Phobias Research Paper

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Phobia derives from the Greek word phobos, meaning “fear.” Phobias are persistent, excessive fear responses to objects or situations that are for most people neutral or only mildly anxiety-arousing. Phobias typically involve fears of the commonplace situations involved in life and, if the feared situation is frequently encountered, can interfere greatly in the general conduct of life. The current classification of phobias includes three types: specific phobia, social phobia, and agoraphobia. They tend to occur frequently, as approximately one in seven adults will experience a phobia at some point in their lives. While we think of the various types of phobias as separate entities, it is not uncommon for a given person to experience more than one type of phobia at the same time. Similarly, individuals who develop phobias are likely to experience other types of mental disorders, among them depression, and other anxiety disorders such as obsessive-compulsive disorder and generalized anxiety disorder. Phobic disorders, in addition to being relatively common, often have a profound effect on the lives of individuals who suffer with them.

In this paper, each of the three types of phobias will be examined. A definition of each type will be provided, followed by an examination of the associated features of the disorder, its typical course and prognosis. Several causal models of each phobia group will be evaluated, followed by a discussion of therapeutic approaches.

Outline

I. Specific Phobia

A. Definition

B. Clinical Features

1. Symptoms and Epidemiology

2. Course/Prognosis and Comorbidity Issues

C. Etiology

1. Genetic Factors

2. Biological Factors

3. Associative Learning

4. Treatment

II. Social Phobia

A. Definition

B. Clinical Features: Symptomatology and Epidemiology

C. Course/Prognosis and Comorbidity Issues

D. Etiology

1. Genetic Factors

2. Biological Factors

3. Environmental Factors

4. Psychological Factors

E. Therapy

1. Psychological Approaches

2. Pharmacological Approaches

III. Agoraphobia

A. Definition

B. Clinical Features: Symptomatology and Epidemiology

C. Course and Prognosis

D. Causal Factors

E. Heredity

F. Biological Factors

G. Psychological Factors

IV. Panic Disorder and Agoraphobia

A. Psychological Approaches

B. Pharmacologic Treatments

V. Bibliography

I. Specific Phobia

A. Definition

The Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, (DSM-IV, the primary source in the United States for defining the various mental disorders) defines specific phobias as irrational and persistent fears of certain objects or animals. Specific phobias have historically been known as “simple phobias,” “monosymptomatic phobias,” or “focal phobias.” The phenomenon of specific phobias has been described for centuries. Hippocrates, for example, described a man displaying an irrational fear of bridges. Detailed discussions of phobic symptoms can be found in the writings of seventeenth- and eighteenth-century authors such as Descartes, Le Camus, and Sauvages.

DSM-IV identifies three central features of specific phobias: (1) fear is directed at a limited set of stimuli; (2) confrontation with these stimuli elicits fear and avoidance behavior; and (3) the fear is unreasonable and excessive to a degree that it interferes with daily life. In addition, the fear persists over an extended period of time.

With the publication of DSM-IV, specific phobias were for the first time differentiated into four highly prevalent types: (1) animal type (e.g., spider phobia); (2) natural environment type (e.g., height phobia); (3) blood-injection-injury type (e.g., dental phobia); and (4) situational type (e.g., claustrophobia). In addition, DSM-IV introduces an “other type” that includes phobias of specific situations not covered above–choking phobia, for example. The validity of such distinctions is supported by data showing that these types tend to differ with respect to age of onset, familial aggregation, and physiological responses to the phobic stimulus.

B. Clinical Features

1. Symptoms and Epidemiology

When not confronting the feared object, individuals with specific phobias are not different from nonphobic individuals in their level of physiological arousal. When confronting the feared situation, however, phobic individuals reported a number of common anxiety-related somatic symptoms such as heart palpitations, trembling, and sweating. In addition, individuals with specific phobias demonstrate similar increases in indices of arousal upon exposure to cues associated with their phobia. Thus, a person with a fear of spiders might become fearful when looking at a picture of a spider or when entering a dusty place where spiders may be present. In addition to physiological arousal, phobic individuals also show increases in subjective level of fear and in their tendency to avoid the phobic object. However, this consistency is not always present as phobic individuals may manifest increases in one or two of these domains and not the other(s).

Blood-injection-injury phobics are characterized by a unique physiological response to their fear cues. These individuals exhibit an initial increase in heart rate and blood pressure, as do most other phobics, followed by a dramatic drop on these measures, often resulting in fainting.

Not much is known about the cognitive symptoms in individuals with specific phobias due to an assumption that any thoughts individuals with specific phobias might have would be related to the feared object. Furthermore, cognitions have not been considered to be important in the etiology of specific phobias. This view~that cognitions are unimportant in the development of specific phobias–is changing. For example, 37% of individuals exposed to a phobic stimulus reported being equally or more concerned with their physical sensations than with the stimulus itself. In addition, many claustrophobics report thoughts of being trapped, suffocating, and losing control, thoughts characteristic of individuals who experience panic attacks.
It was found in a recent national survey of mental disorders that 11.3% of the population will have a specific phobia in their lifetime. Situational and environmental phobias are the most common (13 % of the population), followed by animal phobias (8%), and blood-injection-injury phobias (3 %).
Women are twice as likely as men to be diagnosed with a specific phobia. This is especially true for animal phobias and situational and environmental phobias, but less so for blood-injection-injury phobias.

