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Panic attacks are discrete episodes of terror that begin suddenly and are associated with intense physiological symptoms (e.g., breathlessness, rapid heart rate, dizziness) and thoughts that one is about to die, lose self-control, or “go crazy.”

OUTLINE

I. History of the Concept of Panic Attack

II. Assessing Panic Attacks

III. Panic Attack Variants

IV. The Development of Panic Disorder and Agoraphobia

V. Epidemiology

VI. Biological Aspects of Panic

VII. Psychological Aspects of Panic

VIII. Psychopharmacologic Treatments for Panic

IX. Psychological Treatments for Panic

X. Conclusions

I. HISTORY OF THE CONCEPT OF PANIC ATTACK

In 1959, research psychiatrist Donald F. Klein was studying imipramine, a new drug synthesized by a minor alteration in the chemical structure of the “major tranquilizer” chlorpromazine. Researchers hoped that imipramine, like chlorpromazine, would help people with schizophrenia, whose psychotic symptoms were at that time believed to result from excessive anxiety. Unfortunately, imipramine did not attenuate delusions or hallucinations, but it did alleviate depressive symptoms in schizophrenic patients, and its mood-improving effects were notably dramatic in patients suffering from severe depression.

As evidence for the antidepressant effects accumulated, Klein and his associates struggled to treat a group of highly anxious inpatients who had been diagnosed as “schizophrenic” but who exhibited neither delusions nor hallucinations. Not only had they failed to respond to sedatives and to psychotherapy, their anxiety was not reduced by chlorpromazine. These results were puzzling in light of prevailing theory: chlorpromazine helped typical schizophrenics whose psychotic symptoms supposedly resulted from extreme anxiety, yet it failed to help an atypical group of schizophrenics who were very anxious, but who were not psychotic.

Klein’s decision to prescribe imipramine for these atypical schizophrenics was born of frustration. Other approaches had failed, and the new drug was known to be safe and to have some anxiety-reducing properties. However, after taking imipramine for several weeks, the patients maintained that the drug was ineffective because it failed to attenuate their chronic anxiety. Their psychotherapist concurred, but the nursing staff did not. Before taking imipramine, these patients had been rushing to the nursing station several times a day, terrified, and exclaiming that they were dying. The nurses would reassure them that they were not dying, and their terror would pass after about 20 minutes or so. Despite their claims of lack of improvement, patients were no longer experiencing these terrifying episodes of suddenly feeling on the brink of death. Also, once their sudden, unpredictable episodes of terror (i.e., panic attacks) had ceased, patients became increasingly comfortable, moving freely throughout the hospital unaccompanied by others.

Based on these observations, Klein inferred that imipramine was effective against acute panic attacks, but not against chronic anxiety. Indeed, their chronic anxiety was itself the consequence of panic; they lived in dread of these recurrent episodes of terror. These observations also suggested a qualitative distinction between episodic panic attacks and chronic anticipatory anxiety. Klein reasoned that the effects of imipramine would make no sense if panic were just an extreme form of anxiety. Indeed, why should a drug be effective against the severe form of a disease, but not against its mild form? This paradox would disappear if panic and anxiety arose from different underlying processes rather than being two points on a quantitative continuum of severity. As Klein observed, such apparent paradoxes are common in nonpsychiatric medicine. Bacterial pneumonia and the common cold are respiratory disorders that share many symptoms, and although the former might be mistaken for a severe form of the latter, antibiotics are effective against bacterial pneumonia but are useless against the common cold. Therefore, reasoned Klein, just as bacterial pneumonia does not lie on a continuum of severity with the common cold, panic is not merely a severe form of ordinary anxiety.

Klein’s experience with imipramine not only motivated his distinction between panic and anxiety, it also led him to conclude that agoraphobia was chiefly a consequence of panic attacks. (The “schizophrenic” patients who first responded to imipramine would now be diagnosed as having “panic disorder with agoraphobia” because they fearfully avoided many activities in addition to having panic attacks.) Traditional views conceptualized agoraphobia as a fear of open or public places. But it became apparent that the motivation for avoidance was fear of panicking in situations where escape was not easy or help readily available.

