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Agoraphobia is an anxiety disorder characterized by marked fear of entering crowded, public places; of traveling away from home, especially by public transportation; of feeling trapped or confined; and of being separated from a place or person associated with safety. Sudden, brief episodes of extreme anxiety – panic attacks – are commonly associated with agoraphobia, and may lead to avoidance of situations in which they occur. Often there is a “fear of fear” pattern, in which the bodily sensations of mounting panic are themselves a source of anxiety. Generally more debilitating than specific or social phobias, agoraphobia causes some people to remain entirely housebound. As a syndrome of anxiety elements in physiological, behavioral, and subjective domains, agoraphobia represents a distinct disorder with a typical clinical presentation and course. It usually arises in early adult life, with a prevalence in the Western world of approximately 2.5%; there is a significant preponderance of females in surveys of agoraphobia in clinical and community settings. Since about 1970, clinical researchers have developed effective pharmacological and psychological treatments to reduce or eliminate agoraphobic avoidance behavior and panic attacks.
OUTLINE
I. Agoraphobia: Past and Present
II. Descriptive Psychopathology and Epidemiology
A. Description of Agoraphobia
B. Diagnostic Classification
C. The DSM-IV Classification
1. Panic Disorder with Agoraphobia
2. Agoraphobia without History of Panic Disorder
D. Epidemiology
III. Etiological Theories
A. Biological Theories
B. Psychodynamic and Interpersonal Theories
C. Behavioral and Cognitive Theories
1. Conditioning Theories
2. Cognitive Theories
3. A Comprehensive Model
IV. Assessment and Diagnosis
A. Diagnosis
B. Assessing the Range and Extent of Agoraphobia
V. Treatment
A. Pharmacological Treatment
1. Tricyclic Compounds
2. Monoamine Oxidase Inhibitors (MAOIs)
3. Benzodiazepines and Triazolobenzodiazepines
4. Summary
B. Psychological Treatment
1. Treatment of Agoraphobic Avoidance Behavior
2. Treatment of Panic
3. Comprehensive Treatment of Agoraphobia
VI. Conclusions and Prospects
I. AGORAPHOBIA: PAST AND PRESENT
The term “agoraphobia” was introduced by the German psychiatrist C. F. O. Westphal (1822-1890) in a classic monograph of 1871, Die Agorapbobie. He chose the term to describe the abnormal fears of a series of three men who experienced anxiety episodes when walking alone in public places. Feared situations included city squares, concert halls, churches, open streets and fields, crowded rooms, and traveling by carriage, bus, or train; typical anxiety symptoms were trembling, heart palpitations, and “an immediate breakout of intense anxiety,” or feeling “strange all at once, almost like a ‘hangover.'” Westphal gave prominence to the patients’ fear of walking alone in streets or across squares, and therefore used agoraphobia to denote “fear of spaces”; however, he acknowledged that the term was not exhaustive because it did not embrace all features of the disorder. Contemporary commentators have noted that the Greek “agora” refers to a marketplace or place of assembly, and find Westphal’s choice of term felicitous in aptly describing the chief situational fears associated with agoraphobia today.
Despite the enthusiasm of some American psychiatrists, interest in agoraphobia waned in the years following the publication of Die Agoraphobie. The taxonomist Emil Kraepelin later described a patient similar to those of Westphal, but referred neither to him nor to agoraphobia. The field of psychiatry rapidly became dominated by the psychoanalytic paradigm at the turn of the century, and, while agoraphobia received some attention from psychoanalysts, it was viewed as but one of many psychogenic disorders, not meriting particular notice. Sigmund Freud was more interested in all-encompassing theories of psychosexual development and neurotic symptom formation than in the classification of specific syndromes.
The development of behavior therapy in the 1950s by Joseph Wolpe and others was closely connected with the study of phobias and other anxiety disorders; interest in agoraphobia revived with American and British research on systematic desensitization and related methods in the 1960s, and with the publication of Isaac Marks’ Fears and Phobias in 1969. Systematic desensitization produced disappointing outcomes with agoraphobia, but treatment based on graduated or full-flooded real-life exposure to relevant situations was successful in reducing avoidance behavior and anticipatory anxiety.
The work of Donald Klein on “pharmacological dissection” suggested that benzodiazepines are helpful in relieving anticipatory anxiety, whereas monoamine oxidase inhibitors and tricyclic compounds attenuate panic attacks. Such findings raise the question of different, co-existing anxiety patterns in agoraphobia.
This progress in psychological and pharmacological treatment of agoraphobia in the 1970s influenced the diagnostic classification itself in the United States, so that in 1980 agoraphobia appeared for the first time as a distinct category. Further developments in the 1980s gave prominence to the panic attack as the central feature of agoraphobia and, indeed, of panic disorder, a parallel syndrome not marked by phobic avoidance of situations. Psychological treatment of both syndromes focused on therapeutic exposure to panic sensations, and on encouraging patients to make more realistic and benign ascriptions as to the source of their anxiety; exposure to somatic cues and cognitive therapy have become the leading psychological interventions.
II. DESCRIPTIVE PSYCHOPATHOLOGY AND EPIDEMIOLOGY
A. Description of Agoraphobia
People with agoraphobia usually fear, and often avoid, situations in which it would be difficult or embarrassing to obtain help if overwhelmed by anxiety. Such situations include (a) traveling away from home, especially by bus, train, or car; (b)crowded, public places, such as government buildings, supermarkets, concert halls, shopping malls, and places of worship; and (c) confined places, such as elevators, the dentist’s or beautician’s chair, and—when driving—passing through tunnels, over bridges, or along a limited-access highway. Agoraphobia is commonly associated with highly distressing attacks of panic that appear to arise spontaneously and unpredictably, often—but not always—in the situations typically feared and avoided. When confronted by such typical agoraphobic situations as a large auditorium or a crowded shopping mall, a person with the disorder may experience rapid heartbeat, a compelling urge to escape from the situation, apprehensions about dying or losing control, and a sense of depersonalization or unreality. A “fear of fear” pattern often develops in which the appearance of any bodily sensation associated with anxiety engenders fear of an impending panic attack, thus arousing further anxiety. Some people with agoraphobia restrict their lives substantially, sometimes to the point of remaining housebound, in order to avoid the anxiety or panic aroused by entering public places.