2. Course/Prognosis and Comorbidity Issues

Specific phobias develop at different points in the life cycle. Animal phobias develop earliest (average age around 7 years), followed by blood phobias (average age around 9 years), dental phobias (average age around 12 years), and claustrophobia (average age around 20 years). The differences in age of onset among the specific phobias suggest that different causal factors are at work in their development. The heterogeneity of the diagnostic group is further evidenced when one examines claustrophobia. Claustrophobia may well be descriptively and functionally a less constricting form of agoraphobia, a disorder described later. Support for a link between claustrophobia and agoraphobia comes from (1) a similar age of onset with both developing around 20 years of age; (2) a similar mode of acquisition, with agoraphobia (81% of the time) and claustrophobia (69% of the time) developing after experiencing a stressful event; and (3)the co-occurrence in claustrophobia of uncued/unexpected panic attacks, worry about becoming anxious and panicky, fear of bodily symptoms of arousal (e.g., “fear of fear”), and unpredictability of the fear response in claustrophobic situations, all of which are features of Panic Disorder with Agoraphobia. In contrast, other specific phobias have an earlier age at onset, are less likely to be acquired after experiencing a traumatic event, and are more consistently associated with fear of specific situations than of internal anxiety symptoms.

The natural course of specific phobias is usually chronic and can be characterized by the persistence of mild rather than severe symptoms of anxiety over time. Only 16% of individuals with specific phobias have a complete remission of symptoms over a followup period of 7 years. While specific phobias appear to occur frequently in the general population, few sufferers seek treatment, even though this problem may seriously threaten their social or occupational functioning and in spite of the fact that treatment can be highly successful.

C. Etiology

1. Genetic Factors

The genetic hypothesis contends that a predisposition to develop specific phobias is inherited. Evidence indicates there is a consistent, modest contribution of genetic factors to the development of specific phobias. Furthermore, the genetic factors underlying specific fears appear to be of a general nature, such that what is inherited is a trait that predisposes to anxiety in general rather than inheritance of a specific fear. In some cases, the predisposition is expressed as a specific phobia; in other cases, the complaints may take the form of, for example, social phobia or agoraphobia. However, blood-injection-injury phobia may represent an exception to this pattern. Evidence suggests that in blood-injection-injury phobia, the genetic contribution is much stronger than in other phobias and that what is inherited is the specific vulnerability to develop this phobia.

2. Biological Factors

The preparedness hypothesis suggests specific phobias are an example of evolution-prepared learning. The concept of “preparedness” refers to the observation that anxiety responses are more easily learned to some stimuli than to others and that the ease of learning in any one instance varies from species to species. Most specific phobias involve stimuli that over the course of evolution might have been dangerous to man (e.g., snakes, heights) and are still reacted to as though intrinsically dangerous. Several human and animal studies have tested the preparedness hypothesis under laboratory conditions and found evidence to support it. In one such study, it was found that when conditioned responses to evolution-relevant cues are acquired, they continue to persist much longer than conditioned responses to evolution-neutral cues. A number of studies on monkeys lend further support to the preparedness hypothesis. In these studies, observer monkeys acquired an extremely persistent fear of snakes after they watched model monkeys reacting fearfully to snakes. In contrast, observer monkeys failed to acquire a fear of flowers after they had seen models exhibiting identical fear responses when presented with flowers. These various research studies provide support for the contention that fear responses to some stimuli are much easier to acquire if fear responses to these stimuli were adaptive to our ancestors’ survival.

The “Preparedness” hypothesis specifies that learning a phobic response will occur more easily for some stimuli than for others. An association with a negative unconditioned stimulus is still, however, required. An alternative, nonassociative hypothesis is that certain stimuli are hard-wired to produce fear, that is, they elicit a fear response without a previous negative experience with the stimulus. Darwin noted, after observing his 2-year-old’s nonfearful response to caged animals, that fears are inherited effects of real dangers. When Darwin tried to control his fear response to the strike of a puff adder seated behind a solid glass barrier, he was unable to restrain his automatic recoil from the barrier. Perhaps the best evidence for the biological basis of fear comes from examining the responses of infant rhesus monkeys. Shown slides of monkeys in various poses, these monkeys displayed clear fear responses when shown pictures of threatening, but not of nonthreatening, monkeys. Because these infant monkeys were reared in isolation, they could not have learned this fearful response by experiencing trauma themselves or by watching other monkeys display a fear response. Similar nonlearned fearful responses in human children develop at specific periods in the developmental cycle. Thus, human infants display a fear of strangers from around 4 to 9 months of age, peaking at 12.5 months. Human infants, after they develop locomotion, also display a fear of falling when placed on the edge of an apparatus that looks like a visual cliff. Infants will crawl away from mothers who call to them from across the cliff even after patting the surface to assure themselves of its solidity. Such data indicate that for at least some stimuli there is a built-in readiness to experience fear in their presence.

There are critics of the biological hypothesis. These critics point out that the results of these studies are open to alternative interpretations. One such interpretation is that the tendency for learned responses to some stimuli to persist might be the product of expectancies rooted in culture rather than genes. Such an explanation fails to account for the automatic fear response of infants and of monkeys raised in isolation to specific fear stimuli.

3. Associative Learning

Classical conditioning is a process by which different stimuli, which occur at the same time, come to be associated. The earliest demonstration that humans could learn a fear response via classical conditioning occurred in 1920 when Watson and Rayner produced a fearful response in an 11-month-old infant named Albert. Watson observed that Albert’s response to a white laboratory rat was initially positive–Albert smiled and played with the animal. Subsequently, whenever the rat was present, a loud noise was sounded that startled Albert. The rat, through repeated presentations with the noise, came to be associated with the noise. This association of an initially neutral stimulus (rat) with an aversive unconditioned stimulus (UCS = loud noise) resulted in a conditioned fear response (CR) when only the rat was presented. For some time after this demonstration it was thought that all phobic reactions were obtained via aversive conditioning as in the “Little Albert” study.

