these stimuli are not as dangerous as they had believed.
History
The term “panic” derives from the Greek god Pan, who let out a terrifying scream whenever he was awakened by passersby. Most of the earliest accounts of panic attacks emphasized their physiological nature. In 1871, Jacob DaCosta described a syndrome he termed irritable heart, which was characterized by palpitations, shortness of breath, dizziness, and other symptoms now recognized as typical of panic disorder. DaCosta observed this condition both in Civil War soldiers and in individuals not involved in military combat. Irritable heart syndrome became a frequent diagnosis among anxiety-stricken soldiers in the Franco-Prussian and Boer Wars. Other early names for this syndrome were effort syndrome and neurocirculatory asthenia; again, both of these terms emphasized overexertion of the heart and circulatory system as the principal causes of panic symptoms.
At approximately the same time, Sigmund Freud was describing a syndrome he called anxiety neurosis. Freud noted that this neurosis could occur in a diffuse, long-lasting form (what later would be called generalized anxiety) or in sudden, discrete attacks marked by symptoms such as excessive heartbeat and respiration (what later would be called panic disorder). In contrast to DaCosta and other writers of this period, Freud emphasized unconscious psychological factors as the primary determinants of panic disorder. According to Freud, anxiety attacks resulted from a massive damming up (repression) of sexual impulses. In his later writings, Freud revised his position to assert that anxiety served as a signal to the individual that impulses needed to be repressed. According to this later view, anxiety (including panic) is a cause, rather than a result, of repression and functions as a defense mechanism to ward off trauma. Although many psychologists did not concur with Freud’s conjectures, by World War II, there was increasing appreciation that many of the panic reactions seen among soldiers were largely of psychogenic origin.
The term “agoraphobia” stems from the Greek agora, meaning marketplace. As noted earlier, however, although agoraphobics fear marketplaces and similar situations, their fears tend to be extremely varied. “Agoraphobia” was coined by Alexander Westphal in 1871, who observed that many patients experienced anxiety while walking across open spaces or deserted streets. Interestingly, Moritz Benedikt had observed a similar syndrome in 1870; he labeled it Platzschwindel (dizziness in public places), a term that presaged findings of vestibular dysfunction in some of these patients.
Panic disorder and agoraphobia are recognized as two different, although often overlapping, conditions; however, professional opinion has vacillated on this point. In the third edition of the American Psychiatric Association’s
Diagnostic and Statistical Manual of Mental Disorders
(DSM-III, 1980), for example, panic disorder and agoraphobia were listed as separate disorders. Then, in DSM-IV (1994), the two were specifically linked in three diagnoses: panic disorder with agoraphobia, panic disorder without agoraphobia, and agoraphobia with no history of panic disorder. In DSM-5 (2013), the pendulum of professional consensus swung back the other way, with the two again being listed as separate disorders, in recognition of the sizable number of individuals with agoraphobia who do not experience panic attacks.
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