For many patients, dysphoric mood, somatoform disorders, interpersonal conflict, or substance abuse accompany agoraphobia. Untreated, agoraphobia tends to follow a chronic, fluctuating course. It is common for people with agoraphobia to experience daily variations in anxiety severity; most describe having “good days” and “bad days.” For some patients, there may be weeks or months of near-normal functioning followed by a resurgence of the original symptoms. For others, gradual improvement leading to complete recovery may occur without professional intervention, but this is not typical. In one study, patients interviewed 8 years following successful treatment reported general maintenance of improvement with some interim exacerbations. When agoraphobic problems had reappeared temporarily, the most common context was acute objective stress such as the loss of employment or a bereavement.
B. Diagnostic Classification
The psychiatric taxonomy accepted in the United States is the Diagnostic and Statistical Manual of Mental Disorders (DSM), published since 1952 by the American Psychiatric Association and revised in 1968, 1980, 1987, and 1994. Before 1980, agoraphobia was not listed as a distinct disorder in the DSM classification, but could be found among lists of the Greek names for specific phobias in textbooks on psychiatry and abnormal psychology. By the time the third edition of the DSM was published in 1980 it had become clear that agoraphobia was in no sense a specific phobia– its prevalence, its resistance to treatment, its distressing and disabling consequences, and the broad range of its symptoms all clearly set it apart from such focal fears as phobias of heights, snakes, blood, or the number 13. Agoraphobia does include fear of situations (shopping malls, crowded buses, public meetings, etc.), but patients show varied patterns of specific fears, and there is no standard list of situations that must be feared for the diagnostic criteria to be met. Given that it is quite typical in agoraphobia for the patient to fear having a definite appointment, or even the ringing of the doorbell, it is difficult indeed to specify exactly what external situation constitutes the phobic stimulus. Some commentators note that what is chiefly feared in agoraphobia is the absence of safety signals, not the presence of disturbing objects. Most recently, “fear of the panic attack” (or, in patients who do not panic, fear of limited symptom attacks or circumscribed anxiety episodes) has been cited as a central feature of agoraphobia. The significance of the panic attack in many cases of agoraphobia further sets it apart from the specific phobias.
In the 1980s, with such considerations in mind, the compilers of the DSM considered listing agoraphobia as a distinct diagnostic category. Renewed interest in agoraphobia in turn sparked interest in the panic phenomenon, and it was soon recognized that the overlapping of agoraphobia and panic attacks allowed several possible patterns: Agoraphobia with or without panic attacks, and panic attacks with or without agoraphobia. Accordingly, in the DSM-III of 1980 agoraphobia appeared in two forms, with and without panic attacks, and panic disorder was allotted a distinct category. The most recent changes were seen in the DSM-III-R of 1987 and the DSM-IV of 1994, both of which gave precedence to panic in the syndrome that includes panic attacks and agoraphobia.
C. The DSM-IV Classification
Agoraphobia appears twice in the DSM-IV, as panic disorder with agoraphobia and as agoraphobia without history of panic disorder; both are found among the anxiety disorders. The DSM-IV lists separate criteria sets for “Panic Attack” and for “Agoraphobia.” These are not diagnostic categories in themselves.
1. Panic Disorder with Agoraphobia
The essential elements of this diagnosis are the presence of Panic Attacks and Agoraphobia, as defined in the criteria sets. Panic attacks are recurrent, distinct episodes of extreme anxiety or distress, not explained by the presence of a continuing organic factor. Panic attacks include at least 4 of a 13-item list of typical anxiety symptoms, which by definition are initially unexpected and are not produced in response to stimuli associated with specific or social phobias. The list of typical symptoms in a panic attack includes shortness of breath, dizziness, heart palpitations or rapid heart rate, trembling or shaking, sweating, the sensation of choking, depersonalization or derealization, and fear of dying, losing control, or developing an acute mental illness. By definition, the anxiety symptoms in a panic attack arise suddenly and rapidly increase in intensity. An organic factor may have been influential in early panic attacks (for example, the patient may have experienced dizziness as a result of a viral infection of the vestibular system, or depersonalization following ingestion of an illicit drug) but, by definition, the attacks will have continued despite successful treatment or removal of the initiating organic factor.
To meet criteria for panic disorder with agoraphobia, the patient with this diagnosis also has agoraphobia, of course, which is chiefly defined by fear of situations in which it could be difficult to obtain help if a panic attack arose, leading to avoidance or marked distress. The diagnosis applies even if the person’s fear and avoidance of situations are not attributed to fear of having a panic attack.
2. Agoraphobia without History of Panic Disorder
A person with this disorder has never had problems that meet criteria for panic disorder. Instead, he or she fears, and may avoid, situations in which it would be difficult or embarrassing to leave in the event of the sudden onset of anxiety, which may represent a “limited symptom attack” that would not include the range of symptoms associated with a panic attack. Agoraphobia entails difficulties with travel: either avoidance of travel altogether, or being able to travel only with the aid of a trusted companion, or despite significant discomfort. Finally, it should be noted that patterns meeting criteria for panic disorder but not agoraphobia are classified as panic disorder without agoraphobia; patterns consistent with panic disorder but in which an organic factor initiates and maintains the problems are classified as anxiety disorder due to a general medical condition.
D. Epidemiology
Appropriate methodology requires assessing the prevalence and correlates of agoraphobia in the general community as well as in clinic samples (which tend to be unrepresentative). Because of recent changes in the taxonomy, allowance has to be made for the different terms and criteria in studies conducted in different decades. Accordingly, the most informative studies have separated the agoraphobic syndromes from panic disorder without history of agoraphobia and have used accurate community survey techniques. In the studies cited, about half of the respondents with agoraphobia would be classified as having panic disorder with agoraphobia, and half as having agoraphobia without history of panic disorder. However, in clinical samples of agoraphobia, panic disorder with agoraphobia predominates, justifying extensive coverage of panic in discussions of treatment.