The classical conditioning model of phobias explains why people react with subjective and physiological fear when they are exposed to a learned phobic stimulus. However, it does not account for the persistent avoidance behavior phobics display. A two-stage model explaining the development of the fear response and avoidance behavior was subsequently developed. Classical conditioning explained the learned fear response in the first stage, while instrumental conditioning explained the learned avoidance response in the second stage. Instrumental conditioning in this case refers to the reinforcement of the avoidance response produced by the decrease in anxiety. During classical conditioning, the pairing of a neutral CS and an aversive UCS results in a conditioned fear response to the CS. During instrumental learning, the person learns that the fear response to the CS can be reduced by escaping or avoiding the CS. The reduction in fear levels that follows avoidance reinforces this behavior (a process termed negative reinforcement) and, in time, avoidance behavior becomes an integral part of the phobia. This two-stage theory has been well-documented in the laboratory. However, the two-stage theory has several limitations. First, the conditioning approach fails to explain why specific fears are nonrandomly distributed, that is, why some individuals are more likely to develop phobias than are others. Second, individuals do not always acquire phobias as a result of confronting an aversive stimulus and pairing it with a neutral stimulus. Individuals who have specific phobias, for example, frequently are unable to remember a traumatic event during which they learned to fear the stimulus. Lastly, fearful behavior that is produced via classical conditioning in the laboratory requires repeated pairings of the unconditional and neutral stimuli, a circumstance inconsistent with reports of how specific phobias develop.

Because of the failure of classical conditioning to explain how most specific fears developed, Rachman proposed two additional pathways: (1)vicarious learning (i.e., learning to fear by watching someone else act fearfully toward a stimulus) and (2) acquisition of negative information and the aforementioned associative learning. All three of these explanations for the development of specific fears have in common a cognitive expectancy of threat that is connected to the feared stimulus. People essentially learn through direct or indirect experience that some stimuli pose a threat to them and that fear is proportional to the likelihood and severity of that threat. The vicarious learning hypothesis has been supported by both animal and human laboratory studies that show individuals react fearfully after watching others act fearfully. Negative information provided by significant others, such as parents, or through the media of books or television may give rise to fear of stimuli that are subjects of the negative information.

Support for the three modes of fear acquisition comes from studies that ask individuals with specific phobias to identify what they believe caused their disorder. A proportion of phobic individuals report their phobias began suddenly, following a fear-producing encounter with the stimulus, while a smaller proportion report their fear began when they viewed someone respond fearfully or learned indirectly of the potential danger associated with the object. These three avenues for acquiring phobias through learning occur with different frequencies in the four subtypes of specific phobias. Animal phobics and blood-injection-injury phobics more often ascribe their fears to seeing others respond fearfully and to negative information that do claustrophobics. In contrast, the associative learning pathway is more pronounced in claustrophobia than in animal phobia, blood-injection-injury or height phobia. The acquisition of a fear through modeling or negative information is associated with phobias with an early age of onset. It is also likely that the acquisition of a specific phobia is overdetermined, that is, individuals who acquire a phobia often report negative learning experiences of more than one variety. There are even indications that subjects with “mixed” pathways (e.g., conditioning and modeling) have higher levels of fear.

4. Treatment

It is generally accepted that the most successful treatments for specific phobias employ a reconditioning paradigm. In specific phobias, neutral stimuli such as animals, storms, or blood have become associated with an anxiety response, whether through direct association, vicarious learning, or anxiety-producing information. Presenting the phobic stimulus to the sufferer in the absence of a reinforcing or unconditioned stimulus leads to reductions in the fear response to the stimulus. This has been accomplished using a variety of treatment approaches, including systematic desensitization-both imaginal and “in vivo,” that is, in “real life”–and vicarious learning techniques.

Systematic desensitization refers to a process in which the phobic stimuli are arranged in hierarchical fashion from least anxiety-producing to most anxietyproducing, and these stimuli are systematically paired with a response incompatible with anxiety. Taking as an example an individual with a spider phobia, an item low on the hierarchy might be a picture of a small spider, while an item high on the hierarchy might be holding a jar containing a live tarantula. After constructing the hierarchy, the phobic individual would then be taught a method of inducing relaxation. The final step would involve the phobic individual sequentially confronting items in the hierarchy while remaining relaxed. Phobic items are presented repeatedly until the sufferer reports little or no anxiety when presented with the phobic cue. When this level of comfort is reached, the sufferer proceeds to the next item on the hierarchy until he is able to tolerate all phobic stimuli on the hierarchy with a minimal level of anxiety. In one version of this approach, all the stimuli are presented imaginally, while in another version the sufferer is exposed to the fearful stimuli in vivo. The in vivo approach has been found very successful with improvement rates in excess of 85%.

Vicarious learning techniques are used adjunctively to the above two approaches as well as alone. Vicarious learning is a phenomenon by which organisms learn a response by watching the emotional responses of others to these same stimuli. Children whose parents exhibit fearless responses to a variety of situations are themselves likely to show low fear responses to the same situations. On the other hand, children who observe their parents or peers responding fearfully to certain situations are themselves likely to respond fearfully to these same situations. Used therapeutically, vicarious learning involves corrective information, for example, “the spider is not harmful,” skills on how to handle the feared object, and exposure to models who respond positively to the phobic stimuli. The sufferer is then encouraged to expose himself to the previously feared situations.

Interestingly, individuals with blood-injury phobias can also be treated with exposure techniques, but in this case the phobic stimulus is paired with a muscle-tensing response that is incompatible with the drop in blood pressure characterizing this group of phobias. When this procedure is carried out repeatedly, both the fear of blood-injury and the drop in blood pressure experienced at the sight of blood diminish.