Klein subsequently delineated three types of panic attack. Spontaneous panic attacks are sudden, unexpected surges of terror accompanied by intense (especially cardiorespiratory) symptoms. Spontaneous panics are often accompanied by catastrophic thoughts that one is about to die, “go crazy,” or lose self-control. From the perspective of the panicker, the attacks seem to “come out of the blue,” uncaused by any obvious environmental precipitant. “Spontaneous” does not imply “uncaused”; it implies only the absence of external triggers, not the absence of neurobiological dysregulation. Spontaneous panics are akin to other conditions in medicine that erupt without clear-cut external provocation, like paroxysmal tachycardia, migraine, and vertigo (i.e., rotational dizziness) arising from inner ear disease.

Stimulus-bound panics refer to the sudden surge of intense fear experienced by people with specific phobias (e.g., of animals, of heights) when they encounter, or anticipate encountering, their feared object. These episodes are similar to spontaneous attacks except that the panicker is aware of the external precipitant and is less likely to misinterpret the attacks as a sign of impending insanity.

Situationally predisposed panics occur in some situations more than in others, but are not inevitably or immediately triggered by these external stimuli. For example, people with agoraphobia often panic while in crowded stores, but crowded stores do not inevitably trigger panic with the same predictability that snakes trigger panic in people with snake phobia.

Klein’s work greatly influenced the inclusion of panic disorder as a diagnostic category in the third edition of the Diagnostic and statistical manual of mental disorders (DSM-III), which appeared in 1980. Based partly on his work, DSM-III postulated two types of anxiety neurosis. One type was characterized by repeated spontaneous panic attacks (panic disorder), and the other was characterized by chronic high levels of anxiety that did not erupt into panic attacks (generalized anxiety disorder). In the revised version of DSM-III (DSM-III-R), which appeared in 1987, panic disorder was coded as either panic disorder without agoraphobia or panic disorder with agoraphobia. This important change acknowledged the consensus view among American psychopathologists that although some people with panic disorder do not extensively avoid situations and activities, when people do develop agoraphobia, their avoidance almost always develops as a consequence of panic disorder. Some people, however, develop agoraphobia after having experienced episodes of intense symptoms that do not qualify as full-blown panic attacks (e.g., sudden bouts of dizziness).

Because research has indicated that spontaneous panic attacks occasionally occur in people with other disorders (e.g., social phobia, major depressive disorder), DSM-IV defines panic attacks separately from panic disorder. That is, recurrent spontaneous panics are insufficient for the diagnosis of panic disorder: the person must also alter his or her life to accommodate the attacks, develop a chronic fear of the attacks, or both.

According to current DSM-IV criteria, panic attacks are discrete periods of intense fear or discomfort that begin suddenly and reach peak intensity within 10 minutes. (Most research studies, however, indicate that panic attacks usually reach peak intensity well before 10 minutes have elapsed, and often seem to peak almost instantly.) To qualify as a panic attack, an episode of sudden-onset fear must be accompanied by at least four of the following symptoms: (1) palpitations, pounding heart, or accelerated heart rate; (2) sweating; (3) trembling or shaking; (4) sensations of shortness of breath or smothering; (5) feeling of choking; (6) chest pain or discomfort; (7) nausea or abdominal distress; (8) feeling dizzy, unsteady, lightheaded, or faint; (9) derealization (feelings of unreality) or depersonalization (being detached from oneself); (10)fear of losing control or going crazy; (11) fear of dying; (12) paresthesias (numbness or tingling sensations); and (13) chills or hot flushes. Rapid-onset attacks of fear that are characterized by fewer than four of these symptoms are called “limited-symptom attacks.”

DSM-IV distinguishes three types of panic attack that are approximately equivalent to Klein’s spontaneous, stimulus bound, and situationally predisposed panics. Unexpected (uncued) panic attacks are not triggered by any obvious external stimulus, and seem to occur “out of the blue” for no apparent reason. Situationally bound (cued) panic attacks are triggered by an encounter with a feared (phobic) stimulus or in anticipation of such an encounter. For example, a person with a snake phobia will typically experience a situationally bound panic upon encountering a snake in the woods.
Finally, situationally predisposed panic attacks are triggered by encounters with feared situational stimuli, but are not invariably triggered by such encounters. For example, a person with a fear of driving automobiles will tend to experience panic attacks more often while driving than while doing other things, but driving does not invariably cause panics.