The largest and most authoritative epidemiological investigation to include assessment of anxiety disorders was the Epidemiological Catchment Area study, reported in the 1980s. The fully structured Diagnostic Interview Schedule was used in a survey of 18,572 appropriately sampled adults in five communities in the United States (New Haven, Baltimore, St. Louis, Durham, and Los Angeles). The life-time prevalence of agoraphobia was estimated as 4.8%. A smaller study with similar methodology conducted in the former West Germany showed a life-time prevalence of 5.7% for agoraphobia; a similar Canadian study gave 2.9%. A rate of 6.9% was found for a Hispanic population in Puerto Rico with a Spanish form of the interview schedule. Generally, the estimates of the 6-month prevalence of agoraphobia in these studies were one or two percentage points lower than the life-time estimates.
Overall, the findings on the prevalence of agoraphobia are consistent across countries and cultures in studies using the same instrument and careful sampling procedures. Across studies, the life-time prevalence of agoraphobia, with or without panic attacks, is about 5%; the 6-month prevalence is about 4%. However, by 1997 most experts, including the authors of the DSM-IV, had concluded that these estimates were inflated. A more realistic general prevalence estimate for agoraphobia is 2.5 %. Yet, whichever prevalence rate is accepted, these rates are markedly higher in women than in men; for the five sites in the Epidemiological Catchment Area study the ratio of women to men with agoraphobia was 2.7:1.
Agoraphobia is associated with more severe impairment than other phobias and has a markedly higher comorbidity rate for depression. Substance abuse, hypochondriasis, somatization disorder, and personality disorders are often associated with agoraphobia. The usual course is chronic. The age of onset in agoraphobia varies but is usually in the 20s or 30s with a mean of about 28 years. There is no general agreement on an association between agoraphobia and specific childhood experiences. Maternal overprotection has been studied, but findings are mixed.
The estimated morbidity risk of anxiety disorders in the first-degree relatives of patients with agoraphobia is 32%; there is also a greater risk of an alcohol disorder. Concordance rates for panic disorder with and without agoraphobia are significantly higher in monozygotic than in dizygotic twins; a Norwegian study showed 31% concordance in 32 monozygotic twins but 0% in 53 dizygotic twins. Such results have been taken to indicate some genetic predisposition for agoraphobia and panic disorder.
III. ETIOLOGICAL THEORIES
A. Biological Theories
The observations that anxiety syndromes seem to run in families and that pharmacological treatment can be helpful have understandably led to considerable interest in biological mechanisms underlying agoraphobia and related disorders. Attention has been paid to the heritability of agoraphobia, to possible biological variables increasing vulnerability to agoraphobia, and to potential specific mechanisms that may explain agoraphobia. There is general agreement that a predisposition toward agoraphobia (and panic) may be inherited, but it is not possible to predict who will develop agoraphobia even among people with a number of close relatives with the disorder. (It is also widely accepted that mental disorders in general defy attempts to fit a classical model of single-gene heredity.) Agoraphobia probably conforms to a diathesis-stress model in which an inherited vulnerability is necessary, but not sufficient, for the eventual appearance of the syndrome. That would require the additional operation of certain environmental factors in interaction with the predisposing conditions.
Physiological variables distinguishing agoraphobia from normal functioning, and from less pervasive anxiety disorders like specific phobia, include resting heart rate and forearm blood flow (both higher in agoraphobia) and skin conductance (higher and more variable in agoraphobia). However, such findings have not produced clear conclusions with implications for etiology or treatment.
The most promising candidates for the inherited vulnerability factor (if there is but one) in people with agoraphobia can be described as personality traits such as neuroticism, emotionality, trait anxiety, or “nervousness.” Studies of animals and humans have consistently indicated a genetic component in emotionality; it is well known that rats can be bred for emotional reactivity, for example, and in the human studies, there is even stronger evidence for the heritability of trait anxiety or neuroticism than there is for the heritability of anxiety disorders.
Neuroticism is thought to result from lability of the limbic system, of the autonomous nervous system, or of specific neurotransmitter processes. For example, one animal study showed that rats bred for emotionality had more brain benzodiazepine receptors than rats bred normally. Malcolm Lader has noted that many of the data on panic may be explained by positing an instability or hypersensitivity of central noradrenergic mechanisms centering on locus coeruleus function. Despite these observations, few definite conclusions may be drawn from the many physiological and endocrinological studies. The best-supported generalization is that patients with agoraphobia and related anxiety disorders have chronically overaroused central nervous systems and are slow to habituate to noxious stimuli.
Several physiological processes and physical disorders produce symptoms like those of panic, arousing interest in possible mechanisms for agoraphobia. These include hyperventilation, asthma, limbic seizures, abnormalities of thyroid function, hypoglycemia, and mitral valve prolapse. Of particular interest has been the phenomenon of provocation of panic by sodium lactate infusions; people with a history of panic disorder, but not those without prior experience of panic, tend to react to the infusion with panic. Furthermore, pharmacological treatment by means of imipramine can abolish the lactate provocation of panic. Although such observations may appear to confirm a biological basis for panic disorder (and, therefore, of at least one of the agoraphobic syndromes), the mechanism is a subtle one that interacts with environmental and cognitive factors. The lactate provocation of panic can also be blocked by psychological treatment; hence, it would be misleading to focus exclusively on biological processes in interpreting panic phenomena.
There is as yet no clear evidence of a particular biological variant that explains all of the features of agoraphobia. There is likely to be an inherited predisposition toward a labile limbic or autonomic nervous system, associated with chronic overarousal and slow habituation. This diathesis may in turn interact with certain behavioral and cognitive mechanisms to produce agoraphobic syndromes. David Barlow has pointed out that “The fact that language and meaning structures are the most common stimuli for anxiety in humans requires a complex neurobiological system.”