All the above treatment techniques involve learning a new and incompatible response in place of the fearful response to the phobic stimulus. The process by which the new learning takes place is still a matter of some debate. One explanation is a simple reconditioning model in which either the old fearful response to the phobic stimulus is changed by prolonged exposure without the reinforcement provided by the presence of an aversive stimulus, or a new relaxation response is learned in the presence of the phobic stimulus. Another explanation is provided by the informationprocessing theory of fear reduction. In this model, phobic knowledge that exists in the brain consists of both stimulus (such as images associated with the phobic object) and response propositions, including the behavioral, verbal, and physiological reactions to the phobic object. Change is thought to occur when the individual processes the phobic stimulus and the response to that stimulus thoroughly, thereby altering the fearful images and anxious responses associated with that stimulus.

II. Social Phobia

A. Definition

Although fears in the presence of others have been described for centuries and have been addressed in the mental health literature since at least 1970, social phobia was not considered a diagnosable entity until the publication of the third Diagnostic and Statistical Manual of Mental Disorders, published in 1980. DSM-IV (the current system) identifies the essential feature of Social Phobia (also referred to as Social Anxiety Disorder) as a marked and persistent fear of social or performance situations in which embarrassment may occur. Social phobics fear and/or avoid a variety of situations in which they would be required to interact with others or to perform a task in front of other people. Typical social phobia situations include speaking, eating, or writing in public, using public bathrooms, and attending parties or interviews. In addition, a common fear of social phobics is that other individuals will identify and ridicule their anxiety in social situations. When a person fears a broad spectrum of social situations, it is referred to as Social Phobia, Generalized subtype, whereas fear of one or a few social situations is referred to as Social Phobia, Specific subtype. Individuals with social phobia are aware that their fears and social isolation are unreasonable and excessive, but they feel unable to control these feelings.

B. Clinical Features: Symptomatology and Epidemiology

As in specific phobia, the anxiety of social phobics is stimulus-bound, that is, it occurs only in the presence of the feared situation or when anticipating that situation. When in or anticipating a potentially embarrassing situation, the individual with social phobia experiences profound anxiety, accompanied by a variety of somatic symptoms including palpitations, muscle tension, nausea, and blurred vision. The person with a social phobia experiences symptoms that underscore the fear of public scrutiny, including symptoms such as trembling, shaking, blushing, twitching, and sweating.
Social phobics also experience more negative selfevaluative thoughts and fewer positive thoughts prior to and during social situations than do individuals who do not experience anxiety. Not only do individuals with social phobia experience more negative arousal symptoms compared to nonphobic individuals, social phobics also perform less well in social situations and systematically underestimate their performance. Judging from their response to social situations, social phobics have a variety of information that serves to underpin their fears.

Social anxiety and reports of shyness in the general population are relatively common, occurring in about 40% of college students. Furthermore, social anxiety is a common accompaniment of all anxiety disorders. The most recent National Comorbidity Survey found a given individual had a 13 % chance of developing a social phobia in his/her lifetime.

The distinction between generalized and specific social phobia is a useful one. Individuals with generalized social phobia have a fear of and will avoid a wide variety of interpersonal and performance situations. These may include formal speaking to a group, informal interactions such as going to parties or meeting strangers, assertive interactions and being observed by others. Individuals with specific social phobia typically are afraid only in performance situations or in a limited number of interpersonal situations. Most individuals with social phobia experience anxiety in two or more different social situations. A lack of social skills has been found in the generalized type, with increases in subjective feelings of anxiety being found in the specific type. Individuals with generalized social phobia reported themselves as more shy and, especially for males, less likely to date during the late adolescent period. Differences between the two types are also indicated by treatment studies that attempt to match treatment type to type of social phobia, a distinction discussed further in the section on treatment of social phobias.

Unlike agoraphobia and specific phobia, social phobia has repeatedly been found to have an essentially equal sex distribution or even a slight tendency to affect males more than females. A similar sex distribution has been found among socially anxious college students.

C. Course/Prognosis and Comorbidity Issues

The consensus among individuals who study anxiety disorders is that social phobia typically begins in late childhood or early adolescence, with fewer individuals developing the disorder in early childhood. Onset is generally gradual and, clinically, most social phobics report they cannot specifically remember the beginning of their symptoms. Some social phobics report specific stressful experiences prior to the onset of the disorder. The course of social phobia is often continuous, with duration frequently being lifelong. Social phobia may fluctuate in severity or remit during adulthood, and severity of impairment may fluctuate with life stressors and demands. Social phobia is much more serious and disabling than previously thought and can have severe functional consequences. More than 50% of individuals diagnosed with social phobia are unable to complete high school, more than 70% of these individuals are in the lowest two socioeconomic quartiles, and 22 % of individuals with pure social phobia receive welfare. The majority of individuals with social phobia are unmarried. It is clear from the prevailing information that social phobia is a severe illness with numerous social consequences.

In addition to the social and occupational consequences of social phobia, almost 19% of individuals with social phobia are likely to abuse alcohol, while 13% will likely develop some type of drug abuse. In addition, social phobia is also commonly associated with major depression (16.6 %), dysthymia (chronic low-grade depression) (12.5), obsessive-compulsive disorder (11.1%), and anxiety disorders such as panic disorder (4.7), agoraphobia (4.9%), and specific phobia (59%). In the majority of cases, the onset of social phobia precedes the onset of the second psychiatric disorder, with the exception of specific phobias, by many years. Social phobia, generalized subtype, is viewed as being more severe than social phobia, specific subtype, and thus is associated with more frequent comorbidity.