II. ASSESSING PANIC ATTACKS

Most research on spontaneous panic attacks has been based on the patients’ retrospective self-report. Patients are often asked to recall their most recent, most severe, or most typical attack, and then indicate the presence and severity of the DSM symptoms on some scale. Regrettably, these ratings are subject to unintentional distortion. Research suggests that atypically intense, and therefore memorable, attacks are often described as “typical,” and patients often overestimate the frequency and severity of their attacks when asked about them days or weeks later.

To circumvent this problem, clinical researchers now have patients prospectively self-monitor their attacks and record them in structured diaries designed for this purpose shortly after the attack occurs.

Because classic panic attacks occur unpredictably, they have rarely been captured in the psychophysiology laboratory. Indeed, most laboratory research on panic involves attacks provoked by biological challenges (see below). Nevertheless, about 20 unexpected attacks have been recorded while patients were undergoing various assessments while wired for psychophysiologic assessments. These recorded episodes have indicated that panics do, indeed, begin abruptly, as patients say, and are marked by increases in heart rate, skin conductance (i.e., sweating), facial muscle tension, and hyperventilation.

III. PANIC ATTACK VARIANTS

During the mid-1980s, researchers noted that about one-third of the young adult (nonclinical)population reported having experienced a “panic attack” during the previous year. These nonclinical panic attacks seemed to suggest that a phenomenon so common might not be indicative of psychopathology. Subsequent studies revealed, however, that most of these attacks were not especially severe and nor were many the spontaneous, unexpected attacks that characterize panic disorder. Consensus now holds that between 2 % and 7% of the general young adult population experiences at least one spontaneous panic attack that meets DSM criteria each year. Occasional panic attacks may presage the development of panic disorder in people who also have elevated anxiety sensitivity.

Researchers have described the seemingly oxymoronic condition of nonfearful panic attacks among cardiology patients seeking help for unexplained chest pain. These individuals complain of sudden rushes of somatic symptoms identical to those of panic attacks, but do not experience fearful thoughts about imminent death and so forth. Comparisons between typical panickers and nonfearful panickers on variables such as age of onset, average number of symptoms per attack, duration of disorder, depressive, agoraphobic symptoms, and so forth indicate that the two groups are nearly indistinguishable except for the fact that typical panickers experience terror during their attacks, whereas nonfearful panickers do not. Nonfearful panic indicates that sudden rushes of autonomic symptoms are not equivalent to panic attacks, thereby raising the possibility that a person’s interpretation of the symptoms as threatening may partly determine whether they experience the episode as terrifying.

Although panic attacks most often occur during the daytime, they can also erupt while the person is sleeping. Nocturnal (or sleep) panics are characterized by abrupt awakening, terror, and intense physiological arousal. Because nocturnal attacks emerge during non-REM (rapid-eye-movement) sleep, they are rarely preceded by dreams (which occur during REM sleep). Most attacks occur during the transition from stage 2 to stage 3 sleep (i.e., as the person is going into a deeper stage of sleep). About 5% of college students report having had a nocturnal panic at some point in their lives, and about 69% of panic disorder patients have had at least one nocturnal panic. It is very unusual for a person with panic disorder to have only nocturnal panics, but those who experience nocturnal panics tend to experience more daytime panics as well.

There are similarities and differences between nocturnal panics and night terrors (also known as payor nocturnus in children and incubus in adults). Both erupt during non-REM sleep; both are rarely preceded by dreams; and both are marked by abrupt awakenings, terror, and autonomic arousal. Yet night terrors are more common in children than in adults, and emerge after a sustained period of very deep (stage 4) sleep. Panic attacks, including nocturnal ones, are more common in adults than in children. Furthermore, night terrors begin with a blood-curdling scream, yet the person who experiences a night terror rarely remembers the episode, and easily returns to sleep. Also, a person experiencing a night terror may become combative or run out of the house. In contrast, nocturnal panickers vividly remember their attacks, and often experience difficulty returning to sleep.
The causes of nocturnal attacks are unknown. One possibility is that physiological irregularities waken the person who then panics in response to perplexing symptoms like breathlessness, racing heart, and so forth. Another possibility is that the psychobiological substrate of the emotion of fear does, indeed, begin while the person is sleeping, consistent with patients’ reports that they awoke already in the midst of fear.