B. Psychodynamic and Interpersonal Theories
Psychoanalytic theory proposes that mental experience and behavior are influenced profoundly by the dynamic interaction of largely unconscious intrapsychic forces. All disorders are viewed as having important unconscious determinants, but this is particularly poignant in such disorders as agoraphobia because of the pivotal importance of anxiety to psychoanalytic theory. Early childhood experiences, particularly interactions with parents and other significant people, are given prominence not only because they form the prototypes for adult social interactions, but also because they influence the development of the mental apparatus itself. Particularly relevant to agoraphobia are the person’s inner representations of other people. It is vital to one’s sense of safety and security to develop stable “object relations,” or internal representations of others. If object relations are disturbed, due, for example, to a poor quality or consistency of early actual relationships, then the person may be vulnerable to insecurity and anxiety later in life. Studies have shown that in humans and animals early separation from parents can be linked to agoraphobia-like behavior.
Freud’s initial theory of anxiety dealt with its somatic aspects. He described “anxiety neurosis” as an actual neurosis (“condition of the nerves”), not a psychoneurosis, because it results from undischarged neural excitation (caused by emotional trauma, for example). To Freud, such actual neuroses involve disturbed bodily processes, particularly difficulties in breathing. He later described psychoneuroses in which undischarged tension results from unacceptable ideas rather than from external stimulation.
Eventually Freud turned his attention away from physical explanations of anxiety and emphasized its role as an ego function that is aroused in response to danger, a sense of helplessness when confronted by internal or external threat. Relevant to agoraphobia, Freud’s ideas are consistent with the views that the ego responds with anxiety to (1) real danger, (2) physiological processes involving the autonomic nervous system, and (3) the arousal of emotions like anger or frustration.
An important issue for clinicians taking a psychodynamic approach is to separate manifestations of anxiety that stem from biological disturbances from those that stem from intrapsychic problems, such as an underlying conflict or a disorder of object relations. Psychodynamicists argue that, because environmental stimuli influence neurophysiological reactivity, and because the meaning of those stimuli mediates their impact, there is an important role for psychodynamic hypotheses and therapy in application to agoraphobia.
An integrative theory put forward by Alan Goldstein and Dianne Chambless in 1978 uses behavioral and psychodynamic concepts to explain the various phenomena of agoraphobia, including typical personality factors and interpersonal styles. It is argued that the person with agoraphobia (a) fears panic attacks rather than particular places; (b) has difficulties with self-sufficiency, independence, and assertiveness; (c)is unable to trace the antecedents of emotional feelings when they arise; and (d) develops the initial symptoms of agoraphobia in a climate of interpersonal conflict. The interaction of these factors produces agoraphobia. The typical patient in this model is a woman who feels trapped in a troubled marriage. Although she wishes to leave, she lacks the necessary autonomy, independence, and self-sufficiency to make leaving a realistic option. Dealing directly with her feelings and asserting her opinions toward her husband are unfamiliar and difficult for her, so she attempts to tolerate this unsatisfactory situation. An argument with her husband early in the day elicits dysphoric mood but not a specific, identifiable emotion. Out in public later in the day, she still feels ill at ease, but is unsure of the origin of this feeling. Waiting in line somewhere (or using an elevator, traveling through an underpass, etc.), she feels trapped, and at some level this is reminiscent of being trapped in the unsatisfactory marriage. A panic attack suddenly arises. She later begins to avoid places similar to the site of the panic attack. Eventually becoming housebound, she is no longer able to contemplate leaving her husband, and this has the advantage of settling the matter so that she is no longer troubled by her mixed feelings about leaving.
This view of agoraphobia draws attention to the potential role of adjunctive treatments like assertiveness training, marital therapy, or therapeutic work on recognizing and identifying feeling states. The work of some behavior therapists attests to the value of assertiveness training in programs for agoraphobia, and marital therapy has brought benefit to at least some patients with agoraphobia, as judged by anecdotal reports. However, marital distress has not been shown to have general etiological significance in agoraphobia.
C. Behavioral and Cognitive Theories
1. Conditioning Theories
The most familiar behavioral theory of the etiology of agoraphobia calls attention to classical conditioning as a possible mechanism. According to this view, previously innocuous stimuli such as streets, shops, and crowds acquire fear-eliciting properties through systematic pairing with noxious events. Although these noxious events are usually not specified, there are various plausible possibilities, such as witnessing an accident while in town, or being taken ill while shopping. Suddenly becoming ill, for example, creates reflex responses of distress and discomfort. By their pairing with the stimuli that elicit distress, certain stimuli in the immediate environment could become conditioned stimuli that on later occasions call forth anxiety as a conditioned response.
An immediate objection to classical conditioning as an explanation of agoraphobia is that extinction of the acquired anxiety would be expected when the person encounters the newly feared situations without the original noxious stimuli. However, Mowrer’s two-factor theory posits the operation of a second process, instrumental or operant learning, to explain the persistence of conditioned fear. Once fear is acquired by means of classical conditioning, avoiding the feared situations will be reinforced because avoiding these situations means removing anxiety. At the same time, avoidance of conditioned stimuli prevents the exposure to them that would be necessary to allow extinction to occur.
So many objections have been raised to two-factor theory in this context that it can no longer be supported as a general explanation of agoraphobia. In agoraphobia, levels of fear and avoidance behavior are not closely correlated, yet two-factor theory explains avoidance behavior as motivated by conditioned fear. Conditioning does not explain the common phenomenon of daily fluctuations in anxiety severity, or the fact that general stress is often associated with an exacerbation of agoraphobia. It is not clear from two-factor theory why agoraphobia so often represents a syndrome of fears of travel, crowds, confinement, and so forth, if indeed conditioning takes place haphazardly and involves whichever stimuli happen to be prepotent at the time. Conditioning theories do not obviously explain the comorbidity of agoraphobia with depression or hypochondriasis. Even the survivors of serious accidents or natural disasters do not necessarily develop an anxiety disorder, despite having been subjected to highly anxiety-provoking experiences. By contrast, most people with agoraphobia cannot recall having had an aversive experience with the situation or object they fear. Conditioned fear is very difficult to produce in humans in laboratory experiments, and there are many contradictory findings. Several attempts to replicate landmark studies of classical fear conditioning in humans were notorious failures.