D. Etiology

1. Genetic Factors

It is likely there is a genetic predisposition to developing social anxiety and shyness. The rate for social phobia in first-degree relatives (parents, children, siblings) of individuals with pure social phobia is 16%, compared to 5% in individuals selected randomly from the population. Identical twins were also found to have a higher rate of social phobia (49%) if their cotwin had the disorder than did fraternal twins whose cotwin had the disorder (30%). Such findings have been reported by several different investigators, even when controlling for gender in various studies. It has been estimated that genetic factors account for 30% of the vulnerability for social phobia.

2. Biological Factors

Little research has been conducted on the biological causes of social phobia. One line of research has examined biological differences between anxiety in social phobics and other anxiety disorders. When in social situations perceived as evaluative, 50% of individuals with social phobia symptoms experience a surge of epinephrine (a drug secreted in your body to prepare you for an emergency), distinguishing them from panic attacks in which an adrenaline surge is not regularly seen. Another line of investigation has assessed the relationship between sensitivity to social disapproval and neurotransmitters (chemicals necessary for efficient transmission of nerve signals). These studies have revealed a connection between depletion of specific neurotransmitters and mood responses to social approval and disapproval. The possibility exists that this transmission system is poorly regulated in social phobics and those with atypical depression. Both these groups overreact to criticism or rejection, and greatly benefit from a group of antidepressant drugs—monoamino oxidase inhibitors~ that reduce their sensitivity to rejection and also inhibit the metabolism of specific neurotransmitters.

3. Environmental Factors

In addition to direct conditioning experiences, social phobics report parental behavior that tends to foster dependency and insecurity. Social phobics compared to nonphobic normals perceive their parents as overprotective and low in emotional support. Other research has replicated these findings and additionally found social phobics rated their parents as rejecting. These parental patterns could account for general feelings of insecurity, typical of most individuals who experience anxiety. Other research compared social phobics to agoraphobics. Social phobics reported their parents isolated them from social experiences, overemphasized the opinions of others, and de-emphasized socializing with others as a family. These additional patterns in the parents of social phobics could account for the specific manifestation of anxiety found in these individuals.

4. Psychological Factors

Four types of concerns have been identified among social phobics: (1) perceptions of autonomic arousal; (2) concern with others’ awareness; (3) feelings of social inadequacy; and (4) fear of negative evaluation. Of these, the last three have all been identified as important causal and/or maintaining factors in social phobia.

Awareness of others’ perceptions was one of the earliest areas to be investigated in social phobia. Research studies substantiated increased public selfconsciousness in socially anxious individuals accompanied by a fear of negative evaluation. Increases in self-consciousness led to increased autonomic arousal.

Social phobics believe that compared to others they are deficient in social skills. They combine a belief that others hold high expectations for their performance with the perception of their own inadequacy. Consequently, they anticipate negative evaluations and are predisposed to interpret neutral feedback or even moderately positive feedback in negative terms. This bias in the manner in which information is processed by socially anxious individuals tends to maintain these perceptions as socially phobic individuals tend to “find” the behaviors in others for which they search. When asked to recall their past evaluations, they are more likely to recall negative feedback than are non-socially anxious individuals.

E. Therapy

1. Psychological Approaches

Psychological treatment approaches are both effective and often preferred to medications by people who experience side effects from medications. Relapse rates for social phobics treated by specialized psychological treatments tend to be lower than for those treated with medications.
Specific psychological techniques can be linked to the symptoms and characteristics of social phobias. Aspects of successful interactions that cut across a variety of approaches can be identified. These common elements constitute the basic ingredients of a successful approach. They include:

1. Education regarding the defining characteristics and treatment of the disorder. Social phobics are frequently ashamed of their problem, believe their problem to be unique, and thus have not discussed it with others. Informing such individuals that much is known about the problem and that many people share the problem is very reassuring and anxiety-reducing.
2. Anxiety-reduction techniques such as relaxation training and diaphragmatic breathing (breathing that begins in the diaphragm) can be used to diminish the anticipatory anxiety as well as anxiety within the phobic situation itself. Social phobics experience heightened arousal manifested in a variety of somatic experiences of anxiety. Anxiety-reduction techniques are effective in dealing with these symptoms and in restoring confidence in the ability to decrease arousal in phobic situations.
3. Cognitive-retraining techniques deal with the exaggerated beliefs of being humiliated or ridiculed for having anxiety symptoms. Techniques that challenge such beliefs, invite the sufferer to test his beliefs against reality, and even dismiss or reframe the perceived negative evaluations of others are a critical element of therapy.
4. Training in social interaction techniques and socialskills is important for individuals with generalized social phobia. Sufferers of the generalized form are deficientin assertiveness techniques, in techniques forstarting a conversation or engaging a stranger, as wellas techniques for deepening intimacy. Training in theuse of such approaches and practice with them servesto improve social skills and increase their confidencein the ability to engage in these behaviors.
5. Graduated exposure to the feared situation. It is in this context alone that the social phobic learns to apply the above techniques in real-life situations. Such self-exposure increases the belief that the feared situation can be faced and that the sufferer can reduce the anxiety and cognitions and engage actively in social situations.

2. Pharmacological Approaches

The use of pharmacologic interventions in the treatment of social phobics has been relatively rare until recent times. Some drugs have achieved a high rate of acceptability, in part because of their effectiveness and in part because of their low rate of side effects.