IV. THE DEVELOPMENT OF PANIC DISORDER AND AGORAPHOBIA

Panic attacks usually start in late adolescence or in early adulthood; they rarely begin before puberty or late in life. They typically emerge during periods of life stress such as after the death of a loved one, in anticipation of a major life event (e.g., wedding), after losing a job, and so forth. Occasional panic attacks are not uncommon in the general population, but if individuals become persistently fearful of them or alter their lives in response to them, panic disorder is diagnosed.

The vast majority of people who develop agoraphobia do so as a consequence of their fear of panic attacks. It is very unusual for someone to become agoraphobic without first having had panic attacks. Rarely, clinicians encounter people who appear to have agoraphobia without a history of panic. But close inspection of these cases reveals that such patients fear other forms of sudden bodily incapacitation that do not qualify as panic per se (e.g., diarrhea, migraine headaches).

Some panickers become agoraphobic within days of their first attack; others become increasingly agoraphobic over weeks, months, and years; and still others never become agoraphobic. Researchers have studied what factors predict which panickers develop agoraphobia by comparing panickers with and without agoraphobia. Avoiders and nonavoiders do not differ in their age of onset or duration of panic disorder, and there are few differences in the severity of the attacks themselves: agoraphobic panickers do not seem to have worse attacks than nonagoraphobic panickers. There are no differences in the frequency of attacks. The best predictors of avoidance are cognitive. Predictors of agoraphobic avoidance include expectations of panicking in certain situations, perceived negative consequences of panic, fears of dying or going crazy during attacks, and lack of confidence in one’s ability to cope with panic.

V. EPIDEMIOLOGY

Epidemiology is the study of the distribution and determinants of disease in the population. Interviewing more than 18,000 American adults, the Epidemiologic Catchment Area (ECA) team endeavored to determine the prevalence and incidence of panic disorder and other mental disorders. The ECA data indicated that the annual prevalence rate of DSM-HI panic disorder (without agoraphobia) was 1.2 % in women and 0.6 % in men, and the lifetime prevalence was 2.1% in women and 1.0% in men. Panic disorder was most common among people aged 30 to 44 years, and least common in people older than 65 years old. People with panic disorder sought the services of mental health professionals more than people with any other disorder, including alcoholism and schizophrenia.

The ECA team reported annual prevalence rates for DSM-III agoraphobia of 5.9% for women and 2.1% for men. Surprisingly, however, the ECA team reported that only 7% of the subjects diagnosed with agoraphobia also had panic disorder. This result was dramatically at variance with the observations of clinicians who rarely see agoraphobics without panic disorder. Subsequent reexamination of the “agoraphobia without panic” cases strongly suggested that the ECA team had inadvertently classified many cases of specific phobias (e.g., of flying, driving, crossing bridges) as instances of agoraphobia.

The ECA researchers estimated the annual incidence of panic disorder 2.4 new cases per 1000 persons per year. The estimated incidence of a severe panic attack was 9 per 1000 persons per year.

The ECA team found that 20% of people with panic disorder reported having attempted suicide at some point in their lives. This finding was surprising because panic patients often fear dying in the midst of their attacks, and most studies on patients with the disorder indicate that they are not at high risk for attempting suicide. A reanalysis of the ECA data suggested that the presence of comorbid disorders that independently increase risk for suicide attempt (e.g., schizophrenia, alcoholism, depression) may have been the basis for the apparent connection between panic disorder and suicide attempts. Nevertheless, the presence of panic disorder in a person with, say, depression provides no guarantee that the person will not attempt suicide.