There is the paradox that, although unadorned conditioning accounts of agoraphobia have been discredited, treatments that seem based on extinction procedures have been quite successful. Exposure in vivo, in which the patient learns to confront agoraphobic situations without leaving at the onset of anxiety, can be helpful in overcoming a pattern of avoidance of situations and can attenuate panic attacks. However, the success of such treatment does not confirm a two-factor theory account of the etiology of agoraphobia.
When the panic attack itself is considered to be the noxious event that allows classical conditioning of fear to external situations, the conditioning explanation becomes more credible. That leads to the proposition that it will be most helpful to explain the origin and maintenance of panic attacks. A panic attack may be viewed as the result of a vicious circle or upward spiral in which, at each point, stimuli associated with anxiety elicit conditioned anxiety responses, which in turn produce further anxiety-eliciting stimuli. This is an interoceptive conditioning view in which it is assumed that the conditioned stimuli are the bodily sensations that result from initial anxiety arousal, and that each conditioned response has a greater amplitude than its immediate predecessor. It follows from this view of panic attacks that it will be helpful therapeutically for the patient to confront anxiety sensations themselves rather than simply the external situations in which they commonly arise. If the patient fears the bodily sensations of anxiety (heart pounding, dizziness, shortness of breath, and so forth), then the exposure principle would predict that systematic confrontation of these sensations will ultimately diminish their power to evoke anxiety.
Problems with this view of panic attacks include the following. If any arousal of anxiety leads inexorably to a vicious circle that culminates in a panic attack, then people with panic disorder would never experience limited episodes of mild or moderate anxiety. However, it is usual for panic disorder patients to display moderate levels of generalized anxiety between their panic attacks. The theory also fails to explain who will be vulnerable to the escalation of mild anxiety into panic attacks. The cognitive therapy approach to which we turn next attempts to address this problem.
2. Cognitive Theories
Aaron Beck’s cognitive therapy rests upon several theoretical assumptions that center upon the individual’s appraisal of events. Such appraisals range from fleeting “automatic thoughts” in the form of accessible, though covert, verbalizations (e.g., “Oh, no. I knew I’d get anxious if I came to the mall, and I feel slightly dizzy already!”) to deeper and more enduring “cognitive schemas,” not necessarily verbalized, reflecting a more fundamental attitude (e.g., strange feelings could indicate a serious medical catastrophe).
Central to the application of cognitive therapy assumptions to panic attacks is the patient’s appraisal of the bodily sensations or somatic cues connected with mounting anxiety. David Clark has argued that people with panic disorder have developed cognitive schemas concerning vulnerability to medical catastrophes, and he and others have demonstrated that people with panic disorder show cognitive biases in that direction. (The notion of fear of medical catastrophes as one variant of agoraphobia was introduced by Joseph Wolpe in 1970.) This model complements the conditioning of somatic cues model by indicating who is vulnerable to panic and why not all anxiety episodes culminate in panic. Variations in cognitive appraisals between and within individuals may account for the unpredictability of panic attacks. In Clark’s model, the sequence begins when the client experiences sensations from a flushed face or pounding heart. It is immaterial to the model whether these sensations result from pathological (developing a fever in response to an infection) or normal (having run up the stairs) processes. Next, the patient makes a “catastrophic misinterpretation” of the bodily sensations, viewing them as signals of a medical disaster such as a heart attack. The misinterpretation itself arouses increased anxiety, and the vicious circle continues when further alarming appraisals are made.
3. A Comprehensive Model
Perhaps the most comprehensive contemporary theory is that of David Barlow, who suggests that panic results from activation of an ancient alarm system, and is the basic emotion of fear, while anxiety is a more general cognitive-affective structure. Panic occurs in response to three types of alarm. True alarms are panic attacks elicited by genuine danger. False alarms are panic attacks in the absence of objective danger, and result from a genetically determined predisposition in interaction with an accumulation of general stress. (Anyone may experience a false alarm, not only people with anxiety disorders.) Learned alarms are panic attacks that are triggered by cues, which may be particular objects, as in specific phobia, or internal physiological changes, as in panic disorder. Anxious apprehension also plays a part in explaining the development of anxiety disorders; a cognitive schema containing propositions concerning anxiety elicits negative affect when triggered, and the sequence of events that follows includes directing attention to internal self-evaluations, increased arousal, narrowing of attention, and hypervigilance concerning sources of apprehension.
In summary, Barlow’s model of agoraphobia is his model of panic disorder with the addition of the development of agoraphobic avoidance. Biological vulnerability interacts with objective stress to produce an initial uncued panic attack, or false alarm. The connection of the panic attack with interoceptive cues leads to the development of cued learned alarms. As a result, there is a psychological vulnerability characterized by anxious apprehension about future panic attacks. Next, panic attacks are triggered unpredictably by a combination of autonomic and cognitive symptoms of anxiety with additional somatic cues. Depending on the presence or absence of safety signals and various cultural and environmental factors, avoidance behavior may develop, giving rise to the panic disorder with agoraphobia syndrome.
IV. ASSESSMENT AND DIAGNOSIS
The assessment of agoraphobia in clinical practice proceeds through several stages. First, the diagnosis is established. Second, identification of the specifics of a patient’s level of distress and disability allows development of an individualized treatment plan. Third, evaluating concomitant problems or issues, ranging from diagnosable disorders to matters of life circumstances, permits employment of adjunct treatments or influences the sequence in which treatments for agoraphobia are provided. Fourth, monitoring the patient’s progress throughout the course of therapy is essential in determining response to treatment and alerting the clinician to needed procedural changes.