Beta-adrenergic blockers–beta blockers–have been widely accepted as a treatment for performance anxiety. Fast-acting and with a relatively short presence in the body, beta blockers are used by seasoned performers and amateurs facing their first public appearance as a way of reducing the physiological accompaniments of anxiety. Side effects from using these drugs are negligible. The effectiveness of beta blockers appears to be restricted to social phobics with specific fears such as stage fright. Generalized social phobias are less likely to be helped by this group of medications, perhaps because of the failure of these drugs to reduce the negative cognitions associated with this disorder.

A second class of drugs–an antidepressant group known as monoamino oxidase inhibitors (MAOIs)–have the highest success rates in the treatment of social phobia. This class of drugs was initially found to be effective with a type of depression characterized by interpersonal sensitivity. They were then tried on social phobics who, as previously discussed, also display a high level of interpersonal sensitivity. This class of drugs is successful with both specific and generalized social phobics, and also has beneficial effects for a variety of disorders that frequently co-occur with social phobia, including panic disorder, obsessive-compulsive disorder, and depression. The principal drawback of the MAOIs is that severe side effects are likely to occur, including hypertensive crisis, unless the individual taking the drug eliminates from his diet foods that contain tyramine (including cheeses, wines, beers, and some brans). For this reason, the use of MAOIs in the treatment of social phobia has been restricted.

A new class of antidepressant medication called selective serotonin reuptake inhibitors (SSRIs) has also been used in the treatment of both specific and generalized social phobias. This class of drugs has been found effective with the advantage that the individual taking these drugs experiences few side effects. Because of the frequency with which this class of drugs is well-tolerated, it may well be the first choice of pharmacologic interventions. The level of effectiveness is high even when the social phobia is accompanied by other anxiety disorders or depression, all of which are also responsive to this class of medications.

III. Agoraphobia

A. Definition

The term agoraphobia, which literally means “fear of the marketplace,” was initially used by Westphal in 1871 to reflect the frequent observation that individuals with this problem were afraid of venturing into public places. The diagnosis requires the existence of two primary features: (1) anxiety about being in places or situations from which escape might be difficult (or embarrassing) or in which help might not be available, and (2) avoidance of these situations, enduring them with marked distress or fear of having panic symptoms, or requiring the presence of a companion before entering the phobic situation.

The agoraphobic individual fears the onset of panic attacks (a discrete period of intense fear or discomfort that develops abruptly and reaches its peak within 10 minutes) or panic symptoms and avoids situations associated with such attacks. Four feared situations typically yield the avoidance behavior that occurs in agoraphobia: (1) situations, typically social, from which escape might be difficult, including restaurants, shopping malls, hairdressers, dentist chairs, and so on; (2) travelling where escape is difficult, including strange cities, bridges, tunnels, planes; (3) traveling away from home; and (4) being home alone. The common feature of these situations is the fear of being unable to obtain help in the event of a panic attack, or the possibility of embarrassment if one obtained help. This response has been referred to as the fear of fear.

B. Clinical Features: Symptomatology and Epidemiology

The chief feature of agoraphobia is escape from or avoidance of situations where panic symptoms might occur. While agoraphobia is frequently accompanied by or preceded by panic attacks, many agoraphobics are unable to recall a distinct panic episode prior to developing avoidance behavior. In these individuals, limited-symptom panic attacks (attacks where fewer than four symptoms are present) or fears of putting themselves at risk by leaving their safe base appear to underlie the avoidance behavior. Thoughts of dying, losing control, becoming seriously ill, going insane, or acting in an embarrassing fashion are likely to precede the avoidance behavior.

Recent evidence indicates that the lifetime prevalence for agoraphobia is 6.7%. Agoraphobia tends to develop later in life than specific or social phobias and occurs more than twice as frequently in women as in men. Individuals who are agoraphobic tend to have lower income and education levels, are frequently unemployed, and are more likely to live with someone other than a spouse. It is unknown whether agoraphobics, because of their illness, drift into these less productive circumstances or whether the stress of these circumstances produces agoraphobia. When individuals with agoraphobia are studied in the general community, they are often found to have at least one additional diagnosis, with major depressive disorder, specific phobia, and panic disorder among the most likely of these. While a number of mental disorders tend to co-occur with agoraphobia, it is often less related to substance abuse or dependence, indicating that agoraphobics tend not to medicate themselves with alcohol or street drugs. When unaccompanied by another disorder, agoraphobics tend to perceive little role impairment, which may account for the finding that only about one-fourth of these individuals seek help even when their agoraphobic avoidance is extensive. Having another diagnosable mental illness, and especially the existence of panic attacks, significantly increases the likelihood that agoraphobics perceive themselves as being impaired socially or occupationally, with as many as 70% of these individuals reporting that they have sought help for their problem.

C. Course and Prognosis

Agoraphobia develops from young adulthood through middle life with few instances of agoraphobia beginning in late life. The average age for the onset of this disorder is between 25 and 29. Panic attacks, which frequently are the precursor of agoraphobia, often begin with the onset of puberty. These findings indicate there is a lag between the onset of panic attacks and the development of avoidance behavior.

When agoraphobia is accompanied by panic disorder, long-term outcome is poor. Studies up to 20 years in length reveal 50% of untreated individuals with this problem experience significant social and occupational impairment, with 80% at least occasionally symptomatic. A variety of additional problems either co-occur with this disorder or develop in response to it, including increased depression, suicidality, sexual and marital problems, tranquilizer addiction, unemployment, and financial difficulties. Treatment using one of several recognized approaches improves the long-term adjustment, although a significant portion of sufferers who receive treatment continue to experience symptoms or, in fact, relapse to the level of adjustment prior to treatment. Individuals who at the conclusion of treatment continue to experience occasional panic attacks, or who remain avoidant, are more likely to experience a relapse to their previous level of functioning. Likewise, individuals who experience low levels of social support, problems in their marital relationship, or significant stressors after treatment is completed are likely to suffer a relapse.