The National Comorbidity Survey (NCS), a nationwide DSM-III-R assessment of mental disorders, revealed a lifetime prevalence rate for panic disorder of 3.5%; 1.5% of the respondents had panic disorder at the point of the survey. The NCS indicated that 1.5 % of the population develops panic disorder with agoraphobia at some point in their lives; 0.7% had it at the time of the survey. As in the ECA study, the rate was about twice as high for women as for men. The NCS team also found that those with less than a high school education were more than 10 times as likely to have panic disorder as those who had graduated from college. Because income level, unlike education, was unrelated to risk for panic disorder, the NCS team suggested that lower cognitive ability may be linked to panic. Race/ethnicity was unrelated to panic disorder. Being married (or living with someone) and being employed was associated with reduced risk.

VI. BIOLOGICAL ASPECTS OF PANIC

One early hypothesis was that chronic hyperventilators are prone to panic because they are more likely than other people to experience hyperventilation-induced sensations (e.g., dizziness) that may frighten them, causing further overbreathing, greater fear, and so forth until full-blown panic results.

However, most subsequent research indicates that panic patients are usually not chronic hyperventilators. But excessive ventilation is a common accompaniment of panic attacks and can worsen the symptoms associated with panic. Therefore, hyperventilation does not seem to cause panic attacks, but it does seem to intensify attacks that do occur.

An important tool for studying panic in the laboratory has been the biological challenge test. Biological challenge tests produce intense bodily sensations, and incite panic attacks far more often in panic patients than in patients with other disorders or in healthy subjects. They are designed to stress specific neurobiological systems, and if panic occurs, then dysfunction in the stress system may constitute a vulnerability to naturally occurring panic attacks. A purpose of this research is to identify procedures that will reliably initiate attacks in the laboratory that strongly resemble spontaneous panic attacks. These procedures, in turn, enable researchers to investigate the mechanisms of panic in controlled experimental situations.

However, panic attacks occurring in response to biological challenges have been interpreted in two principal ways. One interpretation holds that challenges directly incite panic by exacerbating a neurobiological dysfunction. The other interpretation holds that they incite attacks merely by generating intense bodily sensations that these patients are prone to fear.

Several challenges have been used. Infusion of sodium lactate occasions panic in about 67% of panic patients, but in only about 13% of healthy control subjects. Controversy persists about whether the response of panic patients differs qualitatively from that of control subjects. For example, panic patients often are more anxious and more physiologically aroused than control subjects before the infusion begins. That is, the reactivity of panic patients is often not greater than that of control subjects (i.e., the magnitude of change is not greater), but patients begin the challenge at a higher baseline level of arousal and anxiety.

Some psychopathologists believe that dysregulation in the noradrenergic system is involved in the genesis of panic attacks. This hypothesis stems partly from the phenomenology of panic itself. Panic attacks are characterized by symptoms indicative of massive autonomic arousal associated with norepinephrine surges, thereby implying an instability in the noradrenergic system. Consistent with this possibility, oral (or infused) yohimbine challenges, which stimulate noradrenergic activity, produce panic in about 63% of panic patients and in about 7% of control subjects.

Carbon dioxide inhalations have also been used as biological challenge tests. One hypothesis is that panic disorder patients are characterized by hypersensitive carbon dioxide receptors in the brainstem such that increases in central carbon dioxide produce an excessive ventilatory response that can initiate panic attacks. A related hypothesis is that panic is attributable to a pathologically low threshold for firing of an evolved suffocation alarm. That is, carbon dioxide receptors in the brainstem may respond to relatively low increases in carbon dioxide as if the person is suffocating. When this alarm fires, the person begins hyperventilating and experiences the terror appropriate to one who cannot breathe. Physiological evidence in support of carbon dioxide receptor hypersensitivity is mixed. In some studies, panic patients have exhibited excessively vigorous ventilatory responses to carbon dioxide inhalation, whereas in others they have not.

Panic disorder appears to run in families, suggesting the possibility of a genetic vulnerability. It is unclear whether this vulnerability is for panic attacks per se, for overactive physiological responding, or for personality traits that may predispose people to react fearfully to bodily symptoms.