A. Diagnosis
People with agoraphobia may be self-referred, referred by friends or relatives, or referred by other professionals. It is not uncommon for a patient to seek treatment having made a self-diagnosis of agoraphobia after reading a magazine article or viewing a television presentation about agoraphobia. It is also quite common for a patient to be referred to a mental health professional by emergency room staff after one or more visits for urgent treatment during panic attacks. Because many people with agoraphobia are either entirely housebound or have a limited range of travel, clinicians working with this disorder become accustomed to making home visits, at least in the early stages of assessment and treatment.
Because there are several physical conditions that give rise to symptoms like those of agoraphobia, it is important that the patient receive a physical examination before mental health interventions begin. If anxiety persists despite successful treatment of a precipitating or complicating physical condition, then treatment of agoraphobia proceeds. It should be noted that having certain physical conditions is not incompatible with having agoraphobia, but accompanying physical disorders demand attention first.
Assessment is needed to identify other psychiatric disorders that may co-exist with agoraphobia, including mood, somatoform, substance use, and personality disorders. Also relevant for assessment are issues like marital conflict, social skills deficits, and difficulty with personal autonomy that may not require a formal diagnosis but may yet be important foci for intervention. By no means do all people who experience anxiety when in public places or who have had panic attacks have problems that meet diagnostic criteria for agoraphobia syndromes. Social and specific phobias may center upon some of the situations commonly avoided in agoraphobia, and panic attacks may occur in mood disorders, psychosis, and in people without psychiatric disorders. Treatments usually employed with agoraphobia may be misdirected in these other diagnostic contexts.
Assessing the Range and Extent of Agoraphobia
Simply applying the appropriate diagnostic label is insufficient to guide treatment. The clinician seeks to know the patient as a unique individual and accordingly conducts the usual psychosocial history and mental status examination. Beyond that, the nature and extent of the agoraphobic problems will need to be charted in sufficient detail to allow formulation of an appropriate individual treatment plan and continued evaluation of progress toward treatment goals.
The Anxiety Disorders Interview Schedule – IV (ADIS-IV) is the most widely used structured interview protocol in the assessment of agoraphobia and other anxiety disorders. Developed by Barlow and his colleagues, the ADIS-W allows detailed and accurate characterization of the person’s anxiety problems and permits authoritative diagnosis in DSM-IV terms. The instrument is primarily employed in research trials to ensure uniformity of diagnostic practices. Although the complete protocol is too lengthy for routine clinical use, subsets of the ADIS-W may be used appropriately and conveniently in most clinical settings.
Self-report questionnaires like the Fear Questionnaire, the Anxiety Sensitivity Index, and the Mobility Inventory are all useful for treatment planning and charting progress in respect of the specific agoraphobic symptoms. Questionnaires on other related issues, such as assertiveness, depression, or marital harmony, are generally helpful in initial evaluations and may be germane to the issues of particular clients throughout the course of treatment.
It is highly desirable to have the patient self-monitor general anxiety, panic attacks, and agoraphobic avoidance daily. Individualized forms may be used so that details of the specifics of the patient’s situation may be accommodated therein. For example, daily ratings may be made of a patient’s degree of avoidance of, fear in, and self-confidence about each item in a customized graded hierarchy of feared situations. Daily ratings of the frequency and intensity of panic attacks allow the patient to record the circumstances surrounding each episode, situational, cognitive, and interpersonal.
The nature of agoraphobia allows the use of a hierarchically ordered behavioral test for most patients. This takes the form of an unaccompanied journey—walking, driving, or using public transportation—to take in as many situations relevant to the patient’s fear and avoidance as is feasible. The clinician asks the patient to proceed as far as possible, and takes the distance actually traveled as a helpful datum in sampling current levels of agoraphobic avoidance.
Physiological monitoring has been a customary component of research trials designed to provide generalizable information on treatment effectiveness, but is far less common in routine clinical practice. The typical finding that measures of anxiety in the different domains–self-report, behavioral observation, and psychophysiological—do not covary as might be predicted should not daunt the clinician unduly. When all such measures are available, it is recommended that treatment proceed until clear reductions have been seen in each measurement modality.
V. TREATMENT
A. Pharmacological Treatment
Pharmacological treatment has several advantages for the patient and significant progress has been made in this area since 1970, improving the general outlook for agoraphobia. Many people with agoraphobia have their first clinical contacts with physicians, either in emergency rooms following an initial panic attack or in family practice settings, and medication is readily available and convenient to use. (Despite this, surveys show that the general public and people with agoraphobia tend to disfavor drug therapy.)
Agoraphobia subsumes anxiety and avoidance behavior, and is often associated with dysphoric mood if not clinical depression. The medications most commonly used, and extensively studied, in the treatment of agoraphobia are those that are generally prescribed for anxiety and depressive symptoms.
1. Tricyclic Compounds
Together with the monoamine oxidase inhibitors, the tricyclic compounds are chiefly used in treating depression, but the term “antidepressants” commonly applied to them may be misleading in this context because there is controversy about their role in agoraphobia treatment (do they attenuate dysphoric mood, facilitating other treatments, or do they act specifically to block panic attacks?).
Imipramine has been the most extensively studied, but the related tricyclics desipramine and clomipramine may be similar in effectiveness. Early studies appeared to show that imipramine reduced panic attacks, but patients continued to avoid agoraphobic situations.
Later studies demonstrated imipramine’s superiority to placebo medication and indicated that it brought additional benefit when added to behavioral treatment. However, this additional benefit was not attributable to the blockade of panic. When imipramine is used in conjunction with the anti-therapeutic recommendation to avoid confronting feared situations, improvement in mood, but not in agoraphobia, is the resuit. Empirically, imipramine plus exposure therapy seems more effective than either treatment alone. It has been argued that inconsistencies in research findings with imipramine may result from marked differences in doseage across studies.