D. Causal Factors

Agoraphobia is best viewed as the endpoint of a series of factors that contribute to the development of this disorder. Genetic factors produce a biological vulnerability that then interacts with stressors and other environmental factors that in turn increase the likelihood one will develop panic disorder and agoraphobia. A strong genetic and biological vulnerability will require fewer environmental factors to produce agoraphobia, while a weak genetic and biological vulnerability will require more and stronger environmental factors before agoraphobia develops.

E. Heredity

There is a demonstratable link between genetic factors and the development of panic disorder, a frequent precursor of agoraphobia. First-degree relatives of individuals with panic disorder are approximately seven times more likely to be diagnosed as panic disordered than are first-degree relatives of individuals with no panic disorder. Similarly, identical twins are twice as likely to share a common diagnosis of anxiety disorder than are fraternal twins, although they are unlikely to share the same diagnosis for the specific type of anxiety disorder. If one twin has a diagnosis of agoraphobia with panic attacks, their identical cotwin is likely to experience panic attacks as well, while their fraternal cotwin is not.
It appears from the limited research in this area that a biological vulnerability exists for panic attacks but not necessarily agoraphobia. A stronger genetic relationship is likely to exist for anxiety problems in general such that what is inherited is a vulnerability to develop anxiety.

F. Biological Factors

If genetic factors play a role in the development of panic, the question remains as to what type of vulnerability is inherited. One possibility is that panic disorder may involve a deficit in the metabolism of factors that inhibit the transmission of anxiety messages in the brain, while another possibility is that there is an increased sensitivity to certain substances. If the latter is true, the introduction of these substances to the bodies of individuals with panic disorder and agoraphobia should produce symptoms of panic, while this response would not be expected in individuals without panic attacks.

These differences in sensitivity to certain substances have been demonstrated in a wide variety of studies. Panic disordered agoraphobics have been shown more sensitive to sodium lactate, adrenalin, caffeine, and hyperventilation. The first of these—sodium lactate~is similar to lactic acid, a substance that increases naturally in the body in response to physical exercise. It is known that agoraphobic individuals possess a sensitivity to increases in physiological arousal such as increased heart rate, respiration, and sweating, body changes common to both exercise and panic attacks. Panic attacks, therefore, may be an alarm reaction to detected physiological changes produced by increases in lactic acid. People suffering from panic disorder show this increased sensitivity by developing panic attacks when injected with sodium lactate, while people who do not have this problem do not show this sensitivity. Similarly, panic-disordered agoraphobics respond with panic attack symptoms when administered a standard hyperventilation procedure, when they drink caffeine, or when they are injected with adrenalin. This response is not typically seen in nonpanickers, thus supporting the biological vulnerability hypothesis.

The finding that panic-disordered agoraphobics have an increased sensitivity to symptoms of physiological arousal may help explain why there is an increase vulnerability to panic in individuals with certain cardiovascular problems. One such line of evidence has shown that individuals with mitral valve prolapse syndrome (MVPS), a problem characterized by chest pain, difficulty in breathing, dizziness, fatigue, and tachycardia are at risk for developing panic disorder. Individuals who experience such symptoms and are psychologically sensitized to them may come to fear them and develop catastrophic cognitions when they occur – the previously identified “fear of fear.”

Further evidence for the role of biological factors comes from panic-disordered individuals who report fluctuations in the frequency and severity of attacks they experience. Recent findings in women indicate increases in panic attacks of as much as 100% occur during the premenstrual period, while there is no change in the degree of anticipatory anxiety or avoidance behavior at these times. Again, the biological contribution is more apparent for panic attacks than for agoraphobia.

G. Psychological Factors

The childhood backgrounds of agoraphobics suggest family experiences play a role in the development of this problem. Lack of maternal care and a general lack of social support, coupled with high intrafamily conflict, have been linked to the development of agoraphobia in adulthood. This deficiency in a warm, supportive parent-child relationship and frequent punishment and criticism produce individuals who view themselves as incompetent and unable to handle challenging situations. This self-view in turn leads to withdrawal and avoidance when faced with challenging situations as an adult.

As many as 80% of agoraphobics report the onset of their panic symptoms was preceded by identifiable stressors or a period of prolonged stress. Interpersonal problems is a frequent precipitant of agoraphobia in adults. Rejection or loss have been reported by a majority of sufferers able to identify a precipitant. Also implicated are marital conflicts in which persons fail to assert themselves, or when they do assert themselves are threatened with loss of the relationship. Loss by death, divorce, or separation, either of a family member or a friend, has been reported as a factor that has led to the development of agoraphobia. The combination of low support and high conflict in childhood and threatened or actual loss of interpersonal relationships in adulthood produces a unique psychological vulnerability to agoraphobia.

Some people who have panic attacks do not become agoraphobic. Women, who tend to value social relationships more than men do, may be uniquely vulnerable to losing such relationships, a fact that may help explain why so many more women with panic than men with panic develop agoraphobia. Two additional factors are predictive of who among panicdisordered individuals develops agoraphobia—how panickers think about their attacks, and how they cope with them. Those panickers who develop agoraphobia believe there is a connection between the situations they avoid and the likelihood they will suffer panic attacks in those situations, while nonavoiders are less likely to make such links. Further, individuals who become agoraphobic believe that if they do have a panic attack, there will be nothing they can do to control itmthe absence of a belief known as selfefficacy. The belief that coping strategies are available that will help control panic attacks is also associated with lower levels of avoidance. The use of coping strategies such as seeking out social support, reasoning out what is happening, controlling one’s breathing and relaxing one’s muscles are specific strategies linked to lower levels of avoidance, while wishful thinking is a strategy linked to higher levels of avoidance.