Rates of panic disorder are higher in the first-degree relatives of patients with panic disorder (17.3 %) than in the first-degree relatives of healthy control subjects (1.8%). Estimates of the heritability of panic attacks and panic disorder vary depending on the population from which the subjects are drawn. In one study involving patients, 31% of the identical twins with panic attacks had a co-twin with panic attacks as well, whereas none of the fraternal twins with panic attacks had a co-twin with panic attacks. In one population study, 23.9% of the identical twins were concordant for panic disorder as compared to 10.9% of the fraternal twins when a psychiatrist made the diagnosis based on the collected data, but the respective concordance rates were nearly identical (14.5 % vs. 14.6 %) when a computer algorithm evaluated the data.

VII. PSYCHOLOGICAL ASPECTS OF PANIC

Psychological theorists hold that physiological symptoms are insufficient to produce the experience of panic. For panic qua panic to occur, the person must react to these bodily sensations with fear. Responding to one’s own bodily sensations as if they were phobic stimuli, panickers worsen these symptoms, and thereby amplify their terror. Moreover, only those people who dread these symptoms will qualify for panic disorder. According to psychological theorists, panic disorder is in large part a “fear of fear” itself.

There have been several versions of the fear-of-fear hypothesis of panic disorder. One view holds that Pavlovian interoceptive conditioning figures in development of panic disorder. Initial panic attacks establish certain bodily sensations (e.g., heart palpitations, breathlessness) as conditioned stimuli that evoke subsequent panic attacks.

Another view holds that panic attacks occur because individuals catastrophically misinterpret certain benign bodily sensations as harbingers of imminent psychological or physical disaster. Thus, a person might misinterpret palpitations as an impending heart attack, become more anxious, and thereby intensifying these sensations until they culminate into a panic attack. According to this view, catastrophic misinterpretations of bodily sensations are necessary for a panic attack to occur.

A third approach emphasizes that not everyone is equally likely to respond fearfully to their own bodily sensations. People who hold mistaken beliefs about rapid heartbeats, dizziness, and so forth are presumably more likely than other people to react fearfully when these sensations occur. This notion is embodied in the anxiety sensitivity hypothesis. Anxiety sensitivity is an individual difference variable that may constitute a cognitive risk factor for panic disorder. It is conceptually and empirically distinguishable from trait anxiety. Trait anxiety refers to a proneness to react fearfully to a wide range of potential stressors, whereas anxiety sensitivity refers to the specific tendency to react fearfully to bodily sensations associated with anxiety. Importantly, people with elevated scores on the Anxiety Sensitivity Index (ASI)~a questionnaire measure of this variable~respond just like panic patients to biological challenges (e.g., carbon dioxide inhalation) even if they have no history of panic attacks or panic disorder. These studies imply that a fearful response to challenge is a marker for the fear of symptoms rather than a marker for panic disorder per se. Longitudinal research indicates that people with elevated ASI scores are at enhanced risk for developing panic and other anxiety disorders.

Implicit in the fear-of-fear construals of panic is the notion that people prone to experience panic attacks process arousal-related information differently than do people who are not prone to experience panic attacks. That is, people with panic disorder seem characterized by cognitive biases favoring the interpretation of threat. A growing body of experimental research indicates that panickers are characterized by interpretive, attentional, and memory biases favoring threat. For example, when asked to provide explanations for ambiguous scenarios (e.g., “You feel discomfort in your chest area. Why?”), panic patients are prone to interpret them in a catastrophic manner (e.g., reacting to chest discomfort as indicative of heart attack rather than indigestion).

Panic patients are also characterized by attentional biases favoring threat, as evinced by their responses on “emotional Stroop” tasks. In these tasks, subjects are shown words of positive, neutral, and negative emotional significance, and are asked to name the colors in which the words appear (on a computer screen) while ignoring the meanings of the words. Delays in color-naming occur when the meaning of the word captures the subject’s attention despite the subject’s effort to attend to the color of the word. In one experiment, panic patients exhibited delayed color naming for words related to fear (e.g., panic), bodily sensations (e.g., breathless), and catastrophe (e.g., insane). In another experiment, they exhibited greater interference for catastrophe words than for positive words of equivalent but opposite valence (e.g., carefree). These studies suggest that panic disorder is characterized by biases for selectively attending to threat cues.