2. Monoamine Oxidase Inhibitors (MAOIs)
The MAOIs phenelzine and iproniazid have received most attention. Whereas some studies have shown little if any difference between phenelzine and placebo in application to agoraphobia, another has shown that phenelzine reduces general disability and avoidance behavior. In that study phenelzine was more effective than imipramine. For reasons that are unclear, phenelzine appears to potentiate self-initiated exposure.
3. Benzodiazepines and Triazolobenzodiazepines
The benzodiazepines are minor tranquilizers that have been extensively prescribed for various forms of anxiety and stress reactions, clinical and subclinical, for decades. Donald Klein’s initial work on imipramine had suggested that it is specific for blocking panic, whereas the benzodiazepines are effective only with generalized or anticipatory anxiety. Later work suggests that high doses of benzodiazepines may be effective in treating panic attacks. The recent development of high-potency benzodiazepines like alprazolam and clonazepam has brought substantial benefit in the treatment of agoraphobia and panic. Alprazolam, a triazolobenzodiazepine, has been the subject of a multi-center world-wide double-blind study of people with panic disorder (with and without agoraphobia). Fifty percent of the alprazolam patients and 30% of placebo patients were panic-free 3 weeks after the start of the trial.
Strong withdrawal reactions after discontinuance of alprazolam pose a significant problem, as does the phenomenon of “rebound panic” in which a minority of patients may experience even worse panic attacks after withdrawal from medication than before treatment.
4. Summary
Imipramine, phenelzine, and alprazolam are helpful in the treatment of agoraphobia. The related medications desipramine, clomipramine, tranylcypromine (an MAOI), and clonazepam have received less attention but may be as helpful. Some medications not noted above, like the beta-blocker propranolol, have been shown ineffective for agoraphobia. By the late 1990s the selective serotonin reuptake inhibitors and other new medications have been widely prescribed for people with agoraphobia, and there is a ferment of pharmacological research activity. The mechanisms underlying successful pharmacological treatment are unclear.
B. Psychological Treatment
Psychodynamic approaches to agoraphobia have received far less attention than biological, behavioral, and cognitive approaches in recent decades, and there is no corpus of empirical research on psychodynamic formulations of etiology or on the results of psychodynamic treatment. However, its proponents suggest that psychodynamic approaches are particularly germane to some of the common clinical issues in agoraphobia, and applying psychodynamic reasoning could be especially fruitful in this context. It is argued that these approaches may be particularly helpful with treatment-resistant patients, in guiding the strategy of supportive psychotherapy, and in using the therapeutic relationship in a supportive context and as a potential therapeutic tool.
Behavior therapists treating agoraphobia in the late 1950s and early 1960s emphasized its commonalities with the phobias, and sought to reduce situational fear and avoidance behavior by means of techniques effective for specific phobia. In the 1970s the differences between agoraphobia and other phobias began to be recognized, and treatment by systematic desensitization was replaced by imaginal flooding and exposure in vivo. Attention was paid to panic attacks as well as to avoidance behavior. Since the 1980s the focus has been on direct psychological treatment of panic attacks.
1.Treatment of Agoraphobic Avoidance Behavior
Despite initial enthusiasm for Joseph Wolpe’s technique of systematic desensitization as a therapeutic breakthrough for phobias, its application to agoraphobia in controlled clinical trials in the 1960s brought disappointing results. The technique was largely abandoned as treatment for agoraphobia when developments in the 1970s established flooding in fantasy and graded practice in real life as effective treatments. Researchers in Vermont led by Stuart Agras showed that graded practice–with or without praise for specific accomplishments–could quickly reduce agoraphobics’ avoidance of unaccompanied journeys away from the clinic. This work converged with that of Isaac Marks in the United Kingdom to identify exposure in vivo as the central ingredient of psychological treatment for agoraphobic avoidance.
Procedural variations such as brief or prolonged exposure duration, massing or spacing of treatment sessions, and terminating exposure at the point of increasing or decreasing anxiety were examined assiduously by clinical researchers, but the consensus is that these technical details are less important than the general recommendation to confront, rather than avoid, feared situations. This exposure principle is as well-founded as any in the entire field of mental health work.
Improved functioning after exposure treatment for agoraphobia has been shown to persist for several years post-treatment. Not all patients accept or remain in exposure treatment; the attrition rate during therapy has been estimated at 12%. Of those who complete a course of treatment, approximately 70% have successful outcomes.
Exposure treatment may proceed intensively and rapidly. In some studies, an entire course of treatment was completed in 2 weeks of prolonged, daily sessions. While the data on adverse complications from rapid treatment are equivocal, particularly those concerning the possibility of social and marital disruptions, gradual treatment is recommended in order to facilitate patients’ thorough consolidation of therapeutic gains at each step. Treatment of avoidance through exposure preferably includes weaning patients from “safety signals,” items like written instructions from the therapist, bottles of minor tranquilizers (even empty ones), or canes or umbrellas that are carried more for their associations with a sense of security than for any more obviously practical benefit.
2. Treatment of Panic
The current diagnostic classification assigns central importance to panic attacks in most cases of agoraphobia seen in clinical settings. If panic is primary, and avoidance behavior a secondary complication thereof, then treatment could logically be directed at panic phenomena. This is not incompatible with treatment of avoidance by exposure, which can itself reduce panic attacks. But, as David Barlow has put it, “treating avoidance behavior will always be necessary. Nevertheless, the primary goal should be the treatment of panic.”
The essential technique in the psychological treatment of panic is exposure to somatic cues, or reproduction of and confrontation by the bodily symptoms that the patient associates with panic attacks. The patient is asked to create sensations of panic deliberately in treatment sessions. Running in place, voluntary hyperventilation, and spinning around in a swivel chair are examples of procedures for creating such sensations. Clinicians match particular procedures to patient’s most troublesome symptoms; someone who is most troubled by dizziness will practice spinning around, while someone disturbed by the sensations of a rapid heart-rate will run up and down the stairs.