IV. Panic Disorder and Agoraphobia

A. Psychological Approaches

Psychological treatments for this disorder target each of the disorder’s components m the panic attacks, anticipatory anxiety, and agoraphobic avoidance. Panic attacks themselves are comprised of several features, each of which is targeted within the treatment program. These features include physiological arousal symptoms and catastrophic cognitions. In addition, panic attacks develop from a baseline of chronically high anxiety and are preceded by high levels of anticipatory anxiety when sufferers face situations where panic attacks have previously occurred. Panic sufferers typically have little information about their problem and considerable misinformation. The first phase of treatment aims at providing an understanding of the disorder as well as factors that may have caused it and serve to maintain it. Subsequently, techniques that reduce the chronically high baseline anxietymsuch as applied relaxation–are taught to the panicker with instructions to frequently practice them. Reducing the level of generalized anxiety decreases the frequency of panic attacks but only infrequently eliminates them completely.

Strategies for dealing with both the physiological and cognitive components of the panic attacks themselves have the greatest positive effects. The physiological symptoms are reduced by using a variety of coping strategies, including diaphragmatic breathing, distraction strategies, and social support strategies. Catastrophic cognitions, which are interpretations of the symptoms and inaccurate predictions of the likely consequences of the symptoms, are reduced by providing accurate information and by teaching the sufferer ways of challenging the negative thoughts. Because one of the principal symptoms that occurs during panic attacks is confusion of thought, and because the panic sufferer does not believe in his ability to use these techniques during the panic attack itself, the techniques are practiced in contexts similar to those experienced during an actual panic attack. As the sufferer gains confidence in the new coping strategies, he is encouraged to enter previously avoided situations and to practice strategies for dealing with attacks prior to entering the phobic situation and when in the situation itself. Mastery of the panic attacks is accompanied by a decrease in anticipatory anxiety and a willingness to enter phobic situations. As the phobic situations are entered absent the panic attacks, the agoraphobia decreases.

B. Pharmacologic Treatments

A variety of classes of psychotropic medications have been evaluated as treatments for panic disorder and agoraphobia. These include (1) three classes of antidepressants–tricyclics, MAO inhibitors, and the SSRIs; (2) two classes of benzodiazepines: low-potency benzodiazepines such as valium and librium, and high-potency benzodiazepines such as alprazolam; and (3) beta-blockers. Both low-potency benzodiazepines and beta-blockers have limited effectiveness with panic attacks and are used infrequently in the treatment of this disorder.

All three types of antidepressants have been studied as treatments for panic attacks. Tricyclics and MAO inhibitors are moderately effective in reducing panic attacks, but each is often accompanied by significant side effects. One principal side effect is an initial increase in panic-like symptoms, a response that leads from 30 to 40% of individuals given these drugs to discontinue their use. Similar problems are encountered with the SSRIs, but less frequently. Another problem occurs when panic sufferers attempt to discontinue their use of these drugs: panic attacks frequently return and the individual is faced with a choice between relapse of panic symptoms or remaining on the medication indefinitely.

High-potency benzodiazepines such as alprozalam are the pharmacologic treatment of choice for panic disorder and agoraphobia. Side effects are few, and approximately 80% of those on a therapeutic dose experience an elimination of their panic attacks. As with the antidepressants, however, stopping use of this drug is frequently accompanied by a return of panic attacks.

A comparison of the best psychological intervention with the antidepressants and high-potency benzodiazepines on the three criteria of treatment dropout, treatment improvement, and treatment relapse seems to favor the psychological approach. Antidepressants produce an unfavorable side effect profile with numerous treatment dropouts. Relapse rates are high after discontinuing treatment. Treatment success rates are comparable for the best psychological treatments and high-potency benzodiazepines—approximately 80% are significantly improved. Relapse rates after concluding treatment are considerably higher for the high-potency benzodiazepines than for the best psychological treatment, however, thus favoring the psychological approach. Another avenue is to combine pharmacologic and psychological treatments. This approach produces treatment improvement rates similar to the best psychological approach alone. Other considerations may lead to choosing this alternative, however, such as the necessity to produce a quick reduction in panic attacks.

In typical clinical practice, panic-disordered and agoraphobic individuals are treated with a combination of medications and psychological interventions. There is some evidence that drugs interfere with the beneficial effects of psychotherapy techniques that involve exposure to phobic stimuli. The individual’s choice of what approach to use–drugs or psychotherapy–often comes down to biases and expectations that exist prior to seeking help. Some who choose drugs do not want to spend the time or make the effort required by psychological treatments. Others do not want the stigma or side effects associated with the use of drugs. Future intervention strategies may take into consideration these basic attitudes and best available treatments in recommending a course of therapeutic action.

Bibliography:

1. American Psychiatric Association (1994). Diagnostic and statistical manual of mental disorders (4th Ed.). Washington, CD: Author.
2. Clum, G. A. (1989). Coping with panic: A drug-free approach for dealing with anxiety attacks. Pacific Grove, CA: Brooks-Cole Publishing Co.
3. Markway, B. (1992). Dying of embarrassment: Help for social anxiety and social phobia. Oakland, CA: New Harbinger.
4. Rosenbaum, J. F., Pollock, R. A., Otto, M. W., & Pollock, M. H. (1995). Integrated treatment of panic disorder. Bulletin of the Meninger Clinic, 59, A4-A27.
5. Sheehan, D. (1983). The anxiety disease. New York: Charles Scribner’s Sons.

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