Finally, other studies have shown that panic patients exhibit superior memory for words related to anxiety and threat. This memory bias for threat appears enhanced when patients are in a state of physiological arousal. Taken together, these results suggest that threat-related material may have preferential access to conscious mentation in these patients.

VIII. PSYCHOPHARMACOLOGIC TREATMENTS FOR PANIC

As noted earlier, the tricyclic antidepressant, imipramine, was the first compound shown effective against panic attacks. Patients need not be depressed for this drug to work against panic. The effects of imipramine are potentiated by combining it with exposure in vivo, a behavior therapy method (see below).

Unfortunately, a substantial minority of panic patients fail to tolerate the side effects of imipramine, which include increased heart rate and jitteriness. Some clinicians suggest slowly increasing dosage until a therapeutic effects are reached as a means of managing side effects.

High-potency benzodiazepines, such as alprazolam, have been used to treat panic disorder. Their side effects are less disagreeable, and these medications begin to exert their antipanic effects within days of commencing treatment in contrast to imipramine, which often takes weeks before benefits begin to appear. Disadvantages of these compounds include their capacity to induce pharmacologic and psychological dependence; panic patients often find it difficult to cease taking alprazolam. This can pose a problem for women who wish to become pregnant, and therefore need to be free of alprazolam. Moreover, cessation of these compounds often results in the return of panic attacks, and sometimes these rebound panics are more intense than the attacks that had been occurring before the patient began taking alprazolam. Some evidence suggests that panic patients with agoraphobia who undergo otherwise effective in vivo exposure treatments do worse at follow-up if they had been taking alprazolam than if they had been taking placebo.

The selective serotonin reuptake inhibitors (SSRIs) have been widely prescribed for many psychiatric conditions in recent years. Originally developed as antidepressants, SSRIs, such as fluoxetine, have been recently used as antipanic agents. Indeed, the study reporting the most impressive evidence for the pharmacologic treatment of panic disorder tested the SSRI fluvoxamine. Although controlled research on the treatment of panic disorder with SSRIs has only recently begun, the consensus among psychopharmacologists is that SSRIs are the drug treatment of choice for panic disorder. The SSRIs appear to have more tolerable side effects than tricyclic antidepressants and they appear to be less likely to produce dependence than high-potency benzodiazepines. Limited data also suggest that relapse upon drug discontinuation may be less likely than relapse following discontinuation of alprazolam and similar compounds.

IX. PSYCHOLOGICAL TREATMENTS FOR PANIC

Despite differences in emphasis, most cognitivebehavior therapists treat panic as follows. Early sessions usually are designed to reduce the patient’s anxiety sensitivity by providing the patient with basic information about panic attacks that counteracts the patient’s catastrophizing tendencies. For example, one approach emphasizes that panic attacks reflect an adaptive, evolved fight-or-flight response that fires at inappropriate times. Under this view, panic attacks are not dangerous events but rather reflect an evolved mechanism for protecting against danger. Patients are also shown how they may inadvertently maintain their disorder by hypervigilantly monitoring their bodies for feared sensations and then misinterpreting them as harbingers of harm.

Some clinicians next train patients to use symptom (or panic) management techniques. These include respiratory control procedures for counteracting patients’ tendencies to hyperventilate during panic attacks (and thus worsening them). Patients are taught to breathe by using their abdomen rather than just their upper chest, and are taught to breathe at a comfortable pace instead of gasping for air and making things worse. They are taught to breathe through the nose, not the mouth, as an additional means of counteracting hyperventilation. Patients are taught a technique called applied relaxation as another means of managing symptoms. This method first involves teaching them how to tense and relax different muscle groups in the clinic and to detect signs of tension. They are then given practice in applying these procedures while they engage in everyday activities. It is unclear whether these methods are effective because they blunt symptoms during episodes of panic, or whether they enhance the patient’s sense of restoring control.

Inspired by the notion that panic attacks are akin to conditioned responses to the phobic stimuli of one’s own bodily sensations, clinicians structure interoceptive exposure exercises. Interoceptive exposure refers to graduated, structured induction of feared bodily sensations done in a fashion so as to reduce the patient’s fear of the sensations. Patients may be asked to run up stairs to increase heart rate, to breathe through a straw to increase breathlessness, and so forth. The rationale is that structured exposure to harmless bodily sensations reduces the patient’s fear of them.