In early trials, this approach has brought the most impressive results yet seen in the treatment of panic and agoraphobia, the success rates approaching 100% in some studies. Advances in methodology that have allowed the daily monitoring of panic attacks have permitted accurate tracking of panic attack frequency. “Percentage of patients panic free” has become a standard datum to report in contemporary treatment trials. The success of exposure to somatic cues as treatment for panic has prompted a reinterpretation of some early studies that lacked a theoretical context at the time. Inhalation of carbon dioxide as treatment for generalized anxiety, the “running treatment” for agoraphobia, the utility of imaginal flooding to phobia-irrelevant themes in reducing phobic sensitivity, and the lactate provocation of panic as treatment for anxiety episodes—all found in the literature of the last few decades—may be readily understood today as consistent with the exposure principle in its most recent application to panic sensations.
The efficacy of exposure to somatic cues has been attributed to various theoretical processes. These include the exposure principle, possibly resting upon the extinction or habituation of conditioned anxiety responses to panic sensations, or upon the development of coping skills by the patient. The success of the method is consistent with the specific hypothesis that chronic hyperventilation underlies panic disorder. It is also consistent with the cognitive therapy view that the patient makes catastrophic misinterpretations of the bodily sensations of panic, ascribing to them morbid significance as harbingers of a medical emergency.
Parallel to exposure to somatic cues is cognitive therapy in the contemporary treatment approach to panic. Consistent with David Clark’s model of an interaction of sensitivity to somatic cues and catastrophic misinterpretation thereof, patients are engaged in a cognitive treatment process of collaborative empiricism in which implicit schemas construing panic sensations as signals of dire illness are carefully assessed, gently challenged, and empirically tested. Cognitive therapy involves exploring, in a sympathetic and accepting way, the specific idiosyncratic cognitions that are assumed to underlie emotional distress. Wherever possible, real-life “experiments” are undertaken in attempting to challenge unrealistic assumptions. There is no standard, structured format that must be applied systematically to all patients; rather, the principles of cognitive therapy guide a creative treatment approach with each individual. The results of preliminary trials of cognitive therapy have been as encouraging as those of exposure to somatic cues, and the combination of these treatments has brought the best outcomes.
3. Comprehensive Treatment of Agoraphobia
In addition to the central psychological treatment approaches of exposure in vivo, exposure to somatic cues, and cognitive therapy, relaxation training and breathing retraining have been found helpful in the treatment of agoraphobia and are recommended as optional components of a treatment plan. There is a consensus that in the typical case of panic disorder with agoraphobia treatment should proceed employing all of these techniques in sequence, beginning with self-paced exposure in vivo. Some authorities argue that, because it is not associated with deleterious side-effects or complications from withdrawal, psychological treatment should be used first, and pharmacological treatment brought in as necessary subsequently.
VI. CONCLUSIONS AND PROSPECTS
Although it is fragmented by the current nomenclature into two distinct disorders, agoraphobia is a coherent syndrome with a range of symptomatology extending far beyond the limited compass of specific phobias. Recognized since 1871 as an unusually debilitating anxiety disorder, agoraphobia has only recently yielded to effective pharmacological, behavioral, and cognitive treatments.
The conclusion of a recent Consensus Development Conference on the Treatment of Panic Disorder, sponsored by the National Institutes of Health and the National Institute of Mental Health in the United States, are pertinent and may be summarized as follows. Although perhaps most patients receiving psychological treatment are also taking medication, little is known about the effectiveness of combined pharmacological and psychological treatment. Not enough is known about the mechanisms of action of contemporary treatments, patient factors predicting success or permitting matching to the most appropriate treatment, the long-term effectiveness of the new treatments for panic, and the value of treatment for associated mental health problems and issues.
Also in need of further attention by clinicians and researchers are the following. Whereas pharmacological treatment is readily available, it is difficult for many patients to gain access to psychological treatment, especially in rural areas. Innovations in service delivery are needed, and studies should address the viability of psychological treatment of agoraphobia from remote sites by means of the latest communications technology. Many communities are underserved by mental health professionals, and people who are housebound by agoraphobia have even greater difficulties than most people in gaining access to needed psychological services.
BIBLIOGRAPHY:
- Barlow, D. H. (1988). “Anxiety and Its Disorders.” Guilford Press, New York.
- Beck, A. T., Emery, G., & Greenberg, R. L. (1985). Anxiety disorders and phobias: A cognitive perspective. New York: Basic Books.
- Chambless, D. L., and Goldstein, A. J. (Eds.) (1982). “Agoraphobia: Multiple Perspectives on Theory and Treatment.” Wiley, New York.
- Gournay, K. (Ed.)(1989). “Agoraphobia: Current Perspectives on Theory and Treatment.” Routledge, London.
- Hecker, J. E., and Thorpe, G. L. (1992). “Agoraphobia and Panic: A Guide to Psychological Treatment.” Allyn and Bacon, Boston.
- Hecker, J. E., Losee, M. C., Fritzler, B. K., & Fink, C. M. (1996). Selfdirected versus therapist-directed cognitive-behavioral treatment for panic disorder. Journal of Anxiety Disorders, 10, 253-265.
- Knapp, T. J. (Ed.) and Schumacher, M. T. (Trans.) (1988). “Westphal’s ‘Die Agoraphobie’.” University Press of America, Lanham, MD.
- Marks, I. M. (1987). “Fears, Phobias, and Rituals: Panic, Anxiety, and Their Disorders.” Oxford University Press, New York.
- Mathews, A. M., Gelder, M. G., and Johnston, D. W. ( 1981 ). “Agoraphobia: Nature and Treatment.” Guilford, New York.
- Thorpe, G. L., and Burns, L. E. (1983). “The Agoraphobic Syndrome: Behavioural Approaches to Evaluation and Treatment.” Wiley, Chichester, UK.
- Walker, J. R., Norton, G. R., and Ross, C. A. (Eds.) (1991). “Panic Disorder and Agoraphobia: A Comprehensive Guide for the Practitioner.” Brooks/Cole, Pacific Grove, CA.
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