Just as the fear-of-fear hypothesis inspired the development of interoceptive exposure, so has the catastrophic misinterpretation hypothesis inspired cognitive techniques for refuting patient’s beliefs about the harmfulness of bodily sensations. These beliefs are treated as experimental hypotheses, and therapists work with patients to evaluate the evidence for and against their catastrophic hypotheses and noncatastrophic alternative interpretations of bodily sensations. This approach entails the conducting of behavioral experiments. If, for example, a patient hypothesizes that dizziness leads one to collapse, the therapist might have the patient hyperventilate while sitting and then have the patient stand up quickly. The failure of the patient to collapse disconfirms the catastrophic hypothesis while confirming the noncatastrophic alternative that intense lightheadedness may produce unsteadiness, but not collapse. The basic notion behind these experiments is that patients often engage in subtle avoidance behavior in the midst of panic attacks that prevents their catastrophic beliefs from being tested and refuted. Thus, if patients always sit down when becoming dizzy and panicky, they will never learn that their feared catastrophe of collapse never occurs. The object of cognitive therapy is to provide these instructive learning experiences.

Finally, most patients with panic disorder have developed varying degrees of agoraphobic avoidance behavior. Although few become entirely housebound, most have restricted their lives to a considerable extent. Therefore, patients are urged to undertake in vivo (i.e., real-life) exposure exercises whereby they practice entering previously avoided situations and engaging in previously avoided activities. The general rule is for patients to remain in these situations until their discomfort has diminished. Although it was once believed that exiting a feared situation in the midst of a panic would automatically worsen the patient’s fear and avoidance, subsequent research has indicated that this is not necessarily true. Even if a patient leaves the feared situation, no lasting exacerbation of fear seems to occur if the patient reenters the situation soon afterward.

The chief goal is to ensure that patients regularly practice engaging in feared activities. It is not essential that the therapist accompany the patient on these forays, but for highly avoidant patients, it is often helpful.

Most early psychological research on the treatment of panic disorder and agoraphobia concentrated on the reduction of fear and avoidance via exposure therapies. Although in vivo exposure does not directly target panic, catastrophic misinterpretations, and so forth, it has been shown to reduce (but not always to eliminate) panic attacks. Some studies have shown that the combination of imipramine and exposure is better than either alone, whereas adding alprazolam to exposure seems to reduce the effectiveness of the latter. There are no data on combined SSRI and behavioral treatment.

During the past several years, researchers have tested the efficacy of the cognitive-behavioral approach described above. This strategy eliminates panic attacks in approximately 80% to 90% of patients, and most retain their gains at follow-ups of 1 to 2 years posttreatment. Indeed, the percentages of patients who are panic-free at posttreatment are comparable and often higher than the percentages of panic-free patients who receive medication. Moreover, rates of relapse are lower after cognitive-behavior therapy than after drug treatment, probably because patients have learned not to react fearfully to bodily sensations and have therefore learned how not to let fear spiral into panic.

Moreover, cost-effectiveness analyses have confirmed that cognitive-behavioral treatment for panic is not only at least as effective in the short term as drug treatment, it is less expensive in the long term, and it does not generate side effects or pharmacologic dependence.

X. CONCLUSIONS

Although most researchers agree that panic attacks constitute emotional phenomena distinct from anxiety, there is no consensus about their cause. Biological researchers have identified several possible pathways that may give rise to unusual bodily sensations (e.g., noradrenergic overreactivity, carbon dioxide hypersensitivity), it is unlikely that one physiologic cause is the source of sensations in all patients. More likely, several different biological abnormalities produce the sensations that patients fear.

Most data indicate that surges of sensations do not produce the emotional phenomenon of panic unless the person reacts to them as threatening stimuli. Taken together, the data suggest that panic disorder comprises abnormalities in both biology and cognition. Fortunately, effective treatments, both pharmacologic and cognitive-behavioral, are available.

BIBLIOGRAPHY:

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